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ANESTHESIA SEMINARS

By

Dr.R.Muthukumar

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TABLE OF CONTENTS

S.NO TOPIC PAGE

NO

1 Neuromuscular junction monitoring 3

2 Preoperative Evaluation and Anesthetic consideration for

patients undergoing thoracic surgery

20

3 Newer inhalational Agents 37

4 Anesthetic Management of Patients with Diseases of

Neuromuscular junction

48

5 Anesthesia for Intra Cranial Vascular Surgery 64

6 Measurement of Temperature and Pressure 78

7 Neuropathic Pain Management 103

8 Fluid and Electrolyte Disorders 130

9 Acid Base Balance 167

10 Pregnancy and Heart Diseases 189

11 Anatomical and Physiological changes in Obstetrics Patients 220

12 Anatomical and Physiological variations in

Neonates,Infants,Children from normal adults

234

13 Anatomy and Physiology of CSF pathway concepts of Intra

Cranial Pressure and Factors determining the ICP

253

3

Neuromuscular Junction Monitoring

Traditionally degree of neuromuscular block during and after anesthesia was

evaluated using clinical criteria which resulted in 42% of patients inadequately

reversed. Monitoring is recommended for 2 issues:

1. Variable individual response to muscle relaxants

2. Narrow therapeutic window

Monitoring permits to determine onset of NMB and sensitivity to relaxants

during inductions

Permits administration of NMBs for optimal surgical relaxation

Permits prompt and reliable reversal with antagonists

Conditions warranting monitor of NMJ

1. Pharmacokinetics of muscle relaxant abnormal as in severe liver, kidney

disease, extremes of age

2. Pharmacodynamics change as in myasthenia gravis, myopathies, upper

and lower motor neuron lesions

3. When postop muscle power is expected to be maximal as in masked

obesity, severe pulmonary disease

4. Continuous infusion / administration of long acting NMBs

5. Patient’s undergoing lengthy surgical procedures and requiring postop

ventilation

In 1958, Christie and Churchill Davidson described use of nerve stimulators.

Principles of Peripheral Nerve Stimulation

Nerve Stimulator

Essential Features:

Square wave impulse, < 0.5msec ,> 0.1msec duration

Constant current variable voltage

Battery powered

Multiple patents of stimulation (Single twitch train of four, double burst, post

tetanic count)

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Optional Features:

Adjustable current output

Polarity output indicator

Audible signal with each stimulus

High output (80 – 100mA) and low output (<5mA) sockets

Ability to calculate and display fade ratio and percentage depression of single

twitch

Battery charge indicator

Alarm for excessive impedance, low battery, disconnection

Features of Neuro Stimulation

Current Intensity: Supramaximal current should be delivered for monitoring

absolute twitch height to ensure constant recruitment of all fibres

2.75 times (20-25%) above the threshold current

Current intensity: 20mA to 50mA – Surface electrodes

5mA to 8mA – Needle electrodes

Stimulators should deliver at least 50 – 60mA (vary between 0-80mA)

Constant current is delivered only when skin resistance is 0-2.5kΩ

Stimulus Frequency: Rate at which each impulse is repeated in cycles per

second (Hertz) 0.1 to 100 Hz.

0.1 Hz – Single twitch – 1 Stimulus every 10 sec

50 Hz – Tetanic stimulation – 50 impulse/sec

Waveform: Rectangular and Monophasic.

Pulse Width: Duration of individual impulse should be <0.5msec3 and 0.1msec

in duration.

Electrodes:

1. Surface Electrodes: Disposable, gel covered conducting surfaces, knob for

attachment to electrical lead.

Conducting area is small (78mm) in diameter

Different thickness than ECG electrodes, smaller chemical buffers to

maintain skin surface

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2. Metal Electrodes: Two metal balls 1 inch apart directly attached to

stimulator.

3. Needle Electrodes: Subcutaneously placed parallel to the nerve, held with

tapes.

Bypass tissue impedance

Local irritation, infection , nerve damage, burns, delivery of excessive

amounts leading to direct muscle stimulation, discomfort , broken needles

Polarity: Maximal effects achieved when negative electrode is placed close to

nerve being stimulated. If electrodes placed <5cm apart, polarity is minimal.

Patterns of Nerve Stimulation

Single Twitch Stimulation

Single supramaximal electrical stimuli are applied at 0.1 to 1 Hz

1 Hz stimulation used

Not applied more frequently than every 10 sec

With both NDMB and DMB there will be progressive depression of

response

Advantages:

Useful in establishing supramaximal stimulus

Identifying conditions satisfactory for intubation

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Disadvantages:

Pre-relaxant control twitch needed

Cannot distinguish between DMB and NDMB

Presence of full-twitch height does not guarantee full recovery from NMB

Train of Four Stimulation

Four supramaximal stimuli are given every 0.5 sec (2 Hz)

Repeated every 10 to 12 sec

With a depolarizing block , equal depression of height of all four twitches

With a non-depolarizing block , there is progressive depression of twitch

height (FADE)

Train of Four Ratio : ( TOFR ; Tr% ; T4 : T1 )

Ratio of magnitude of fourth response to that of first

Expressed as a percentage or a fraction

Control response : TOFR is 1.0

Partial Non-Depolarizing block : TOFR decreases and is inversely

proportional to degree of blockade

Partial Depolarizing block : TOFR is 1

Fade in TOF after Sch : Phase II block

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Levels of NMB and TOF Response

Intense Neuromuscular blockade: Period of no response

Moderate or Surgical blockade:

Begins when first response to TOF stimulation appears

One response detectable – degree of NMB : 90 to 95%

Fourth response reappears – NMB : 60 to 85%

One or two response In TOF : Sufficient Relaxation for most Surgical

Procedures

Recovery: Return of fourth response in TOF

Correlation between TOF Ratio and Clinical Observat ion

TOFR: 0.4 or less

patient is unable to lift the head or arm

Tidal volume – Normal

Vital capacity inspiratory force – Reduced

TOFR: 0.6

Patient is able to lift the head for 3 seconds

Vital capacity inspiratory force – Reduced

TOFR: 0.7 to 0.75

Patient can open eyes widely, stick out the tongue, cough sufficiently and lift

the head for at least 5 seconds

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TOFR: >0.8

Vital capacity inspiratory force – Normal

Clinically TOFR of 0.7 to 0.75 has been thought to reflect adequate recovery of

neuromuscular function.

Phase II Block

Occur in genetically normal patients after prolonged infusion of

Succinylcholine

Patients with genetically determined abnormal plasma Cholinesterase

activity

Fade in response to TOF

Fade in response to Tetanic Stimulation

Occurrence of Post - Tetanic Facilitation of Transmission

Advantages of TOF:

Sensitive indicator of residual NMB than single twitch

No control twitch is needed

Distinguishes between DMB and NDMB

Detects Phase II blockade

Less painful than tetanic stimulation

Disadvantages of TOF:

Not possible to detect fade reliably using visual or tactile methods

Since TOFR requires that four twitches be present, it cannot be used to

monitor deep NMB

Tetanic Stimulation

Rapidly repeated stimulus (30, 50, 100 Hz)

50 Hz stimulation is most commonly used

Duration of 5 sec is standard

Should not be repeated more often than every 2 min

Depolarizing block – tetanus will be depressed in amplitude but sustained

Non Depolarizing block and Phase II block with Succinylcholine,tetanus is

depressed in amplitude and there is non-sustained / fade in contraction

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Profound block – No response to tetanic stimulation

Post Tetanic Facilitation

During partial non-depolarizing blockade, titanic nerve stimulation is followed by

a transient augmentation of response to stimulation of 1 Hz seen in EMG

recording. Maximal in 3 seconds lasts up to 2 min.

Mechanism:

Fade in response to tetanic stimulation

Tetanic stimulation – large amounts of Ach released from stores in nerve

terminal

Stores depleted , equilibrium between mobilization and synthesis of Ach

Muscle response to stimulation is maintained as release of Ach is greater

than that required for response

Later there is decrease in release of Ach and occupancy of free Cholinergic

receptors in post synaptic membrane by NDMB agent (impaired mobilization

of Ach)

FADE

PTF occurs because of increase in mobilization and synthesis of Ach caused by

tetanic stimulation continues for some time after discontinuation of stimulation.

Disadvantage: Painful and not acceptable in awake patients

Moderate non-dep block with Tetanic and Post Tetani c Facilitation

Moderate non-dep block Moderate dep block

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Post- Tetanic Count

Used in profound block where there is no response to single twitch or TOF

Procedure: Single stimuli at 1Hz are given followed by tetanic stimuli of

50Hz for 5sec. After a pause of 3sec single twitch of 1Hz is repeated and

number of post tetanic responses is counted.

Inference: Profound block – no response to tetanic or post-tetanic

stimulation

As the block dissipates - before the first response to TOF stimulation, the

first response to Post titanic twitch stimulation occurs

Time until return of first response to TOF is related to number of post titanic

twitch at a given time (PTC)

PTC = 0 to eliminate coughing / bucking in response to tracheobronchial

stimulation

Double Burst Stimulation

Used to detect shallow degrees of residual neuromuscular blockade.

DBS33 and DBS 32 – DBS consists of 2 short bursts of 50Hz tetanic

stimulation separated by 750msec.

DBS33 - commonly used burst of three 0.2msec impulses at 50Hz followed

750msec later by an identical burst.

Repeated at intervals of > 12sec

In non paralysed muscle 2 contractions are equal in strength

In partly paralysed muscle 2nd response is weaker than first

Advantage: superior to visual or tactile evaluation of TOF during recovery

Disadvantage: discomfort in awake patients

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Summary of Patterns of Neuromuscular Stimulation

Feature ST TOF Tetanus DBS PTS

Current Strength Supra maximal Supra/ Sub Supra/Sub

maximal

Supra/ Sub Supra/Sub

maximal

Frequency 0.1 to 1Hz 2Hz four

stimuli

30 to 50Hz

for 5sec

3 impulses at

50Hz

repeated after

750msec

5Hz for

5sec, 3sec

later ST at

1Hz

Pre Relaxant control Needed Not

Needed

Not

Needed

Not Needed Not

Needed

Pain on Stimulation - - / + + + + + +

Sensitivity of Manual

Detection

Not Sensitive Not

Sensitive at

TOFR

0.4 – 0.7

Sensitive Highly

Sensitive

Sensitive

Alteration of subsequent

Responses

Not Altered Not Altered Altered

(Post -

tetanic

facilitation)

Not Altered Altered

Interval Between Stimuli 5Sec 12Sec 6min 12 - 15sec 6min

Receptor occupancy 75 - 90% 70 - 90% 70 - 90% 70 - 90% > 90%

Sensitivity for Detection

of Subtle Block

Not Sensitive Sensitive Sensitive Sensitive Not

Applicable

Monitoring of Profound

Block

Not useful Not useful Not useful Not useful Useful

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Monitoring Sites

Different muscle groups have different sensitivity and onsit time for NMB

Causes: Fiber composition, number of NMJ (innervate ratio), blood flow,

muscle temperature, margin of safety of NMJ.

Extrajunctional receptors in paretic muscles are relatively resistant to NDMBs

resulting in exaggerated evoked responses

Diaphragm is more resistant (1.4 - 2 times) than adductor pollicis but onset

time is shorter and recovers quickly than peripheral muscles

Relative Sensitivities of muscle groups to NDMR

Muscle Sensitivity

Vocal Cord Most Resistant

Diaphragm

Orbicularis Oculi

Abdominal Rectus

Adductor Poillics

Masseter

Pharyngeal

Extra - Ocular Most Sensitive

1. Ulnar Nerve: Commonly used for monitoring because of accessibility for

visual, tactile and mechanograph assessment.

Adductor pollicis stimulation at wrist - thumb adduction and flexion of

fingers

Stimulation at elbow produces hand adduction as well. Preferable in

children to avoid direct muscle stimulation

At wrist, 2 electrodes are placed along the ulnar aspect of distal forearm, 2

cm proximal to junction of hand and wrist, 2-3 cm apart

At elbow, electrodes are placed over the sulcus of medial epicondyle of

humerur and other at wrist, especially in children, where active negative

electrode is at wrist to ensure maximal response

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2. Median Nerve: Stimulated at wrist by placing electrodes medial to that for

ulnar nerve thumb adduction noted

3. Posterior Tibial Nerve: Electrodes are placed behind medial mallcolus

(negative) and anterior to Achilles tendon stimulation causes plantar flexion of

big toe.

Useful when hand is inaccessible (burns, infection)

Patients with PVD, metabolic neuropathies, foot deformities have poor

evoked responses

4. Peroneal Nerve: Electrodes placed near the popliteal fossa, lateral to neck of

fibula stimulation causes dossiflexion of foot.

5. Facial Nerve: Negative electrode is placed anterior to inferior part of earlobe

and the other electrode is placed just posterior or inferior to lobe. The

frontalis, orbicularis oculi observed for twitch. Facial muscles like diaphragm

are resistant to NMB so there is greater relaxation than limb muscles. So

caution required during recovery as significant NMB may be present even

responses show complete recovery.

6. Mandibular Nerve: Stimulated by placing negative electrode anterior and

inferior to zygomatic arch and positive electrode on the forehead.

Stimulation causes closure of jaw.

Onset of NMB is faster than hand muscles

Sensitive to both NDMR/DMR

Diaphragm most significant of all muscles to both DMR/NDMR (1.4 - 2)

times muscle relaxant as adductor pollicis

Onset time is shorter for diaphragm than for adductor pollicis

Diaphragm recovers more quickly than peripheral muscles

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Evoked Contractive Response

Isometric (Mechanomyography)

Non-Isometric (Accelarography)

Compound Muscle Action Potential

Tactile Recording Devices

Assessment of responses

Visual

Methods of Assessment of Evoked Responses of

Neuromuscular Transmission

Methods of Evaluating Evoked Responses

1. Visual:

Count the number of responses in TOF

Detect the presence of fade with TOF or DBS or post-tetanic facilitation

with tetanic stimuli

To determine post tetanic count

Disadvantages:

Difficult to determine accurately the TOFR

Difficult to compare single twitch height to its control

2. Tactile:

Placing the evaluator’s fingerstrips on the muscle to be stimulated so that

there is a slight preload and feeling strength of contraction

Determines presence or absence of responses and fade with TOF, DBS,

tetanic stimulation, PTC

Disadvantages:

Difficult to detect fade unless TOFR < 40%

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Difficult to determine single-twitch depression

3. Mechanomyogram:

Measuring thumb movement after applying a resting tension (200 - 300g)

that is preload to thumb to align contractile elements

The force of contraction on stimulation is transmitted to a force -

displacement transducer attached to the thumb

The force of contraction is converted to electrical signal, which is amplified

and displayed on a monitor screen or recorded on a chart

Difficulties:

Requires isometric conditions and application of a constant preload

Thumb should always apply tension along length of transducer

Arm should be fixed rigidly

Overloading of transducer should be avoided

4. Electromyography:

Records the compound action potential produced by stimulation of a

peripheral nerve

Often obtained from muscles innervated by ulnar or median like 6thenar,

hypothenar, first dorsal interosseous muscle of hand

2 stimulating electrode

3 electrodes (Recording)

Active receiving electrode - motor area

Reference electrode - over tendon

Grounding electrode - between the two stimulating and recording

Best Signal: Electrodes in contact with skin for 15 min before calibration,

limb fixation and constant pre-tension to the muscle

Evoked EMG is filtered, amplified and displayed

Measurements made: Peak amplitude, Sum of positive and negative

deflections, area under the curve T4 ratio can be accurately measured

Advantages:

No need of bulky apparatus near muscle being monitored

No need of transducer orientation

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Electrodes can be applied earlier

Can be measured from muscles that are not accessible for mechanical

recording

Site of stimulation need not be accessible

T4 ratio can be accurately measured

Disadvantages:

Sensitive to electrical interference

Response varies according to muscle used

5. Accelerography:

Measures acceleration of thumb after stimulation of a peripheral motor

nerve

Based on Newton’s second law Force = mass x acceleration

Uses a piezo electric ceramic wafer having electrodes on both sides. It

gets distorted by movement of crystal inlaid transducer applied to finger -

electric current produced - output voltage proportional to deformation of

crystal

Muscle must be free to move as this is a non-isometric measurement

No preload is necessary

Advantage: T4 / T1 ratio similar to force translation

Electrodes to Record EMG

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Disadvantages:

Recording of tetanic responses is not possible because of movements

Control of TOF ratio is slightly higher than mechanical and so effect of

small doses of NDMR cannot be compared

Relaxograph

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Clinical Application of Neuromuscular Monitoring

Check functioning of neuromuscular monitor

Choose nerve-muscle to be monitored

Electrodes site should be dry, free of excessive hair, not placed over scar

tissue, lesion, erythema

Skin is wiped with ether, dried and rubbed briskly with a dry guaze pad

Monitoring is started before administration of muscle relaxant but after

induction

Select supramaximal current (turn current slowly during repetitive single

twitches until maximum plateau is achieved and then increase current

level by 20%)

Keep the monitoring sites warm

Piezoelectric Film

Accelerography

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Summary of Application of Neuromuscular Junction Mo nitoring

Clinical Objective Site Twitch Modality Target Resp onse

Fast onset or Tracheal

Intubation

Orbicularis

Oculi

Single twitch or TOF 0 twitches

Profound blockade Adductor Polli

Orbi Oculi

PTC

TOF

PTC = 0 at thumb

Adequacy of relaxation

(Abdominal surgery)

Adductor

Pollicis

TOF count one to two twitches

present

predicting reversible block

(When no TOF response)

Adductor

Pollicis

PTC Relaxant dependent

Detecting reversible block Adductor

Pollicis

TOF At least t two twitches

present

Detecting Adequate

Neuromuscular function

Adductor

Pollicis

DBS No fade present

Limitations of Neuromuscular Monitoring

Neuromuscular responses may appear normal despite persistence of

receptor occupancy by NMBS

Wide individual variability in evoked responses

Increased skin impedance from perioperative hypothermia limits the

interpretation of evoked responses

The cut off values for adequate recovery do not guarantee adequate

ventilatory function or airway protection

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For Patients Undergoing Thoraxic Surgery

Pre Op Consideration Intra Op Consideration

Post Op Consideration

Cardiopulmonary

Evaluation

Optimal Pulmonary

Preparation

Monitoring

Requirements

Choice of Anesthesia

Respiratory

Physiology of Lat.

Decubitus position

One lung ventilation

and Anesthesia

Indication and

Techniques of OLV

Analgesia

Respiratory care

maneuvers

Mechanical

Ventilation

Pre Operative Evaluation and Anesthetic Considerati on for Patients Undergoing Thoraxic Surgery

Preoperative Evaluation

Respiratory System Evaluation

History:

Majority of lung resections and repair are done for cancer and benign masses.

History of heavy smoking and recent weight loss are the prominent history in

many of them (10% occur in non smokers)

History of working in chemical industries (Uranium mines)

Average age is 60 - 70 years. Rare in persons < 30 years of age

5% of patients are asymptomatic

Symptoms may be related to

1. Bronchopulmonary

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2. Extrathoraxic nonmetastatic

3. Extrapulmonary Intrathoraxic

4. Non specific

Bronchopulmonary Symptoms: are due to involvement of lung, bronchial

irritation, ulceration and obstruction or infecton.

1. 75% of patients had cough

Common stimulus is formation of sputum

Common among smokers - morning cough

Sputum-purulent in injective pathology

Blood stained (small streaks to hemoptysis) warrents malignancy

Quality and quantity of sputum

2. 40% chest pain

Mild constant, dull aching on the side of the tumour

Pleuritic pain - direct extension of tumor into pleura- worse on breathing

and coughing

Mediastinal masses can cause retrosternal poorly localized pain

3. 30% Dyspnea

Patients with severe dyspnea have decreased ventilatory reserve that is

FEV1 <1500ml.These patients require post op ventilatory support

In patients with lung Cancer - abrupt onset with less functional impairment

In COPD patients - chronic complaints and dyspnea is seen only when

reserves are severely impaired

4. 10% Wheezing

Localized to one side of tumor

Stridor is seen if trachea is involved

Extra pulmonary Intrathoraxic: are due to involvement of

1. Pleura - effusion- dyspnea

2. Chestwall - pain

3. Esophagus - Dysphagia

4. SVC - SVC syndrome

5. Pericardium - Pericarditis

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6. Brachial plexus – Horner’s Syndrome

7. Recurrent laryngeal nerve – Hoarseness

Extra thoraxic metastatic: Metastatic spread outside the thorax are in the

decreasing order of brain> skeleton> liver> adrenals> GIT> kidneys> pancreas.

Histories with regard to these organs are extremely important

Extrathoraxic Non Metastatic Due to

Para neoplastic syndrome (15% of patients)

Cushings syndrome

ADH secretion

Carcinoid syndrome

Hypercalcemia

Hypoglycemia

Eaton Lambert Syndrome – neuromuscular manifestation

HPOA (hypertrophic Pulmonary osteoarthropathy) – skeletal

Scleroderma, acanthosis nigrans – dermatologic

Thrombophelibitis – vascular

Non specific:

Weight loss, malaise, anaemia, lethargy, Anorexia

Physical Examination

1. Inspection

Respiratory pattern and rate

Cyanosis and clubbing

Movement of chest wall and expansion

Accessory muscle aiding respiration

2. Palpation

Tracheal deviation

Difficult intubation

3. Percussion

Dullness – collapse consolidation

Resonant – Hydropneumothorax

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Shifting dullness

4. Ausculation

Bronchial breathsounds

Added sounds

Investigations

Complete blood count – Polycythemia – in chronic smokers decrease in SaO2 Leucocytosis – active infection

Sputum gram’s stain and cytology – metastatic lesions

Liver and Bone Enzymes – metastatic lesions

BUN, Creatinine and urine analysis – metastatic lesions

CXR – far most useful common investigation

When a tumor of lung is first detected on CXR it has completed ¾ of its natural

history. By the time bronchial Cancer becomes symptomatic, CXR is abnormal in

98% of all patients.

Radiographic Criteria for differentiating malignant / benign lesions

More likely Malignant

More likely benign

Intermediate or Noncontributory

Opacity > 3 cm

Speculated

margins

Non calcified

Doubling time 30

to 490 days

Stable for 2 yrs (major)

Doubling time<30days or >490days

Well circumscribed

Benign pattern of calcification

Small < 2 cm

Nearby satellite lesions

Cavitated with thin walls or with fluid levels

Age of lesion is

unknown

Non calcified or

eccentric

calcification

Size of 2-3 cm with

smooth margins

Presence of 2 or 3 criteria has greater impact than one alone.

Radiologic Features with Anesthetic Implications

1. Tracheal deviation, obstruction

2. Mediastinal mass

3. Pleural effusion – low FRC

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4. Cardiac enlargement

5. Balloons cyst (rupture)

6. Air-fluid levels (abscess – infection)

7. Consolidation, atelectasis, edema, low V/Q mismatch and intrapulmonary

shunt

8. Raised hemidiaphragm

Pulmonary Function Testing

Pulmonary function test can determine how much lung tissue can be safely

removed without rendering the patient a pulmonary cripple – carried out in 3

phases

Testing phase PFT Increased Operative risk result

Whole lung tests ABG (FiO2 0.21)

Spirometry

Lung volume study

Diffusion of CO study

PaCO2 > 46 mm Hg

PaO2 < 60 mm Hg

FVC < 50% or 1.5 ml/kg

FEV1 < 50%

VC < 2L

MVV < 50% or < 50ml/min

RV/ TLC > 50%

DLCO < 50%

Split lung function Regional spirometry

with radio isotope

Xe133 or Tc99

Predicted post resection FEV1 < 800ml

Blood flow to the resected lung > 70%

Unilateral pulmonary artery

occlusion

Done with

supplemented

oxygen

Mean pulmonary artery pressure > 40

mmHg

Severe breathlessness

PaCO2 > 60 mm Hg

PaO2 < 45 mm Hg

Unilateral balloon occlusion of

bronchus (R) or (L) of the lobe or

lung to be resected

Oxygen

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Minimal PFT Criteria for Pulmonary Resections

Test Unit Normal Pneumonectomy Lobectomy Segmentectomy

MBC % of

predicted

100% > 55% > 40% > 35%

FVC % of

predicted

100% > 51 to 64

FEV1 % of

predicted

100% > 55 to 65% > 40 to 50% > 40%

FEF 25-75% % of

predicted

Liters

100

2

> 60

> 1.6

0.6 to 1.6

> 0.6

Flow Volume Loops

Displays same information as spirometry

More convenient for measuring specific flow rates

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In general patients with obstructive lung disease like asthma, bronchitis,

emphysen have reduced FEV1/ FVC ratios because of increased airway

resistance and fall in FEV1. PEFR and MVV reduced

TLC increases due to increase in RV. In these patients the effort independent

portion of flow volume curve is markedly depressed inward with reduction of

flow rate at FEF 25-75%

In patients with restrictive lung disease like pulmonary fibrosis there is fall in

FVC, normal FEV1 and FEV1/ FVC is normal.TLC is reduced. MVV and FEF

25-75% - Normal

Flow volume curves are normal in shape but the lung volumes and peak flow

rates are lower

Significance of Bronchodilator Therapy

PFT are usually performed before and after Bronchodilator therapy to assess

the reversibility

After treatment with a bronchodilator increases in PEFR compared with

baseline indicate reversibility of airway obstruction- asthmatic

A 15% improvement in PFT after bronchodilator considered being a positive

response to therapy and that this therapy should be instituted before surgery

Overall prognosis of COPD is better related to the level of spirometry after

bronchodilator therapy than to the baseline

Cardio Vascular System Evaluation

These patients with pulmonary tumors have long history of smoking and

COPD. The pathologic changes lead on to increased pulmonary vascular

resistance followed by RV dilation and hypertrophy – COR PULMONALE

Rigid pulmonary vascular bed cannot accommodate even a small increase in

pulmonary blood flow – leads to development of post pneumonectomy

pulmonary edema

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Non Invasive Diagnosis of PAH, RVH and Corpulmonale

Ausculatory

Signs (PAP high

and PVR high)

Radiographic

Signs

ECG signs of RA

and RVH

Additional signs

of corpulmonale

High P2 of 2nd

heart sound

Dilation of main

pulmonary artery

R axis deviation Pulmonary

diastolic murmur

Loss of normally

split S2

Fullness of Atrial

pulmonary vessels

High R and High S

wave V2 to V6

3rd heart sound

4th heart sound RV comprises L

and R heart

border – globular

shaped heart on

P-A film

Inverted T in V1 to

V6

Prominent R

sternal border

pulsation and

retraction over left

chest

High pitched early

ejn systolic click

pulmonary area

Lateral film shows

encroachment of

retrosternal air

(RV dilation)

Low S-T in V2 to

V6

RH failure

Dependent edema

large tender liver

Ascites + high

JVP (large a

waves)

High P in LII and

LIII biphasic in V1

Echo: In COPD patients without waking hypoxemia – corpulmonale can be

detected twice as sensitively and frequently by ECHO.

Invasive diagnosis of PAH

PCWP using PA catheter at various levels of cardiac output

Operative risks are increased if PVR > 190 dyne/s/cm3

Left Ventricular Function Testing

Causes of LV dysfunction in patients with lung diseases – CAD + Syst HTN

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Presence of carboxyhemoglobin

Systemic hypoxemia + acidosis

Alteration in intrathoraxic pressure

RV dysfunction

Myocardial Ischemia and Infarction

Occur during surgery and on the 3rd day after surgery

1st peak – Due to intraop hemodynamics

2nd peak – Hypoxia, pain, withdrawal of drug therapy

Strong suspicion of patient having angina though exercise test prove to be

negative are canditates for angio.

Echo – Used for LV function estimation

Significant CAD – Patient needs CABG before pulmonary resection

Lesser CAD – Appropriate medical therapy initated prior to lung resection

History of angina or ECG changes like Q waves, LBBB, ST

elevation, ST depression, T inversion, Positive U wave (LA infarct)

is suggestive of further pre op evaluation of coronary function

Non Invasive Exercise Testing (Dobutamine Stress Echo test)

(Limitations of Decreased Pulmonary reserve)

N I

Surgery Thallium Exercise Test

I

Coronary Angiography

N

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If patient needs CABG and lung resection is small – Both procedures can be

done

If patient needs CABG and pneumonectomy or lobectomy – not to be done in

same sitting – CABG to be done 1st wait for 4 to 6 weeks and lung resection

done

Preoperative Preparation

Three major reasons for post op pulmonary complications are

1. Preop lung conditions

2. Operative compression of nondependent or dependent lung – causing edema

3. Painful incision causes restriction of deep breathing and coughing so retained

secretions, atelectosis and pneumonia

Five prolonged regimen of preoperative preparation – aimed at improving pre

existing lung disease – implemented in parallel fashion

1. Stop smoking

2. Dilate airways

B2 agonist

Theophylline

Steroids

Cromolyn sodium

3. Loosen Secretions

Airway hydration (Humidifier/Nebulizer)

Systemic hydration

Mucolytic and expectorant drugs

Antibiotics

4. Remove secretions

Postural drainage

Coughing

Chest physiotherapy (Percussion and vibration)

5. Increased education, motivation and facilitation of post op care

Psychological preparation

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Incentive spirometry

Exposure to secretion removal maneuvers

Exercise

Weight loss or gain

Stabilize other medical conditions

Logic behind these regimens

Stopping smoking terminates the stimulus for production of secretions and

broncho constrictions

Airway dilation facilitate removal of secretions

Thick tenacions adherent secretions loosened by adequate hydration

Once the airway is dilated and secretions are loosened, it can be removed by

physical maneuvers

Discontinuing Smoking

1. Cessation for > 4 to 8 weeks

Decreases postoperative pulmonary complications

2. Cessation for > 1 to 2 weeks

Improve ciliary beating

Decrease the amount of secretions and airway irritability

3. Stopping for 12 to 48 hrs

31

Decrease carboxy Hb and increases hemoglobin available for O2 transport

Decreases Nicotine induced tachycardia

Dilating Airways

B2 sympathomemitic drugs, Methyl xanthines, Theophylline Aminophylline –

act via CAMP and causes broncho dilation. Increases diaphragmatic force of

contraction

Steroids – Decreases mucosal edema and prevent release of broncho

constricting substance

Two different approaches are used in asthma and COPD

Approach I: Bone etal

Step Asthma COPD

1 Inhaled B2 agonist Inhaled Antich

2 Inhaled Anticholinergics Inhaled B2 agonist

3 Inhaled Steroids + cromolyn Theophylline and steroids

4 Theophylline Theophylline and steroids

5 Oral or IV steroids Theophylline and steroids

Approach II: Newhouse etal

Step Asthma COPD

1 Inhaled Steroids Inhaled Steroids / cromolyn

2 Inhaled B2 agonist Inhaled B2 agonest (rarely Antich)

3 Inhaled Anticholinergics Oral / IV steroids /Theophylline

4 Theophylline Oral / IV steroids /Theophylline

5 Oral / IV steroids Oral / IV steroids /Theophylline

Loosening Secretions

Mainly by adequate hydration

Radioactive tracer study – dehydration decreases and rehydration increases

mucous transport velocity

32

Common method – jet humidifier or ultrasonic nebulizer – produces a heated

sterile water aerosol that is delivered by a close fitting mask for 20 min to a

spontaneously breathing patient

Systemic hydration by oral inhale or IV fluids

Infections if present should be treated according to culture and sensitivity by

broad spectrum antibiotics

Forced expiration Technique (FET)

Regarded as most effective in removing secretions than cough

Called “HUFF COUGH” – consists of one or two forced expiration of low lung

volume without closure of glottis followed by diaphragmatic breathing and

relaxation

Advantage as it is performed without closure of glottis and without

compressive phase as in cough. (radioaerosal)

Useful in patients prone for airway collapse during coughing – Emphysema,

Cystic fibrosis, Bronchioctasis

Positive Pressure Adjuvant

Helpful in mobilizing secretions and treat atelectasis

1. CPAP

2. EPAP (Expiratory Positive Airway Pressure)

3. PEP (Positive Expiratory Pressure)

High Frequency Compression/Oscillation

Oscillations refer to rapid vibratory movement of small volume of air back and

forth in the respiratory tract.

External

HFCC

Internal

Flutter Valve

Intrapulmonary Percussive Ventilation

High Frequency Oscillation

33

Removal of Secretions

Combination of postural drainage (different positions may be required) chest

percussion and vibrations coughing or suctioning.

Chest percussion and vibrations

Application of mechanical energy to chest wall using either hands a

pneumatic devices

Manual percussion with hands in cupped position with fingers and thumb

closed – traps a cushion of air – applied over the segment that is to be

drained

Striking force may be against the skin or a thin layer of cloth that does not

prevent the transmission of energy

Slower and most relaxing rates are better tolerated

Avoid tender areas, never percuss over bony landmarks

Vibration: is used together with percussion but limited to application during

exhalation

Cough: is alone effective in clearing central airway. Thus chest physiotherapy

moves the peripheral bronchial secretions to central that can be cleared by

coughing

Positioning during coughing: sitting, inward rotation of shoulder, neck slightly

flexed, arms relaxed.

Electrica lly powered mechanical percussor/vibrator Cross Section of a flutter valve

34

Contrandications for chest physiotherapy

Lung abscess

Metastasis to ribs

History of significant hemoptysis

Not tolerating the postural drainage positions

1. Head and neck injury

2. Hemodynamic instability

3. High ICP

4. Spinal surgery/ injury

5. Empyema / Bronchopleural fistula

6. Active hemophysis

Movement of Cupped hand at wrist to Percuss Chest

Chest Vibration

35

Patient Position for Postural Drainage

36

Complications of Postural Drainage Therapy

Hypoxemia

Increased intracranial pressure

Acute hypotension during procedure

Pulmonary hemorrhage

Pain or injury to musckes, ribs, or spine

Vomiting and aspiration

Bronchospasm

Dysrhythmias

References

1. Ronald.D.Miller: Anesthesia, 5th edition, Volume 2, Chapter 48. Churchill

Livingstone 2000.

2. Paul G.Barash, Bruce F.Cullen, Robert K.Stoelting: Clinical Anesthesia, 4th

edition, Chapter 30. Lippincott Williams and Wilkins, Philadelphia 2001.

3. Robert L.Wilkins, James K.Stoller: Egan’s Fundamental of Respiratory Care,

7th edition, Chapter 36, 37. Mosby.

37

Newer Inhalational Agents

A) Desflurane

History: Between 1959 and 1966, Terrell and associates at Ohio medical

products synthesized more than 700 compounds in order to develop a better

volatile anesthetic agent.

The 653rd compound (The Desflurane) was discarded at the time of synthesis as

it involved potentially explosive step with elemental flourine and because of its

vapour pressure close to atmospheric pressure, it could not be used in

conventional vaporizers.

Reinvestigation of this compound in 1987, suggested that because of its stability

and low solubility it could be used as anesthetic agent for short ambulatory

surgeries.

Structure:

Chlorine atom in Isoflurane is replaced by fluorine.

Halogenated methyl ethyl ether

Physical Properties:

Molecular Weight 168.0 Da

Boiling Point 22.8 oC

Vapour Pressure at 20 oC 664 mmHg

MAC in O 2 6 to 9% in 70% N2O 2.5 to 3.5%

Blood gas solubility 0.42 (lowest)

Oil gas Solubility 19

Boils at very close to room temperature – So requires sophisticated vaporizer

that is heated and pressurized by electrical supply system – So the vaporizer

38

is larger, heavier but more accurate – direct flow meter vaporization is

required

It is a clear, slightly pungent liquid

It is much stable in heat, light and with soda lime

Now corrosive and non inflammable in clinical conditions

Pharmacokinetics

Low Blood gas solubility makes it a faster induction agent if pungency does

not limit its rate of increase of inspired concentration

Blood gas solubility is similar to N2O but FA/FI of N2O rises rapidly due to

concentrating effect and its low tissue solubility

Oil gas Solubility – 19- Diminished potency compared to halothane and

isoflurane

Reawakening time is twice as fast as isoflurane related to depth of anesthesia

rather than exposure time

Elimination and metabolism:

Resists biodegradation as it is halogenated solely with fluorine

No significant increase of Serum Fluroide ions were detected

Cytochrome P450 metabolises Desflurane

Toxicity:

Organ specific toxicity is minimal or absent

39

Pharmacodynamics

Potency:

MAC of Desflurane is 4.6 to 7.25% in O2

MAC decreases 50% with 60% N2O

MAC awake is 2.42%

Respiratory Effects:

Mild airway irritant – inhalational induction may produce marked secretion

coughing and occasional laryngospasm at high FI of 6-7%

Airway support may be required at 2 to 3%

Causes dose dependent depression of respiration

Depresses respiration primarily by reducing tidal volume; increased

ventilatory frequency does not compensate and so PaCO2 increases

Bronchodilator

Cardio Vascular effects:

Like isoflurane decreases SVR and mean arterial pressure

Does not alter the cardiac index even with deep anesthesia (1.66 mAC)

Sustained cardiac output and resistance to depression of contractibility may

result from better sustained autonomic activity

Unchanged Cardiac output in the presence of increased heart rate, low SVR

suggests the myocardial depression is less than other halogenated

anesthetics

Prolonged desflurane anesthesia produces return of cardio vascular events

towards pre anesthetic values – reason appears to be increased β

sympathetic activity or due to products of metabolism

Tachycardia and hypertension at induction

Tachycardia at deep levels

Stable cardiac rhythm

Does not sensitize myocardium to catachelamines

CNS effects:

Produces a pattern of increasing cortical depression

Significantly suppresses EEG activity

40

Prominent burst suppression is seen at 1.24 mAC

Increase in CBF with increase in PaCO2 finds to be less than isoflurane

CMR is depressed in close related manner approx isoflurane

Somato sensory evoked potentials are decreased in close related manner

(1.5 mAC produces 45% depression)

No epilephiform activity is seen

Less cognitive function impairment, drowsiness, confusion in early post op

period

Rapid emergence is associated with delitrium. So concomitant administration

of opioids is needed

Neuromuscular effect:

Depresses neuromuscular function and augments NDMR and DM relaxants

Capable of producing malignant hyper pyroxie

Renal effects:

No nephro toxicity due to increased fluoride concentration

Hepatic effects:

No hepato toxicity is described. However small amounts of trifluroacetate are

found in urine and blood. Hence caution should be exercised in patients at

risk for halothane hepatitis

Other effects:

Increase in white cell neutrophil count

Increase in blood glucose concentration – but return to normal in 24 hrs

No mitagenic changes reported

Anesthetic Implications:

Rapid induction and recovery makes it choice of agents for day care surgery

Irritant nature precludes its use as sole inhalational agent in pediatric patients

Attained only less favour due to bulky vaporizers

Suited for low flow or closed circuit anesthesia as it is very stable

Minimal effect on ozone depletion

41

B) Sevoflurane

History:

In early 1970, Regan, a research pharmacologist at Travene laboratories, Illinois,

identified fluorinated isopropyl ether, sevoflurane as a potent anesthetic agent

with low solubility in blood.

Structure: C4H3F7O

Methyl Propyl ether Fluromethyl 2-2-2 trifluro methyl ether

Physical Properties:

Molecular Weight 200.053

Boiling Point 58.5oC

MaC Value 1.71 to 2.02 in O2

0.66 % with N2O

S.V.P 21.3 KPa or 160 mmHg at 20 oC

Blood Gas Solubility 0.6 to 0.68

Oil Gas Solubility 47 to 53

Colourless volatile, liquid noted for its low pungency

Less chemically stable – Degraded by soda lime, in increasing amounts with

increase in temperature.

22 oC – degraded at 6.5% per hour – Increasing 1.6% per hour/degree

increase reaching 57.4% per hour at 54 oC

Baralyne degrades sevoflurane even at greater rate

Two main degradation products are studied –with no evidence of toxicity

Non Inflammable in concentrations used in anesthesia

Pharmacokinetics:

Low blood gas solubility makes it induction faster

42

Tissue / blood partition coefficient is greater for sevoflurane than desflurane

and Isoflurane but less than halothane, suggests that cerebral concentration

is moderately well correlated with inspired concentration

Elimination and Metabolism:

Approximately 1 to 5% of absorbed sevoflurane is biotransformed

The α carbon is most likely site of oxidation

Non volatile organic fluride formed in humans are hexafluroisopropanol -

detected in blood and urine

This compound is not further degraded but conjucated with glucomide

Metabolism enhanced by cytochrome P450 and Cytochrome b5 hepatic

enzymes

Decomposition with Soda lime:

Two products are formed in closed circuit

Compound A - Pentafluroisopropenyl fluromethyl ether

[CF2 = C (CF3) OCH2F]

Removal of H+ from isopropyl group

Compound B - Difluorobromochloroethylene [CH3OCF2CH (CF3) OCH2F]

Addition of methoxide ion (CH3O-) at isopropyl group is another compound

from interaction of sevoflurane with soda lime

Methoxide ion - formed from methanol + soda lime and added to Compound A

Toxicity:

Clinical studies show that sevoflurane concentration often peak above

50µmol/L even when administered for average duration. Because of its low

blood gas solubility and its rapid elimination F- concentration falls quickly after

surgery and renal toxicity are not reported

Sevoflurane administered to hypoxic rats with induced hepatic enzymes both

with and without soda lime - results in hepatotoxicity similar to isoflurane. No

elevation of liver enzymes

43

Compound A:

1. Nephrotoxic - Corticomedullary tubular necrosis

2. All studies on sevoflurane suggest that it has little potential for

nephrotoxicity, a conclusion supported by its apparently safe

administration to many millions

Compound A:

B catalysed degradation of sevoflurane in CO2

Its production is enhanced in low flow or closed circuit breathing systems

and by warm or very dry CO2 absorbents

Barium Hydroxide lime produces more compound A than does soda lime -

attributed to slightly higher temperature

Compound A is itself is not toxic to organs. Rather the biodegradation of

compound A to cystine conjugates and the further action of renal enzyme

B-lyase - on these conjucates forms toxic thiol

This metabolism in humans is far less extensive than in rats(8 - 30 times

less active)

Thus compared with rats humans receive low doses of Compound A and

metabolise lower fractions via renal B layse - accounting for lower toxicity

compared to rats

However caution when using in renal failure patients

44

Compound A

Via P450

No Toxicity

Glutathrone S Conjucate

Cysteine S Conjucate

N Acetylation

Mercapturic acid (Rapid renal elimination)

No toxicity

Returned to plasma

Nacetylation

Excretion

No toxicity

Plyase

Thioacyl Alkalide

Nephrotoxin

Inhaled Compound A concentration during administrat ion of sevoflurane at

different flow rates in humans

45

Pharmacodynamics

Potency: MAC of 2 with O2 decreases to 0.66% with 63% N2O.

Respiratory Effects:

No breath holding or coughing - not irritant

Twice as respiratory depressant as halothane in dose related manner

In humans 1.1 MAC produced same degree of respiratory depression as

halothane at 1.4 MAC

Respiratory Defects:

Increase in PaCO2 increases respiratory rate but insufficient to maintain

minute volume

Rapid elimination reduces the post op respiratory depression

Bronchodilator-less effective than halothane

HPV not inhibited at 1 MAC

Cardio Vascular Effects:

Effects are similar or more desirable than isoflurane

Causes lesser decrease in MAP (Diastolic is decreased > systole)

Bradycardia may result but myocardial contractibility is better preserved with

sevo than with halothane

MVO2 is decreased without decreasing myocardial blood flow

Coronary artery dilator

Not Arrhythmogenic

Used for pheochromocytoma resection in humans

CNS Effects:

Has effects on CBF/CMRO2 and ICP similar to isoflurane

No ECG or motor evidence of seizure activity has been noted

Neuromuscular effects:

Good muscle relaxant - potentiates NDMR

Sufficient degree to produce tracheal intubation without muscle relaxants

Induces malignant hyperthermia

46

Renal effects:

Combined effect of minimal metabolism of sevoflurane in kidney (contrast to

methoxyflurane) and rapid elimination reduces the risk of nephrotoxicity even

after prolonged administration (at 1 MAC hr for 3-4 hrs)

Hepatic Effects:

No report of clinical hepatotoxicity seen over 2 million people

Animal studies showed hepatotoxic features - decreased blood flow

In animal studies - decreased protein synthesis is clinically relevant

concentration

Not mutagenic

No effect on ozone depletion

Anesthetic Implications:

Advantage:

Used in pediatric anesthesia more extensively

Disadvantages:

Cost and not used with circle system

In neuromuscular diseases where relaxants are not preferred for intubation

In patients with hemodynamic instability - difficult airway

Xenon:

Inert gas

Difficult to obtain so expensive

Has many characteristics of ideal inhalational anesthetics

Blood gas coefficient - 0.14

Provides some degree of analgesia

MAC in humans is 71% - limiting factor

Non explosive, non pungent and odorless - inhaled with ease

Does not produce significant myocardial depression

Because of its scarcity and high cost, Anesthetic systems need to be

developed to provide recycling of xenon

47

References

1. Ronald.D.Miller: Anesthesia, 5th edition, Volume 1, Chapter 4. Churchill

Livingstone 2000.

2. Prys Roberts, Brown: International practice of Anesthesia, Volume 1, Chapter

11. Butterworth Heinemann, Oxford OX2 8DP - 1996.

3. Paul G.Barash, Bruce F.Cullen, Robert K.Stoelting: Clinical Anesthesia, 4th

edition, Chapter 15. Lippincott Williams and Wilkins, Philadelphia 2001.

48

Anesthetic Management of Patients with Diseases of Neuromuscular Junction

Myasthenia gravis is an autoimmune disease caused antibody and t-cell attack

on the nicotinic ach receptors on the muscle endplate

Clinical course

Insidious in onset and presents as fluctuating weakness of voluntary muscles

that is exacerbated by exercise and is improved after a period of rest.

The characteristic distribution of weakness - extraocular, bulbar, neck, limb

girdle, distal limb, and trunk muscles in decreasing order of involvement

Diplopia is the commonest complaint. Ptosis is the next common presenting

problem, may be unilateral, bilateral and it alternates between right and left

Dysarthria, difficulty in swallowing, chewing are the symptoms of early bulbar

involvement

15 to 20% presents with extremity weakness. Respiratory muscle weakness

is much rarer

Disease progression is slow if symptoms remain localized to the eyes for >2

years

Exacerbated by injection, physical (surgical), emotional stress, hyperthyroid,

drugs like quinidine, aminoglycoside antibiotics

Differential diagnosis

Thyrotoxicosis, neurasthenia, progressive external opthalmopleg, Restricted

myopathies, Musclular dystrophies, Brain tumors, Eaton lambert syndrome,

amyotrophic lateral sclerosis, D-penicillamine administration.

Incidence of MG

Relatively rare disease with incidence of 1 in 30,000 2/3 of patients are

women

Age at which the disease manifests varies with the gender

Women most commonly present between 10-40 yrs

Men manifests > 40 yrs

49

Patients younger than 16 yrs - 10% of all cases

Clinical Classification

Osserman and Genkins Classification

Class I: Ocular myasthemia (15 - 20%)

Class I A: Ocular symptoms with EMG evidence of peripheral muscle

Class II A: Mild generalized weakness (30%)

Class II B: Moderately severe generalized symptoms without respiratory failure

(20%)

Class III: Acute fulminant disease (11%) Severe bulbar symptoms with

respiratory failure

Class IV: Late severe disease (respiratory failure and burnt out disease ) - no

responses to anticholinesterases

Pediatric MG

Neonatal transient - the neonate born to MG mother have transient symptoms

lasting 1 to 2 months and require treatment

Neonatal persistant - Onset is at 2 to 3 months of age. The diagnosis is often

difficult and is not associated with antibiotics to Ach receptors

Juvanile MG- Occuring in younger patients similar to adult

Pathophysiology

The antibodies demonstrated against the Ach recertors at endplates (85%)

These antibodies do not bind to Ach receptors, but close to them causing

destruction of the receptors

The resulting decrease in Ach receptors, results in decreased efficiency of

transmission of nerve impulses

Characterized by the period of remission and exacerbation

It is likely that the reduction in binding of Ach is not the major mechanism of

action of the antibody since antibody titers frequently do not correlate with

disease severity

50

30 to 50% of patients associated with thymoma or thymic hyperplasia

70 to 80% of patients thymic hyperplasia improve after thymectomy only 25 to

30% of patients with thymoma shows improvement

Associated with other autoimmune disorders like rheumatoid arthritis,

Hashimoto’s thyrorditis

Diagnosis of MG

Diagnosis is primarily by history and is confirmed by diagnostic tests

1. Electromyographical (Electrophysiology)

2. Pharmacological

3. Serological

1. Electrophysiological: Testing involves testing a peripheral nerve, by

stimulating it with a supramaximal stimulus of 2Hz 4 times over 2 seconds in

Train-of-four pattern.

Decrease in twitch response to stimuli of >10% (T4/T1 ratio) when 4th response is

compared with 1st is diagnostic of MG. They also show less post titanic facilitation

during this examination than their healthy counterparts.

2. Pharmacological: Testing involves administering edrophomium (2.5 to 5ml)

IV .there is dramatic improvement of symptoms in MG patients

Curare test:

Can be done as regional or systemic

Regional is safer

Involves risk of respiratory arrest

Tourniquet applied to the arm to be tested and other arm as a control

In one arm 0.2mg d -Tc is 20ml NS is given IV and in other arm 20ml NS

alone is given

Muscle function tested before, during and every few minutes with

electromyography until 16 minutes after administration

Decreased response to twitch in arm receiving d-Tc is seen

51

3. Serological: acetylcholine receptor antibodies are elevated up to 95% -

demonstrated by radio - immuno assay. However they may be absent in mild

disease or in pediatric MG

Other tests: Suigle fibre electromyography, reflexometry and nystagraphy

Medical management of MG

Available medical treatments are:

1. Anticholinesterases

2. Immune suppression

3. Plasmapheresis

1. Anticholinesterases:

Used in treatment of MG since 1934

Prolong the duration of Acetylcholine at the post synaptic membrane of the

NMJ

Patients response to these agents are tremendously variable, so patients

education and maximal involvement are required for their optimal use

a. Pyridostigmine (Mestinon)

Commonly used - fewer side effects than neostigmine

After oral administration

Onset - 15 to 30 min Peak effect - 1 to 2 hrs Duration - 3 to 4 hrs

Available doses 10,60,180mg

Common daily doses 30 to 120 mg/day 3 to 6 administrations

b. Neostigmine (Prostigmin)

Lasts only 1 to 2 hrs

May be given parentrally

Muscarinic side effects are more than pyridostigmine

c. Edrophorium (Tensilon)

5 to 10mg IV

Used to differentiate the patient who is in cholinergic/ myasthenic crisis

2. Immuno suppression:

Corticosteroid therapy used to complement anticholinesterase therapy

52

Appear to cause a reduction in number of antibodies to Acetylcholine

Receptors

Clinical improvement - may take weeks to manifest

Side effects of generalized immuno suppression like infections, cataract,

myopathy etc are seen

Azothioprine, methrotrexate, actinomycin or cyclophosphomide can be used

with steroids

11% remissions and 50% clinical improvement have been reported with

medications

ACTH has been used when steroid treatment fails

3. Plasmapheresis:

Method of obtaining short term relief

Time consuming and lead to depletion of Pseudocholinestarase and cause

electrolyte abnormalities

Showed to shorten post op ventilatory requirement and intensive care stay

Surgical Management - Thymectomy

Thymectomy has been used in treatment of MG since 1939

Described by Blalock

Role of thymus in pathogenesis of MG is unclear but 75% of patient with MG

has thymoma or thymic hyperplasia

Only 30% patients with thymoma have symptoms of MG

50% of patients will show improvement clinically after thymectomy

Stress of surgery - may precipitate an acute attack. So may require ICU for

respiratory failure

Disagreement between transcervical and transsternal approach for

thymectomy

Blalock - 1941-reported that total thymectomy to be performed

Trans - sternal Trans - cervical

More complete removal Not possible

Post op mortality/ morbidity Less because of minimal invasive

53

The rates of remission with both are comparable

Response of Anesthetic agents in MG

Muscle Relaxants

Decreased Acetylcholine receptors

Extremely sensitive to NDMR (< 1/10 the intubating dose)

Sensitivity has been shown to exist in patient with only ocular symptoms or

even in subclinical MG

Long acting NDMR are avoided

Intermediate acting NDMR like vecuronium and atracurium ED - 95 (effective

dose in 95% of normal patients) has been reduced by 45 to 55% in MG

patients

Chan et al showed that spontaneous recovery characteristics in MG patients

show greater TOF fade with vecuronium than atracurium

So atracurium may be preferred to vecuronium

Sensitivity to mivacurium - recovery after mivacurium in patients receiving

anticholinesterases is prolonged which can also inhibit pseudocholinesterase

that metabolic mivacurium

Metabolism and elimination of these relaxants are not affected

Resistant to depolarizing muscle relaxant (suxamethorium) due to decreased

receptors

ED95 - 2.5 times the normal dose for scoline

Higher propensity to develop phase II block with even single repeat dose or

with single intubating dose

Plasma cholinesterase intubated by pyridostigmine may prolong the duration

of blockade by suxa and mivacurium

Inhalational Agents

Halothane, Isoflurane, Enflurane and Desflurane have muscle relaxing

properties

54

Exaggerated in patients with MG and produces sufficient relaxation for

intubation

TOF depression with isoflurane is shown to be twice as much with equilpotent

concentration of halothane and enflurane

Servoflurane and desflurane in equi MAC concentration has been shown to

have similar relaxant effect as isoflurane

Intravenous Anesthetics

Most IV anesthetics do not affect the induction, recovery in MG patients

Propofol has advantage of rapid and clear recovery

Opioids

Do not produce neuromuscular depression but cause central respiratory

depression and precipitate respiratory failure

Extremely sensitive to ventilatory depressant effect of parental opioids

So shorter acting opioids are preferred in small doses

Drugs to be avoided in Myasthenia Gravis

Antibiotics Neomycin, Kanamycin, Gentamycin, Tetracyclines,

Erythromycin, Lincomycin

Cardiovascular drugs β Blockers, Quinidine

CNS drugs Diphenyl hydantoin, chlorpromazine, Lithium

Antirheumatic penicillamine, Chloroquine

Local anesthetics Procaine, Lidocarine

Others Magnesium

Local Anesthetics and Regional Anesthesia

Local anesthetics potentiate neuromuscular blocking drugs by decreasing the

sensitivity of post junctional membrane to Acetylcholine

So high blood levels cause muscle weakness

Though regional analgesia can be safely used in MG patients dose has to be

reduced to avoid blood concentration

55

Ester LA are metabolized by cholinesterase and hence anticholinesterase

therapy may result in high blood concentration of ester Local Anesthetics

So RA should be performed with Amide Local Anesthetics

Spinal analgesia has advantage of lower drug dosage compared to epidural

analgesia

Anesthesia for Patient with MG

1. Pre-Operative Assessment: Should be assessed for

Severity of the disease/duration

Treatment regimen

Presence or absence of bulbar involvement and respiratory failure

Presence or absence of cholinergic or myasthenic crisis

2. Pre-Op Laboratory data:

Electrolyte abnormalities apart from routine lab investigations

Arterial blood gas values - preop

Pulmonary function test and their percentages from the predicted values

(low FVC, FEV1 , FEF 25-75% PEFR )

Lowered inspiratory and expiratory pressure

Xray chest/neck - to rule out compression of thymoma on its adjacent

structures

3. Pre-Op Cholinestarase Therapy:

Pre op anticholinesterase increases the requirement of muscle relaxants

Increase the vagal response

Increases the duration and efficiency of opioids

Decrease the metabolism of Ester LA

Withdrawing on the day of surgery may cause respiratory difficulty in patients.

Requirement of muscle relaxant is decreased and post op anticholinesterase

therapy can be easily adjusted.

Intubation can be done under inhalational and IV anesthetics.So patients

with mild disease or ocular symptoms are allowed to withdraw the drugs 3

56

to 6 hours before surgery but patients requiring high dosage (>750

mg/day) are asked to continue

Patients receiving steroids should have adequate steroid cover

In severe cases, post op condition can be improved by preop

plasmapheresis

4. Premedication:

Patient should neither sedated too much nor too anxious

Preoperative counseling about post op ventilation often decreases the

need for anxiolysis

Antisialogogue - Atropine or glycopyrolate - useful in reducing oral

secretions due to anticholinesterase therapy

5. Intra-Operative Monitors:

ECG

NIBP (Arterial)

SaO2

Esophageal temperature

ETCO2

If post op ventilation is mandatory or if intrathoraxic procedure is done - arterial

line is must.

A nerve stimulator should be used to monitor muscle strength whether or not

patient receives muscle relaxant intra operatively. This is because inhalational

anesthetics have been shown to cause twitch suppression in the absence of

muscle relaxants

Anesthetic regimen for a patient with MG

Aimed at least interferance with both ventilatory and neuromuscular function

Controversy exists regarding best induction agents

Any IV agents could be used - propofol may be preferred as recovery is rapid

Recently sevoflurane 6 to 7% with limited hemodynamic changes is preferred

- seem to reduce the requirement or totally eliminates the need for muscle

relaxants during intubation and maintenance

57

Muscle relaxants are rarely required for laryngoscopy and intubation if level of

anesthesia is deep

Vocal cords sprayed with 4% xylocaine if relaxants are not used

Some patients may reqire relaxants

Suxa is avoided

Intermediate acting atracurium/vecuronium is used

Narcotics – Short acting fentanyl, Remifantanyl preferred

Extubation and Post Operative Ventilation - (Variab le)

Many institutions prefer to continue ventilation in the post operative period for

24 to 48 hrs to allow spontaneous recovery

Patient should be awake, responsive. TOF showing all 4 responses same as

preop, able to generate negative inspiratory force of at least 20cm H2O

Should be able to maintain narmocapnea / oxygenation prior to extubation

Tital volume > 5ml/kg during unarrested spontaneous breathing

Neostigmine for reversal may produce cholinergic crisis (most common in

patients with only ocular symptoms) incremental doses with NMJ monitoring

Preoperative Conditions requiring post operative ve ntilation

Leventhal et al- assigned a scoring system to 4 factors found to be predictive

1980

Duration of >6 yrs 12 points

H/O chronic obstructive pulmonary disease 10 points

> 750 mg/d of pyridostigmine 8 points

VC < 2.9 liters 4 points

Score of < 10 - extubated immediately post op

Score of > 12 - required post op support

This system has failed to substantiate in patients who underwent thorocotomy

and upper abdominal surgery. (Sensitivity of 43%)

Other preop conditions requiring post op ventilation are:

Duration of surgery > 3 hrs

58

Patients with bulbar involvement and respiratory failure

H/O myesthenic crisis/ cholinergic crisis

Expiratory force < 40 cm H2O

Inspiratory force < 30 cm H2O

Presence of respiratory infections

Bowel surgeries - fear of anestamotic dehiscence

Upper abdominal and thoraxic surgeries

Multivariate discriminant analysis identified 7 risk factors (sensitivity of 88.2%)

Risk factors correlated with the need for post op v entilation No

FVC and percentage of predicted value 2

FEF 25-75% (forced mid exp flow) and its percentage 2

MEF 50% (max exp flow at 50% of FVC ) and its percentage of predicted value 2

Sex 1

Totally 7

Myasthenia in Pregnancy

Pregnancy is a stress to Myasthenia patients

Symptoms respond unpredictably to pregnancy

As pregnancy advances, the symptoms worsen

Patient return to their pre pregnant state of weakness immediately post

partum

Antinatal:

Regular monitoring of muscle strength and adjustment of oral anticholinesterase

drug throughout the course of pregnancy

In labour:

During labour, increase in weakness is expected

This increases the risk of respiratory insufficiency and aspiration

Maternal expulsive efforts may be markedly decreased and end up in

instrumental delivery or cesarean section

59

Oral medication of anticholinesterase can be continued throughout labour

unless the disease is very severe and gastric function is in doubt where

parental medication is substituted

Both myasthenic and cholinergic crisis may occur

Labour analgesia:

Regional analgesia with 0.125% bupivacaine + fentanyl epidurally has been

documented to minimize the stress of labour without causing detoriation of

symptoms and prevents use of sedation.

Caesarean section:

In well controlled MG, LSCS may be performed under RA (spinal)

If not well controlled, the risk of respiratory impairment and aspiration with

high spinal must be weighed against the risk of post op ventilatory support

following general anesthesia

Myasthenic Crisis

Exacerbation of existing myasthenic symptoms

Either directly from increased muscle weakness or it can be secondary to

infection

Oropharyngeal weakness predispose to respiratory injection - aspiration of

the secretions

Increased secretions, respiratory infection and muscle weakness will produce

a vicious cycle leading to respiratory failure

Response to anticholinesterase may not be satisfactory and ventilatory

support is needed for these patients

There is marked reduction in vital capacity accompanied by restlessness,

anxiety or tremor

Common cause of sudden death in MG patients

Management:

Entiles timely intubation and mechanical ventilation

Plasma pheresis to hasten recovery and weaning from the ventilator

Immuno adsorption and immuno globulins are useful alternatives

60

Anticholinergic drugs are best withdrawn

Patient may respond in 1 or 2 days or may take weeks to slow recovery

Anticholinesterase and steroids are reintroduced prior to weaning

In patients who donot recover for more than a week, other possible causes

like steroid induced myopathies, concomitant thyroid disorder has to be ruled

out

Cholinergic Crisis

Some times difficult to distinguish from myasthenic crisis and is result of

overtreatment with anticholinesterase agents

It is not just increased cholinergic symptoms like secretion and bradycardia

but worsening of myasthenic syndrome that could easily be treated with

Atropine

This occurs more commonly in ocular myasthenia. As the ocular muscles are

relatively resistant to treatment with anticholinesterase, we tend to over treat

to get adequate relief of ocular symptoms. (Individual muscle sensitivity to

anticholinesterase agents varies)

This overtreatment of other muscle groups results in weakness - fasciculation,

sweating, miosis, lacrimation, abdomen colic

Tensilon Test:

Differentiated by giving 10mg edrophonium in 70kg patient

Improvement in muscle strength - myasthenic crisis

No increase in muscle strength or if respiratory distress worsens - Cholinergic

crisis

Management:

Elective mechanical ventilation after intubation in ICU

With holding anticholinesterase drugs

Treatment with anticholinergic drugs - like Atropine or glycopyrolate

Eaton - Lambert Myasthenic Syndrome (ELS)

A rare disorder affecting NMJ

Resembles MG - in low neuromuscular transmission

61

Differ from MG in many ways

Myasthenic Gravis Eaton - Lambert Syndrome

Sex Females > Males Males > Females

Presenting

Symptoms

Extra Ocular, Bulbar and

facial muscle weakness

Proximal limb weakness (Legs > Arms)

Other

Symptoms

Fatigue with activity Myalgias

uncommon Reflexes Normal

Activity increase strength Myalgias

common Reflexes reduced or absent

EMG Initial action potential with

normal amplitude.

Decremental response to

repetitive stimulation (<10Hz)

Initial action potential with abnormally

small amplitude. Decremental response

to low frequency (<3Hz) and

incremental response to high frequency

(20 to 50HZ)

Response to NMB Sensitive to NDMR

Resistant to Depolarizers

Sensitive to both depolarizers and

NDMR

Response to

anticholinesterase

Good Poor

Associated

Pathologies

Thymoma (25%)

Thymic Hyperplasia (75%)

Small cell Cancer of lung

Pathophysiology

Most cases associated with small cell (oat cell) Carcinoma of brochus. It has

also been associated with other tumors like Cancer prostate, breast, stomach

and rectum

In 1/3 of the patients, the tumour is not identified (ELS preceeds the

presentation of tumour as early as 2 years)

Defect is in presynaptic acetylchlorine release quanta of Acetylcholine

released per nerve impulse is reduced due to down regulation of voltage

gated Ca2+ channels

Auto antibodies have been identified against these calcium channels

62

Clinical Features

Muscle weakness and hyporeflexia - proximal limb muscles improves with

exercise

Ocular and bulbar muscle not involved

Autnomic dysfunction - dry mouth, impaired lacrimatre, impaired sweating,

urinary retention, constipation, orthostatic hypotension

ECG - decreased RR interval with respiration

Neuromuscular monitoring shows increase in twitch and tetanic response with

increased frequency and duration

Management:

Corticosteroids and azathiopine have been shown to improve the condition -

used with caution - accelerate tumour growth

Plasma pheresis in reducing acute effect

Respons to anticholinesterase therapy is poor

3,4 diaminopyridines given alone or in combination with pyridostigmine or

neostigmine

It prolongs the duration of action potential by blocking the membrane K+ efflux

Ca2+ channel remain open for longer period resulting in increased release of

quanta of acetylcholine

Anesthetic management:

Preoperative search for primary tumour. This often calls for biopsy and

surgical excision of tumour requiring anesthesia

Pre op evaluation, pre medication and investigations and intra op monitors

are as required for MG

No relaxants is used - if to be used - atracurium is the choice

Neuromuscular blockade monitored and residual paralysis is reversed with

3,4 diaminopyridine and or neostigmine or pyridostigmine

Post op ventilation - in most of the cases

Extubation criteria is same as in MG

They are sensitive to Narcotics, BZD and other sedatives

63

References:

1. Robert K. Stoelting, Stephein F.Dierdorf: Anesthesia and Co-existing

Disease, 3rd edition, Chapter 26.Churchill Livingstone, Philadelphia 1993.

2. Paul G.Barash, Bruce F.Cullen, Robert K.Stoelting: Clinical Anesthesia, 4th

edition, Chapter 28. Lippincott Williams and Wilkins, Philadelphia 2001.

64

Anesthesia for Intra Cranial Vascular Surgery

Intracranial Aneurysm

Epidemiology:

World wide incidence of 10.5 per 100000 people per year

In India 2 to 4 per 100000 persons /year

Female : male is 1.3 :1

Incidence of Subarachnoid hemorrhage due to aneurysmal rupture is 6 to 8

per 100000 persons/year

Peak incidence of SAH is in the 5th and 6th decade of life

Etiology:

Inherent structural weakness of cerebral vessels

Absence of external elastic lamina

Unique branching and pulsatile hemodynamic bombardment

Increased sheer stress at the bifurcation

Common at branching

Associated with collagen vascular diseases

Types and Location:

Saccular (berry aneurysm) found usually on the major arteries at the apex of

branch points (85 to 95%)

Anterior communicating artery- 30%

Posterior communicating artery -25%

Middle Cerebral artery -20%

Fusiform aneurysm common in vertibrobasillar system- 5 to 15 %

Presentation and Clinical Features

Headache- sudden and severe. May be mild due to warning leak (sentinal

hemorrhage)

LOC with headache (97%)

Meningismus (52%)

Confusion and coma due to rupture causing hydrocephalus and ischemia

65

Focal neurological deficits –21%

Mass effect – gaint aneurysm(>24mm)

Potential risk factors for Aneurysmal rupture

Smoking

Hypertension

Alcohol consumption

Cocaine and Amphetamine abuse

Oral contraceptives

Plasma Cholesterol > 250mg/dl

Associated adult PCKD

Familial (1st degree relatives)

Predictors of outcome after Aneurysmal rupture

Hunt and Hess (Boterall) grading:

0 Unruptured aneurysm

1 Asymptomatic or minimal headache with slight nuchial rigidity

2 Moderate to severe headache, nuchial rigidity, no neurological deficits

other than cranial palsies

3 Drowsiness, confusion, mild focal deficits

4 Stupor, mild/severe hemiperesis, early decerebrate rigidity, vegitative

disturbances

5 Deep coma, decerebrate rigidity, moribund appearance

Serious systemic diseases like HTN, DM, Atherosclerosis, COPD, Severe

angiospam on angiography increase the grade by one level.

World federation of neurosurgeons’ grading:

WFNS GCS motor deficit

I 15 absent

II 14-13 absent

III 14-13 present

IV 12-7 present/absent

V 6-3 present/absent

66

Poorer the grade on hospital admission, worse the prognosis.

Surgical mortality and morbidity in relation to gra ding:

Grade H and H mortality % morbidity%

0 0-2 0-2

1 2-5 2

2 5-10 7

3 5-10 25

4 25-30 25

5 40 –50 35-40

Pathophysiology of rupture of cerebral aneurysm

Raised ICP-blood, CSF outflow obstruction, arteriolar dilatation, vasoparalysis

Reduction in CBF-hematoma, hydrocephalus, edema, vasospasm

Reduction in CMRO2 (25%)-decrease in CBF and direct effects of

subarachnoid blood

Increased CBV-vasodilation, microcirculation

Impaired auto regulation with right shift

Impaired CO2 reactivity in reducing ICP

Increased sympathetic activity with activation of coagulation and fibrinolytic

system

Increased excitatory Amino Acids, cellular apoptotic pathway, lactic acidosis

Medical complications following SAH

1. Blood Volume and Electrolyte Disturbances:

HypoNatremia – found in 10 to 34% of patients due to Atrial Natriuretic

Peptide and also attributed to SIADH

HyperNatremia - poor prognosis

HypoVolumia - bed rest, diuretics, negative N2 balance, blood loss, raised

catacholamines

Treatment - isotonic saline solution-normovolumia delays incidence of

ischemia

67

2. Cardiovascular Effects:

ECG changes (50%)-Q waves, ST elevation/depression, T inversion,

arrythmias

Hypokinetic LV, subendocardial damage

Echo correlates clinical grading than ECG

Hypertension-catacholmines, cushings reflex

TMP=MAP-ICP/ CPP==TMP

So MAP not decreased < 20%of baseline values

3. Pulmonary Complications:

Aspiration

Neurogenic pulmonary edema(13%,1st week)

Embolism

Bronchospasm

Due to increased sympathetic out flow and pulmonary capillary

endothelium disruption

4. Deep Venous Thrombosis:

50% in patients not receiving prophylaxis

Compression stockings

LMWH (21% -14%)

Intermittent calf compression

Surgical Complications following SAH

1. Rebleeding:

Most common cause of mortality (25%)

4% on 1st day, 1.5%daily for 13 days

7 to 20% rebleed by 1 month

35% of them die

Early surgery is the choice

Advantage: Prevent rebleed, vasospasm, hydrocephalus

Disadvantage: Edema causing difficult exposure, rupture

Safe drugs, good monitors, microscopes– early surgery feasible

68

2. Hydrocephalus:

Acute phase has negative impact on outcome

Chronic (6-67%)

Shunt dependence due to increase age, intraventricular hemorrmage,

thick SAH

3. Vasospasm:

Focal or diffuse narrowing of large arteries

Hemiperesis, visual disturbances, alt consciousness

Onset 4-14 days peak at 7th day after bleed

Not before 72 hrs and resolves by 2 weeks

Oxyhemoglobin, endothelin, BNP

Diagnosised by TCD, EEG, angio, xenon study, PET or SPECT scans

Trt:Nimodepin, balloon angioplasty, intraarterial papavarine, triple H

therapy.(hemodilution, hypertension, hypervolumia)

Evaluation and investigation

1. CT- Scan:

Detects SAH in 95% < 48 hrs

Assess the amount of blood in cisterns

Location in 70%

Fisher grading of CT scan:

Grade CT Scan Findings

1 No blood detected

2 Diffuse thin layer of subarachnoid blood (vertical layers<1mm)

3 Localized clot or thick layer >1mm thick

4 Intracerebral or Intraventricular blood with diffuse or no SA blood

2. Lumbar Puncture:

Most sensitive, false positive are common

CSF flow under high pressure, non-clotting blood stained CSF

RBC count > 100000/mm3

High proteins and normal glucose

69

3. MRA (Magnetic Resonance Angiography):

86% sensitivity, only for screening

Cerebral 4 vessel angio

4. Cerebral Angiogram:

Gold standard for evaluation of cerebral aneurysm

Demonstrates size, site and direction of aneurysm

Helps to visualize the presence of vasospasm and adequacy of collateral

flow

Anesthetic considerations

Goals:

Prevent intraop rupture

Prevent cerebral ischemia

Provide cerebral protection

Provide lax brain

Maintain Cerebral Perfusion Pressure

Preoperative assessment:

Patients neurological status

Systemic dysfunction and medical disorders

Optimization and correction of physiological disturbances

Review of CT and angio

Investigations: CBC, RBS, BUN, Creatinine, ECG, CXR

Special investigations: LFT, Coagulation profile, ECHO in high risk and poor

grade patients

Premedications:

Anti convulsants, calcium channel blocker, and steroids to be continued

Heavy sedatives avoided

Good grade and unruptured aneurysm may require anxiolytic doses of

Benzodiazepines

Intubated patients are given muscle relaxants to prevent coughing

Antisalogague (Atropine or glycopyrdate)

70

Monitoring for aneurysm clipping

Before induction: ECG, SaO2, ETCO2, NIBP, Intraarterial BP.

After induction: CVP/PCWP, Temperature, neuromuscular block monitor; urine

output, ABG, blood glucose

Special monitoring : SjVO2, TCD, EEG, Brain tissue oxygen tension monitoring,

SSEP, BAEP

Induction

Goal is to prevent rupture (< 1%)

TMP = CPP = MAP - ICP

Pre-oxygenated

Induction with

Thiopentone 3-5 mg/kg

Propofol 1.5-2.5mg/kg

Etomidate 0.3-0.5 mg/kg

Narcotics for suppression of sympathetic response

Morphine 0.1-0.2mg/kg

Fentanyl 3-5mg/kg

Sufentanyl 0.3-0.7mg/kg

Relaxants: Scoline, NDMR

β blockers - esmolol - 300 to 500mcg/kg

Lidocaine 1.5mg/kg + add thio or propofol

Isoflurane /sevoflurane.

No GTN /SNP

Maintenance

Goals:

Provide lax brain

Maintain CPP

Cerebral protection during temporary clipping

71

Early recovery following surgery

Techniques: Inhalational, Intravenous and combination

1. Inhalational: servoflurane / isoflurane(up to 2 mac)

2. Intravenous: propofol+fentanyl/alfentanyl dose 5-8mg/kg/hr for maintenance,

500mcg/kg/min for burst suppression.

MAP maintained with inotropes / IVF.

Brain relaxation

Mannitol 0.25 - 1gm/kg for 20 min

Onset within 10 min; peaks at 30 min ;( rises TMP)

CSF drainage by LP- excessive drainage causes rebleed and herniation,

20 –30 ml can be drained before dural opening at 5 ml/min

Optimal ETCO2 of 30 –35 mmhg is mandatory

Deliberate hypo tension

Advantage: To prevent rupture to make dissection easy and neck pliable for

clipping

Disadvantage: worsen ischemia

Absolute Contraindication in vasospasm

Relatively in carotid artery stenosis, CAD, Anemia, hypovolumia,

hypertension uncontrolled

BP reduced not more than 20% of baseline,mostly during brief period of

clipping

Temporary clipping and cerebral protection

Done to overcome the disadvantage of hypotension

Advantages:

Reduces TMP more effectively

Reduces rupture of aneurysm intraop

Disadvantage:

Causes cerebral infarction and ischemia

Safe Occlusion time <10 min (< 1.5 % stroke)

72

Intraoperative Cerebral Protection:

Mild to mod hypertension + hemodilution (Hct –32%)-for perfusion thro

collaterals

Brain protection with thiopentone(5-10mg/kg) or propofol to produce burst

suppression

Hypothermia:

Deep 15 to180C TCA up to 60 min under CPB

Mild 32-330C CMRO2 falls by 15% prevents free radical and excitatory

AA formation

Intra operative rupture of aneurysm

Incidence of leak- 6%, frank rupture –13%

Sudden and sustained hypertension with or without bradycardia

Surgery postponed or rescue clipping done

Outcome depends on timing of rupture (good in later stages of surgery) and

amount of blood

Treatment:

Reduce MAP with NTG

Rapid craniotomy and clipping

blood loss replacement

Indication of DHCA

Atherosclerotic gaint aneurysm

Partially thrombosed gaint aneurysm

Gaint aneurysm adherent to vital structures

Basilar artery aneurysm

Ophthalmic artery aneurysm

Emergence

Uneventful procedure for grade 1 and 2– extubation in OT

Grade 3 ventilated based on post op neurological status

Grade 4 and 5 ventilated electively, aggressive management in ICU

73

Complications

Delayed recovery due to anesthesia or surgery (global or focal deficits)

Seizures due to brain retraction

Pnemocephalus - repeat CT

Hydrocephalus, ischemic neurological deficits, infections, hyponatremia

ArterioVenous Malformations

Tangle of congenitally malformed blood vessels

Arterial afferent to venous efferent -ischemic injury to the brain

Incidence:

One tenth as aneurysm

Male : female 1:1

Development of AVM

Congenital: during embryo genesis-high flow low resistance vessels shunting

blood and increase in size

Trauma and occlusion of arteries or venous sinuses producing increase in

perfusion pressure

Pathogenesis:

Endothelial dysfunction and /or aberrant angiogenesis

Angiogenic growth factors

Anatomic components of AVM

Nidus

Arterial feeders ( MCA or dural)

Arterial collaterals

Venous outflow channels -superficial, deep

Location:

Supratentorial (70-90%)

Posterior fossa (10%)

Basal ganglia and internal capsule (7%)

74

Dural (10%-15%)

Neural elements of spine

Co-existence of Aneurysm

4 – 10% of AVM

Occurs at Nidus (psedoaneurysm) hemorrhage

Feeding arteries (flow related) 37% -95%

Theories:

a. Coincidence finding

b. Generalized vascular maldevlop

c. Flow causing degeneration

Treatment:

a. Nidus and distal regress with AVM

b. Anesthetic precaution

Signs and symptoms

Seizures and headache(20 –40 yrs of age)

20% asymptomatic

SAH followed by seizures and focal neurological deficits in young adults

Hydrocephalus and high output failure in infants with vein of galen AVM

Incidence declines > 50 yrs

Clinical and angiographic factors for hemorrhage

Deep venous drainage

Intranidal or multiple aneurysm

Small AVM < 3 cm

High feeding artery or draining venous pressure

Diffuse morphological findings

Age> 40 yrs

Feeding by arterial perforators

75

AVM in Obstetrics

Maternal ICH 0.01 –0.05% of all pregnancies

23-50% of ICH results from AVM rupture

Pregnancy is not a risk factor for hemorrhage

Unruptured or stable post hemorrhagic allowed till term

Caesarean / vaginal delivery has no influence on maternal or fetal outcome

Grading system for AVM Spetzler and Martin:

Features points

Size: small <3cm 1

med 3-6cm 2

large >6cm 3

Eloquence of adj brain:

No-eloquence present 0

Eloquence present 1

Pattern of venous drainage:

Superficial 0

Deep 1

Management of AVM

Surgical excision

Embolization (single or multi staged) reduces the risk of intra op bleeding and

post op hyperemic complications

Steriotactic radio surgery (small AVM in critical location)using Co 60

Conservative (grade 5 or 6)

Risk of unfavorable surgical outcome

Age> 50 yrs

Recruitment of perforating vessels

Large size >5 cm

Depressed total CBF

76

H/o pre op hemorrhage

Co-existing aneurysm

Hyperemic complication

Anesthetic consideration for Embolization

General vs conscious sedation

Intra op neurologic testing

Controlled ventilation(ICP)

Ability to still for long periods

Fluid and electrolytes

Contrast dye complications

Radiation precautions

Complications

New neurological deficits

Seizures

Pul embolism

Acute bleeding

Hyperemic complication

Anesthetic consideration for surgical resection

Pre op: preexisting medical conditions

Neurological status

Fluid and electrolyte and coagulation

Diagnostic studies

Monitors and induction:

Maintenance:

Choice –neurological testing and stability

Brain protection

Deliberate hypotension

Emergence:

BP control

77

Evaluate neurological status

Complications:

New neurological deficits

Hyperemic complications(normal perfusion pressure breakthrough syndrome)

Severe bleeding

Hyperemic complication:

Definition: cerebral hyper-perfusion with normal perfusion pressures (spetzler

1978)

Mechanism:

Chronic hypo perfusion or ischemia in surrounding brain tissue(mech

weakness and instability)

Vasomotor paralysis of vascular smooth muscle

Neuropeptides in perivascular area

Left shift of auto regulatory curve

Complete venous and incomplete arterial obstruction

Prevention:

Staged removal via embolization

Carotid artery clamping

Barbiturate trt

Treatment:

Control ICP- high dose thio

Mannitol

Hyperventilation

Hypotension

Hypothermia

References:

1. James Cottrell, David Smith: Anesthesia and Neurosurgery, 4th edition,

Chapter 19, 20. Mosby 2001.

2. Paul G.Barash, Bruce F.Cullen, Robert K.Stoelting: Clinical Anesthesia, 4th

edition, Chapter 28. Lippincott Williams and Wilkins, Philadelphia 2001.

78

Measurement of Temperature and Pressure

Concept of heat and temperature

Heat is the form of energy transferred from hotter to colder substance.

Temperature is the thermal state of a substance which determines whether it will

give heat or receive heat.

Temperature Scales

When heat is added to a substance, not only temperature changes, but changes

in other physical properties also occur. Eg: Substance may expand; its electrical

resistance may change. These properties are made use in measuring the

temperature and in the design of temperature scales.

Mercury which is a liquid metal with lowest specific heat changes (expands and

contracts) with temperature and was the first substance used by Fahrenheit to

construct temperature scales.

Non Electrical Techniques of temperature measuremen t

1. Mercury Thermometer

2. Alcohol Thermometer

3. Dial Thermometer

1. Mercury Thermometer:

Principle: Utilizes the changes in volume of mercury with temperature.

Advantages:

Maximum reading thermometers

Used in wide varieties of range and accuracies

Used for calibrating electric thermometer

It is made to read maximum reading from an

angulated construction at the lower parts of mercury

column which splits the column after it has reached its

maximum readings. This prevents the mercury above

79

from contracting into the bubble until the thermometer

is shaken.

This can also be made by including a small metal index

above the surface of mercury. When the column

contracts back, this index is left behind to make the

level.

Disadvantages:

Breakage

Slow response, due to relative high thermal capacity

Unsuitable for recording and for remote readings

Difficulty in using intracavity - chances of rectal

perforation in children because of its rigidity

2. Alcohol Thermometer:

Alcohol is sometime used instead of mercury

Cheaper and more suitable for low temperature as mercury solidifies at -

39oC

It is unsuitable at high temperature - boils at 78.5 oC

Tends to be less linear than mercury

3. Dial Thermometer:

Bimetallic strip

Bourdon gauge

Bimetallic Strip

Two dissimilar metals fixed together in a coil. As

the temperature rises, metals expand by different

amounts and coil tightens to move the lever

clockwise over the scale.

80

Bourdon gauge type thermometer

Bourdon gauge is a device

really used for measuring

pressure. It is attached to a

sensing element containing

small tube of mercury or a

volatile fluid.

Variation in temperature causes

volume or pressure changes in the sensing fluid and this is recorded on the

Bourdon gauge which is calibrated in units of temperature.

Electrical techniques of temperature measurement

1. Resistance thermometer

2. Thermistor

3. Thermocouple

1. Resistance Thermometer:

Resistance Thermometer is based on the fact that the electrical resistance of a

metal increases linearly with temperature.

A simple resistance thermometer could incorporate a platinum wire resistor, a

battery source of electrical potential and an ammeter to measure current which

could then be calibrated to indicate temperature.

This simple system would not be very sensitive and it is better to incorporate the

temperature sensitive resistor into a Wheatstone bridge circuit containing array of

resistors.

R4 - strain gauge transducer or

resistance thermometer

R3 - Variable resistance that can be

adjusted until galvanometer reads 0

Here when the bridge is balanced

ie. no current

flows through

P

G

81

the galvanometer and G shown 0.

In practice, the output is amplified and is connected to a recorder or oscilloscope

in place of G and the extent to which the bridge goes out of balance is recorded.

Disadvantage:

Physical size of the coil

Slow response time

Smaller probes not available for oesophageal / rectal thermometer

Current through the coil (100Ω) must be limited to avoid self heating

2. Thermistor:

The thermistor is a semiconductor element consisting of a heavy metal oxide

which has a large negative temperature coefficient of resistance. Oxides of

Nickel, Cobalt, Iron and Zinc are used.

Thermistors are produced by compressing such oxides in powder form to beads,

rods or disc and sintering the mixture at high temperature into a solid mass. For

biological use, minute beads ranging in diameter from 0.015 to 0.25cm are

available which may be sealed into the tip of hypodermic needles.

Here the resistance of the semiconductor beads - unlike the platinum resistance

thermometer - falls exponentially as temperature increases.

Disadvantage:

Most thermistors show an ageing as

an increase of resistance with time

over a period of months

Calibration is liable to change if

subjected to a large temperature

fluctuations (>10o/min)

3. Thermocouple:

Thermocouples work on the principle of

seebeck effect. When a circuit made of 2 dissimilar metals has the 2 junctions

maintained at different temperatures an emf is developed. This arrangement of

metals is called a thermocouple. The effect is called seebeck effect.

82

Required Temperature Ice Reference Temperature

Constantan

Copper

Metals such as copper and constantan (alloy of copper and nickel) may be used.

For thermocouple to be used as thermometer, one of the junction is kept at

constant temperature while measuring junction acts as temperature probe.

Advantages:

The junction may be very small and versatile

Measuring probe can be manufactured and used in the form of a needle

Respond rapidly on account of their low thermal capacity

Accuracy is adequate

Disadvantages:

Voltage output / oC is only about 50mv

The reference junction temperature should be kept constant that is difficult in

operation theatre

Faulty readings

Liquid Crystal Thermometer

Liquid crystal contains Organic compounds in thermal transformation from solid

to liquid state passes through an intermediate phase that exhibits optical activity.

When light shines on such material, crystal at a certain temperature scatter some

light and transmit some light producing some colors. Thus by encapsulating

these liquid crystals - the colors form letters and numbers.

83

LCT consists of a flexible adhesive backed strip or disc with plastic cased liquid

crystals on a black back ground.It is used by removing the adhesive and the strip

is placed on the skin.

Two forms are available:

One displays the skin temperature

Other has built in offset that displays core temperature

Advantages:

Convenient

Gives fast continuous reading

Non invasive

No electric circuitry involved

Easy to apply and read

Can be applied before induction and transferred with patient

Unbreakable

Disposable

Non irritating

Inexpensive

Disadvantages:

Less accurate

Extremes of ambient temperature, humidity, air movement introduce

inaccuracy

Only skin temperature

Sunlight, freezing, infrared lamps can interfere with readings

Clinical Applications

Sites for temperature measurement

Factors influenzing temperature at any given site include

Tissue’s heat production

Blood flow through the area

Amount of insulation from environment

Any external influence on the site

84

Core temperature reflects the amount of heat generated in the most central and

vital body organs. Core tissues contribute 80 to 90% thermal input to the

thermoregulatory systems. Sites differ in how well they reflect core temperature

and this may depend on the rate of change of temperature.

Skin:

Correlation of skin temperature with core temperature is controversial

Devices used are LCD, flat metal discs containing thermocouples or

thermistors

Readings are affected by ambient temperature, use of skin surface warming

devices and regional vaso constriction

Use of an opaque dressing and / or tape over the sensor may decrease the

effect of environmental factors on the reading

Commonly measured over the forehead - fairly good blood flow and not much

underlying fat

Forehead temperature gives better correlation with core temperature than

neck temperature

Useful in evaluating quality of nerve block (Increase in temperature -

successful)

In micro vascular surgery - viability of the tissue - rise in temperature

Disposable Probe for measuring skin temperature

Axilla:

Probe positioned over the axillary artery and the arm adducted

Equilibration may take 10 to 15 minutes

Convenient, non invasive and carries little risk of perforation in infants and

children

Influenced by contact of the probe with skin (perfusion)

Correlation with core temperature is controversial

85

Nasopharynx:

Sensor is in contact with posterior pharyngeal wall - close to hypothalamus

(thermostat) (easily accessible)

In intubated patients, readings not affected unless there is leak around the

tracheal tube

Cannot be used in non intubated patients (inspired cool air)

Correlation with core temperature is good in most number of studies but

shows less satisfactory in some studies

Epistaxis may follow after insertion

Urinary bladder:

Correlates well with core temperature but may lag behind during rapid

warming or cooling

Urinary catheters with a temperature sensor near the patient end are

available

Useful in patient who need urinary catheter post operatively

Esophagus:

Measured using a simple probe, esophageal stethoscope with temperature,

sensor, gastric tube with sensor

Measured with sensor located in the lower 1/3 or ¼ of esophagus. Where

esophagus lie between the heart and descending aorta. This placement will

minimize the effect of temperature of respired gas

If high - reading is low by inspired gas

If low - recorded high reflecting liver metabolism

Ideal position calculation

In adults 38 to 46 cm below the central incisions 45 cm from the nostril

In children ideal distance in cms below the corniculate cartilage is

approximated by the following formula

10 + (2 x age in yrs)/3 cm

Brain temperature may adequately be reflected by esophageal temperature

during mild but not profound hypothermia

86

Easily accessible, probes easily inserted without significant risk and relatively

inexpensive

Contrandications:

Procedures on the face , oral cavity, nose, airway or esophagus

Uncomfortable and poorly tolerated in awake patients

Chances of displacing is common

Continuous gastric suction lowers the reading

Sitting or prone position, oral secretion can track down and collect between

the probe and monitor cable - incorrect reading

Tympanic membrane

Anatomical position of tympanic membrane - placed deep within the skull and

separated from ICA by only the narrow air filled cleft of the middle ear and a

thin shell of bone

Temperature measured by inserting a thermistor or thermo couple probe into

external auditory canal until it contacts with membrane (anterior lower part)

Danger of perforation but readings are inaccurate if the probe does not touch

the membrane

The probe is enclosed in soft foam, and is advanced into the canal till the reading

is stabilized.

Infrared Thermometer

Non invasive device

Sensing the infrared radiation emitted by the warm object ™

Can be used (Otoscope like)

87

High accuracy

Well tolerated

Stable over wide range

Correlation with core temperature is good but may not be accurate in sudden

change of temperature and profound hypothermia

Ambient air influence can be minimized by correct placement

Cerumen renders the reading incorrect with probe but not in infrared

thermometer as cerumen is transparent to infrared energy

Acute Otitis of its media - increase in temperature

Advantage:

Cleanliness, convenience, tolerated by conscious patients

Accessible

Disadvantage:

Trauma - perforation of TM

Change of position when head is moved

Contrandications:

Skull

ISOM

Any abnormalities of ear

Pulmonary artery:

Through Swan Ganz Catheter

Correlates with brain temperature even with rapid coding and rewarming

Poor correlation is seen in DHCA

Not reliable during thorocotomy or bypass (no flow)

Directly affected by cardioplegia used during cooling

Oral cavity:

Probe placed in one of the pockets on either side of frenulum of the tongue -

proximity to lingual artery

Mouth to be closed and equilibration takes few minutes

Not influenced by respiration rate, presence / absence of teeth, warm or cold

substance in the mouth

88

Rectal temperature:

Commonly measured

More than core temperature

Readings affected by the blood from lower limbs

Peritoneal lavage and cystoscopy

Disadvantage:

Equilibrates with body temperature very slowly

Discomfort for patients

Relative inaccessibility

Bacterial contamination

Contraindications:

OBG procedure

Risk of Para rectal abscess

Usage of Probes:

Thoroughly cleaned and distinguished between uses

Wear and tear checked before use

When extreme temperature readings are seen, accuracy to be verified by

other means

Water proof tapes recommended

Cables to be kept dry

Hazards of Thermometry:

Damage to the monitoring site

Burns - if the probe acts as the ground for electro surgical apparatus

Incorrect readings

Esophageal stethoscope and temperature probe

Gastric tube with temperature probe

Urinary catheter with temperature sensor near the patient end

89

Measurement of blood pressure

Pressure at the heart

BP arises from the force of contraction of myocardium

acting on the blood in the ventricles.

The concept of pressure = F/A is less clear because the

force of contraction acts tangentially at the surface. This

force gives rise to Tension. Tension being force/length and

Laplace law applies P = 2T/R

Practical application of Laplace law:

Distended failing heart has a large radius than the normal and the pressure

produced falls unless the muscle contracts more forcefully. In the normal heart

increase in radius - lengthening of muscle fiber - increase force of contraction (by

starlings law) pressure is maintained.

Pressure is the circulation:

Circulation is a system of tubes filled with liquid, hydrostatic effects is present.

A tall man who is standing - mean BP varies from 53 mmHg at his head to 202

mmHg at his feet with mean BP of 90 mmHg at his heart.

Standard reference patient is taken as that of heart

level

BP also depends on caliber of vessel and distance

from heart

Mean pressure is the arterioles is lower than

arteries

Diurnal variations are seen in blood pressure

Blood pressure = peripheral resistance X cardiac output

So in patients with

Normal or decreased PR (warm pink skin) - high BP is due to high CO and in

patients with increased PR (cold pale skin) - high BP is not due to high CO.

So mean BP = diastolic BP + 1/3 of pulse pressure

90

Techniques of measuring blood pressure

Simplest non invasive system of BP consists of an inflatable cuff (Riva Roci cuff)

connected to a manometer

Cuff:

Cuff must be positioned so that the centre of

its bladder is on the medial side of the arm

over the brachial artery

Width of the cuff - 20% greater than the

diameter of the arm

Should be leak proof

Manometer:

Mercury type manometer - must read zero before use

Should be vertical unless it is of the type calibrated to be used at an angle

Partial block of the air vent or the connection tubing may lead to inaccurate or

sluggish readings

Aneroid gauges are more portable, have to be calibrated regularly

Effect of slope in manometer tube:

Mercury manometer:

Denser liquid - used for measuring high pressure (atmospheric pressure)

13.6 times denser than water so force exerted by its weight is proportionately

greater

7.5 mmHg = 10.2 cm H2O (13.6 x 7.5) = 1 Kpa

It is essential that the top of a manometer tube is open

91

In the mercury manometers used for BP measurements, a disc of material

permeable to air is placed at the top of the tube to prevent spillage of the

mercury

It can create problem if gets obstructed - gives faulty readings

Mercury barometer:

It has a sealed upper end with vacuum above the mercury

Absolute pressure is recorded

Bourdon gauge:

In conditions where pressure higher

than 1 bar is present, Bourdon gauge

is used. Here the gas at high pressure

causes tube to uncoil and in doing so it

moves a pointer over a scale on a dial.

Advantage:

No liquid spill (called aneroid gauges)

Another form is based on bellows or capsule which expands and contracts

depending on the pressure across it. More specialized detector system for

measuring pressure

92

Oscillometric System:

Earliest techniques of BP measurement

As BP cuff is detected from above systolic pressure the needle on an aneroid

gauge will start to oscillate when systolic pressure is reached

Electronic oscillometric apparatus has now proved to be more convenient and

accurate and has the added advantage to give automated measurements

Automated Oscillometric Technique:

Also known as NIBP (Non invasive Blood Pressure) monitors

93

Uses single cuff

Pressure transducers measures both the pressure and the oscillations

Strain Gauge Pressure Transducer:

It works on the principle that when a wire

is stretched it becomes longer and thinner

and its resistance increases. Such

resistors are called strain gauges.

In this transducer, movements of the

diaphragm with changes of pressure after

the tension in the resistance wire thus

changing its resistance.The changes of current flow through the resistor can be

amplified and displayed as a measure of pressure change.

The processing unit analyses the signal from the transducer to detect the

onset of oscillations at systolic pressure and the point of maximum oscillation

as mean pressure and to give an indication of the diastolic pressure

There is provision for automatic inflation of cuff at preset intervals to a suitably

high value (160 mmHg) or its repeated readings to 25 mmHg above previous

systolic BP

Released at the bleed value at 2 to 3 mmHg/sec

Frequency of cuff inflation - permit readings at a max rate of 1/minute even

this may be too great for long term use - cause impeded blood flow

Maximum frequency of every 2 min is preferable except for short term

monitoring

Reliable readings if appropriate cuff is used

Less accurate when patient has dysrhythmias, BP < 50 mmHg, rapid

fluctuations of BP

Penaz Technique:

Measurement of finger blood pressure

Finapress - is the apparatus

94

The technique resembles the electronic oscillometric technique and is its

initial calibration detects the mean pressure from the point of max oscillation

Differs from oscillometric by using at cuff, an infrared light emitting diode and

a photocell

The photocell measures absorption at an infrared wavelength appropriate for

arterial blood and so detects the volume of arterial blood in the finger under

the cuff

Volume varies according to the degree of distention of arteries during systole

An electronic processor analyses the photoplethysmograph to determine the

volume at a point set according to mean BP,then the servo control value at

the air pump acts as a feed back mechanism, continuously inflating/deflating

the finger cuff in order to maintain the photoplethysmograph output constant

at this set point

Pressure at the transducer gives continuous tracing

Perfusion of finger continues despite continuous inflation of finger cuff but it

remains to be seen if this perfusion is adequate for long surgeries

Invasive Arterial Pressure Monitoring

Invasive measurements of arterial pressure are used in preference to non

invasive methods when arrhythmias are present, in patients whom rapid changes

95

of BP are likely eg: Sudden blood loss, operations for pheochromocytoma, or

during controlled hypotension. Beat to beat variability has to be recorded.

Procedure of Cannulation:

Peripheral artery is chosen so that the whole limb is not threatened if a clot or

hematoma forms. Before cannulating the radial artery modified Allen test is

carried out

Patients hand is clenched and radial and ulnar arteries are occluded

Patient is asked to relax his clenched fist and ulnar artery pressure is

released

Flushing < 5 seconds - good collaterals

Local anesthesia is required in conscious patient

Percutaneous route is usually satisfactory than open exposure

Rarely causes thrombosis if cannula is of Teflon, short with parallel smooth

surface

Fixation of cannula should be free of leak - may lead to serve blood loss

Intermittant flushing with hepainized saline to prevent clotting

Here the high pressure generated by 2ml syringes can damage arterial walls

or the diaphragm of the transducer

Care should be taken when catheters are being flushed

Syringes smaller than 5ml should not be used

For longer term recording and continuous flushing system (Infra flow) is used

Here the hepainized saline is kept in a pressurized container (300mmHg). It is

passed through a drip chamber through a constriction, which does not allow >

4ml/hr of flow rate.

96

Equipments used:

It uses an arterial cannula, catheter, transducer, an amplifier and a display /

recorder. Pressure changes in the artery are transmitted through the saline in the

catheter to the transducer, where they cause the flexible diaphragm to move.

This movement is detected by strain gauge transducer that consists of an

electrical resistance connected to the diaphragm. The circuitry required to

measure the change of resistance (Wheatstone bridge) is incorporated in the

transducer body. In some model the resistor and associated circuitry are built into

single silicon chip to form a “semiconductor strain gauge”. For analysis purpose

catheter and transducer is considered a single unit -arterial manometer.

Arterial Pressure Waveform:

Arterial pressure waveform is a periodic complex wave which can be reproduced

by Fourier analysis. Fourier analysis technique is that which recreates the

original complex pressure wave by summing a series of simpler sine waves of

various amplitude and frequencies.

1

The original pressure wave has a characteristic periodicity called fundamental

frequency equal to its pulse rate

Sine wave that sum to produce the complex wave have frequencies that are

multiples (harmonics) of fundamental frequency

If the original arterial pressure waveform contains high frequency components

(like step systolic upstroke) higher frequency sine waves (more harmonics)

are needed to produce adequate reproduction of most arterial waveforms

97

So if faster the heart rate, steeper the systolic upstroke, greater will be the

dynamic response required from the monitoring system

Alternatively, venous pressure waveform do not have steep waves or high

frequencies, so monitoring system do not require dynamic response (high

frequency response)

Arterial Pressure Recording:

Here the final waveform produced can be displayed on an oscilloscope or a

recording tracing

The pressure waves become narrower and increases in amplitude as the

blood flows to the periphery

So even in supine position, systolic pressure is Dorsalis Pedis artery is higher

than in the radial, which in turn, is higher than in the aorta

This modification is due to change in diameter, elasticity and possibly also

because of reflection of wave pattern from the vessel walls

The systolic and diastolic pressure are easily identified on a tracing

At radial artery systolic BP > 5 mmHg higher with arterial than with indirect

NIBP diastolic BP is 8 mmHg lower

Dicrotic notch caused by intra aortic vibrations

Frequency range of various biological signals like ECG - 0.1 to 100Hz, EEG -

15 to 60Hz

Similarly in case of arterial pressure waves the frequency range is 0 to 40Hz

98

So the apparatus used for arterial pressure measurement must be able to

respond adequately to this range of frequencies

Usually recorders and amplifiers are of no problem may arise with the

transducer (diaphragm) and the connection to the cannula

Resonance and Damping:

The pressure measuring system consisting of a transducer diaphragm,

catheter and saline column possesses a resonant frequency at which

oscillations can occur (just as the weight on the end of a spring)

If this is less than 40Hz, it falls within the range of frequencies present in

blood pressure waveform

The phenomenon of resonance occurs if the natural frequency of the system

is super imposed by the harmonic input from the blood pressure wave forms

For the measurement system, resonance is undesirable, as it introduces both

amplitude and phase distortion

There are 2 approaches to avoid this type of distortion which can be used

separately or together

1. To arrange the resonant frequency of the instrument well above the

frequency of the highest significant harmonic in the blood pressure

waveform - difficult to achieve (fo)

2. The second method is to increase the damping (β) which could be done

by increasing the length of the catheter or decreasing its radius fo = r/2 √

(E /Πρl) β = 4µ/r3 √ (l / ΠρE)

Under Damping

Over Damping

99

Factors which tend to increase the resonant frequency (fo) larger radius,

increased elasticity and small length tends to decrease the damping.

Damping could also occur if there is restriction to the transmission of the

pressure from artery to transducer diaphragm.

Air bubbles in the catheter, transducer chamber

Clot formation in the cannula, catheter or transducer

Both reduce the deflection of diaphragm.

Adjustment of frequency response in a monometer:

To achieve a frequency response suitable for all clinical purpose - 1st method of

using manometer of higher natural frequency is preferred - principle behind

catheter tip transducer. fo 0f 40KHz .But they are expensive and fragile.

Conventional catheter transducer systems has intrinsic natural frequency of

200Hz

Addition of catheter, taps and cannulas, lowers the natural frequency

This systems are usually under damped

So correct adjustment requires a method for increasing the damping (β) while

leaving fo unchanged. It is necessary to assess the frequency response of a

manometer system to check that resonant is sufficiently high and that the

damping factor is optimum.

Invasive Arterial Pressure Non Invasive Pressure

Greater accuracy Less accurate

Reliable pressure readings in

hypotensive and shocked patients

Less reliable below certain

minimum readings

Gives continuous record of beat to

beat variability of blood pressure

Intermittent record

Advantage

Better reliability in patients where

BP is continuously varying

Risk of arterial damage No damage

More costly Cheaper

Disadvantage

Requires technical skill Can be done by paramedics

100

Transducer setup: zeroing, calibrating and leveling

Zeroing:

Zeroing the transducer means actually the transducer is exposed to

atmospheric pressure via an open stopcock affixed to the transducer

The monitor should be inspected to ensure that the pressure trace overlies

the zero pressure on the display screen and the digital pressure value equals

zero

If the stopcock is exposed to atmosphere and pressure is not equal to zero,

then baseline drift of the transducer’s electrical circuit may have occurred

This transducer drift is caused by problems with memb dome coupling to

electronic pressure transducing elements - electrical cables or with monitor

itself

Uncommon as many disposable transducers are available

Calibration:

Calibration is an adjustment of a system gain to ensure the proper response to a

known reference pressure value.

Using mercury manometer

Disposable transducers - no need for calibration

So avoiding air embolism, infections

Levelling:

Midchest position in midaxillary line in supine

More important in CVP / PWP monitoring than arterial monitoring

“The only factor that contributes to measured hydrostatic pressure with fluid filled

catheter- transducer system is the level of the transducer relative to the upper

most fluid level in the chamber in which pressure is measured”

To remove hydrostatic pressure influence, the transducer should be placed level

to the top of fluid column in the chamber or vessel being measured.

101

Vasotrac System

Apparatus and Principle:

Consists of a reusable circular sensor strapped over the radial artery at the

wrist

The sensor is supported by a control mechanism a digital signal processor

and a display screen. The raw information collected from the sensor is

processed and displayed graphically

The pressure transducer is placed directly over the radial artery at the distal

end of radius.

A disposable adhesive backed vasoguide strip helps to position and hold the

sensor over the radial arterial site

Activation of the unit, the control mechanism actively compresses the

pressure transducer over the radial artery in a non occlusive manner (not

circumferential but only anterior) until the radial pressure waveform is

detected by the transducer

Compression of the transducer on the radial pulse stops as soon as the

maximum energy transfer between radial artery and the sensor has been

achieved

An external safety transducer provides a feedback to the control mechanism

and prevents the application of unsafe pressure

Measures only the pulsatile energy perpendicular to the artery

Cyclical compression and decompression measures several parameters

The pressure requires 12 to 15 consecutive beats without interference

(movement artifacts) to obtain adequate energy information to generate a

pulsatile calibrated beat. (one of the 15 pulsation)

Thus when used in the continual mode, single calibrated waveforms along

with BP/HR are displayed is an uninterrupted fashion every 12 - 15 beats

Sensor check / calibration:

Sensor is zero adjusted when simply exposed to atmospheric pressure.

Accomplished by activating a zero key on the monitor ensures that there is no

surface pressure on the transducer.

102

As this measures the anterior pulsatile energy, precise positioning of the

transducer is essential for its accuracy.

Advantages:

In healthy volunteers, resulted in accurate measurement of BP, that very

closely matched measurements obtained directly via radial arterial line

(invasive)

It was able to track the rapid and drastic changes in BP same as IABP

No H/O significant compression injuries when compared with NIBP measured

every 30 seconds

Finapress (Penaz) needs no frequent calibration, gives beat to beat BP

readings with arterial waveform but may cause troublesome venous

congestion when used for long periods - not seen in vasotrac

Zeroing is easy compared to invasive

Unaffected by damping, air bubbles, clots and other artifacts of IABP

Disadvantages:

Accuracy is positioning of the sensor on the radial artery

Not suitable in hemorrhage, hypothermia, sig vaso constriction but BP can be

measured accurately if hypotension is due to vasodilatation

Not suited for infants and children (too large)

Not suited in some rare congenetial anomalies (absence of radius)

Not suited when patients are on non pulsatile CP bypass

Arterial samples –impossible

References:

1. G.D.Parbrook, P.D.Davis, G.N.C.Kenny: Basic Physics and Measurement in

Anesthesia, 4th edition, Chapter 9 and 17, Butterworth Heinemann 2002.

103

Neuropathic Pain Management

Definition

Painful condition resulting from current or past damage to the peripheral or

central nervous system and is due to aberrant processing of information in the

PNS or CNS.

Initially neuropathic pain affects sensory nerves. Smaller sensory nerves are

affected before the larger nerves and motor nerves are affected in later stages

(DM).

In crush / traumatic injuries both nerves are equally damaged and symptoms

develop simultaneously.

The unmyelinated C fibers and smaller myelinated Aδ fibers are mostly

susceptible to injury.

Pathophysiology

Damaging or trapping of a nerve will obviously cause an immediate acute pain.

After damage, there are several ways in which it results in continuing pain.

Damaged nerves are apt to fire spontaneously giving pain

If the peripheral nerves are cut or damaged they regenerate by sprouting, so

that, they innervate the denervated regions. This process leads to hyper

algesia (Increased response to normal Noxious stimuli)

In some cases, if the spouting nerve endings cannot successfully innervate

the tissues, forms a tangle of nerve fibers – neuroma.These damaged nerve

endings and the neuromas have altered elecrophysiological properties of

conducting nerve impulse and may become very sensible to normal

mechanical or chemical stimulation (Tinel’s sign)

Damage to the myelin sheath can also intensify the pain arriving at the

demylinated patch

Pharmacology and Physiology of neuropathic pain

Spontaneous sensations from the afferents from neuroma and ganglion cells,

could be due to clustered or altered Na+ channels

104

Trauma nerve lesion

Trophic changes due to various cycles

Abnormal state of afferent nerve

Distorted processing in spinal cord

Deregulation of sympathetic activity

Insertion of coupled receptors into sprouting nerve endings and growth of

sympathetic terminals into neuroma provides possibility of sympathetic

activity along the afferent axonal activity

Dorsal root ganglion changes after injury - it gets hyperinnervation with type A

ganglion and C cells. Post ganglionic sympathetic terminals proliferate and

form basket like projections around the DRG

AB fibres - large myelinated carrying low threshold information ends in Lamina

III and IV

Aδ and C fibres - small myelinated / unmyelinated - high threshold information

ends in Lamina I, II, and V. After injury, there is spontaneous sprouting of AB

from LIII to LI and LII. So even the low threshold is sensed as pain

Loss of GABA ergic or glycenergic tone leads to allodymia (pain due to low

intensity stimulation)

Enhancement of glutamate and aspartate has been postulated as the cause

of post nerve injury pain. Increase in spontaneous firing activity and loss of

inhibitory interneuron functions

105

Sites of generation of spontaneous activity in PNS

1. Axon conduction (myelin sheath damage)

2. Spontaneous activity in injured fibers

3. Neuroma fixing

4. DRG

5. Glutamate evoked excitation

Signs and Symptoms

Spontaneous pain (continuous or paroxysmal):

This type of pain is described as being felt in skin, muscles or bones - can be

episodic paroxysmal with short duration often described as “shooting” or “shock

like” .It is said that pain is always present though its intensity may wax and wane.

Eg: In patients with central pain in RSD phanthom pains.

Abnormal evoked pain:

Hyperalgesia Allodynia

Painful sensation of abnormal severity

following Noxious stimuli

Pain produced by normal and innoxious

stimuli

Can be from deeper tissues following

injury

Light touching of the skin

i. Mechano allodynia

ii. Warm allodynia

iii. Cool allodynia

Exists in single or in combination

106

Res

pons

es

Intensity

Pain Threshold

Pain Threshold

Intensity

Res

pons

es

Hyperpathia: Presence of abnormal pain despite some degree of sensory loss

(less than anesthesia). Persistence of pain even after the stimuli

Hyperesthesia: Increased response to mild stimulation.

Dysesthesia: unpleasant or abnormal sensation with or without noxious

stimulus.

Parasthesia: Abnormal sensation perceived without an apparent stimulus.

Paroxysmal evoked pain:

It is a stimulus evoked pain with qualitative and spatial characteristics

These are discrete foci called trigger points when stimulation produces

shooting, lancinating pain. These are often described as “burning”, “dull

acting”, “boring”, “sharp shooting”, and “lancinating”.

Types of Neuropathic pain

1. Traditional etiological classification:

Trauma: Phanthom limb - spinal cord injuries

Ischemic injury: Central pain (Thalamic infarct), DM neuropathy

Infection / Inflammation: Post herpetic neuralgia (neuralgia - pain in

distribution of a nerve or group of nerves)

Cancer: Invasion - compression of nerves

Compression: sciatica - Trigeminal neuralgia

Idiopathic: TGN - Multiple sclerosis

107

SMP

Neuralgias Herpes Zoster V

isce

ral P

ain

CR

PS

Pha

ntho

m

Li

mb

Met

abol

ic

Neu

ropa

thy

2. Anatomical classification:

PNS: Sympathetically maintained pain (SMP) [RSD]

a. Due to trauma, surgery or entrapment

b. Compression brachial or lumbar pluxes

c. Metabolic - DM, uremic

d. Deafferentiation - stump pain, phanthom pain

Spinal root or ganglion lesion

a. Cervical - Thoraxic Rhizopathy

b. Lumbosacral Rhizopathy (including Cauda eqinq syndrome)

c. Post herpitic neuralgia

Spinal cord: MS - post cordotomy dysesthesia

Central pain: thalamic infarct

Reflex Sympathetic Dystroy (RSD) and Causalgia

Mitchell first used the term causalgia for chronic pain syndrome

In 1916 French surgeon Leriche linked sympathetic system to causalgia

Term RSD was introduced by Evans

108

Various other terminologies used were:

Algoneurodystrphy

Chronic traumatic edema

Post traumatic dystrophy

Shoulder hand syndrome

Sudeck dystrophy

Sympathalgia

Traumatic vasopasm

According to the classification of chronic pain by the International Association for

the study of pain (IAPS) these syndromes are now called Complex Regional Pain

Syndrome (CRPS).

CRPS I

II

RSD without identifiable nerve lesion

RSD without identifiable nerve lesion

CRPS SMP

SIP

Sympathetically maintained pain - respond to sympathetic block

Sympathetically independent pain - unresponsive

Signs and symptoms

Pain associated with hyperalgesia to cutaneous stimuli

Symptoms are not limited to the territory of a single peripheral nerve and are

disproportionate to the initiating event

Stage I:

a. Edema, skin blood flow abnormality, abnormal pseudomotor activity are

seen in the painful region after the initiating event - early hyperemic phase

b. Cardio vascular effects:

Early hot phase - skin is warm, red and swollen

Late cold phase - skin is cool, clammy and cyanosed

Finally this vasomotor instability may disappear but the skin still remains

shiny, swollen and discolored.

Stage II:

Burning pain with cold skin, mild cyanotic with moderate stiffness

(dystrophic / Ischemic)

109

Nociceptors

Cutaneous Stimuli Injury

Spinal Cord

Central pain Signaling Neuron

Pain

Low Threshold Mechano Receptors AB

Modulator LIII - LI

Sympathetic Neurons

α Adrenergic

To Thalamus

Hyperalgesia

On going pain

CNS PNS

Stage III: Severe burning pain with cold cyanotic skin with severe stiffness

and atrophic changes

Diagnosis:

It is very difficult to judge which patient with CRPS is associated with SMP or SIP

by clinical presentation.

SMP is diagnosed by relief of pain by sympathetic blockade by LA or α

adrenergic blockade by phentolamine infusion.

Other diagnostic tools: are

IV regional blockade with guanethidine acts along Noradrenaline system.

Prolonged pain relief 2 to 5 weeks – SMP.

No relief or minor < 5 days – SIP.

Ischemic Test: Interruption of circulation to a region with BP cuff, reduces

the pain in that region.It is due to obstruction to microvascular flow to deep

somatic tissues, reduces the activity of Aδ and c fibres.

If positive means SMP.

Thermography: Difference of > 2oC between affected and normal limb

Treatment for CRPS

Release of NA from CNS produces Nociception and pain.

110

In patients with SMP principle treatment is sympathetic blockade. Patients with

SIP require other treatment modalities with pharmacological adjutants. Many

patients have both SMP and SIP components and require simultaneous

treatment for both.

Treatment of underlying cause ( Pain generator) like Neuroma

Physiotherapy to encourage movement and to prevent muscle atrophy

Chronic pain associated with anxiety and depression is to be treated at the

earliest stages

Techniques of sympathetic blockade

Interventional

Medications

Local Anesthetic sympathetic blockade

Cranial nerve blockade - GLN and TGN

Upper extremity block - Stellate ganglion block, Intercostal

Lower extremity block - Paravertibral, celiac pluxes block, subarachnoid,

superior hypogastric

Stellate Ganglion Block:

1st Thoraxic and Inf cervical sympathetic ganglion at the level of C6 - C7

Most common site is in front of the anterior tubercle of the transverse process

of C6 vertibra - Chassaignac’s tubercle

Chance of pneumothorax and intra arterial inj are less with C7 level

Technique: Ant Paratracheal technique at C6 level - Leriche

IV access mandatory

Position - supine with a pillow below shoulder with full neck extension

Land mark - Carotral artery and shoulder muscle retracted laterally ant.

tuberscle of C6 palpated just lateral to Gricord Cortiage

Wheel raised over the skin with 1 ml of 1% xylo

22G needle passed till it touches the transverse process

Needle is withdrawn slightly and after negative aspiration 1% or 3.75%

xylocaine or Bupivacive 8 to 10 ml is injected

111

Success of the block is confirmed by presence of HORNER’s syndrome

Increase in skin temperature (at least 1.5oC)

Good pain relief > 50% from basal level

Sometimes hoarness of voice

Neurolysis:

Phenol 6% 5 to 8 ml

alcohol 100% 3 to 4 ml

Complication:

Intravascular injection

Intra arterial - vertebral artery

Intradural - Total spinal

Pneumothorax

Hematoma and LA - Compression on Reccurrent Laryngeal nerve and Phernic

nerve

Lumbar sympathetic block (LSB)

Anterolateral side of vertebral bodies, separated from somatic nerves by

Psoas fascia and muscle at L2 to L5 level

Single injection of large volume 20 to 25 ml at L3 is sufficient

Use of fluoroscopy is mandatory

Position: Prone or lateral

Landmark: 7 to 10cm lateral to spinous process of L3

20-22G 15 to 20 cm needle directed towards upper or middle 1/3 of L3

When the needle comes in contact with the vertebral body the angle of insertion

is changed to allow the tip to slip off the vertebral body.

Loss of resistance using saline / air

15 to 20 ml of 0.375 Bupi or 1% xylo injected

Neurolysis with 6% phenol or 100% alcohol (8-10ml)

Complictaions: Intravascular junction - Aorta or IVC, Somatic nerve damage,

Uretral stricture

Efficiency 40 to 80%

112

Medicational Sympathetic blockade

1. Phentolamine injections ( α1 / α2 blocker)

Informed consent

Monitoring of ECG, BP, HR, skin temperature

IV access

Recording of baseline pain level (VAS)

Propranalol 1-2 mg/IV

Infusion of phentolamine 1 mg/kg over 10 minutes

Continue sensory testing every 5 minutes for 15 to 30 minutes

After stopping of infusion - vitals to be monitored for ½ to 1 hr

2. IV guanethedine, reserpine and bretylium

3. Topical clonidine

4. Oral sympatholytics: Prazocin / Terazocin - postural hypotension

Continuous Sympathetic Blockade and Surgical Sympathectomy (International)

Series of LA blocks are indicated if pain relief duration is prolonged with each

block. If not prolonged then trial of continuous infusion or surgical

sympathectomy is considered.

Epidural infusion

LA of lower concentration to have continuous sympathetic blockade without

motor blockade

Infusions of clonidine has been reported to be of benefit in RSD

Surgical Sympathectomy

Surgical sympathectomy is considered if diagnosis is clearly established and

other options provide only transient pain relief.

Failures of surgical sympathectomy to provide long term pain relief are attributed

to collateral reinervation of post ganglionic efferent fibres or failure to extend

sympathectony over adequate level.

Revision sympathectomy and collateral sympathectomy should be considered in

patients with recurrent SMP of lower extremity.

113

For upper extremity endoscopic T2/4 sympathectomy

Radiofrequency percutaneous sympathectomy - as out patient procedure

Other Interventional Approach:

Intrathecal pumps for continuous infusions of opioids and dorsal column

stimulators are used.

Electrical stimulation:

Based on gate control theory of pain transmission

If one could activate the larger forces, the gate would remain closed and

Noxious stimuli via small fibres could not reach higher centres

Spinal cord stimulation (SCS)

Many theories are proposed to explain

Gate control theory

Activation of supraspinal mechanism

Neurochemical alteration in CNS

Blockade of spinothalamic tract and inhibition of sympathetic nervous system

tone resulting in vasodilation

Spinal cord is stimulated with tiny electrical signals

Affected area feels gentle tingling

SCS is reversible procedure that does not damage the spinal cord and nerves

Two types - Fully implanted system , partially implanted system

Brain stimulation

Different parts of brain like intracerebral, motor cotex are selectively

stimulated

Facility of steriotactic procedures and experienced medical team is mandatory

Intracerebral stimulation can be of sensory thalamic to treat some forms of

central pains

114

Pharmacological Management of Neuropathic pain

Categories Mechanism of Action Example Comments

Opioid

analgesics

µ receptors Morphine 30mg/day

Codeine 15mg bd

Transdermal or

Sublingual

Bupinorphine

Drug dependence

Side effects of constipation

Non opioid and

NSAIDS

Prostaglandin inhibitors

Seratotin, Adrenalin -

uptake inhibitor

COX II

Celicoxib100mg

Roficoxib 25mg

Tramadol 50 mg

Contradicted in CRF/BA

patients

gastric ulcer/Nephrotoxic

Nausea/vomiting

Adjuvants to Analgesics

Tricyclic

Antidepressants

NA and seratonin

reptake blockers

Modulate descending

Nociceptive inhibition

Nortryptaline 25mg/day

Amitriptyline 10 mg/day

Fluoxetine 10mg

Sedation mental clouding

Anticholinergic side effects on

cardiovascular / GIT/system

urinary

Less CVS side effects

(selective setatonin)

Traditional

Anticonvulsants

Na+ channel blockade

GABA agonist

(hyperpolarization)

increase K+ decrease

Ca++ conductance

Carbamazepine 400mg

8th hrly

Phenytoin 300mg

Valporate 750mg 8 hrly

Baclofen 15-20mg/pdd

Clonazepam 2-4mg/d

Bone marrow depression,

Agranulocytosis, Leucopenia,

hepato toxicity

Alaxia, confusion, sedation

(long ½ life) monitoring blood

levels needed

Enzyme induction

Toxicity: drowsiness, increase

seizure activity

Tolerance develops - slow

withdrawal

115

Long term intrathecal therapy

Noval

Anticonvulsants

Ca2+ blocker analog of

GABA

NMDA and Na+ blocker

and Ca++ channels

Gabapentine 600mg 8th

hrly

Lamotregine 100mg 8th

hrly

Ataxia, headache and tremors.

Does not induce hepatic

enzyme (3mg/dl) dizziness,

headache, diplopia, nausea,

skin rashes.

Typical hypersensitivity

reaction

Phenothiazines Dopaminergic receptor

blockade also have

5HT2 and α1 antagonism

Chlorpromazine 100mg

Haloperidol 2mg

Clozapine 50mg

Extrapyramidal side effects

Anticholinergic effects

Antiarrythmias Na+ channel blockers

Mexiletine 500mg/d

Lidocaine 1mg/kg/hr

Nausea/vomiting if

S.concentration > 2 mcg/d

Require close monitoring

Contraindicated in patients

conduction defects

Adrenergic Α2 agonist centrally

acting

Clonidine 0.2 mg/day

Transdermal (skin

reaction)

Dry mouth, hypotension,

sedation, drug interaction with

TCA

Less sedation but

hypersensitivity withdrawal

symptoms

NMDA

antagonist

Non competitive NMDA

blockade of glutamate

Dextromethorphan

60mg 8th hrly

Sedation

Steroids

Gluocerticostero

ids

Inhibition of

phospholiphase Α2 and

the Arachedonic acid

cascade pathway of

inflammatory mediators

Prednisolone

1-2mg/kg/day

If used > 2 weeks

Mainly in PHN

Adreno cortical suppression

Increase catabolic effects -

osteoporosis low muscle man

Increase glucose levels/

cushings syndrome

116

Response of vascular/

bronchial SM to

catacholamines is decreased in

absence of steroids

GI ulcers, behavioral changes

Calcium

channel

blockers

Abarrent Ca++

conduction blockade at

the injured n terminals

Nefidepin 10 to 30mgpo Hypotension

Peripheral Neuropathisis

Etiology: Trauma, surgical, entrapment

Metabolic: Diabetic, uremic, alcoholic

Deafferentiation: Anesthesia dolorosa, Phanthom pain, stump pain

Causes: 3 types -

Axonal degeneration

Demyelinating disorders - segmental

Mixed disorders

Differentiated from:

Cauda eqina syndrome - bladder and bowel

Posterior column lesion - Intact reflex / babenski

Peripheral Vascular insufficiency - Intact reflex and no atrophy

Signs and Symptoms

Symmetrical distribution in DM/ uremic/ alcoholic

Pain - Continuous/ intermittent and Spontaneous discharging

Burning, tingling, parasthesie, sharp and shooting, electric shock like -

hyperalgesia and allodynia may be present

Glove and stocking distribution of sensory loss/ dysesthesia deep tendon

reflexes - loss

Weakness of peripheral muscles and atrophy of muscles

Autonomic dysfunction are also seen in metabolic disorders like postural

hypotension, gastroperesis, gustatory sweating, diarrhea

117

Emotional components - anxiety, depression, insomnia

Treatment

Central Pain Syndrome

Sites of CNS pain

Spinal cord

Brain stem

Brain

Types:

Spontaneous pain: Constant varying in intensity influenced by emotion,

climates etc

Hyperesthesia: Poorly localized - unpleasant and intermittent on stimulus

Theories of central pain:

Results from an abnormal firing of sensory neurons that have lost their

sensory input and have become deafferentiated

Results from hyperactivity of reticulothalamic pathways that have lost their

sensory afferent

Spinal cord lesions

Etiology:

Traumatic

Disc lesions - prolapse / bulge

Vascular

AVM

Apart from symptomatic treatment of pain with medical and surgical approaches,

these patients should be looked for bladder and bowel abnormalities, nutrition

and psychological treatment is also needed.

Diabetic Alcoholic Uremic

Control of DM

Anti depressants

Anti convulsants

Vitamin B complex

Substitution Nutritional

Hemodialysis

118

Brain stem lesions

Wallenberg’s sign or lateral medullary syndrome is the most common

Other causes - syringobulbia / hematobulbia associated Ipsilateral cranial

nerve dysfunction

Loss of taste

Palatal and pharyngeal weakness

HORNER’s syndrome

Vocal cord palsies

Diminished reflex

Lhermitte’s sign - Electric shock produced in all four extremities on neck flexcan -

seen in multiple sclerosis.

Brain lesion

Dejerine Roussy syndrome or thalamic pain syndrome - Ischemic

Seen in patients who had developed stroke and hemiplegia pain may start

several months after an attack

Experiences pain on the affected side of the body

Other causes : AVM, neoplasm, Abscess, trauma, degeneration

Treatment

Medical Surgical

Barbiturates

Anti depressants

Anti convulsants

Anti arrhythmic - mexilitine (No opioids)

Removal of the

triggering focus

Thalamectomy

119

Acute Herper Zoster and Post Herpitic Neuralgia

Hyper zoster

Localized disease characterized by unilateral radicular pain and vascular

cutaneous eruption limited to dermstome innervated by single cranial/ spinal

sensory ganglion

Reactivation of V.Z.V infection triggered by trauma, surgery irradication,

immuno suppression

Pain of acute Herpez Zoster often preceeds and generally accompanies the

characteristic rash. If the pain persists even after 1 month of acute phase

(healing of the crusts) - post herptic neuralgia

Common Site Incidence

Thoraxic 50%

Bilateral <1%

Trigeminal n distribution (ophthalmic) 3 to 20%

Cervical 10 to 20%

Characteristics of Pain

Varies from superficial, itching, tingling or burning to severe deep boring or

sharp stabbing and lancinating pain

May be constant or intermittant

Hyperesthesia and allodynia may be present

Mimics pain due to MI, pleurisy, DU, Cholecystites, Renal/ Bilicuar colic,

Appendicitis, or early glaucoma

Treatment

Acyclovic 10mg/kg - 8th hrly and (Topical / oral)

Steroids 60mg/day - prednisolone to stop the inflammatory response

Anti depressants

Anti convulsants

Analgesics - (nonadditive, mild additive, strong additive)

120

Sympathetic neural block - Immuno compromised patients / unresponse to

Acyclovir (ophthalmic TGN)

Somatic Neural block - inter costal N block

1. Continuous epidural infusion

2. Intrapleural catheter with LA -thoraxic

3. Only in patients resistant to conservative measures

Local infiltration (Subcutaneous steroids Triamicinalone 0.2%)

Post Herpitric Neuralgia

Usually seen in elderly (>60 yrs) age group even after the rashes has heated (ie)

after all crusts have fallen off and re epithelization is complete. (>1 month)

3 types of pian:

Spontaneous - constant deep burning

Intermittant sharp stabbing, shooting, lancinating

Dysesthetic - Allodyma / hyperesthesia

Factors for developing PHN

Age>60 yrs - common. Rare is age < 40 yrs

Patients with severe pain during acute phase

Patients in whom sensory abnormalities are seen during acute phase

Failure to initiate antviral therapy < 72 yrs of rash onset

Pathology

Acute Phase:

Diffuse lymphocytic infiltration

Focal hemorrhage

Axonal degeneration

Demyelination

Followed by scarring, loss of axons and myelin sheath in the sensory nerve with

fibrosis and loss of axons and myelin in the sensory ganglion.Leads to atrophy of

the Ipsilateral dorsal horn.

121

Treatment:

Medical Surgical

Anti depressants

Local anesthetics

Anti convulsants

NMDA antagonists

Local infiltration - 10 to 12 days of steroids

Somatic blockade - prognosis

Neurolysis - 95% absolute alcohol, 6% Phenol

Complication is neuritis infection hematoma

Ammonium SO4 - 10%

Cryoanalgesia - ice, solid CO2, ethyl chloride

Neuroabalative procedure -

not usually recommended

Neuro stimulatory - TENS/

Acupuncture

TENS:

High frequency / low

intensity - AB fibres

Dorsal column stimulation

122

Trgeminal Neuralgia

Most frequent cranial neuralgia Female: Male = 2 : 1

It presents with brief paroxysms of stabbing or lancinating pain often in the

distribution of mandibular and maxillary division of trigeminal nerve -TIC

DOULOUREUX

Mostly unilateral (> 95%) bilateral seen in multiple sclerosis

Trigger zones - along the distribution of trigerminal nerve

Etiology and Pathngenesis:

Caused by compression of central axons of trgeminal nerve either by vessel

or tumor at the root entry zone

Vascular - 55% Tumor - 11% (Acquestic neuroma, cholesteatoma)

Demyelination of TGN - 2 to 4% - in M.soluosis

Infection at the root entry zone

Diagnosis:

Accurate history

Character of pain - sharp, shooting, electric shock like, superficial

Moderate to severe with wincing of face (TIC)

Provoked by high touch such as eating, chewing, talking and wash the face

Duration < 2 minutes

Frequency - single to several times/day - mostly day time and patient enjoys

pain free periods between attacks

Site - distribution of TGN

Relieving factors - sleep and anti convulsant drugs

DD:

Atypical facial neuralgia

Dental pain

Post herpitic dyesthesia

Cluster headache

Migraneous pain

TM joint Arthrosis

123

GLN neuralgia

Spheno palatine neuralgia

Investigation for TGN Neuralgia: History

MRI / CT - for compression by tumors

Vertibral angio, MR angio - vascular compression

Management of Trgeminal Neuralgia

Destructive Procedure Pharmacotherapy

Surgical Non Surgical

Non Destructive

Procedure

Monotherapy with

one anticonvulsants

- CPZ or phenytoin

Avulsion of

TGN branches

Peripheral chemical neurolysis

(to branches) with phenol in

glycerin (1:16)

Decompression

Procedure

MVD - Retro mastoid

approach

Combined therapy

with more than 1 AC

CPZ + Clonazepam

Avulsion of

TGN ganglion

Anhydrous glycerol

Phenol in wax

70 to 80% have

complete pain relief

for > 10 yrs

Add on therapy

usually with novel

anti convulsants

Complications

Permanent

deficit

hematomas

infarctions

Gasserian gangliolysis

Anhydrous glycerol (0.5 ml)

Chemical meningitis - antibiotics

Compression

technique

Micro compression of

TGN ganglion by

precutaneous Trans

ovavale

Insertion of Fogarty

catheter and inflation

of balloon

Pain relief > 5 yrs and

80% less side effects

Polytherapy Ac + add

on therapy + anti

depressants +

Procedure

18G- 18cm long needle through

foramenovale with fluoroscopy/

Gamma knife radio

surgery

70Gy - complete pain

124

anxiolytics imaging assistant

Confirmed by pain and CSF flow

Pain relief > 2 yrs

Percutaneous radio frequency

thermo coagulation of TGN

sensory roots (70o, 80 o, 90 oC

for 60 sec)

Pain relief is 65% for 1 yr, 49%

for 2 yrs, 26% for 11 yrs

LA

Mandibular and maxillary nerve

block with 1% xylocaine or

0.375% Bupivacine

relief

Acute Herpes Zoster Post Herpitic Neuralgia

Pharmacological

Antiviral: Acyclovir 10mg/kg 8th hrly

Cytabarin, vidaratrine, Idoxuridine - inhibits DNA

synthesis and viral replication

Analgesia is with anti depressants, anti

convulsants.

Antiviral and opioids are not much helpful

Newer Antiviral: Sorivudine, Valacyclovir,

famicyclovir - OD dosage

Steroids: Oral predisolone 60mg/day

Steroids + Antiviral (Newer) reduces the

inflammatory response

Analgesics: Non additive NSAID

Additive- moderate - Pentazocine

Strong - Morphine, Pethidine

Nerve Blocks

Local Infiltration: Subcutaneous -

Trimiainolone 0.2% - single injection

Multiple sittings 10-12 injections combined with

LA

Somatic Nerve block: Brachial pluxes,

Paravertibral intercostals nerve block

Usually as prognostic before neurolysis

125

Sympathetic blockade of Stellate ganglion:

Trigerminal herpes

Temporary relief

Central: Epidural only LA Steroids - Temporary

No neurolytic or surgical Neurolysis :Ethyl alcohol 50% - Neuritis

Absolute alcohol 95%, Phenol 6%

Neuritis: incomplete Neurolysis

Ammonium sulphate 10% + LA

- Local hemorrhage

-Infection

Other: TENS Other : TENS

Cryoanalgesia - Ice, Ethyl chloride, Solid CO2

Acupuncture

Surgical : Neuroabelative procedures

Rhizotomy, cardotomy, deep brain stimulation in

intractable pain

Phanthom Pain

It was first described by a French Surgeon Ambroise Pare in 1551

Phanthom limb sensation is the perception of the continued presence of

amputated limb. This sensation is non painful

Phanthom limb pain describes painful sensations that are perceived to

originate in the amputated position

Stump pain - localized pain originating from the amputated stump

Phanthom limb Sensation:

Universal occurrence - during 1st month of surgery

Strongest is the above elbow amputations and weakest in below knee

amputations. More frequent in the dominant limb of double amputees

Incidence increases with age of the amputees

85% to 98% begins with in 3 weeks and resolve after 2 to 3 years if they are

not associated with pain

126

Signs and Symptoms:

Strongest sensation comes from the body parts that has largest brain cortical

representation

Phanthom limb undergoes Telescoping - patient looses sensation gradually

Telescoping is more common in the upper extremity

During telescoping the last disappearing part is the one with the highest

cortical representation (Thumb, Index finger, big toe)

Only painless phanthom undergoes telescoping and lengthening occurs if

pain returns

Telescoping. The phantom hand gradually approaches the residual limb and

eventually becomes located inside the stump.

Phanthom limb Pain:

Initially incidence were <10% but now >60%

127

More common is 1st month after amputation 85 to 97%

At 1 year - 60%

After 2 yrs - <10%

Symptoms and Signs:

Burning, aching or cramping

Knife like or stitching are commonly used - immediately

Burning or sqeezing - Pain beyond immediate POP

Feelings of unusual positions of the phanthom limb like tightly clenched fist

with fingernails digging into the palms

Exacerbations with trivial physical, emotional stimuli

4 groups based on frequency and severity and to degree to which it interferes

with patients life style

Group I: Mild intermittent parasthesias that do not interfere with normal work

or sleep

Group II: Parasthesias - uncomfortable and annoying but do not interfere with

routine activities

Group III: Pain with sufficient intensity and duration that interferes with

activity intermittently but responds to conservative treatment

Group IV: Constant pain that interferes with normal activity and sleep

Usual course of Phanthom pain is to remain unchanged or to improve. So any

pain worsening or beginning after 1 year has to be investigated. Neuromas are

found to be the cause only in 20%,

Various Theories

1. Peripheral Theories: Pain originates from the cut ends of the nerves that

innervated the extremity - Neuromas, scar tissues, abscess associated with

sympathetic Nervous System. Draw back is complete sensory blockade does

not provide pain relief

2. Central Theories (Gate Control theory): Following destruction of sensory

neurons, WDR neurons are free from central inhibitory control. So self

128

sustaining neuronal activity occur in spinal cord neuron. If this exceeds the

critical level, pain occurs in phanthom limb

3. Psychological Theories (Characterization): Rigid, compulsive and self

reliant personalities are prone

Treatment:

Physical therapy: Conditioning of stump and preparation of prosthesis

Nerve stimulation: TENS, Acupuncture

Psychological:

Medical: Anti depressants, Anti convulsants

Nerve blocks: Trigger patient or direct stumping of LA, sympathetic blockade

(SMP), Intrathecal opioids

Surgical: Stump revision, Neuro Stimulation - Dorsal column, Neuroabalation

Stump Pain:

Signs and Symptoms: Pain may be spontaneous or as a result of pressure of

prosthesis. Sharp and Satabbing. Neuroma / Stitch abscess. Increase

Sympathetic activity

Causes:

Poor fitting Prosthesis

Ulceration / Blistering - infection

Bonespurs - Osteomyelits

Myofascial trigger points

Vascular insufficiency - DM

Treatment:

Local injuries and infection - prevention

Fitting prosthesis

Sympathetic blockade

TENS

Surgical removal

129

Signs and Symptoms of CRPS

Course of CRPS

Stage I

Acute /

hyperemic

Stage II

Dystrophic / ischemic

2 to 6 mo from onset

Stage III

Atrophic Stage > 6 mo after

the onset Permanent

Burning pain Moderate Severe Severe

Allodynia Moderate Severe Severe

Edema Severe Moderate Mild

Skin Temp Warm Cool Cold

Skin

Discoloration

Red Mildly cyanotic and pale Severely cyanotic and pale

Pseudomotor Mild Moderate Severe

Stiffness Mild Moderate Severe

Trophic changes None Mild to Moderate Severe

Sympathetic

block

Effective May be Ineffective

References:

1. John D.Loser, Steven H. Butler, C. Richard Chapman, Dennis C. Turki:

Bonica’s management of pain, 3rd edition, Lippincott 2001.

2. P.Prithivi Raj: Practical Management of Pain, 3rd edition, Masby 2000.

130

Fluid and Electrolyte Disorders

Fluid and electrolyte disturbances are more common in perioperative period and

in Intensive care units that can cause impairment of CNS, CVS and

neuromuscular functions.

Some common Terminologies in use

Mole: One mole of a substance is its atomic weight in grams.

Molarity: Molarity is the SI unit of concentration of a solution that gives the

number of solute per litre of solution.

Molality: Molality is the alternative form that gives number of moles of solute per

kilogram of solvent.

Eqivalency: Commonly used for substance that ionizes. Given by number of

moles multiplied by its changes.

Conversion of mEq/L to mg/dL:

MEq/L = (mg/dL x 10 x valancy) / atomic weight

Eg: For Na+ = 140 mEq/L valancy = 1

140 x 23 / 10 x 1 = 322 mg/dL

1 Osmole = 1 mole for nondissociatable solution. For dissociatable molecules like

NaCl, 1 mole produces 2 Osmoles of ionic species.

Osmosis: Movement of water across semi permeable membrane as a result of

difference in non diffusible solute concentration between 2 sides.

Osmotic pressure: Pressure on the side of more solute that prevents water from

moving down its concentration gradient. (1osmole exerts pressure of about

19.3mmHg/L) Osmotic pressure = osmolality X 19.3mmHg mosm/L/kg

Plasma Osmotic pressure and osmolality:

mosm/kg Osmotic pressure

Sodium chloride (140mEq/L) 280 5404

BUN (11.2mg/dl) 4 79

Glucose (108 mg/dl) 6 116

Proteins (7 g/dl) 1.2 23 (0.4%)

291.2 5620

131

Fluid Compartments

Distribution:

Compartments Body weight% TBW% Volume in L

Intracellular 36 60 25

Extracellular

Interstetial 19 32 13.5

Intravascular 5 8 3.5

Composition of fluid Compartments:

Components g/molwt In ICF In IV in IS

[Na+] mEq/L 23 10 145 142

[K+] mEq/L 39.1 140 4 4

[Ca++] mEq/L 40.1 <1 5 2.5

[Mg++] mEq/L 24.3 50 2 1.5

[Cl-] mEq/L 35.5 4 105 110

[HCO3-] mEq/L 61.0 10 24 28

Phosphate mEq/L 31.0 75 2 2

Protein g/dL 16 7 2

Interstetial fluid pressure is negative (-5mmHg)

As IS fluid volume increases pressure becomes positive and edema develop

Protein content is < 2 g/dl because small quantities cross the capillary cleft

and most of them are returned to vascular system by lymphatic

Most of the electrolytes can pass freely between plasma and interstitium

resulting in identical composition

So plasma proteins are only osmotically active solutes in fluid exchange

between plasma and interstitium called ONCOTIC pressure or colloid osmotic

pressure

Exchange of fluids:

Fluid exchange between the compartments is governed by osmotic forces due to

non diffusible solutes. So fluid moves from hypo osm hyper osm compartment.

132

Fluid exchange across the capillaries differs from cell membrane as they are

governed by hydrostatic pressure in addition to oncotic pressure.

Arterial end Venous end

Capillary hydrostatic pressure 30 Capillary hydrost atic pressure 10

Int hydrostatic pressure 5 Int hydrostatic pressu re 5

Int Oncotic Pressure 6 Int Oncotic Pressure 6

41 21

Disorders of water balance and sodium content:

Total body water at birth is 75% of body weight. By 1 month, the value decreases

to 65% and by adult it is 60% for males and 50% for females (due to increase in

fat content). Since obesity and old age have decrease in TBW.

Normal water balance:

Daily water intake - 2500ml

Water loss = 2500ml - (1500ml as urine, 400ml in respiration, 400ml in skin

evaporation, 400ml in sweat, 100ml in faces)

41-28=13 21-28= -7

Plasma Oncotic Pressure = 28mmHg

133

ECF volume is directly proportionate to total body sodium content. Since [Na+]

indicates change in water balance rather than in sodium content.

Relation between plasma Osmolality and sodium and T BW

Osmolality of ECF = sum of concentration of all dissolved solutes

Na+ and Cl- forms 90% of ECF solutes

Since plasma Osmolality = 2 X plasma conc of Na+ (2 [Na+])

As ICF and ECF are in equilibrium, plasma [Na+] generally reflects total body

osmolality

Total body Osmolality = (Extracellular solutes + Intracellular solutes)/TBW

In pathological states glucose and urea can contribute to Osmolality

Plasma Osmolality = 2 [Na+] + BUN/2.8 + glucose/18

= 280 + 11.2/2.8 + 108/18

= 290mosm/kg

Here plasma Na+ concentration decreases 1mEq/L for 62mg/dL increase of

glucose.

Factors Controlling Sodium Balance and ECF Volume

Volume Regulation Osmo Regulation

Purpose Control of ECF volume ECF osmolality

Mechanism Na+ excretion (Renal) Water intake

Water excretion (Renal)

Sensors in

intravascular

Aff Renal arterioles

Carotid Baro receptors (high)

Atrial stretch receptors (low)

Osmo Receptors in lateral

Hypothalamus (shrink of

cells with increase in Osm)

Effectors RAA system

ANP

ADH

Thirst

ADH

Because of these relationships between ECF volume and [Na+], regulation of one

is tied to another.

134

In the absence of renal disease, diuretic therapy, urinary Na+ concentration

reflects effective intravascular volume.

Urinary [Na+] < 10mEq/L decrease in IV volume and sec Na+ retention by

kidney.

Both ADH and aldosterone levels are elevated during anesthesia and

surgery, independent of circulating volume

Effective adaptation requires

Intact vasometer reflex arc (carotid baro receptors)

Intact kidneys

Adequate aldosterone and ADH

Various drugs, anesthetic procedures may impair these sympathetic and

humeroid mechanism for monitoring the integrity

For eg in trauma patients with hypo volumia may be normo tensive because

of increased sympathetic bone

During induction with thiopentone (5mg/kg) - venodilator - may cause fall in

BP and cardiac output

GA blunts the neuronal input to vasomotor centre and diminishes the efferent

vasoconstrictor signals

Causes of True Hypo Volumia Causes of Relative Hypo Volumia

Hemorrhage

Small bowel obstruction

Pyloric Stenosis

Intestinal obstruction

Renal Insufficiency

DI/DM

Burns

Long bones

Hemothorax / Hemoperitonium

Cirrhosis + Ascites

Hypertension on Diuretics

Patient on Anti hypertensives like Ca++ channel

blockers, ACE inhibitors, NTG, α methyl dopa

Spinal cord injury

Diabetic autonomic dysfunction

Sepsis

Cirrhosis liver (Liver failure)

Hypo / Hyper thyroid

Pregnancy (SHS)

Pheochomocytoma

Malignant hyperthermic

CCF / Cardiac tamponade

135

HyperNatremia and HyperOsmalility

Hyper Natremia is [Na+] > 145 mEq/L - causes are:

Loss of both Na +& H2O

H2O > Na+ (Low total body Na +)

Loss of water with normal

[Na+]

Increased Na + intake

(increased total body Na +)

Renal: ( Urinary

Osmolality<800mosm/kg)

Osmotic diuresis

Hyperglycemia

(For every 100mg/dL increase in

plasma glucose - [Na+] decreases by

1.6mEq/L)

Mannitol

High protein intake

Extrarenal: (Urinary

Osmolality>800mosm/kg)

Gastrointestinal

Osmotic diarrhoea

Insensible / sensible water loss

Insensible: prespiration practically

contains pure water occurs in both cold

and warm weather.

Sensible: or visible sweat occurs with

increased heat production is usually

hypotomic with NaCl of 30-70mEq/L

and with little of K+

Heat Cramps, Heat Exhaustion and

Heat Stroke

Treatment:

Replace isotonic fluid loss

Replace water deficit

1. Inadequate water intake in

comatose patients, old age

head injury and low thirst

2. Renal:

DI - central (low ADH)

Nephrogenic (low

response)

Essential hyper Na+

(reset osm receptors)

3. Extrarenal: Water loss

through lungs

Tracheostomy

hyperventilation

4. Burns

Treatment:

Replace water deficit with

5% D

[Na+] is decreased at a rate

of 0.5mEq/L/hr (If

decreased rapidly causes

cerebral edema)

Symptom and sign:

Loss of weight

Oligurea

Plasma osm> 340mosm/kg

Hct > 55%

1. Massive salt ingestion by

ryles tube feeding in ICU

2. 3% hypertonic saline

administration

3. Increased NaHCO3

therapy

4. Primary

hyperaldosteronism

5. Cushing’s syndrome

Treatment:

Replace water deficit

Loop diuretics to excrete

Na+ - [Na+] is low at rate

of 0.5mEq/L/hr

Symptom and sign:

Weight gain

Polyurea

Plasma Osm>340mos/kg

Hct = 45%

If polyurea occurs

SG - 1.010 - 1.030

Osm ≈ 250 - 300 mos/kg

136

Symptoms and sign:

Dehydrated / Oligurea plasma osm

increases > 300mosm/kg

Urinary Na+ > 20meq/L in Renal

In DI if polyurea occurs

urinary osm ≈50-150mEq/kg

SG < 1.005

Heat Cramps

Loss of water in athletes is due to increased sweat and evaporation from skin

with little of electrolyte loss

Manifests as spam of calf muscles and abdominal muscles

Treatment:

Removal from direct sunlight

Rest and ice packs to affected muscles

Replacement of water mainly

Prevention:

To take adequate water during strenuous exercises. Using so called athletic

drinks and sports beverages to replace loss causes increase in electrolytes and

sweatness that are hypertonic and are slowly absorbed from stomach producing

satiety and decreases water intake.

Heat Exhaustion

Due to loss of water and electrolytes causing decrease in ECF volume. Mainly

occurs in patients on diuretics or in patients with inadequate water intake in hot

climate.

Symptoms:

Weakness, visual disturbances, vertigo, headache, syncope, hyperventilation,

confusion, agitation, weak pulse, fall in BP and temperature may be normal or

elevated.

Treatment:

Removal from sunlight, rest, plenty of oral fluids. If patient is unconscious IVF is

necessary. (To replace electrolyte loss)

Heat Pyrexia (Heat Stroke) Rectal temperature > 42oC

This is of 2 types - Exertional and Non exertional

137

Exertional - in young people exposed to hot climate and deprived of salt and

water doing strenuous exercise, body is not able to dissipate heat produced. (In

obese persons, in persons with inadequate acclimatization to physical exertion)

Non exertional (Classic) - Occurs in older persons.

Eg. Patients with CCF on diuretics, alcoholics, malnourished, when exposed to

hot environment and deprived of salt and water.

Eg. Patients taking drugs that decrease sweating (AntiCh, AntiHist).

Eg. Patients taking drugs like antiparkinson, antipsychiatrics like halopindol have

decreased thirst sensation.

Symptom / Sign:

Patient complains of weakness, headache, dizziness, confusion, cramps,

deliruim, generalized conclusions and coma.

Rectal temperature > 41oC

Skin is hot, dry and ashen colored

Heart rate increases greater than 200/min

Rapid shallow respiration

ECG - non specific ST, T changes

Complications:

Acute renal failure due to Rhabdomyolysis (muscle protein breakdown in

exertional type)

DIC, Necrosis of levicells in non exertional type and abnormal LFT -

exertional type

Other electrolytes part from Hyper Na+ Hypo K+, Hypo Ra+, Hyper K+

Respiratory alkalosis Non exertional type - Hyperventilation

Lactic acidosis in exertional type.

Treatment:

If rectal temperature > 41oC ice water tub bath until temperature is down to

38.8oC when the active cooling should be stopped

IVFluids is determined by other electrolyte abnormalities

Stabilize cooling by air conditioned room

138

IVF fluids should not be used until temperature is lowered because there is

vasodilation at higher temperature and on cooling there is vasoconstriction

If patient is in state of shock - (due to profound peripheral pooling) - Inject

Dopamine/ Isoprotrenol can be used as infusion and adrenergic

vasoconstriction decreases heat dissipation, so should not be used if

temperature is high.

In ARF - dialysis

Diabetic Insipidus

Characterized by marked impairment of renal concentrating ability due to

decreased ADH (Central DI) or failure of renal tubula to respond normally to

ADH. (Nephrogenic)

Central DI:

Lesions in and around hypothalamus / pituitary stalk following neurosurgical

procedures and head injuries

H/O polyurea > 6 litres/ days , polydypsea in absence of hyperglycemia and

compulsive water drinking (where S.Na+ is less than normal)

In pre op / post op

If polyurea without glycosurea (> 200 to 300ml/hr)

Urinary Osm < plasma osm

SG - 1.003 to 1.005

In head injury and ICU patients, absence of thirst leads to hypovolumia

Confirmed by increase in urine osm following administration of aqueous

vasopressin 5 units sc 4th hourly.

Treatment:

Vasopressin in oil 0.3ml 1M/day - long lasting but likely to cause water

intoxication

Desmopressin - Synthetic analogue of ADH with 12 to 24 hrs duration

Available as transnasal preparation 5 to 10mcg

139

Nephrogenic DI

1. Congenital

2. Secondary to other causes:

CRF/ Electrolyte disorders Hypo K+, Hypo Ca++

Sickle cell disease

Hyperprotenemias

3. Drugs:

Amphotericin B

Methoxyflurane

Demeclocycline

Mannitol

Confirmed by failure of increase in urine Osm following administration of

Exogenous ADH.

Treatment:

Treat the underlying disorder

Replace water deficit with 5% Dextrose

Chlorpropamide - OHA potentiates ADH effect on renal tubules

Clinical Manifestation of HyperNatremia

Neurologic manifestation predominates due to cellular dehydration,

restlessness, irritability, lethargy, hyperreflexia, seizures, coma

Symptoms correlate more closely with rate of movement of water out of brain

cells

Rapid decrease of brain volume can cause rupture of cerebral veins and

result in focal intracerebral or subarachnoid hemorrhage

Chronic hyper Na+ are better tolerated than acute

Clinical manifestation of total body water deficit reflects loss of fluid from all body

compartments.

Skin

Dry mucous membrane

Loss of skin turgor

140

CVS

Decrease in Bp increases pulse rate - severe dehydration

Peripheral cyanosis due to sluggish circulation

CNS

CNS dysfunction

Renal

BUN / S. creat increases cardiac output decreases and BP causes

decrease in GFR

Hct remains the same

Calculating water deficit:

Total body water deficit can be calculated if hyper Natremia is considered purely

due to water loss

Normal TBW X 140 mEq/L = present TBW X Plasma [Na+]

If plasma [Na+] = 160mEq/L is a 70kg adult

70 X 0.6 X 140 = x X 160

x = 70 X 0.6 X 140 / 160 = 36.7L

So TBW deficit = 42 - 36.7 = 5.3litres

5300ml over 48hrs ≈ 110ml/hr corrected by D5%

This formula excludes other isotonic fluid deficits.

Anesthetic Consideration for hyper Na +

Increase in MAC of inhalational agents

141

Hypovolumia accentuates vasodilatation or cardiac depression by anesthetic

agents

Decrease in Vd for the drugs given IV necessitates reduction of dose while fall

in cardiac output enhances uptake of inhalational agents

Elective surgery should be postponed in significant hyper Na+ (>150mEq/L)

until established cause of fluid deficit is corrected

HypoNatremia and HypoOsmolality:

Hypo Natremia is [Na+] < 135mEq/L

Rarely hyponatremia does not reflect hypo - Osmolality (Pseudo hyponatremia

causes of pseudohyponatremia)

With normal plasma Osmolality:

1. Asymptomatic

Marked hyperlipedimia

Marked Hyperprotenemia

2. Symptomatic

TURP - Irrigation fluid absorption

With elevated Osmolality:

Hyperglycemia

Maximal administration

142

HypoNatremia

Water and Na loss Water Excess Syndrome Sodium Exce ss

Decrease in ECF volume

Water loss < Na+ loss

Renal:

1. Diuretics

2. Salt loosing

Nephropathies

3. Renal Tubular acidosis

4. After Transplant

5. Polyuric ARF

Extra Renal:

CNS: Salt washing

syndrome

GIT:

Diarrhoea (VC) vomiting

Surgical and 3rd space loss

Fistulas

Burns - more in wet burns

and scalds

Normal increase in ECF

volume

Normal Na+ content

No edema

1. SIADH

2. Adernocortical (insufficiency

with patients on long term

steroids)

3. Myopathysoidism

4. Drug induced

Chlorpropamide

Carbamzapine

Cyclophosphomide

Vircristine

Increase in

ECF volume

1. CCF

2. Cirrhosis

3. Nephrotic

Syndrome

4. Renal failure

Diagnosis and Treatment

Renal:

Urinary Na+ > 20 mEq/L

Extra Renal:

Urinary Na < 10mEq/L

Replace isotonic deficit

Replace Na+ deficit

In 1

SIADH UNa > 20mEq/L

Restrict water Hypertonic saline

In 2 & 3 - Cortisol or Thyroid

hormone

In 1,2 & 3

UNa < 20mEq/L

Restrict H2O

Loop diuretics

In 4

UNa > 20mg/kg

Restrict water

143

Increased ADH

Increased Na+ loss through kidneys (increased Uosm)

Increased ANP (atrial stretch receptors) and decreased aldosterone secretion

Increased ECF volume Water Retention (decreased Plasma osm)

Syndrome of Inappropriate ADH secretion

Causes:

CNS disorders:

Head injuries, Hypopituitarism, SAH, Encephalitis, Brain abscess, Gulhain bane

syndrome, ECT therapy

Stress:

Fear, pain, surgery

Drugs:

Chlorpropanide, Tolbutamide/OHA, Tricyclic antidepressants, Anti psychiatrics,

Anesthetic drugs - morphine and mepredine, oxytocin

Malignancy:

Oat cell Ca, Erwing’s Sarcoma, Ca Pancreas

Inflammatory:

Tuberculosis, status asthmaticus

Pathophysiology

Inappropriate or Excess secretion of ADH:

Diagnosis:

Rule out Addisons disease, Hypothyroid, Hypopituitarism

Urine Na+ > 40mEq/L despite HypoNatremia

Urinary Osm > Plasma Osm (except if Na+ intake is low)

Normal renal function test

Absence of dehydration, hypotension (signs of hypovolumia)

Absence of clinical edema

Improvement in clinical condition with fluid restriction

144

Treatment:

Hypertonic saline 5% or 3% can be used (severe cases [Na+] < 110mEq/ L)

1 meq/L of Na+ = I ml of 5% NaCl and 1 meq/L of Na+ = 6 ml of 0.9% NaCl

S [Na+] should not be raised rapidly (> than 0.5mEq/L/hr) should be

discontinued when S [Na+] = 125mEq/L

Loop diuretics enhances water excretion and to prevent latrogenic salt

overload in extreme cases

If lesser symptoms are present, restrict water intake (<500ml/day) and

increases salt in diet

Surgical resection of malignant tumors (oat cell ca)

Drug therapy:

Phenytoin - inhibits ADH secretion

Demeclocyclin - Interfere with renal action of ADH (takes several days for

effect to be noted clinically).

Clinical manifestation of HypoNatremia

Primarily neurological - due to increase in Intracellular water. Severity

depends on rapidly developing hypo osmolality

Patients with Na+ > 125mEq/L are asymptomatic

Early symptoms are Anorexia, nausea, vomiting, weakness, headache,

fatigability, general sense of exhaustion

CNS - Progressive Cerebral edema - seizures - coma

Serious manifestations with plasma [Na+] < 120mEq/hr

In chronic hyponatremia, compensatory loss of Intracellular solute restore cell

volume to normal

Treatment of HypoNatremia:

Acute symptomatic hyponatremia should be treated promptly.In such cases [Na+]

upto 130mEq/L is usually sufficient to allivate symptoms.

Calculation of Na + deficit:

Na+ deficit = TBW X (Desired [Na+] - Present [Na+])

For eg: 80 kg female with [Na+] of 118 TBW = 50% of 80 kg

[Na+] deficit = 80 X 0.5 X (130 - 118) = 480mEq/L

145

0.9% NaCl contains 154mEq/L.

So patient should receive 480/154 = 3.12 litres of 0.9% NS.

For correction at the rate of 0.5meq/L/hr saline should be administered over 24

hrs (3120/24) = 130ml/hr.

Very rapid correction is associated with demyelination of pons.

Cerebellopontine Myelinolysis - leading to permanent neurological damage.

So rapidity with which Hypo Na+ to be corrected are

Mild symptoms 0.5mEq/L/hr

Moderate 1 mEq/L/hr

Severe 1.5 mEq/L/hr

Hypertonic saline - For more rapid correction in patients who are markedly

symptomatic with plasma Na+ <110mEq/L and must be given cautiously as it

cause pulmonary edema.

Anesthetic Implications:

Plasma [Na+] > 130mEq/L - Safe for patients for GA - for all elective procedures

even in the absence of symptoms

Hypertonic Fluids

Advantages Disadvantages

Hypertonic Crystalloids

Inexpensive Hypertonicity

Promotes urinary flow Ppt of SDH

Requires small initial volume Transient effect (30 to 60 min)

Improved myocardial contractility

Reduced Peripheral edema

Lower ICP (BBB permeable to Na+)

Arteriolar Dilatation

Hypertonic Crystalloid + Colloid

More sustained hemodynamic response Expensive

Reduced subsequent volume requirements Complications of colloids

146

Characteristics of Colloids

Colloid Composition Concenta

-tion %

Mol wt KD % Intra

Vascular

Colloid Osm

pressure(mmHg)

I.V ½ life

(hrs)

Albumin Albumin 5 69 80 20 >24

Dextran 70 Polysacchride 6 70 (20-175) 100 40 6 -12

Dextran 40 Polysacchride 10 40 (15-75) 100 2-3

HES Amylopectin 6 450 100 30 > 24

Pentastarch 10 264 100 40 10

Advantages and Disadvantages of colloid / crystallo id fluids

Solution Advantage Disadvantage

Colloid Smaller infused volume Expensive

Prolonged increase in Plasma

volume

Coagulopathy (Dex > Hes)

Minimal peripheral /

pulmonary edema

Pulmonary edema in capillary leak

state like burns, trauma, ARDS

Higher oxygen delivery Low Ca2+

Lowers ICP as BBB is

impermeable

Low GFR

Osmotic Diuresis (Dex 40)

Crystalloid Less expensive Short lived hemodynamic

improvement

Greater Urinary flow Large quantities cause pulmonary

edema

Replaces 3rd space loss Dilutional hypoNa+ (D5)

147

Flu

ids

Glu

cose

g/dl

Sod

ium

mE

q/L

Chl

orid

e

mE

q/L

P

otas

sium

mE

q/L

Cal

cium

mE

q/L

Mag

nesi

um

mE

q/L

Bicarbonate

mEq/L as

lactate or

Citrate Pho

spha

te

mE

q/L

Ace

tate

mE

q/L

Osm

olal

ity

PH

D5W 50 - - - - - - - - 252 4.5

D10W 100 - - - - - - - - 505 -

D5RL 50 130 109 4 - - 28 - - 525 5.0

RL 130 109 4 3 0 28 - - 273 6.5

0.9 NaCl 154 154 - - - - - - 308 6.0

0.45

NaCl

77 77 - - - - - - 154 -

0.33

NaCl +

D5W

50 56 56 - - - - - - 365 -

Isolyte E 140 103 10 5 3 8 (as citrate) - 47 320 -

Iso P 50 25 22 20 - 3 - 3 23 375 -

Iso M 50 40 35 40 - - - 15 20 425 -

3% NaCl 513 513 - - - - - - 1026 -

5% NaCl 855 855 - - - - - - 1710 -

6% HES 154 154 - - - - - - 310 5.9

0.5% alb

+0.9%

NaCl

154 154 - - - - - - 330 7.4

25% alb 154 154 - - - - - - 330 7.4

10%

dexran40

50 - - - - - - 255 4.0

148

Disorders of Potassium Balance

Normal K + Balance:

Dietry intake averages 80 mEq/day in adults (40 to 140 mEq/day)

Renal excretion varies between 5 and 100 mEq/day

All potassium filtered through glomeruli is normally reabsorbed in PCT and

loop of Henle. So K+ excreted is the result of DCT secretion and due to

aldosterone action on CT

A fall in Serum.K+ from 4mEq/L represents 100mEq/L to 200mEq/L deficit of

total body K+ while fall of K+ below 3mEq/L represent deficit of 200 to

400mEq/L

Hypokalemia:

Defined as plasma K+ less than 3.5mEq/L

Inter Compartmental shift cell Increased K + loss Decreased K + Intake

1. Alkalosis (ECF ICF)

2. H ↔K K+ conc changes

0.6mEq/L/0.1 unit change in

PH (0.2 - 1.2)

3. Circulating insulin -

enhanced Na+ K+ at pase

(Liver and skeleton muscle)

4. Sympathetic Stimulation

Enhancing Na+ K+ ATPase

β2 agonist and α2 agonist

5. Hypothermia - increased

uptake

6. Familial periodic paralysis

HypoK+ variant

7. Treatment of Megaloblastic

anaemia

8. Transfusion of frozen red

cells

Renal:

1. Diuretics

2. Increased

MinaraloCorticorcoid

activity

1o hyper aldosteronism

2o hyper aldosteronism

- Renin Sec tumor

- Reno Vascular HT

Minaralo Corticoid tumor

Cong adrenal Hyperplasia

Increased GlucoCorticoid

excess (17α and 11β

hyroxylase)

3. Renal Tubular acidosis

4. Ketoacidosis

5. Salt wahing Nephropathis

6. Hypo mg2+

Because of enormous

ability of kidney to

reabsorb K+, this

occurs only at very low

intake of K+ coupled

with increased loss.

149

7. Urinary diversion with ileal

loop

8. Amphotericin β therapy

Extra Renal:

GI:

Diarrhoea- villousadenoma

Vomiting/ryles tube

suctioning

Laxative abuse

Fistulas

Uterosigmoidostomy

Skin:

Sweat with decreased intake.

Dialysis with decreased K+

dialysate

Uremia acidosis Low

intracellular K+ On dialysis

hypo K+

Uk+ < 20mEq/L - Extra Renal

> 20mEq/L - Renal

wasting

Clinical effects of hypokalemia: Most patients are asymptomatic till 3mEq/L

CardioVascular:

ECG changes -primarily due to delayed ventricular repolarization - in the

order of T wave inversion or flat, prominent U waves, decreased ST,

Increased P amplitude, prolonged PR

150

Dysrhythmias - Increased automaticity and delayed repolarization

Myocardial fibrosis

Causes autonomic dysfunction and so labile BP

Neuromuscular: < 2.5mEq/L

Skeletal muscle weakness (Quadriceps)

Ileus

Rhabdomyolysis

Tetany and muscle cramping

Renal:

Impaired concentrating ability - resistant to ADH and polyurea

Sodium retention and increased HCO3- absorption - alkalosis

Increased production of ammonia result in impairment of urinary

acidification.Increased ammonia production is due to intracellular acidosis. As

K+ is lost in urine, H+ moves into cells

Met - alkalosis and ammonia increases causing encephalopathy in patients

with advanced liver disease

Hormonal:

Hypo K+ impairs Insular secretion and antagonizes its peripheral effects

leading to hyperglycemia even in non diabetics

Decrease in GH secretion and decrease in Aldosterone secretion

Metabolic:

Negative nitrogen balance - altered protein metabolism during chronic hypo K+

Treatment of Hypokalemia:

Depends on severity and presence of any associated organ dysfunction

ECG monitoring is mandatory

Muscle strength should be assessed in patients with weakness

Oral replacement is generally safe - 60 to 80mEq/day - patients on Digoxin +

diuretics - Replacement take several days.

151

IV therapy:

Goal is to move the patient from immediate danger and not to correct the

entire K+ deficit

Peripheral IV replacement should not exceed 8mEq/hr as it is irritative

Dextrose containing solutions should be avoided due to further lowering of K+

Faster IV replacement requires central venous catheter (10-20mEq/hr)

Much higher replacement will be safe through femoral vein as very high

localized K+ concentration may occur within the heart with standard up should

not exceed 240mEq/day

Availability:

Available as potassium chloride 10mldrugs with 20mEq/10ml for IV

Oral - potassium chloride - tablets syrups causes gastritis

Usually KCl is preferred in alkalosis (met) because Cl- deficit is also corrected

potassium acetate/ citrate producing bicarbonate is used for met acidosis

potassium phosphate for patients with hypophosphotemia in DKA.

Anesthetic Consideration:

Preoperative: Elective surgery should be postponed if K+ < 3mEq/L.

In general mild hypokalemia (3 to 3.5mEq/L) without ECG changes does not

cause any anesthetic risk except in patients on Digoxin in whom K+ values < 4 is

not desirable.

Intraoperative: It requires ECG, neuromuscular monitoring

Glucose free solutions should be given

KCl - IV to be given with NS diluted to 50 times its volume

Avoid hyperventilation

Dose of muscle relaxants to be reduced by 25 to 50%

Hyperkalemia

Plasma [K+] > 5.5mEq/L

Rearely occurs in normal individual because of kidney’s tremendous capacity

to excrete K+. (upto 500mEq/day)

Causes of Pseudohyperkalemia :

Invitro red cell lysis - prolonged tourniquet application

152

Marked leukocytosis - if WBC > 70,000 cells/NL - Release of K+

Marked thrombocytosis platelets > 10,00,000/NL - Release of K+

Inter Compartmental shift Decreased Renal Excretion Increased K + intake

ICF ECF

1. Acidosis

H+ ICF

ECF K+

2. Hyper Osmolality “Solvent

drag” - Increased Na+,

Increased Glucose,

mannitol

3. Succinylcholine - Increased

K+ by 0.5mEq/L/50mg in

burns/trauma/spinal cord

injuries

4. Tissue breakdown

Chemotherapy

Rhabdomyolysis

Severe exercise

5. β blockers/over dosage of

Digoxin

6. Arginine HCl used for

Alkalosis

Arg ↔ K+

7. Hyper K+ variant of periodic

paralysis

Renal Failure:

1. Decrease in GFR < 5ml/min

2. Decreased Aldo sterone

3. Decreased K+ secretion in

DCT

Decreased Minaralo

Corticoid Activity:

Pri Adrenal insufficiency

- Addison’s disease

- B/L Adrenelectomy

Cong Adrenal Hyperplasia

(21 Hydroxylase decreases)

HypoReninemic

Hypoaldosteronism (Type

IV RTA) DM + Renal

impairment

Competitive K+ sparing

diuretic - spironalactone

ACE inhibitors

NSAID - PG - Renin

Heparin - Increased in large

dose

Decreased K+ Secretion in

DCT:

Pseudo hypoaldosteronism

Non competitive K+ sparing

diuretics - Amiloride

(30mEq in 21 day)

1. Transfusion of old

whole blood

2. Iatrogenic K+ load

3. Increased fruit

drinks with high K+

content

4. PRBC can be used

to prevent / reduce

hyper K+ with whole

blood multiple

transfusion

153

Triamterine

Sickle cell disease

SLE

Obstructive Uropathy

Cyclosporine nephropathy

in transplanted kidney

Clinical manifestation of Hyperkalemia:

Skeletal Muscle: Weakness is not seen until [K+] > 8mEq/L causes

hyperpolarization and inactivation of sodium channels of muscle membrane

(similar to suxa) resulting in ascending paralysis.

Cardiac:

ECG findings is in the order of

1. Symmetrically peaked T waves (with short QT interval) - 6 or 7mEq/L

2. Widening of QRS complex - < 8mEq/L

3. prolonged PR interval - < 8mEq/L

4. Loss of P wave - lies between 8mEq/L and 9mEq/L

5. Loss of R amplitude - < 9mEq/L

6. ST increases or decreases - < 9mEq/L

7. Sine wave - < 9mEq/L

8. VF or Asystole (in diastole) - 10mEq/L

Presence of peaked T waves is not itself pathognomonic sign of increased K+ as

it can occur with MI, Intracranial hemorrhage, and cardiac tamponade.

Treatment of Hyperlkalemia:

S [K+] > 6mEq/L should be treated.

154

Goal of therapy:

Reversing cardiac manifestation - emergency

Skeletal muscle weakness

Restoring [K+] to normal

Emergency treatment:

Hypertonic Dextrose (25%) + 1 unit of regular insulin per 4 to 5g dextrose in

central vein. Takes ½ to 1 hr for peak effect and S.[K+] remains lowered for 4

to 6 hrs.Risk: hypertonic Dextrose causes endogenous insulin secretion and

stopping suddenly causes hypoglycemia.

Calciumgluconate (5 to 10ml of 10% solu) - IV

Calciumchloride (3 to 5ml of 10% solu)

a. Here the serum K+ conc remains unchanged

b. ECG signs of increased K+ disappears - indication for stopping calcium

c. Contrandicated in hyper K+ patients receiving Digoxin - Potentiates

Toxicity

Hypertonic (7.5%) NaHCO3 - most likely in patients with metabolic

acidosis/CRF with in 15 minutes

β agonist - Increased cellular uptake - useful in massive transfusions

Eg: Low dose of epiniphrine (0.5 to 2mcg/min)

Hemodialysis or peritoneal dialysis in refractory Hyper K+ .

Hemodialysis is faster and more effective - 50mEq/hr can be removed

when compared to 10 to 15mEq/hr through peritoneal dialysis.

Non Emergency Treatment:

A sodium polystyrene sulfonate (Kayexalate) Resin - removes K+ from color.

Given orally or rectally.

Each gram of resin binds 1mEq of k+ and releases 1.5mEq of Na.

Na+ in resin is replaced by K+ and is excreted through faces.

Oral Dose:

20-30g in 100ml of 20% sorbitol

1 to 4 times daily sorbitol causes mild diarrhea

Rectal dose:

155

30g in 200ml of water or 10% Dextrose

Enema should be at body temperature - retained for 4 to 10hrs

Not as effective as oral administration

Disorders of Magnesium

Magnesium is basically an intracellular cation most abundant next to

potassium

Responsible for activation of over 300 enzymes in the body including those of

TCA cycle in ATP production

Involved in production of DNA, RNA and protein synthesis

It is physiologically calcium antagonist

Uptake of calcium by sarcoplasmic Reticulum is highly Mg++ dependent and

thus Mg++ deficiency predispose to intracellular Ca++ overload.

Mg++ also activates Na+/K+ ATPase pump and blocks the K+ efflux from the

cell by blocking specific K+ channels

Average intake by adult - 20 to 30mEq/day (240 to 370mg/day) ½ of Mg++

concentration is present in bones and 20% in skeletal muscle and only 1% is

extracellular. (Plasma) protein bound.

Renal excretion is 120 to 150mg/day in patients with normal diet. Reabsorbed

in PCT (25%) and Asc loop of henle (50 - 60%)

Determined by fluctuations in calcium, total inorganic phosphorus, Alkalosis

and Acidosis

Normal Plasma concentration - 1.5 to 2.1mEq/L (1.7 to 2.4mg/dl)

Hyper Magnesaemia: > 2.5mEq/L

Increased intake MgSO4 therapy Mg++ antacids and laxatives

Decreased excretion CRF where GFR < 30ml/hr

Hypothroid

Lithium

Clinical manifestation of Hyper Mg ++

Central Nervous System:

Causes depression of CNS and sedation - NMDA glutamate receptor antagonism

- causing 60% reduction of MAC.

156

But Mg2+ penetrates BBB poorly and its level in CSF is controlled by active

transport and so when given IV - no major CNS depression is noticed.

Controversy exists in eclamptic patients about the anticonvulsant action of Mg++

Alternative explanation for Anticonvulsant action - cerebral vasodilator action -

reverses the cerebral vasospam thought to be the principal cause of convulsions

in PET.

Neuromuscular Junction:

Antagonism with Ca2+ presynaptically - inpains Ach release (5mmol/L)

Potentiates and prolongs the action of even the shortest acting muscle

relaxants. Nondepolarising relaxants must be reduced in doses and increased

in dosing intervals in hyper Mg++ patients. (Nerve stimulator) Calcium may be

used in reversing motor functions

Mg++ does not decrease the onset time of NDMR. Prolongation of action of

Suxa in PET patients is not due to Mg++ but due to reduced cholinesterase

Acute hyper magnesia does not affect the duration of single dose of

Suxamethonium

Patients treated with MgSO4 do not demonstrate fasciculations and

administration of MgSO4 prior to use of Suxamethonium appears to prevent

potassium release (Can be used in risk of increased K+)

Mg++ may also reduce the incidence and severity of Suxamethonium induced

muscle pains

Can precipitate severe muscular weakness in patients with Myasthenia

Gravis and Eaton-Lambert syndrome

Does not affect the duration of single dose of suxa n obstetrics patients

Patient treated with MgSO4 does not show fasciculation to suxa and increase

in K+ efflux due to suxa is also suppressed

Autonomic Nervous System:

At S.conc > 5.0mEq/L causes progressive inhibition of catecholamine secretion

from Adrenergic terminals. It can be used for preventing Intubation response,

phechromocytoma causes ganglion blockade at increased levels.

Cardiovascular:

157

Vascular: Decreases vascular tone by

Direct action on smooth muscles by inhibiting Ca2+ and as α antagonist

Inhibition of catachotamine secretion

Causes vasodilation - decrease in PVR

Cardiac:

As Ca2+ antagonist, theoretically it should produce decrease in contractility

In intact subjects decreases in PVR offsets any decrease in contractility

Evidence of cardiac depression is very minimal

Doesn’t impair the cardiotonic action of Adrenaline even at concentration

causing catecholamine suppression

Variable and unpredictable action on HR

Expected to cause bradycardia but causes tachycardia

Inhibits Ach release by vugus and decresed PVR

At higher conc > 5mEq/L - AV conduction is slowed

Antiarrythmic property -

a. Treatment of VT, VF, Digitoxicity, MI, Hypo K+, Multifocal atrial

Tachycardia

b. Arrythmias due to Adrenalin and Bupivacaine

Respiratory System:

No central respiratory depression but due to neuromuscular blockade

Effective bronchodilator in patients with β2 agonist induced arrythmias

Inhibits histamine release from mast cells

Ach release from nerves

Treatment:

Stop the infusion/oral intake

IV Calcium gluconate 3 - 5ml of 10% solution

Loop diuretics with NaCl 0.5% in 5% D - infusion with increase or decrease

(0.9% NaCl is not used as it causes hypocalcemia)

Fluid loading

Dialysis

Anesthetic management:

158

Acidosis and dehydration should be prevented

Patient should be ventilated mechanically if there is hypoventilation

Hypoxia and Hypercartia:

Monitors: ETCO2 / SaO2 / ABG / ECG / Urine output and neuromuscular

monitoring

Cardiac depression and hypotension of anesthetic agents is potentiated

Hypomagnesemia: < 1.5meq/L

Causes:

Inadequate Intake Increased GI

absorption

Increased Renal

loss

Multifactorial

Nutritional

(Prolonged fasting)

Patient on TPN

Malabsorption

syndrome

Post Surgical

Inflamatory Bowel

disease

Small Bowel / Biliary

fistulas

Prolonged NG suction

Severe diarrhoea

Diuretics

Hyperglycemia

Diuretics

DKA

Hyperparathyroid

Hyperaldosteronism

Drugs

Cisplatinum

Alcohol

Aminoglycosides

Post obstructive

diuretics

Ch.

Alcoholism

PCM

Hyperthyroid

Pancreatites

Burns

Diagnosis:

Severe Hypoalbunemia should be excluded as 30% of serum Mg2+ content is

protein bound

Better determined in serum rather than plasma, as anticoagulants may

interfere with esturation

Always associated with K+, Ca++ deficiency

Clinical Manifestation of Hypomagnesemia

CardioVascular:

159

ECG changes are non specified - Widening QRS and peaked T waves. In

severe prolonged PR and QT - Reflects Hypo Ca++

Development of arrhythmias - both SVT and ventricular are seen

Myocardium is extremely sensitive to all arrythmias, especially those with

digitalis and catacholamines. Probably through its actions in determining Na+,

K+ and Ca2+ fluxes.

Digoxin induced arrythmias and Tosedes de pontis responds well to Mg++

therapy

Central Nervous System:

Personality and psychiatric manifestations have been described like

depression, agitation, confusion, anxiety and delirium

Seizures are seen but infrequent

Mg++ deficiency may contribute to the seizures of alcohol withdrawal

Neuromuscular:

Competes with calcium in excitation - Contraction coupling

Mg++ deficiency may produce frank Tetany and Chvostik’s and Trousseau’s

sign

Muscle weakness and Hyporeflexia -respiratory depression interferes with

weaning of the patient

Treatment (MgSO4 therapy):

In 50% solution (1g of MgSO4 = 4 mmol of Mg++ or 8mEq)

Patient at risk are persistant Hypo K+, Hypo Ca, significant arrhythmias

Parental way is the only way to achieve increase in S.Mg++ levels

Vd of Mg2+ = ECF. So loading dose of approximately 16mmol (4g of MgSO4)

required to raise plasma concentration by 1mmol/L

IV: 4g IV followed by infusion of 15 to 30mg/kg/hr (Emergency cases)

IM: 1% solution 10ml of 50% MgSO4 + 490ml of 5%DW . 5gm in MgSO4

followed by 2.5gm every 4th hourly for 48 hours (MgSO4 therapy in PET) (4ml

of 50% solution = 2gm) painful

Comes in

50% solution - 2ml ampules - each ml = 500mg (2ml = 1g)

160

25% solution - 2ml ampules - each ml = 250mg (2ml = 1/2 g)

Anesthetic Management:

No specific anesthetic interactions are described

Coexistant electrolytes disorders to be corrected

Isolated Mg++ deficiency should be corrected before elective procedures

161

Disorders of Calcium

Normal Ca2+ Balance: 98% of Ca2+ is in bones - ECF cations

Involved in all biologically important functions - muscle contraction, Release

of neurotransmitters and harmones, blood coagulation

Ca++ intake in adults is 600-800mg/day, requirement is 0.65gm of elemental

Ca++/day

Renal excretion - 50 to 300mg/day - 98% filtered Ca++ is reabsorbed. Ca2+

reabsorption parallels sodium reabsorption in PCT and loop of Henle

Reabsorption is augmented in DCT by PTH

Significance of S.Calcium Concentration:

Normal plasma Ca++ concentration = 8.5 to 10.5mg/dl (4.5mEq/L) in which 50 to

75% is in the ionized form and 40% is protein bound to albumin. 10% is

complexed to citrate and Amino acids.

Free Ionised calcium that is physiologically more important concentration of free

ionized Ca++ is 4.5 to 5mg/dl can be measured using special Ca++ ion electrodes.

Relation with S.Albumin: (% of Protein bound Ca+=0.8 X alb + 0.2 globulin + 3)

Increase or decrease of S.alb by 1g/dl [above normal (4 to 5g/dl)] is associated

with increase or decrease of S.Ca++ by 0.8mg/dl (1mg/dl) increase in S.alb

more of Ca++ becomes bound to it decrease in ionized Ca++ symptoms of

Hypo Ca++.

Changes in PH: affects the degree of protein binding and thus ionized calcium

concentration.

Ionized Ca++ increases 0.16mg/dl for 0.1 unit decrease in PH

Alkalosis Decreases ionized calcium Tetany

Acidosis Increases ionized calcium No tetany

Regulation of ECF [Ca ++] concentration:

Parathyroid harmones

a. Increases reabsorption from bones, Renal tubules (DCT)

b. Increases Phosphate excretion - enhances Vitamin D3 action

162

Vitamin D3

a. Increases Interstinal reabsorption of Ca++

b. PO4- excretion by kidneys = facilitates PTH action

Calcitonin

a. Decreases S.Ca++ level by inhibiting bone reabsorption

b. Increases urinary excretion

Hypocalcemia < 8mg/dl (4.0mEq/L)

Calculated on the basis of plasma ionized Ca++ concentration

When not available total Ca++ concentration is corrected for decrease in

plasma albumin (approximately 1mg/dl is added to S.Ca++ for every g/dl

decrease of S.protein < 4g/dl)

Hypopara thyroid Vitamin D Defeciency Ppt of Ca ++ Chelation of Ca +

1. Surgical (Thyroid)

2. Idiopathic (adreno

Cortical insuffeciency or

Perineceous anemia)

3. MEN disease

(Medullary thyroid)

4. Hypo Mg2+ (Prevent

PTH action on bone)

5. Sepsis

6. Burns

Pseudo Hypoparathyroid

Genetic lack of response of

renal tubules to PTH.

Pseudo Pseudo

Hypoparathyroid

Similar to above but S.Ca++

Nutritional

Malabsorption

Post Surgical

Inflamatory Bowel

disease

Ch pancreatitis

Altered Vitamin D

metabolism

Renal insufficiency

Hepatic failure

Drugs - Phenytoin,

Phenobarbitone

(Interferes with OH

of vitamin D3)

Hyper Phosphatemia

Chronic Renal

Pancreatitis

Rhahdoncyolysis

Fat embolism

Multiple Transfusion

Liver disease

Hypothermic

Rapid large

volume of

albumin

Less Common

Causes:

Calcitonin

secreting tumor

Osteoblastic

metastasis of

breast, prostate

Heparin,

protamine and

glucagon

Cholecalciferol 250H CHF (Liver)

1, 25, Dihydroxy CHF (Calcitriol) (Renal)

163

and PO4- are normal failure

Acute

lymphoblastic

Leukaemia (after

chemotherapy)

Loop diuretics

Clinical Manifestations:

Most characteristic sign of Hypo Ca++ -tetany (<7mg/dl). Also due to increase

in PH (Alkalosis). Does not appear in metabolic acidosis due to CRF even in

decreased Ca++

Carpopedal spasm, Trousseau’s sign, Chvostek’s sign

Parasthesia, convulsions and laryngeal spasm

Cardiac irritability - arrythmias

Decreased Cardiac contractility

Decreased response to Digitalis and β-agonists by myocardium

ECG prolonged QT (does not necessarily correlate with decreased Ca++

severity)

Mental changes - emotional depression, confusion hallucination and delirium

Treatment of Hypocalcemia:

Tetany - Lowering the PH if alkalosis is present or if Ca++ is low

Calcium gluconate 10 to 20ml of 10% solution given IV slowly not exceeding

the rate of 2ml/min. If not responding may be due to decreased Mg2+

Symptomatic hypo Ca++ is medical emergency treated with IV CaCl2 (3 to 5ml

of 10% solution) or Calcium Gluconate (10-20ml of 10% solution)

10ml of 10% CaCl2 272mg of Ca2+per ml

10ml of 10% Caglu 93mg of Ca2+ per ml

Continuous infusion of (Ca++ - 1 to 2mg/kg/hr) may be given

Oral salts of calcium -

Calcium Lactate - 13% Ca++

Calcium Gluconate - 9% Ca++

Calcium Carbonate - 40% Ca++ Gastric CO2 formation

164

Vitamin D replacement should be considered

Thiazide diuretics - increases S.Ca++ concentration

Anesthetic Implications:

Alkalosis should be avoided

IV calcium followed by rapid and massive blood transfusion > 50ml/70kg/min

There may be potentiation of negative ionotropic effects of anesthetic drugs

Response to muscle relaxant is inconsistent and requires neuromuscular

monitoring

HyperCalcemia: (> 11mg/dl)

Causes:

Hyperparathyroidism Malignancy

Primary and secondary (CRF, maln)

Tertiary (autonomus PTH)

Excessive Vitamin D/A intake (> 50,000 IV/day for

several days)

Pagets disease of bone

Prolonged inmoblization

Drug induced:

Thiazides, Lithium, Oral Iso trenitoin for Acne

Skeletal metastasis

Multiple myeloma

Sarcordosis/TB

Lymphomas

165

Clinical Manifestation of Hyper Ca ++:

Muscular:

Muscle weakness with or without in coordination. Hypotomia with Hyper Reflexia,

muscle pains, Ataxia.

CNS:

Distributed conciousness, head aches and irritability coma. If concentration >

16mg/dl.

GI:

Anorexia, nausea, vomiting and constipation, severe abdomen pain, distension

and ileus.

Cardiac:

Short ST segment and short QT interval. Increase in cardiac sensitivity to digitalis

and catacholamines. Incomplete or complete heart block may occur - cardiac

stand still at S. conc of 18mg/dl.

Renal:

Polyurea/Polydipsia with water loss due to renal tubular function disturbance

Azotemia may develop

Hypercalcemic crisis occurs when S Ca++ increases greater than 17mg/dl where

Ca+ salts precipitates in kidneys and other organs.

Treatment of Hypercalcemia:

Serum Calcium conc < 12mg/dl - treatment can be postponed unless Azotemia

or hypercalcemic symptoms are present

>12mg/dl - Should be treated

>15mg/dl - emergency treatment

Symptomatic patients require rapid treatment:

Blisk diuretics (urinary output of 200 to 300ml/hr) with IV saline and a loop

diuretic to accelerate Ca2+ excretion

Replacement of K+ and Mg2+

Surgical resection of parathyroid tumor - Rebound hypocalcemia

In S.Ca++ > 15mg/dl - Potassium Biphosphates can be used

166

Mechanism: Inhibits bone reabsorption and forms Ca - PO4 complex that is

deposited in soft tissues or bones.

Contraindicated is renal failure and vitamin D intoxication

Investigational: Calcitomin / Diphosphonates (Pamidronate 60mg)

References:

1. Emanuel Goldberger, Jeffrey M. Brensilver: A.Primer of water, Electrolyte and

Acid Base Syndromes, 8th edition, Jaypee Brothers 1996.

2. Ronald.D.Miller: Anesthesia, 5th edition, Volume 1, Chapter 45. Churchill

Livingstone 2000.

167

Acid Base Balance

Introduction

All Biochemical reaction in the body is dependent on physiological Hydrogen

ion concentration

Regulation of [H+] is called Acid-Base Balance

Changes in ventilation and perfusion affects this balance

Definitions

Acid - Donates H+ ion at a given PH

Base - Accepts H+ ion at a given PH

Buffer pair - is a weak acid in equilibrium with a weak conjugate base

PH - Puissance Hydrogen - Negative logarithm to base 10 of [H+] in

moles/liter

Arterial [H+] = 40 nmol /L = 40 x 10-9 mol/L

PH = - log10 (40 x 10-9)

= 7.4

Neutral PH - Equal number of [H+] and [OH]-

Electro neutrality of water at 25oC occurs at PH - 7

Electro neutrality of water at 37oC occurs at PH - 6.8

Blood PH – 7.4 (alkaline)

Acid Generation and Measurement

Intracellular [H+] varies among tissues and is less variable than that in the

blood

Exerts powerful mechanism of intracellular function regulation

Intracellular [H+] is difficult to evaluate, so indirect measurement by PH gives

the Acid Base status

168

Endogenous generation - by high energy phosphates, carbohydrates,

ingested acids and metabolism of AA

Hydration of CO2 to bicarbonate generates the largest amount of [H+] per

day

Relationship of [H+] and PH

PH [H+]

6.70 200

6.80 158

6.90 126

7.00 100

7.10 79

7.20 63

7.30 50

7.40 40

7.50 32

7.60 25

7.70 20

7.80 16

7.90 13

8.00 10

1 unit change in PH changes [H+] by factor 10

7.7 – 20 6.7 – 200

0.3 unit change in PH changes [H+] by factor 2

7.0 – 100, 6.7 – 200, 7.3 – 50

0.1 unit change in PH changes [H+] by factor 0.8

7.4 – 40, 7.5 – 32, (40 x 0.8)

7.3 – 50 (40 / 0.8)

169

CO2 Transport in Acid Balance Base

Tissue CO2 production and H+ production are linked by carbonic acid that helps

H+ to interconvert with CO2

This reaction is important because

It indicates that, largest single [H+] source under physiological condition is

tissue CO2 production

It allows flexibility of [H+] – more quickly and effectively removed as CO2

Carbon dioxide removal keeps in pace with production

Compensatory Mechanism for [H +] Changes

Physiological response to changes in [H+] is characterized by 3 phases:

Immediate chemical buffering normalizes arterial PH in seconds or minutes

Respiratory compensation in hrs

Renal compensation in days , more effective , normalizes arterial PH even if

the pathological process exists

Tissues Plasma RBC Lungs

Kidney

170

Immediate Compensation

Buffers:

Solutions containing weak acid and its conjugate base, acts by donating and

accepting [H+]

Minimizes drastic changes in PH

Henderson-Hasselbalch Equation

CO2+ H2O <=> H+ + HCO3-

By the Law of Mass Action:

Ka = [H+]. [HCO3-] / [CO2]. [H20]

Ka x [H2O] = [H+]. [HCO3-] / [CO2]

[CO2] = 0.03 x pCO2 (by Henry’s Law) [where 0.03 is the solubility coefficient] K'a

= 800 nmol/l (value for plasma at 370C

[H+] =(800 x 0.03) x pCO2/ [HCO3-] = 24 x pCO2 / [HCO3

-] nmol/l

pH = log10(800) - log (0.03 pCO2 / [HCO3-] )

pH = 6.1 + log ( [HCO3] / 0.03 PCO2 )

Important Body buffers:

Bicarbonate (H2CO3/HCO3)-PK =6.1; ECF 15 to 20 min

Hemoglobin (HHb/Hb)-PK=6.8 ; RBC, ECF

Intracellular proteins (Hpr/Pr)-PK =6.8, ICF 2 to 4 hrs

Phosphates (H2PO4/HPO4-) urinary buffer PK =6.8

Ammonia (NH3/NH4+)

Bicarbonate Buffer System (PK=6.1)

Biochemically weak ,but made powerful because open at both ends

a. Presence of carbonic anhydrase

b. Ability of kidney to synthesize new HCO3 and excrete excess

c. Effective removal by lungs as CO2

Acute dependence on albumin would displace hormones and drugs from

binding sites causing endocrine dysfunction and drug toxicity

Excessive dependence on Hb decreases its ability to carry O2

171

Hemoglobin Buffer System (PK=6.8; RBC, ECF)

Rise in tissue CO2 increases HCO3 release by erythrocytes

PaCO2/HCO3 ratio is balanced

Quantification of ECF Buffer:

Base excess

Acid or base added to return the blood PH to 7.4 when PaCO2 is 40 mmHg at full

O2 saturation and 370 c

Normal 0 to +/- 2mmol/L

Bicarbonate correction

Buffer base

Sum of charges on all strong base (non buffering cations) minus sum

of charges on all strong acids (buffering anions)

Bb=∑ (SIn*źSIn) ---Σ (Bin*źBIn)

Strong ion difference:

SID = (the sum of all the strong cation concentrations in the solution) minus

(the sum of all the strong anion concentrations in the solution).

SID = [Na+] + [K+] + [Ca++] + [Mg++] - [Cl-]+ [Other strong anions-]

SIDapp = [Na+] + [K+] + [Ca++] + [Mg++] - [Cl-]+ [lactate-]

SIDa has a normal value of 40 to 42 mEg/l

SIDeff=[HCO3-] (albumin g/dl*2.6)+(inorganic phosphates *18mmol/L)

Erythrocyte Plasma Tissue

Chloride shift

172

SIDe has a normal value of 36meq/l

SIDa-SIDe >10 meq/l indicates increased plasma anions (pathogenic)

Important to evaluate acid base status during marked hypo-albuminemia or

phosphate deficiency

Anion gap: (Analog of SID)

Defined as difference between major measured cations and anions

AG = [Na+] + [K+] - [Cl-] - [HCO3-] = 140 – (104 + 24) = 12 meq/l

Albumin accounts for largest fraction of AG

AG decreases by 2.5 meq/l for every 1g/l reduction in plasma albumin

concentration

AG (corrected)=AG +2.5 (normal albumin–observed albumin)

Urinary anion gap: (Batlle et al)

Urinary Anion Gap = (UA - UC) = [Na+] + [K+] - [Cl-]

Negative UAG suggests GIT loss of bicarbonate

Positive UAG suggests impaired distal renal acidification (RTA)

Increase in NH4 in bowel loss of bicarbonate so UAG decreases

Delta ratio:

Increase in Anion Gap / Decrease in bicarbonate

Normal delta ratio = 1

Base deficit / excess gap:

BDE NaCl= ([Na+] - [Cl-]) - 38

BDE alb =0.25 (42- albumin in g/dl)

BDE NaCl - BDE alb =calculated BDE

BDE -calculated BDE = BDE gap

The effect of unmeasured cations or anions

173

Delta Ratio Assessment Guideline

< 0.4 Hyperchloraemic normal anion gap acidosis

0.4 - 0.8 Combined high AG and normal AG acidosis BUT note that the ratio is often

<1 in acidosis associated with renal failure

1 to 2 Usual for uncomplicated high-AG acidosis

Lactic acidosis: average value 1.6

DKA more likely to have a ratio closer to 1 due to urine ketone loss

(especially if patient not dehydrated)

> 2 Suggests a pre-existing elevated HCO3 level so consider:

a concurrent metabolic alkalosis, or

a pre-existing compensated respiratory acidosis

Osmolality of a solution is the number of osmoles of solute per kilogram of

solvent

Measured in the laboratory by machines called osmometers

Units of osmolality are mOsm/kg of solute

Osmolarity of a solution is the number of osmoles of solute per litre of solution

calculated from a formula which represents the solutes which under ordinary

circumstances contribute nearly all of the osmolality of the sample

(1.86 x [Na+]) + glucose/18 + BUN/2.8 + 9

Units of osmolarity are mOsm/litre of solute

Osmolar gap = Osmolality – Osmolarity (used in detecting methanol toxicity)

Respiratory Compensation

Changes in alveolar ventilation is responsible for PaCO2 changes

Mediated by chemoreceptor in brain stem in response to CSF PH

Minute ventilation is increased 1 to 4 L/min for every 1 mmHg rise in PaCO2

174

Hypoxymia stimulates ventilation so PaCO2 never rises >55mmHg

Renal Compensation

Increased reabsorption of filtered HCO3

Activated immediately but takes 12 -24 hrs for manifestation

PCT reabsorbs 80% of bicarb filtered ,DCT remaining 20%

For every bicarb entering the circulation 1 H+ is secreted

In metabolic alkalosis large amount of bicarbonate is excreted

Metabolic Acidosis

Stimulate medullary centers

Hyperventilate

PaCO2

Metabolic Alkalosis

Increase in arterial PH

Hypoventilation

PaCO2

175

Increased excretion of titratable acids

After HCO3- reserve is exhausted H+ combines with HPO42-

This occurs till urinary pH is 4.4

176

Increased formation of ammonia

Deamination of glutamine within mitochondria of PCT is principle source of

NH3 production in kidneys

Active when phosphate buffer is exhausted

177

Hepatic Compensation

Liver is the principal organ for lactic acid clearance

Lactic acid metabolized in 2 ways oxidization and gluconeogenesis

Accompanied by 1:1 consumption of H+

Each molecule of urea synthesized consumes 2 HCO3-

2 NH4+ + 2HCO3 UREA + CO2 +H2O

Lactic acidosis inhibits urea synthesis

178

Primary Acid Base Disorders

Acid-base

imbalance

Plasma

pH

Primary

disturbance

Compensation

Respiratory

acidosis

low increased pCO2 increased renal net acid excretion with

resulting increase in serum bicarbonate

Respiratory

alkalosis

high decreased pCO2 decreased renal net acid excretion with

resulting decrease in serum bicarbonate

Metabolic

acidosis

low decreased HCO3- hyperventilation with resulting low PCO2

Metabolic

alkalosis

high increased HCO3- hypoventilation with resulting increase

in PCO2

pH remains unchanged in chronic respiratory changes

179

Guide Lines for Interpreting Acid –Base Status

Decide whether arterial or venous

a. Appreciated best by person drawing

b. SvO2 < 75% and PaO2 < 40 mmHg

c. Clinical correlation

Steady state of oxygenation and ventilation

a. 20 min before sampling after changing FIO2

b. 30 min for PaO2 and PCO2 to attain steady state after changing

ventilator settings

Assessment of hypoxic state (FIO2 *5)

Adequacy of ventilation (PCO2)

180

181

182

Acidosis and Alkalosis

Physiologic Effects of Acidosis:

Decreased myocardial contractivity,increase threshold for VF

Increased PVR Increased PHT

Decreased SVR Decreased BP

Impaired response of Cardiovascular system to endogenous and exogenous

catacholamines

Compensatory hyperventilation

183

Potentiate the Depressant actions of anesthetics

Right shift of ODC curve, increase oxygen to tissues

Hyper K+(0.6 meq/L for 0.1 decrease in PH )

Respiratory Acidosis

(PH < 7.35 and PaCO2> 45 mmHg)

Acute Chronic

Absence of Renal HCO3- Compensation Renal retention of HCO3

- returns PH normal

< 6 - 12 hrs 12 to 24 hrs – peaks up to 3 - 5 days

Causes

Decrease in minute Ventilation Increase in CO2 Production

CNS depression Hyper catabolic status

Peripheral muscle weakness Sepsis

COPD Fever

Acute Respiratory failure Poly trauma

Malignant hyperthermia

Hyper alimentation (increase in CO2)

Treatment

Increase in alveolar ventilation (Bronchodilation)

Reduction of CO2 production (paralysis, carbohydrate)

Buffers like THAM , carbicarb containing nil CO2

Metabolic Acidosis (pH <3.5 and HCO3 <21meq)

Causes

a. Consumption of bicarbonate by strong volatile acids

b. Renal and GI wasting of bicarbonate

184

c. Rapid dilution of ECF by bicarbonate free fluids

Fall in bicarbonate without proportionate reduction in PaCO2 causes fall in pH

Pulmonary compensation by hyperventilation

DD for metabolic acidosis is by calculating anion gap

Acidosis with acid gain (wide AG) Acidosis with HCO 3 loss (normal AG)

Increased production of non-volatile acids

• Keto acidosis, lactic acidosis

Decreased or no excretion of volatile acids

Renal failure (GFR <20ml/min)

Ingestion of nonvolatile acids

Salicylate poisoning

Methanol poisoning

Ethylene glycol poisoning

Increased GI loss

Diarrhea, small bowel fistulas,

uretrosigmoidostomy, obstructed ileal loop

Increased renal loss

Renal tubular acidosis

Carbonic anhydrase inhibitors

Hypoaldosteronism

Other causes

Dilutional

TPN

Increased chloride containing solutions

Lactic Acidosis:

Hypoxic Non hypoxic Drugs and toxins

Shock - sepsis, MI, hemorrhage

Respiratory failure

Anemia, CO poisoning

Increased demand and

decreased supply

Leukemia

Lymphoma

Poorly controlled

diabetics

Severe hepatic failure

Fructose in TPN

Phenformin

Methanol, ethanol

poisoning

Pathophysiology of lactic acidosis:

Deficient oxygen impairs electron flow through cytochrome transport chain

ATP lowers and cell redox pair NADH/NAD is shifted to reduced state ie.,

NADH > NAD. This activate enzyme Phosphofauctokinase in regulatory

glycosis

Pyruvate +NADH lactate +NAD +H+

185

Treatment:

Stop the source of production

Correct hypoxia

Maintain adequate perfusion

Avoid vasoconstrictors (dopa)

Tips to Treat Metabolic Acidosis:

Correct respiratory acidemia control respiration if necessary

Bicarbonate if pH<7.2, half correction based on base deficit

Given diluted through central line

Use in cardiac arrest and low flow states causes cellular acidosis

Raising pH from 7.2 to 7.3 is sufficient

Profound acidosis needs bicarbonate dialysis

Serial blood gas to be done to avoid Na overload and alkalosis

Physiological Effects of Alkalosis

Left shift of ODC , impaired oxygen to tissues

Hypokalemia – extrusion of H+ for K+

Hypocalcaemia – increase binding sites for Ca++

Coronary vasospasm and bronchospasm

Increases SVR and decreases PVR

Reduces CBF

Potentates neuromuscular blockade

Prolongs the respiratory depression of opoids

Respiratory Alkalosis (PaCO2<35, pH >7.45)

Central stimulation Peripheral stimulation

Pain

Anxiety

Fever

Infection

Hypoxemia

High altitude

Pulmonary disease

asthma

pulmonary edema

pulmonary emboli

186

Other causes:

Ventilator induced

sepsis

Metabolic Alkalosis (pH>7.45, HCO3>27 meq/l)

Chloride sensitive

(urine cl- <10mmol/l)

Chloride resistant

(urine cl- >20 mmol/l)

GI

vomiting

villous adenoma

gastric lavage

Renal- diuretics

Sweat – cystic fibrosis

High minarolocorticoid activity

cushings

batters

Other causes:

Massive blood transfusion-citrate toxicity

Alkali therapy

Hypercalcemia-metastasis

Treatment of Alkalosis:

Treat the underlying disorder

Patients on ventilator decrease minute ventilation

Chloride sensitive alkalosis – 0.9% NaCl

Avoid Ringers lactate

Avoid hyperventilation

Potassium supplement

Aldosterone antagonist (spironalactone)

Azetazolamide in edematous patients (decreased reabsorption of HCO3 in

PCT)

Temperature Correction

Changes in temperature directly affects the measurements of PaCO2 and

PaO2 and indirectly the PH

187

Decrease in temperature lowers the partial pressure of a gas in solution even

though total gas content does not change

Both PaCO2 ,PaO2 therefore decrease during hypothermia but PH increases

because temperature does not alter [HCO3- ]

Since blood gas tension and PH in vitro are measured always at 37oC

controversy exists over whether to correct the measured values to the

patients actual temperature (Hypothermic Cardiac Surgery)

Two school of thought exists regarding the ideal body PH at lower

temperature where CO2 solubility is increased

PH Stat:

PCO2 must be maintained to preserve the PH

Here the ABG analysis measured with electrodes at 37oC is corrected to the

patients temperature of CO2 during hypothermic CPB

Edmark suggested that patients PH should be reduced 0.0147 units for each

degree centigrade decrease in temperature below 37oC

True PH = PH (37o) + (37- t) X 0.0147 where t – patients temperature

Eg: t = 25oC PH= 7.0 at 37oC

True PH= 7 + (37 – 25) x 0.0147

= 7 + 12 X 0.0147 = 7 + 0.186 = 7.186

Since here patient’s temperature has been lowered by 12oC, Normal PH from

7.4 should also be decreased. This normal PH at lower temperature is

calculated by 7.4 – 12 X 0.0147 = 7.22 9 Normal PH. So the patient is slightly

acidic and PH should be raised only slightly.

α Stat:

It is not the PaCO2 that is to be maintained during hypothermia but the ratio of

ionized to unionized imidazole ring on histidine

Imidazole ionization does not change with temperature, here there is no

correction made for patients temperature during interpretation of arterial blood

gases determined at 37oC.

188

PH Stat Management α Stat Management

Greater cerebral blood flow during this

management

Reported to limit myocardial damage, better

presence of sensitivity to adrenergic

stimulation during CPB

Increase in total CO2 content ; uncoupling

of CBF and CMRO2

Total CO2 content maintained same; CBF

and CMRO2 are appropriately coupled

In children PH stat is beneficial because

of developmental milestones are not

affected especially during DHCA

Lower incidence of post op cognitive

dysfunction in CABG patients under

hypothermic CPB

References:

1. Emanuel Goldberger, Jeffrey M. Brensilver: A.Primer of water, Electrolyte and

Acid Base Syndromes, 8th edition, Jaypee Brothers 1996.

2. Barry A. Shapiro, Ronald A. Harrison, Roy D. Cane: Clinical Application of

blood gas, 4th edition, Year Book Medical Publishers 1989.

3. Ronald.D.Miller: Anesthesia, 5th edition, Volume 1, Churchill Livingstone

2000.

4. Edward G. Morgan, Maged S.Mikhail, Micheal J.Murray: Clinical

Anesthesiology, 3rd edition, Chapter 30. Mc Graw- Hill 2002.

189

Pregnancy and Heart Diseases

Over a 30 year period, the incidence of heart disease during pregnancy has

declined from 3.6% to 1.6%.Rheumatic heart disease, despite declining

incidence still accounts for most cases.Incidence of congenital heart disease in

pregnant patients is steadily increasing as greater number of women with CHD

reach the child bearing ages due to improved medical and surgical therapies.

Incidence and Mortality of RHD and CHD in pregnant patients

% Mortality RHD % of Distribution

Maternal Fetal

MS 90 1 to 17 3.5

MR 6.5

AR 2.5

AS 1.0

% Mortality CHD % of Distribution

Maternal Fetal

VSD 7 to 26 7 to 40 2 to 16

ASD 8 to 38 1 to 12 1 to 12

PDA 6 to 20 5 to 6 17

TOF 2 to 15 4 to 12 36 to 59

Eisenmenger 2 to 4 12 to 33 30 to 54

Coarctation of aorta 4 to 8 3 to 9 10 to 20

AS 2 to 10 22

PS 8 to 16 4

PPH 1 to 2 53 7

Cardio vascular changes during pregnancy

Circulatory changes during pregnancy may have adverse effects over the

cardiovascular system. Increase in cardiac output by 40 - 45% and an additional

190

rise of 35 to 45% during labour and delivery can precipitate a failure in already

diseased heart.

Relief of Aortocaval compression contributes to increased venous return and

central volume resulting in further increase in cardiac output above pre labour

values.

Decrease in SVR in pregnancy is also important in some patients with valvular

heart disease with potential for R L shunts.

Hypercoagulability associated with pregnancy increase the need for adequate

anticoagulatits in patients being at the risk of thromboembolism. And the use of

anticoagulants increases the risk of post partum hemorrhage.

Mother with mild cardiac disease will usually adapt to the volume shifts and

changes in cardiac output. But with more severe cardiac disease risk of

decompensation peaks during 3rd trimester, is parturition and in immediate

peurperium.

Signs and Symptoms in heart disease in pregnant wom an

Many of the signs and symptoms of normal pregnancy can mimic those of

cardiac disease

Dyspneoa due to pulmonary edema due to LVF may be difficult to distinguish

from laboured breathing typical of normal pregnancy

Leg edema due to CCF may be mistaken for venous stasis due to aortoeaval

compression

Presence of CCF is diagnosed by raised JVP and hepatomegaly that are

absent during normal pregnancy

It may be difficult to differentiate a heart murmur due to organic lesion from

the one due to increased blood blow

Rotation of maternal heart due to elevation of diaphragm as pregnancy

progresses can be mistaken for cardiac hypertrophy

The grading of dyspneoa anf fatigue caused by heart failure is often still

classified using old functional NYHA classification (1973)

191

Class I No limitation of physical activity

Class II Slight limitation of physical activity, symptoms with ordinary activity

Class III Marked limitation of physical activity, symptoms with less than ordinary

activity

Class IV Unable to carry out any physical activity without discomfort symptoms

even at rest

Changes that occur in heart sounds normally in preg nancy

In a study of 50 normal pregnant women at varying steps of pregnancy, a

phonocardiographic study found that the first heart sound may have an

exaggerated split with increased loudness of both components

In upto 84% of pregnant patients, 3rd heart sound is evident

Functional systolic murmur occur in > 90% of women

Soft transient diastolic murmur occur in 20% of these women and 10% have

continuous murmur apparently arising from the breast vasculature

An Overview of Anesthetic Consideration

Anesthesia for cardiac disease in pregnancy requires the understanding of

the type, severity and progression of the disease in the context of normal

cardiovascular adaptations to pregnancy

For most cardiac disease no one technique is exclusively indicated or

contraindicated

Primary concern of anesthesiologist is to avoid and/or treat the specific

pathophysiological changes that can exacerbate the disease form

Cardiac medications are to be continued on the day of surgery

Prophylactic antibiotics to be given to prevent infective endocarditis

Care should be taken to minimize sudden changes in BP, PR, BV

Patient should be placed left lateral or sit up right position

Adequately oxygenated during pain, apprehension and uterine contractions

Prolonged 2nd stage of labour should be avoided as valsalva maneuver

produce fall in BP, when released and bearing down efforts increase the CVP

and systolic BP

192

Adequate analgesia is to be provided as catacholamine release may increase

the SVR, BP and Cardiac output

So forceps or vacuum extraction is advocated

Following delivery IV syntocinion (oxytocin) should be administered carefully

Intensive monitoring to be continued postpartum also

Monitoring in Pregnancy with Cardiac disease

The pre operative requirements are:

a. Detailed history and physical examination

b. Exercise tolerance test

c. X ray chest if pulmonary edema is suspected

d. ECG, pulse Oximeter / ABG and

e. Serial echo

Intra op, they are to be monitored with usual monitors like NIBP, SaO2, ECG,

Oesophageal steth, Temperature, ETCO2, neuromuscular monitor

The decision of invasive monitors (Radial arterial line, CVP, PCWP catheter)

depend on severity and progression of disease

Patients with NYHA class I and II do not routinely require invasive monitoring

Most asymptomatic patients who show no disease progression and have no

signs of impaired RV or LV performance will have an uneventful cause and do

not require any invasive monitoring

Exceptions are patients, even if asymptomatic with pri PHT, R L shunt

dissecting aneurysm, coarctation of aorta, severe AS require invasive monitor

Though PCWP monitor is time consuming, requires expertise and have been

associated with morbidity and mortality, at is delivered that information

derived from PCW monitoring in the presence of severe cardiac disease is

worth the imposed risk

Management of Complications

Treatment of various complications involves drugs like digoxin, propranalol,

lidocaine, SNP, metaramiol. These drugs may have outbound fetal ill effects.

193

Their use depends on severity of maternal impairment and consideration

whether; the risk of fetal morbidity overweighs the maternal morbidity associated

with forgoing therapy.

Here the philosophy is to correct immediately any severe maternal impairment

even though the therapy may cause fetal morbidity.

194

Valvular Heart Disease

Rheumatic Heart Disease

It is a diffuse inflammatory disease affecting the heart, joints and

subcutaneous tissues following group A B hemolytic streptococcal injections

Clinical picture usually includes migratory poly arthritis with or without carditis

Polyarthritis is self limiting whereas carditis is progressive and can cause

permanent damage to heart

Due to extensive use of prophylactic antibiotics, the incidence has come

down much rapidly, but still the mitral valve stenosis seems to be the common

RHD in pregnant patients

Mitral Stenosis

Rheumatic fever occurs 1st in 6-15 yrs old children. If carditis occurs - MR

ensues, followed in about 5 yrs by MS. They are asymptomatic for 15 yrs.

Pulmonary congestion, RVF with PHT develops 5 to 10 yrs after appearance of

symptoms in normal persons.

Clinical manifestation:

Fatigue, breathlessness on exertion, PND, orthopneoa and dyspneoa at rest

Hemoptysis with rupture of broncho pulmonary varices and pulmonary and

systemic arterial embolisation

In severe MS, atrial fibrillation, pulmonary embolism and pregnancy may

cause rapid decompensation

Physical examination may reveal a middiastolic murmur with presystolixc

accentuation. If faint will be heard only when the patient lies on her left side.

An opening snap is also heard

Intensity of murmur correlates poorly with the degree of stenosis because of

other hemodynamic effects like decreased cardiac output, blood flow through

the valves

Test Indicators:

X ray chest - Straightening of left heart border in long standing cases

ECG - Broadening of P wave (P mitrale) in V1 showing LA enlargement

® Axis is deviation showing RV enlargement

195

PCWP - 25 to 30mmHg (normal 0 -12mmHg) if mitral valve onface < 2cm2

Diastolic pressure gradient is the hallmark of this condition. (Normal is

5mmHg) (Increases > 25mmHg)

Pathophysiology:

Decrease in mitral valve onface impairs LV filling

Initially LA may overcome the obstruction, but ventricular filling decrease, LA

volume and pressure increase, causing rise in RV and pulmonary capillary

wedge pressures

Transudation of fluids into pulmonary interspace

Pulmonary compliance decreases, work of breathing increases producing

progressive dyspneoa on exertion with pulmonary HT.Pulmonary vascular

resistance becomes permanently elevated

RV hypertrophy, dilation and failure may follow, leading to TR, hepatic and

peripheral congestion

Atrial fibrillation, Tachycardia and increased metabolic demands can

exacerbate this process

Pregnancy Induced Changes:

With pregnancy, an automatically moderate stenosis can become functionally

severe

Pregnant patients with MS have increased incidence of pulmonary congestion

25% atrial fibrillation (7%) PSVT (3%)

LV dysfunction is uncommon with pure MS and its pressure suggests an

associated MR or AR

Major complications in pregnant patients Incidence percentage

LVF/ RVF 8 - 5

Atrial arrhythmias 6.5

Systemic/ Pulmonary anabolism 1.6

Infective endocarditis 0.4

196

Anesthetic Consideration:

Asymptomatic patients without evidence of pulmonary congestion have minimally

increased risk. Thus they do not require any additional invasive monitoring but

should be attended with caution.

Presence of marked symptoms warrents invasive monitoring.

Specific factors to be considered are:

1. Prevent rapid ventricular rates: Neither sinus tachycardia, nor AF with rapid

ventricular response is well tolerated

Digoxin therapy is used to control atrial fibrillation prior to pregnancy is

continued with readjustment of dose if necessary to maintain ventricular

beats < 110/min

Development of AF with rapid ventricular response may decrease cardiac

output and produce pulmonary edema

Treatment of AF with cardio version starting with 25 watt sec

Fetal safety of cardio version is well documented

If cardio version is unavailable propanalol (o.2 to 0.5mg) every 3 minutes

can be used to lower the pulse rate. This should be discontinued if the

total dose exceeding 0.1mg/kg or if there is increase in PCW and

evidence of CCF

Digitalization is used in stable situations where prolonged but not

immediate ventricular rate control is necessary.

2. Precipitating factors like hypoxia, hypercapnia, acidosis, pain, light GA should

be avoided to present sinus tachycardia

3. Marked increase in central blood volume is poorly tolerated. Overtransfusion,

Trendlenberg position, Autotransfusion via uterine contraction can precipitate

RVF. CVP monitoring may be used to assess the increase in blood volume

4. Marked decrease in systemic vascular resistance is poorly tolerated. In

patients with severe MS, decrease in SVR is compensated by increase in HR

as there is fixed stroke volume. SVR could be maintained by IV infusion of

mephenteramine. Ephedrine is contrandicated due to tachycardia

197

5. Pulmonary hypertension should be avoided: Any degree of PaCO2, hypoxia,

acidosis, lung hyperinflation, increased lung water can cause increased

pulmonary vascular resistance

Postaglandins are used with caution

Treatment of increased PHT - Dopamine (3 to 8Hg/kg/min) and low dose

SNP (0.1 to 0.5 Hg/kg/min) causing pulmonary vasodilation

If hemodynamic and pulmonary complications occur then mechanical

ventilation is prolonged

Anesthesia for Vaginal Delivery:

Segmental Lumbar epidural analgesia is used for labour and vaginal delivery.

This eliminates pain and tachycardia with uterine contractions. (Diluted LA +

opioids)

Perineal analgesia (Pudental block) stops the urge to push and thereby

prevents exertion, fatigue and deleterious effect of valsalva maneuver

Delivery is facilitated by vacuum extraction or outlet forceps

Hypotension is prevented by continuous left uterine displacement and

judicious fluid infusions

Prophylactic ephedrine, rapid hydration should be avoided

Anesthesia for Cesarean section:

Regional Anesthesia:

A continuous LEA is preferred to spinal because it produces more controlled

hemodynamic changes. The level of block should be established slowly by

titrating the LA through the epidural catheter.

Epinephrine is omitted from LA as it causes potential tachycardia and

peripheral vasodilation

If hypotension occurs, monitoring of CVP is needed to correct fluid

replacement

General Anesthesia:

Drugs that produce tachycardia like atropine, pancuronium mepridine,

ketamine should be avoided

198

Patients with mild MS, may be managed by IV thiopentone (titrated) induction,

intubation and balanced GA

Those with moderate to severe MS may require high opioid induction and

post op ventilation

Tachycardia, hypertension due to intubation response is prevented by β

blockers or by increasing anesthetic depth

High opioid - inhalational anesthetic induction increases the risk of maternal

aspiration or neonatal depression. But the benefits overweighs these hazards

Post Operative Care:

ICU monitoring and ventilatory care may be required. ABG, Pulmonary

mechanics, X ray chest are to be done and respiratory adequacy must be

assessed before weaning.

Mitral Regurgitation / Insufficiency

It is the 2nd most common valvular defect in pregnancy. Left ventricular work

increases. As the complications usually occur late in life (ie) after child bearing

age, most patients with MR tolerate pregnancy well. There is

5.5% of Pulmonary Congestion during pregnancy

4.3% of atrial tachy arrhythmias

2.8% of pulmonary embolism

8.8% of Infective endocarditis

Clinical manifestation:

Principle symptom of advanced MR is those of LVF. Cardinal sign is a pan

systolic murmur of blowing quality, loudest at the apex, radiating to axilla and

infrascapular areas. Atrial fibrillation occurs approximately in 1/3 of the patients.

Test Indictors: ECG - normal but may reveal signs of LVH or RVH in long

standing cases.

Pathophysiology:

Mitral valve insufficiency causes regurgitation of blood from LV to LA with

chronic MI; LA adapts to increase in blood volume by dilating and by

increasing the compliance

199

When LA pressure increases, pulmonary venous and capillary pressure also

rises causing edema, which does not occur till late course of the disease

LV dilation also occurs because of increase in preload by hyper volumic LA

Forward ejection of blood through aortic valve can be impaired by as much as

50 to 60% and depends on the ratio of resistance through the aortic valve to

the resistance through the insufficient mitral valve

Reduction in LV afterload can therefore play an important role in decreasing

the amount of regurgitant blood and increase the cardiac output

Pregnancy Induced Changes:

With pregnancy there is increase in intravascular blood volume that may be

intolerable to the chronically compromised LV

Changes in SVR palys an important role

Decrease in peripheral vascular resistance in pregnancy may improve

forward flow at the expense of regurgitant flow

In contrast, pain apprehension, uterine contraction or surgical stimulation

associated with labour and delivery may increase SVR by augumenting

sympathetic activity. This causes decreased forward flow and increased

regurgitant fraction

It should be noted that murmurs of MI / AI are decreased during pregnancy

Anesthetic Consideration:

Asymptomatic patients with mild MI and an unchanging murmur throughout

pregnancy may be approached in a routine but cautious manner

Special consideration to be given to symptomatic patients

Marked raise in SVR can cause acute LVF (due to pain of labour and

surgery). Treatment consists of LV after load reduction with low dose SNP

AF can cause LVF

Myocardial depressant are not well tolerated

Bradycardia is poorly tolerated. Maintenance of normal to slightly increased

HR is advised to maintain cardiac output

200

Anesthesia for vaginal delivery and Cesarean sectio n:

Regional Anesthesia:

For labour and vaginal delivery LEA is recommended. This technique will prevent

peripheral vaso constriction associated with the pain of labour and will increase

the forward flow of blood.

However RA will increase the venous capacitance and requires administration of

IV fluids to maintain filling volume of LV.

Constant left uterine displacement, vasopressors like Ephedrine are useful in

preventing and treating hypotension.

General Anesthesia:

General anesthesia with N2O/O2/ inhalational agents can cause peripheral vaso

constriction.

However when combined with low dose SNP, it may be useful in patients with

LVF as it avoids myocardial depressant and maintains elevated HR. Halothane

can be used in patients without LV compromise.

Mitral Valve Prolapse

Barlow’s disease, Systolic click murmur, Bellowing mitral valve, Tachycardia -

Bradycardia syndrome

Most common congential valvular lesion occurring is 5 to 10% of population

and most prevalent in younger females, during child bearing age

85% of patients with MVP - asymptomatic 15% develop MI over 10 - 15 yr

period Parturients without MI tolerates pregnancy well

Complications are reported only with MVP existing with MI or other coexisting

disease like PIH

Clinical Manifestation:

Patient presents with diverse clinical manifestation like anxiety, palpitation,

dyspneoa, chest discomfort, light headedness, emotional disturbances, and

orthostatic hypotension, indicative of autonomic dysfunction.

Cardial sign of MVP is mid to late systolic click occurring after the beginning of

upstroke of carotid pulse. It is some times accompanied by mid to late crescendo

201

systolic murmur with murmur duration reflecting and severity of MI.If MVP is

severe click occurs early and murmur becomes holosystolic.

Test Indicators:

ECG may be normal or show T wave and non special ST changes in inferior

leads.

PSVT - common arrhythmia, Brady arrythmias are also seen

ECHO is definitive diagnostic method

Pathophysiology:

With MVP Chordac Tendinae are p elongated causing mitral leaflets to

prolapse into LA when ventricular volume decreases during mid to late

systole

A systolic click is produced by sudden tensing of the elongated chordae

tendinae and prolapsing leaflets

The crescendo systolic murmur represents retrograde flow during systole

from LV to LA

Conditions that decrease LV volume such as hypovolumia, venodilation,

increased AW pressure, Tachycardia cause earlier prolapse of leaflets during

systole and increase the regurgitant flow

Conditions that increase the LV volume like bradycardia, after load increase

by peripheral vaso constriction, hypervolumia, etc delay the systolic click and

murmur and decrease the regurgitation. Sometimes may mask the signs of

MVP

Pregnancy Induced Changes:

Normal physiological changes appear to have little effect on patients with MVP

when no other cardiac abnormalities are present.

Anesthetic Consideration:

Patients with MVP + MI managed as MI alone. Special considerations are

Avoid decrease in preload

Continue anti arrhythmic drugs

Avoid decrease in LV volume

Minimize sympathetic stimulation

202

No particular anesthetic technique appears to be superior in MVP patients with

mild or no MI.

Infective endocarditic prophylaxis is to be considered as this potentially serious

complication accounts for 10 - 15% of cases.

Aortic Stenosis

Appears to be dominant valve lesion in 0.5 to 3% of parturients

Symptoms are CHF, syncope, angina

Clinical Manifestation:

Cross sectional area of Aortic valve in normal adults is 2.6 - 3.5cm2

A 25 to 50% decrease in the area results in loud aortic systolic murmur.

Narrowing less than 1cm2 increase the LVEDP areas < 0.75cm2 produce

exertional dyspneoa, angina, and syncope

ESM is 2nd intercosal space ® 1.5cm from sternum and radiating to neck.

Decrease in cardiac output and ejection velocity decrease the intensity of the

murmur

Test Indicators:

ECG - LVH, LBBB, X ray - cardiomegaly

Systolic pressure gradient between aorta / LV of ≥ 50mmHg indicates severe

stenosis except in patients with CHF, where reduced LV stroke volume

produce only 30mmHg even with severe MS

Anesthetic Consideration:

In healthy parturients, fall in SVR is compensated by increased stroke volume

and HR. In A.S stroke volume is fixed and patients must rely on HR to

increase the BP

Elevation of HR > 140/min will decrease the diastolic filling and cardiac output

Brady cardia is poorly tolerated, as it may produce increase in LVEDP and

may produce ischemia

Avoid fall in systemic vascular resistance

Avoid Brady and tachy arrythmias

Maintain venous return and LV filling

203

Due to increased and fixed after load, left ventricular stroke volume will be

maintained only if LVEDV is adequate

Anesthesia for Vaginal delivery and Cesarean Sectio n:

Patients with aortic stenosis do not tolerate hypotension.

For labour and vaginal delivery, systemic analgesia, inhalational anesthetics,

prudental block are utilized.

Neuroaxial blockade is desired - intrathecal opioids alone are given or it is

coadministered with dilute concentration of local anesthetic epidurally. (CSE)

For Cesarean section, general anesthesia with standard Nitrous oxide relaxants/

opioids technique is recommended.

Myocardial depressants and drugs producing fall in SVR are avoided.

Aortic Insufficiency (Chronic)

Characterized by widened pulse pressure, decreased diastolic pressure and

bounding peripheral pulse.

Clinical Presentation:

Moderate to severe AI produces widened pulse pressure with diastolic pressure

≤ 60mmHg.

EDM is heard in left sternal border in 2nd intercosal space. Duration of diastolic

murmur depends on severity.

Test Indicators:

ECG - LV strain pattern is seen

X ray chest - LV dilatation

Pathophysiology:

LV volume overload occurs in AI.This volume overload depends on the area

of regurgitant onface duration of diastole, diastolic pressure and LV - Aorta

pressure gradient

With chronic LV overload - compliance of LV increases

LVEDP remains normal for several years

LV can usually tolerate this chronic increase and can become markedly

distended without evidence of CHF

204

However once LV starts failing, stroke volume decreases LVEDP and volume

increases above normal. Pulmonary congestion edema follows

Pregnancy Induced Changes:

The decrease in systemic vascular resistance and increase in HR during

pregnancy may reduce both the regurgitant flow and intensity of murmur.

In contrast, increase in intravascular volume throughout pregnancy and increase

in SVR with stress lead to LV dysfunction.

Anesthetic Consideration:

Asymptomatic patients without signs of CHF are at minimal risk

Symptomatic patients with increased murmur intensity, decreased diastolic

BP are at increased risk

Elevated systemic vascular resistance can be corrected by titrated low dose

vasodilator (SNP)

Anesthesia for Vaginal delivery and Cesarean sectio n:

Anesthetic management of parturients with AI is comparable to that for patients

with MI.

Continuous LEA will prevent peripheral vaso constriction due to stress/ pain

during labour and vaginal delivery.

For C.S regional/ GA as in MI may be used.

Congenital Heart Disease (CHD)

Major categories of CHD are L R shunt (ASD, VSD, PDA) R L shunt

(TOF, Eisenmenger’s syndrome) and congenital valvular and vascular lesions

(Co - arctation of aorta, AS, PS)

Pregnancy in women with CHD may be affected by several factors including

cardiac status, anatomic diagnosis, co-existing PHT, type of surgical repair

and residual post op impairment

Avoid marked raise in SVR

Avoid sudden decrease in HR

Avoid drug induced myocardial depression

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Left to Right Shunt (Acyanotic CHD)

Atrial Septal Defect:

Occurs in 17.5% of adults with CHD and it is the most common CHD. Cardiac

arrythmias, pulmonary hypertension, LVF, RVF are not seen till 4th to 5th

decade

Most women with uncorrected ASD tolerate pregnancy well. However risk of

LVF increases during pregnancy

Clinical Manifestation:

Signs and symptoms:

Clinical examination reveals fixed expiratory splitting of 2nd heart sound and

systolic ejection murmur at left upper sternal border and its intensity varies with

degree of shunt.

Investigations:

ECG - Right axis deviation with OS defect

X ray chest - shows LVH, Pulmonary hypertension is seen as prominent arterial

markings and bronchovascular markings

Pathophysiology:

L R shunt increases pulmonary blood flow and right ventricular preload and

right ventricle work. However a compensatory decrease in pulmonary vascular

resistance keeps the pulmonary arterial pressure normal. Chronically increased

pulmonary blood flow increases pulmonary vascular resistance and causes PHT.

Pregnancy Induced Changes:

Pregnancy accelerates these changes by increased blood volume and cardiac

output with consequent increase in L R shunt. Right and left ventricular

volume and work also increases. Pulmonary blood flow increases with faster

development of PHT. Right atrial and left atrial distension may cause PSVT, AF

and other atrial arrhythmias.

Anesthetic Consideration:

Prevent or treat SVT immediately

Avoid increase in Systolic vascular resistance

Avoid decrease in Pulmonary Vascular resistance

Patients with PHT, avoid further increase in pulmonary vascular

206

Most asymptomatic patients without evidence of PHT or RV compromise do

not require unusual care

Symptomatic patients require invasive monitoring

Supra Ventricular Tachyarrythmias increases L R shunt. Medications for

chronic SVT to be continued. Acute SVT to be treated by DC cardio version

or β blockers

Systemic Vascular resistance increases L R shunt by increasing aortic

impedance (outflow) relative to impedance of ASD (fixed)

Fall in pulmonary vascular resistance increases L R shunt causing

decreased cardiac output and hypotension

In patients with pulmonary HT, increase in pulmonary vascular resistance

precipitates RVP

Anesthesia for Vaginal delivery and Cesarean sectio n:

Lumbar epidural anesthesia (continuous) is preferred for labour and vaginal

delivery and even for C.S as this avoids the hazards of increase in systemic

vascular resistance due to pain and anxiety. General anesthesia can be used if

above anesthetic considerations are followed.

Ventricular Septal Defect

Occurs in 7% of adults with CHD

Size of VSD and degree of pulmonary HT determines the course of patients

with VSD

In most adults, VSD is small with minimal L R shunt, insignificant PHT and

no symptoms. Pregnancy is usually uneventful but rarely may be complicated

by bacterial endocarditis or CHF

Few patients with uncorrected large VSD usually display growth retardation,

recurrent RTI, Pulmonary HT, LV and RV compromise. Their mortality during

pregnancy is 7 to 40%

Severe RVF with shunt reversal is the major complication

Operative correction of VSD before pregnancy does not increase maternal or

fetal morbidity or mortality during pregnancy

207

Clinical Manifestations:

Small VSD produces a mild pansystolic murmur in 4th and 5th intercosal space

along the left sternal border.

Moderate to large VSD produce low pansystolic murmur with expiratory splitting

of 2nd heart sound.

Cyanosis and clubbing could be seen in case of reversal of shunt.

ECG - RBBB

CXR - right and left ventricular hypertrophy (Cardiomegaly)

Pathophysiology:

L R shunt with small VSD, there is increase in pulmonary blood flow and

secondarily decreased pulmonary vascular resistance, thereby presenting normal

pulmonary arterial pressure.

With larger VSD, the greater shunt marked with increased pulmonary blood flow

but, pulmonary vascular resistance cannot compensate for this increased flow

and pulmonary HT develops.

Increase in LV work leads to LVF

Increase in pulmonary capillary wedge pressure and pulmonary HT leads to RVF

Pregnancy Induced Changes:

In pregnancy increase in HR, cardiac output, Intravascular volume may increase

the L R shunt, exacerbate pulmonary HT, and the onset time of LVF and RVF.

Increase in vascular resistance (sys) is response to stress of labour and surgery

increases the right and left ventricular dysfunction. Bidirectional or R L shunt

may result.

Anesthetic Consideration:

Small VSD in an asymptomatic patient with normal LV function does not require

specialized monitoring.

In symptomatic patients specific precautions are to be considered.

Avoid marked increase in systemic resistance

Avoid marked increase in heart rate

In patients with pulmonary HT, avoid fall in SVR and increase in pulmonary VR

208

Marked increase in SVR and HR may increase L R shunt causing

pulmonary HT and LVF. Therefore adequate analgesia and anesthesia is

essential to prevent sympathetic response to pain.Vasodilation with drugs

(SNP) to reduce shunting

In patients with pulmonary HT and RVF marked decrease in systemic

vascular resistance is poorly tolerated. It causes R L shunt and cyanosis.

In these patients hypotension due to RA should be avoided

In these patients, factors that increase pulmonary vascular resistance are to

be avoided (acidosis, hypoxia, hypercapnia)

Anesthesia for vaginal delivery and Cesarean Sectio n:

LEA permits control of systemic vascular resistance and painful stimuli in

vaginal delivery

For cesarean section, either GA or RA can be used. If RA is selected,

continuous LEA will ensure slower changes in systemic resistance and allows

more time for correction of pressure changes

General anesthesia that combines inhalational opioid, minimizes the rise in

SVR and myocardial depression

Complications:

Peripheral cyanosis with increased cardiac output denotes R L shunt. Treated

with 100% oxygen and increasing systemic vascular resistance.

Peripheral cyanosis with decreased cardiac output denotes right and left

ventricular failure. Treated with 100% oxygen, withdrawal of anesthetics and use

of ionotopes.

Patent Ductus Arteriosus

Constitutes 15% of CHD. Current practice of early surgical correction makes this

a rare finding during pregnancy. Patients with small PDA usually have a benign

clinical course during pregnancy.

Ductus of larger (ID > 1 cm) may produce growth retardation, RTI, Pulmonary HT

and CHF during pregnancy.

209

Clinical Manifestation:

PDA produces continuous murmur enveloping the 2nd HS with lateral systolic

accentuation, terminating in the late or mid systole and radiating to 1st left

intercosal space.

Investigations:

ECG - May be normal or show LVH / RVH with larger ductus

X ray may be normal or show LA / or LV enlargement

Prominent Broncho vascular markings indicates PHT

Pathophysiology:

L R shunt of aortic blood via ductus to pulmonary increases the central

circulatory flow at the expense of peripheral blood flow

Both the length and cross section of ductus determines the resistance to flow

and the amount of shunt

Small ID < 1cm, moderate ID 1 to 2cm, Large ID > 2cm

Pregnancy Induced Changes:

Increase in Intravascular volume associated with pregnancy can increase the

shunting, PHT and LV work

In addition increase in HR, stroke volume, will increase myocardial oxygen

consumption and may compromise LV function during stress

Decrease in SVR lead to shunt reversal and cyanosis with large PDA

Anesthetic Considerations:

Symptomatic patients require invasive monitors and special precautions

Anesthesia for vaginal delivery and Cesarean Sectio n:

Continuous LEA in labour and vaginal delivery prevents increase in SVR

associated with pain. For cesarean section continuous LEA can be employed. If

GA is selected increase in SVR should be rapidly treated or avoided.

Avoid increase in systemic vascular resistance

Avoid marked increase in blood volume

In patients with pulmonary HT, decrease in SVR or increase in PVR may cause

reversal of shunt

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Monitoring concerns for PDA:

Use of simultaneous oxygen saturation monitors of right hand (radial) and foot

(Dosalis pedis) is useful

Blood flow to right arm is predominantly preductal and SaO2 in right arm

reflects FiO2, pulmonary function and cardiac output

SaO2 of right foot changes inversely with amount of R L shunt through

PDA if SaO2 of right arm is constant

Cardiac Lesions causing right to left shunts (cyano tic CHD)

Tetrology of Fallot (TOF)

This constitutes 15% of all CHD and is most common cyanotic CHD.

Anamoly characterized by right ventricular outflow obstruction, VS, RVH and

overriding of aorta. Many women do not reach the child bearing age in olden

days. Nowadays due to increased antibiotics and palliative corrective surgery,

increased number of parturients are presenting with corrected or uncorrected

TOF

Pregnancy increases the morbidity and mortality of uncorrected TOF

particularly in patients with history of syncope, polycythemia decreased SaO2

(<80%) RV hypertension

Cerebral thrombosis, SABE are common

Most complications develop immediate PP where SVR is lowest, thus

exacerbating R L shunt

With uncorrected TOF - 40% of parturients sustain CHF, and 12% die. Fetal

death rate is 36%

Maternal mortality is not increased with corrected TOF but fetal mortality can

still be as high as 25%

Clinical manifestation:

Uncorrected TOF causes cyanosis, clubbing and a systolic thrill at the left

sternal border - 2nd IC space

Degree of pulmonary HT, pulmonary blood flow determine the loudness of the

thrill

ECG - RVH X ray - Enlarged heart. Pulmonary oligemia PCWP - decreased

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Pathophysiology of TOF:

The increased resistance to RV outflow promotes R L shunting via VSD.

Therefore cyanosis depends on the size of VSD, outflow obstruction and

ability of the RV to outcome the obstruction

The obstruction may result fixed pulmonary stenosis or dynamic infundibular

hypertrophy

If Infundibular hypertrophy exists, increase in myocardial contractility or

decrease in RV volume increases the outflow obstruction

If significant hypertrophy is not there, maintenance of RV contractility is

important for preservation of pulmonary blood flow and peripheral

oxygenation

Regardless of the type of RV outflow obstruction, decrease in SVR may

exacerbate shunting producing cyanosis

Pregnancy Induced Changes:

Stress of labour increases the pulmonary vascular resistance and increases

the R L shunting

Fall in SVR in pregnancy and is puerperium, increases the R L shunt.

Patients with infundibular obstruction are at increased risk during labour,

when the contractility of myocardium is the highest

Anesthetic Consideration:

If TOF is not corrected and if patient survives till term pregnancy (which is very

unusual). Special precautions with all invasive monitors are required.

In patients with corrected TOF may have residual RVF and may require special

consideration.It is necessary to

Avoid fall in SVR

Avoid decrease in blood volume (Hyovolumia)

Avoid the decrease venous return (Uterine displacement)

Avoid myocardial depressants

212

Anesthesia for labour and vaginal delivery:

These are best managed in parturient with TOF with systemic medications,

inhalational anesthesia, Paracervical and pudental block. Regional anesthesia

(LEA) is usually avoided as it may cause a fall in SVR.

In cesarean section - GA is mostly preferred. Induction agent - ketamine is the

drug of choice. Maintenance with 50% N2O +O2

Inhaled anesthetic agents - because of decreased pulmonary blood flow

induction is faster and adverse effects of fall in BP / SVR is greater.

Pancuronium is muscle relaxant of choice though other drugs can also be used.

Because of coexisting poly cythemia it is not necessary to consider blood

replacement until 20% of blood volume is lost. Care should be taken not to inject

air into the tubings of IV line to present air embolization. α agonists like

phenylephonine must be available to increase the SVR.

Eisenmenger’s Syndrome

Consists of pulmonary HT with reversal of shunt or bidirectional shunt with

peripheral cyanosis

3% of all patients with CHD are reported to have Eisenmenger’s syndrome.

Prognosis is poor

Maternal and fetal prognosis depends on severity of PHT

Pathophysiology:

Degree of R L shunt depends on 3 factors

Severity of pulmonary HT and size of R L circulatory communication

Relationship between pulmonary and systemic vascular resistance

Contractile state of RV (Progressive RVF can cause decreased pulmonary

blood flow and increase of shunt)

Pregnancy induced changes:

Pregnancy is not well tolerated in patients with Eisenmenger’s syndrome.

Pulmonary vascular resistance is fixed and unaltered by the physiology of

pregnancy.

However in Eisenmenger’s syndrome patients in pregnancy, the usual fall in SVR

occurs and the reversal of shunt increases.

213

With the elevated shunt, rise in HR, stroke volume, increases the RV, Oxygen

consumption and in the presence of relatively desaturated blood may produce

RV compromise.

Anesthetic Consideration:

Anesthesia for vaginal delivery and cesarean section is identical to that of

patients with TOF. However diurersis usually occurs following delivery increasing

the hematocut, decreasing blood viscosity and pulmonary blood flow.

Adequate crystalloids to maintain Hct < 55% are recommended. If epidural

analgesia is selected, epinephrine is not added to LA as it would cause decrease

in SVR by its peripheral β agonistic effect.

Pregnancy after Valvular Surgery

Mitral Valvulotomy:

Patients with previous mitral valvulotomy have increased maternal and fetal

mortality due to pulmonary embolism and atrial fibrillation. These complications

may be related to residual right and left ventricular dysfunction, residual

pulmonary HT and dilated compliant LA.

Anesthetic Consideration:

Assessment of the status of valvulotomy should be made throughout and prior to

labour and delivery.

Changes in signs and symptoms with pregnancy and exercise are particularly

important because they indicate residual dysfunction or new lesion.

Residual pulmonary HT may exist despite correction of valvular lesion

Residual right and left ventricular dysfunction may also coexist. These may be

subtle and symptoms associated with low cardiac output may precipitate only

with exercise or stress

Chance of atrial fibrillation and systemic embolization are common

All patients require invasive monitoring

Avoid fall in SVR

Avoid fall in venous return

Avoid increase in pulmonary vascular resistance

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Mitral valve Replacement

Maternal mortality, fetal mortality and malformations are significantly increased

as compared to patients after valvulotomy. In non pregnant population, mitral

valve replacement is associated with number of chronic post op complications

like

Thromboembolism

Paravalvular regurgitation

Hemolysis

Infective endocarditis

These patients may also have low resting cardiac output and subnormal increase

in cardiac output with exercise, residual pulmonary vascular disease and some

degree of right and left ventricular dysfunction.

Pregnancy aggravates these complications further because of increased

intravascular volume, increased myocardial oxygen consumption and increased

risk of Thromboembolism.

Anesthetic Consideration:

Invasive monitoring is recommended in symptomatic patients with evidence of

LV compromise or pulmonary HT

Coumarin (Warfarin) anticoagulants are replaced with heparin during

pregnancy

One anesthetic approach is to continue heparin therapy throughout labour

and delivery, avoiding all forms of RA and using GA with inhalational and

opioid

The second approach is to discontinue heparin therapy immediately (6 - 12

hrs) prior to labour or administer protamine until coagulation normalizes.

Regional analgesia can be conducted and heparin to be resumed 24 hrs after

the removal of epidural catheter

Aortic Valve replacement

They have lower incidence of complication than those of mitral prosthesis.

215

Reason for this difference can be attributed to the difference in myocardial

function and more restricted use of anticoagulants in patients with aortic valve

prothesis

Generally cardiac output at rest and in response to exercise is normal in

patients with aortic valve prosthesis and ventricular function is better

Compared to patients with mitral valve replacement risk of thromboembolism,

residual pulmonary HT left and right ventricular compromise is lower

But pregnancy may aggravate these complications

Anesthetic Considerations:

All patients should be assumed to have some degree of residual myocardial

dysfunction.

Cardiomyopathy of Pregnancy

Pregnant women may have pre-existing cardiomyopathy or may develop

cardiomyopathy of pregnancy (peripartum cardiomyopathy PPCM)

Cause of pre-existing cardiomyopathy are diverse - infection, sarcoidosis,

amyloid, toxins (alcohol, cocaine) - commonest is hypertrophic obstructive

cardiomyopathy (HOCM)

Classic criteria for diagnosis of PPCM:

Development of cardiac failure in last month of pregnancy or within 5 months

of post partum

Absence of clear specific etiology for CCF

Absence of cardiac disease before last month of pregnancy

Some physicians extend these criteria to include CCF developing in 3rd TM for

which no cause can be found.

Patients with PPCM have dilated cardiomyopathy. Incidence is 1 in 3000 - 4000

patients. Most common symptoms are of CCF - Dyspneoa, orthopneoa, PND,

cough, palpitations.

Pathophysiology:

These patients have reduced myocardial contractility involving both ventricles,

manifested as decreased cardiac output and increase in LV filling pressures

216

Ventricular dilatation is so marked, that there may be functional MR or TR or

both

Test Indicators:

ECG - shows LVH, ST, T changes, 1st degree AV block, BBB, Cardiac

arrhythmias are frequent and include VPC’s and atrial fibrillation

X ray chest shows cardiac enlargement involving all 4 chambers and signs of

interstitial pulmonary edema

ECHO - shows ECF of < 0.4 (40%) dilated hypokinetic LV mild to moderate

mitral regurgitation

These patients are prone for systemic embolisation reflecting the formation of

mural thrombi in hypokinetic cardiac chambers. This is further accentuated by

pregnancy state of hypercoagulability. Prognosis is poor with only 25 to 40% of

patients surviving 5 yrs after definitive diagnosis.

Treatment:

Avoidance of unnecessary physical activity

Treatment of CCF with Digoxin and Diuretics, oxygen, vasodilators therapy or

ionotropes with vasodilator properties like Amrinone may be useful (decrease

the after load)

Cardiac arrhythmias treated with antiarrythmics

Anticoagulants like warfarin to treat embolization

If CCF is advanced cardiac transplant is indicated in patients with no

pulmonary HT or other systemic illness

Anesthetic Consideration:

Goals for management of anesthesia in the patients with dilated CM

• Failure of the expected sedative response to the intravenous injection of an

induction agent may reflect slow circulation time, making the patient

vulnerable to a drug overdosage

Avoidance of drug induced myocardial depression

Maintenance of normovolumia

Prevention of increase in ventricular after load

217

• Dose dependent direct myocardial depressant action of inhalational

anesthetics must be considered

• Opioids though have benign effect on myocardium, when used alone, may

not produce unconciousness. When used with Benzodiazipine may produce

sudden unexpected myocardial depression

• Stress of labour and surgery can cause increase in HR and SVR

precipitating CCF. It can be treated with β antagonists with caution

• Regional (LEA) analgesia is ideally preferred in these patients. LEA produce

changes in preload and after load that mimic pharmacological goals in the

treatment of this disease

• IV infusion of crystalloids / blood should be guided by CVP monitors to

decrease the chances of volume overload. PCWP may facilitate early

recognition for need for ionotropes

• Intraop hypotension is logically treated with drugs such as ephedrine that

provide some degree of β stimulant

Ischemic Heart Disease in pregnancy

Nowadays, there is increase in number of MI during pregnancy. This is related to

smoking, use of illegal drugs, and increase in child bearing age of women.

Post partum MI has alone been reported as complication of pre eclampsia.

Diagnosis:

High index of suspicion is necessary. Angina may not be considered in a DD of

pregnant women with chest pain. (Atypical)

Clinical examination and investigations may also be difficult to interpret such that

T changes are common ECG findings in normal healthy women.

Mode of Delivery: vaginal delivery is ideal. Cesarean only for obstetric

indications.

Monitoring: Invasive arterial line, SaO2, ECG are mandatory.

Anesthesia and Analgesia during labour and delivery :

During labour and delivery continuous LEA minimizes the hemodynamic

instability caused by pain and stress of labour. For cesarean if GA is preferred

care should be taken against

218

Intubation response

Life threatening arrythmias (VT,VF)

Post op ventilatory support if high opioid induction is used

Neonatal recuscitation

Oxytocic Drugs:

Ergometrine is contraindicated

Large IV bolus dose of oxytocin causes hypotension and so continuous

infusion is preferred

Puerperium:

Hemodynamic instability is more common in early puerperium

ICU monitoring for 48 hrs is mandatory

Post op analgesia is must

Prophylactic anticoagulants are to be continued for 3 to 6 months after

delivery

Arrhythmias in pregnancy:

During pregnancy, there is increased incidence of both benign arrhythmias and

arrhythmias with cardiac disease. Any abnormal rhythm causing maternal

hemodynamic instability causes fetal compromise and treatment is instituted

immediately.

None of antiarrhythmic drug is considered safe during pregnancy but none are

contrandicated.

During pregnancy, the lowest dose of the safest drug that will achieve therapeutic

effect should be used.

Common Arrhythmias during pregnancy:

Sinus Tachycardia: Normal during pregnancy. May be superimposed SVT

can occur. Underlying organic disease is unlikely and reassurance to be given

to avoid precipitating factors ( caffine, tobacco)

PSVT: More common in pregnancy, rarely indicates underlying organic

disease. Palpitations, dizziness, syncope may occur and may terminate

spontaneously with rest. Persistant tachycardia treated either with anti

arrythmics (Adenosis or viapred) or with DC cardioversion.In chronic cases,

219

ablation of abnormal conduction pathways may be indicated (usually done

after delivery)

Atrial Fibrillation: Associated with MS/MR/ Cardiomyopathy. Major risks

involved are thromboembolic phenomenon and pulmonary edema.

Prophylactic anticoagulation is must. Full anticoagulation during and after DC

cardio version. It is important to monitor therapeutic plasma levels of

antiarrythmic agents throughout pregnancy

Ventricular Ectopics are relatively uncommon during pregnancy only

reassurance when it occurs as palpitations

Ventricular Tachycardia or fibrillation may occur with underlying organic

heart disease. In such situation pregnancy is of secondary concern

Management:

In general, pregnant women with arrythmias should be treated as non pregnant

women.

All commonly used antiarrythmics crosses the placenta. There are reports of

using Digoxin, Lignocaine, procainamide, Flecanide, β blockers, amiodarone,

virapamil, bretylium and adenosine during pregnancy. But there are no well

designed controlled studies of any of these during pregnancy.

Antiarrythmics makes fetal heart rate tracing difficult due to fetal bradycardia. If

DC cardio version is to be performed during pregnancy, it is important to protect

Airway

Hypotension due to Aortocaval compression

Prophylactic anticoagulation

References:

1. Samuel C. Hughes, Gershan Levinson, Mark A. Rosen, Sol. M. Shnider:

Anesthesia for Obstetrics, 4th edition, Chapter 26.Lippincott 2002.

220

Anatomical and Physiological changes in Obstetrics Patients

Introduction

Pregnancy produces profound physiological and anatomical changes that are

adaptive and useful to mother in tolerating the stress of pregnancy, labour and

delivery. These changes alter the usual response to anesthetic techniques and

drugs. Therefore it is necessary to consider these factors while anesthetizing a

pregnant woman for labour, vaginal delivery or cesarean section.

Physiological Changes in mother during pregnancy: Pregnancy affects

virtually every organ system.

Parameters Average Change %

Volume and Capacities

Total Lung Capacity 0 to -5

Inspiratory Lung Capacity +5

Functional Residual Capacity (FRC) -20

Expiratory Reserve Volume -20

Residual Volume -20

Vital Capacity and Closing Volume No change

Mechanics of Ventilation

Minute Ventilation +50

Alveolar Ventilation +70

Tidal Volume +40

Respiratory Rate +15

Dead Space No change

Airway resistance -36

Total Pulmonary Resistance -50

Total Compliance -30

Only Lung Compliance No change

Only chest wall Compliance -45

FEV1 No change

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Diffusing Capacity -5

Blood Gases

PaO2 +10mmHg

PaCO2 -10mmHg

Serum HCO3- -4meq/L

PH No change

O2 Consumption +20

Most notable changes in maternal lung capacities and volume occurs in FRC

which decreases by 15 to 20 times at term

Vital capacity remains unchanged throughout pregnancy

Transverse and AP diameter of chest increases to compensate for elevation

of diaphragm. The diaphragm moves freely at term. However, as pregnancy

progresses abdominal breathing decreases and thoracic breathing is seen

About 1/3 of the parturient have airway closure during normal - tidal

ventilation that is closing volume > FRC and may develop atelectasis that is

increase in oxygen alveolar arterial gradient

Oxygen uptake increases by 20% during pregnancy due to increase in

maternal metabolism and work of breathing and fetal metabolism

Most earliest and dramatic change is the increase in minute ventilation by

50% as a result of increase in tidal volume and slight increase in RR

As a result of increase in alveolar ventilation at term, PaCO2 < 32mmHg but

PH is normal because of compensatory decrease in serum carbonate (26 to

22 meq/L)

PaO2 is slightly increased due to increased minute ventilation

ODC curve shifts to right during normal pregnancy due to increase in P50

allowing greater volume of O2 to be unloaded to fetus at a given arterial PaO2

222

Status P 50 in mmHg

Pregnancy 1st Trimester 27.8

2nd Trimester 28.8

3rd Trimester 30.4

Normal woman 26.7

Pre Eclamptic 25.1

An increase in circulating levels of progesterone is presumed to be the

stimulus for increase in minute ventilation

Opioid induced depression of ventilation seem to be less in parturient

reflecting the stimulation effects of progesterone increase

During labour, particularly 1st and 2nd stage, the pain from episodic uterine

contractions produce corresponding increase in maternal minute ventilation

(>300%) and in O2 consumption. Maternal hypocarbia and alkalemia results.

Hypocarbia can lead to hypoventilation between uterine contractions,

resulting in intermittent hypoxemia particularly in obese patients (or) who

have received parental opioids. Epidural analgesia eliminates these pain

induced increase in O2 consumption and minute ventilation

223

Decrease FRC/ and increase in O2 consumption can lead to faster

desaturation during Apneoa (Intubation). This can be avoided by 100% O2

preoxygenation

In order to maximize the fetal benefit of Preoxygenation this should be

continued for 6 minutes as this is the estimated time required for maternal -

fetal equilibration

Mean increase in umbilical vein PO2 of 22mmHg to 28mmHg is expected

within this 6 minutes

During pregnancy, capillary engorgement of mucose occurs throughout the

respiratory tract, potentially causing edema in the nasopharynx, oropharynx,

larynx and trachea. Therefore manipulation requires extreme care

Suctioning of orophrynx, insertion of airways, laryngoscopy may cause further

edema and bleeding

Because the area of false vocal cords may be swollen a small cuffed ETT (6.5

to 7.0) is recommended

Repeated attempts at Laryngoscopy during difficult airway must be avoided or

minimized to prevent obstructing airway edema

Cardio Vascular System

This system is progressively stressed during pregnancy and parturition

Many of these changes appear during 1st TM of pregnancy where there is

increase in CO of 22% and decrease in SVR by 30% at 8 weeks of gestation

These changes continue to 2nd and 3rd TM (early) of pregnancy when CO

increases 30-40% of non pregnant values

Increase in cardiac output, during pregnancy is primarily a result of increase

in stroke volume (by about 30%) with a more modest increase in HR (10 to 15

beats/min) is noted

Arterial BP do not change during pregnancy because of decrease in

peripheral vascular resistance, however there may be mild decrease in

diastolic BP and to lesser extent systolic BP

224

Parameters % of change from normal to Pregnant woma n

Intravascular fluid volume +35

Plasma volume +45

Erythrocyte volume +20

Cardiac output +40

Stroke volume +30

Heart rate +15

Peripheral circulation No change

Systolic BP -15

Diastolic BP -15

SVR No change

CVP No change

Maternal blood volume increases markedly during pregnancy. Near term

blood volume has increased 30-40% (>1000ml)

Plasma volume also increases from 40ml/kg of pre pregnant value to 70ml/kg

during late pregnancy

RBC volume increases from 25ml/kg to 30ml/kg

This increase of plasma volume in excess of RBC mass increase causes

dilutional anaemia of pregnancy

However Hb% remains 10-11gm/dl

In terms of tissue oxygen delivery, the decrease oxygen carrying capacity of

the blood is offset by several complementary factors

a. Increase in PaO2

b. Decrease in blood viscosity

c. Increase in cardiac output

d. Shift in ODC (increase in P50)

Maternal blood volume increases by 1000 - 1500ml in most woman allowing

them to easily tolerate blood loss associated with delivery

Average blood loss during vaginal delivery is 400 - 500ml compared to 800 -

1000ml for cesarean section

225

Blood volume does not return to normal up to 1 to 2 weeks of post partum

Increase in blood volume and cardiac output may produce changes in cardiac

examination of pregnant patients

Auscultation may reveal a wide, loud split S1 and a soft systolic murmur

caused by increased blood flow and vasodilatation

Position of heart is altered by the elevated diaphragm at term

ECG shows axis deviation, minor non specific ST, T and Q wave changes

and begin arrhythmias

Signs of significant heart disease in pregnancy include true cardiac

enlargement, severe arrhythmias, systolic murmur more than grade 3 with a

thrill or significant diastolic murmur

Onset of pain and apprehension of labour adds to cardiac work during

pregnancy and increase the stroke volume and CO by 45% of prelabour

values

BP also increases during labour. Uterine contractions can cause an effect of

auto transfusion

226

With each uterine contraction blood from the body of the uterus is pushed into

central circulation causing 10-25% increase in blood volume and CO. This

auto transfusion can occur after delivery

In addition to increase in central blood volume, obstruction to IVC is released.

As a result there is marked increase in stroke volume and CO (80% of pre

labour value) in the immediate postpartum. Patients with limited cardiac

reserve may experience cardiac failure during this period

Supine Hypotension and Aortocaval Compression (SHS)

Despite increase in blood volume and cardiac output, the parturient at term is

susceptible to hypotension when supine. Supine hypotension syndrome (SHS) is

a decrease in maternal blood pressure that occurs in about 20% of parturient

after 28 weeks of pregnancy (before the presenting part is fixed in pelvis).

When the patient is supine, the gravid uterus partially or completely compresses

the aorta and IVC leading to decreased venous return, decreased cardiac output,

hypo tension and reduced uterine blood flow. It is characterized by hypotension

with pallor, sweating, nausea and vomiting.

Most parturient are able to initiate compensatory responses that offset the

potential adverse hemodynamic sequale of this phenomenon. For eg: Increased

venous pressure below the level of IVC obstruction serves to direct venous blood

from lower half of body through para vertibral venous pluxes to azygos veins and

to right atrium to maintain CO and BP

This cause inadvertent IV injection of local anesthetic during an attempted

lumbar epidural anesthetic can result in bolus delivery to heart causing cardiac

depression.

Another compensatory response that offset IVC obstruction is increase in

peripheral vascular resistance. Permitting maintenance of BP despite fall in CO

(BP = CO X PVR). This compensation is inspired by the regional anesthesia.

Aortocaval compression results in uteroplacental insufficiency, fetal asphyxia,

due to decreased uterine blood flow in spite of healthy uteroplacental unit.

Lateral Angiogram from two women lying supine

227

Non Pregnant Pregnant

There is clear gap between vertebral

column and the aorta.

Aorta is displaced dorsally encroaching

the shadow of the supine.

Uniform width of aorta is seen. Aorta is narrowed at the level of lumbar

landosis

Decrease in maternal BP < 100mmHg persisting 10-15mts may be associated

with progressive fetal acidosis and bradycardia.

The incidence of SHS is reduced by nursing the parturient in lateral position.

Methods to increase maternal BP should be instituted when

Systolic BP pressure below 100mmHg in previous normotensive

20 to 30% decrease in BP of previous normotensive

FH suggestive of uteroplacental insufficiency

Therapeutic measures are:

Intravenous fluid replacement

Left ward displacement of uterus

Intravenous ephedrine

Leftward displacement of uterus can be done

Manually by lifting and displacing uterus to left

15o tilt of the table to left

Elevating the right buttock 10-15 cm with a blanket or foam rubber wedge

228

Maternal C.V.S changes during Pregnancy and labour on patients in lateral

and supine position

Central Nervous System:

Many animal studies have shown that requirement of inhaled anesthesia is

decreased in pregnancy. Decrease in MAC has been demonstrated in humans in

early pregnancy around (10-12 weeks) and in immediate PP (24-36 hrs)

Changes in MAC of various inhalational agents

Agent Non Pregnant Pregnant % change

Halothane 0.97 ± 4.04 0.73 ± 0.07 -25

Isoflurane 1.58 ± 0.07 1.01 ± 0.06 -40

Methoxyflurane 0.26 ± 0.02 0.18 ± 0.01 -32

The sedative effects of increased progesterone were posed as a mechanism of

this decrease in MAC in animal studies. However in animals MAC value returned

to non pregnant values within 5 days of PP when progesterone levels were still

elevated.

Pregnancy induced activation of B.endorphin is likely a major contributor for

decrease in MAC.

229

Regardless of mechanism, the important clinical implication is that the alveolar

concentration of the inhaled anesthetic that would not produce unconsciousness

in nonpregnant patient may approximate anesthetizing concentration in

parturient.

This degree of CNS depression may also impair protective upper airway reflexes

and subject the patient to hazards of pulmonary aspiration.

At term pregnant patients displays enhanced sensitivity to local anesthetics -

either hormonally mediated or related to engorged venous pluxes epidurally.

Increased intragastric pressure as pregnancy progresses and shunting of blood

through para vertebral venous pluxes due to compression of IVC results in

engorgement of epidural veins. This engorgement decreases the size of epidural

space and try compression may also reduce the volume of CSF in subarachroid

space.

This engorged veins produce pumping like effect, resulting in the spread of

local anesthetic in epidural space over more segments than would normally

be expected

Exaggerated lumbar lardosis of pregnancy may contribute to cephalad spread

of local anesthetic

These changes are consistant with 30 to 50% reduction in dose requirements

of LA needed for epidural and SAB in pregnant woman compared to non

pregnant

Reduced plasma HCO3- in compensation for hyperventilation could reduce

buffer capacity and contribute to enhanced action of LA

230

Increased plasma and CSF progesterone concentration parallel the

augmented dermational spread of LA in Sub arachnoid space

Distension of epidural veins is likely to be maximum in sitting position and

pressure in epidural space is also more in sitting position

During contraction, blood expelled from uterus passes epidural venous pluxes

and the pressure in epidural space may rise to 4-10cm water. It is for this

reason, injection of LA should be with held during uterine contraction as

spread may be unpredictable

Gastrointestinal System Alterations:

Gastro Intestinal changes makes the parturient vulnerable to regurgitation of

gastric contents and to the development of acid pneumonitis if pulmonary

aspiration occurs

They are initially related to progesterone effect with smooth muscle relaxation

and secondary effects from the physical effects of enlarging uterus

The early effects of relaxation prolong the GI transit time with slower gastric

emptying and frequent constipation. LES tone is decreased and causes heart

burn

Pain, anxiety and use of opioids during labour contribute to delayed gastric

transit time

231

Enlarging uterus changes the angle of gastro esophageal junction leading to

relative incompetence of LES. Intragastric pressure is increased during

pregnancy

These changes emphasize that the parturient are prone to silent regurgitation

even in the absence of sedative drugs or GA

Contribution of factors like decrease LES tone, increase IGP, delayed gastric

transit time, increase the risk of aspiration during inductance and emergence.

The history of heart burn in term pregnant woman should warn the anesthetist

and necessary precaution to be taken to prevent aspiration

During pregnancy, gastric acid secretion is increased due to elevated levels of

hormone gastrin produced by placenta.

Pulmonary reaction increase progressively as the PH of the aspirate decreases

less than 2.5 and volume as small as 25ml. 55% of parturient at term has gastric

volume >40ml and PH < 2.5 of gastric contents.

Hepatic functions alteration in pregnant women

Liver blood flow is unaltered during pregnancy. Acute fatty liver of pregnancy is a

rare but potentially fatal disorder that manifests about 35 weeks of gestation.

Management of anesthesia for caesarean in the patients is with epidural

anesthesia.

Decrease in S proteins is due to dilutional effect and liver output of proteins

remains unchanged.

S alkaline phosphatase is elevated due to its secretion by placenta.

Plasma pseudo cholinesterase activity is decreased by 25 to 30% but this rarely

produces significant prolongation of succinylcholines action. This activity may not

return to normal till 6 weeks of PP.

Renal function adaptations

Renal blood flow and GFR, increases about 50% by month of gestation reflecting

the changes in concentration. During the 3rd TM, these values return to normal.

As reflection of these changes, normal upper limit of BUN, creatinine

concentration is reduced by 50%.

232

S creatinine is 0.5-0.6mg/dL, BUN - 8-9mg/dL, and amino acids is common and

often results in mild glycosuria. (1 to 10g/day) or protunuria (<300mg/day).

Progesterone effect relaxes the renal pelvis, ureters and increases the maternal

susceptibility to UTI.

Alteration in Coagulation factors

As pregnancy progresses, coagulation function tends to incline towards

increased coagulation (hyper coagulable state). Platelet count remains to be

within normal limits but 20% of decrease in platelet count may be encountered

during 3rd TM. Increase in all coagulation factors particularly Fibrinogen factor VII,

VIII, X. Plasminogen activation is slightly reduced. These changes protect the

mother at parturition, when the placenta separates by increasing the

coagulability, so as to reduce the bleeding.

They have additional side effects of deep vein thrombosis.

Metabolic and Hormonal changes

Altered carbohydrate, fat and protein metabolism favours fetal growth and

development

These changes resemble starvation, because blood glucose and amino acid

levels are low whereas free fatty acids, ketones and triglycerides levels are

high

Pregnancy is a diabetogenic state; insulin levels steadily rise during

pregnancy

Secretion of human chorionic soma to mammotropia (HCS) previously called

H.placental lactogen by the placenta is probably responsible for relative

insulin resistance associated with pregnancy

Pancreatic β cell hyperplasia occurs in response to an increased demand for

insulin secretion

Secretion of HCG and elevated estrogen levels promote hypertrophy of

thyroid gland and increase thyroid binding globulin. Although T4 and T3 levels

are elevated free T3 and free T4 and TSH remains normal

233

References:

1. Edward G. Morgan, Maged S.Mikhail, Micheal J.Murray: Clinical

Anesthesiology, 3rd edition, Chapter 43. Mc Graw- Hill 2002.

2. Ronald.D.Miller: Anesthesia, 5th edition, Volume 2, Chapter 58. Churchill

Livingstone 2000.

3. Robert K. Stoelting, Stephein F.Dierdorf: Anesthesia and Co-existing

Disease, 3rd edition, Chapter 31.Churchill Livingstone, Philadelphia 1993.

234

Anatomical and Physiological Variations in Neonates , Infants, Children from normal adults

Introduction

Pediatric patients present unique anatomical, physiological and pharmacological

variations for management of anesthesia. Neonates (<28 days) Infants (1-12

months) and Children (1 - 12 yrs) are not merely small adults. The unique

characteristics that differentiate them from adults necessitate modification in

anesthetic techniques, drugs and dosages.

Anatomy of the airway in pediatric patients and its difference from adults

1. Large Occiput

2. Narrow nares

3. Small Pharynx

4. Large tongue

5. Mobile epiglottis

6. Larynx - C3 - anterior- funnel shaped

7. Obligate Nasal breathers

235

Airway of the infants differs in 5 different ways f rom adults

Relatively larger size of the infant tongue in relation to the oropharynx

Higher located larynx at C3 makes the straight blade more convenient

The epiglottis is shaped differently being short and stubby and angled over

the laryngeal inlet, control with laryngoscope blade is therefore difficult

Vocal cords angled, so blindly passed endotracheal tube may easily lodge in

anterior commissure rather than sliding into trachea

Infant larynx is funnel shaped, narrowest portion occurring at the cricoid

cartilage whereas in adult the glottic opening is the narrowest portion

Therefore in infants and children, an ETT that passes the vocal cord may be tight

in the subglottic region.

For this reason, uncuffed endotracheal tube is the preferred choice for the

patients younger than 10 yrs of age.

Anatomical variations of head and neck also influence the anesthetic techniques

(intubation). Large occiput tends to place the head in flexed position. This is

corrected by slightly elevating the shoulders with towels and placing the head on

a doughnet shaped pillow.

Specially contoured mask minimizes the dead spaces. Compression of

submandibular soft tissue should be avoided during mask ventilation to prevent

airway obstruction.

236

Internal diameter of the ETT is calculated by (4 + age/4) in mm (Rough guideline)

except in premature (2.5 - 3.0) and is full term (3.0 to 3.5 mm) correct size is

confirmed by easy passage into larynx and development of audible leak.

ETT length calculated by (12+ age/2) in cm. Convenient method to assess the

depth of insertion - 6+ weight in kg cms distance from the lip of the neonate.

In older children prominent adenoid and tonsillar tissue can obstruct visualization

of vocal cords.

Variations in Respiratory Physiology and their anes thetic

implication

Respiratory immaturity of preterm is well known

Production and secretion of surfactant (a complex phospholipids of lecithin) is

of paramount importance

Pulmonary capillaries approximate the primitive alveolar sacs at 24 weeks of

gestation

Type II alveolar cells begin to differentiate at 24 weeks but they start

synthesizing and secreting mature surfactant only at 34-36 weeks of gestation

Most important factor that physiologically distinguishes pediatric patients from

adult is OXYGEN CONSUMPTION

Oxygen consumption in Neonate is 6ml/kg/min that are twice that of adult. To

satisfy this increased demand alveolar ventilation is doubled

CO2 production is also raised, but increase in alveolar and minute ventilation

maintains near normal PaCO2

Since the tidal volume on weight basis is the same, the rate of respiration, is

increased in Neonate and Infants to compensate for increase in alveolar

ventilation

237

Parameters Neonate Adult

O2 consumption (ml/kg/min) 6.4 3.5

CO2 production (ml/kg/min) 6.0 3.0

Exhaled minute volume (ml/kg/min) 210 90

Alveolar ventilation (ml/kg/min) 130 60

Respiratory rate Br/min 35 15

Tidal volume (ml/kg) 6 6

Vital capacity (ml/kg) 35 70

FRC (ml/kg) 30 34

FRC/VA ratio 0.23 0.57

TLC (ml/kg) 63 86

Anatomical dead space (ml/kg) 2.5 2.0

Physiological DS/TV 0.3 0.3

Tracheal diameter (mm) 4 16

Tracheal length (mm) 57 120

PaO2 is low immediately after birth due to low FRC and fluid filled alveoli. So PH

is acidic and PaCO2 is high.

Normal arterial PH/ blood gas tension/ Hct in Neona tes and Infants:

Age

Parameters 1 hr 24 hrs 1 to 24 months

1 Arterial PH 7.33 7.37 7.40

2 PaCO2 (mmHg) 36 33 34

3 Base excess (mEq/L0 -6.0 -5.0 -3.0

4 PaO2 (mmHg) at Fi O2 of 0.21 63 73 83

5 Hct 53 55 35

Ribs are soft, non calcified and perpendicular to vertebral body in infants/

neonates.

In adults calcified and bucket handled - causing chest wall in infants/ neonates

more compliant.

238

FRC is less because of more complaint chest wall and less complaint lungs. So

the smaller airway tends to close at end expiration. This decrease in FRC, limits

the oxygen reserve during the period of apneoa (Intubation). FRC reached to

adult level (30ml/kg/min) at about 4 days of age.

In awake state, the infant uses the active mechanism such as glottic closure

(laryngeal breaking) and premature ceasation of expiration to maintain FRC

above its normal resting value. However these mechanisms are not available

under anesthesia and airway closure may result in absorption atelectasis with

V/Q mismatch and hypoxemia.

This can be prevented by controlled mode of ventilation in neonates and

infants

Hypoxic and hyper capneric ventilatory drives are not well developed in

neonates and infants, but they cause respiratory depression

Another factor is the composition of diaphragmatic and intercostals muscles

Type I muscle fibers are deficient neonate and infant which help in performing

repeated exercise. So any factor that increases the work of breathing

contributes to the early fatigue of respiratory muscles

Fatigue --- apneoa --- CO2 retention --- respiratory failure

Narrow acute angle formed by diaphragmatic with abdomen wall and protuberant

abdomens are also causes of respiratory failure due to match insufficient.

Composition of diaphragmatic and intercostal muscles changes during first 2 yrs

of life.

239

Variations in CVS and their Anesthetic Implications

240

Birth and spontaneous ventilation initiates circulatory changes that permits

the neonate to survive extra uterine environment

Fetal circulation is characterized by high PVR and low SVR R---L shunting of

blood through Foraman ovale and Ductus arteriosis

Onset of spontaneous ventilation increases pulmonary blood flow and

decreases PVR and increases LA pressure. This causes functional closure of

Foraman ovale. Anatomic closure occurs at 3 months to 1 year. 20 to 30% of

adults have probepatent FO

Functional closure of DA is at 10 to 15 hrs after birth. Anatomic closure takes

2 to 3 weeks

Increase in PaO2 is responsible for closure of DA but successful closure

requires arterial muscle tissue which is poorly developed in premature infants.

Alv may account for high PDA

During this critical period of 2 - 3weeks infants reverts readily from adult to

fetal circulation. This state is called Transitional Circulation.

Many factors that produce reversal of this circulation eg. Hypoxia, hypercapnia,

acidosis, anesthesia and infection induced. Rise in PVR, hypothermia, causing

cyanosis/ hypoxemia.

Persistent fetal circulation is seen in some conditions like - diaphragmatic hermia.

Meconium aspiration, pulmonary injection, polycythemia. This can be confirmed

by measuring PaO2 from preductal and post ductal arteries. A difference of

greater than 20mmHg verifies the diagnosis.

Anatomy of heart

In fetus, the work of circulation is shared by both ventricles, so the wall thickness

is same in both RV and LV. After birth there is increase in SVR and so increase

in LV wall thickness consequently development of myofilaments and cross

bridges causing LVH within 3 months.

Cardiac output in neonates and infants is dependent on heart rate, as the stroke

volume is relatively fixed by noncompliant and poorly developed LV

241

Age related changes in vitals

Arterial Blood Pressure mmHg Age Respiration

Rate br/min

Heart Rate

beat/min Systolic Diastolic

Neonate 40 140 65 40

12 months 30 120 95 65

3 yrs 25 100 100 70

12 yrs 20 80 110 60

Anatomy of Arteries and veins and cannulation

Canulation of tiny pediatric veins can be very difficult especially 1 yr old with

extensive subcutaneous fat. Usually long sephaneous vein around the ankle is

felt than seen. Scalp vein can also be used. 24G needle catheters from the

extension line should be removed since a high incidence of patient FO, increase

the risk of Paradoxic air embolism.

In emergency where IV line is in accessible fluids can be given through 18G

needle through medullary sinusoids within titral bone (Introsseous Infusion)

Arterial cannulation - usually ® radial artery is chosen (CVP) as it is preductal.

Central and autonomic nervous system

Autonomic Nervous System:

Parasympathetic system is well developed whereas sympathetic control is

immature. This reduced sympathetic activity is responsible to reflex bradycardia

and hypo tension to various anesthetic menuvous like (laryngoscopy, intubation,

0 2 4 6 8 10 12 16 Adult

Car

diac

Out

put m

l/K

g/m

in

1

00

2

00

242

tracheal suction, traction on eye muscles, viscera) and to anesthetic drugs like

succumethorium, halothane and neostigmine

Low level of baroreceptor activity in infants may reduce their ability to adapt to

hypotension by increasing the heart rate. (10% fall in intravascular volume

causes 15 to 30% fall in BP)

Central Nervous System

The Neonatal brain receives approximately 1/3 of the cardiac output to the adult

brain which receives 1/7th of

Central Nervous System variations and Anesthetic Im plications

Features that distinguish the CNS of neonate from adult are

Soft pliable cranium

Non fused sutures

2 open fontanelles (A F - open till 18 months, PF- 6 to 9 months)

Brain, structurally complete but incompletely myelinated up to 2 yrs

Spinard cord at L ¾ in neonates as compared to adults at L1

Fragile and subependymal vessels

Composition of brain changes dramatically during early infancy. In the neonate

the predominant constituent of brain is water. This water content decreases

throughout infancy as myelination and protein concentration increases. As this

water content decreases, the partition coefficient of inhalational anesthetics

increases.

Central blood flow (CBF) in healthy neonate is 30 - 40ml/100g of brain/min

which is less than the adult (55ml/100gm/min) and children (65ml to

100ml/100g/min)

A cerebrovascular change CO2 in response to PaCO2 and PaO2 is attenuated in

neonate.

Blood brain barrier is less mature in neonates and permits larger lipid soluble

molecules to pass.

The Neuro endocrine response to stress and surgery in neonates were similar to

those observed in adults.

243

Variations in Renal parameters and body fluids

Renal functions are markedly diminished in preterm and neonates because of

low perfusion pressure and immature glomerular and tubular functions.

Nearly complete maturation of GFR/Tubular function occurs by 20 weeks after

birth and complete maturation by 2 yrs of age.

Neonates are obligate Na+ losers and their concentrating ability in water

deprivatrion is 800 - 900 mogm/l) (35% less than adult levels)

Renal function in pediatric

GFR (ml/min/1.7 m 2)

Preterm 16

Term 20

3 - 5 mo 60

1 yr 80

Adult 120

GFR is markedly impaired at truth but develops rapidly during 1st year of life.

Half life of the drugs eliminated by kidney is prolonged in Neonates. As neonates

excrete water volume load more slowly, they are more susceptible for volume

overload. ½ NS or ¼ NS are ideal fluids of choice in neonates because of this

limited ability in handling sodium loads.

Distribution of body fluids

Total body water and ECF volume are increased proportionately in Neonate.

TBW contributes 75% in neonates compared to 50-60% in adults. ECF volume

equivalent to 40% of body weight in neonates compared to 20% in adults. By 18

to 24 months of age ECF volume relative to body weight is similar to adults.

244

Average Blood Volume

Recommended fluid often contains glucose as neonate / infants are more

susceptible for hypoglycemia. This increased ECF volume in neonates / infants

make them tolerant to greater volume of distribution for highly ionized drugs

Percentage of Body Volume:

Age Vessel Rich Group Muscle Group Fat Group

New born 22.0 38.7 13.2

1 Yr 17.3 38.7 25.4

4 yrs 16.6 40.7 23.4

8 yrs 13.2 44.8 21.4

Adult 10.2 50 22.4

Premature 95 ml/kg

Full term 85 ml/kg

Infants 80 ml/kg

Adults men 75 ml/kg

Adults women 65 ml/kg

245

Thermoregulation:

Neonate and infants are perpendicularly vulnerable to hypothermia because of

both large ratio of body surface area to weight and limited ability to cope up with

cold stress like immature sweat glands, poor insulation, and inability to move

from adverse environment.

Premature infants are even more susceptible because of very thin skin and

limited fat stores.

Infants compensate for cold by either shivering or non shivering thermo

genesis

Shivering mechanism appears only after 6 months. Minimal ability for

shivering makes the neonates to adapt to non shivering thermo genesis

Non Shivering or Thermo genesis is by which the neonate burns the brown fat

(located in the posterior neck, inter scalpular area, vertebral areas, around

kidney and adrenals) producing heat

Intact sympathetic nerves release catacholamines stimulating fat hydrolysis

Heat lost through radiation (most important mechanism of heat loss in

opening room) is decreased by using double shelled incubator for transport.

Heat lost through conduction is minimized by warm mattress warming the

opening room and that through conviction of gases and warming fluids

Critical temperature is the ambient temperature below which an unclothed/

anaesthetized person cannot maintain core temperature

Neutral Thermal state temperature is the ambient temperature at which

oxygen consumption of the person is minimal. In neonate, the oxygen

consumption is minimal when the difference between skin environment

temperature < 2 to 4o C

Neutral o C Critical o C

Preterm 34 28

Term 32 23

Adult 28 1

246

Hematological Variations:

The principal differences in fetal and neonatal RBC compared with those of older

infants are content of fetal Hb and relatively low 2, 3, DPG. Fetal Hb binds more

readily to O2 than HbA and combined with lower 2, 3 DPG results in left shift of

ODC.

P50 on day one is 20mmHg by 12 months due to high RBC concentration of 2,3

DPG. This along with change of HbF HbA results in right ward shift from fetal

to adult positions of ODC.

The high affinity of O2 in neonates is magnified as decreased O2 release to

peripheral tissues. This is offset by high Hb% concentration in neonates.

Age Hb% g/dl Hct%

1 day 19 61

2nd week 17.3 54

1st month 14.2 43

2nd month 10.7 31

6th month 12.3 36

247

1st yr 11.6 35

6th yr 12.7 38

10-12 yrs 13.0 39

Physiological anaemia results by 2-3 mo of age. Hb% and Hct increases

progressively after 3rd mo and reaches the adult value by 4 to 6 mo of age.

Thermal stress can increase catacholamines causing increase in PVR and

SVR, metabolic academia causing return of fetal circulation

Radiant heaters are used for warming after induction and before draping.

These should not be placed too close and should not exceed > 40oC to

prevent thermal burns

Hepatic Variations

At term functional maturity of liver is somewhat incomplete

Most enzyme systems for drug metabolism are developed but are not induced

As the infant grows the ability to metabolize increases rapidly by 2 ways.

1. Hepatic blood flow increases and more drug is delivered to the liver

2. Enzyme system maturation occurs

The microsomal enzyme system in neonate is absent.

Phase I reactions for drug elimination like oxidation and reduction are week in

neonates but increases to adult levels in a week

Phase II conjucation reactions take 1 to 3 months to develop. From 3 months

to 3 years drug metabolism equals that of adults

Premature neonate liver has minimal glycogen stores and is unable to handle

protein loads. This accounts for hypoglycemia and acidemia in high protein

diets

Pl. albumin and other S.proteins for drug binding are less in neonates making

free drug to increase in plasma

Vitamin K is deficient in neonates causing neonatal coagulopathy

Gastro Intestinal

At birth gastric PH is alkalotic, by 2nd day of life PH is in the normal range

(physiological) as per old patients. The ability to coordinate swallowing with

248

respiration does not fully mature until the infant is 4 to 5 mo. Therefore the

incidence of gastro-esophageal reflex is high in new born.

In view of decreased cardiovascular reserve and left shift of ODC, it is useful to

maintain neonatal Hct close to 40% rather than 30% often accepted for older

children.

Coagulation tests with exception of bleeding time are often abnormal in neonate.

Vit k dependent coagulation factors (II, VII, IX, X) are decreased leading to

increase in prothrombin time and partial thromboplastis time.

Fibrinogen and factor V are same as adults. Despite these laboratory

abnormalities, blood of a term neonate coagulates normally or at an increased

rate because of deficiency in naturally occurring anticoagulants.

Pharmacological variations in pediatric patients

Major variations for anesthetic consideration in ne onates

Greater volumes of body water and ECF in neonates’ results in larger Vd for

water soluble drugs like muscle relaxants. This leads to need for larger initial

doses per unit mass to obtain specific responses in neonates compared with

older child

Body composition differs considerably between neonate / infant and adult.

Vital organs constitute 18% in neonate in contrast to 5% in adult. So much

larger fraction of dose will be distributed in high perfused vital organs

Low albumin in preterm and increased bilirubin alter the drug binding in

neonates

Drugs with high lipid solubility like opiods, barbiturates diffuse more readily

into neonatal brain than into that of older child or adult because of higher

permeability of neonatal blood brain barrier. More over, high proportion of

cardiac output is dedicated to CBF (34% vs 14% in adult). So virtually all

drugs reach the brain

Hepatic enzyme systems in neonates are inactive and immature so drug

metabolism is delayed. Half life is prolonged.

Renal system shows low GFR and low tubular functions causing delayed

elimination of drugs

249

Older children tend to have mature renal, hepatic functions, normal adult

values for proteins and their fat and muscle content approximates adult

values. Most of the cardiac outputs are directed towards liver and kidney.

These factors mean that most medications have shorter half life in older

children (> 2yrs of age) than the adults. As child approaches adulthood half

life of most drug lengthens

In general half life of a drug in premature and infant is prolonged and it is

decreased in child > 2 yrs to early teen and again prolonged in terms to adults

Inhalational Anesthetics

Uptake and elimination of inhaled anesthetics are more rapid in children than

in adults

Principal reason for this is that pediatric patients have a larger minute volume

of ventilation and lower FRC, so more of gas in the lungs is exchanged with

each breath and also anesthetics are less soluble in blood of peadiatric

patients

Also the increased cardiac output in children increases the rate of anesthetic

equilibration in the tissues and this may be the reason for more rapid

appearance of cardiovascular side effects such as bradycardia and

hypotension.

Low incidence of halothane hepatitis in children than in adults even after

repeated usage

MAC Values of different inhalational agents

Agents Neonates Infants Small Children Adults

Halothane 0.87 1.1 to 1.2 0.87 0.75

Sevoflurane 3.0 3.3 2.5 2.0

Isoflurane 1.6 1.8 to 1.9 1.3 to 1.6 1.2

Desflurane 8 to 9 9 to 10 7 to 8 6.0

MAC value is highest in infants of 3 to 6 months of age.

250

Muscle Relaxants

Morphologic and functional maturation of the neuromuscular junction is not

complete until about 2 months of age

With respect to nondepolarising, infants are three fold sensitive to these drugs

Because of the larger Vd the initial dose of NDP muscle relaxants calculated

on the basis of infants body weight is not different from adults

Immaturity of hepatic or renal function could prolong the duration of action of

muscle relaxants that are highly dependent on these mechanism for

clearance

In contrast with other NDP muscle relaxants, plasma clearance of Atracurium

is greater in infants compared with older children. This is because of

Hoffmann hydrolysis of this drug (Non organ route)

Neonates and infants require more of succinyl choline on a body weight basis

than do the older children due to increased TBW/ ECF volume and increased

251

Vd . Infants require 3mg/kg and children 2mg/kg to produce reliable condition

for intubation

Children are more subject to cardiac arrhythmias, myoglobnemia.

Hyperkalemia, malignant hyperthermia, masseter spasm after succinylcolnine

than adults

So, succinylcholine is better avoided for routine elective surgeries in children

and adolescent patients

Neostigmine:

After a standard dose of neostigmine, antagonism of NDP blockade is faster in

pediatric patients than in adults.Infants and children require ½ to 2/3 as much

neostigmine as adults to antagonize muscle paralysis.ED50 for neostigmine was

13.1 mcg/Kg - children, 15.5 mcg/kg - Infants, 22.0 mcg/kg for adults.

Intravenous Agents:

Thiopentone remains the standard intravenous induction agent for children. The

dose varies with age.

The effective dose GD50 in neonates is 3.5mg/kg increases to 7 mg/kg in infants

of 1 to 6 months and during throughout and in childhood it is 5-6 mg/kg.

The reduced requirement in neonates to old infants is due to decreased plasma

protein binding.

252

The increased requirement in infants and children when compared to adults (4-5

mg/kg) is due to increase in their, cardiac output as this would reduce the 1st

pass concentration at brain.

References

1. Edward G. Morgan, Maged S.Mikhail, Micheal J.Murray: Clinical

Anesthesiology, 3rd edition, Chapter 44. Mc Graw- Hill 2002.

2. Ronald.D.Miller: Anesthesia, 5th edition, Volume 2, Chapter 60.Churchill

Livingstone 2000.

3. Robert K. Stoelting, Stephein F.Dierdorf: Anesthesia and Co-existing

Disease, 3rd edition, Chapter 31, Churchill Livingstone, Philadelphia 1993.

253

Anatomy and Physiology of CSF pathway, Concepts of Intracranial Pressure and Factors Determining the I CP

Anatomy and Physiology of CSF Pathway

Cerebrospinal fluid (CSF) plays a major role in protecting the brain and the

spinal cord, as well as in providing an optimal physiochemical environment for

functioning of neural tissues. It also helps in transport of nutritive substances

metabolic products and neurotransmitters

CSF affects the Intracranial pressure which in turn determines the cerebral

perfusion pressure (CPP=MAP-ICP/CVP)

These functions are greatly influenced by the rates of CSF formation,

absorption and circulation CSF dynamics

CSF Formation

CSF is formed by the combination of ultra filtration and secretion of plasma by

choroid plexus in the lateral ventricles. Its composition differs from plasma and

ECF in other tissues.

SG - varies greatly from 1.003 to 1.007 which is much lower than the plasma

Concentration of glucose - 60% of the blood and protein < 0.5% that in

plasma

Na+, Cl-, Mg++ more than in plasma

K+, Ca++, HCO3-, PO4

2-are less than in plasma

Concentration of these substances in CSF vary depending on the site of

sampling, showing the transport of solute to and from the CSF occurs as it

passes towards the site of absorption. Ca++, HCO3-, K+ concentration are lower

while protein is higher in Lumbar CSF than in cisternal CSF.

CSF is formed in choroid plexus (CP) and extrachoroidally

Capillary endothelium of choroid plexus is fenistrated unlike the rest of the

cerebral vasculature

The epithelial cells are joined together by “tight junctions” which produces a

blood CSF barrier

254

Fluid is forced through this by hydrostatic pressure in other words CP

perfusion pressure and this contributes to ultra filtration

There are also ATP dependent membrane pumps which carry out active

transport of Na+, Cl-, HCO3- into CSF and K+ out of CSF

40-70% formed in CP

30-60% CSF formed extrachoroidally by ultra filtration in the cerebral capillary

endothelium through the ‘tight junction’

These cells have specialized pin ocytic vesicles which aid in transport of

number of solutes and water

Astrocyte layer around the endothelium also takes part in active transport

CSF is produced at the rate of 0.35 - 0.40ml/min or 21ml/hr or 500ml/day

Total volume is 100-150ml in adults and this volume is replaced by fresh CSF

in 5-7 hrs that is turn over is 3 ½ times/day

CSF Circulation

The main driving force for CSF flow

is the hydrostatic pressure of CSF

formation and the gradient between

ventricular pressure and

subarachnoid pressure over the

concavity of hemisphere called

transmantle pressure.

Other factors which promote the

movement are ciliary action of

ependymal cells in the ventricles,

respiratory variations and vascular

pulsations of cerebral arteries and

choroid plexus.

255

CSF Absorption

Takes place in the Arachnoid villi and granulations located within the dural wall

enclosing the superior sagital sinus and other venous sinuses intracranially and

dural sinusoids of dorsal nerve roots of the spinal cord. Normally 90% of CSF

absorbed within the cranium and 10-15% spinally.

Other pathways of absorption: Through lymphatics of nasal mucosa via

periolfactory and optic nerve sheaths (pathological)

Driving force of CSF absorption is mean CSF pressure to superior sagital

sinus pressure gradient (Normal = 6cm H2O)

High velocity blood flow produces venturi effect maintaining CSF absorption

despite postural variations

Lateral Ventricles

Foramina of Monro

3rd Ventricles

Aqueduct of Sylvius

4th Ventricles

Cerebello Pontine Cistern Cistern Magna

Foramen of Luschka (Paired) Foramen of Magendie

(midline)

Spinal Cord

Anterior

Inferiorly

Ven

tral

ly

Basilar Cistern

Cerebral hemispheres

Superior Sagital Sinus

Absorbed

Dorsally around Cerebellar Hemisphere

256

CSF absorption is directly proportional to ICP and inversely to cerebral

venous pressure

CSF Dynamics

The term CSF Dynamics include the rates of formation and absorption of CSF

and resistance to absorption and interaction of these parameters with intracranial

pressure.

Assessment of CSF dynamics necessitates measurement of all these

parameters (in animals initially and later in humans with appropriate

modifications)

1. Ventriculocisternal perfusion

2. Manometric Infusion

3. Volume Injection or Withdrawal

1. Ventriculocisternal perfusion

Introduced in 1960’s, mainly in goats

Cannulae are placed in one or both lateral ventricles and in cisterna

magna

Labelled mock CSF is infused into ventricles and CSF is continuously

sampled through cisternal canula

The concentration of labelled substance that is sampled is less than that

infused (Co < Ci) and this difference depends on the rate of CSF formation

(Vf) since the freshly formed CSF dilutes the infusate. Thus

Vf = Vi (Ci - Co) where Vi - rate of infusion, Ci - Concentration of label in

infusate, Co - Concentration of label in sample,

Rate of fluid entry into system = Vf + Vi

If Vo is rate of sampling then Va (rate of absorption) Va = (Vf+vi) - Vo

Resistance to CSF absorption - Ra = Va/ICP

=Rate of absorption / Intracranial Pressure

2. Manometric Infusion:

Requires a manometric infusion device which can simultaneously infuse fluid as

well, measure the pressure at the site of insertion.

257

This instrument is inserted into subarachnoid space and basline pressure

(Po) is noted

The mock CSF is infused at steady state whileCSF pressure is monitored

Once the pressure (Ps) is stabilized, the corresponding (Vi) rate of

infusion noted

This process is repeated at different infusion rates to obtain Vi : Ps values

These are plotted on a semilog graph and a linear slope is esctrapolated

to the left

The value of Vi corresponding to the baseline pressure po is considered to

be Vf (rate of formation of CSF)

Compliance can be calculated from C=Vi / (dp/dt) where dp/dt - rate of

increase of CSF pressure during infusion

3. Volume Injection and withdrawal:

In this method, ventricular or spinal subarachnoid catheter is inserted. After

recording the baseline pressure Po a Known volume of fluid DV is injected or

withdrawn from the catheter and a timed recording of CSF pressure is made.

Pressure-Volume Index PVI = DV / (log Pp/Po)

Where Pp is the peak CSF pressure reached

Intracranial Compliance is calculated from C = (0.4343 X PVI) / Po

In normal adults 25ml of DV is required to raise the Po by factor of 10.

So PVI = 25ml In Infants PVI = 10ml

Intr

a C

rani

al P

ress

ure

Vi - Rate of Infusion

P0

Vf

Intr

a C

rani

al P

ress

ure

Vi - Rate of Infusion

P0

dp /dt

258

Modification of CSF Dynamics study in human

Ventriculo cisternal perfusion - sampling catheter is placed in lumbar

subarachroid space rather than in the cisterns

CSF pressures are monitored closely to avoid any abrupt increase in CPP

Techniques most commonly used in humans is volume infusion or withdrawal

because

a. Here various parameters are determined with single injection or

withdrawal of fluid

b. CSF withdrawal may be therapeutic in patients with increased ICP

c. As this is closed system risk of injection is minimized

d. Repeated assessment could be made

Non invasive assessment of CSF dynamics

MR imaging Normal volunteers CSF flow was found to occur synchronously

with arterial pulse wave which was thought to provide the main impulse for CSF

flow and mixing.

Cine-MRI and retrospective cardiac gated MRI were found to be helpful in the

evaluation of conditions with altered CSF flow as in syringomyelia and

hydrocephalus.

Color Doppler - in babies. Also used in diagnosis of ICH / ventriculitis.

Physiological Factors affecting CSF Dynamics

Vf-Rate of formation of CSF

Increase in ICP decreases CPP Decreased Vf

Adrenergic stimulation vasoconstriction and low carbonic anhydrous Decreased Vf

Cholinergic stimulation - Muscaranic Increased Vf

Peptidergic stimulation - VIP/P vaso dilation Increased Vf

Hypothermia - low metabolic activity of CP and low blood flow to CP Decreased Vf

Hypocapmia - acute Decreases Vf returns to normal

Hypocapmia - chronic Increases Vf

Hypercapmia Normalizes Vf if it was low at

normocapnia

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Effect of Pharmacological agent on CSF dynamics

Concepts of ICP and factors determining it

ICP refers to CSF pressure within the cranial cavity

Variation in ICP is influenced by CSF dynamics, cerebral circulation and

Intracranial abnormalities

Cerebral perfusion pressure is the driving force that permits blood flow

through the brain tissues

Cerebral Perfusion Pressure = MAP - ICP or Cerebral Venous Pressure

which ever is greater

Hence isolated increase in ICP or decrease in MAP may decrease CPP -

cerebral ischemia, neuronal injury and neuronal death

260

Increase in ICP also causes herniation of brain structure causing cell injury

and neuronal death

Determinants of ICP

Murro Kellir doctrine states (1783) that pressure inside the closed cranial cavity is

determined by

1. Volume of brain tissue

2. Blood flow

3. Cerebrospinal fluid is called intracranial volume (ICV) and is relatively

constant.

Normal ICP in supine human is 5 - 15mmHg

Any increase in ICP that exceeds the intracranial space result in increase

in ICP

Increase in ICP also occurs if IC space is decreased (eg) in depressed

#skull or if ICV is increased eg (High brain substance, high CBF, high CSF

volume or space occupying lesions like foreign body, air)

Changes in ICV of 0.1 to 0.5% - Increases ICP by 40 - 50mmHg

Interactions between CSF dynamic and ICP

Increase in ICP decreases CPP and perfusion pressure in choroids plexus.

This decreases the filtration pressure required for CSF formation (Vf)

A fall in CPP < 70mmHg (N=100mmHg) due to increased ICP either alone or

in combination with decrease in MAP results in decreased Vf

Rate of absorption (Va) increases with increase in ICP, since ICP is the

driving force for reabsorption

Resistance to absorption (Ra) remains fairly constant till ICP increases to 30

cm water. With further increase in ICP / Ra declines and Va is increased. This

fall in Ra is due to increase in number and size of pinocytic vesicles in the

Arachnoid villi and opening up of additional channels for reabsorption

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Normally rate of absorption is balanced by rate of formation so ICP remains

constant

Lumbar CSF pressure is normally 70 - 180mm of CSF (cm water) within this

range CSF formation is independent of interventricular pressures

Absorption as it by bulk flow is proportional to pressure

At pressure 112mm CSF Va = Vf below at 68mm CSF absorption stops

Large amount of CSF accumulate when reabsorptive capacity of

arachnoid villi is decreased - communicating or external hydrocephalus

Fluid also accumulates proximal to the block with in the ventricles - Non

communicating or internal hydrocephalus

Pressure- Volume Compliance Curve (PVC)

Pressure Volume curve reflects the

changes produced by an expanding

intracranial tumor. It measures the

change in intracranial pressure in

response to change in intracranial

volume.

For the region from 1 to 2:

Normally increase in ICV is well

compensated by

Initial displacement of CSF fluid from cranium - spinal

Increase in rate of absorption Va

Flo

w m

l/m

in

0

.4

0.8

1.2

68 112 200 Pressure Outflow (mmcsf)

Absorption

Formation

262

Decrease in rate of production Vf

Decrease in CBV (Venous)

For the region from 2 to 3:

Beyond a point, a small increase in volume produces rapid and large increase in

ICP.

Testing of volume / pressure relationship

Patient’s position on the PVC can be elicited by injecting small volumes (0.1 to

1ml) of normal saline into ventricular catheter while measuring ICP.

Resulting ICP gives an index of severity of IC compression

If the increase is small, patient is on flat part (1 to 2) on the curve

Jugular vein compression and measurement of amplitude of pulse wave are

other methods of measuring position of the patient on PVC

ICP Waveforms

These are the indicators of the conditions within the cavity and may provide

information about the state of compliance and stiffness of the brain

Actually the down slope of the wave provides the greatest information about

the brain stiffness

Slow decay - stiff non compliant brain

Sinusoidal with multiple harmonics - slack compliant healthy

There are 3 distinct pathological wave forms

A wave - Plateau waves - significant prognostically in patient’s management

B wave - 1 / min wave

C wave - 6 / min wave are less useful in this regard

A Waves:

Intr

acra

nial

P

ress

ure

(mm

Hg)

Minute

50-100mmHg

263

Characterized by sudden increase in ICP followed by rapid decrease to less

than or to baseline level

Pressure increase from baseline to 100mmHg makes the patient sympathetic

and hyperventilating for 10 - 20 minutes

Mechanism - Increase in blood volume

Events causing are 1. Anxiety, 2. Pain, 3.Induction of anesthesia

Represent failure of auto regulation

B Waves:

0.5 to 2 / min frequency / amplitude < 50mmHg

Brain stem failure, head injury, chynestrokes breathing

C Waves:

4 - 8 / min frequency / amplitude < 20mmHg

May be exaggeration of normal systemic pressure

May also signal brain stem dysfunction if persists for long periods

Monitoring of ICP

Indications for ICP monitoring - Comatosed patients

CNS causes are:

Head injury

Subarachroid hemorrhage (SAH)

Post operative ICP monitoring

Hydrocephalus especially normal pressure HC

Non CNS cause

Liver failure and Hepatic transplantation for fulminant hepatitis

Head Injury:

Patients without CT indicators of increased ICP and without H/O hypoxic and

hypotensive episodes should not undergo ICP monitoring

ICP monitoring is a useful indicator in patients with mass lesions after head

injury

In patients with multiple injuries and on artificial ventilation, ICP monitoring is

a good indicator of delayed hypoxic neuronal damage

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SAH:

When SAH is massive and GCS is 13 or less, placement of ventricular

catheter indicated for dual purpose - drainage and ICP monitoring

Post operative management of brain swelling by osmotic agents and

ventilation and also aids in making hypertensive therapy safer in patients with

vasospasm after SAH

Post operative ICP monitoring

Indicated following prolonged or difficult resection of glioma, Aneurysm

surgery etc

Useful in early detection of post operative hematoma and tension

pneumocephalin

Hydrocephalus:

Helpful in differentiating normal pressure hydrocept from dementra due to

brain atrophy

Outcome:Liver failure and Hepatic Transplantation

Increase in ICP due to encephalopathy but coagulopathies make hazardous

Methods of monitoring - Devices used

Devices can be classified according to whether transducer is located inside the

cranial vault or externally. Methods are:

a. Fluid coupled transducer with catheter - External

b. Transducer tipped systems - Internal

a. Fluid Coupled Catheters:

Here transducers are placed externally. Depending on the site they are of 3 types

1. Ventricular catheter

2. Subarachroid screw and bolt

3. Subdural catheter

1. Ventricular catheter:

Catheter placed inside the ventricle (lateral) through a burr hole

Standard method

Relatively safe

Can also be used to withdraw CSF

265

Inject saline to test compliance

Disadvantage:

If anatomy is distorted, there is difficulty in placement - there are risks of

insertion and hemorrhage

2. Subarachiord screw and bolt:

Leed bolt, Mcdowel screw, Richmond screw

Inaccuracy is 41%

Small leaks and obstruction at high ICP are common

3. Subdural Catheter:

Throat cup catheter - ribbon like catheter placed in sub dural space at

craniotomy

Inaccuracy is 40% at high ICP

Leaks , obstruction to lumen are common

b. Transducer Tipped Systems:

Transducer is within the vault. This can minimize the problem of leaks,

obstruction or infection.

1. Ladd ICP monitor

2. Gaeltec monitor

3. Camino system

1. Ladd ICP monitor:

Detects changes in ICP by deflection of a mirror which in turn alters return

of fiber optically transmitted light

Can be placed either in epidural or sub dural space

Disadvantages:

Cannot be calibrated or zeroed

No waveforms for visual monitoring

Erroneous readings due to break in fiber optic cable

2. Gael Tec ICP monitor:

Contains a strain gauge transducer at its tip, one side being coupled to

atmospheric pressure by a rigid walled tubing and other reflecting ICP

through a thin membrane

266

Advantages:

Generates electrical signal that can be easily visualized on external

monitor

Zeroed in vivo by injecting 0.3ml of air to open the potential space to

equalize the pressure on 2 sides

More accurate in sub dural space than fluid filled catheter

Gaeltec monitor is placed mostly epidurally

Disadvantage:

Electrical disconnections

Pneumocephalus - rupture of membrane

3. Camino system:

Miniatured fiber optic intracranial pressure monitor determines pressure

directly from the amount of light reflected off the pressure sensitive tip

Does not require counter pressure or pneumatics

Can be calibrated but not zeroed

Safe, accurate and reliable

Sites of Monitoring

Intra Ventricular

Intra Parenchymal

Subdural

Subarachnoid

Extradural

Lumbar

267

Duration of ICP monitoring

Based on the risk of infection / hemorrhage Vs benefit to be obtained from

continuous measurement.

If ICP is low - discontinued < 24 hrs

If ICP is high - used to guide therapy

Signs and Symptoms of raised ICP

The clinical presentation varies with time course of increase in ICP

Sudden massive increase present with coma

In sub acute presentations - headache, vomiting, irritability or a personality

change (children)

Detectable papill oedema takes 2 weeks to develop physical findings

depends on age of presentation and site of obstruction to CSF flow

In Infants - Increase in ICP presents as hydrocephalus associated with

disproportionate increase in head circumference bulging anterior fontanelle

and dilated scalp veins

In older children visual tracking deficits due to oculomotor /gaze paloy

268

Shift of Intracranial contents occur when asymmetrical increase in pressure

create pressure gradients across 1. Falx, 2.Tentorium, 3.Foramen magnum

resulting in herniation of brain contents.

Increase in Supratentorial pressure:

Tentorial herniation or uncal syndrome

Typical eye and motor signs

Eye signs:

vertical gage palsy (sunset sign)

Dilated unreactive pupil - sign of brain stem compression

Post cerebral artery compression - irreversible blindness

Motor signs:

Hemiplegia - cerebral peduncle

Exterior hypertomia, decrebrate rigidity, decorticate posturing, ophisthotonus,

hypotomia - midbrain especially in children

Further midbrain compression - hypertension / bradycardia/ tachypneoa

Brady Apnoea coma

ICP from intratensional lesions

Cerebellum out of foramen magnum or upward through Tentorium.

Medullary coning: Ocalomotor signs, vomiting, cranial abnormalities

Miotic fixed pupils - Central hyperventilation

Transcalvanal

Cingulate gyrus under flaxcerebris

Obtitration of ventricles

Uncinate gyrus under Tentorium cerebelli

Cerebellar Tonsil through foramen magnum

Sup

rate

ntor

ial

Infr

aten

toria

l

269

Methods to decrease intracranial pressure

General Principles:

Patient airway, adequate oxygenation, hyper ventilation - Ventilation to

Normocapnia is the integral part in Intensive management of head injury patients.

(PaCO2 of 35-40mmHg). It is suggested that hyper ventilation is employed in

patients in whom other modalities that is surgery Normoventilation, osmotic

therapy and Barbiturates have failed to control ICP.

Pharmacological Measures:

Sustained increase in ICP of 20mmHg has to be treated (or) 20mmHg with

decreased IC compliance is also to be treated.

Central Dehydration:

Osmotic Diuretics:

Mannitol 0.25 to 1 g/kg IV over 15 - 30 mts removes 100ml of water from the

brain S.osmolarity should be maintained less than 320 mosm/L and CVP -

12 to 15cm water. Decrease in ICP is seen within 30 mts and max effect with

in 1 to 2 hrs

Urine output increases by 1 to 2 l/hr. Electrolytes and volume should be

replaced appropriately

Duration of 6 hrs contraindicated in CCF/ before opening of dura in aneurysm/

A-V malfunction / old age

No incidence of rebound increase in ICP, or cerebral venous thrombosis

Do not penetrate blood brain barrier

Loop Diuretics:

Furosemide 1mg/kg IV - Hypokalemia is common. Decrease in ICP by decreased

CBV and decreased CSF formation.

Advantages over Osmotic diuretic:

Lack of initial volume expansion

Lack of initial increase in ICP

Absence of peripheral vasodilation

Choice in patients with CCF

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Corticosteroids:

Restoration of B-B barrier by stabilization of capillary membranes

Reduction of CSF formation

Dexa 4 to10mg/stat 4mg every 6th hourly

Postural:

Elevation of 30oC increase in the venous outflow decreases ICP extreme flex ion

or extension and restrict jugilan venous outflow and increases ICP.

Surgical - CSF drainage, VP shunts - diversion, decompression

Intracranial Compartments and their techniques for manipulation of their volume

Compartment Volume Control Method

Cells (glia, neurons, tumors, hematoma) Surgical removal

Fluids - ICF, ECF Diuretics, Steroids

CSF Drainage

Blood - Arterial, Venous Low CBF high venous drainage

References

1. James Cottrell, David Smith: Anesthesia and Neurosurgery, 4th edition,

Mosby 2001.

2. Wylie, Churchill Davidson: Practice of Anesthesia, 6th edition, Chapter 30, 32,

Edward Arnold 1995.