respiratory physiology during anesthesia
DESCRIPTION
RESPIRATORY PHYSIOLOGY DURING ANESTHESIA. Presenter – Hitesh Gupta Moderater – Dr Anil Ohri. Anesthesia - impairment in pulmonary function whether patient is breathing spontaneously or ventilated mechanically after muscle paralysis . - PowerPoint PPT PresentationTRANSCRIPT
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RESPIRATORY PHYSIOLOGY DURING ANESTHESIA
Presenter – Hitesh GuptaModerater – Dr Anil Ohri
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• Anesthesia - impairment in pulmonary function whether patient is breathing spontaneously or ventilated mechanically after muscle paralysis.
• 20% of patients may suffer from severe hypoxemia(spo2 81% for up to 5 minutes)
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• GA produces
1. Fall in FRC
2. Fall in lung compliance
3. Uneven distribution of ventilation
4. Increased physiological dead space
5. Increased P(A-a)O2
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• FRC reduced by
0.8 to 1.0 L - changing body position from upright to supine
another 0.4- to 0.5-L - when anesthesia is given.
• Muscle paralysis and mechanical ventilation cause no further decrease in FRC.
• average reduction corresponds to around 20% of awake FRC
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• Cranial shift of diaphragm and a decrease in transverse diameter of the thorax contribute to lowered functional residual capacity (FRC).
• Decreased ventilated volume (i.e. in atelectasis and airway closure ) is a possible cause of reduced lung compliance (CL).
• Decreased airway dimension by the lowered FRC should contribute to increased airway resistance (Raw).
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Causes of reduced FRC• General anesthesia:
• due to loss of respiratory muscle tone, which shifts the balance between the elastic recoil force of the lung and the outward force of the chest wall to a lower chest and lung volume.
• Maintenance of muscle tone( ketamine anesthesia) does not reduce FRC
• Supine Position: • FRC decreases by 0.8-1.0L• Diaphragm cephalad displacement
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. Immobility, excessive intravenous fluid administration:
• Dependent areas below the heart (zone3-4) are susceptible to edema
• this will happen after being immobile (5 hour or more) in supine position with excess volume administration
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. Surgical position:1. Supine : FRC
2. Trendelenburg: FRC
3. Steep trendelenburg: FRC
4. Lateral decubitus : FRC in dependent lung and FRC in un dependent lung (overall FRC )
5. Lithotomy : FRC more than supine
6. Prone : FRC
Prone> lateral decubitus > supine > lithotomy> trendelenburg> steep trendelenburg
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Ventilation pattern:
• Rapid shallow breathing occurs due to reduced compliance - FRC
• This can be prevented by•Periodic large mechanical inspiration•Spontaneous sigh•Peep
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. Decreased removal of secretion:
Increasing viscosity & slowing mucocilliary clearance
1. Tracheal tube (low or high pressure cuffs any place in trachea)
2. High FiO23. Low moisture4. Low temperature 5. Halogenated anesthetics
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Compliance and Resistance of the Respiratory System
• Static compliance(lungs and chest wall) is reduced – from 95 to 60 mL/cm H2O during anesthesia
• static lung compliance- 187 mL/cm H2O awake to 149 mL/cm H2O during anesthesia
• Resistance( total respiratory system and lungs)increases both spontaneous breathing and mechanical ventilation
• increased lung resistance reflects reduced FRC during anesthesia
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Causes of decreased lung compliance • Atelectasis
• 15% to 20% of lung is collapsed at the base of lung during uneventful anesthesia.
• thoracic surgery and cardiopulmonary bypass > 50% of the lung can be collapsed.
• decreases towards apex of lung
• increases with BMI but is independent of age
• COPD patients show less atelectasis
• Risk factors:
High FiO2
Low V/Q ratio
Longer time exposure of high FiO2 to low V/Q
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• ZONE A – ventilation > perfusion resulting in dead space like effect
• ZONE B – perfusion > ventilation leading to low Va/Q and caused impaired oxygenation of blood due to intermittent airway closure
• ZONE C – there is complete cessation of ventilation (atelectasis) but still perfusion is there (shunt)
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Prevention of atelectasis
• Positive end expiratory pressure (PEEP)
• Application of 10 cm water PEEP can open collapsed lung but it recollapses on cessation of peep
• Gen PEEP of 10 cm H2O squeezes perfusion to lower lung
• Selective application of PEEP to lower lung might lead to redistribution to upper lung
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• Maintenance of muscle tone
• Anesthetic that allows maintaince of respiratory muscle tone will prevent atelectasis e.g ketamine
• Pacing of diaphragm through phrenic nerve stimulation prevents atelectasis ,but is too complicated
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• Recruitment maneuvers
• Sigh maneuver
• Double VT
airway pressure of 30 cm of H2O decrease atelectasis by 50 % of initial size
for complete reopening 40 cm of H2O is req.
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Prevention of atelectasis
•VC maneuver
Vital capacity maneuver is the volume inflated to the maximum breath by the awake subject before anesthesia.
Inflation of lungs to +40 cm H2O maintained for no more then 7 to 8 sec re expand all previously collapsed lung tissue
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Prevention of atelectasis
• Minimising gas resorption
• 100% O2 - collapse reappears faster but using 40% O2 in nitrogen, atelectasis appears slowly
• Avoidance of preoxygenation procedure (ventilation with 30% O2) eliminates atelectasis formation during induction and subsequent anesthesia
• CPAP of 10 cm H2O can prevent atelectasis even with 100 % O2
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Prevention of atelectasis
• Postanesthetic oxygenation
• Postanesthetic oxygenation (100% O2) 10 minutes before termination of anesthesia together with a VC maneuver at the end of anesthesia will not protect against atelectasis at the end of anesthesia
• VC maneuver followed by a low O2 concentration, 40% keeps the lung open after recruitment until end of anesthesia.
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Airway Resistance• Increase airway resistance,
leads to airway collapse
• Factors:• Decreases in FRC
• ETT
• Upper and lower airway passages
• External anesthesia apparatus
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Uneven distribution of ventilation
• Uneven distribution
• Right > left
• Nondependent > dependent
• PEEP increases dependent lung ventilation
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Distribution of Lung Blood Flow(Perfusion)• Uneven distribution
Base> apex
• successive increase in perfusion down the lung, from the ventral to the dorsal aspect.
• PEEP impede venous return to the right heart and therefore reduce cardiac output.
• PEEP causes a redistribution of blood flow toward dependent lung regions.By this upper lung regions may be poorly perfused,causing a dead space–like effect.
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V/Q ratios• V/Q ratio: 0.8
• Shunt: V/Q ratio =0, perfusion only
• Dead space: V/Q ratio =infinity, ventilation only
• Perfusion increases at a greater rate than ventilation• Apical area: higher V/Q ratio
• Basal area: lower V/Q ratio (shunt)
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• during anesthesia
increased VA /Q mismatch
increased Venous admixture (approx 10% cardiac output).
increased alveolar dead space
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Hypoxic Pulmonary Vasoconstriction
• Normally PaO2 decrease will cause HPV
• inhaled anesthetics inhibit HPV . Aggravate an existing V/Q mismatch
• no such effect seen with intravenous anesthetics (barbiturates)
• isoflurane and halothane depress the HPV response by 50% at 2 MAC
• Direct: nitroprusside ,NTG, Isoproterenol ,inhaled anesthetics, hypocapnia
• Indirect: MS , fluid overload, high fio2 , hypothermia ,emboli, vasoactive drugs, lung disease
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Effect of depth of anesthesia on respiratory drive
• Inhaled anaesthetics and barbiturates reduce sensitivity to CO2 and the effect is dose dependent.
• due to impeded function of intercoastal muscles
• Anaesthesia also reduces response to hypoxia due to effect on carotid body receptors
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Effect of depth of anesthesia on respiratory pattern
• Less than MAC
vary from excessive hyperventilation to breath holding
• 1 MAC (light anesthesia)
regular pattern with larger VT than normal
• More deep
end inspiration pause (hitch) – active and prolong expiration
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Effect of depth of anesthesia on respiratory pattern
• More deep (moderate)
faster and more regular – shallow –no pause – Inspiration = Expiration
• Deep 1. Narcotic- N2O : Deep and slow2. Volatiles : rapid & shallow (panting)
• Very deep
all inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only diaphragmatic respiration) just like airway semi obstruction or partial paralysis
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Effect of depth of anesthesia on spontaneous minute ventilation
• Minute ventilation decreases progressively as depth of anesthesia increases
• ET CO2 increases as depth of anesthesia increases
• Increase of CO2 caused by halogenated anesthetics
(<1.24 MAC) enflurane > desflurane =isoflurane > sevoflurane > halothane
(>1.24 MAC) enflurane = desflurane > isoflurane > sevoflurane
• Ventilation response to CO2 increase is decreased
• Apnea threshold is increased
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Factors That Influence RespiratoryFunction During Anesthesia
• Spontaneous Breathing
• FRC is reduced to the same extent during anesthesia
• atelectasis occurs to almost the same extent in anesthetized spontaneously breathing subjects as during muscle paralysis.
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Increased Oxygen Fraction
• As Fio2 is increased, shunt is also increased
• explained by attenuation of HPV response with increasing Fio2 or further development of atelectasis and shunt in lung units with low VA /Q ratios
Body Position
• FRC is reduced in supine position
• Lateral position causes severe impairment in arterial oxygenation in some patients.
• ventilation distribution was more uniform in anesthetized subjects who were in the prone position
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Age
• arterial oxygenation is impeded with increasing age of the patient
• shunt is independent of age 23 to 69 years
• There is increasing VA /Q mismatch with age
• major cause of impaired gas exchange during anesthesia at ages younger than 50 years is shunt, whereas at higher ages mismatch becomes increasingly important.
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Obesity
• worsens the oxygenation of blood
• markedly reduced FRC, which promotes airway closure to a greater extent than in a normal subject
• PEEP , CPAP or near-VC inflations followed by PEEP ventilation
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Preexisting Lung Disease
• Smokers and patients with lung disease have severe impairment of gas exchange in the awake state as well as during anesthesia
• smokers with moderate airflow limitation have less shunt, however, considerable Va /Q mismatch with a large perfusion fraction to low Va /Q regions
• Reason - chronic hyperinflation which changes the mechanical behavior of the lungs and their interaction with the chest wall such that the tendency to collapse is reduced
• these low Va /Q ratios can be converted over time to resorption atelectasis.
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Regional Anesthesia
• extensive blocks (thoracic and lumbar segments)-inspiratory capacity is reduced by 20% and expiratory reserve volume approaches zero.
• Diaphragmatic function is often spared, even in sensory block up to the cervical segments.
• Arterial oxygenation and carbon dioxide elimination are well maintained
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Thankyou