mechanical ventilation.1e.2015.pdf

Mechanical Ventilation

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Series EditorsAnupam Sachdeva

Krishan ChughAjay GambhirSatinder Aneja

AP DubeyShyam Kukreja

Guest EditorsSanjeev Kumar Krishan ChughSoonu Udani

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First Edition: 2015

ISBN: 978-93-5152-771-8

Printed at

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Contributors

Amit Vij

Sanjeev Kumar

Vikas Taneja

Manish Kori

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Preface

Mechanical Ventilation, while not a primary treatment application for disease states, is an extremely valuable respiratory support system. Every Pediatrician, who is confronted with critically ill children, needs to be familiar with the basics of intubation, bag mask ventilation, and the principles of stabilisation and transfer of a child.

With a growing number of independent Intensive Care Units in the country, the basic tools, language and culture of “ventilation” has become rather widespread. Now there is a keen desire to move forward and � ne-tune old skills and learn new ones.

� is workshop is designed with just that in mind. � e importance of using noninvasive ventilation, wherever feasible, will

be emphasised. � is is actually seen as a step up rather than a step down in the intensivists’ skill in ventilation technique. High frequency still exists in the armamentarium of the intensivist as a rescue measure, where advanced ventilation techniques are considered and shall be covered.

Besides this, a number of advanced modes of ventilation have also come in with the sole purpose of making the ventilation gentle and avoid asynchrony. � e use of ventilatory graphics has also put us in a better position to understand the physiology and mechanics of patient ventilator interactions in the diseased lung.

� is manual is intended for intensivists and pediatricians, who wish to delve into details. Special focus has been kept on ventilatory graphics, high frequency ventilation as well as noninvasive ventilation.

We hope it meets with your expectations.

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Contents

1. Basics of Mechanical Ventilation 1 2. Pediatric Airways and Oxygen Delivery Devices 14 3. Disease Speci� c Ventilation 29 4. Interpretation of Graphic Displays on Ventilators 37

Amit Vij

5. High Frequency Ventilation 50Sanjeev Kumar

6. Non-invasive Ventilation in Children 59 7. “Bubble CPAP” for Neonates 64 8. Newer Modes of Ventilation 71 9. Humidi� cation and Mechanical Ventilation 86 10. Complications of Mechanical Ventilation 93

Vikas Taneja

11. Troubleshooting and Monitoring DuringMechanical Ventilation 104

12. Extracorporeal Membrane Oxygenation 109Manish Kori

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Applied Physiology of Ventilation

Mechanical ventilation in children and neonates is different from adults. While basic principles of physics and gas flow apply to all age groups, anatomical and physiological differences play a significant role in selecting the type of ventilator as well as ventilatory modes and settings.

The upper airway in infants is cephalad, funnel shaped with its narrowest area being at the subglottic region (at the level of cricoid ring as compared to the relatively tubular adult airway. Airway resistance increases inversely by 4th power of the radius; i.e. in an already small airway even 1 mm of edema or secretions will increase the airway resistance and turbulent flow markedly necessitating treatment of airway edema, suctioning of secretion, measures to control secretions. Low functional residual capacity (FRC: Volume of air in the lungs at end of expiration) reduces the oxygen reserve and hence the time that apnea can be tolerated by a child.

Respirations are shallow and rapid due to predominant diaphragmatic breathing, and inadequate chest expansion due to the more horizontal alignment of the ribs in infancy giving less play in the bucket handle movement of the ribs during inspiration. Therefore, a child tends to get tachypneic rather than increasing the depth of respiration in response to hypoxemia. Oxygen consumption per kg body weight is higher therefore tolerance to hypoxemia is lower.

Susceptibility to bradycardia in response to hypoxemia is also higher due to high vagal tone. Pores of Kohn and channels of Lambert (bronchoalveolar and interalveolar collaterals) are inadequately developed making regional atelectasis more frequent. Closing volumes are lower and airway collapse due to inadequate strength of the cartilage in the airways is common making a child particularly susceptible to laryngomalacia, and tracheobronchomalacia as well as lower airways closure.

Therefore, children tend to require smaller tidal volumes, faster respiratory rates, adequate size uncuffed endotracheal tube, adequately suctioned clear airway for proper management of mechanical ventilation. Other important factors for choosing the ventilatory setting include the primary pathology, i.e. asthma, acute respiratory distress syndrome (ARDS), pneumonia, air leak syndrome raised intracranial tension, neuromuscular weakness, neonatal hyaline membrane disease, or neonatal persistent pulmonary hypertension (PPHN).

Chapter

1Basics of Mechanical Ventilation

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Mechanical Ventilation2

Basic Physiology

Gradient between the mouth and pleural space is the driving pressure for the inspired gases, and this gradient is needed to overcome resistance and to maintain the alveoli open, by overcoming elastic recoil forces. Therefore, a balance between elastic recoil of chest wall and the lung determines lung volume at any given time. Normal inspiration is actively initiated by negative intrathoracic pressure driving air into the lungs. Expiration is passive.

VentilationVentilation washes out carbon dioxide from alveoli keeping arterial PaCO

2

between 35–45 mm of Hg. Increasing dead space increases the PaCO2.

PaCO2 = k ×

Metabolic production

Alveolar minute ventilation

Alveolar MV = Respiratory Rate × Effective Tidal VolumeEffective TV = TV—dead spaceDead Space = Anatomic (nose, pharynx, trachea, bronchi) + Physiologic

(alveoli that are ventilated but not perfused)Adequate minute ventilation is essential to keep PaCO

2 within normal

limits.

OxygenationPartial pressure of oxygen in alveolus (PaO

2) is the driving pressure for gas

exchange across the alveolar-capillary barrier determining oxygenation.PaO

2 = [(Atmospheric pressure – water vapor) × FiO

2] – PaCO

2/RQ

RQ = respiratory quotientAdequate perfusion to alveoli that are well ventilated improves oxygenation.Hemoglobin is fully saturated 1/3 of the way through the capillary.

Hypoxemia can occur due to:• Hypoventilation• V/Q mismatch (V– ventilation, Q– perfusion)• Shunt (Perfusion of an unventilated alveolus, atelectasis, fluid in the

alveolus)• Diffusion impairments

Hypercarbia can occur due to:• Hypoventilation• V/Q mismatch• Dead space ventilation

Gas ExchangeHypoventilation and V/Q mismatch are the most common causes of abnormal gas exchange in the PICU.

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Basics of Mechanical Ventilation 3

One can correct hypoventilation by increasing minute ventilation.One can correct V/Q mismatch by increasing amount of lung that is

ventilated or by improving perfusion to those areas that are ventilated.

Compliance = Δ volume/Δ pressure à the change of unit volume over a change of unit pressure applied is the compliance of the lung.

The pressure used for this calculation is the transpulmonary pressure, which is equal to the difference between the alveolar pressure (P

alv) at the end

of inflation and the pleural pressure (Ppl

or Pes

). • P

plat àsubstituted for P

alv

• The tidal volume àsubstituted for a change in lung volume (Clung

):• Therefore the C

lung = Vt/(P

plat – P

es)

• Since True esophageal measures are not available à So usually not measured accurately

Importance of compliance when using pressure and volume modes1. When a gas is delivered at a set pressure à Tidal Volume ∝ compliance If for the same Pressure change VOLUME increases à Compliance is GOOD If for the same Pressure change VOLUME decreases à Compliance is POOR2. When a gas is delivered at a set volume à Pressure 1/µ compliance If For the same VOLUME pressure DECREASES à Cl is GOOD If For the same VOLUME pressure INCREASES à Cl is POOR

Time constant and inspiratory timeThe time constant is the time taken for the airway pressure (and volume) changes to equilibrate throughout the lung à It is proportional to the compliance and resistance of the respiratory system.

Time constant = Compliance × Resistance

One time constant that fills an alveolar unit to 63% of its capacity. It takes three time constants to fill an alveolus to 90% capacity and up to 5 Tc to fill it to 95%.

To calculate a full term neonates Tc who has a compliance of 0.004 L/cm and a R of 30 cm H

2O/L/sec the Tc will be:

–C = 0.004 L/cm H2O; R = 30 cm H

2O/L/sec

–T = 0.004 × 30 = 0.12 sec.

If we want to set the inspiratory time with this knowledge, then we need 3–5 Tc to fill the alveolus so 0.12 × 4 = 0.48 secs. If we are dealing with RDS/ARDS we could use a lower Ti like 0.4 secs and if we are dealing with an obstructive disease requiring more time we could use a higher Ti like 0.55 secs.

An adult has a Tc of about 0.3 so the Ti is set around 0.9–1 sec commonly.

Indications of mechanical ventilationIndications remain essentially clinical and may not be always substantiated by objective lab parameters such as blood gas analysis. Common indications include:

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1. Respiratory failure − Apnea/respiratory arrest − Inadequate ventilation − Inadequate oxygenation − Chronic respiratory insufficiency with failure to thrive

2. Cardiac insufficiency/shock − Eliminate work of breathing − Reduce oxygen consumption

3. Neurologic dysfunction − Central hypoventilation/frequent apnea − Patient comatose, glasgow coma score (GCS) <8 − Inability to protect airway

Commonly used Nomenclature

Airway pressures• Peak inspiratory pressure (PIP)• Positive end expiratory pressure (PEEP)• Pressure above PEEP (PAP or δP)• Mean airway pressure (MAP or Paw)• Continuous positive airway pressure (CPAP)

Inspiratory time TiI:E ratio,

Frequency (F): Ventilatory rate or RR (usually F is what is set on the machine and RR refers to the total rate of machine plus patient).

Tidal volume (Vt): Amount of gas delivered with each breath. (Vti will be the Inspiratory vol and Vte will be exp vol. the Vte will be the accurate patient volume as leaks occur during inspiration and the machine checks the actual delivered volume during exhalation).

There are five basic breaths that are used. These are shown below. Various modes are then permutations and combinations of these breaths.

It is essential to be familiar with the appearance of the wave forms that are seen in the flow and pressure scalars of these basic breath types. The volume scalar always looks the same.

By convention, the pressure scalar is always the top one followed by the flow scale (Fig. 1.1).

Modes of Ventilation

Control ModesMinute ventilation is determined entirely by the set respiratory rate and tidal volume/pressure.

The patient does not initiate additional breaths above that set on the ventilator (Figs 1.2 and 1.3).

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Fig. 1.1: Basic types of breaths: Comparison on pressure, flow and volume time scalars

Fig. 1.2: Controlled mode—pressure control ventilation

volume control ventilation (VCV): flow-targeted volume-cycled breathspressure control ventilation (PCV): pressure-targeted time-cycled breaths

In this mode every breath is fully supported by the ventilator. In classic control modes, patients were unable to breathe except at the controlled set rate. Difficult to wean and asynchrony is a major issue. Patients on control modes will need sedation and/or paralysis. This is usually set with some leeway for patient triggering either SIMV + PSV or in the AC or assist control mode so when the patient awakens and breaths there is adequate flow and to avoid flow hunger and asynchrony.

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Assist-control centilation (ACV)• Volume assist-control ventilation (VACV): flow-targeted volume-cycled

breaths• Pressure assist-control ventilation (PACV): pressure-targeted time-cycled

breaths• Guarantees a set number of positive-pressure breaths. • If respiratory rate exceeds this, breaths are patient-triggered breaths (VA

or PA). If respiratory rate is below guarantee, ventilator delivers mandatory breaths (VC or PC breaths).

Synchronized intermittent mandatory ventilation (SIMV) (IMV no longer used) (Fig. 1.4)• Set ventilator breaths: set minimum minute ventilation with respiratory

rate + tidal volume (volume SIMV) or inspiratory P (pressure SIMV)• Ventilator breaths are synchronized with patient inspiratory effort • Patients increase minute ventilation by additional spontaneous breaths,

which can be unassisted or pressure suppart (PS).

Pressure Support

• Flow-limited mode of ventilation (not volume-limited or pressure-limited) • Delivers inspiratory pressure until the inspiratory flow decreases to ~25%

of its peak value.• Clinician sets inspiratory pressure, applied PEEP, and FiO

2.

• Patient triggers each breath• Comfortable mode, good for weaning, can be combined with SIMV

Fig. 1.3: Controlled mode—volume control ventilation

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• Not good for full ventilatory support, high airway resistance, or central apneaPressure support can decrease work of breathing by providing flow during

inspiration for patient triggered breaths. It can be given with spontaneous breaths in IMV modes or as stand alone mode without set rate, as well as for weaning to retrain coordination of respiratory muscles in patients on ventilation for longer than few weeks.

Continuous Positive Airway Pressure

• Continuous level of positive airway pressure. • Pt must initiate all breaths• Functionally similar to PEEP • Good for OSA, cardiogenic pulmonary edema

Bilevel positive airway pressure • Mode used during NPPV• Delivers set IPAP and EPAP• Tidal volume is determined by difference between IPAP-EPAP

Pressure-regulated volume control (PRVC)• A form of PACV that uses tidal volume as a feedback control for continuously

adjusting the pressure target• Combines volume ventilation and pressure control—(for mech., time-cycl.

breaths only)• Set Vt is “targeted”• Ventilator estimates vol./ press. relationship each breath• Ventilator adjusts level of pressure control breath by breath• Dual mode with flow in the pressure regulated mode, i.e. decelerating.

Fig. 1.4: SIMV mode—volume control ventilation

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Way to use:1. Set PC limit and target Vt, e.g. Vt 100 PIP 28. PEEP 7 Ti 0. 8 seconds2. First breath = 5–10 cm H

2O above PEEP= 11–15 PIP àbut 100 ml not

delivered3. V/P relationship measured—Next 3 breaths, pressure increased to 75%

needed for set TV4. Then up to +/– 3 cm H

2O changes per breath

5. Insp. Time ends inspiration (phase variable)

PRVC – Considerations• Like PC, flow varies automatically to varying patient demands • Constant press. during each breath—variable press. from breath to breath• Time is cycling method; delivered Vt can vary from set.• If Vt

target not met, dial up PC limit gradually

But check patient—may not need that VtIndications:• Patient who require the lowest possible pressure and a guaranteed

consistent Vt• ALI/ARDS• Patients requiring high and/or variable insp. flow• Patient with the possibility of C

L or Raw changes

• Advantages of PRVC• Maintains a minimum PIP• Guaranteed Vt and VE• Patient has very little WOB requirement• Allows patient control of respiratory rate• Variable flow and pressure to meet patient demand• Decelerating flow waveform for improved gas distribution• Breath by breath analysis

Disadvantages and risks:• Varying mean airway pressure• May cause or worsen auto-PEEP• When patient demand is increased, pressure level may diminish when

support is needed• May be tolerated poorly in awake non-sedated patients• A sudden increase in respiratory rate and demand may result in a decrease

in ventilator support

Basic Fundamentals of Ventilation

Ventilators deliver gas to the lungs using positive pressure at a certain rate. The amount of gas delivered can be limited by time, pressure or volume. The duration can be cycled by time, pressure or flow.

If volume is set, pressure varies; if pressure is set, volume varies according to the compliance.

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Following are three main expectations from the ventilator• Ventilator must recognize patient’s respiratory efforts (trigger)• Ventilator must be able to meet patient’s demands (response)• Ventilator must not interfere with patient’s efforts (synchrony)• Whenever a breath is supported by the ventilator, regardless of the mode,

the limit of the support is determined by a preset pressure or volume.• Volume limited: Preset tidal volume• Pressure limited: Preset PIP

Pressure vs Volume ControlGoal is to ventilate and oxygenate adequately. Both pressure and volume control modes can achieve it. Important requirements include adequate movement of the chest and minimal barotrauma or volutrauma.

One must have a set up of high/low pressure alarms in volume cycling and, low expired tidal volume alarm when using pressure cycling.

Pressure Limited VentilationVentilator stops the inspiratory cycle when set PIP is achieved.

Caution: Tidal volume changes suddenly as patient’s compliance changes. .Ventilator delivers a decelerating flow pattern (lower PIP for same Vt).

This can lead to hypoventilation or overexpansion of the lung. If endotracheal tube is obstructed acutely, delivered tidal volume will decrease. This mode is useful if there is a leak around the endotracheal tube.

For improving oxygenation, one needs to control FiO2 and MAP, (I-time, PIP,

PEEP) and to influence ventilation, one needs to control PIP and respiratory rate.

Volume Limited VentilationVentilator stops the inspiratory cycle when set tidal volume has been delivered.

One can control minute ventilation by changing the tidal volume and rate. For improving oxygenation primarily FiO

2,

PEEP, I-time can be manipulated.

Increasing tidal volume will also increase the PIP, hence affecting the oxygenation by increasing the mean airway pressure. It delivers volume in a square wave flow pattern. Square wave (constant) flow pattern results in higher PIP for same tidal volume as compared to pressure modes.

Caution: There is no limit per se on PIP (so ventilator alarm will have to be set for an upper pressure limit to avoid barotrauma). Volume is lost if there is a circuit leak or significant leak around the endotracheal tube, therefore an expired tidal volume needs to be monitored and set. Some ventilators will alarm automatically if the difference between set inspired tidal volume and expired tidal volume is significant (varies between the ventilators).

Trigger/SensitivityTrigger means sensitivity setting of the ventilator.

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Ventilators have a negative pressure sensor which can be set at various levels of sensitivity to initiate a breath usually based on patient effort (negative pressure) or elapsed time before the next breath in the event of respiratory depression or apnea. The patient’s effort can be “sensed” as a change in pressure or a change in flow in the circuit (flow triggering). A setting of greater than 0 makes it too sensitive (meaning the triggered breath from the ventilator will be too frequent). A negative setting (negative 1 or negative 2) setting is usually acceptable. Too negative setting will increase the work of the patient (to generate a negative pressure) to trigger a ventilator breath.

Initial Ventilator SettingsOne should always have the general idea regarding what initial ventilatory settings to choose when initiating the ventilation. Parameters to chose include:

Rate: start with a rate that is somewhat normal; i.e. 15 for adolescent/child, 20–30 for infant/small child, 30–40 for a neonate.

FiO2: 1 (100%) and wean down to level <0.5.

PEEP: 3–5 cm of H2O (higher if ARDS, low compliance disease, lower if Asthma,

high compliance disease.

Inspiratory time (I-time or I:E ratio): 0.3–0.4 sec for neonates, 0.5–0.6 sec for children, 0.7–0.9 in older children. Normal I:E ratio = 1:2–1:3

Higher I-times may be needed to improve oxygenation in difficult situations (Inverse ratio ventilation) increasing the risk of air leak.

Control every breath (Assist control) or some (SIMV)Choose the mode: Pressure limited: PIP is set depending upon lung compliance and pathology:• Neonates: 18–22 cm H

2O

• Children 18–25 cm H2O

Volume limited:Tidal volume 6–8 ml/kg.

Adjustments after initiation: usually based on blood gases and oxygen saturationsFor oxygenation: FiO

2, PEEP, I-time, PIP (tidal volume) can be adjusted

(increase MAP) (Fig. 1.5).For ventilation: Respiratory rate, tidal volume (in volume limited) and PIP

(In pressure limited mode) can be adjusted.PEEP is used to help prevent alveolar collapse at end inspiration; it can

also be used to recruit collapsed lung spaces or to stent open floppy airways

Gas exchange related problems:• Inadequate oxygenation (hypoxemia)• Inadequate ventilation (hypercarbia)

Inadequate oxygenation: low PaO2

Important guidelines:

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1. Don’t just increase FiO2

2. Increase tidal volume if volume limited mode, PEEP, inspiratory time (Ti).3. Increase peak inspiratory pressure (PIP)/PEEP/Ti if pressure limited mode4. If O

2 worse, get chest X-ray to rule out air leak, if lungs show worsening

(increase PEEP further)5. Do not forget other measures to improve oxygenation:

− Normalize cardiac output (if low output) by fluids and/inotropes − Maintain normal hemoglobin − Maintain normothermia − Deepen sedation/consider neuromuscular block

Determinant of Paw = area under the curve (Mean Airway Pressure) and therefore oxygenation: 1. Inspiratory flow rate 2. Peak inspiratory pressure 3. Inspiratory time4. PEEP

Inadequate Ventilation: High PaCO2

Common reasons include hypoventilation, dead space ventilation (too high PEEP, decreased cardiac output, pulmonary vasoconstriction),

Increased CO2 production: hyperthermia, high carbohydrate diet,

shivering.Inadequate tidal volume delivery (hypoventilation): will occur with

endotracheal tube block, malposition, kink, circuit leak, ventilator malfunction.

Fig. 1.5: Mean airway pressure (area under the pressure time curve) and oxygenation (1: increase inspiratory rise time, 2: increase PIP/ VT, 3: increase inspiratory time, 4: increase PEEP, 5: increase rate)

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Measures for High PaCO2

Guidelines1. If volume limited: Increase tidal volume (Vt), increase frequency (rate) (F)2. If asthma: Increase expiratory time, may need to decrease rate to achieve

an I:E ratio >1:33. If pressure limited: Increase peak inspiratory pressure (PIP), decrease PEEP,

increase frequency4. Decrease dead space (increase cardiac output, decrease PEEP, vasodilator)5. Decrease CO

2 production: Cool, increase sedation, decrease carbohydrate

load6. Change endotracheal tube if blocked, kinked, misplaced or out, check

proper placement7. Fix leaks in the circuit, endotracheal tube cuff, humidifier

Measures to Reduce Barotrauma and VolutraumaFollowing concepts are being increasingly followed in most pediatric intensive care units:1. Permissive Hypercapnia Higher PaCO

2 are acceptable in exchange for limiting peak airway

pressures: as long as pH >7.22. Permissive Hypoxemia PaO

2 of 55–65; SaO

2 88–90% is acceptable in exchange for limiting FiO

2

(<60) and PEEP, as long as there is no metabolic acidosis.Adequate oxygen content can be maintained by keeping hematocrit >30%.

Patient ventilator dyssynchrony: Incoordination between the patient and the ventilator: Patient fights the ventilator!!

Common causes include hypoventilation, hypoxemia, tube block/kink/ malposition, bronchospasm, pneumothorax, silent aspiration, increased oxygen demand/increased CO

2 production (in sepsis), inadequate sedation.

If patient fighting the ventilator and desaturating: Immediate measures.

Use Pnemonic: DOPE

D–displacement, O–obstruction, P–pneumothorax, E–equipment failure1. Check tube placement. When in doubt take the endotracheal tube out, start

manual ventilation with 100% oxygen2. Examine the patient: is the chest rising? Breath sounds present and

equal? Changes in exam? Atelectasis, treat bronchospasm/tube block/ malposition/pneumothorax? (consider needle thoracentesis). Examine circulation: shock? sepsis?

3. Check arterial blood gas and chest X-ray for worsening lung condition, and for confirming pneumothorax.

4. Examine the ventilator, ventilator circuit/humidifier/gas source

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5. If no other reason for hypoxemia: increase sedation/muscle relaxation, put back on ventilator.

Sedation and muscle relaxation during ventilationMost patients can be managed by titration of sedation without muscle relaxation.

Midazolam (0.1–0.2 mg/kg/hr) and vecuronium drip (0.1–0.2 mg/kg/hr) is most commonly used. Morphine or fentanyl drip can also be used if painful procedures are anticipated.

Routine ventilator management protocolThe following protocol is commonly followed:1. Wean FiO

2 for SpO

2 above 93–94%

2. ABG 1 hour after intubation, then am and pm schedule (12 hourly), and after major ventilator settings change, and 20 minutes after extubation

3. Pulse oximetry on all patients, end-tidal carbon dioxide (EtCO2)/graphics

monitoring if available4. Frequent clinical examination for respiratory rate, breath sounds,

retractions, color5. Chest X-ray every day/alternate day/as needed

Respiratory care protocol1. Position change 2 hourly right chest tilt/left chest tilt/supine position.

Unless highly unstable2. Suction 4 hourly and as needed (In line suction to avoid de recruitment/

loss of PEEP/desaturation if available)3. Physiotherapy 8 hourly 4. Percussion, vibration and postural drainage. No physiotherapy if labile

oxygenation such as ARDS and PPHN5. Nebulization: In line nebulization is preferred over manual bagging.

Metered dose inhalers (MDIs) can also be used.6. Disposable circuit change if soiled or >96 hours7. Humidification/in line disposable humidifier.

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The following chapter focuses on basic physiology and anatomy of pediatric airways and the adjuncts and techniques used to support oxygenation and ventilation. Let us start with understanding the clinical implications of differences between pediatric and adult airways (Fig. 2.1).1. The infant’s nose is short, soft and flat with small circular nares which are

easily occluded by secretions, edema or compression.2. The upper airway of infants is smaller in diameter which markedly increases

the airflow resistance and hence, works of breathing.3. A larger tongue relative to oropharyngeal space, with lower anterior

compressibility makes intubation difficult in infants.4. The larynx in an infant, and more so in a neonate, is anterior and is placed

at a higher level (epiglottis at birth is at the level of first cervical vertebrae, moves down to third at the age of 6 months, and further down to fifth or sixth cervical vertebrae in the adults). The higher and anterior position of larynx results in an acute angle between the base of the tongue and the glottis opening. As a result straight (Miller) blades are used for intubation, which entrap the epiglottis and create a direct plane for visualization of

Fig. 2.1: Difference between adult and child airway

Chapter

2Pediatric Airways and

Oxygen Delivery Devices

Ch-02.indd 14 1/19/2015 3:54:34 PM

pediatric airways and Oxygen Delivery Devices 15

the glottis. The entrapping of epiglottis is important as it is long, floppy and is angled away from the long axis of trachea in infants.

5. Other significant anatomical and physiological differences are narrow subglottic region, smaller airways, decreased cartilage in airways, increased chest wall compliance, fewer alveoli, high metabolic rate and increased O

2

consumption in infants.

Approach to Airway Management

The basic requirement in any patient is a functional airway providing adequate ventilation and oxygenation. Following are the steps involved in establishing a functional airway. 1. Opening a collapsed airway2. Oxygen delivery3. Bag and mask ventilation4. Airway adjuncts and alternative airways5. Intubation/RSI

Maneuvers to Open Airway

Clearing the mouth of blood, secretions, broken teeth and debris, etc. along with lateral decubitus helps is opening an obstructed airway.

Head-tilt and Chin lift: By extending the neck and pulling the mandible forward, tongue may be lifted from the posterior pharyngeal wall. Hyperextension of the neck must be avoided in small infants since it may lead to compression of the soft tracheal cartilage (Fig. 2.2).

Jaw-thrust: This maneuver can be attempted with the patient in any position by placing two or three fingers at each angle of the jaw and then lifting the chin and jaw forward. It is generally accompanied by head tilt and helps to maintain

Fig. 2.2: Maneuvers to open the airway: Head tilt and chin lift method

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airway patency. If cervical trauma is suspected, jaw thrust should be applied without head tilt to avoid spinal dislocation or further injury (Fig. 2.3).

Oxygen Delivery

The FiO2

delivered depends upon O2 flow and patient’s minute volume, and

on the type of delivery device used (low/high flow) (Fig. 2.4).

Fig. 2.3: Maneuvers to open the airway: Jaw thrust method

Fig. 2.4: High flow and low flow devices

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• Low flow devices: in these devices, oxygen flow is less than the patient’s total minute volume, and there is mixing of room air to provide patient with adequate minute ventilation. Hence FiO

2 delivered is less than 100%. The

oxygen concentration delivered depends on the patient’s minute ventilation and the gas flow rates (range 23–80%). Examples of low flow devices are Simple face masks, nasal cannula, and partial re-breathing masks (Fig. 2.5).

• High flow devices: deliver flow rates that are more than the entire ventilatory minute volume requirement, so that the breathing pattern does not affect the FiO

2 ex.

Non-rebreathing masks, venturi masks and Oxygen

hoods (Fig. 2.6).

Bag and Mask VentilationBag-mask ventilation can be as effective as endotracheal intubation and safer when providing ventilation for short periods. Important considerations while ventilating through this method are: selecting the correct size mask, opening the airway, making a tight seal between the mask and face (EC Clamp technique), delivering effective ventilation, and assessing its effectiveness (Fig. 2.7).

Bag-Mask Valve DevicesVentilation bags can be self-inflating (AMBU) or Flow inflating (Anesthesia bag). A self-inflating bag is available in three pediatric sizes viz. Neonatal

Fig. 2.5: Low flow devices

Fig. 2.6: High flow devices

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(250 cc), infant and child (500 ml) and for a larger child (750 ml). It delivers only room air unless supplementary oxygen is attached, but even with an oxygen inflow of 10 L/min, the concentration of delivered oxygen varies from 30–80%. To deliver a high oxygen concentration (60–95%), an oxygen reservoir may be attached. Flow inflated bags require a constant gas flow (Oxygen or air-oxygen mixture) to keep them inflated. There is a standard 15 mm and 22 mm connector at patient end (for mask/tube). It has a pressure release valve, but does not contain a non-rebreathing valve; hence the concentration of inspired gas depends upon the flow. Also, if the pressure release valve in this system is set too tight, it may lead to high inspiratory pressures and its complications.

Airway Adjuncts and Alternative Airways

Oropharyngeal Airways (Geudel’s airway)Parts: Flange (short bite-block segment) and a curved body.

Purpose: To hold the base of tongue and other hypo-pharyngeal structures away from the posterior pharyngeal wall.

Size: With flange at the mouth, the tip should be at or near the angle of the mouth (4–10 cm in length; Geudel sizes 0–4)

Technique of insertion: should be inserted following the curve of the tongue and the palate while using a depressor to hold the tongue to the floor of the mouth. No rotation is required (Fig. 2.8).

Contraindication: Patient with intact cough and gag reflexes, oral airway is better avoided.

It is important to note that an adequate size is used. If selection is too small, it may push the tongue posteriorly and cause more obstruction. A larger oropharyngeal airway may cause laryngospasm or injury.

Recently, a new oral airway suitable for adolescent and young adults, COPA (Cuffed Oro-Pharyngeal Airway) has been clinically evaluated. The method of insertion of this device is the same that of a standard oral airway. After proper insertion has been achieved, the balloon is then inflated so as to ensure a close fit to oropharyngeal structures.

A B

Fig. 2.7: EC clamp technique of ventilating using Bag and Mask ventilation

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Nasopharyngeal AirwaysParts: soft rubber or plastic tube (acts as a conduit from nose to pharynx).

Size: appropriately sized airway extends from external nares to the ear lobule or tragus and does not cause blanching of skin surrounding the nares.

Technique: lubricate properly, insert through nostril in posterior direction perpendicular to the plane of the face, along the floor of the nasopharynx (Fig. 2.9)

Complications: Nasal trauma and bleeding, damage to the adenoids, nasal ulceration, perforation of cribriform plate.

Contraindications: Coagulopathy, CSF leak, basilar skull fractures.

The advantage of nasopharyngeal airway is that it can be used in semiconscious patients with intact cough and gag reflexes as well as in a neurologically impaired patient with poor pharyngeal tone.

Fig. 2.8: Oropharyngeal airways

Fig. 2.9: Nasopharyngeal airways

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Laryngeal Mask Airway

The laryngeal mask airway (LMA) allows avoidance of intubation and maintenance of airway patency. The main principle behind its use is to place the tip of LMA in the beginning of the upper esophagus to occlude it, so that the portion of LMA superior to the upper end of esophagus outlines the glottis thereby placing a mask on the larynx (laryngeal mask airway). It can be used for passage of a flexible bronchoscope as well as passing a suction catheter. Various adult and pediatric sizes are available. It is contraindicated in patients with full stomach and in patients requiring intubation due to airway obstruction due to inflammation or edema (Table 2.1).

Insertion technique: the cuff is deflated before insertion and the posterior surface is lubricated with Lignocaine jelly. The airway is then advanced with mask facing the tongue, into the hypopharynx until resistance of upper esophageal sphincter is encountered. Cuff is then inflated which forms a seal around the laryngeal outlet. See that the longitudinal black line on the shaft should be aligned in the midline against the upper lip (Fig. 2.10).

Table 2.1: LMA size selection

LMA size Patient selection information Max. Inflation vol. (ml)LMA-ClassicTM

1 Neonates/infants up to 5 kg 4

1½ Infant 5–10 kg 7

2 Infants/children 10–20 kg 10

2½ Children 20–30 kg 14

3 Children 30–50 kg 20

4 Adult 50–70 kg 30

5 Adult 70–100 kg 40

6 Large adult over 100 kg 50

LMA-FlexibleTM

1 Neonates/infants up to 5 kg 4

1½ Infant 5–10 kg 7

2 Infants/children 10–20 kg 10

2½ Children 20–30 kg 14


4 Adult 50–70 kg 30

5 Adult 70–100 kg 40

6 Large adult over 100 kg 50

LMA-UniqueTM


4 Adult 50–70 kg 30

5 Adult 70–100 kg 40

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Fig. 2.10: LMA insertion technique

Endotracheal Intubation

Main indications for tracheal intubation are airway obstruction, respiratory failure requiring assisted ventilation, cardiopulmonary resuscitation or administration of general anesthesia (Fig. 2.11).

Fig. 2.11: Sniffing position for ET intubation

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Ideal position for endotracheal intubation is the sniffing position with flexion at the neck and extension at the atlanto-occipital joint. To align the oral, pharyngeal and tracheal axes neonates and infants, due to a relatively large occiput in, require a shoulder support. So is the requirement of a head support in larger kids.

Selection of Endotracheal TubeParts: Cuffed or Uncuffed

Adapter for BMV device or ventilator Murphy’s eye a side opening on the right side (Decreases the chances

of complete tube block and atelectasis of the right upper lobe Vocal cord guide

Size: Cole’s formula (Based on internal diameter)

ID (mm) Uncuffed Age (years)

+ 4 4

Cuffed Age (years)

+ 3.5 4

Depth of insertion (cm) Age (years)

+ 12 2 Or 3 × ID (internal diameter)

Important:• Cuffed tubes to be used in children 8-10 years or older (in younger children,

narrowing at the level of Cricoid cartilage, provides a functional cuff)• With normal lung compliance and airway resistance an audible air leak

should develop when ventilation is delivered to a pressure of 20–30 cm H2O

LaryngoscopyThere are two types of Laryngoscopy blades, straight and curved. As stated earlier, the larynx in an infant, and more so in a neonate, is anterior and is placed at a higher level (epiglottis at birth is at the level of first cervical vertebrae, moves down to third at the age of 6 months, and further down to fifth or sixth cervical vertebrae in the adults). The higher and anterior position of larynx results in an acute angle between the base of the tongue and the glottis opening. As a result straight (Miller) blades are used for intubation, which entrap the epiglottis and create a direct plane for visualization of the glottis. The entrapping of epiglottis is important as it is long, floppy and is angled away from the long axis of trachea in infants. Nowadays there are Fiberoptic and video Laryngoscopes to assist intubation (Fig. 2.12).

Intubation TechniqueOrotracheal intubation is preferred over nasotracheal route as it is easier and faster. Hold the handle of Laryngoscope in the left hand and insert the blade

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into the oral cavity following the contour of the tongue. Move the blade to the right side of the mouth and then sweep the tongue to the left. This provides a space/channel in the right side of the oral cavity to pass the ET tube (Fig. 2.13). After the blade is properly positioned, traction is exerted upwards in the direction of its long axis and upwardly. This displaces the base of tongue and epiglottis anteriorly, exposing the glottis. Application of Cricoid pressure (Sellick’s maneuver) by an assistant may facilitate visualization. Once glottis opening is seen, ET tube is inserted, with its depth guided by the vocal cord indicator (Fig. 2.14).

Difficult Intubation: When proper placement of ET tube with conventional laryngoscope requires >3 attempts or more than 10 minutes, it is called difficult airway/intubation. Intubation should always be approached with a specific plan with a backup strategy in mind. Extra equipments like forceps,

Fig. 2.12: Types of laryngoscope blades

Fig. 2.13: Direction of force applied during intubation

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extra ET tubes, standby Flexible bronchoscope if feasible, tracheostomy and Cricothyrotomy trays and personnel as needed.

Grading of Difficult Intubation

Cormack and Lehane Classification (Fig. 2.15): describes the best view of larynx on laryngoscopy:• Class I - Vocal cords visible• Class II - Vocal cords partially visible (or posterior commissures visible)• Class III - Only epiglottis is seen• Class IV - No glottic structures visible

Mallampati Classification: (modified by Sampson and Young) Based in anatomical structures seen on examination of oral cavity:• Grade I - Faucial pillars, soft palate and uvula• Grade II - Faucial pillars and soft palate, uvula masked by base of tongue

Fig. 2.15: Cormack and Lehane classification

Fig. 2.14: Sellick’s maneuver

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• Grade III - Only soft palate visualized• Grade IV - Soft palate not seenNB: This rarely applies in the picu setting where the child is not in a situation to voluntarily open the mouth. It is meant for a routine preop evaluation.

Thyromental Distance: Distance from the thyroid notch to the tip of jaw with head extended.• >6.5 cm – Normal• If <6.5 cm – Intubation may be difficult• If <6.0 cm – Intubation impossible

Sternomental Distance: Distance from sternum to the tip of mandible with head extended.• >12.5 cm – Normal• ≤12.5 cm – Difficult intubation

Nasotracheal Intubation

Nasotracheal Intubation is preferred only when long-term ventilation is required. Its main disadvantage is chronic sinusitis caused by obstruction of the ostia draining nasal sinuses. It is performed electively via one of the nostrils. After proper lubrication the tube is passed via the nostril, until it is visualized in the pharynx by oral laryngoscopy. Force should not be used in inserting the tube as this may result in severe bleeding from the nasal turbinates. Once visualized in pharynx, the tip of the tube is guided towards the vocal cords by grasping it with Magill’s forceps. It is contraindicated in patients with basilar skull fracture, maxillofacial trauma and coagulopathies. It should never be performed when emergency intubation is required, when there is hypoxemia, airway compromise or by inexperienced hands.

Rapid Sequence Intubation

Rapid sequence intubation (RSI) is a standard (ED) procedure applied for facilitation of intubation and prevention of aspiration. It also prevents the patient from experiencing the psychological trauma of an awake intubation a procedure that’s been described as the “mouth being held open with a wrench. The use of pharmacologic agents to assist intubation seems to decrease complications however RSI is not a simple “one-size-fits-all” procedure. The drugs selected to perform an RSI are tailored to the specific scenario and individual patient. It is imperative that the clinician be familiar with an array of pharmacologic options for emergent endotracheal intubation (Tables 2.2 to 2.6).

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Table 2.2: Rapid sequence intubation

Timeline of Rapid Sequence Intubation

1. Preparation—assemble all necessary equipment, drug, etc. 2. Preoxygenation—replace the nitrogen in the patient’s functional reserve with oxygen–

“’nitrogen wash out–oxygen wash in” 3. Pretreatment—ancillary medications are administered to mitigate the adverse

physiologic consequences of intubation 4. Paralysis with Induction—administer sedative induction agent via IV push, followed

immediately by administration of paralytic via IV push5. Positioning—position patient for optimal laryngoscopy; Sellick’s maneuver, if desired,

is applied now6. Placement with proof—assess mandible for flaccidity; perform intubation, confirm

placement7. Postintubation management— long-term sedation/analgesia/paralysis as indicated

Table 2.3: Pretreatment agents should be given 3 minutes prior to intubation (can be given in any order)

Drug Dose Indication Other notes

Lidocaine 100 mg Head injury, traumatic brain injury, unknown mechanism of injury, elevated ICP

Lidocaine will help protect the patient from increases in intracranial pressure caused by intubation

Fentanyl 2–3 µg/kg Elevated ICP, cardiovascular disease (ischemic coronary disease, aneurismal disease, great vessel rupture or dissection, intracranial hemorrhage)

Fentanyl helps decrease catecholamine discharge secondary to intubation, thus decreasing the risks associated from BP increases in patients with CV disease, aortic dissections, etc. Be careful if the patient is already hypotensive

Rocuronium defasciculation)

0.1 mg/kg (e.g. 7 mg in a 70 kg patient)

Head injury, traumatic brain injury, unknown mechanism of injury, elevated ICP

Defasciculation no longer routinely recommended. May consider if patients with head injury to be paralyzed with succinylcholine (SCh). SCh causes transient muscle fasciculation (twitch) which theoretically may increase intracranial pressure

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Table 2.4: Paralytic summary – depolarizing

Agent Usual emergency induction dose

Onset (sec)

Duration (min)

Indications Adverse effects

Comments

Succi-nylcho-line

1.5 mg/kg IV Increase to 2 mg/kg IV in myasthenia gravis 4 mg/kg IM (only in life threaten-ing situa-tions)

45 6–10 Essentially all patients except those with: Malignant hyperthermia Hyperkalemia >5d after burn, crush, denervation, severe infec-tion

Hyper-kalemia Muscle fascicu-lations Elevated lop

Bradycar-dia may occur after repeated doses, have atropine ready in the event it occurs

Table 2.5: Paralytic summary – nondepolarizing


Onset (sec)

Duration (min)


Comments

Rocu-ronium

1 mg/kg 60–75 40–60 RSI when suc-cinylcholine contraindi-cated

No, clinically significant ADEs

Ensure contin-gency plan in place in the event of failed airway

Vecuro-nium

0.01 mg/kg priming dose followed 3 minutes later with 0.15 mg/kg

120– 180

45–65 Not recom-mended for RSI unless a nondepolar-izing agent is indicated and rocuronium is not available

No clinically significant ADEs

Ensure contin-gency plan in place in the event of failed airway

Table 2.6: Summary of induction agents


Onset (sec)

Duration of action (min)


Comment

Thio-pental

3 mg/kg I.V < 30 5–10 Patients with elevated ICP or status epi-lepticus who are hemo-dynamicaly stable

Histamine release Myocar-dial de-pression Venodila-tionHypoten-sion

Not rou-tinely usedAvoid intra-arterial injection (may cause gangrene) Pregnancy category C

Contd...

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Onset (sec)

Duration of action (min)


Comment

Mida-zolam

0.2–0.3 mg/kg IV

6.0–90 15–30 Not routinely recommend-ed For RSI. May use for post-irituba-tion manage-ment

Respira-tory de-pression Apnea Paradoxi-cal agita-tion

Not recom-mended for RSI. Patient response may be extremely variable

Etomi-date

0.3 mg/kg IV 10–15 4–10 Used in almost all patients for emergency RSI. May consider alternative agent if pa-tient is septic or in status epilepticus

Adrenal insuffi-ciencyPain on injectionMyoclonic activity

Commu-nicate to subsequent ‘providers that patient received etomidate if patient septic

Keta-mine

1–5 mg/kg IV 45–60 10–20 Good option for patients with reactive airway dis-ease or who are hypov-olemic, hem-orrhaging, or in shock

Increased: EIF’HRIntraocu-lar pres-sure

Not recom-mended in hyperten-sive or nor-motensive patients. Use caution in patients with car-diovascular disease

Propo-fol

2.5 mg/kg IV 15–45 5–10 Hemody-narnkally stable patients with reactive air-way disease or in status epilepticus

Hypoten-sionMyocar-dial de-pression Reduced cerebral perfusion pressure Pain on injection

Ultra-short acting Negative CV effects lim-its use for induction in RSI

Contd...

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Status Asthmaticus

• Mainindicationsareclinicaldeteriorationdespitemaximaldrugtherapy.• RisingPaCO

2(40–45mm)fromalowPaCO

2(25–30mm)

• Fatigue,lethargy,deterioratingmentalstatus• Mixedrespiratoryandmetabolicacidosis• Bradycardia,neararrest

Initiation of Ventilation

• Controlledintubationusesedationandmusclerelaxation(short-actingmusclerelaxantsuchassuccinylcholine

• Usecuffedendotrachealtubeiffeasible• Ketaminewithmidazolamare good sedatives for initiation and

maintenanceofmechanicalventilation

Mechanical Ventilation in Asthma is Associated with High Morbidity and MortalityRisks:• Barotrauma(airleak)duetodynamichyperinflation• Impairedvenousreturn(tamponade)andlowcardiacoutputdueto

hyperinflation(pulsusparadoxus)• Hypotensionandcardiacarrest• Asynchronyand• SuddenriseofPaCO

2withdropinRRfrompatientsownhighrateto

controlledrateStrategies thatminimizeendexpiratoryvolume, intrinsicpeep,and

maximizeexpiratorytime,usinglowertidalvolumesandrespiratoryrateswithpermissivehypercapniahavebeenshowntobeassociatedwithlowermortality.

Ventilation StrategiesControlled hypoventilation using SIMV or assist control:• Volumeorpressurelimitedmode• Plateaupressurelimitmustbe<30cmwater

Chapter

3Disease Specific Ventilation

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• Tidalvolume4–6ml/kg<8ml/kg/8–14/min,or1/3ofexpectedrate.PEEP3–4cmH

2O

Support modes:volumeorpressuresupport• Patientdetermines(f )rateandinspiratorytime(Ti)• Patientcandeterminetherespiratorycycle,frequencyandflowpattern

thereisactiveexhalationanddecreasedendexpiratorylungvolume• WatchPPlandPIPcloselyinallmodes.Nottoallow>30cmH

2O.

Use of PEEP

Inconsciouspatientsnotonmusclerelaxants,onassistcontrolmode,PEEPcan be used in physiological levels (3–4 cmH

2O). Application of extrinsic

PEEP (at levels less than intrinsicPEEP)helpsdecreaseworkofbreathingandeasierpatient triggering (theamountofPEEP tobeapplied isanareaofgreatdebateinthefieldofcriticalcareandnooneanswerissatisfactory).

Modes

Both pressure control or volume control can be used as long as plateaupressuresdonotexceed30,ratesareat8–14(I:Eratio1:3ormore),useofprolonged expiration to avoid intrinsic PEEP and delivered tidal volume6–10ml/kg.InvolumecontrolmodePIPmaygotoohigh.ThePIPmaybeanindicatorofinitialairwarresistanceandthedifferenceinthePIPandPplisthereforeimportant.Ifthedifferenceis>6–7thenitcanbeattributedtoRratherthantothecompliance.Effectivebronchodilatortherapywillnarrowthedifference.

Advantageofthepressurecontrolmodeisthatadeceleratingflowdeliversvolumeatalowerinspiratorypressure.

Strategies of permissive hypercapneaandpermissivehypoxemiaaregenerallyacceptabletominimizebarotraumaandairleak.

In Summary for Obstructive lung Disease

• Keeppeakalveolarpressure<30cmH2O

• Setsensitivitytotriggerat<1.5cmH2O

• Withvolumetarget,setpeakflowtopreventconcavepressurewave-form• Inspiratorytimemayneedtobelengthenedbeyond1.0seconds• WithSIMV,addPSV5–8cmH

2O

• I:Eratio1:3ormoretoallowadequatetimeforexpiration

Acute Respiratory Distress Syndrome

Indications for ventilation in acute respiratory distress syndrome (ARDS) are essentially based on clinical evidence of hypoxemia, and include:1. Increasingrespiratorydistress2. Tachypnea, tachycardia,accessorymuscleuse(in latestageapnea/

bradycardia)

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Disease Specific Ventilation 31

3. Increasingoxygenrequirementwithdesaturationonmaximaloxygen4. Respiratoryfatigue/lethargy5. Toreduceworkofbreathing

Goals of Ventilation in ARDS

• Ventilationshouldbedeliveredwithminimalvolutraumatolungs(usinglowtidalvolumes:6-8ml/kg)

• MinimaltolerableinspiredoxygenwithpositiveendexpiratorypressuretoachievePaO

255–80mmHg

• MaximaltolerablearterialPCO2(50–60mmHg)witharterialpH>7.25

(permissivehypercapnia)• Absenceofmetabolic(hypoxic)acidosis.

Conventionalventilationisthemostreadilyavailablemodality.Earlierstandardapproachusedtobe:Volumeventilationwithtidalvolumes10–15ml/kgwithpositiveendexpiratorypressure.Adequatefillingpressureswithuseoffluidandgoodcardiaccontractilitywithinotropicsupporttopreventlowcardiacoutput.

Problemswithconventional10–15ml/kgtidalvolumeandPEEPareasfollows:

Barotrauma,volutrauma,airleak(pneumothorax),chroniclungdisease,delayedrecovery,poorcardiacoutput,prolongedventilationandnosocomialinfections

Inviewofproblemswithconventionaltidalvolumeventilation:Lowtidalvolumestrategyisrecommended(NIHARDSNetworkstudy).

Thiswasaprospectiverandomizedmulticentertrialof240patientswithtwogroupsusing12ml/kgvs6ml/kgtidalvolume,PEEP5–18cmofH

2O,FiO

20.3to

1,showed25percentreductioninmortalityin6ml/kggroup.Inanotherstudy,useofhigherpositiveendexpiratorypressurewithlowertidalvolumes(openlungapproach)hasbeenusedwithimprovedresults.GattinonietalinadultsandMarraroinpediatricARDSpatients,showedthatchestcomputerizedtomography(CT)maybeusefultoseetheextentofpulmonaryinvolvement.GattinonistudiedbenefitsofpronepositioninginpatientswithARDSwithunderventilatedposteriorzones.Pronepositioningisbeingrecommendedalthoughtransientimprovementinoxygenationoccursbutnorealeffectonimprovinglongtermoutcomeshasbeenshown.Problemsassociatedwithpronepositioningincludedifficultyinnursingmanagementandmonitoring(chancesofaccidentalextubation,especiallyduringX-rayexaminationandphysiotherapy).

PediatricstudiesareavailableontheuseofpronepositioninginARDSpatientsandtheeffectsareessentiallyrelatedtoimprovedoxygenationandnotoverallmortality.

Summary for ARDSa. Pressureorvolumetargetacceptableb. UsehighPEEP“openthelungandkeepitopenstrategyfromthebeginning’

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c. Fullventilatorysupportduringacutephased. Partialventilatorysupportduringrecoveryphasee. VTsetat6–8ml/kgf. PressuretargetsettoallowVTof6–10ml/kgg. Setrateaccordingtoage,avoidairtrappingh. SetPEEPatoraboveinflectionpointonP-Vloop,8-12cmH

2O

i. IncreaseinspiratorytimetoincreasePawasalastresortinverseratio;avoidcreatingauto-PEEP

Air Leak Syndrome

Pneumothorax, Bronchopleural FistulaVentilationforairleaksyndromeischallenging.Chesttubesarefrequentlyrequired.

Ventilation strategiesUsinglowmeanairwaypressures,lowpeakinspiratorypressures,lowPEEP,lowertidalvolumes,andlowerinspiratorytimesareneeded.

Other Modes Useful in Air Leak Syndrome• Highfrequencyoscillatoryventilator(HFOV)deliverssmalltidalvolumes

athighfrequencywithlowerpeakandmeanairwaypressures• Patienthastobemusclerelaxed• Patientcannotbesuctionedfrequentlyasdisconnectingthepatientfrom

theoscillatorcanresultinvolumelossinthelung• Likewise,patientcannotbeturnedfrequentlysodecubitusulcerscanoccur.• Patientshouldbeturnedandsuctioned1–2times/dayifhe/shecan

tolerateit

Most Bronchopleural Fistula Do Not Require Surgery

Postoperative Ventilation Following Open Heart SurgeryGeneralprinciples:Oneneedstounderstandthecardiacphysiologyassociatedwiththelesionandcorrectivesurgeryaswellascardiopulmonaryinteractionsinthepostoperativeperiod.

Hypoxiaandhypercarbiashouldbeavoided topreventpulmonaryhypertensionthat increasesrightventricularafter load/chancesofRightventricularfailure.

ExcessivesystemicvasoconstrictionshouldbeavoidedtopreventincreaseinLVafterload.

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Volume/Pressure Limited Ventilation• Modeofventilationhasnotshowntomakeanyrealdifferenceinoutcomes.• ExcessivePEEPandexcessivemeanairwaypressuresshouldbeavoided

topreventtamponade/lowcardiacoutput.• Pulmonaryandsystemicvascularresistancecanincreasewithpaincausing

increasedafterloadontheheart• Considernitricoxideinpatientswithseverepreoperativepulmonary

hypertension,inpostoperativeperiod.

Chronic Lung Disease/Neuromuscular Weakness• Tracheostomyisusuallyperformedifrecoveryisexpectedtotakeseveral

weeks• OneneedstoassessneedforDay/Night/homeventilation• Generallylowventilatorsettingsareneeded.Non-invasivepositivepressure

VentilationcanalsobetriedtodeliverPSandCPAPviatightfittingmask(BiPAP:bi-levelpositiveairwaypressure).Onecanseta“backup”rateincaseofapnea.

Raised Intra Cranial Pressure (ICP)Followingpointsshouldbekeptinmind:1. AvoidsuccinylcholinemorphineastheseagentsMayraiseICP.2. Midlineheaduppositionisideal.3. Adequatesedationandmusclerelaxationisrequiredtopreventcoughing

andbuckingontheventilator(leadstoraisedICP)andadequateanalgesiaduringpainfulprocedures

4. LowPEEP(avoidanceofexcessivePEEP)topreventICPfromgoingup.5. IfhighPEEPisneededforrefractoryhypoxemia,anICPmonitormaybe

ofbenefittobesttitratetherapy.6. Goalofventilation tokeepnormalPaO

2 andPaCO

2 30–35mmHg;

hyperventilationisnolongerrecommended.

Neonatal Ventilation

Continuous positive airway pressure (CPAP):Acontinuousflowofheatedhumidifiedgasiscirculatedpasttheinfant’sairwayatasetpressureof3–8cmofH

2Omaintaininganelevatedendexpiratorylungvolumewhiletheinfant

breathesspontaneously.CPAPisusuallydeliveredbymeansofnasalprongsornasopharyngealtube.Itimprovesoxygenationbyanincreaseinthefunctionalresidualcapacity.However,overrelianceonCPAPmaybedangerousanditshouldonlybeusedifinfantsshowadequaterespiratoryeffort,appeartobetoleratingtheprocedurewellandmaintainadequatearterialblood(PCO

2<50

mmHg,pH>7.25,PaO2>50)

WithallCPAPdevicessomeairmaygetintothegutandcausegastricdistension.Thiscanbepreventedbyusinganopenendedoro-gastrictube-

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in-situ.CPAPeffectivelysplintsthechestwall,keepstheairwayspatenttherebypreventingobstructiveapneasandatelectasis.VariousstudieshavedocumentedtheefficacyofCPAPinrespiratorydistress(Hyalinemembranedisease)ofmildtomoderatedegree.Recentlytrialshavebeenconductedonusingnasalintermittentpositivepressure(NIPPV)andithasbeenfoundtohavesimilarresultsasCPAP.

Conventional Neonatal Ventilation

Pressure Limited Time Cycled VentilationThecommonesttypeofventilationusedforneonatesispressurelimited,timecycledventilationwhereapeakinspiratorypressureissetandgasisdeliveredtoachievethattargetpressure.Afterthetargetisreached,theremainderofthegasvolumeisreleasedintotheatmosphereasaresultthetidalvolumedeliverywitheachbreathisvariabledespitetherecordedpeakpressurebeingconstant.Inspirationalsoendsafterapresettimeperiod.

Incontrastinvolumelimitedmodes,apresetvolumeisdeliveredwitheachbreathregardlessofthepressurethatisneeded.Someventilatorsalsouseairwayflowasthebasisofcyclinginwhichinspirationendswhenflowhasreachedacriticalloworpresetlevel(flowcycledventilation).

Inpressurelimited,timecycledcontinuousflowventilatorsfollowingparametersaresetattheoutset:• Peakinspiratorypressure(PIP)• Peakendexpiratorypressure(PEEP)• Inspiratorytime(Ti)• Rate

Thissystemisrelativelysimpleandmaintainsgoodcontroloverrespiratorypressures.

Disadvantages

• Poorlycontrolledtidalvolume• Doesnotrespondtochangesinrespiratorycompliance• Spontaneouslybreathinginfantsmayreceiveinadequateventilationand

areatincreasedriskforairleaks

Weaning From Mechanical Ventilation

Processofweaningbeginsatthetimeofinitiationofventilation(i.e.minimalventilatorysettings tokeepbloodgasesandclinicalparameterswithinacceptablelimitsalthoughthesesettingswillbeveryhigh).

If suchprocedure is followed thenventilatory settingswouldbereducedoncetheprimarypathology/conditionthat ledtoventilationisimproving.

Ch-03.indd 34 1/19/2015 3:53:53 PM


How do we know if the condition is improving?• Improvinggeneralcondition,fever,etc.• DecreasingFiO

2requirement

• Improvingbreathsounds• Decreasingendotrachealsecretions• ImprovingchestX-rays• Decreasedchesttubedrainage,bleeding/airbubbles(asthecasemaybe)• Improvedfluidandelectrolytestatus(nooverloadordyselectrolytemia)• Improvinghemodynamic status• Improvingneurologicalstatus,musclepower,airwayreflexes/control

Describedweaningcriteriasuchasmaximalnegativeinspiratoryforce,vitalcapacitymeasurementareusuallyimpractical.Inpediatricsandneonatalagegroupweaningcriteriaaregenerallyclinical.

Weaning MethodologyTherearenosetprotocolssupportedbyanypediatricstudies.Protocolfollowedatauthorsinstitutionisasfollows:• WhenFiO

2requirementisdownto0.4,improvementinsecretions,and

chestXrays,improvingclinicalcondition,musclerelaxantdripisstoppedandsedationcanbeslowlyweaned.

• Oneshouldchangecontrolmode(orPRVC)toSIMVmodewithpressuresupport.Pressuresupportcanbesetat10–15cmabovePEEPsothatthespontaneousbreathscanbeadequatelysupported.Triggersensitivityshouldbe0-tonegativeone.

• Spontaneousbreathing trialscanbegivenconnecting toC-circuit(anesthesiabag)foravariableduration(15minutesto1hour)toassessadequacyofspontaneousrespirations

Followingweaningguidelinescanbefollowed:1. DecreaseFiO

2tokeepSpO

2>94

2. DecreasethePEEPto4–5graduallybydecrementsof1–2cmH2O

3. DecreasetheSIMVrateto5–10(by3–4breath/min)4. DecreasethePIP(to20cmH

2O,byreducing2cmH

2Oeachtime/Tidal

volume,tonolessthan5ml/kgtopreventatelectasis(usuallyguidedbybloodgases)

5. VentilatorrateandPIPcanbechangedalternately.6. Ifatanypointpatient’soxygenrequirementincreasesgreaterthan0.6,or

spontaneousventilationisfastordistressedwithaccessorymuscleuse(increasedworkofbreathing),patientgetslethargic,hypercarbiaonbloodgas,weaningprocessshouldbepausedandthesupportlevelincreased.Patientmaynotbeready.

7. Goalistodecreasewhattheventilatordoesandseeifthepatientcanmakeupthedifferencewithoutdesaturations/hypercarbia/significanttachypneaandrespiratorydistress(ifpatientsSIMVwasreducedfrom20/minto15/minandthepatientsspontaneousrateisincreasedfrom25–50,thispatientmayneedmoretimeontheventilator).

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Extubation

MostpatientscanbeweanedtoSIMVof5andextubated,somewillneedpressuresupport5–10abovePEEPwithCPAP,whileothersmayneedCPAP5cmH

2Obeforeextubation,withorwithoutspontaneousbreathingtrialswith

C-circuitorTpiece.

Extubationcangenerallybeperformedwhenfollowingcriteriaaremet:1. Controlofairwayreflexes,minimalsecretions2. Patentupperairway(airleakaroundtube?)3. Goodbreathsounds4. Minimaloxygenrequirement<0.3withSpO

2>94

5. Minimalrate5/min6. Minimalpressuresupport(5-10abovePEEP)7. “Awake”patient

Summary

1. Remembershockandpostresuscitationareimportantindicationsforventilation,inadditiontorespiratoryfailureandneuromusculardisease.

2. Clinicalmonitoringofadequatechestriseandoxygensaturationsisveryimportant(regardlessofvolume,pressureortimecycledmode)

3. Ifventilatorfails,orwhenindoubt,removeendotrachealtubeandtrybagmaskventilation.

4. Thinkaboutpneumothoraxinapatientonmechanicalventilation.5. PulseoximetryandABGfacilityisnecessaryforventilation.6. Hypoxiashouldberuledout/correctedbeforesedatinganagitatedchild.7. Donotmusclerelax/sedatepatientwithupperairwayobstructionunless

veryconfidentinendotrachealintubation.8. Lowtidalvolume ispermitted toprevent lung trauma(permissive

hypercapnia)9. EndtidalCO

2monitoringandpulmonarygraphicsmonitoringisdesirable

ifavailable.

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Uses

Confirm mode functions:• Detect auto-PEEP• Determine patient-ventilator synchrony• Assess and adjust trigger levels• Measure the work of breathing• Adjust tidal volume and minimize overdistension • Assess the effect of bronchodilator administration• Detect equipment malfunctions• Determine appropriate PEEP level

measured parameters are Time on the X-axisFlow, volume, pressure on the Y-axis

Definitions

• Inspiratory flow time: beginning of flow to end of flow during inspiration• Inspiratory pause time: time in inspiration where flow is zero• Inspiratory phase time: Insp. flow time + insp. pause time• Expiratory flow time, Exp. pause time exp. phase time• Inspiratory flow rate: rate at which gas flows into the patient expressed as

volume per unit of time• Peak pressure : max. pressure during the insp. phase time• Plateau pressure: resting pressure during the insp. pause• Resistance: ratio of the change in driving pressure to the change in flow

rate cm H2O/L/sec

• Compliance: ratio of a change in volume to a change in pressure

Basic Shapes of Waveforms

• Square wave: − Represents a constant or set parameter. − For example, pressure setting in PC mode or flow rate setting in VC

mode.

Chapter

4Interpretation of Graphic

Displays on VentilatorsAmit Vij

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• Ramp wave: − Represents a variable parameter − Will vary with changes in lung characteristics − Can be accelerating or decelerating

• Sine wave: − Seen with spontaneous, unsupported breathing

Waves in pressure control modes: PRVC SIMV (PRVC) SIMV (press. control) including pressure support volume support.

Flow is decelerating but the pressure is constant• In pressure modes, the shape of the pressure wave will be a square shape.• This means that pressure is constant during inspiration or pressure is a

set parameter.

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Interpretation of Graphic Displays on Ventilators 39

Waves in volume control: Volume control, SIMV VC. In volume modes, the shape of the pressure wave will be a ramp for

mandatory breaths.

The baseline for the pressure waveform will be higher, when PEEP is added. There will be a negative deflection just before the waveform with patient triggered breaths.

Uses of the Pressure Waveform

• Air trapping (auto-PEEP)• Airway obstruction• Bronchodilator response• Respiratory mechanics (C/Raw)• Active exhalation• Breath type (pressure vs. volume)• PIP, P-plat• CPAP, PEEP• Asynchrony• Triggering effort

The area under the entire curve represents the mean airway pressure Paw/ MAP

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At the beginning of the curve (above) the airway resistance contributes to the pressure. Then the main part is the alveolar distending pressure. The first peak gives the peak inspiratory pressure and the flat portion shows the plateau pressure.

A B

A—Increase in airway resistance (Raw) causes the PIP to increase, but P-plat pressure remains normal.

B—A decrease in lung compliance causes the entire waveform to increase in size. (More pressure is needed to achieve the same tidal volume). The difference between PIP and P-plat remains normal.

Decreased ComplianceCauses• ARDS• Atelectasis• Abdominal distension• CHF• Consolidation• Fibrosis• Hyperinflation• Pneumothorax• Pleural effusion

How to identify it on the graphics?• Pressure wave: PIP and plateau both increase• Pressure/Volume loop: lays more horizontal

Auto-PEEP: During an expiratory hold maneuver, trapped air will cause the waveform to rise above the baseline, auto-PEEP should be <5 cm H

2O

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Volume waveforms: used to assess:• Air trapping• Leaks• Tidal volume• Active exhalation• Asynchrony

Typical curve will generally have a “mountain peak” appearance at the top. It may also have a flattened area at the peak of the waveform if there is

inspiratory hold.

Leak detection: what volume goes in comes out, except if there is a leak.If Gas is trapped in the lung the exhalation volume will not return to zero

and the appearance will be the same.

Flow Time Waveforms

In volume modes, the shape of the flow wave will be square.This means that flow remains constant or flow rate is a set parameter. In

pressure modes, the shape of the flow waveform will have ramp pattern which shows a decelerating flow. The decelerating flow pattern may be preferred over the constant flow pattern. The same tidal volume can be delivered, but with a lower peak pressure.

Flow waveforms are used for the assessment of:Air trapping (auto-PEEP)• Airway obstruction• ronchodilator response• Active exhalation• Breath rype (pressure vs. volume)• Inspiratory flow• Asynchrony• Triggering effort

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Auto-PEEP: If the expiratory portion of the waveform doesn’t return to baseline before the start of the next breath starts, there could be air trapping (emphysema, improper I:E ratio).

Causes:• Insufficient expiratory time• Early collapse of unstable alveoli/airways during exhalation

How to Identify it on the graphics?• Pressure wave: while performing an expiratory hold, the waveform rises

above baseline.• Flow wave: the expiratory flow doesn’t return to baseline before the next

breath begins.• Volume wave: the expiratory portion doesn’t return to baseline.• Flow/Volume loop: the loop doesn’t meet at the baseline• Pressure/Volume Loop: the loop doesn’t meet at the baseline• How to Fix.• Give a treatment, adjust I-time, increase flow, add PEEP.

Airway Resistance

The expiratory limb is seen as short and there is a longer duration to return to baseline. An improvement after bronchodilator treatment can be seen with an increased exp. peak flow and a shorter time to touch the baseline.

Air trapping and short peak flow with delayed decay may be seen in the same graph as in asthma.

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Inspiratory rise time: (How quickly is the pressure reached?) determines the amount of time it takes to reach the desired airway pressure or peak flow rate. It is measured as a percentage of the breath cycle. The less the percentage the faster the time to reach peak pressure. It’s adjusted to meet the flow demands of the patient, especially in the pressure support mode. If rise time is too fast, you can get an overshoot in the pressure wave, creating a pressure “spike”. If this occurs, you need to increase the rise time. This makes the flow valve open a bit more slowly.

If rise time is too slow, the pressure wave becomes rounded or slanted, when it should be more square. This will decrease Vt delivery and may not meet the patient’s inspiratory demands. If this occurs, you will need to decrease the rise time to open the valve faster.

Too slow giving less Vt Too fast giving pressure spike

Flow cycle off:The inspiratory cycle off determines when the ventilator flow cycles from inspiration to expiration, in pressure support mode.Also know as–• Inspiratory flow termination• Expiratory flow sensitivity• Inspiratory flow cycle %• E-cycle, etc.

Flow cycling is important for tidal volume delivery as well as patient comfort.

100% flow, i.e. stops when flow reaches 30% (set value) : If 10 L/minute is the peak flow, when the flow comes down to 3 L/min, the flow will stop.

A. If the cycle off percentage is too high, cycling off too soon. This makes the breath too small (not enough Vt).

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B. If the cycle off percentage is too low, making the breath too long. This forces the patient to actively exhale (increase WOB). creating an exhalation “spike”.

Setting the Ti: The equation Vt = Flow X insp. time (Ti) is used but the Ti is often set arbitrarily using the age and disease state. To check the adequacy of the Ti, the flow time wave can be used.

A. Short Ti: flow stops too early. resulting in low Vt and flow hunger.B. Normal Ti: flow stops just before or at end insp.C. Long Ti: flow stops but insp. goes on. In the PRVC mode, when the decided Vt is not met by the PIP limit set,

an increase in Ti (within limits) may be a better option than increasing pressure.

A scooping of the inspiratory limb of the wave denotes a very low set flow. A breathing effort may be seen on either limb when asynchrony occurs

Loops

Pressure and Volume• Volume is plotted on the Y-axis, pressure on the X-axis.• Inspiratory curve is upward, expiratory curve is downward.• Spontaneous breaths go clockwise and positive. MV breaths are shown

anti-clockwise

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• The bottom of the loop will be at the set PEEP level. It will be at 0 if there’s no PEEP set.

• If an imaginary line is drawn down the middle of the loop, the area to the right represents inspiratory resistance and the area to the left represents expiratory resistance.

Can be used to assess:• Lung overdistention• Airway obstruction• Bronchodilator response• Respiratory mechanics (C/Raw)• WOB• Flow starvation• Leaks• Triggering effort

Best used in the volume control setting as it becomes almost square shaped in pressure modes because of pressure limiting (constant), during the inspiration. Whereas in VC there is a relationship between P and V that can be seen.

PRESSURE (X-axis) VOLUME (Y-axis)PC mode normal loop: May be extrapolated as being the plateau pressure

Therefore only in VC can any inflection points be seen and measured.

VC mode: Normal loop.

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Compliance changes: Increased compliance: surfactant, emphysema (till beaking)

Overdistention. Initial good Cl, then no change in vol for P inc

Airway Resistance

As airway resistance increases, the loop will become wider.• An increase in expiratory resistance is more commonly seen

Ch-04.indd 46 1/19/2015 3:53:37 PM


Flow–Volume Loops

A normal Flow-volume loop begins on the X-axis (volume axis): at the start of the test both flow and volume are equal to zero. After the starting point the curve rapidly mounts to a peak. Peak (expiratory) Flow: After the PEF the curve descends (= the flow diminishes) as more air is expired. A normal, non-pathological F/V loop will descend in a straight or a convex line from top (PEF) to bottom (FVC).

The forced inspiration that follows the forced expiration has roughly the same morphology, but the Peak Inspiratory Flow (PIF) is not as distinct as PEF.

In a PFT, the inspiratory limb is always on the negative side (as flow is detected as decreasing in the circuit) and the exhalation is detected as a positive flow in the circuit. However, the ventilator graphics may not always be oriented this way. Most machines show a spontaneous breath as being clockwise and a machine breath as being anti-clockwise. The insp. limb is usually on the upper side. Square appearing insp. limb exponentially decreasing exp. limb after initial peak flow which is almost straight.

Used for Air trapping:• Airway obstruction• Airway resistance• Bronchodilator response• Insp./exp. flow• Flow starvation• Leaks• Water or secretion accumulation• Asynchrony

Starting type of loops seen:

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• Obstructive pattern• Scooping of the exp. limb with a very low peak flow• With bronchodilators, this will reverse

The shape of the insp limb will match the flow wave form:• Constant flow will be flat• Deceleration flow will be sloping down

If there is a leak, the loop will not meet at the starting point where inhalation starts and exhalation ends. It can also occur with air-trapping.

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Leaks: Causes

• Expiratory leak: ETT cuff leak, chest tube leak, BP fistula, NG tube in trachea• Inspiratory leak: loose connections, ventilator malfunction, faulty flow

sensor

Recognition• Pressure wave: Decreased PIP• Volume wave: Expiratory side of wave doesn’t return to baseline• Flow wave: PEF decreased• Pressure/volume loop: exp. side doesn’t return to the baseline• Flow/volume loop: exp. side doesn’t return to baseline

How to fix it• Check possible causes listed above• Do a leak test and make sure all connections are tight

Asynchrony

Causes (flow, rate, or triggering):• Air hunger (flow starvation)• Neurological injury• Improperly set sensitivity

Recognition• Pressure wave: patient tries to inhale/exhale in the middle of the waveform,

causing a dip in the pressure• Flow wave: patient tries to inhale/exhale in the middle of the waveform,

causing erratic flows/dips in the waveform• Pressure/volume loop: patient makes effort to breath causing dips in loop

either Insp./exp.• Flow–volume loop: patient makes effort to breath causing dips in loop

either insp./exp.

How to fix it?• Try increasing the flow rate, decreasing the I-time, or increasing the set

rate to “capture” the patient.• Change the mode—sometimes changing from partial to full support will

solve the problem• If neurological, may need paralytic or sedative• Adjust sensitivity

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In this chapter, we will mainly discuss high-frequency oscillatory ventilation (HFOV), which is rarely used in PICUs. Theoretically, HFO is an ideal tool for lung-protective ventilation as it allows effective pulmonary gas exchange with the delivery of a very small tidal volume (Vt) below dead space while keeping the lung open at a constant distending pressure akin to a high PEEP and diminished risk of atelectrauma. Some trials have done and others are going on but till date none of them had showed survival benefit (Table 5.1).

Key features of HfOV

• Highfrequency: It utilized much high respiratory rates (up to 900/min) then conventional ventilator (CV).

• Amplitudeorpower:Ventilation is much more dependent on amplitude (a determinant of tidal volume). Amplitude controls the force with which the piston moves. Appropriate amplitude creates a “chest wiggle factor (CWF)”. In contrast to CV, very small tidal volume (below dead space volume) is delivered at supra physiological rate.

Chapter

5High frequency Ventilation

Sanjeev Kumar

Table 5.1: Comparison of high frequency (HFOV/HFJV) and conventional ventilatorConventional HFOV 1Hz = 60 HFJV (Jet)

Frequency 2-60 Up to 900 Up to 600

Delivered tidal volume

More than dead space (VD)

< VD < VD

Expiration Active Passive Passive

Potentiation of intrinsic PEEP

+1 +2 +3

Peak pressure Peak < Conventional < Conventional

Mean pressure (Paw)

MAP < or > Conventional < or > Conventional

Minute ventilation

R X TV > Conventional > Conventional

ET tube Normal Normal Special double lumen ET tube

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high Frequency Ventilation 51

• Activeexpiration: In contrast to other ventilator, expiration is also active processes. Gas is actively pushed and withdrawn into the lung. It enables control of lung volumes, decreasing the risk of air trapping and over distension of airspaces.

• Highermean airway pressurewith lower peak pressure:The continuously high distending pressure provides better oxygenation via improved alveolar recruitment.

• Decouplingofoxygenationandventilation—in contrast to CV, oxygenation and ventilation are handled independently.

• Minuteventilation:It is equal to rate x VT

n rather than rate × tidal volume.• LessVILI:In comparison to conventional ventilator the entire cycle of HFO

operates in the “safe window” and avoids the injury zones. Peak airway pressure is characteristically lower in HFOV compared to conventional ventilation so less barotrauma. Tidal volume is below dead space volume, so less volutrauma. Smaller differences between inspiratory and expiratory pressures prevent atelectrauma which usually associated with cyclical alveolar collapse and distension.

• Specialventilator:HFOV can be delivered only by esp. ventilators with oscillator. The ventilator delivers a constant bias flow, while a valve creates resistance to maintain airway pressure, on top of which a piston pump oscillates at supra physiological rate (Fig. 5.1). A flow of warmed humidified gas (bias flow) is run across the proximal

end of the endotracheal (ET) tube at 20–40 liter/min. An oscillatory piston pump vibrates this bias flow of gas so that a portion of the gas is pumped into and out of the patient. Thus, in contrast to CV, inspiration and expiration are both active processes in HFOV. The ventilator delivers a constant flow (bias flow), while a valve creates resistance to maintain airway pressure, on top of which a piston pump oscillates at frequencies of 3–15 Hz (180–900/min). This creates a constant airway pressure with small oscillations. For appropriate amplitude “CWF” is assessed clinically. Oxygenation is achieved with high mean airway pressure to achieve lung recruitment and ventilation is achieved with an oscillating piston that creates cycles of pressure above and below the mean airway pressure at supraphysiologic respiratory rates, resulting in small

Fig. 5.1: Showing that MAP is identical or slightly high in HFOV but amplitude (DP) of the oscillations is much smaller than the difference between PIP and PEEP in conventional ventilator.

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tidal volumes (1–2.5 mL/kg). Exhalation is active rather than passive process as occurs in all other conventional and high frequency mode. In this mode control of oxygenation and ventilation are independent.

Lung volume changes with each breath are therefore minimized during HFOV, with volume being maintained above functional residual capacity during all phases of the respiratory cycle.

Mechanismsofgas transport inHFO:Bulk convection is the major mechanism for gas transport on conventional ventilator. A number of different mechanisms have now been identified as having a contributory role in promoting gas exchange during HFOV, including bulk convection, asymmetric velocity profiles, pendelluft, cardiogenic mixing, Taylor dispersion and turbulence, molecular diffusion, and collateral ventilation. Bulk convection plays a relatively small role in gas transport during HFOV, especially ventilatory exchange in the most proximal gas exchange units.

Indications: In contrast to neonatal practice, HFOV is not however recommended as a first line ventilatory strategy in pediatric and adults. The main potential indications for use of HFOV in critical care patients remain the treatment of patients with severe ARDS, bronchopleural fistula, pulmonary hemorrhage and acute chest syndrome in sickle cell disease. Indications of HFOV in ARDS are especially when plateau pressures are above 35 and oxygenation index is more than 13–15 (Table 5.2 and Fig. 5.2).

Contraindications:HFOV should not be used in patients with shock, severe airway obstruction, intracranial hemorrhage, or refractory barotraumas. It must be used cautiously with severe acidosis, because CO

2excretion may be limited.

Table 5.2: Initial ventilatory setting in ARDSFiO2 Bias flow Ti Hz Paw Power

Neonate (not preterm)

1.0 20 L/min 33% 13–12 3-5 cm above CMV Paw

0–2

<10 kg 1.0 20 L/min 33% 12–10 0–4

10–30 kg 1.0 20–30 L/min 33% 12–8 4

>30 kg 1.0 > 30 L/min 33–(50)% 6 4–6

Fig. 5.2: Showing settings of different parameters on HFOV.

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InitialventilatorsettingsinHFOV:It does depend on age, type and severity of the disease.

Adjustment: After initial ventilator settings, the oxygenation and ventilation are adjusted independently.

Ventilation:Ventilation in HFO is much more dependent on amplitude (a determinant of tidal or cycle volume) rather than the frequency. Cycle volume is synonymous with delivered tidal volume. This is controlled by the distance the piston pump moves in and out, the amplitude of oscillations. We will adjust the amplitude while targeting permissive hypercapnia. CO

2 elimination is

increased by adjusting the amplitude and decreasing frequency on machine. Amplitude controls the force with which the piston moves and the frequency controls the time allowed (distance) for the piston to move. A clinically useful measure of tidal volume is the ‘CWF’. Appropriate amplitude creates a CWF.

MonitoringofCWF:It refers to visible movement of the patient generated by the oscillations. It should be visible from the clavicles to mid-thigh; it must be evaluated upon initiation and followed closely during whole ventilation. CWF may be used as a surrogate marker of tidal volume and sudden changes (asymmetrical/absent/decreased) in observed CWF should prompt urgent patient evaluation (Table 5.3).

Frequency: in HFOV, lowering frequency (Hz) paradoxically improves CO2

removal by achieving larger tidal volume (greater volume displacement) (Fig. 5.3).

Stepwiseapproachtoimproveventilation1. Amplitude (Power)2. Frequency (Hz)3. Inspiratory time (Ti)4. Cuff leak-washed by bias gas flow but monitor for a loss in Paw with the air

leak created by deflating the cuff.

Fig. 5.3: Showing increase volume displacement with decrease frequency

Table 5.3: Monitoring of amplitude chest wiggle factorAsymmetrical chest wiggle factor No chest wiggle factor

� Pneumothorax � Displaced ET tube

� ET tube disconnect � Secretion in ET tube � Improper amplitude settings � Severe bronchospasm

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Oxygenation:As conventional ventilator oxygenation is mainly depends on mean airway pressure (Paw) and FiO

2. PaW is adjusted to achieve target

saturation of >90%.

Step Wise Approach to Increase Oxygenation

1. Paw or MAP (mean airway pressure) – Initial PaW is set at 3–5 cm H2O

more than the MAP on conventional ventilator. After initial settings we will adjust MAP while targeting permissive hypoxemia, keeping in mind that excessive Paw can impair ventilation by over distension. Optimal lung volume is determined by the increase in saturation (PaO

2/SaO

2) and

diaphragm is at ~T9 on chest radiograph. Ensure adequate intravascular volume and cardiac output while increasing Paw. Consider fluid bolus or inotropes infusion as per hemodynamic status.

2. FiO2—we will start at FiO

2 1.0 and wean the FiO

2 until ≤0.60 after achieving

adequate Paw. 3. Bias flow: If the Paw adjust control knob is maximised with less bias flow is

at 20–30 L/min, then by further increasing the bias gas flow, a higher Paw

can be achieved. 4. Alveolar recruitment maneuver (RM): If we are unable to wean off FiO

2

despite adequate Paw, then RM (sustained inflation) can be tried. 5. Frequency may sometimes effect oxygenation6. Inspiratory time (Ti): Increasing % Ti (33–50%) may also affect lung

recruitment by increasing delivered Paw.

Recruitmentmaneuver(RM):It should be conducted only after assessment of adequacy of cardiovascular function and volume status. If oxygenation is poor prior to commencing HFOV it is advisable to perform a recruitment maneuver such as an inspiratory hold, 30–40 cm H

2O for 40 seconds. This should be

aborted if hemodynamic instability occurs (Table 5.4).

Biasflow:It is usually set at 20 liter/min but it may be increased when an increased bias flow is required to compensate for a leak in order to achieve a desired MAP, e.g. physiotherapy, suctioning, severe ARDS, and pathological air leak (bronchopulmonary fistula).

Table 5.4: Monitoring while recruitment maneuverRecruitment maneuver Monitor Post procedure

� Set high airway pressure alarm to 50 cm H2O

� Inflate cuff to occlude leak � Set HFOV to standby (stop

oscillator) � Increase Paw to 40 cm H2O

for 40 sec.

� Watch BP and SpO2 � Stop immediately if

fall >20 mm Hg or MAP <50 mm Hg

� Return Paw to previous or high setting

� Reset cuff leak � Restart piston � ABGs 10 minute after RM � Repeat RM up to max of

3 cycles

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Pistoncentering:It is unique feature of ventilator especially in Sensor medics A (Pediatric). • Any change in setting can affect position of the piston, so it should be

adjusted.• If it is displaced in either direction, the max. Oscillatory motion which can

be produced will be limited by closer of the two mechanical stops at front and back wall of cylinder.

• It works by applying an adjustable direct electrical counterforce to piston coil to maintain piston centering.

Weaning:The first priority in weaning HFOV is to decrease FiO2 from toxic

levels. The gradually Paw and amplitude is adjusted. After reaching target MAP and FiO

2, we continue HFOV for at least 12–24 hours. ABG and clinical

monitoring continued throughout weaning period. In comparison to neonates who can be directly extubated from HFO, pediatric patients were switch back to conventional ventilator.

Target values for switch back to conventional ventilator:• Reversal of disease process• MAP <15 (12–18 cm H

2O)

• FiO2 <0.5 (0.4–0.6)

• Adequate gas exchange and improving pulmonary function

Monitoring on HfOV (Table 5.5)

HFOcircuit:These are different from usual ventilatory circuits and have additional diaphragm and water trap. All packaged tube are disposable and for single use only. Long and short circuit tubing were connected directly to patient and ET tube. Color coded lines are placed as per their distance (place the shortest line to the closest cap). Usually inline suction is attached to the circuit. Ensure that HFOV circuit does not kink. Humidification Chamber must be MR290 HFV type and it should not be empty.We can use additional expiratory and inspiratory filter with HFO circuits as per institutional recommendations.

EndotrachealsuctiononHFOV:Ideally appropriate size close (In-line) suction should be attached to the ET and circuit.Close suction prevents derecruitment and VAP.Suction should be done whenever there is clinical (decreased or absence CWF, visible ET secretions) or blood gas deterioration

Table 5.5: Monitoring on high frequency occilation ventilatorClinical monitoring Chest X-ray (CXR) Blood gas

� Chest Wiggle Factor

� Auscultation � Vitals (HR, BP) � SpO2 /TcCO2

� CXR after 30-60 minutes – Check posterior rib – Air leak

� Initial ABG after 30 min – PaO2 and PaCO2/pH

� Recheck ABG 15–30 minutes after each adjustment or so

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(Desaturation/hypercarbia). Denitrogenation (FiO2-1) is advisable before

suctioning. Suction passes should be limited maximally to 10–15 seconds. After completion of suction, Paw could be increased by 3 cm H

2O for approximately

30 minutes (depend on severity of disease) (Fig. 5.4).

EmergencyscenariosassociatedwithHFOV(Table5.6)• Hypotension may be caused by increased Paw on HFOV causing reduced

cardiac preload. This is exacerbated by coexistent hypovolemia. • SubtotalobstructionofETtube will lead to progressive hypercapnia.

Abrupt increases in PaCO2, loss of CWF and a change in observed amplitude

may all indicate an obstructed airway. • PneumothoraxandETtubedisplacement are difficult to recognize in

patients receiving HFOV. A high index of suspicion is required for both clinical situations. There may be a change in amplitude, loss of oscillations

Fig. 5.4: Showing HFOV circuit with in-built oscillator

Colour–Circuit attachementBlue–Limit ValveGreen–Paw control valveRed–Dump valveWhite–Paw sensor port

Contd...

Table 5.6: Trouble shootingon high frequency occilation ventilatorSource gas low alarm

Battery low alarm

Oscillator overheated alarm

Oscillator stopped alarm

High Paw alarm

Low Paw alarm

� If high pressure gas sup-plies fall < 30 PSI.

� This will activate the visual indicator only

� Check gas supply if activated

� If the 9 volt alarm battery needs replaced

� This will activate a visual indicator only

� If the linear mo-tor temp exceeds 150°C

� This will activate a visual indicator only

� If the oscillatory amplitude is at or below 7 cmH2O and the oscillatory system is pressur-ized

� Activation of this alarm will trigger the Auto Limit System

� The Auto Limit System will open the “blue” limit valve on the circuit and vent pressure

� Activa-tion of this alarm will only provide audible and visual alarms. The visual alarm will automati-cally reset after the

Ch-05.indd 56 1/19/2015 3:53:24 PM


on the side of pneumothorax or area no longer ventilated after ET tube displacement as well as an abrupt rise in CO

2. Hypoxia and hypotension

may also ensue.

Sedation,analgesiaandneuromuscularblockingagents:To facilitate ‘capturing’ the patient, additional sedation and intermittent neuromuscular blockade may be required.

Evidence for HfOV

Different nonrandomized trials has found no differences in survival or duration of mechanical ventilation between the 2 groups while comparing conventional and HFOV, but few children who receive HFOV remained dependent on supplemental O

2 at 30 days. It has been suggested that HFOV should be

employed early in the course of severe ARDS.Till now, two randomized controlled trials investigating the effect of HFOV on patient outcome have been performed and the larger of these included only 58 children. The main finding of this study was that HFOV did not significantly improve survival (66% with HFOV versus 59% with conventional MV) or total ventilator days (20 ± 22 days with HFOV versus 22 ± 17 days with conventional MV). As a consequence, HFOV is not universally employed in pediatric critical care. This means that well-designed observational studies are needed to shed light on some of the

Contd...

Source gas low alarm

Battery low alarm

Oscillator overheated alarm

Oscillator stopped alarm

High Paw alarm

Low Paw alarm

� Both audible and visual indicators will be activated

� The valve will then re-pressurise to its normal operational state unless it pressure reaches Paw > 60 cm H2O before the issue is resolved

� If this hap-pens the circuit pres-sure will vent to ambient, the oscillator will stop and you will need to recruit

fault con-dition has resolved unless the pressure drops to Paw < 5 cm H20 before the fault is resolved. If this happens the circuit pressure will vent to ambi-ent, the oscillator will stop

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many other aspects of pediatric HFOV which remain to be explored, including the identification of patients who are most likely to benefit from HFOV, the timing of HFOV (early versus rescue) and optimal oscillator settings.

further Reading1. Arnold JH, Anas NG, Luckett P, et al. High-frequency oscillatory ventilation in

pediatric respiratory failure: a multicenter experience. Crit Care Med. 2000; 28(12):3913-9.

2. Arnold JH. High-frequency ventilation in the pediatric intensive care unit. Pediatr Crit Care Med. 2000;1(2):93-9.

3. Dos Santos CC, Slutsky AS. Overview of high-frequency ventilation modes, clinical rationale, and gas transport mechanisms. Respir Care Clin N Am. 2001;7(4):549-75.

4. Duke PICU Handbook (revised 2003).5. High Frequency Oscillation in ARDS trial (OSCAR), www.oscar-trial.org. 6. Priebe GP, Arnold JH. High-frequency oscillatory ventilation in pediatric patients.

Respir Care Clin N Am. 2001;7(4):633-45.7. Ritacca FV, Stewart TE. High frequency oscillatory ventilation in adults a review of

the literature and practical applications. Critical Care. 2003;7:385-90.8. Slutsky AS. Lung Injury Caused by Mechanical Ventilation. Chest. 1999;

116(1):9S-14S.9. The Oscillation for Acute Respiratory Distress Syndrome (ARDS) Treated Early

(OSCILLATE) Trial, Canadian Critical Care Trials Group.

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Introduction

Non-invasive ventilation (NIV), involves the delivery of mechanically assisted breaths without the use of an invasive artificial airway (endotracheal or tracheostomy tube).

The concept of NIV is not new. Dr Philip Drinker (a pediatrician), developed and used the negative pressure ventilator popularly known as “iron lung”—to treat patients with poliomyelitis in 1920s. This fell out of practice as invasive mechanical ventilation became popular in 1960s which still remains a standard practice for management of children with acute hypoxemic respiratory failure. However, during the last decade NIV has been used increasingly to provide ventilatory support to various groups of patients. Most of the experience originates from the adult patients. Most of the pediatric data is still in the form of case reports. The conditions or diseases reported are heterogeneous. Hence, there are no generally accepted guidelines for NIV in pediatric population.

The standard strategy for treating children in respiratory failure is by invasive mechanical ventilation which is associated with a number of pulmonary and extra-pulmonary complications. NIV can often eliminate the need for intubation or tracheostomy and preserve normal swallowing, speech, and cough mechanisms. The use of NIV in acute/chronic hospital settings has been increasing in the past few years. Children with chronic conditions needing ventilatory support at home are increasingly put on NIV therapy (“home” ventilators).

Modes and Mechanism of Action

The NIV can be in the form of volume or pressure controlled. Volume controlled ventilators are not well tolerated because of variable pressure generation.

Non-invasive “Positive” Pressure Ventilation (NPPV)1. CPAP2. BiPAP

Chapter

6Non-invasive

Ventilation in Children

Ch-06.indd 59 1/19/2015 3:53:07 PM


“Negative” Pressure Ventilation

Continuous Positive Airway PressureContinuous positive airway pressure (CPAP), is a mode of ventilation, in either spontaneously breathing or mechanically ventilated patients, in which airway pressure is maintained above atmospheric pressure throughout the respiratory cycle by pressurization of the ventilatory circuit.

CPAP circuit may use demand valve or continuous fresh gas flow. Demand valve may be flow triggered or pressure triggered. The disadvantage of demand valve system is that work of breathing is increased by need to trigger valve.

Biphasic Positive Airway PressureBiphasic positive airway pressure (BIPAP) is a pressure controlled mode of ventilation with cycling variations between two continuous positive airway pressure levels, allowing spontaneous breathing during every ventilatory phase. The mandatory breaths are pressure controlled and the spontaneous breaths can be pressure supported.

The major advantages of NPPV are related to the effects generated by the increase in intrathoracic pressure. These benefits include increases in functional residual capacity and oxygenation, reduction in the work of breathing, and reductions in preload and afterload.

Negative Pressure VentilationNegative pressure ventilation (NPV) works by exposing the surface of the chest wall to sub-atmospheric pressures resulting in the expansion of the lungs and drawing in of air. Both the inspiratory and expiratory phases can be fully controlled by modifying the negativity of the air pressure.

Three commonly used modes of NPV are:1. Continuous Negative Extra-thoracic Pressure (CNEP): It increases the

lung volume by creating continuous negative chamber pressure whilst the patient is breathing spontaneously.

2. Respiratory Synchronized Mode: This mode allows the patient to breathe at their own rate. The patient’s inspiratory and expiratory efforts are triggers for the respirator and thus full synchronization with their respiration is achieved. The trigger sensitivity can be set and is patient dependant.

3. Secretion Clearance (‘physio mode’): This is a physiotherapy tool used to enhance clearance of secretions from the lungs using two alternating modes. The “vibration” mode loosens secretions and “Cough” mode creates a cough like effect to eliminate secretions. This is achieved by high frequency oscillations around a negative baseline followed by an artificial cough that has a prolonged inspiratory phase followed by a forced short expiratory phase.

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Non-invasive Ventilation in Children 61

Indications

There are no strict guidelines to initiate NIV in children. Also, the choice of NIV mode depends largely on the availability and clinical expertise of the staff at bed side. The role of respiratory physiotherapists cannot be overemphasized. Following might prompt the clinician to consider NIV in children: 1. Acute or chronic respiratory distress 2. PaCO

2 greater than 45 mm Hg and pH < 7.35 (but > 7.10)

3. PaO2 and fraction of inspired oxygen (FiO

2) ratio < 200

Some of the specific disease categories/conditions include:a. Respiratory: RDS in newborn babies, pneumonia, acute severe asthma,

bronchiolitis, CLD, Brochiectasis, cystic fibrosis, sleep apnoea syndromeb. Thoracic wall deformities: kyphoscoliosis, thoracic dystrophyc. Neuromuscular disorders: DMD, congenital myopathyd. Cardiac: Congestive heart failure, persistent ventricular dysfunction post

Cardiac surgery (following extubation)e. Immunocompromised patients: leukemia, severe combined immune

deficiency; to reduce hospital acquired infectionsf. Neurological: Central hypoventilation syndrome, bulbar dysfunction g. Patients ‘not for intubation’h. Post extubation period: stridor, persistent respiratory distress, severe failure

to thrive (can “buy time” to improve nutritional status)

Contraindications

1. Respiratory arrest 2. Hemodynamic instability or life-threatening arrhythmia 3. High risk of aspiration 4. Uncooperative or agitated patient 5. Life-threatening refractory hypoxemia (alveolar-arterial difference in

partial pressure of oxygen [PaO2] < 60 mm Hg with FiO

2 of 1)

6. Impaired mental status 7. Facial or upper GI surgery8. Craniofacial injuries

Relative contraindications 1. Inability to use mask because of trauma or surgery 2. Excessive upper airway secretions3. Claustrophobia

An alternative mode (such as negative pressure ventilation) may be considered in these conditions.

Interfaces

Interfaces are devices that connect the ventilator tubing to the face (or chest wall, in case of negative pressure ventilation) facilitating ventilation. Nasal,

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oro-nasal masks and mouth pieces are currently available. A “jacket” around chest wall is used for Hayek (negative pressure) ventilator. The interface should have minimal dead space and a soft inflatable cuff to provide a seal with the skin. Face masks and nasal masks are the most commonly used interfaces. Nasal masks are used most often in chronic respiratory failure while face masks are more useful in acute respiratory failure (may prevent air leaks). Transparent models should be preferred which help in inspecting mouth and nostrils as secretions often occlude upper airway. Unfortunately, unavailability of appropriate sized interface is a very common limiting factor in using NIV in children.

Whilst a good seal is imperative for better functioning, care should be taken to prevent pressure sores.

Humidifiers

Dryness of the upper airways is a common side effect of NIV. Heated humidifiers are much more efficient than pass over humidifiers. The addition of a humidifier will add to the resistance of the circuit, and may interfere with triggering and possibly pressure delivery.

Initiating NIV

There are no data from current studies of any kind on how to initiate NIV in children. A good understanding of underlying problem/diagnosis, and a well-defined baseline profile is desirable before NIV is instituted. Parents and if possible, the child should be counselled regarding the indication, possible duration and side effects (potential discomfort) of NIV. If the child is heading for long term home ventilation, formation of a “core” group (pediatrician, nurses, physiotherapists) as well as training the parents is very essential.

Following may help as general principles: 1. NIV should be started on an elective/semi-elective basis. 2. Choose appropriate position for the patient. 3. Choose appropriate size mask/jacket; avoid “tight” fit. 4. Choose appropriate type of mask (nasal/facial). 5. If possible, explain to the child about the ventilation process. 6. Start with low pressures and gently titrate to avoid patient-ventilator

mismatch. 7. Evaluate the adequacy of ventilation periodically (bilateral air entry, chest

wall movement, improvement in dyspnea, improved respiratory rate, and good comfort for the patient)

8. A backup rate may be provided in the event the patient becomes apneic. 9. Set the ventilator alarms and backup apnea parameters.10. Monitor with oximetry, and adjust ventilator settings after obtaining

arterial blood gas results in initial phase. Clinical parameters may be more important than blood gases later in the course.

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Non-invasive Ventilation in Children 63

11. Consider alternative modes during the course (CPAP to BiPAP, use of Hayek ventilation)

12. Always have a back up plan (invasive ventilation, “not for” re-intubation).

Weaning

Again, no fixed guidelines! One might discontinue the NIV altogether or progressively reduce the pressure support before discontinuing NIV support. Alternatively, patient may be “trained” by discontinuing the NIV support for brief periods and duration of “time off” can be increased progressively. This largely depends on underlying conditions (e.g. children with neuro-muscular disorders may need a slow wean over days to weeks).

Complications

1. Nasal and pharyngeal dryness2. Vasomotor rhinitis3. Air leaks4. Skin irritation on the nasal bridge5. Gastric distension6. Air flow-induced arousals7. Possible increase in work of breathing in user machine8. Impaired growth of facial bony structures

Summary

NIV in the paediatric population is being used increasingly both as an elective as well as rescue mode of respiratory therapy. The technique has proved effective both in the acute setting and in relation to long-term ventilation, with respect to improvement of arterial blood gases, survival and probably to quality of life. Centers lacking experience in the application of these devices should make efforts to educate their respiratory care staff. More clinical research is needed before NPPV can be used to its greatest advantage.

Further Reading1. Caples SM; Gay PC. Noninvasive positive pressure ventilation in the intensive care

unit: a concise review. Crit Care Med. 2005;33(11):2651-8.2. Deep A, Munter CD, Desai A. Negative pressure ventilation in pediatric critical care

setting. Indian J Pediatr. 2007;74:483-8.3. Antonelli M, Pennisi MA, M Luca. Clinical review: Noninvasive ventilation in the

clinical setting–experience from the past 10 years. Critical Care. 2005;9:98-103.4. O. Nørregaard. Noninvasive ventilation in children. Eur Respir J. 2002;20:1332-42.5. Samuels MP, Southall DP. The role of negative pressure ventilation. Arch Dis Child.

1998;79:94.6. Shekerdemian LS, Bush A, Shore DF, Lincoln C, Redington AN. Cardiopulmonary

Interactions after Fontan Operations. Augmentation of Cardiac Output Using Negative Pressure Ventilation. Circulation. 1997;96:3934-42.

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Introduction

A primary goal of respiratory assistance is to improve gas exchange and reduce the work of breathing (WOB) of patients with acute respiratory failure, without causing iatrogenic lung injury. Continuous positive airway pressure (CPAP) is a method of delivering positive end-expiratory pressure with air-oxygen mixture to the airway of a spontaneously breathing patient. This helps to maintain lung volume during expiration, reducing atelectasis, alleviating respiratory fatigue and improving oxygenation.

Bubble continuous positive airway pressure (B-CPAP) has been used for the treatment of respiratory distress syndrome in newborn infants for over 30 years by Wung et al.1 It has attracted the most clinical interest over the 20 years following the reports of Avery and colleagues2 and, more recently, VanMarter and associates,3 highlighting the low incidence of chronic lung disease in preterm infants at the Columbia Presbyterian Medical Center in New York, where B-CPAP has been a cornerstone of clinical treatment practice since the 1970s. The way the pressure is generated is very simple and does not require expensive ventilators. Nasal prongs are placed into the baby’s nose, and the pressure is developed from tubing placed underwater at a particular depth. Bubble CPAP system produces a positive pressure by placing the expiratory limb under water. It was first reported in 1971 for supporting breathing of preterm neonates.4

CPAP in the Premature Newborn

CPAP has been proven to be of use in the management of RDS in the preterm newborn. Even in the pre-surfactant era when antenatal steroid usage was uncommon; there was some evidence that early application of CPAP might reduce subsequent use of mechanical ventilation and the associated adverse outcome.5 CPAP has proven to be of use in neonates with RDS weaning from the ventilator. Infant’s extubated to nasal CPAP experienced a reduction in respiratory failure necessitating re-intubation.6

Chapter

7“Bubble CPAP” for Neonates

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“Bubble Cpap” for Neonates 65

CPAP Circuit

The CPAP system consists of a source of humidified blended oxygen, the pressure generator and the airway interface device. The air oxygen blender, humidifier and airway interface devices are as per standard specifications.

Pressure can be generated from the following three ways.7

• Through the ventilator: the expiratory valve of the ventilator is used to adjust the expiratory pressure.

• Secondly, the pressure is generated by adjusting the inspiratory flow or altering the expiratory resistance.

• Thirdly, the B-CPAP system produces a positive pressure by placing the far end of the expiratory tubing under water. B-CPAP system produces a positive pressure by placing the expiratory limb under water. The pressure is adjusted by altering the depth of the tube under the surface of the water.

Components of Bubble CPAP

Essentially the B-CPAP system consists of three components: a continuous gas flow into the circuit, an expiratory limb with the distal end submerged into water to generate positive end-expiratory pressure and the nasal interface connecting the infant’s airway with the circuit via the expiratory limb.

Oxygen blender which is connected to wall oxygen and compressed air supply is used for supplying appropriate concentration of inspired oxygen. Optimal gas flow of 5–10 L/min is maintained with a flow meter to prevent re-breathing of carbon dioxide, increased work of breathing related to insufficient flow available for inspiration and to compensate for leakage in the CPAP system. Pressure in the B-CPAP system is created by placing the distal expiratory tubing in water. Designated pressure is determined by the length of expiratory limb being immersed.8 When the pressure is delivered to the baby without leakage, it results in continuous bubbling and the pressure oscillates in the circuit. Short bi-nasal prongs are commonly used for the nasal interface between the circuit and the infant’s airway as they are found to have the lowest resistance9 and their use has been supported by a meta-analysis as the better device for delivery of effective CPAP.10 Choosing the right prong and keeping it in place not only increase the effectiveness of CPAP support but can also prevent nasal trauma. The resistance increases proportionately with increasing length of the prongs and exponentially with decreasing radius. Shorter and wider bi-nasal prongs that can fit snugly in the nares without causing blanching of the skin are a good option. Hudson prongs are anatomically curved, or Argyle prongs can also be used.

Physiology of Bubble CPAP

The B-CPAP provides a dual mode of action. The CPAP helps to stabilize airway, recruit alveoli, increase FRC and helps maintain oxygenation. During B-CPAP,

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mechanical oscillatory vibrations are created which are transmitted into the chest secondary to the non-uniform flow of gas bubbles across a downstream underwater seal. The resulting bubbles create pressure oscillations that are transmitted back to the airway opening. The noisy nature of the pressure waveform delivered to the airway opening generates broadband frequency composition and oscillatory pressure amplitudes that are in the order of 4 cm H

2O around the mean pressure. Although this noisy component may

contribute to gas mixing in a similar fashion to mechanisms present during high-frequency oscillatory ventilation.11

Two studies have examined the effect of B-CPAP on gas exchange. Lee and colleagues11 randomized a group of infants ready for extubation to receive either B-CPAP or ventilator-derived (constant pressure) CPAP (CP-CPAP) for a period of 15 minutes before crossover to the alternative treatment. Although there were no differences in PaCO

2 between B-CPAP

and CP-CPAP groups, the babies treated with B-CPAP had lower respiratory rates and lower minute volumes, suggesting more efficient ventilation. More recently, Morley and colleagues reported a crossover study of clinically stable infants treated with CPAP in the neonatal intensive care unit.7 They found no differences in transcutaneous measurements of arterial CO

2 or in oxygen

saturation between CPAP with and without bubbles over the brief 30-minute study epochs. Both studies tested the effect of B-CPAP on clinically stable infants in the recovery stage of neonatal respiratory illness, and focused predominantly on the concept that the bubble component was likely to influence CO

2 clearance.

Nursing Care for Bubble CPAP

Nursing care is important for the success of applying B-CPAP to premature infants. Proper positioning of the prongs, which fits snuggly into nares, that can be secured by putting on an infant bonnet (Fisher and Paykel®) which covers the lower part of the infant’s ears and across his forehead with the circuit fastened on it. It remains static on the infant’s head, otherwise the circuit and the prong will move with the motion of the loosely fit bonnet. Nasal trauma is common when the prong rests on the septum of the nose or on the columella. Application of a soft, pliable nasal prongs with jelly with chin strap (Fisher and Paykel®) can prevent nasal trauma/soft tissue necrosis of immature nares. Suctioning of nares is important to keep airways clear.

Lightweight ventilator circuits with heated wire and servo-regulated humidification system is necessary for the delivery of warm and humidified inspired gas to the CPAP supported infant. Condensation affects the gas flow and resistance. It should be checked and drained regularly. Consistent bubbling is important to recruit alveoli, maintain functional residual capacity, and reduce airway resistance and work of breathing, especially in the early acute phase of respiratory distress. If the bubbling stops it means that there is a pressure leak in the system, usually around the nostrils. It has been reported that the pharyngeal pressure drops markedly when the CPAP supported infant

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opens his mouth.12 The use of chin strap or pacifier has been recommended to reduce mouth leak for effective CPAP support.13 However, it should not be so tight as to prevent the infant from yawning or crying but tight enough to prevent leaking at rest.

The infant’s respiratory status has to be assessed at regular interval. CPAP has to be temporarily interrupted during chest auscultation as the bubbling sound may interfere with hearing lung and heart sounds.

Gastric distension is common in the CPAP supported infant (CPAP Belly Syndrome). Frequent decompression of the stomach with an oro-gastric tube is necessary to promote comfort, preventing the distended stomach from splinting the diaphragm and compromising respiration.

Why Bubble CPAP is Vital

Most respiratory diseases of the neonate occur as a result of the immaturity of the premature neonate’s lungs. Despite stimulation, the normal process involved in the first breath does not occur. Bubble CPAP with the combined effects of CPAP and pressure oscillations from the bubbles provides a lung protective, safe and effective method of respiratory support to spontaneously breathing neonates. Reduced days on mechanical ventilation and postnatal steroid use in the NICU for ELBW infants was been demonstrated by Narendra V et al.14 Bubble CPAP has the advantage of being simple and inexpensive.

AdvantagesBubble CPAP effectively maintains functional residual capacity (FRC).14 It helps reduce the infant’s WOB. In a prospective randomized cross over trial performed by Lee, Dunn et.al. Comparing B-CPAP with ventilator-derived CPAP, results showed that there was a decrease in the infant’s minute volume and respiratory rate with bubble CPAP. They observed chest vibrations caused by the pressure oscillations from the bubbling. This physiologic effect of B-CPAP may help improve gas exchange and reduce the infant’s work of breathing.11

Bubble CPAP may reduce the need for intubation and mechanical ventilation,15 in the multicenter comparative study of Avery et.al. it was noted that the use of B-CPAP avoided the need for intubation reducing the possibility of airway injury, aspirations and secondary infection associated with the use of the ET tube.15,2 Results also showed significant reduction in the need for mechanical ventilation that may minimize the possible incidence of barotraumas.15,2

Bubble CPAP tends to reduce the incidence of chronic lung disease (CLD).15 It also improves non-pulmonary outcomes. Improved non-pulmonary effects have also been observed in clinical trials such as the tendency to increase mean weight at 36 weeks corrected gestation, increase mean length and head circumference, reduction in time to reach full oral feeds and average length of stay.14

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Early initiation of CPAP combined with tolerance for elevated PCO2 levels

has reduced the incidence of CLD to <6% at Morgan Stanley Children’s Hospital. In 2004, there was a 27.7% CLD rate for infants in the same weight bracket in hospitals participating in the Vermont Oxford Network 2– a non-profit group comprised of 485 NICUs from around the United States. The B-CPAP system delivers a simple and inexpensive form of HFV. Physiologic effects of bubble CPAP include a decreased contribution to the minute volume by the infant and decreased respiratory rate with no effect on blood gas parameters. There may be role of B-CPAP in weaning a premature infant from positive pressure ventilation, since it has capacity to deliver CPAP and simulates HFV with the possible effect of decreased effort of breathing and susceptibility to fatigue. Large randomized clinical trials are necessary to compare B-CPAP with other modes of ventilation, especially with regards to incidence of chronic lung disease.

Evidence for Bubble CPAP

Narendran et al has convincingly proved in their study of Outcomes of all infants between 401 and 1000 g born in a level 3 neonatal intensive care units (NICU) between July 2000 and October 2001(period 2) were compared using historical controls (period 1). Early bubble (CPAP) was prospectively introduced in the NICU during period 1. Univariate and adjusted comparisons were made across time periods. Delivery room intubations, days on mechanical ventilation and use of postnatal steroids decreased (p < 0.001) in period 2, while mean days on CPAP, number of babies on CPAP at 24 hours (p < 0.001) and mean weight at 36 weeks corrected gestation also increased (p < 0.05) after introduction of early B-CPAP. Conclusions were early B-CPAP reduced delivery room intubations, days on mechanical ventilation, postnatal steroid use and was associated with increased postnatal weight gain with no increased complications.14

Study conducted at a neonatal unit in developing country by Lanieta Koyamaibole, Joseph Kado et al found not only the requirement of mechanical ventilation for preterm babies come down by 50 % but also that mortality remained same or little less.16

Costs

In a study16 of retrospective evaluation of prospectively collected data from two time periods: 18 months before and 18 months after the introduction of B--CPAP. The introduction of B-CPAP was associated with a 50 per cent reduction in the need for mechanical ventilation; from 113 of 1106 (10.2 per cent) prior to B-CPAP to 70 of 1382 (5.1%) after introduction of CPAP. In the 18 months prior to B-CPAP there were 79 deaths (case fatality of 7.1%). In the 18 months after B-CPAP there were 74 deaths (CF 5.4%), relative risk: 0.75. Nurses could safely apply B-CPAP after 1–2 months of on-the-job training. Equipment for B-CPAP cost 15% of the cost of the cheapest mechanical ventilator. The introduction

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of B-CPAP substantially reduced the need for mechanical ventilation, with no difference in mortality. B-CPAP has the potential for being available at even lower cost than the current commercially available bubble systems.

Costs to patient decreases as the need of mechanical intubation is averted with further number of days of ventilation are reduced. There is decrease in hospital stay of the infant. Costs to the hospital/private nursing home reduces as it costs 15% lesser than the standard low cost mechanical ventilator. Indigenous B-CPAP can also be prepared.

In summary, if early B-CPAP initiated in the delivery room can be safe, inexpensive and an effective way to avoid intubations in the delivery room.

Clinical Practice Guidelines

1. Initiate Bubble CPAP early in RDS – soon after birth2. Check and keep ready CPAP circuit, with humidifier and blender3. Ensure correct size of nasal prongs, good application, use bonnet chin strap

as needed4. Monitor the baby clinically and with blood gases5. Increase or decrease CPAP as indicated clinically, radiologically and as per

blood gasses.6. Use B-CPAP after extubation in VLBW7. Surfactant may be administered even when the baby is on CPAP (INSURE)

References 1. Wung JT, Driscoll JM Jr, Epstein RA, Hyman AI. A new device for CPAP by nasal

route. Crit Care Med. 1975;3:76-8. 2. Avery ME, Tooley WH, et al. Is chronic lung disease in low birth weight infants

preventable? A survey of eight centers. Pediatrics. 1987;79:26-30. 3. Van Marter LJ, Allred EN, Pagano M, et al. Do clinical markers of barotrauma and

oxygen toxicity explain interhospital variation in rates of chronic lung disease? The Neonatology Committee for the Developmental Network. Pediatrics. 2000;105: 1194-201.

4. Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, Hamilton WK. Treatment of the idiopathic respiratory-distress syndrome with continuous positive airway pressure. N Engl J Med. 1971;284:1333-40.

5. Ho JJ, Subramaniam P, Henderson-Smart DJ, Davis PG. Continuous distending pressure for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev. 2002;(2):CD002271.

6. Davis PG, Henderson-Smart DJ. Nasal continuous positive airways pressure immediately after extubation for preventing morbidity in preterm infants. Cochrane Database Syst Rev. 2003;(2):CD000143.

7. Halamek LP, Morley C. Continuous positive airway pressure during neonatal resuscitation. Clin Perinatol. 2006;33:83-98.

8. Polin RA, Sahni R. Newer experience with CPAP. Semin Neonatol. 2002;7:379-89. 9. Aly HZ. Nasal prongs continuous positive airway pressure: a simple yet powerful

tool. Pediatrics. 2001;108:759-61.

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10. De Paoli AG, Morley C, Davis PG. Nasal CPAP for neonates: what do we know in 2003? Arch Dis Child Fetal Neonatal Ed. 2003;88:F168-72.

11. Lee KS, Dunn MS, Fenwick M, Shennan AT. A comparison of underwater bubble continuous positive airway pressure with ventilator-derived continuous positive airway pressure in premature neonates ready for extubation. Biol Neonate. 1998; 73:69-75.

12. Chilton HW, Brooks JG. Pharyngeal pressures in nasal CPAP. J Pediatr. 1979;94: 808-10.

13. De Paoli AG, Lau R, Davis PG, Morley CJ. Pharyngeal pressure in preterm infants receiving nasal continuous positive airway pressure. Arch Dis Child Fetal Neonatal Ed. 2005;90:F79-81.

14. Narendran V, Donovan EF, Hoath SB, Akinbi HT, Steichen JJ, Jobe AH. Early bubble CPAP and outcomes in ELBW preterm infants. J Perinatol. 2003;23:195-9.

15. AM de Klerk, RK de Klerk. Nasal continuous positive airway pressure and outcomes of preterm Infants. J Paediatr. Child Health. 2001;37:161-7.

16. Koyamaibole L, Kado J, Qovu JD, et al. An evaluation of bubble-CPAP in a neonatal unit in a developing country: effective respiratory support that can be applied by nurses. Journal of Tropical Pediatrics. 2006;52(4):249-53.

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Need of Newer Modes of Ventilation

The need for newer modes is unclear. None have been shown to improve oxygenation or mortality. Many are designed to improve patient ventilator synchrony. This removes the reliance on sedation and paralysis and allows greater use of spontaneous and triggered modes to be used from early in the disease on awake patients. Mobility is enhanced with less VAPs and dependant atelactasis. It also leads to easy weaning. Not all of these have been successfully demonstrated usefulness in children as sedation is still a requirement, cooperation not being very forthcoming.

In the Table 8.1 may help understand the basic separation of the modes with the sequence of delivery of the trigger and control vis a vis patient and machine. It is only a reference tool and not to be studied in detail.

Table 8.1: Newer modes of ventilationClassification of modes of ventilation

Breath Se-quence

Volume Pressure

Continuous mandatory ventilation

Intermittent man-datory ventilation

Continuous mandatory ventilation

Intermittent mandatory ventilation

Continuous sponta-neous ventilation

Breath sequence-volume

Target-ing Scheme

Continuous mandatory ventilation Intermittent mandatory ventilation

Set point Dual Adaptive Set point Dual Adaptive

Volume control,VC-A/C,CMV, (S)CMV,Assist/Con-trol

CMV + pres-sure limited

Adaptive flow

SIMV, VC-SIMV SIMV + pres-sure lim-ited

Auto Mode (VC-VS), mandatory minute volume

Contd...

Chapter

8Newer Modes of Ventilation

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Breath sequence-pressure

Target-ing Scheme

Continuous man-datory ventilation

Intermittent mandatory ventilation

Continuous spontaneous ventila-tion

Set point Adap-tive

Set point

Optimal Adap-tive

Set point

Dual Ser-vo

Adap-tive

Intelli-gent

Pressure control (PCV),PC-A/C, AC PCV,high-pressure oscil-latory ventila-tion(HFOV)

Pres-sure-regu-lated volume control(PRVC), VC+AC, AMV+ Auto Flow

Airway pressure -release ventila-tion(APRV),SIMV-PCV,Bi Level, PCV+

Adaptive support ventila-tion(ASV)

VC + SIMV, V V + SIMV APVS-IMV,SIMV+ Auto Flow, Auto mode (PRVC-VS)

(C-PAP),pres-sure sup-port(PSV)

VAPSVA

PAVATC

Vol-ume sup-port(VSV)

Smart Care

Abbreviations used in this article: PCV—Pressure control ventilation, VCV—Volume control ventilation, ACV—Assist control ventilation, SIMV—Synchronized intermittent mandatory ventilation, PSV—Pressure support ventilation, CPAP—Continuous positive airway pressure, BIPAP—Bi-level positive airway pressure, PRVC—Pressure regulated volume control, ASV—Assist control ventilation, VAPS—Volume assured pressure support, PAV—Proportional assist ventilation, NAVA—Neurally Adjusted Ventilatory Assist, PA—Pressure Augmentation, VSV—Volume support ventilation

Pressure Regulated Volume Control

Key FeaturesPressure regulated volume control (PRVC) ventilation is an old example of a dual control ventilation mode, also known as hybrid modes of ventilation. This mode is a form of closed loop ventilation that has combined the features of volume and pressure ventilation. First introduced on the Servo 300 ventilator, it is now available on most modern ventilators under different names, e.g. Autoflow (Drager Evita), Volume Guarantee (Datex-Ohmeda, Drager Babylog), Adaptive pressure ventilation (Hamilton Galileo), Variable pressure control (Venturi). (Each of these may have variations in the delivery of volume and pressure and the algorithms used will vary according to their own patents)

Being a very commonly used mode, it has been dealt with in the first chapter.

Airway Pressure Release Ventilation

Key Features• Bi-level ventilation—Two level of CPAP applied for set period of time.• Spontaneous mode—Spontaneous breathing is allowed at both levels of

pressures.

Contd...

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Newer Modes of Ventilation 73

• Oxygenation—Better oxygenation is achieved by constant mandatory pressure with inverse ratio ventilation.

• Low peak pressures with high MAP—Better alveolar recruitment with less VILI and hemodynamics effect.

• Ventilation—Tidal volume is depending on change in airway pressure from inspiratory to expiratory phase and lung-thorax compliance. This is a SPONTANEOUS mode. It has also been identified as safe mode

of ventilation for acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) and called the “poor man’s HFO”. It has been described as continuous positive pressure ventilation (CPAP) with intermittent, regular and brief release of pressure. The release phase results in alveolar ventilation and removal of carbon dioxide (CO

2), aided by the spontaneous efforts of the

patient. Airway pressure release ventilation (APRV), unlike CPAP, facilitates both oxygenation and CO

2 clearance and originally was described as an

improved method of ventilatory support in the presence of ALI and inadequate CO

2 ventilation. Technically, APRV is a time-triggered, pressure- limited, time-

cycled mode of mechanical ventilation (Figs 8.1 an 8.2).

Physiological Effects

Oxygenation is better with APRV with spontaneous breathing than with mechanical ventilation alone. This effect is at least attributable to recruitment of collapsed lung tissue and increased aeration in dependant areas of lung. Putensen et al showed improved ventilation perfusion matching and increased systemic flow in APRV with spontaneous breathing. APRV with

Fig. 8.1: Airway pressure release ventilation

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Fig. 8.2: Differences between APRV and Biphasic PAP mode: APRV (top) and biphasic positive airway pressure (bottom) are forms of pressure controlled intermittent mandatory ventilation in which spontaneous breaths can occur at any point without altering the ventilator-delivered breaths. The difference is that the time spent in high pressure is greater in airway pressure-release ventilation.

spontaneous breathing increased ventilation in the juxta-diaphragmatic regions, predominantly in the dependent areas. Spontaneous breathing had a significant effect on the spatial distribution of ventilation and pulmonary perfusion. APRV has been shown to improve cardiac output, renal blood flow, glomerular filtration, and achieve high mean airway pressure (MAP) with low Peak airway pressure. APRV was associated with increases in lung compliance and oxygenation and reduction of shunting.

Initial Ventilator Settings

There are four commonly used terms in APRV: pressure high (P High), pressure low (P Low), time high (T High), and time low (T Low). • Phigh:It is the baseline airway pressure and is higher of the two airway

pressure. Initial P high is kept same as plateau pressure measured on volume control mode provided if it is lower than 30 cm H

2O.

• Plow:It is the airway pressure level resulting from pressure release. Another authors have described P low as the PEEP level, the release pressure, or the P2 pressure. It is usually set at 0 cm of H

2O.

• Thigh:It is the time during which P high is maintained. It is set at 3-4 sec. then adjusted if necessary.

• Tlow:It is the time for which P low is held or pressure is released. It is probably the most difficult variable to set because it needs to be short enough to avoid de-recruitment but still long enough to allow alveolar ventilation. It is usually set at 0.6–0.8 seconds.

Adjustments (Table 8.2)

Hypoxemia—adjusttheseventilatorsettingstoimproveoxygenation• Increase pressure gradient (P high minus P low)—increase P high by 2–5

cm H2O.

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• Airway pressure release frequency = 60/cycle time (T high + T low), Decrease frequency (prolong T high by 0.5–1 sec) (if T low remains constant)

• Increase FiO2

Hypercapnia—Adjusttheseventilatorsettingstorelievehypercapnia• Tolerate “permissive hypercapnia” (pH ≤7.15)• Reduce T high by 0.5–1 sec; it may affect recruitment by lowering the Paw.

BiphasicPositiveAirwayPressure(BiPAP):Other names for BiPAP used by different manufacturers are: Bi-level (Puritan Bennett), BiPAP (Drager, Europe), Bi-Vent (Siemens), Bi-Phasic (Avea, Inc, Dublin, OH), and PCV + (Drager Medical). In North America, BiPAP (Respironics) and Bi-level are used to refer to noninvasive modes of ventilation.

Volume Support Ventilation

Key Features• Spontaneous mode—every breath is trigger by patient. Same as PSV,

inspiratory time and rate is determined by patient.• Constant tidal volume with lowest pressure support.• Automatic weaning—automatic weaning of pressure support as long as

tidal volume matches minimum required tidal volume.• Automode—In case of apnea, automatically switch to PRVC.

In volume support ventilation (VSV) patient triggers every breath. Ventilator automatically adjusts the inspiratory pressure to ensure the lowest possible inspiratory pressure to deliver the preset tidal volume. Tidal volume is used as feedback control to adjust the pressure support level. Inspiratory pressure is maintained constant during inspiration. Inspiratory flow is decelerating. Patient determines the breathing rate and the inspiratory time. If there is apnea,

Table 8.2: Summary of advantages and disadvantages of airway pressure release ventilation

Advantages Disadvantages

High MAP with low Peak pressureMaintain normal cyclic decrease in pleural pressureAllow inverse ratio ventilation, Increases oxygen deliveryAugment venous return, increases cardiac indexReduces need for sedation/paralysisImproves renal perfusion, increase osmolar clearance, increases urine outputDecreased basal atelectasis, may decrease dead spaceImprove patient ventilatory synchrony with spontaneous respiration

Pressure targeted mode, variable tidal volume deliveryCO2 elimination depends on spontaneous breathsIncrease in airway resistance hampers CO2 eliminationIncrease work of breathing with asynchrony between spontaneous and pressure release breatheLarge bronchopleural fistulaIncrease intracranial pressureLimited experienceAuto-PEEP is usually present, contraindicated in high expiratory resistance

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there is automatic back-up with PRVC mode of ventilation. Inspiration stops and expiration starts when the peak flow drops to 5-15% of initial flow (as per setting). As the upper pressure limit is reached, the ventilator immediately changes to expiration and gives alarm for “high airway” pressure. If the difference between the upper pressures limit and peak airway pressure is less than 5 cm of H

2O, a “limited pressure” alarm is given. The tidal volume

delivered will be less than the preset. Maximum inspiratory time is 80% of the respiratory cycle. VSV indicated in post-op patient recovering from anesthesia, Spontaneous breathing patient who require minimum tidal volume, Patients who are asynchronous with the ventilator, and as a weaning mode especially in patient with neuromuscular weakness (Fig. 8.3).1. Test breath (5 cm H

2O)

2. Pressure is increased slowly until target volume is achieved3. Maximum available pressure is 5 cm H

2O below upper pressure limit

4. VT higher than set VT delivered results in lower pressure5. Patient can trigger breath6. If apnea, ventilator switches to PRVC (Automode)

Advantages:Provide the positive attributes of PSV with constant exhaled tidal volume. Automatic weaning of pressure support as long as tidal volume matches minimum required tidal volume

.

Disadvantages:Sustain spontaneous effort required, tidal volume selected may be too large or small for patient, auto-PEEP may affect proper functioning, varying mean airway pressure with each breath, sudden increase in respiratory rate and demand may result in a decrease in ventilator support.

Proportional Assist Ventilation

Key FeaturesChanging inspiratory pressure—Unlike PSV (constant inspiratory pressure) this mode delivers a proportional amount of inspiratory pressure. Ventilator generates pressure in proportion to patient’s effort.

Fig. 8.3: Breath to breath analysis of patient in pressure time and flow time waveform with volume support ventilation

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More synchronized—It reduces the work of breathing with better synchronization; automatically adapt to changing patient lung mechanics and effort.

Patients who have normal respiratory drive but who have difficulty in sustaining adequate spontaneous ventilation are often subjected to pressure support ventilation (PSV), in which the ventilator generates a constant pressure throughout inspiration regardless of the intensity of the patient’s effort. In 1992, Younes and colleagues developed proportional assist ventilation (PAV) as an alternative in which the ventilator generates pressure in proportion to the patient’s effort. PAV became commercially available in Europe in 1999 and was approved in the United States in 2006, available on the Puritan Bennett 840 ventilator. PAV has also been used for noninvasive ventilation. Other names for PAV are Proportional Pressure Support (Drager Medical) (Fig. 8.4).

Both PSV and PAV are spontaneous modes. The patient controls the timing and size of the breath. There are no preset pressures, flow, or volume goals, but safety limits on the volume and pressure delivered can be set. With PSV, the pressure applied by the ventilator rises to a preset level that is held constant until a cycling criterion is reached. The inspiratory flow and tidal volume are the result of the patient’s inspiratory effort, the level of pressure applied, and the respiratory system mechanics. In contrast, during PAV, the pressure applied is a function of patient effort: the greater the inspiratory effort, the greater the increase in applied pressure. The operator sets the percentage of support to be delivered by the ventilator. The ventilator intermittently measures the compliance and resistance of the patient’s respiratory system and the instantaneous patient-generated flow and volume, and on the basis of these it delivers a proportional amount of inspiratory pressure.

Ventilator Settings in PAV• Airway type (endotracheal tube, tracheostomy)• Airway size (inner diameter)• Percentage of work supported (assist range 5–95%)• Tidal volume limit• Pressure limit• Expiratory sensitivity (normally, as inspiration ends, flow should stop; this

parameter tells the ventilator at what flow to end inspiration).

Fig. 8.4: Breath to breath analysis of patient with varying inspiratory efforts. Volume delivery adjusted proportionally to the patient’s effort in PAV mode.

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Advantages:In theory, PAV should reduce the work ofbreathing, improve synchrony, automaticallyadapt to changing patient lung mechanics andeffort, decrease the need for ventilator interventionand manipulation, decrease the needfor sedation, and improve sleep. The probability of spontaneousbreathing without assistance was significantlybetter in critically ill patients ventilated withPAV than with PSV. No trial has reported theeffect of PAV on deaths.

Volume Assured Pressure Support

Key FeaturesClosed loop ventilation with inter-breath variation-character of breath changed within the breath from pressure control to volume control if minimum tidal volume has not been achieved.

Volume assured pressure support (VASP) is also based on closed loop ventilation but in this mode the initial pressure control breath will change to volume control if minimum tidal volume has not been achieved. It combines high initial flow of pressure-limited breath with a constant volume delivery of volume-limited breath within the same breath.

The type of breath will depends on the adequacy of the patient’s effort. If the patient has adequate respiratory effort, then a pressure supported breath will be delivered. If inadequate respiratory effort, then a controlled breath (flow targeted and volume cycled) will be delivered rather than a pressure supported breath (Fig. 8.5 and Table 8.3).

Advantages:Patient will receive minimum pressure support and peak flow to achieve minimum tidal volume.Decrease work of breathing in comparisons to conventional ventilation.

Fig. 8.5: Pressure, volume and flow time waveforms (scalar) in VASP mode

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Disadvantages:Target tidal volume is achieved by physiological decelerating flow pattern in initial part of breath with only deficiency being met when rest of tidal volume is achieved by constant flow toward the end of inspiration. There is risk of increasing the total inspiratory time, which can lead to gas trapping (Auto-PEEP). There is also risk of barotrauma esp. at the end of inspiratory phase when peak pressure override to achieve target tidal volume. Appropriate setting of pressure support is important to ensure adequate augmentation of patient’s inspiratory effort. Otherwise ventilator will switch back to VC resulting in asynchrony with V/Q mismatch.

Adaptive Support Ventilation

Key Features• Closed loop ventilation with synchronization—every breath is synchronized

with patient effort if such an effort exists, and otherwise, full mechanical ventilation is provided to the patient.

• Target minute ventilation- this mode automatically selects the appropriate tidal volume and frequency for mandatory breaths and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and target minute alveolar ventilation.

• Target tidal volume—it is achieved with either pressure control or pressure support breath (decelerating flow).

• Automatic weaningAdaptive support ventilation (ASV) is a closed-loop controlled form that

uses minute ventilation. Mandatory minute ventilation is a mode that allows the operator to preset target minute ventilation, and the ventilator then supplies mandatory breaths, either volume/pressure controlled, if the patient’s spontaneous breaths generate lower minute ventilation. ASV automatically selects the appropriate tidal volume and frequency for mandatory breaths

Table 8.3: Comparisons between different modes of ventilationPressure regulated volume control

Volume support ventilation Volume assured pressure support

Inter-breath variationUse the set tidal volume as the “target” for each breathNormal cycling may stop inspiration below or above set tidal volumePressure used based on mechanics measurements

Inter-breath variationUse the set tidal volume as the “target” for each breathNormal cycling starts when the peak flow drops to 5–15% of initial flowIf inspiratory demand decreases, ventilator can increase up to 150% of set tidal volume in next breath by increasing inspiratory pressure up to a limittidal volume/pressure mechanics measured

Intra-breath variation Use the set TV as a minimumNormal cycling occurs at or above the set tidal volumeCharacter of breath changed within the breath from pressure control to volume control if minimum tidal volume has not been achievedTidal volume mechanics not measured

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and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and target minute alveolar ventilation. In the ASV mode, every breath is synchronized with patient effort if such an effort exists, and otherwise, full mechanical ventilation is provided to the patient. Targeted tidal volume will be given as pressure control or pressure support breaths (Fig. 8.6).

Initialventilatorysettings: It is first commercially available mode that automatically selects all the ventilator settings except PEEP and FiO

2.

• Sex and height (to calculate the ideal body weight)• Percent of normal predicted minute ventilation goal. Delivers 200 mL/min/

kg of minute ventilation for children. It can be set from 20–200%. • FiO

2

• PEEP• High-pressure alarm: 5 cm H

2O above PEEP to 10 cm H

2O below set P max

Advantages: It provides decelerating flow waveform to improved gas distribution with guaranteed tidal volume. It also decreases work of breathing. Automatic weaning is possible with disease reversal.

Neurally Adjusted Ventilatory Assist

Key Features• Unique mode based on neural respiratory output—neurally adjusted

ventilatory assist (NAVA) ventilation is controlled by diaphragmatic electrical signals.

• Fine synchronization—The electrical signals allow fine synchronization of ventilation to spontaneous breathing efforts of a child, as well as permitting pressure assistance proportional to the electrical signal. Pressure assistance varying with the needs of the child. It is a unique mode of ventilation which is based on neural respiratory

output. The act of taking a breath is controlled by the respiratory center in the

Fig. 8.6: Differences between PRVC (APC) and ASV mode. Adaptive support ventilation (bottom) automatically selects the appropriate tidal volume and frequency for mandatory breaths and the appropriate tidal volume for spontaneous breaths on the basis of the respiratory system mechanics and the target minute ventilation.

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brain, which decides the characteristics of each breath, timing and size. The respiratory center sends a signal along the phrenic nerve, excites the diaphragm muscle cells, leading to muscle contraction and descent of the diaphragm dome. As a result, the pressure in the airway drops, causing an inflow of air into the lungs. The implementation of NAVA requires the introduction of a catheter to measure the electrical activity of the diaphragm (EAdi). NAVA relies, opposite to conventional assisted ventilation modes, on the EAdi to trigger the ventilator breath and to adjust the ventilatory assist to the neural drive. The amplitude of the ventilator assist is determined by the instantaneous EAdi and the NAVA level set by the clinician. The NAVA level amplifies the EAdi signal and determines instantaneous ventilator assist on a breath-to-breath basis. With NAVA, the EAdi is captured, fed to the ventilator and used to assist the patient’s breathing in synchrony with and in proportion to the patient’s own efforts, regardless of patient category or size. As the work of the ventilator and the diaphragm is controlled by the same signal, coupling between the diaphragm and the ventilator is synchronized simultaneously. As the work of breathing increases and the respiratory center ask the diaphragm for more effort, the neurally controlled system increases the amount of ventilator support (Fig. 8.7).

Fig. 8.7: Neuroventilatory coupling from health to disease

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Experimental and clinical data suggest superior patient-ventilator synchrony with NAVA. With NAVA, the reliance on the EAdi signal, together with an intact ventilatory drive and intact breathing reflexes, allows integration of the ventilator in the neuroventilatory coupling on a higher level than conventional ventilation modes. The simple monitoring of the EAdi signal alone may provide the clinician with important information to guide ventilator management, especially during the weaning process (Fig. 8.8).

Paw = NAVA level × EAdi

• Where Paw is the instantaneous airway pressure (cm H2O), EAdi is the

instantaneous integral of the diaphragmatic electrical activity signal (μV), and the NAVA level (cm H

2O/μV or per arbitrary unit) is a proportionality

constant set by the clinician.• In NAVA, the EAdi is captured, fed to the ventilator and used to assist the

patient’s breathing in synchrony with and in proportion to the patient’s own efforts, regardless of patient category or size.

• As the work of the ventilator and the diaphragm is controlled by the same signal, coupling between the diaphragm and the ventilator is synchronized simultaneously.

• As the work of breathing (WOB) increases and the respiratory center ask the diaphragm for more effort, the neurally controlled system increases the amount of ventilator support.

Fig. 8.8: Neurally adjusted ventilatory assist by diaphragmatic electrical signals

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Although, until now, little evidence proves the superiority of NAVA on clinically relevant end points, it seems evident that patient populations (e.g. COPD and small children) with major patient-ventilator asynchrony may benefit from this new ventilatory tool.

AdvantagesPatient–ventilator synchrony is improved with NAVA; the children may require lower doses of sedation with this mode of MV, which could reduce the time of MV.

Disadvantages• Cost of sensor• Infants take a very small TV, have a rapid RR, have a limited chest wall

musculature, and have variable and fluctuating lung compliance.• In most neonates and small children use uncuffed tracheal and air leak is

always present, making reliable measurements and triggering problematic. • Ventilators that are efficient in adults are not systematically efficient in

children and infants, mainly because the inspiratory triggers are not sufficiently sensitive for early detection of infants’/children’s inspiratory effort.

Auto Mode

This mode design to allow the ventilator to be interactive with the patient’s needs by making breath-by-breath adjustments in both control and support modes. In the absence of triggering, the machine functions in a control mode. When the patient begins to make satisfactory inspiratory efforts (two consecutive triggered breaths), the ventilator switches to the support mode. All breaths are patient triggered, pressure limited, and flow cycled. A switching of modes is indicated by a blinking light. Ventilator automatically shifts between controlled, supported, and spontaneous ventilation as required. When patient was shifted from time cycled to flow cycled ventilation, which can lead to decrease in mean airway pressure and hypoxemia.

Conclusion

Regardless of the mode, our goals are to avoid lung injury, keep the patient comfortable, and wean the patient from mechanical ventilation as soon as possible. Conventional modes are passive and operator dependant, but newer modes are adaptively interactive, goal oriented and patient centerd. Further clinical trials are needed to make a recommendation for various modes of ventilation according to disease and patient status.

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Further Reading 1. Amato MB, Barbas CS. Volume-assured pressure support ventilation. A new

approach for reducing muscle workload during acute respiratory failure. Chest. 1992;102(4):1225-34.

2. Arnal JM, Wysocki M, et al. Automatic selection of breathing pattern using adaptive support ventilation. Intensive Care Med.2008;34:75-81.

3. Balke B, Ware RW. Basic principles of ventilator machinery. In: Tobin MJ, editor. Principles and practice of mechanical ventilation. 2nd edition, Philadelphia, McGraw-Hill. 2006:77-8.

4. Baum M, Benzer H, et al. Biphasic Positive Airway Pressure (BiPAP) - a new form of augmented ventilation. Anaesthetists. 1989;38:452-8.

5. Bollen CW, van Well GT, Sherry T, et al. High-frequency oscillatory ventilation compared with conventional mechanical ventilation in acute respiratory distress syndrome: a randomized controlled trial. Crit Care. 2005;9:430-9.

6. Chan V, Greenough A. Randomised controlled trial of weaning by patient triggered ventilation or conventional ventilation. Eur J Pediatr. 1993; 152: 51-54.

7. Chatburn RL. Classification of ventilator modes; update and proposal for implementation. Respir Care. 2007;52:301-23.

8. Derdak S, Mehta S, et al. High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults. Am J Respir Crit Care Med. 2002;166:801-8.

9. D’Angio CT, Chess PR, Kovacs SJ, et al. Pressure regulated volume control ventilation vs synchronized intermittent mandatory ventilation for very low birth weight infants. A randomized controlled trial. Arch Pediatr Adolesc Med. 2005;159:868-75.

10. Falkenhain SK, Reilley TE, et al. Improvement in cardiac output during airway pressure release ventilation. Crit Care Med. 1992;20:1358-60.

11. Gruber PC, Gomersall CD, et al. Randomized controlled trial comparing adaptive support ventilation with pressure-regulated breathing mode with automode in weaning patients after cardiac surgery. Anesthesiology. 2008;109:81-7.

12. Guldager H, Nielsen SL, et al. A comparison of volume control and pressure-regulated volume control ventilation in acute respiratory failure. Crit Care. 1997;1:75-7.

13. Heulitt MJ, Wolf GK, et al. Mechanical Ventilation. In: Nichols DG, Ackerman AD, Argent AC, et al. editors. Rogers’ Textbook of Pediatric Intensive Care, 4th edition, Philadelphia: Lipincott Williams and Wilkins. 2008:508-31.

14. Holt SJ, Sanders RC, et al. An evaluation of Automode, a computer-controlled ventilator mode, with the Siemens Servo 300A ventilator, using a porcine model. Respir Care. 2001;46(1):26-36.

15. Kallet RH, Campbell AR, et al. Work of breathing during lung-protective ventilation in patients with acute lung injury and acute respiratory distress syndrome: A comparison between volume and pressure-regulated breathing modes. Respir Care. 2005;50:1623-31.

16. N Ambrosino, A Rossi. Proportional assist ventilation (PAV): a significant advance or a futile struggle between logic and practice? Thorax. 2002;57:272-6.

17. Navalesi P, Costa R. New modes of mechanical ventilation: proportional assist ventilation, neurally adjusted ventilatory assist and fractal ventilation. Curr Opin Crit Care. 2003;9:51-8.

18. Oakes DF, Shortall SP, eds. Ventilator Management: A Bedside Reference Guide. 2nd ed. Orono: Health Educator Publications. 2005.

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19. Piotrowski A, Sobala W, Kawezynski P. Patient-initiated, pressure regulated, volume controlled ventilation compared with intermittent mandatory ventilation in neonates: A prospective, randomized study. Intensive Care Med. 1997;23:975-81.

20. Putensen C, Mutz NJ, et al. Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 1999;159:1241-8.

21. Sachdev A, Chugh K, Gupta D, et al. Comparison of two ventilation modes and their clinical implications in sick children. Ind J Crit Care Med. 2005;9:205-10.

22. Scott O, Bonnie J, et al. A crossover analysis of mandatory minute ventilation compared to synchronized intermittent mandatory ventilation in neonates. Journal of Perinatology. 2005;25:643-6.

23. Siau C, Stewart TE. Current role of high frequency oscillatory ventilation and airway pressure release ventilation in acute lung injury and acute respiratory distress syndrome. Clin Chest Med. 2008;29:265-75.

24. Sinderby C, Beck J. Proportional assist ventilation and neurally adjusted ventilatory assist-better approaches to patient ventilator synchrony? Clin Chest Med. 2008; 329-42.

25. Sinderby C, Beck J. Proportional assist ventilation and neurally adjusted ventilatory assist- better approaches to patient ventilator synchrony? Clin Chest Med. 2008; 329-42.

26. Stock MC, Downs JB. Airway pressure release ventilation: a new approach to ventilatory support during acute lung injury. Respir Care Clin N Am. 1987;32:517–24.

27. Sydow M, Burchardi H, et al. Long-term effects of two different ventilatory modes on oxygenation in acute lung injury. Comparison of airway pressure release ventilation and volume-controlled inverse ratio ventilation. Am J Respir Crit Care Med. 1994; 149:1550-6.

28. Hasan A. Editor. Understanding mechanical ventilation. Mechanical ventilation. 2nd edition, Philadelphia, Springer. 2010:72-109.

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Introduction

Humidification of respired gases during mechanical ventilation is a standard of care. Delivery of cool, anhydrous gases from institutional compressed air and liquid oxygen systems to the patient with an instrumented airway, bypassing the normal mechanisms of warming and humidification, has dire consequences.

The addition of heat and moisture to inspired gases delivered to the patient during mechanical ventilatory support via an artificial airway is known as humidification. There is agreement among clinicians that heating and humidifying inspired gases is required. The level of heat and humidity, type of device, duration of use, impact on ventilator-associated pneumonia and optimal characteristics are widely debated, however. Clinical decision-making regarding the use of humidification devices requires an understanding of pathophysiology and equipment. Clearly, the selection of the device to be used on a given patient must be based on the patient’s lung disease, ventilator settings, intended duration of use, and other factors (e.g. the presence of leaks and body temperature).

A lot has changed over the last few years. It is now not considered whether gases delivered to patients should be humidified, but by how much (optimum humidity); not whether we should be concerned about removal of microbes from gases delivered to patients, but what level of performance can be expected from the devices in use.

In general the artificial humidification process can be described by two means:• Determining the moisture output of the humidifying device• Determining the water loss from the airways using the humidifying device

Physiology

The main function of upper airway is to condition inspired gases so when they reach the alveoli, they are warm, humidified, and free of foreign material. The mucociliary elevator on the inner surface of the highly vascular mucosa lining the airway is responsible for this specialized function. Ambient air inspired

Chapter

9Humidification and


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humidification and Mechanical Ventilation 87

through the nose and upper airway is heated to 37°C and humidified to 100% relative humidity.

The nose and upper airway act as an efficient countercurrent heat and moisture exchanger that conditions inspired air and retains heat and moisture on expiration. There is a point below the carina in the upper airway, the isothermal saturation boundary (ISB), at which inspired air reaches body temperature and 100% relative humidity. Above the ISB, the airway acts as a heat and moisture exchanger; below it temperature and humidity remain constant. The exact position of the ISB varies slightly according to the volume, temperature, and relative humidity of inspired air.

When the upper airway is by-passed by an artificial airway (tracheal tube or tracheostomy), air or medical gases are delivered directly into the trachea. The ISB may be shifted down, i.e. at level of 3rd subsegmental bronchi or may be up according to the amount of heat and moisture present in the inspired gases; hence the airway structure or function may be modified. Even in extreme conditions, however, it does not fall to the level of the respiratory bronchioles or alveoli, so that gas in the functional residual capacity of the lungs has a stable water content and temperature that is in equilibrium with blood and tissues.

Under normal conditions, about 250 ml of water are lost from the lungs each day to humidify inspired gases.

It generally is accepted that tracheal intubation, mechanical ventilation, and anesthesia may damage the respiratory epithelium and alter mucociliary function. These abnormalities have been attributed notably to local trauma caused by:• Tracheal tube or suction catheter• Drugs• High oxygen concentrations• Local inflammatory phenomenon• Infection• The pressure effect of mechanical ventilation.

Therefore, during ventilation of intubated or tracheostomized patients, the gases entering the trachea should mimic physiologic conditions as closely as possible.

Consequences of ventilation without conditioning of inspired medical gases:Cyto-morphological airway modifications• Decrease in sol phase depth• Hyperviscosity of airway secretions• Tracheal inflammation• Deciliation, epithelial ulceration, and then necrosis

Functional airway modifications• Decrease in the humidification capabilities• Downward shift of ISB • Decrease in mucus transport velocity, secretions retention• Decrease in bronchospasm threshold• Alteration of the ciliary function, ciliary paralysis• Airway obstruction and increase in airflow resistance

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Pulmonary, mechanical and functional alterations • Atelectasis• Decrease in FRC and compliance• V/Q mismatching, increase in intrapulmonary shunting, hypoxemia• Pulmonary infection

Devices for Humidification of Inspired Gases

Devices that are used for humidification of inspired gases must ensure physiologic conditions in the respiratory tract. That means that pulmonary water losses of greater than 7 mg/L that are due to ventilation with dry gases should be avoided as well as ventilation with oversaturated gases or gases that are warmer than body temperature. It should be taken into account that all systems that are used for this purpose influence the inspiratory and expiratory resistance as well as the functional dead space in different ways. This is especially important in spontaneously breathing patients to avoid hypercapnia and additional work of breathing. Therefore, the additionally imposed inspiratory and expiratory resistance of the system must be known. Similar to the added resistance, the increased functional dead space that is caused by addition of a humidifying device (e.g. HME) must be considered when used with patients who are unable to compensate by increasing their ventilation, which thereby causes CO

2 accumulation.

Types of HumidifiersActive humidifier: Adds water vapor, and heat to the inspired gases (e.g. heated humidifiers).

Passive humidifier: Uses exhaled heat and moisture to humidify inspired gases (e.g. HMEs).

Devices for Non-intubated PatientsSpontaneously breathing patients without a tracheal tube or tracheostomy necessarily do not require additional strategies for conditioning of respiratory gases. But because of the subjectively unpleasant concomitant phenomena that are due to the respiration of dry gases by way of a facemask or oxygen tubing, it is advisable to humidify the gases to normal conditions.

Devices for Intubated Patients• Heat and moisture exchangers• Humidification

Simple Humidifiers

These do not employ heat and the amount of water added to the inspired gas is inadequate for intubated patients. Simple humidifiers operating at 20°C

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and 100% relative humidity deliver only 17 mg water/L of gas. In distal trachea gas should contain 37 mg water/L. This difference should be now supplied by airway epithelium leading to loss of heat and water from epithelium and thereby it’s drying (Table 9.1).

Heated Humidifiers

These deliver more water to airways by heating the inspired gas. The temperature of gas that is delivered to the patient is regulated by a servo device that measures gas temperature at airway and adjusts the heater output of the humidifier. These are used when gases are being delivered via an artificial airway and mechanical ventilator.

Heating the water causes a larger number of water molecules to gain sufficient kinetic energy to enter the gaseous state, thereby the vapor content of inspired gas is increased (Table 9.2).

Heat and Moisture Exchangers

Placed on the distal end of the tracheal tube, heat and moisture exchangers (HMEs) store a portion of the humidity from the expired volume and return

Table 9.1: Types of simple humidifiersType Method of humidification EfficiencyPass-over Gas flows over the surface of the water and then to the

patientLow

Bubble Gas flows through a diffuser into water, generating bubbles that increase the surface area for humidification; gas then flows to the patients

Moderate

Jet Gas flow produces and aerosol that disperses water particles in the gas steam, increasing the surface area for humidification. Baffles prevent deliver of particulate water to the patient.

High

Table 9.2: Types of heated humidifiersType Method of humidification EfficiencyCascade Gas is forced through a grid that is covered by a film of

heated water. The forth that is generated humidifies the stream of gas to the patient. Gas temperature delivered to the patient can be regulated by a servo.

High

Bubble Gas flows through a diffuser into heated water generating bubbles that increase surface area for humidification. The heated and humidified gas then flows to the patient.

High

Wick Gas flows past wick (blotting paper or sponge) that remains saturated with water by capillary action. The wick is surrounded by heaters. Wick humidifiers do not bubble gas through water or grids and have a very low resistance to flow.

High

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this to the inspired air. They function as passive respiratory air humidifiers, which do not depend on a supply of external energy or source of water. Because their mode of operation is related to the nasal operating principle, they also are called ‘‘artificial noses’’. A HME can only return as much heat and humidity as has been stored reversibly from the previous breath. Therefore, the quantity of inspiratory humidity is determined by the moisture content of the expired air, which is defined by the patient temperature, and by the thermodynamic properties of the HME materials (specially designed paper, cellulose or polyurethane foams).

To improve the heat- and moisture-conserving qualities of the HME material, a hygroscopic coating, such as magnesium, calcium, or lithium chloride, is used. These compounds reversibly adsorb water molecules and thus increase the water retention capacity. After a few breaths HMEs are at almost full effectiveness and reach steady state within a few minutes. Subsequently, the moisture-returning properties of the HME depend only on ventilatory parameters, the most important of which is tidal volume, such that the moisture-returning performance decreases as the tidal volume increases.

HMEs always result in an elevation of the inspiratory and expiratory airway resistances; this should be considered especially in cases that involve spontaneous respiration. The internal volumes of HMEs should be as small as possible so that they do not increase the effective dead space too much. A combination of HMEs and catheter mounts results in a further increase in the dead space, and therefore, must be considered critically, especially in cases that involve spontaneous respiration. If a catheter mount is necessary to add flexibility to the breathing system, the HME preferably should be connected directly onto the tracheal tube with the catheter mount behind it; otherwise, the humidification efficiency of the HME will be reduced by condensation in the catheter mount. Children should be ventilated with special HMEs that have a small internal volume.

Contraindications for Use of an HME

• Patients with thick, copious, or bloody secretions. • Patients with an expired tidal volume less than 70% of the delivered

tidal volume (e.g. those with large bronchopleurocutaneous fistulas or incompetent or absent endotracheal tube cuffs).

• Patients with body temperatures less than 32°C.• Patients with high spontaneous minute volumes (>10 L/min).• An HME must be removed from the patient circuit during aerosol

treatments when the nebulizer is placed in the patient circuit.• Non-invasive ventilation

Hazards and complications associated with the use of humidification devices include:• Hypothermia and/or hyperthermia; • Thermal injury to the airway from heated humidifiers; burns to the patient

and tubing meltdown if heated-wire circuits are covered or circuits and humidifiers are incompatible;

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• Underhydration and impaction of mucus secretions; • Hypoventilation and/or alveolar gas trapping due to mucus plugging of

airways; • Possible increased resistive work of breathing due to mucus plugging of

airways; • Possible hypoventilation due to increased dead space (HME); • Inadvertent overfilling resulting in unintentional tracheal lavage (heated

humidifiers); • The fact that when disconnected from the patient, some ventilators generate

a high flow through the patient circuit that may aerosolize contaminated condensate, putting both the patient and clinician at risk for nosocomial infection (heated humidifiers);

• Inadvertent tracheal lavage from pooled condensate in patient circuit (heated humidifiers);

• Elevated airway pressures due to pooled condensation (heated humidifiers); • Patient-ventilator dysynchrony and improper ventilator performance due

to pooled condensation in the circuit (heated humidifiers); • Ineffective low-pressure alarm during disconnection due to resistance

through HME.

The following variables should be recorded during equipment inspection: • Humidifier setting (temperature setting or numeric dial setting or both):

During routine use on an intubated patient, a heated humidifier should be set to deliver an inspired gas temperature of 33 ± 2°C and should provide a minimum of 30 mg/L of water vapor.

• Inspired gas temperature: Temperature should be monitored as near the patient’s airway opening as possible, if a heated humidifier is used.

− Specific temperatures may vary with patient condition, but the inspiratory gas should not exceed 37°C at the airway threshold.

− When a heated-wire patient circuit is used (to prevent condensation) on an infant, the temperature probe should be located outside of the incubator or away from the direct heat of the radiant warmer.

− Alarm settings (if applicable): High temperature alarm should be set no higher than 37°C, and the low temperature alarm should be set no lower than 30°C.

• Water level and function of automatic feed system (if applicable). • Quantity and consistency of secretions. Characteristics should be noted

and recorded. When using an HME, if secretions become copious or appear increasingly tenacious, a heated humidifier should replace the HME.

Infection Control

Reusable heated humidifiers should be subjected to high-level disinfection between patients. Clean technique should be observed when manually filling the water reservoir and sterile water should be used. Condensation from the patient circuit should be considered infectious waste and disposed of according

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to hospital policy using strict universal precautions. Because condensate is infectious waste, it should never be drained back into the humidifier reservoir.

Humidification Devices and VaP

Breathing systems used with heated humidifiers are associated with a rapid and high level of bacterial colonization. This colonization is considerably reduced with the use of HMEs. They do not need to be changed during the entire ventilation period of a given patient unless they are visibly soiled or mechanically malfunctioning. The incidence of VAP is not influenced by the type of humidification device (heated humidifier or HME) or by the duration of use of HMEs or the type of HME, but prolonging the use of a HME further reduces the risk of cross-contamination and results in considerable cost savings. Because breathing systems become rapidly and heavily contaminated when used with heated humidifiers, even with the use of heated delivery tubes and because HMEs efficiently prevent this contamination, some people strongly believe that HMEs should be preferred to heated humidifiers in a global policy against nosocomial infection and cross-contamination.

In addition, there now are substantial data indicating that HMEs can be used as efficiently as heated humidifiers for long-term mechanical ventilation of most ICU patients. This policy reduces staff workload, reduces the potential risk of cross-contamination, and enables substantial cost savings (Fig. 9.1).

Fig. 9.1: Algorithm for choosing humidification devices in ICU

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Complications can occur at any stage of mechanical ventilation and can be life threatening if not attended to in time. Although this section is intended to deal with complications of classical mechanical ventilation, many aspects are common to high frequency oscillatory ventilation. They can be discussed under the heading of the etiology and pathophysiology. Broadly, these are related to 1-process of intubation 2-infection, aspiration 3-hemodynamic.

Intubation and Artificial Airway1

Immediate ComplicationsIntubation and artificial airway management in the occupational therapy (OT) is done in relatively stable patients, under controlled environment, in well-equipped surroundings. Consequently, airway related complications are much less in the OT as compared to in an ICU where airway management is urgent and often little or no help is available. The incidence of difficult intubation scenario is more in the intensive care unit (ICU), which may be related to both inexperienced operator and difficult circumstances.

Hypotension, Hypoxia, Cardiac Arrest and DeathThese are the most common reported immediate complications of intubation in the ICU. Hypovolemia may be masked in patients with significant adrenergic drive arising from pain or fear. In these patients, the combination of a vasodilating sedating agent such as midazolam, together with the loss of sympathetic tone brought about by unconsciousness, rapidly lead to profound hypotension. It may take several minutes before the peak action of the commonly used drugs in RSI such as fentanyl and rocuronium; hence unnecessary repeat doses should be avoided. Drugs like midazolam and propofol should be avoided in conditions with impaired perfusion. Muscle relaxation should only be used once the ability to mask ventilate properly has been established otherwise in case of difficult intubation one may land up in a “cannot intubate cannot ventilate” scenario.1

Although hypoxia may be the initial problem that has precipitated the need for intubation, severe hypoxia during intubation is usually a consequence of

Vikas Taneja

Chapter

10Complications of


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poor manual ventilation with bag-mask or prolonged attempts at intubation. Usually the patients can be supported on manual bag mask ventilation with proper care taken to prevent aspiration, till help arrives or patient starts breathing spontaneously. Esophageal intubation may be mimicked in patients with severe bronchospasm, following intubation of the right main bronchus, or with unilateral pulmonary pathology, but these usually produce a normal ETCO

2 trace. If the tube enters the right main bronchus, an acute

intra-pulmonary shunt with resultant hypoxemia may occur. This may lead to left-sided lung collapse and right-sided hyperinflation with the risk of pneumothorax. The cuff portion of the tube should be passed only 3 to 5 cm beyond the cords. The tip of the tube should be at least 3 cm above the carina to prevent carinal stimulation or intermittent endobronchial intubation with ventilation. If there is any doubt as to the location of the tube, it should be removed and the patient re-intubated. The final confirmation of correct tube positioning is by inspection of a plain chest radiograph to ensure that the tip of the tracheal tube is midway between the carina and the larynx. ET should always be placed under direct visualization of the tube passing through the vocal cords.2

Regurgitation and Aspiration

In an elective intubation, this is prevented by keeping the patient NPO for 3–4 hours before the procedure. However, in an emergency scenario, RSI should be used and Sellick’s maneuver used during intubation to decrease the risk of aspiration. If a NG tube is in place, it should be aspirated to empty the stomach before bag mask ventilation is begun.

Complications that can occur during placement of an endotracheal tube include upper airway and nasal trauma, tooth avulsion, oral-pharyngeal laceration, laceration or hematoma of the vocal cords, tracheal laceration, perforation, hypoxemia, and intubation of the esophagus. Inadvertent intubation of the right main stem bronchus is common. Aspiration rates are 8–19% in intubations performed in adults without anesthesia. Sinusitis, tracheal necrosis or stenosis, glottic edema, and ventilator-associated pneumonia may occur with prolonged use of endotracheal tubes (Table 10.1).

Reduction of Immediate Complications

Acute airway management should be done by experienced operators. Proper preparation should be done in case of known difficult airway scenario. Help

Table 1: Signs to confirm correct placement of the endotracheal tubeLow resistance to inflation

Normal end-tidal carbon dioxide trace

Normal and symmetrical movement of the chest wall

Bilateral breath sounds on auscultation

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Complications of Mechanical Ventilation 95

should be available in terms of experienced personnel and equipment like intubation bougie, LMAs in proper sizes should be available. Nursing staff should be periodically retrained in terms of handling and assisting with intubation.

Complications Arising in the Medium and Long-term

Injuries to the Face, Lips and OropharynxWithout proper care, prolonged intubation results in trauma to the lips or cheeks from the tube tie and can provoke perioral herpes. Injuries to the tongue can occur if the tongue becomes trapped between the endotracheal tube and the lower teeth. Pressure injuries to the palate and oropharynx are uncommon (Fig. 10.1).

Maxillary Sinusitis and Middle Ear EffusionsMaxillary effusions have been noted in patients ventilated for more than 7 days, more so in patients having nasogastric tubes as compared to orogastric tubes. About 60% of these effusions become secondarily infected, most commonly with gram-negative enteric organisms, and may contribute to the development of ventilator-associated pneumonia.

Pharyngolaryngeal DysfunctionPost-extubation discomfort is common and it is independent of duration of intubation. Hoarseness is reported in about 52% cases in short-term intubation and 70% in patients with prolonged intubation. This is supposed to be related to glottic edema. These problems are usually short lasting and resolve in 24 to 48 hours. Another important complication is disturbed swallowing mechanism, slowing of the swallowing reflex leading to increasing the chances of silent aspiration.

Laryngeal InjuriesDespite advance in tube material, laryngeal and tracheal injuries are still seen. The posterior part of the vocal cords is particularly prone to ulcer formation. Granuloma formation has been seen as early as 7 days post-intubation (Fig. 10.2).

Fig. 10.1: Injuries to the face, lips and oropharynx

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Tracheal InjuriesIncidence of significant tracheal injury is not high with attention to cuff pressure and use of high volume and low pressure cuffs. Mild tracheal injuries such as ulceration, edema and submucosal hemorrhage are common but usually resolve without complications. Tracheal stenosis, however, is a serious complication, it may be at the level of the cuff, or at tracheostomy site, but the exact site is usually unclear. CT and bronchoscopy are required to make the diagnosis. Some patients require tracheal reconstruction. In ventilator dependent patients, repeated bronchoscopic dilatation is an option. Other options are laser, cryotherapy and metallic stent implantation where facilities are available.

Accidental extubation: This can be a serious adverse effect. It is of two types, self extubation, where the patient himself pulls out the tube, it usually indicates inadequate sedation and is less dangerous than accidental extubation by members of the staff during positioning, sponging, etc. Incidence of self- extubation is more than accidental extubation.

Hemodynamic Effects of Mechanical Ventilation3

Positive pressure ventilation increased mean intrathoracic pressure. It leads to a decrease in right heart filling, decreased venous return as the pressure gradient for right heart filling is reduced. This may result in a drop in cardiac output and decrease in arterial blood pressure. Optimum fluid administration is needed to maintain good venous return. Vasoactive drug infusion requirement may increase to maintain blood pressure and target urine output. Another effect of positive pressure ventilation is fluid retention and decreased urine output due to increased release of antidiuretic hormone (ADH) and decreased release of atrial natriuretic peptide (ANP). Care should be taken to avoid administration of excessive free water in ventilated patients. Isotonic restricted maintenance fluids should be used to avoid dilutional hyponatremia which can be catastrophic.

Figs 10.2A and B: Laryngeal injuries

A B

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Ventilator-induced Lung InjuryThis is of the following four types:• Volutrauma• Atelectrauma• Biotrauma• Oxygen toxicity.

With ventilator-induced lung injury, the alveolar epithelium is at risk for both barotrauma and volutrauma.

Barotrauma4

Rupture of the respiratory epithelium is the central factor. It can result in air leaking either into the lung parenchyma, or into the pleural space. Air leak into the lung parenchyma is usually along the bronchovascular sheath and is trapped in the mediastinum (pneumomediastinum) and may leak into the pericardium (pneumopericardium) or peritoneum (pneumoperitoneum). Air leak from the distal airway into the pleural space causes pneumothorax. These two air collections are collectively called Barotrauma. The term suggests that high airway pressure is the etiology, but this is not always the case. Actually, rupture of the respiratory epithelium can result from all, high pressures, iatrogenic or even spontaneously in some patients. Cases of recurrent spontaneous pneumothoraces have been reported. Congenital anomalies in the pleural surface like pleural blebs is usually the cause. But high ventilatory pressures are definitely the most common cause of pneumothorax in ventilated patients. High pressures lead to stretching of the epithelium, predisposing to rupture. However, in cases where the primary disease process is active, like in staphylococcal pneumonia causing necrotizing pneumonia, ruptures occur in absence of high pressures. Pneumomediastinum does not usually require active intervention. The incidence of pneumothorax has decreased over the years with the use of lung protective ventilatory strategies. It is clinically suspected when there is a sudden drop in saturation and low tidal volumes. Radiographs usually show the site. Sometimes pressure continues to build in the air pocket leading to sudden cardiorespiratory collapse (tension pneumothorax). Under such circumstances, emergency needle decompression should be done, followed by insertion of chest tube.

Technique of needle decompression: In the mid clavicular line on the affected side, palpate two rib spaces below the clavicle, and while keeping your finger in the space, insert a large bore intravenous cannula perpendicular to the skin, below your finger, until it touches the anterior surface of the rib. Then attach a syringe to the cannula and advance it into the space while aspirating until you get feel of entry into the pleural space, sudden aspiration of air will be obtained. In case of tension pneumothorax, air escaping could be felt. This should be followed by chest tube insertion on the affected side.

Correct chest tube insertion is indicated by bubbling in the underwater seal system and respiratory swings in the drain column. The position should

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be confirmed by radiograph as soon as possible. If there is a non-expansion of the lung or persistent bubbling after 48 hours of chest tube placement, a bronchopleural fistula is indicated. Negative suction should be used in such cases. Ventilatory pressures must be minimized to promote healing. In cases of non-resolution, advanced management options are single lung ventilation, targeted bronchial obstruction, high frequency oscillatory ventilation (HFOV) or rarely surgical correction.

The adjustments that can be done in the settings to minimize barotrauma are: I:E ratio can be adjusted by increasing the inspiratory flow rate, by decreasing the tidal volume, and by decreasing the ventilatory rate. Attention to the inspiratory-to-expiratory ratio is important to prevent barotrauma in patients with obstructive airway disease (e.g. asthma and chronic obstructive pulmonary disease). Encouraging spontaneous respiratory efforts, minimizing positive end-expiratory pressure (PEEP) and reducing resistance to gas flow by judicious use of bronchodilators and timely suction is also vital to reducing pressures around the air leak.

Volutrauma/ VILI1

This section deals with ventilator induced lung injury (VILI), also known as ventilator associated lung injury (VALI). The incidence of VILI is directly related to the use of high tidal volumes, which causes excessive stretch of the respiratory epithelium. It had beginnings in the 1950’s when use of high tidal volumes to maintain normal oxygenation indices on blood gases was the norm. It was after the publication of Webb and Tierney’s paper in 1974 which showed the lethal effects of using high pressures in rats that some headway into the low tidal volume or lung protective ventilation was made. Few more RCT’s demonstrated the beneficial effects of using low tidal volume strategy till 2000. But no definite conclusion was made. After the publication of the acute respiratory distress syndrome (ARDS) net study in 2000, which demonstrated a clear mortality benefit of using low tidal volume strategy, the practice around the world changed. Because of the heterogeneous nature of the lung in ARDS, using low tidal volume only cannot guarantee against over distension of certain areas which may have normal compliance. Hence, it is necessary to keep a check on the maximum pressure to which the alveoli are exposed.

The pathophysiology of the damage is related to two processes, there is an acute phase characterized by interstitial and pulmonary edema with surfactant dysfunction, followed by the later phase of increased inflammation.

Volutrauma refers to the local over distention of normal alveoli. Volutrauma has gained recognition over the last 2 decades and is the impetus for the lung protection ventilation with lower tidal volumes of 6–8 mL/kg. Computed tomography scans have demonstrated that ARDS has a heterogeneous pattern of lung involvement. Abnormal consolidated lung is dispersed within normal lung tissue. When a mechanical ventilation breath is forced into the patient, the positive pressure tends to follow the path of least resistance to the normal or relatively normal alveoli, potentially causing over distension. This over

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distension sets off an inflammatory cascade that augments or perpetuates the initial lung injury, causing additional damage to previously unaffected alveoli. The increased local inflammation lowers the patient’s potential to recover from ARDS. The inflammatory cascade occurs locally and may augment the systemic inflammatory response as well.

Another aspect of volutrauma associated with positive ventilation is the sheer force associated with the opening and closing effects on collapsible alveoli. This has also been linked to worsening the local inflammatory cascade. PEEP prevents the alveoli from totally collapsing at the end of exhalation and may be beneficial in preventing this type of injury. Since Volutrauma was recognized, lung-protective ventilation strategy is recommended in all patients with ARDS or acute lung injury.

Oxygen ToxicityOxygen toxicity is a function of increased FIO

2 and its duration of use. Oxygen

toxicity is due to the production of oxygen free radicals, such as superoxide anion, hydroxyl radical, and hydrogen peroxide. Oxygen toxicity can cause a variety of complications ranging from mild trachea-bronchitis and absorptive atelectasis to diffuse alveolar damage that is indistinguishable from ARDS.

Oxygen at 100% is definitely associated with lung injury.5 No consensus has been established for the level of FIO

2 required to cause oxygen toxicity,

but this complication has been reported in patients given maintenance FIO2

of 50%. The clinician is encouraged to use the lowest FIO2 that accomplishes

satisfactory oxygenation.The medical literature suggests that the clinician should attempt to attain

a FIO2

of 60% or less within the first 24 hours of mechanical ventilation. If necessary, PEEP should be considered a means to improve oxygenation while a safe FIO

2 is maintained. When PEEP is effective and not contraindicated

because of hemodynamics or other reasons, the patient can usually be oxygenated while the risks of oxygen toxicity are limited.

Ventilator-associated PneumoniaVentilator-associated pneumonia (VAP) is a life-threatening complication with mortality rates of 33–50%. It is reported to occur in 10–25% of patients given mechanical ventilation. The risk of VAP is highest immediately after intubation. VAP is estimated to occur at a rate of 3% per day for the first 5 days, 2% per day for next 5 days, and 1% per day thereafter. VAP occurs more frequently in trauma, neurosurgical, or burn units than in respiratory units and medical intensive care units.

The VAP is defined as a new infection of the lung parenchyma that develops within 48 hours after intubation. The diagnosis can be challenging. VAP should be suspected when a new or changing pulmonary infiltrate in seen in conjunction with fever, leukocytosis, and purulent tracheobronchial secretions. However, many diseases can cause this clinical scenario. Examples

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include aspiration pneumonitis, atelectasis, pulmonary thromboembolism, drug reactions, pulmonary hemorrhage, and radiation-induced pneumonitis. Qualitative and quantitative cultures of protected brush and bronchoalveolar lavage specimens may help with the diagnosis, but the utility of these techniques is still debated.

Microorganisms implicated in VAP that occurs in the first 48 hours after intubation are flora of the upper airway, including Haemophilus influenza and Streptococcus pneumonia. After this early period, gram-negative bacilli such as Pseudomonas aeruginosa; Escherichia coli; and Acinetobacter, Proteus, and Klebsiella species predominate. Staphylococcus aureus, especially methicillin-resistant S. aureus (MRSA), typically becomes a major infective agent after 7 days of intubation and mechanical ventilation. Most of the medical literature recommends initial therapy with broad-spectrum antibiotics that cover pathogens resistant to multiple drugs until the sensitivities of the causative organism are identified. Knowledge of organisms that cause VAP in the individual ICU and the pattern of antibiotic resistance is imperative. Choices of antibiotics should be tailored to the microorganisms and the antimicrobial resistance observed in each ICU.

Age Specific VAP Diagnostic Criteria

About 1–12 year of age.

At least 3 of the clinical criteria• T >38.4 C or <37 without other recognized cause• WBC <4000 or >15000• New onset purulent sputum or change in character of sputum or increase

secretions• New onset or worsening of cough, dyspnea or tachypnea• Rales or bronchial breath sounds• Worsening ventilation or oxygenation

Plus radiographic criteria:• At least 2 serial chest X-rays with new or progressive and persistent infiltrate

or consolidation or cavitation that develops >48 hours after initiation of mechanical ventilation.

• For infants less than 12 months of age, worsening gas exchange is essential for diagnosing VAP. Other criteria are similar.

Pediatric VAP Bundle

Following are the prevention items specific to PICU for VAP prevention, these are slightly different than the adult “VAP BUNDLE”. These have been categorized based on the various etiologies of VAP.10 1. Items to prevent iatrogenic spread of infection: This includes proper hand

hygiene practices, universal precautions for all patients and isolation based on the organism.

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2. Prevention of aspiration of gastric contents: This is very important as aspiration of gastric secretions is a common cause of VAP. Head of bed elevation to 30–45 degrees is an absolute must. Regular monitoring and drainage of gastric contents is desirable. Some ET tubes are available with a subglottic drainage port.

3. Oral hygiene: Regular oral rinsing and cleaning with chlorhexidine (0.12%) and use of toothbrushes and oral swabs.

4. Endotracheal tube: Tube related factors: Use of inline suction where available and suction of hypopharynx prior to ET suction and any repositioning is vital and perhaps the most ignored part of care (Fig. 10.3).

5. Respiratory equipment related: Dedicated oropharyngeal suction equipment should be used. Condensation in the ventilator circuit should be avoided and care should be taken not to inadvertently drain the condensate into the patient. Traps should be regularly cleared of secretions. Contamination of ventilator equipment should be avoided.

6. Duration of ventilation: Perhaps the best method to prevent VAP is to avoid ventilation in the first place. Nonetheless, all effort must be made to decrease the duration of mechanical ventilation. Daily readiness to extubate trials along with sedation holidays should be given.

Intrinsic PEEP, or auto-PEEP6-8

Intrinsic positive end-expiratory pressure (PEEP) or auto-PEEP is a complication of mechanical ventilation that most frequently occurs in patients with obstructive disease like asthma who require prolonged expiratory phase of respiration. These patients have difficulty in exhaling the tidal volume to the baseline before the onset of the next inspiration, resulting in stacking of breaths and further worsening of hyperinflation. If this goes unrecognized, the patient’s peak airway pressure may increase to a level that results in barotrauma, volutrauma, hypotension, patient-ventilator dyssynchrony, or death (Fig. 10.4).

Fig. 10.3: Contamination routes for the lower respiratory tract in the acquisition of ventilator-associated pneumonia. A. The para-cuff route, with endogenous contaminants pooling in the sub-glottic space arising from the oropharynx, stomach, nose and sinuses; B. The trans-luminal route, with exogenous contaminants coming from the surface of the endotracheal tube, catheter mount, suction equipment, nebulizer equipment, and ventilator circuit

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The flow to time waveform demonstrating auto–positive end-expiratory pressure (auto-PEEP).

Manometry performed by using an esophageal balloon to record changes in pleural pressure is the most accurate way to recognize intrinsic PEEP. However, this technology is not available at most institutions. Therefore, clinicians must anticipate this complication and carefully monitor the measured peak airway pressure. When intrinsic PEEP is diagnosed, the patient should temporarily be released from mechanical ventilation to allow for full expiration. The ventilator can then be adjusted to shorten inspiration by decreasing the set tidal volume, increasing the inspiratory flow rate, or reducing the frequency of respirations.9 These maneuvers, if performed properly, can increase the expiratory time. The normal inspiratory to expiratory ratio (I:E ratio) is 1:2. In patients with obstructive airway disease, the target I:E ratio should be 1:3 to 1:4.

Troubleshooting

This section is to review the common bed side problems encountered during mechanical ventilation and their solution.11

1. Alarms: Perhaps the commonest sound you hear is the alarms. It can range from high pressure, low tidal volume, high O

2, humidifier alarm,

etc. No alarm should ever be ignored. The nurse should be told about the particular ventilator settings and expected targets of maximum pressure and tidal volumes. Do not keep the alarm range wide to avoid frequent alarms. Usual limit of P Max is 35 cm H

2O, which may have to be exceeded

when recruiting the lung for the first time or after a break for suction or in severe restrictive lung pathology. Tidal volumes are kept at 6 ml/kg in most cases to comply with lung protective ventilation.

2. Sudden collapse of patient—DOPE: Such a situation should be preempted by paying careful attention to the ventilatory pattern. If, however, a patient collapses suddenly, he should be manually ventilated to ascertain whether the cause is with the patient or the ventilator. Rule out – DOPE systematically. Look for displacement of the tube by comparing the mark

Fig. 10.4: Flow time scalar showing expiratory flow doesnot return to zero before the next breath is given

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at lip, and auscultate for air entry. Rule out obstruction, do suction if secretions seen or suggested by auscultation/ graphics. Pneumothorax presents as sudden increase in pressure requirement to achieve the same tidal volumes. Its management has been already discussed. Lastly, equipment failure, there may be a fault in the ventilator.

3. Asynchrony: This is very common. One needs experience of having been at the bedside of ventilated patients to become comfortable with handling asynchrony. This can manifest as an irregular breathing pattern, variable tidal volumes, increased RR or increased pressure requirement. The commonest causes are inadequate sedation, condensation in the circuit, incomplete exhalation, high flow demand of the patient, secretions, etc. Inadequate sedation can be diagnosed by clinical examination of the patient and should be optimized. Condensation in the circuit can lead to auto-triggering and can cause significant asynchrony and patient discomfort; this should be removed from time to time. Incomplete exhalation leads to breathe stacking and can be diagnosed by looking at the flow-time scalar. This can be tackled by judicious use of bronchodilators and adjusting the RR to allow more time for exhalation. Secretions are usually obvious on bed side examination and also can be seen on the graphics, suction should be done only if there are secretions. Large difference in the Peak pressure and the plateau pressure suggests increased resistance.

References 1. Mackenzie I. Core topics in mechanical ventilation. 2. Macintyre NR. Mechanical ventilation, Jones and Bartlett learning. 3. Zimmerman. Pediatric Critical Care. 4th edition. LWW 4. Dreyfuss D, Suvmen G. Ventilator induced lung injury: lessons from experimental

studies. Am J Respir Crit Care Med. 1998;157:294-323. 5. Durbin CG, Wallace KF. Oxygen toxicity in the critically ill patient. Respir Care. 1993;

38:739-58. 6. Pepe PE, Marini JJ. Occult positive end-expiratory pressure in mechanically

ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Respir Dis. 1982;126:166-70.

7. Ranieri VM, Grasso S, Fiore T, Giuliani R. Auto-positive end-expiratory pressure and dynamic hyperinflation. Clin Chest Med. 1996;17:379-94 .

8. Oddo M, et al. Management of mechanical ventilation in acute severe asthma: practical aspects. Intensive Care Med. 2006;32:501-10.

9. Brenner B, et al. Intubation and mechanical ventilation of the asthmatic patient in respiratory failure. J Allergy Clin Immunol. 2009;124:S19-28.

10. Curley MA, Schwalenstocker E, Deshpande JK, et al. Tailoring the Institute for Health Care Improvement 100,000 Lives Campaign to pediatric settings: The example of ventilator-associated pneumonia. Pediatr Clin North Am. 2006;53(6): 1231-51.

11. Bekos Vasileios, MDa, John J. Marini, MD, Monitoring the Mechanically Ventilated Patient. Crit Care Clin 2007; 23: 575-611.

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Troubleshooting and monitoring is an important part of ventilator handling. One needs to be alert and aware of the various alarms as it guides to the proper management of the ventilated patient. For troubleshooting various types of alarms are there in the ventilator and can be divided into the following types: 1. Pressure alarms2. Volume alarms3. Respiratory rate alarms4. Positive end-expiratory (PEEP) alarms5. Oxygenation alarms.

The causes of various alarms are as follows: 1. Pressure alarms

− Low pressure alarms − Loss of system pressure

- Power failure - Source gas failure - Air compressor failure.

− Loss of circuit pressure - Circuit disconnection - Loose circuit/humidifier connection - Leak around ET tube.

− Inappropriate ventilatory settings - Low pressure limit set too high - Excessive rates with insufficient peak flow.

− High pressure alarms − Increase in airflow resistance—mechanical factors

- Kinking of circuit/ET tube - Water in the circuit - Bronchial intubation - High pressure limit set too low.

− Increase in airflow resistance—patient factors - Bronchospasm - Coughing - Patient ventilator asynchrony - Secretions.

Chapter

11 Troubleshooting and Monitoring During Mechanical Ventilation

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troubleshooting and Monitoring During Mechanical Ventilation 105

− Decrease in lung or chest wall compliance - Tension pneumothorax - Atelectasis - Pneumonia/ARDS.

2. Volume alarms − Low expired minute volume alarm − Loss of system pressure

- Power failure - Source gas failure - Air compressor failure.

− Loss of circuit volume - Circuit disconnection - Loose circuit connection - Loose humidifier connection - Leak around ET tube.

− Inappropriate ventilatory settings - Low minute volume limit set too high - Inappropriate sensitivity settings.

3. Respiratory rate alarms − High respiratory rate alarm

- Patient experienced tachypnea—need to increase ventilation - Inappropriate sensitivity settings—increase trigger sensitivity.

− Apnea alarm - Set to insure a minimum number of breaths to be delivered - Disconnection of ventilator circuit from ET tube - Respiratory depression - Respiratory muscle fatigue - Use of muscle paralyzing agents - Some ventilators switch to back up ventilation.

4. Positive end-expiratory (PEEP) Alarms − Auto PEEP (Intrinsic PEEP, inadvertent PEEP) − Causes

- Significant airway obstruction with air trapping - Rapid respiratory rates - Small expiratory time.

− Auto PEEP increases work of breathing - Ventilator initiates breath when the –ve pressure reaches the

sensitivity setting - If auto PEEP present, the work of breathing is increased because

the level of auto PEEP must first be overcome before the sensitivity setting is to be reached.

− Strategies to reduce auto PEEP - Improve ventilation and reduce air trapping by bronchodilators - Decrease the respiratory rate and prolong the expiratory time.

− Using PEEP to reduce the effects of auto PEEP - Increase PEEP to 85% of the measured auto PEEP level

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5. Oxygenation alarms − Low FiO

2 alarm

- Oxygen source failure - Oxygen sensor failure - Faulty oxygen blender.

− High FiO2 alarm

- Air source failure - Faulty oxygen blender

Monitoring

Monitoring during mechanical ventilation is important from many aspects: • Patient’s clinical status in PICU changes often rapidly and unpredictably.• Besides the underlying illness, ventilatory settings also affect the patient’s

status.• Trends can be established to assess progress or deterioration of patient’s

condition.

Various parameters that need monitoring during mechanical ventilation include:1. Vital signs

− Heart rate, BP, respiratory rate, temperature.2. Chest inspection and auscultation3. Pulse oximetery4. Arterial blood gas

− Assessment of oxygenation status − Assessment of ventilatory status.

5. End tidal CO2

1. Vital Signs − Heart rate

i. Tachycardia - Pain - Awake state - Hypoxia - Fever - Low cardiac output - Anxiety and stress - Medications (Ionotropes).

ii. Bradycardia - Hypoxia - Vagal stimulation during ET suctioning - Hypothermia - Arrhythmias - Medications (Morphine, midazolam)

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troubleshooting and Monitoring During Mechanical Ventilation 107

− Blood pressure i. Hypertension

- Pain - Anxiety and stress - Awake state - Fluid overload - Increased ICT - Drugs (Ionotropes).

ii. Hypotension - Hypoxia - ET suctioning (Vagal) - Decreased venous return due to PPV - Hypothermia - Arrhythmias - Drugs (Morphine, midazolam, vasodilators—SNP, NTG).

− Temperature i. Hyperthermia

- Over heated humidifier - Infection (VAP) - IV fluids - Sepsis - Drugs - After cardiopulmonary bypass.

ii. Hypothermia - No humidification - Low cardiac output states - Drugs (Adrenaline) and toxins - After cardiopulmonary bypass - Induced.

− Respiratory rate i. Tachypnea

- Pain - Hypoxia/hypoventilation - Pneumothorax - Hypovolemia - Fever - Low cardiac output - Pulmonary embolism.

2. Chest inspection and auscultation − Important to rule out

- ET tube position - Collapse/consolidation - Pneumothorax - Excessive secretions - Wheezing/crepts.

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3. Pulse oximetery − Advantages

- Measures the oxygenation status - Noninvasive - Serial measurements can help in adjusting ventilatory settings - Weaning from the ventilator.

− Limitations - SpO

2 becomes less accurate when SaO

2 falls

- Inaccurate measurement due to motion artefact, - Inaccurate measurements due to low perfusion states, dyshemo-

globinemias.4. Arterial blood gas

− Assessment of oxygenation - PaO

2

- A-aDO2

- PaO2/FiO

2 ratio

− Assessment of ventilation - PaCO

2

− Assessment of the acid-base status - Acid base status - Anion gap - Electrolyte status - Sugars and lactate - Hemoglobin/Hematocrit.

5. End tidal CO2 − Advantages

- Accidental esophageal intubations - Endotracheal tube cuff leaks - Airway obstructions - Weaning - Cardiopulmonary resuscitation.

− Limitations - Dead space ventilation - Positive pressure ventilation - Decreased cardiac output - Cardiac arrest.

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Extracorporeal membrane oxygenation (ECMO) in simplest form is a modification of the conventional cardiopulmonary bypass technique for prolonged cardiopulmonary support. After initial use in the 1970’s in acute respiratory distress syndrome (ARDS) in adults and few polytrauma patients, its use declines until interest was revived after Dr Robert Bartlett described a neonatal survivor, baby Esperenza.1 After that its use was associated with a high rate of bleeding complications and slowly its use declined till the results of the CESAR trial showed a beneficial effect and more recently good results when ECMO was used during the 2009 H1N1 pandemic in Australia and New Zealand.5

Introduction

The ECMO is an invasive technique in which blood is drained from the venous system, pumped through an artificial organ (oxygenator), and then re-infused to the patient. This process augments the exchange of CO

2 and O

2

and permits the reduction of potentially injurious ventilator settings. There are two methods: Veno-arterial, which supports both cardiac and pulmonary function; and Veno-venous, which supports pulmonary function. It is being used mostly in specialized centers in patients not responding to conventional therapeutic measures. The indications are various and are age specific and are discussed later.

Advantages

Various advantages of ECMO that have been experienced over the years are the ability of providing both cardiac and pulmonary support, support of either both ventricles or left ventricle function (LVF), rapidity of initiation (within 30–60 minutes in specialized centers), applicability in complex cardiac conditions and extensive experience now in ECMO centers.2,3 But, on the other hand, a number of disadvantages of ECMO have been experienced: Significant risk of hemorrhagic or thrombotic complications in spite of strict anticoagulation, infection and end-organ dysfunction with prolonged support, massive transfusion requirement and risk of allosensitization, lack of patient mobility due to cannula positioning and the bulk of the ECMO circuit, etc. ECMO is the

Chapter

12Extracorporeal Membrane

OxygenationManish Kori

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preferred option for mechanical circulatory support versus ventricular assist devices (VAD) for potentially reversible conditions like acute myocarditis, or pump failure postcardiac surgery, also in a situation with rapid deterioration in patient’s condition because of rapidity of initiation. In conditions requiring more prolonged cardiac support, e.g. as a bridge to heart transplantation, VAD’s are more appropriate.4

Physiology and Fundamentals

The ECMO is only useful in cases where the primary lung is not affected by oxygen toxicity and barotrauma due to mechanical ventilation, also, the etiology must be potentially reversible. Criteria often cited for ECMO use are when the predicted mortality approached 80–90% with conventional treatment. Some of the oxygenation indices with >80% predicted mortality are: OI >40 or >35 for 4 hours, ventilation index >90 for 4 hours, alveolar- arterial gradient >600–624 mm Hg, PaO

2 <50 mm Hg for 2–12 hours (on 100 % FiO

2). It is

important to initiate ECMO before setting in of terminal ventilator induced lung injury, which typically occurs in 7 days in patients with high pressure settings.

Extrocorporeal Membrane Oxygenation Circuit

The basic components of an ECMO circuit include a roller pump, a membrane oxygenator, a heat exchanger, tubing made of polyvinyl chloride, connectors and a blood reservoir. Blood is driven through the membrane by the roller pump or centrifugal pump and it is allowed to drain passively by gravity from the venous side through a siphon height of 100 cm or more into a collapsible bladder that acts as a compliant reservoir. The bladder has a proximity switch attached and acts to regulate the roller pup by turning it off as the bladder deflates. The roller pump draws blood from the bladder and pushed it through the membrane oxygenator and then through a heat exchanger before finally returning it to the patient. The bladder and pump are regulated by a trip-switch system so that if the pump flow exceeds venous drainage, bladder collapses to inhibit pump flow. The blood flow within the circuit requires systemic heparin administration to prevent thrombus formation. The pediatric septic shock guidelines recommend a flow rate of 110 mL/kg/minute although improved survival has been noted with flow rates up to 150–200 mL/kg/min (Fig. 12.1).6,7

Venoarterial ECMO

In venoarterial ECMO oxygen-depleted blood is drained from the right side of the heart and oxygenated blood is pumped back into the systemic side, resulting in both, gas exchange and supporting cardiac function. Veno-arterial ECMO is more commonly used in neonates, particularly when both heart and lung function is compromised. This is accomplished via cannulation and ligation of the carotid artery, which is tolerated in neonates because collateral circulation develops. Venoarterial ECMO is used to support patients in cardiac failure—a

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extracorporeal Membrane Oxygenation 111

growing use of ECMO in neonates, pediatrics, and adults. The cannulation route may be transthoracic, as in patients who have undergone palliative and corrective cardiac surgery. In the immediate postoperative period the chest can be easily accessed, with the right atrium cannulated for drainage and the aorta for reinfusion. There are issues like upper body hypoxemia with VA ECMO as the ventricle output perfuses the upper body, mainly the coronary and cerebral circulation.

ECMO in Neonates

Bartlett and colleagues reported the first case series of 28 patients (14 children, 14 adults) who were treated with ECMO in 1977. Although only 5 of 28 patients were long-term survivors, the successes led to the first trials of ECMO therapy for respiratory failure in neonates. 11 high-risk patients were treated with ECMO, all survived (1 patient had cerebral hemorrhage), while the single patient who received conventional therapy did not survive. Another trial reported 100% survival in newborns treated for pulmonary hypertension and respiratory failure. Another randomized, controlled trial was completed in 1996 involving 185 neonates with respiratory failure.8 The mortality rate decreased from 59 to 32% with the usage of ECMO. Subsequently, ECMO has been commonly used in neonatal ICUs for the treatment of respiratory failure due to primary pulmonary hypertension of the newborn, meconium aspiration syndrome, persistent fetal circulation, congenital diaphragmatic hernia, and other reversible lung diseases, yielding good survival rates except in the case of CDH.9,10 Therapies such as HFOV, surfactant, and iNO have reduced the need for ECMO. Nonetheless, ECMO continues to be a viable therapy for refractory neonatal pulmonary failure.

Fig. 12.1: ECMO circuit

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ECMO in Pediatrics

Common indications have been pneumonia, ARDS and pulmonary hemorrhage. First main study regarding use of ECMO in children came from a multicentre retrospective chart review study from the Pediatric Critical Care Group, involving 331 children, the results showed that ECMO, but not high-frequency ventilation, reduced mortality as a result of this disease from 47 to 26%.11 Pediatric ECMO cases kept on increasing till 1994, when improvement in mortality due to safe ventilation strategies led to a decline. There has been resurgence in its use after the H1N1 pandemic in 2009 and the CESAR trial results. 5,12

Cardiac Failure

Congenital heart disease remains a challenge for pediatric intensivists. Surgical correction/palliation has improved outcomes, but some children are too sick to undergo surgery or develop LCOS in the postoperative period, or have grown past the ability of their restructured heart to function. Also, cardiac failure can result from noncongenital medical conditions such as viral myocarditis/ cardiomyopathy. For such patients, ECMO is the option for short-term cardiac support while waiting for either native heart recovery or as a bridge to transplantation. Survival rates for all diseases requiring cardiac support is 38% for neonatal patients and 43% for pediatric patients. In pediatric patients post cardiac surgery, survival rates up to 50% have been achieved by implementing ECMO earlier.13,14 As ventricular assist devices are being adapted for children, need of ECMO may reduce in the future.

Adult ECMO

Indications (Table 12.1)• Post-cardiotomy

− When unable to get patient off cardiopulmonary bypass following cardiac surgery

• Post-heart transplant − Usually due to primary graft failure

Table 12.1: Criteria for respiratory ECMO in adults15

PaO2/FiO2 ratio, <100 on FiO2 of 1.0,

P(A-a)O2 of >600 mm Hg,

Murray lung score of <3.0, 35 or uncompensated hypercapnea with a pH of >7.20

Age <65 years

Receipt of mechanical ventilation for <7 days

No known contraindication to limited anticoagulation

Patients who are not moribund and do not have contraindication to full intensive therapy

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• Severe cardiac failure due to almost any other cause − Decompensated cardiomyopathy − Myocarditis − Acute coronary syndrome with cardiogenic shock − Profound cardiac depression due to drug overdose or sepsis (Fig. 12.2).

Respiratory Indications

• Adult respiratory distress syndrome (ARDS)• Pneumonia• Trauma• Primary graft failure following lung transplantation. • ECMO is also used for neonatal and pediatric respiratory support

− This is where most of the research on ECMO has been done.

Outcome in Pediatric ECMO: Predictors of Survival

• Younger age (23 vs 49 months)• Ventilator days pre-ECMO (5.1 vs 7.3)• Lower PIP, lower A-a gradient (Moler, et al. CCM, 1993)• No difference in survival if >2 weeks on ECMO (Green, et al. CCM, 1995)• Lung biopsy not necessarily predictive.

Patient Selection for Pediatric/Adult ECMO

Basic Principles• Is the pulmonary/cardiac disease life threatening?• Is the disease likely reversible?• Are other diseases relative to prognosis?• Is ECMO more likely to help than hurt?

Fig. 12.2: Size of circuit components based on weight

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• Is preoperative support warranted??• VA or VV.

Results from the CESAR trial:5 Multicenter retrospective trial comparing early referral to an ECMO center versus conventional management showed a significant improved survival without severe disability at 6 months in patients referred to an ECMO center.

Suggested Pediatric Indications

• Oxygen requirement greater than FiO2 >0.6.

• Mean airway pressure more than 20 cm H2O on conventional ventilation

or 25–35 cm H2O with high frequency ventilation.

• Presence of air leak or evidence of barotraumas• Oxygenation Index (= 100 × mean airway pressure × FiO

2/ PaO

2)

• Duration of mechanical ventilation of 7–14 days.• Evidence for reversibility of disease• Reasonable medical certainty of a reasonable quality of life• No condition associated with bleeding diathesis• Inability to remove carbon dioxide.

The ECMO has recently been used in patients undergoing CPR. Extracorporeal cardiopulmonary resuscitation has recently been demonstrated to be associated with good survival rates to hospital discharge (34 to 38%) in pediatric patients (Table 12.2).

Table 12.2: Extracorporeal life support results by age, organ system and survival to discharge in United States (January 2009)16

Group Percent (%) [Survival to transfer or discharge]

Cases

Neonatal

Respiratory 76 19982

Cardiac 39 3089

CPR 38 386

Pediatric

Respiratory 53 3021

Cardiac 44 3442

CPR 39 639

Adult

Respiratory 52 1025

Cardiac 32 499

CPR 37 139

Total 64 32228

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Technical Issues

The ECMO is a very intensive therapy and hence it should ideally be used only in the centers with adequate expertise in its use. This may not be practical given the decreasing requirement of ECMO since the usage of lung protective ventilation and implantation of aggressive sepsis management. Given the overall critical scenario in which it is used, support staff should be familiar with and be able to identify and handle circuit failure in time. Route of cannulation must be determined after the patient has been listed for ECMO. VA cannulation (usually via the carotid artery and jugular vein) is used in patients who require cardiac support in addition to respiratory support. In patients with pure respiratory failure, VV cannulation (usually via the femoral vein and internal jugular vein) is preferred. As there is no arterial cannula in VV ECMO, risk of arterial embolic complications is reduced. This is more significant in adults where strokes are a major complication with VA ECMO. Along with ECMO, all supportive therapies should continue like lung protective ventilation and aggressive implementation of all standard ICU guidelines. More recently ECMO use has increased, perhaps due to some technical improvements, such as nonporous hollow fiber devices, which allow low resistance to blood flow, and polymethylpentene fibers that, combined with nonthrombogenic coatings, decrease the need for platelet transfusion and continuous heparin infusion. Also, recently introduced wire-reinforced walls of vascular access devices allow very thin cannula walls, reducing resistance to blood flow.

VV ECMO technical: Oxygenated blood from the return cannula that passed into the ECMO drainage cannula is called “recirculation”. It does not contribute to oxygenation. Usually there is mixing of oxygenated blood from the ECMO return cannula and normal venous return (deoxygenated), hence a normal arterial saturation is not achieved, more so in cases where the lungs are not functioning well. Common target SaO

2 for VV ECMO is

86–92%. If ECMO circuit flow is at least 70% of cardiac output and most of the ECMO return cannula blood passes through the lungs, this target SaO

2 can be

achieved. Hence, for example in an adult, a circuit flow of at least 3–6 L/min is required to achieve the target SaO

2. In practice, some recirculation always

occurs; it depends on the position of the drainage and the return cannula, intravascular volume, ECMO flow, cardiac output and patient position. A high preoxygenator SO

2 in combination with low patient SaO

2 suggests clinically

significant recirculation. Also, during VV ECMO, the preoxygenator SO2 gives

us the reference systemic venous oxygen saturation (Table 12.3).

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Table 12.3: Differences between VV and VA ECMO17

VA ECMO VV ECMO

Cannulation site � Vein – Internal jugular – Femoral

� Artery – Right common carotid – Axillary – Femoral – Aorta

� Single cannulation – Internal jugular – Right atrium

� Double cannulation – Jugular-femoral – Femoro-femoral – Sapheno-saphenous

Arterial PO2 6–150 mm Hg 45–80 mm Hg

Indicators of O2 sufficiency mSVO2PaO2Calculated oxygen consumption

SaO2 and PaO2Cerebral venous saturationPre membrane saturation trend

Cardiac effects Preload-decreasedAfterload-increasedPulse pressure-lowerCVP-variesCoronary O2-variesLV blood desaturatedCardiac stun syndrome

May reduce RV afterload Rest unaffected

O2 delivery capacity high Moderate

Circulatory support Partial to complete No direct support, increase O2 delivery to coronary and pulmonary circuit → improving cardiac output

References 1. Bartlett RH, Gazzaniga AB, Jefferies MR, et al. Extracorporeal membrane

oxygenation (ECMO) cardiopulmonary support in infancy. Trans Am Soc Artif Intern Organs. 1976;22:80-93.

2. Cabrera AG, Prodhan P, Cleves MA, et al. Interhospital transport of children requiring extracorporeal membrane oxygenation support for cardiac dysfunction. Congenit Heart Dis. 2011;6:202-8.

3. Extracorporeal Life Support Organization: ECLS Registry Report. International Summary. Ann Arbor, MI, Extracorporeal Life Support Organization. 2012.

4. Jaquiss DBR, Bronicki AR, et al. An overview of mechanical circulatory support in children. Pediatr Crit Care Med. 2013;14:S3-S6.

5. Peek GJ, Mugford M, Tiruvoipati R, et al. For the CESAR trial collaboration. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicenter randomized controlled trial. Lancet. 2009;374:1351-63.

6. Brierley J, Carcillo JA, Choong K, Cornell T, et al. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. Crit Care Med. 2009;37:666-88.

7. MacLaren G, Butt W, Best D, Donath S. Central extracorporeal membrane oxygenation for refractory pediatric septic shock. Pediatr Crit Care Med. 2011;12: 133-6.

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8. UK Collaborative ECMO Trail Group. UK collaborative randomized trial of neonatal extracorporeal membrane oxygenation. Lancet. 1996;348:75-82.

9. West KW, Bengston K, Rescorla FJ, et al. Delayed surgical repair and ECMO improves survival in congenital diaphragmatic hernia. Ann Surg. 1992;216:454-60.

10. Shanley CJ, Hirschl RB, Schumacher RE, et al. Extracorporeal life support for neonatal respiratory failure: a 20-year experience. Ann Surg. 1994;220:269-80.

11. Green TP, Timmons OD, Fackler JC, et al. The impact of extracorporeal membrane oxygenation on survival in pediatric patients with acute respiratory failure: pediatric Critical Care Study Group. Crit Care Med. 1996;24:323-9.

12. Davies A, Jones D, Bailey M, Beca J, Bellomo R, et al. Extracorporeal membrane oxygenation for 2009 influenza A (H1N1) acute respiratory distress syndrome. JAMA 2009;302:1888-95.

13. Kolovos NS, Bratton SL, Moler FW, et al. Outcome of pediatric patients treated with extracorporeal life support after cardiac surgery. Ann Thorac Surg. 2003;76: 1435-41.

14. Sachweh JS, Tiete AR, Fuchs A, et al. Efficacy of extracorporeal membrane oxygenation in a congenital heart surgery program. Clin Res Cardiol. 2007;96: 204-10.

15. Douglas JE, et al. ECMO: current clinical practice, coding and reimbursement. Chest. 2008;134:179-84.

16. Custer JR. The evolution of patient selection criteria and indications for extracorporeal life support in pediatric cardiopulmonary failure. Organogenesis. 7 (1):13-22

17. Chauhan S, et al. Extracorporeal Membrane Oxygenation, an anaesthesiologist’s perspective: physiology and principles part 1. Annals of Cardiac Anaesthesia. 2011.

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