`Neonatal
`Mechanical
`
`
`
`Pediatric and Neonatal
`
`Mechanical Ventilation
`
`
`
`Also available....
`
`Practical
`Approach to
`Pediatric
`intensive Care
`
`Praveen Khilnani
`
`7
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`I
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`.l.atI7lC Intensive Care
`" diwf-5f% Praveen Khilnani
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`Pediatric ancl Neonatal
`Mechanical Ventilation
`
`Praveen Khilnani
`MD FAAP (USA) FCCM (USA)
`
`Senior Consultant Pediatric, Intensivist
`and
`
`Pulmonologist
`Apollo Hospital
`New Delhi
`
`Foreword by
`
`RN Srivastav
`
`3
`
`JAYPEE BROTHERS
`MEDICAL PUBLISHERS (P) LTD
`
`
`
`
`
`
`to my rnother
`Late Shrimati Laxmi Dem’ Khilnani
`
`who left for heavenly abode on May 2001.
`She always knew I could do it whenever I thought I couldn't.
`She was the one who fought me to always be optimistic and
`hardworking.
`God will take care of the rest.
`
`Late Smt Laxrni Devi Khilnani
`
`
`
`Published by
`
`Jitendar P Vij
`Jaypee Brothersfledical Publishers (P) Ltd_
`EMCA House, 23/238 Ansari Fioad, Daryaganj
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`Pediatric and Neonatal Mechanical Ventilation '
`
`© 2006, Praveen Khilnani
`All rights reserved. No part of this publication and interactive CD ROM should be
`reproduced, stored in a retrieval system, or transmitted in any form or by, any means:
`electronic, mechanical, photocopying, recording, or otherwise, without the prior written
`permission of the author and the publisher.
`
`
`This book has been published in good faith that the material provided by author is
`
`original. Every etfort is made to ensure accuracy of material, but the publisher, printer
`
`
`
`
`and author will not be held responsible for any inadvertent error(s). In case of any
`dispute, all legal matters are to be settled unde'r,_ Delhi jurisdiction only.
`
`First Edition:
`
`2006
`
`ISBN 81-8061-726-2
`
`_
`
`
`
`''-..>...rs:...*....;—r.....,._,.;______7_
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`
`
`
`
`
`Author of this book Pediatric and Neonatal Mechanical Ventilation is
`an experienced pediatric intensivist with over 20 years of experience
`and expertise in the field of anesthesia, pediatrics and critical care.
`He has been involved in training and teaching at various
`conferences and mechanical ventilation workshops in India as well
`as at an international level. The text presented is intended to be a
`practical resource, helpful to beginners and advanced pediatricians
`who are using mechanical ventilation for newborns and older
`children.
`
`Prof RN Srivastav
`
`Senior Consultant
`
`Apollo Centre for Advanced Pediatrics
`
`IP Apollo Hospital
`New Delhi
`
`
`
`ii
`
`
`
`
`
`As the field of pediatric critical care is growing, the need for a
`simple and focused text of this kind has been felt for past several
`years in this part of the world for pediatric mechanical ventilation.
`Effort has been made to present the method and issues related to
`mechanical ventilation of neonate, infant and the older child. Basic
`
`and some advanced modes of mechanical ventilation have been
`
`described for advanced readers, topics like high frequency
`ventilation, ventilator graphics and inhaled nitric oxide have also
`been included. Finally some commonly available ventilators and
`their features and utility in this part of the world have been
`discussed. I hope this book will be helpful to pediatricians, residents
`and neonatal pediatric intensivists who are beginning to work
`independently in an intensive care setting, or have already been
`involved in care of critically ill neonates and children.
`
`Praveen Khilnani
`
`
`
`
`
`
`
`-
`
`Besides a description of available evidence and using my personal
`experience of mechanical ventilation of neonates and children for
`past 20 years I have taken the liberty of using the knowledge and
`experience of my teachers such as Prof HL Kaul (Professor of
`Anesthesiology, AIIMS, Delhi), Prof I David Todres (Professor of
`Anesthesiology and Pediatrics, Harvard University, Boston, MA),
`Prof William Keenan (Director of Neonatology, Glennon Children
`Hospital, at St Louis University, St Louis, MO), Prof Uday
`Devaskar (Director of Neonatology UCLA, CA), and authorities
`such as Dr George Gregory (CA), Dr Alan Fields (PICU, Childrens
`National Medical Center, Washington DC), Dr Robert Krone (PICU
`Boston Childrens Hospital, and ‘Director, Harvard International,
`Boston, MA), Robert Kacemarek (Director Respiratory Care at
`Mass, General Hospital, Boston, MA) and Dr Shekhar
`Venkataraman (PICU, Pittsburgh Childrens Hospital, Pittsburgh,
`
`PA).
`I would like to give special acknowledgement to my esteemed
`colleagues such as Dr S Ramesh (Anesthesiologist, Chennai),
`Dr Ramesh Sachdeva (PICU, Childrens Hospital of Wisconcin,
`Milwaul<ie,WI), Dr Meera Ramakrishnan (PICU, Ohio),
`Dr Sankaran Krishnan (Pediatric Pulmonologist, Cornell
`University, New York), Dr Balaramachandran (PICU, KKCT
`Hospital, Chennai), Dr Krishan Chugh (PICU, SGRH, Delhi), Dr
`S Singhi (PGIMER, Chandigarh), Dr S Udani (Hinduja Hospital,
`Mumbai), Dr S Ranjit (Apollo Hospital, Chennai), Dr Y -Govil
`(KGMC, Lucknow, UP), Dr S Deopujari (Nagpur), Dr Rajesh
`Chawla (MICU, IP Apollo Hospital, Delhi), Dr RK Mani (MICU,
`IP Apollo Hospital and Delhi Heart and Lung Institute, Delhi), Dr
`Rajiv Uttam (PICU, IP Apollo Hospital, Delhi), Dr Anjali Kulkarni
`
`
`
`xii Pediatric and Neonatal Mechanical Ventilation
`
`and Dr Vidya Gupta'(Neonatology, IP Apollo-Hospital, Delhi) and
`many other dear colleagues for constantly sharing their knowledge
`and experience in the field of neonatal and pediatric mechanical
`ventilation and providing their unconditional help with various
`national level pediatric ventilation workshops and CMEs.
`Finally, the acknowledgement is due to my family without whose
`wholehearted support this task could not have been accomplished.
`
`3 3
`
`
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`1
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`'
`
`
`
`
`
`1. Structure and Function of a Conventional Ventilator ...... ..1
`
`2. Mechanical Ventilation: Introduction and Physiology ....11
`
`3. Basic Fundamentals of Ventilation .......
`
`.............................1'7
`
`4. Initiation of Ventilation .......................
`
`...........................,.....22
`
`5. Maintenance of Ventilation ................................................. ..25
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`.6. Disease Specific Ventilation ..................................................29
`
`'7. Neonatal Ventilation ........................................_........................38
`
`8. Ventilator Management and Respiratory Care .................61
`
`9. Weaning from Mechanical Ventilation ...............................80
`
`10. Complications of Mechanical Ventilation ..........................85
`
`11. Advanced Modes of Ventilation ...........................................90
`
`12. Ventilator Graphics and Clinical Applications .............. 101
`
`13. High Frequency Ventilation ................................................ 125
`
`14. Noninvasive Ventilation .........
`
`......................................... .. 135
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`15. Inhaled Nitric Oxide ........................................................... ..'148
`
`16. Comrnonly Available Ventilators ...................................... 159
`
`Index ........................................................................................ .. I81
`
`
`
`P
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`
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`This chapter is intended to get the reader familiar with basic aspects
`of the ventilator as a machine and its functioning. This has
`important bearing in the management issues of a critically ill
`neonate and child requiring mechanical ventilation.
`
`VENTILATOFI
`
`A ventilator is an automatic mechanical device designed to move
`gas into and out of the lungs. The act of moving the air into and
`out of the lungs is called breathing, or more formally, ventilation.
`Simply, compressed air and oxygen from the wall is introduced
`in to a ventilator with a blender, which can deliver a set FiO2. This
`air oxygen mixture is then humidified and warmed in a humidifier
`delivered to the infant by the ventilator via the breathing circuit.
`Q’ The peak inspiratory pressure (PIP) or tidal volume (Vt), positive
`end expiratory pressure (PEEP), inspiratory time (Ti) and respiratory
`rate are set on the ventilator.
`‘
`‘ The closing of the exhalation valve initiates a positive pressure
`mechanical breath. At the end of the preset inspiratory time, the
`exhalation valve is opened, permitting theinfant to exhale. If this
`end is partly occluded during expiration a PEEP is generated in
`_ ‘tljieicircuitiproximal to the occlusion (or CPAP if the infant is
`breathing spontaneously). Expiration is passive and gas continues
`toiflowidelivering -the set ‘PEEP.
`
`Ventilator
`.[C§€§‘hii2té$§9r.-.
`
`
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`'5
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`
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`to provide a source of compressed air. An in—built
`
` “of lcornpréssed air, if’ available, can be used instead. It
`
`001
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`
`
`2 Pediatric and Neonatal Mechanical Ventilation
`
`draws air from the atmosphere and delivers it under pressure (50 _
`PSI) so that the positive pressure breaths can be generated.
`The compressor has a filter which should__be washed with tap
`water daily or as directed. If this is not done; it greatly increases
`the load on the compressor. The indicator on the compressor should
`always be in the green zone. It should not be placed too close to
`the wall as it may get overheated. There should be enough space
`to permit air circulation around it.
`
`3
`
`Control Panel
`
`The controls that are found on most pressure-controlled ventilators
`include the following:
`0 FiO2
`0 Peak inspiratory pressure: PIP (in pressure-controlled
`ventilators)
`0 Tidal volume / rnjnute volume (in volume-controlled ventilators).
`0 Positive end expiratory pressure (PEEP)
`0 Respiratory rate (R) '
`0
`Inspiratory time (Ti)
`0 Flow rate.
`
`The other parameters displayed on the ventilator include mean
`airway pressure (MAP), I:E ratio (ratio of the inspiratory time to
`expiratory time). The expired tidal volume will be displayed in all
`volume-controlled ventilators and some pressure-controlled
`ventilators.
`
`Newer ventilator models have digital display controls some
`ventilators also display waveforms, which show the pulmonary
`function graphically (see Chapter on Ventilator Graphics).
`
`Humidifier
`
`Since the endotracheal tube bypasses the normal humidifying,
`filtering and warming system of the upper airway the inspired
`gases must be warmed and humidified to prevent hypothermia,
`inspissation of secretions and necrosis of the airway mucosa.
`
`Types of humidifiers available
`1. Simple humidifier: It heats the humidified inspired gas to a set
`temperature, without a servo-control. The disadvantage is
`excessive condensation in the tubings with reduction in the
`
`I
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`..~.-.i.-.....»...¢:.-....,-..-.p.:a=.m.r--
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`002
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`Chapter 1: Structure and Function of a Conventional Ventilator 3
`
`humidity along with cooling of the gases by the time they reach
`the patient.
`2.. Servo-controlled humidifier with heated wire in the tubings.
`These prevent accumulation of condensate while ensuring
`adequate humidification. Optimal temperature of the gases
`, should be 36-37°C and a relative humidity of 70 percent at 37°C.
`the baby is nursed in the incubator temperature, monitoring
`must take place before the gas enters the heated field. At least
`some condensation must exist in the inspiratory limb which
`. shows that humidification is adequate. The humidifier chamber
`must be changed daily. It should be adequately sterilized or
`disposable chambers may be used.
`
`Breathing Circuit
`
`It is’ preferable to use disposable circuits for every patient. Special
`pediatric circuits are available in the market with water traps. If
`reusable circuits are used, they must be changed if visible soiling is
`seen. Reusable circuits are sterilized by gas sterilization or by
`immersion in 2 percent glutaraldehyde for 6-8 hours and then
`thoroughly rinsing with sterile water. Disposable circuits may be
`changed if visible soiling is seen.
`
`Terminology
`
`Ventilatory controls that can be altered in mechanical ventilation
`include the following:
`. Inspired oxygen concentration (FiO2)
`. Peak inspiratory pressure (PIP)
`. Flow rate (X./*)
`. Positive end—expiratory pressure (PEEP)
`. Respiratory rate (RR), or Frequency (f)
`. Inspiratory/expiratory Ratio (I:E Ratio)
`. Tidal volume (in volume—control1ed ventilators) (Vt)
`. Pressure support (PS)
`. Inspiratory time (Ti).
`
`Manipulation of Controls on the Ventilator
`
`An improvement in oxygenation may be accomplished either by
`increasing the inspired oxygen concentration (FiO2) or by different
`
`003
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`4 Pediatric and Neonatal Mechanical Ventilation
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`1. Increasing peak inspiratory pressure (PIP)
`2. Increasing inspiratoryl expiratory ratio (I:E Ratio)
`
`FiO2
`
`FiO2 is adjusted to maintain an adequate PaO2. High concentrations
`of oxygen can produce lung injury and should be avoided. The
`exact threshold of inspired oxygen that increases the risk of lung
`injury is not clear. A FiO2 of 0.5 is generally considered safe. In
`patients with parenchymal lung disease with significant
`intrapulmonary shunting, the major determinant of oxygenation
`is-lung volume, which is a function of the mean airway pressure.
`With a shunt fraction of > 20 percent oxygenation may not be
`substantially improved by higher concentrations of ‘oxygen.
`The administration of oxygen and its toxicity is a clinical problem
`in the treatment of neonates, especially low—birth weight infants.
`The developing retina of the eye is highly sensitive to any
`disturbance in its oxygen supply. Oxygen is certainly a critical factor
`(hyperoxia, hypoxia), but a number of other factors (immaturity,
`blood transfusions, PDA, vitamin E deficiency, infections) may
`interact to produce various degrees of retinopathy of prematurity
`(ROP).
`Another complication of oxygen toxicity induced by artificial
`ventilation in the neonatal period is a chronic pulmonary disease,
`bronchopulmonary dysplasia (BPD), mostly seen in premature
`infants ventilated over long periods with a high inspiratory peak
`pressure and high oxygen concentration.
`High oxygen concentration may play a role in the pathogenesis
`of BPD (bronchopulmonary dysplasia), but recent studies have
`shown, that the severity of the disease is correlated to the peak
`inspiratory pressure (PIP) during artificial ventilation rather than
`to the doses of supplementary oxygen (leading to stretch injury,
`volutrauma).
`
`Peak lnspiratory Pressure (PIP)
`
`Peak inspiratory pressure in the major factor in determining tidal
`volume in infants treated with time—cycled or pressure—cycled
`ventilators. Most ventilators indicate inspiratory pressure on the
`
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`‘9
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`004
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`
`Chapter 1: Structure and Function of a Conventional Ventilator 5
`
`The starting level of PIP must be considered carefully. Critical
`Factors that must be evaluated are the infants weight gestational
`degree of maturity), the type and severity of the disease
`mechanics such as lung compliance and airway resistance.
`The lowest PIP necessary to ventilate the patient adequately is
`In most cases, associated with increased tidal volume,
`lncreasned CO2 elimination and decreased PaCO2 will occur. Mean
`airway pressure will rise and thus improve oxygenation.
`, If,PIP is minimized, there is a decreased incidence of baro-
`trauma, air leak (pneumothorax and pneumomediastinum) and
`bronchopulmonary dysplasia (BPD).
`Hacker et at demonstrated that more rapid ventilator rates and
`lower PIP are associated with a decreased incidence of air leaks: a
`mode of ‘ventilation, which may be recommended in infants with
`congenital diaphragmatic hernia.
`High PIP may also impede venous return and lower cardiac
`output.
`
`Flow Rate (Cr)
`
`The flow rate is important determinant during the infant's
`mechanical ventilation of attaining desired levels of peak inspiratory
`pressure, wave form, l:E ratio and in some cases respiratory rate.
`In general, a minimum flow at least two times the minute volume
`ventilation is usually required. Most pressure ventilators operate
`at flows of 6-10 liters per minute.
`If low—flow rates are used, there will be a slower inspiratory
`time (Ti) resulting in a pressure curve of sine wave form and
`lowering the risk of barotrauma.
`Too low-flow relative to minute volume may result in
`hypercapnia and accumulation of carbon dioxide in the system.
`High inspiratory flow rates are needed if square wave forms
`are desired and also when the inspiratory time is shortened in order
`to maintain an adequate tidal volume. Carbon dioxide retention
`in the ventilator tubing will be prevented at high-flow rates.
`A serious side effect of high-flow rate is an increased risk of
`alveolar rupture, because maldistribution of ventilation results in
`a rapid pressure increase in the non-obstructed or non-atelectatic
`alveoli.
`
`005
`
`
`
`6 Pediatric and Neonatal Mechanical Ventilation
`
`Positive End Expiratory Pressure (PEEP)
`
`Positive pressure applied at the end of expiration to prevent a fall
`in pressure to zero is called positive end expiratory pressure (PEEP).
`PEEP stabilizes alveoli, recruits lung volume and improves the
`lung compliance." The level of PEEP depends on the clinical 3.
`circumstances. Application of PEEP results in a higher mean f
`airway pressure, and mean _lung volumes.
`'
`The goals of PEEP are:
`1. Increasing FRC above closing volume to prevent alveolar collapse
`2. Maintaining stability of alveolar segments
`3. Improvement in oxygenation
`4. Reduction in work of breathing.
`The optimum PEEP is the level at which there is an acceptable ‘Ii
`balance between the desired goals and undesired adverse effects.
`-
`The desired goals are:
`a. Reduction in inspired oxygen concenti-ation—nontoxic levels
`(usually less than 50%)
`b. Maintenance of Pa02 or Sa02 of > 60 mm Hg or > 90 percent
`respectively
`c. Improving lung compliance
`d. Maximizing oxygen delivery.
`Arbitrary limits cannot be placed to determine the level of PEEP
`or mean airway pressure that will be required to maintain adequate
`gas exchange. When the level of PEEP is high, peak inspiratory ;
`pressure may be limited to prevent it from reaching dangerous
`levels that contribute to air leaks and barotrauma. In children with
`
`=:
`
`tracheomalacia or bronchomalacia, PEEP decreases the airway
`resistance by. distending the airways and preventing dynamic
`compression during expiration.
`The compliance may be improved. Improved ventilation may
`result (improvement in ventilation/ perfusion ratio) by preventing
`alveolar collapse.
`Low levels of PEEP (2-3 cm H20) are often used during weaning
`from the ventilator in conjunction with low IMV rates only for a
`short amount of time.
`_
`-Medium levels of PEEP (4-7 cm H20 are commonly used in
`moderately ill patients).
`High levels of PEEP (8-10 cm H20 and higher benefit
`
`006
`
`
`
`
`
`Chapter 1: Structure and Function of a Conventional Ventilator 7
`
`volume, and PaO2 increases. Higher PEEP level can also reduce
`blood pressure and cardiac output explained by a reduced preload.
`high levels of PEEP result in over distention and alveolar
`leading to increased incidence of pneumothorax and
`1:}-1"=é'g_i>1(111omediastinum.
`Respiratory Rate (RR) or Frequency (f)
`Respiratory rate, together with tidal volume, determines the minute
`trentilation. Depending on the infant's gestational age and the
`urfderlydng disease, the resulting pulmonary mechanics (resistance,
`compliance), the use of slow or rapid ventilatory rates may be
`needed.
`(‘Moderately high ventilator rates (60-80 breaths per minute)
`employ a lower tidal volume and, therefore, lower inspiratory-
`pressures (PIP) are used to prevent barotrauma.
`3 High rates may also be required to hyperventilate infants with
`pulmonary hypertension and right—to left—shunting to achieve an
`' increased pH and reduced PaCO2 thereby reducing pulmonary
`arterial resistance and shunting associated with increased PaCO2.
`Respiratory rate is the primary determinant of minute ventilation
`and hence CO2 removal from lungs.
`Minute ventilation = Tidal volume x RR
`
`Increasing the RR lowers the PaCO2 level. A respiratory rate of
`‘40-60 is usually sufficient in most conditions. High rates are
`necessary in meconium aspiration syndrome (MAS) where CO2
`retention is a major problem. It must be recognized that increasing
`the RR while keeping the Ti the same shortens expiration and may
`lead to inadequate emptying of lungs and inadvertent PEEP.
`One of the major disadvantages in using the high ventilator
`rates is an insufficient emptying time during the expiratory phase,
`resulting in air trapping, increased functional residual capacity
`(FRC), and thus decreased lung compliance.
`_
`A slow ventilation rate combined with a long inspiratory time
`both in animals and infants with RDS resulted in fewer bronchiolar
`histological lesions, better lung compliance and in infants, a
`reduction in the incidence of BPD.
`
`007
`
`
`
`8 Pediatric and Neonatal Mechanical Ventilation
`
`
`
`
`
`1»;‘~:~.._._-_':_‘:'Jv‘
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`
`Ratio of lnspiratory to Expiratory Time (t:E Ratio)
`One of the most important ventilator controls and it is the ratio of
`inspiratory to expiratory time (I:E ratio). This ventilator control
`has to be adjusted depending on the pathophysiology and the course ‘
`of the respiratory disease, always with respect to pulmonary
`mechanics, such as compliance, resistance and time constant.
`In infants with, respiratory distress syndrome with decreased
`compliance but normal resistance, resulting in shortened time
`constants; inspiratory times (Ti with I:E ratios 1:1 are usually used).
`Reversed l:E'ratios, as high as 421 have been shown to result in i
`improvement in oxygenation and in a retrospective study decreased
`the incidence of BPD. Other investigators also advocated the use
`of prolonged inspiratory time, since infants in the ’2:1’ group
`required less inspired oxygen and a lower expiratory. pressure to
`achieve satisfactory oxygenation. Extreme reversed I:E ratio with
`a short expiratory time will lead to air trapping and alveolar
`distension. In addition, prolonged inspiratory time may adversely
`affect venous return to the heart and decrease pulmonary and
`systemic blood flow. The concept becomes especially important
`when higher respiratory rates are used.
`If inspiratory time is shorter than three to five time constants,
`inspiration will not be complete and tidal volume will be lower
`than expected except in patients receiving rates faster than 5 min.
`If expiratory time is too short, expiration will not be complete which
`will lead to air trapping.
`A Ti of 3-0.5 sec is sufficient for most disorders. In low
`compliance condition like RDS (respiratory distress syndrome) use
`closer to 0.5 sec. In disorders with increased airway resistance like
`MAS use shorter Ti._ Once set, Ti
`is usually not changed unless
`there is persistent hypoxemia unresponsive to changes in PIP and
`FiO2.
`Increasing the Ti shortens the expiratory time increasing the I:E
`ratio. Normal ratio is 1:3. Avoid 1:1 ratio to prevent air trapping.
`While ventilating a case of lower airways obstruction (asthma,
`bronchiolitis) use short Ti and slow rate as there is gas trapping
`and increased risk of air leaks.
`
`008
`
`
`
`
`
`Chapter 1: Structure and Function of a Conventional Ventilator 9
`
`'-lTidAal..Volume (Vt)
`lijiifiiiiost volume cycled ventilators tidal volume of 8 to 10 ml /kg
`set, or a particular flow rate and minute ventilation can be
`get a particular tidal volume. Siemens Servo 300 ventilator
`f:i'ieél"su.res expired tidal volume and gives a display. If set tidal
`15-20 percent higher than the expired tidal volume then
`leak or an endotracheal leak should be looked for and
`corrected.
`
`Piressure Support Ventilation
`"I
`Pressure support ventilation (PSV) is a form of assisted ventilation,
`where the ventilator assists a patient’s spontaneous effort with a
`mechanical breath with a preset pressure limit. The patient’s
`spontaneous breath creates a negative pressure, which triggers the
`ventilator to deliver a breath. The breath delivered is pressure-
`limited; very high inspiratory flow results in a sharp rise in inspi-
`ratory pressure to the preset pressure limit. The inspiratory pressure
`is'held constant by servo-control of the delivered flow and is
`_ terminated when a minimal flow is reached (usually < 25% of peak
`flow), just before spontaneous exhalation begins. Pressure-support
`"ventilation depends entirely on the patient’s effort, if the patient
`becomes apneic, the ventilator will not provide any mechanical
`_ breath. Pressure-support ventilation allows better synchrony
`between the patient and the ventilator than IMV, volume-assisted
`ventilation, or pressure control ventilation. Pressure-support allows
`ventilatory muscle loads to be returned gradually during the
`weaning process like IMV techniques. Since each breath is assisted,
`it alters the pressure volume relationship of the respiratory muscles
`in such a way as to improve its efficiency. With ventilatory muscle
`fatigue, muscles can be slowly retrained and titrated more efficiently
`than IMV and thus promote the weaning process. The emphasis
`with weaning with pressure support ventilation is endurance
`training of the respiratory muscles, especially, the diaphragm. The
`parameters that can be manipulated to the titrate the muscle
`loading are the magnitude of the trigger threshold and the preset
`pressure limit. PEEP is provided to maintain FRC and prevent
`alveolar collapse. The amount of pressure-support to be provided
`depends on the clinical circumstance. A pressure—lirnit that delivers
`
`009
`
`
`
`10 Pediatric and Neonatal Mechanical Ventitation
`
`level respiratory work can be reduced to zero. It is not necessary to
`provide PSV max at the beginning. The level of pressure support
`selected should allow for spontaneous respiration without undue
`exertion and still result in normal minute ventilation. No strict
`criteria can be established; it has to be applied and ‘titrated on an
`individual basis. Weaning of pressure-support ventilation is
`accomplished by reducing the pressure-lirnit decrementally. With _
`each wean, the effect of weaning on muscle loading has to be
`evaluated clinically. Increase in respiratory rate isan early
`indication of increasing muscle load. Retraction and use of
`accessory muscles would indicate a more severe muscle load. If
`respiratory rate increases during the weaning process, the level of
`pressure-support should be increased until there is reduction in
`the respiratory rate. While this method of weaning is attractive
`theoretically, its benefit in the weaning process is yet to be
`established in infants and children. A relative contraindicatiortto
`the use of pressure-support ventilation is a high baseline
`spontaneous respiratory rate. There is a finite lag time involved
`from the initiation of a breath to the sensing of this effort and from
`the sensing to the delivery of a mechanical breath. In infants
`breathing at a relatively fast rate (40 to 50 breaths/minute), this
`lag time may be too long and result in synchrony between the
`patient and the ventilator. Pressure—support has been mainly used
`to wean adult patients off mechanical ventilation. Its use in
`pediatrics is gaining popularity. When used at our institution, we
`tend to keep a base line low SIMV rate (5 to 6 per min) along with
`pressure support before extubation.
`‘
`
`SUMMARY
`
`Understanding the structure and the capability of the ventilator is
`important. One should get familiar with the control panel to set
`the initial ventilator settings without hesitation. Turning on, off,
`connecting the ventilator tubings and humidifier, and setting the
`alarms is essential part to be mastered by all users.
`
`010
`
`
`
`
`
`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 the ventilatory
`modes and settings.
`Upper airway in children is cephalad, funnel—shaped with
`narrowest area being subglottic (at the level of cricoid ring), as
`compared to adults where the upper airway is tubular with
`narrowest part at the vocal cords} Airway resistance increases
`inversely by 4th power of radius; i.e. in an already small airway
`' even one mm of edema or secretions will increase the -airway
`resistance and turbulent flow markedly necessitating treatment of
`. ' airway edema, suctioning of secretions, measures to control
`« secretions (Fig. 2.1). Low functional residual capacity (FRC: Volume
` 0f_.air in the lungs at end of expiration) reduces the oxygen reserve,
`reduces‘ the time that apnea can be allowed in a child.
`‘_‘Respirations are shallow and rapid due to predominant
`breathing, and inadequate chest expansion due to
`inadequate costovertebral bucket handle movement in children.
`'lfl'leg;efore,_a child tends to get tachypneic rather than increasing
`of respiration in response to hypoxemia. Oxygen
`.%gn§Emp_fion/ kg body weight is higher, therefore, tolerance to
`is lower.
`to bradycardia in response to hypoxemia is also
`i to high vagal tone. Pores of Kohn and channels of
`
` I -""-".‘—.1p;4;1l3.f-.?-r.”c;'-1.;(bronchoalveolar and interalveolar collaterals) are
`an
`5...-'5
`'
`linadéquately developed making regional atelectasis more frequent?
`volumes are lower and airway collapse due to inadequate
`
`
`
`
`
`011
`
`
`
`12 Pediatric and Neonatal Mechanical Ventilation
`
`
`
`(A) Adult airway (cylindrical) and (B)
`(b) Infant airway (funnei-shaped)
`
`{
`
`A)
`
`Normal
`
`Edema
`
`1 mm
`
`Resistance
`
`)(-Sect
`
`1
`<R='';;a'r;;a''')
`16):
`
`“'83
`
`1 75%
`
`‘$1
`
`I
`
`1 44%
`
`I 3x
`
`Fig. 21: Pediatric airway resistance diiterence (from adult)
`
`_
`
`particularly susceptible to laryngomalacia, and tracheo—broncho- _
`malacia 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 :7‘:
`ventilatory setting include the primary pathology, i.e. asthma,
`ARDS, pneumonia, airleak syndrome raised intracranial tension,
`neuromuscular weakness, neonatal hyaline membrane disease, or
`neonatal persistent pulmonary hypertension (PPHN).
`
`1.
`T‘;
`ii
`;i
`
`012
`
`
`
`
`
`Chapter 2: Mechanical Ventilation: Introduction and Physiology 13
`
`Basic Physiology“
`
`Gradient between mouth and pleural space is the driving pressure
`for the inspired gases, and this gradient is needed to overcome
`resistance and to maintain alveolus 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.
`
`Ventilation
`
`Ventilation washes out carbon dioxide from alveoli keeping arterial
`PaCO2 between 35-45 mm of Hg. Increasing dead space increases
`the PaCO2.
`
`PaCO =
`2
`
`k x Metabolic production
`Alveolar minute ventilation
`
`Alveo