2018 ventilator book

Medicineisanever-changingdisciplineandthesubjectmatterofthisbookisno
exception. While the author has done his best to ensure that this book reflects
contemporary evidence-based practice, new developments in the field may
supersede the material published here. Only properly trained and licensed
practitioners should provide medical care to patients with respiratory failure.
Nothing in this book should be construed as advice regarding the care of a
specificpatientorgroup.
Copyright©2018,2012byWilliamOwens,MD
Allrightsreserved.Thisbookoranyportionthereofmaynotbereproducedor
used in any manner whatsoever without the express written permission of the
publisherexceptfortheuseofbriefquotationsinabookreview.
SecondEdition
CoverDesignbyLorienOwens
PublishedbyFirstDraughtPress
Columbia,SC
ISBN978-0-9852965-4-4
PrintedintheUnitedStatesofAmerica


ToLorien,mybestfriendandwife,
AndtoWilliam,Zach,andAmelia,thebestkidsIcouldeverhopetohave.


TableofContents
Introduction

PhilosophyofMechanicalVentilation
Chapter1:InitialSettings
Chapter2:QuickAdjustments
Chapter3:Troubleshooting
Chapter4:TheElevenCommandmentsofMechanicalVentilation
Chapter5:AcuteRespiratoryFailure
Chapter6:MonitoringoftheVentilatedPatient
Chapter7:ArterialBloodGasAnalysisfortheCompleatIdiot
Chapter8:Assist-ControlVentilation
Chapter9:SynchronizedIntermittentMandatoryVentilation
Chapter10:PressureSupportVentilation
Chapter11:PEEPandCPAP
Chapter12:TriggerandFlow
Chapter13:HighFrequencyOscillatoryVentilation
Chapter14:AirwayPressureReleaseVentilation
Chapter15:LiberationfromMechanicalVentilation
Chapter16:ProlongedRespiratoryFailure
AppendixofUsefulKnowledge
References
Acknowledgements
AbouttheAuthor


Introduction
So, here you are in the Intensive Care Unit at 3:30 in the morning. The
Emergency Department has just admitted a patient to your service—a young
manwitharathersuddenonsetoffever,rigors,andrespiratorydistress.Hehad
tobeintubatedintheEDandtheventilatorseemstobealarmingwithanerveracking frequency. His chest X-ray looks horrible, with diffuse infiltrates and
consolidations.TheICUrespiratorytherapistlooksatyouandasksthequestion
youhavebeendreadingsincethepatientarrived—“Doctor,whatventsettings

doyouwant?”
ThisisafamiliarstoryforthoseofuswhospendalotoftimeintheICU,
andanexperiencethatjustabouteveryresidenthasatleastonceduringhisor
her training. Mechanical ventilation can be intimidating—it has its own
terminology,notallofwhichmakessense;it’salife-sustainingtechnology,and
misapplication can have serious consequences; and practitioners of mechanical
ventilationtendtotalkinesotericwaysaboutwhattheventilatorisdoing.This
canconfuseeventhesmartestresidentormedicalstudent.
To make things worse, there aren’t a lot of practical resources for busy
physicianswhojustneedsomequickguidanceonhowtoadjusttheventilator.
Don’t get me wrong—there are plenty of great textbooks on mechanical
ventilation. And, if you have the time, they are well worth reading. The
operative word, however, is “time.” Reading a hundred pages on the pros and
cons of pressure control ventilation may be a good use of an afternoon in the
library but it’s wholly impractical while taking care of patients in a busy ICU.
What’snecessaryisahow-toguide,andthat’swhyI’vewrittenthisbook.Since
there’sonlyoneauthor,thisbookwillbebiased.Nottoomuch,Ihope,butI’m
not delusional enough to think that my approach is completely objective and
basedinfact.Likeeveryoneelseinmedicine,personalanecdoteandexperience
hasshapedmypractice.
The first part of this user’s manual is designed to help you make good
decisions quickly. It is broken down into clinical problems with a proposed
approach for each. This is something that you can use on the fly. It closes out
withtheElevenCommandmentsofMechanicalVentilation.
The second part of the book is intended to teach you about mechanical
ventilation. The chapters are short, and each can be read easily within 15-20


minutes. Here, you’ll learn to speak the language and understand the rationale
forwhythingsworkandwhyintensivistsdowhattheydo.

Atthispoint,it’snecessaryformetopointoutthatwhilethisbookischockfull of great advice, none of it is specific to the care of any individual patient.
Haveanyofyourfacultyevertoldyouthatthepatientsdon’treadthetextbook?
They’reright.Everypatientneedsanindividualizedapproach.Believeitornot,
mylawyerdidn’tmakemewritethis.It’sjustcommonsense.


Philosophyof
MechanicalVentilation
TheartofmedicineconsistsofamusingthepatientwhileNaturetakesitscourse.
—Voltaire
Mechanicalventilationisawonderfultool.Thebirthofmodern-daycritical
care occurred in Copenhagen in 1952, when Bjorn Ibsen realized that positive
pressureventilationcouldsavelivesduringapolioepidemicwhentheironlungs
(a negative pressure ventilator) were failing. The most common reason for
admissiontoamedicalintensivecareunitistheneedformechanicalventilatory
support. The combination of endotracheal intubation and positive pressure
ventilationhaslikelysavedhundredsofthousands,ifnotmillions,oflives.
Likewise,artificialventilationhasprolongedthelivesofthousandsofpeople
afflicted with spinal cord injuries and devastating neuromuscular diseases.
Ventilators attached to wheelchairs permit patients with these conditions to
engageinlife,topursuetheirinterests,andtogenerallylivelivesthatwouldnot
have been possible a half-century ago. Truly, this invention has had a positive
effectonmany,manypeople.
As is the case with any technology, however, there is the potential for
misuse. It is essential that anyone working in an intensive care unit remember
the Third Commandment—that the ventilator is a means of support, and not a
cureforanycondition.Inotherwords,itisfollytobelievethattheapplicationof
mechanicalventilationcanreversechroniclungdisease,malignancy,congestive
heartfailure,oranyofthemyriaddiseasesandinjuriesthatresultinrespiratory
failure.Theventilatorexiststomaintaintherespiratoryandmetabolicfunctions

ofthelungsuntilthepatientrecoversfromhisorherillness.Itcannotmakethe
patient better by itself. This is actually a point lost on many physicians, who
believe that small tweaks and adjustments to the ventilator will accelerate the
patient’srecoveryfromacuterespiratoryfailure.
If it is important for physicians to understand the natural history and
trajectoryofapatient’sdisease,itisequallyimportantthatthephysicianpresent
this information to the patient and his family in concise, understandable, and
evenbluntterms.Alifespentconnectedtoaventilatormaybeacceptabletoa
patient with amyotrophic lateralizing sclerosis, who may require mechanical


ventilationbutcanotherwisespeak,interact,andengageinwhatheconsidersan
acceptablequalityoflife.Itisadifferentmatterentirelyforapatientsuffering
from a massive intracerebral hemorrhage who is comatose, and is expected to
remaincomatosefor,ifnottherestofhislife,agreatdealofit.Whilethepatient
or his family may consider this to be a worthwhile existence, it behooves the
physician to inform them of the stark realities of preserved life on a ventilator
(including the medical, social, and financial ramifications) before they pursue
thistreatmentoption.
So,whatisadedicated,caringphysician,nurse,orrespiratorytherapist
todo?Unsubstantiatedoptimismcanbeharmful,butsocanoverlypessimistic
nihilism. Most patients with respiratory failure who recover from the inciting
illness or injury will recover; true ventilator dependence, meaning a need for
mechanicalventilationmorethanayearafterward,israre.Here’swhatwecan
do:
1. Protectthelungfromiatrogenicinjury.Useanevidence-andphysiologybasedapproachtoventilatorsettings.
2. Promptlyandaggressivelytreattheincitingillnessorinjury.
3. Nodiseaseiseffectivelytreatedwithstarvation.Propernutritionalsupport
isveryimportant.
4. Peoplearen’tmeanttolieinbedallday.Unlessthepatientiscomatose,in

shock,orhasprofoundrespiratoryfailure,it’stimetostartgettinghimout
ofbedandintoachair.Walking,even.I’lladdthatthis,ofcourse,requires
astrongdoseofcommonsense.Mobilizingapatientwithanopensternum
mightnotbeagoodidea.But,it’ssurprisinghowmanypatientslieflaton
theirbacksfortheirentireICUstay.Nothealthy.
5. Whenthepatientseemstoberecovering,startassessinghisreadinessfor
extubationeveryday.
6. Bepatient.Itmighttakelongerthanyouthink.
7. Onceit’sevidentthatthepatientwillrequireprolongedmechanical
ventilation,getonwiththetracheostomy.There’snoneedtowaitan
arbitrarynumberofdays.
8. PayattentiontothelittlethingslikeDVTprophylaxis,skincare,and
preventingdelirium.
9. Bepatient.And….
10. Rememberthatyourpatientisafellowhumanbeingwithwants,needs,
cares,andconcernsthatmaybestrikinglysimilartoyourown.Hedeserves
tobespokento,evenifhecan’tspeakback.Hedeservesrespect,even
thoughhemaynotbeabletoreturnthatrespect.Hedeservesthebasicsof


humankindnessandtouch.Rememberthathehasplacedhislifeinyour
hands.Yourjobisnotaneasyone,andnotonethatmostpeoplecando.
Therecognitionthatyouhavepositivelyaffectedthelifeofanotherperson
inawaythatfewcanisthegreatestrewardofthisgreatprofession.


Chapter1
InitialSettings
*Note on measurements—unless otherwise specified, all airway pressures are
measured in cm H 2O. All tidal volumes are expressed as mL/kg of predicted

bodyweight(PBW).

ModesofVentilation
There are several different modes of ventilation, and each ventilator
manufacturer has its own (usually trademarked) name for them (PRVC, VC+,
CMVwithAutoflow,ASV,PAV,VolumeSupport,andthelistgoesonandon).
Thiscanbeintimidatingatfirst—who’stoknowwhattopick?Fortunately,like
medications,allofthesehaveagenericnameaswell.That’sallyoureallyneed
toknow,becauseallofthemodesonthedifferentventilatorsavailableforsale
willbeessentiallythesame(justwithadifferenttradename).
Each mode of ventilation has its strengths and weaknesses. No mode is
perfect, and no mode is useless. It’s best to pick the mode that best suits the
patient’sneedsatthetime.Eachofthesemodesisdiscussedinmoredetailinthe
followingchapters,buthere’sabriefoverview.

Assist-ControlVentilation
Assist-ControlVentilationisthemodeofchoiceinmostcircumstances.Itallows
the ventilator to essentially take over the work of breathing and is preferred
whenapatienthasacutecardiacorrespiratoryfailure.Itprovidesfullrespiratory
support.Ifthepatientwantstobreatheoverthesetrate,hecan;whenhetriggers
theventilator,hegetsthefullbreathwithminimaleffort.
Upside: Takes over the work of breathing; clinician can choose to set a tidal
volume(volumecontrol)oraninspiratorypressure(pressurecontrol).
Downside:Atachypneicpatientwillgetthefulltidalvolumeoneverybreath,so
without adequate sedation this could lead to significant respiratory alkalosis or


airtrapping.ThiscanbeaprobleminpatientswithCOPDorasthma.

SIMVwithPressureSupport

SIMValsocanprovidefullventilatorsupportandisaverypopularmode.Like
AssistControl,thecliniciancanchooseatidalvolumeoraninspiratorypressure.
ThemajordifferencebetweenSIMVandAssistControliswhathappenswhen
thepatientinitiatesabreath—inA/C,hegetsthefulltidalvolume;inSIMV,he
getswhateverhecanpull(usuallywiththehelpofpressuresupport).
Upside: Can take over the work of breathing but allows the patient more
spontaneousbreathingthaninassist-control.Canbeusefulforweaningsupport
gradually.
Downside:Ifthemachinerateisnotsethighenough,anunstablepatientcanget
fatigued due to excessive work of breathing. If the pressure support is not set
highenough,spontaneousbreathsmaybefastandshallow,whichalsoleadsto
fatigue.

PressureSupportVentilation
PSVdoesn’thaveasetrate—instead,itallowsthepatienttobreatheonhisown
and “boosts” each breath with a pressure that the clinician selects. It’s used in
conjunctionwithCPAPtoimprovealveolarrecruitment.PSVisusedinpatients
who are either intubated for reasons other than cardiac or respiratory failure
(altered mental status, jeopardized airway) or for weaning. It can also be used
when the patient has a severe metabolic acidosis—if he has a pH of, say, 6.88
andaHCO3of4,hisrespiratorydrivewillbemarkedlyelevatedandamodelike
assist-controlmaynotbeabletomeethismetabolicdemands.
Upside:Allowsthepatienttosethisownrateandpatternofbreathing,whichis
morecomfortable;spontaneousbreathinghassalutaryeffectsonhemodynamics
andVQmatching.
Downside: There’s no backup rate, so if the patient goes apneic nothing will
happenuntilthealarmssound.Unstablepatientswillfatiguerapidlyifthework
ofbreathingisimposedonthem,evenwithhighlevelsofpressuresupport.

UnconventionalModes
Airway pressure release ventilation (APRV) and high frequency oscillatory
ventilation (HFOV) are used to treat severe hypoxemia. They are seldom the
first-line option for acute respiratory failure and will be discussed later in the
book.Fornow,justfocusonthemodesalreadylisted(A/C,SIMV,PSV).

VentilatorSettingsBasedonPathophysiology
RestrictiveLungDisease
Examples: ARDS, aspiration pneumonitis, pneumonia, pulmonary fibrosis,
pulmonaryedema,alveolarhemorrhage,chesttrauma
Restrictive lung diseases are associated with a reduction in respiratory system
compliance.Thelungswanttocollapse.Inotherwords,it’shardtogetairinand
easy to get air out. The ventilation strategy is to recruit vulnerable alveoli,
prevent cyclical alveolar closure, provide adequate oxygenation, and to
minimizevolutraumafromoverdistension.
The initial mode should be one that takes over the work of breathing for the
patient. Assist-control, using either volume-controlled or pressure-controlled
ventilation,isthemodeofchoice.
Forvolume-controlledventilation:
1. Tidalvolumeof6mL/kgPBW
2. Rateof14-18breathsperminute,withadeceleratingflowpattern
3. FiO2100%atfirst;reduceto60%ifSpO2≥88%
4. PEEPof5-10cmH2O,dependingonthedegreeofhypoxemia.Remember,
themoreopacificationinthelungsonthechestX-ray,themorePEEPwillbe
neededtoreduceintrapulmonaryshunting.
5. Ifhypoxemiapersists,increasethePEEPuntiltheSpO2is88%orbetter.
Don’texceed20.
6. AfteradjustingthePEEP,checktheplateaupressure.IfthePPLATismore
than30cmH2O,decreasethetidalvolumeuntilthePPLATislessthan30.
Don’tgobelow4mL/kgPBW.

Forpressure-controlledventilation:
1.
2.
3.
4.
5.

PEEPof5-10cmH2O,dependingonthedegreeofhypoxemia
FiO2100%;reduceto60%ifSpO2≥88%
Drivingpressure(orinspiratorypressure)of15cmH2O
Rateof14-18breathsperminute
InspiratorytimeadjustedtokeeptheI:Eratio1:1.5orhigher.TheI-timeis
usually1.0-1.5seconds.Arateof20andanI-timeof1.0secondshasanI:E
ratioof1:2(onesecondinspiration,twosecondsexpiration).Arateof15
withan
I-timeof1.5secondshasanI:Eratioof1:1.67(1.5secondsinspiration,2.5
secondsexpiration).Thisisdisplayedontheventilatorscreen.
6. Ifhypoxemiapersists,increasethePEEPuntiltheSpO2is88%orbetter.
Don’texceed20cmH2O.
7. Lookattheexhaledtidalvolume.Ifitexceeds6mL/kg,lowerthedriving
pressureuntilthetidalvolumeisinthe4-6mL/kgrange.
Afterinitiatingventilation,checkanarterialbloodgas.15-20minutesisenough
timeforgasexchangetoequilibrate.
MakechangesintherespiratoryratetochangethePaCO2(ahigherratelowers
thePaCO2 , and vice versa). Leave the tidal volume in the 4-6 mL/kg range,
keepingthePPLAT(volume-control)orPINSP(pressurecontrol)at30cmH2Oor
less.Rememberthatlungprotectionismoreimportantthannormalventilation—
a pH of 7.15 or better is acceptable and it’s not worth injuring the lungs with

overdistension(intheformofhightidalvolumes)togetanormalpHorPaCO2.
Lower the FiO2 , keeping the PaO2between 55 and 70 mm Hg and the SpO2
between 88% and 94%. There’s nothing to gain from keeping the PaO2above
thisrange,withfewexceptions.Patientswithtraumaticbraininjurysometimes
require a higher PaO2 , usually in conjunction with brain tissue oxygen
monitoring.Victimsofcarbonmonoxidepoisoningalsobenefitfrombreathing
100%oxygen.

ObstructiveAirwaysDisease
Examples:COPD,Asthma


Obstructive lung disease is associated with an increase in respiratory system
compliance and an obstruction to expiratory airflow. It’s easy to get air in, but
hardtogetitout.
The ventilation strategy is to rest the respiratory muscles, provide adequate
oxygenation,andreducehyperinflation.
Assist-control ventilation is usually the mode of choice, and volume-control is
preferabletopressure-control.SIMVwithPScanalsobeused,however,aslong
as the rate and PS are set high enough to prevent tachypnea and fatigue. High
airwayresistanceandhighpeakinspiratorypressurescharacterizeexacerbations
ofCOPDandasthma,eventhoughthePPLATmaybesignificantlylower.Using
pressure-controlinthissituationleadstoverylowtidalvolumes.Volume-control
guaranteesthatthedesiredtidalvolumewillbedelivered.
1. Tidalvolumeof8mL/kgPBW.Lowertidalvolumescanleadtoairtrapping
andworseninghyperinflation.
2. Rateof10-14breathsperminute
3. InspiratorytimeadjustedtokeepanI:Eratioof1:3orhigher.Inobstructive
airwaysdisease,airgetsineasilybuthasahardtimegettingoutdueto
narrow,inflamedbronchiolesandbronchi.Givetheairsometimetoescape.

4. Withasthma,appliedPEEPwillworsenhyperinflation.WithCOPD,PEEP
canbeusedtosplintopenairwaysthatarepronetocollapse.Thisisbecause
COPDischaracterizedbydynamicairwayobstruction,whiletheobstruction
isfixedinanasthmaexacerbation.AgoodstartingpointforbothisaPEEPof
0,orZEEP—zeroappliedend-expiratorypressure.
5. FiO2of100%tostart;lowerthisto60%aslongastheSpO2remains88%or
better.
Sometimes, patients with COPD or asthma will remain tachypneic despite
adequatesedation.Inassist-control,everypatient-triggeredbreathdeliversafull
tidalvolume,andthiscanleadtoairtrappingorsevererespiratoryalkalosis.If
thisisthecase,switchingthemodetoSIMVmayhelp.

SevereMetabolicAcidosis
Examples: Salicylate poisoning, septic shock, toxic exposures, acute renal
failure,diabeticketoacidosis


The normal response of the respiratory system in the setting of metabolic
acidosis is to hyperventilate. CO2 is a volatile acid and the lungs can rapidly
eliminatethisacidfromthebodyinanattempttobringthepHclosertonormal.
InapatientwithaHCO3of4mEq/L,forexample,thePaCO2willbe14-15mm
Hg if there’s appropriate respiratory compensation. This requires a very high
minuteventilationtoaccomplish.
Itisverydifficulttosettheventilatortoprovideahighminuteventilation,even
ifyousettheratetobe30-35andthetidalvolumetobe800-1000mL.Patients
with severe metabolic acidosis will often breathe in when the vent is trying to
breathe out, and vice versa—this leads to significant patient-ventilator
dyssynchrony and alarming of the machine. More consequentially, the volume
and pressure alarms that are normally helpful will actually work against the
patientbylimitingtheminuteventilationthatcanoccur.

Consider the aforementioned example—a patient who has a pH of 6.88 and a
HCO3of4needsaPaCO2of1415.Ifhe’sintubatedandsedated,andthevent
settingsareputinthe“usual”range,hisPaCO2mayriseto25-30.Inthesetting
ofsevereacidemia, thisincreaseinCO2will cause his pH to fall to 6.6 or so,
whichwillmostlikelyleadtoacardiacarrest.
The best way to deal with this situation is to let the patient’s naturally high
respiratorydriveworkinhisfavor.
1. Usethebareminimumofsedationtointubateandavoidneuromuscular
blockersentirely.
2. SettheventmodetobePressureSupportVentilation.
3. CPAP(a.k.a.PEEP)5-10cmH2O,dependingonthedegreeofhypoxemia
4. PressureSupport(PS)of10-15cmH2O.Adjustifneededtoallowthepatient
tobreathecomfortably;mostofthetime,10cmisenoughPS.
5. Allowthepatienttohaveaminuteventilationof18-25L/min.Don’tbe
alarmedtoseehimpullspontaneousvolumesof1000-2000mL.Thehigh
minuteventilationwillkeepthepHupwhilethecauseofthemetabolic
acidosisisbeingtreated.

KeyVentilatorConceptsforOtherClinicalSituations
TheleftventriclelikesPEEP—increasingtheintrathoracicpressurelowers


preloadandafterload,whichisbeneficialinacutecardiacfailureduetoleft
ventriculardysfunction(eithersystolicordiastolic).
The right ventricle, on the other hand, doesn’t care for PEEP very much.
Increasedintrathoracicpressurecanincreasepulmonaryvascularpressures
and stress the thin-walled RV. In situations where RV failure is present
(massive pulmonary embolism, worsening pulmonary hypertension), use
moreFiO2andlessPEEP(ideally10cmorless)tomaintainoxygenation.
Whenthereisacutebraininjury,beitfromstroke,hemorrhage,trauma,or

somethingelse,theprioritywithmechanicalventilationisthemaintenance
of adequate oxygenation. Aim for an SpO2of 94-98% and a PaO2of 80100mmHg.PEEPmayincreasetheintracranialpressure,butitseemstobe
significant only when the PEEP is 15 cm or higher. Hypoxemia, on the
otherhand,definitelyincreasesintracranialpressure.Therefore,usewhatit
takestomaintainadequatecerebraloxygenation.
Hyperventilation(PaCO2<32)lowersintracranialpressure,butitworksby
causing cerebral vasoconstriction. In other words, it works by making the
brainischemic.Thismaybehelpfulifapatientisabouttoherniateandyou
need 5 minutes to get the mannitol in, or 10 minutes to get to the OR.
Prolongedhyperventilation,ontheotherhand,worsensbrainischemiaand
hasnolastingeffectonintracranialhypertension.Aimforanormal(35-40)
PaCO2.


Chapter2
QuickAdjustments

These are ways to adjust the ventilator based on the arterial blood gas.
Obviously, the patient’s condition should dictate what’s done. The adjustments
areinorderofpreference.

PaO2TooLow
Assist-Control,SIMV:increasePEEP,increaseFiO2
APRV:increasePHIGH,increaseTHIGH,increaseFiO2
HFOV:increasemeanairwaypressure,increaseFiO2

PaCO2TooHigh
VolumeAssist-ControlorSIMV:increaserate,increasetidalvolume
PressureAssist-ControlorSIMV:increaserate,increasedrivingpressure
APRV: increase the gradient between PHIGH and PLOW , decrease THIGH ,

increaseTLOW
HFOV:decreasethefrequency,increasetheamplitude,increaseTI%,allowa5
cmcuffleak

PaCO2TooLow


VolumeAssist-ControlorSIMV:decreaserate,lowertidalvolume
PressureAssist-ControlorSIMV:decreaserate,lowerdrivingpressure
APRV:increaseTHIGH,lowerPHIGH,decreaseTLOW
HFOV:increasethefrequency,lowertheamplitude,decreaseTI%


Chapter3
Troubleshooting

These are problems that you’ll be called about. As always, the first thing you
should do is examine the patient. Remember your ABCs and use this guide to
helpyoufigureoutwhat’swrong.

Problem:HighPeakAirway(PAW)Pressures
Yourfirststepshouldbetoperformaninspiratorypauseandmeasuretheplateau
pressure (PPLAT ). The plateau pressure represents the alveolar pressure, while
the peak pressure is a combination of the alveolar pressure and airway
resistance.