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Figure7-7 Algorithmfortheevaluationofsyncope.ARVD,arrhythmogenicrightventriculardysplasia;EPS,electrophysiology
study;ICD,implantablecardioverter–defibrillator.(ModifiedfromStrickbergerSA,BensonDW, Biaggioni I,et al.AHA/ACCF
scientific statement on the evaluation of syncope from the American Heart Association Councils on Clinical Cardiology,
Cardiovascular Nursing, CardiovascularDisease inthe Young, and Stroke, andthe Quality of Care andOutcomes Research
InterdisciplinaryWorking Group; andtheAmericanCollegeof Cardiology Foundation inCollaboration withthe Heart Rhythm
Society. J Am Coll Cardiol. 2006;47(2):473-484. Copyright © 2006 American College of Cardiology Foundation. With
permission.)
TREATMENT
Therapy is tailored to the underlying etiology of syncope with goals of preventing recurrence and
reducingriskofinjuryordeath.
Neurocardiogenicsyncope
Counsel patients to take steps to avoid injury by being aware of prodromal symptoms and
maintainingahorizontalpositionatthosetimes.
Avoidknownprecipitantsandmaintainadequatehydration.
Employisometricmusclecontractionduringprodrometoabortasyncopalepisode.
Evidencesuggeststhatβ-adrenergicblockersareprobablyunhelpful;selectiveserotoninreuptake
inhibitorantidepressantsandfludrocortisone havedebatable effect;midodrine(initiatedat5 mg
PO tid and can be increased to 15 mg tid) is probably helpful in treatment of neurocardiogenic
syncope.
33-35
Ingeneral,PPMshavenoprovenbenefitinthemanagementofneurocardiogenicsyncope.However,
permanent dual-chamber pacemakers with hysteresis function (high-rate pacing in response to a
detectedsudden drop inheartrate) have beenshowntobe useful inhighly selected patients with
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recurrentneurocardiogenicsyncopewithaprominentcardioinhibitorycomponent.
36
Cardiacpacingforcarotidsinushypersensitivityisappropriateinsyncopalpatients.
Ingeneral,neurocardiogenicsyncopeisnotassociatedwithincreasedriskofmortality.
Orthostatichypotension
Adequatehydrationandeliminationofoffendingdrugs.
Saltsupplementation,compressivestockings,andcounselingongradualpositionchanges.
Midodrineandfludrocortisonecanhelpbyincreasing systolic BPandexpanding plasma volume,
respectively.
Cardiovascular(arrhythmiaormechanical)
Treatment of underlying disorder (valve replacement, antiarrhythmic agent, coronary
revascularization,etc.)
Cardiacpacingforsinusnodedysfunctionorhigh-degreeAVblock
DiscontinuationofQT-prolongingdrugs
CatheterablationproceduresinselectpatientswithsyncopeassociatedwithSVT
ICDfordocumentedVTwithoutcorrectablecauseandforsyncopeinthepresenceofsignificantLV
dysfunctionevenintheabsenceofdocumentedarrhythmia
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16. TchouP,YoungP,MahmudR,etal.Usefulclinicalcriteriaforthediagnosisofventricular
tachycardia.AmJMed.1988;84:53-56.
17. AntiarrhythmicsVersusImplantableDefibrillators(AVID)Investigators.Acomparisonof
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ventriculararrhythmias.NEnglJMed.1997;337:1576-1583.
18. MossAJ,HallWJ,CannomDS,etal.Improvedsurvivalwithanimplanteddefibrillatorinpatients
withcoronarydiseaseathighriskforventriculararrhythmia.MulticenterAutomaticDefibrillator
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20. MossAJ,ZarebaW,HallWJ,etal.Prophylacticimplantationofadefibrillatorinpatientswith
myocardialinfarctionandreducedejectionfraction.NEnglJMed.2002;346:877-883.
21. DorianP,CassD,SchwartzB,etal.Amiodaroneascomparedwithlidocaineforshock-resistant
ventricularfibrillation.NEnglJMed.2002;346:884-890.
22. HjalmarsonA,ElmfeldtD,HerlitzJ,etal.Effectonmortalityofmetoprololinacutemyocardial
infarction.Adouble-blindrandomisedtrial.Lancet.1981;2:823-827.
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25. DargieHJ.Effectofcarvedilolonoutcomeaftermyocardialinfarctioninpatientswithleftventriculardysfunction:theCAPRICORNrandomisedtrial.Lancet.2001;357:1385-1390.
26. AjijolaOA,LelloucheN,BourkeT,etal.Bilateralcardiacsympatheticdenervationforthe
managementofelectricalstorm.JAmCollCardiol.2012;59(1):91-92.
27. CuculichPS,SchillMR,KashaniR,etal.Noninvasivecardiacradiationforablationofventricular
tachycardia.NEnglJMed.2017;377:2325-2336.
28. StrickbergerSA,BensonDW,BiaggioniI,etal.AHA/ACCFscientificstatementontheevaluation
ofsyncopefromtheAmericanHeartAssociationCouncilsonClinicalCardiology,Cardiovascular
Nursing,CardiovascularDiseaseintheYoung,andStroke,andtheQualityofCareandOutcomes
ResearchInterdisciplinaryWorkingGroup;andtheAmericanCollegeofCardiologyFoundation:in
collaborationwiththeHeartRhythmSociety.Circulation.2006;113:316-327.
29. SoteriadesES,EvansJC,LarsonMG,etal.Incidenceandprognosisofsyncope.NEnglJMed.
2002;347:878-885.
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30. ChenL,ChenMH,LarsonMG,etal.Riskfactorsforsyncopeinacommunity-basedsample(the
FraminghamHeartStudy).AmJCardiol.2000;85:1189-1193.
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examination,andelectrocardiography.ClinicalefficacyassessmentprojectoftheAmerican
CollegeofPhysicians.AnnInternMed.1997;126:989-996.
32. LinzerM,YangEH,EstesNAIII,etal.Diagnosingsyncope.Part2:unexplainedsyncope.Clinical
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33. SheldonR,ConnollyS,RoseS,etal.PreventionofSyncopeTrial(POST):arandomized,placebocontrolledstudyofmetoprololinthepreventionofvasovagalsyncope.Circulation.
2006;113:1164-1170.
34. SamniahN,SakaguchiS,LurieKG,etal.Efficacyandsafetyofmidodrinehydrochloridein
patientswithrefractoryvasovagalsyncope.AmJCardiol.2001;88:A7,80-83.
35. KuriachanV,SheldonRS,PlatonovM.Evidence-basedtreatmentforvasovagalsyncope.Heart
Rhythm.2008;5:1609-1614.
36. ConnollySJ,SheldonR,ThorpeKE,etal.Pacemakertherapyforpreventionofsyncopeinpatients
withrecurrentseverevasovagalsyncopesecondVasovagalPacemakerStudy(VPSII):a
randomizedtrial.JAmMedAssoc.2003;289:2224-2229.
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8
CriticalCare
DavidB.Rose,MarinH.Kollef
RespiratoryFailure
GENERALPRINCIPLES
Definitions
Hypoxemic(type 1) respiratory failure: Occurs when normal gas exchange is seriously impaired,
causing hypoxemia (arterial oxygen tension[PaO2] <60mmHg or arterial oxygen saturation[SaO2]
<90%). Usually associated with tachypnea and hypocapnia; however, progression can lead to
hypercapnia as well. Acute respiratory distress syndrome (ARDS) is an important form of
hypoxemicrespiratoryfailurecausedbyacutelunginjury.Thecommonendresultisdisruptionofthe
alveolocapillary membrane, leading to increased vascular permeability and accumulation of
inflammatorycellsandprotein-richfluidwithinthealveolarspace.
TheARDSDefinitionTaskForcedefinedARDSasfollows1:
Onsetwithin1weekofaknownclinicalinsultorneworworseningrespiratorysymptoms;
Bilateralopacitiesnotfullyexplainedbyeffusions,lobar/lungcollapse,ornodules;
Respiratoryfailurenotfullyexplainedbycardiacfailureorvolumeoverload;and
ImpairedoxygenationwithlowPaO2tofractionofinspiredoxygen(FIO2)ratio(PaO2/FIO2≤300
mmHg).
TheseverityofARDSisstratifiedbasedonPaO2/FIO2.
Mild:200<PaO2/FIO2≤300mmHgwithpositiveend-expiratorypressure(PEEP)orcontinuous
positiveairwaypressure(CPAP)≥5cmH2O
Moderate:100<PaO2/FIO2≤200mmHgwithPEEP≥5cmH2O
Severe:PaO2/FIO2≤100mmHgwithPEEP≥5cmH2O
Hypercapnic(type 2) respiratory failure: Occurs with acuteelevation of carbondioxide (arterial
carbondioxidetension[PaCO2]>45mmHg),producingarespiratoryacidosis(pH<7.35).
Postoperative(type3)respiratoryfailure:Occurswhenpatientsdevelopatelectasisfrompainorthe
useofsedativespostoperatively.Inreality,thisisasubsetoftype1or2respiratoryfailure;however,
asthisissocommon,itisoftenclassifiedasitsowntypeofrespiratoryfailure.
Respiratory failure from shock (type 4): Respiratory failure where the metabolic demands of the
patient aretoohighfortherespiratorysystemtocompensatefor(e.g.,fromsepsisorfever).Patients
are often intubated in the process of resuscitation to off-load the respiratory system and decrease
oxygenconsumption.
Mixedrespiratory failure: Most commonly, respiratoryfailure is due to multiple pathophysiologic
processesthatcanleadtobothhypercarbiaandhypoxemia.
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Pathophysiology
Hypoxemicrespiratoryfailure(type1):Usuallyistheresultofthelung’sreducedabilitytodeliver
oxygenacrossthealveolocapillarymembrane.Theseverityofgasexchangeimpairmentisdetermined
bycalculatingtheP(A–a)O2gradient(A-agradient)usingthealveolargasequation:
whereFIO2=thefractionofinspiredoxygen,P
ATM
=atmosphericpressure,
=watervaporpressure,andR=therespiratoryquotient.Hypoxemiaiscausedbyoneofthefollowing
fivemechanisms:
Ventilation–perfusion(V/Q)mismatch:Occurswhen perfusiondoesnot compensatefora change
inventilationorviceversa(e.g.,emphysema,pneumonia,pulmonaryedema,pulmonaryembolism).
V/Qmismatchleads toanelevatedA-a gradient.Administrationofsupplementaloxygen increases
PaO2 (of note, supplemental oxygen paradoxically worsens V/Q mismatching in emphysema via
reversinghypoxicvasoconstrictionofpulmonarycapillariessupplyingpoorlyventilatedalveoli).
Shunt:Occurswhenmixedvenousbloodbypasseslungunitsandenterssystemicarterialcirculation
without receiving oxygenation. Shunts can be congenital (e.g., intracardiac shunt) or acquired
(atelectasis, hepatopulmonary syndrome). Shunt leads to an elevated A-a gradient. In pure shunt,
administrationofsupplementaloxygendoesnotincreasePaO2.SeeTable8-1fordifferentcausesof
shunt.
TABLE8-1
CAUSESOFSHUNT
Cause Examples
PulmonaryShunts
Pus Pneumonia
Water Cardiogenicpulmonaryedema
Acutemyocardialinfarction
Systolicordiastolicleftventricularfailure
Mitralregurgitationorstenosis
Noncardiogenicpulmonaryedema
Primaryacuterespiratorydistresssyndrome
Aspiration
Inhalationalinjury
Neardrowning
Secondaryacuterespiratorydistresssyndrome
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Sepsis
Pancreatitis
Reperfusioninjury
Upperairwayobstructionpulmonaryedema
Neurogenicpulmonaryedema
High-altitudepulmonaryedema
Blood Diffusealveolarhemorrhage
Atelectasis Pleuraleffusionwithatelectasis
Mucouspluggingwithlobarcollapse
Cardiacshunts Patentforamenovale
Atrialseptaldefect
Ventricularseptaldefect
Vascularshunts Arteriovenousmalformation
Diffusionabnormality: Occursowingtoabnormalitiesofthe interstitiumwhereinthetimeittakes
forgasequilibrationislongerthantheredbloodcelltransittimethroughthepulmonarycapillaries
(e.g.,pulmonaryfibrosis,pulmonaryhypertension).DiffusionabnormalitiesleadtoanelevatedA-a
gradient.AdministrationofsupplementaloxygenincreasesPaO2.
Hypoventilation: Occurs owing to a decrease inminute ventilation that results in an increase in
PaCO2 (see the causes of hypercapnia under “Hypercapnic respiratory failure [type 2]”) and
displacementofoxygen.TheA-agradientisnormal.Primarytreatmentisdirectedatcorrectingthe
causeofhypoventilation.AdministrationofsupplementaloxygenincreasesPaO2.
Lowinspiredoxygen:Occursowingtoalowpartialpressureofinspiredoxygen(e.g.,high-altitude
travel).A-agradientisnormal.AdministrationofsupplementaloxygenincreasesPaO2.
Hypercapnicrespiratoryfailure(type2):Primarilyoccursowingtoventilatoryfailure,resultingin
anelevatedPaCO2>45mmHg:
whereCO2=CO2production,VA=alveolarventilation,VE=expiredtotalventilation,andVD=dead
spaceventilation.Thecauseofhypercapniaisgenerallyfailureofoneofthefollowingcomponentsof
therespiratorysystem:
Disorders of the central nervous system: An impaired respiratory drive causes a decreased
respiratoryrate(“won’tbreathe”);e.g.,opiate overdose, central apnea/hypoventilation,metabolic
alkalosis,centralnervoussystem(CNS)infection.
Disordersofanterior horncells,peripheralnervoussystem,ormuscles: Neuromuscular failure or
muscle weakness causesdecreased tidalvolume (“can’tbreathe”);e.g.,Guillain–Barré syndrome,
myastheniagravis,amyotrophiclateralsclerosis,musculardystrophies,myopathies.
Disorders of the thoracic cavity: Anatomic abnormality causes decreased tidal volume; e.g.,
kyphoscoliosis,morbidobesity,pleuraleffusions,abdominaldistention,diaphragmaticinjury.
Disorders of the airway or lung parenchyma: Lung pathology causes increased dead space; e.g.,
asthma,chronicobstructivepulmonarydisease(COPD),severeARDS.
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Hypermetabolic states can cause increased CO2 production and lead to hypercapnia; e.g., sepsis,
seizure,thyrotoxicosis,serotoninsyndrome.
NoninvasiveOxygenTherapy
GENERALPRINCIPLES
Nasal cannulas: Most commonly used, but the exact FIO2 delivered is unknown because it is
influenced by peak inspiratory flow demand. Each additional liter of flow increases FIO2 by
approximately4%(e.g.,2L/mindelivers 28%).Flowratesshouldgenerallybelimitedto≤6L/min.
Anoxygenreservoirdevicecanincreaseoxygendelivery.
Simplefacemask:DeliversoxygenatFIO2of35%–55%usingflowsof5–12L/min(lowerflowrates
shouldbeavoidedtopreventbreathinginexpiredCO2).
Venturi masks: Allow theprecise administration ofoxygen via a facemask by delivering a mix of
ambientairwithoxygen.UsualFIO2valuesdeliveredare24%,28%,31%,35%,40%,and50%.As
FIO2increases,totalflowdecreases.
Nonrebreathingmasks: Use a reservoir bag to achieve higher oxygen concentrations(up to 80%).
Flow ratesaregenerallyatleast8–15L/min.A one-wayvalvepreventsexhaled gasesfromentering
thereservoirbag,maximizingtheFIO2thatisinspired.
Heatedhumidifiedhigh-flownasalcannula(HFNC):Deliversheatedandhumidifiedoxygenathigh
flows andconcentrationssuch thatit flushes outa significant amount of nonoxygenated air from the
upper airway. The system can be titrated up to 60 L/min and 100% FIO2 and may provide a small
amountofPEEPathighflowrates.
TheuseofHFNCdeviceshasincreasedrecentlywithsomestudiesshowingencouragingbenefits.In
one open-label trial, patients with hypoxemic non-hypercapnic respiratory failure were randomly
assigned to HFNC versus standard oxygen therapy or noninvasive positive-pressure ventilation
(NPPV). Intubation rates were similar between groups; however, there was a significant
improvement in 90-day mortality in patients who received HFNC as compared with other
modalities.
2
In a meta-analysisofninetrialscomparingHFNCtolow-flow oxygeninpatientswithhypoxemic
respiratoryfailure,HFNCdecreasedtheneedforbothintubationandescalationofoxygentherapy.
3
TheroleofHFNCfollowingextubationisdiscussedin“MechanicalVentilation.”
NPPV:Deliversrespiratorysupportwithpositiveairwaypressureviaasealedfacemask,nasalmask,
or helmet device. NPPV most commonlyrefers to continuous positive airway pressure (CPAP) and
bilevel positive airway pressure (BiPAP) ventilation. NPPV can be delivered by home devices or
ventilators.
CPAP:Delivers continuouspositive airwaypressurethroughouttherespiratorycycleandprevents
alveolarcollapseduringexpiration.CPAPisoftenusedinthetreatmentofobstructivesleepapnea
andpulmonaryedema.Initially,5cmH2Oofpressureshouldbeapplied,andifhypoxemiapersists,
thelevelshouldbeincreasedby3–5cmH2Ouptoalevelof10–15cmH2O.
BiPAP: Delivers two different airwaypressures during inspirationandexpiration to decrease the
work of breathing. BiPAP is often used for COPD exacerbations, weaning, and neuromuscular
weakness.Aninspiratorypressuresupportof5–10cmH2Oandanexpiratorypressureof5cmH2O
are reasonablestarting points.Ventilationis determinedbythedifference betweeninspiratoryand
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expiratorypressures(i.e.,“drivepressure”),andinspiratory pressurescanbeuptitratedtoachieve
adequatetidalvolumesandminuteventilation.
BenefitsofNPPV: NPPV decreases theneed formechanical ventilation in appropriately selected
patients.4 The benefits of NPPV are particularly strong in patients with neuromuscular disease,
COPD, pulmonary edema, andpostoperative respiratoryinsufficiency.5 A 2016 single-center trial
foundthatNPPVdeliveredviaatransparenthelmetdevicecoveringtheentireheadreducedtheneed
forintubationandimprovedsurvivalinpatientswithARDS.
6
There has been conflicting evidence over the years regarding the use of NPPV in severe acute
exacerbations ofasthma. A recent retrospective analysis of>50,000 patientsfoundthat theuseof
NPPVwasassociatedwithloweroddsofreceivinginvasivemechanicalventilationandin-hospital
mortality.
7
Potential harms of NPPV: NPPV is generally safe but can cause skin damage, eye irritation,
claustrophobia, and aerophagia and can be difficult to tolerate for some patients. Use should be
limited to patients who are conscious, cooperative, able to protect their airway, and
hemodynamicallystable.8NPPVuseshouldbelimitedtothosewithananticipatedshortduration
ofrespiratoryfailure.Closemonitoringisrequiredduringitsuse.
AirwayManagementandEndotrachealIntubation
GENERALPRINCIPLES
AirwayManagementBeforeIntubation
Headandjawpositioning:First,theoropharynxshouldbeinspected,andallforeignbodiesshouldbe
removed.Ifthepatientis unresponsive,theheadtilt–chinliftmaneuvershould be performed.If neck
immobilizationisrequired,jawthrustshouldbeperformed.
Oralandnasopharyngealairways:Airwayadjunctdevicescanbeusedtomaintainapatentairway.
Initiallyinsertedwiththeconcavecurveoftheairwayfacing toward theroofofthe mouth.Theoral
airwaythenisturned180degreesasitisinsertedsothattheconcavecurveoftheairwayfollowsthe
natural curve of the tongue.Careful monitoring ofairwaypatency isrequired, as malpositioningcan
pushthetongueposteriorlyandresultinoropharyngealobstruction.Nasopharyngealairwaysaremade
ofsoftplasticandpassedeasilydownoneofthenasalpassagestotheposteriorpharynxaftertopical
nasallubricationandanesthesiawithviscouslidocainejelly.
Bag-valve-maskventilation:Ineffectiverespiratoryeffortscanbeaugmentedwithsimplebag-valvemaskventilation.Properfittingandpositioningofthemaskusingthe“EC”handposition—thumband
index fingerforming a “C”around themask,andthe remainingfingersformingan“E” tosupportthe
jaw—ensureatightsealaroundthemouthandnose.Thismaneuvershouldbeusedinconjunctionwith
properpositioningandairwayadjuncts(e.g.,anoralairway).Ifpossible,twohandsshouldbeusedto
optimizeseal whileasecondclinicianventilates thepatient.Bag-valve-maskventilationisacritical
skillinairwaymanagementandisfrequentlyincorrectlyperformed.
Laryngeal mask airway (LMA): The LMA is a supraglottic airway device shaped like an
endotracheal tubeconnected to an elliptical mask.It is designed to be insertedover the tongue and
seatedinthehypopharynx,coveringthesupraglotticstructuresandrelativelyisolatingthetrachea.Itis
atemporaryairwayandshouldnotbeusedforprolongedventilatorysupport.LMAscanbelifesaving
inestablishinganairwaywhenendotrachealintubationcannotbeeasilyachieved.
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EndotrachealIntubation
Indications: Refractory hypoxemic respiratory failure, hypercapnic respiratory failure, airway
protection(e.g.,intoxication,headtrauma,severeupperGIbleedingwithhematemesis),upperairway
obstruction (e.g., angioedema, tumor), severe metabolic acidosis or shock (e.g., type 4 respiratory
failure, severe diabetic ketoacidosis), and need for hyperventilation as a treatment for increased
intracranialpressure.
Beforeendotrachealtubeintubationisattempted:
Ensure that monitoring equipment is working (including pulse oximetry, telemetry, and blood
pressuremonitoring)andthatthepatienthasadequateworkingintravenous(IV)access.
Ensure that all necessary equipment is at the bedside including working suction equipment,
endotrachealtube(withstylet,lubricant,andballoontested),10mLsyringetofillendotrachealtube
balloon, oral or nasopharyngeal airway, bag-valve-mask connected to15 L/minoxygen,direct or
video laryngoscope, end-tidal CO2 monitor, medications for intubation, and tape or endotracheal
holder.
Have the plan articulated and the equipment at the bedside (e.g., tracheal tube introducer and
supraglotticdevice)incaseofadifficultairway.
Evaluateheadandneckpositioning:Oral,pharyngeal,andtrachealaxesshouldbealignedbyflexing
the neck and extending the head, achieving the “sniffing” position. Obese patients may require a
shoulderrollorramp.
Theselectedagentsforintubationincludingneuromuscularblockingagents,opiates,andanxiolytics
should be chosen based on their respective advantages and disadvantages in the given clinical
situation.CommonlyusedagentsforintubationarelistedinTable8-2.
TABLE8-2
DRUGSTOFACILITATEENDOTRACHEALINTUBATION
Drug Action Dose(IV) Onset
(s)
Duration
(min)
Comment
Propofol Sedation,
amnesia
Unstable:
0.5mg/kg
Stable1–1.5
mg/kg
30–60 5–10 Causeshypotension
andbradycardia;
beneficialinseizures
Midazolam Sedation,
amnesia
0.02–
0.08mg/kg
(generally1–
5mginadult)
30–60 15–30 Causeshypotension;
beneficialinseizures
Fentanyl Analgesia 2µg/kg 15 30–60 Causeshypotension;
usedatlowerdosesas
anadjunctiveagent
Etomidate Sedation Unstable:
0.15mg/kg
Stable0.3
mg/kg
15–45 3–12 Hemodynamically
neutral;inhibitscortisol
synthesis;decreases
seizurethreshold
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