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upper gastrointestinal (GI) bleeding, which can be prevented by appropriate use of pharmacologic
prophylaxis.
Theprimaryindicationsforstressulcer prophylaxisarethepresenceofasignificantcoagulopathy
(platelets<50k,internationalnormalizedratio>1.5,orpartialthromboplastintime>2upper limits
ofnormal) or the use of mechanical ventilation >48 hours. Theother indications for prophylaxis
includeahistoryofanupperGIbleedinthelastyear,presenceofbrainorspinalcordinjury,orany
two of the following: occult bleeding for ≥6 days, use of high-dose steroids (>250 mg of
hydrocortisone),sepsis,oranintensivecareunit(ICU)stay>1week.
Ahistamine-2receptorantagonistorproton pumpinhibitorcanbeusedforprophylaxiswithsome
controversyonwhatagentispreferred.
Theuseofulcerprophylaxismayincreasetheriskofnosocomialinfections,butbenefitsarelikely
greaterthanrisksintheabovepatients.
Oxygentoxicity:BreathinghighFIO2canleadtoexcessivefreeradicalgenerationandresultinlung
injury.
Reducing FIO2tothelowesttolerableoxygensaturation (O2saturationof90%or PaO2 of65 mm
Hg) is advisable. There is evidence that tolerating hyperoxia after intubationmay worsen patient
survival.
13
LiberationFromMechanicalVentilation
Parametersdemonstratingreadiness towean:Dailyassessment ofreadinessforextubationshould
be done once the underlying disease process begins to resolve and minimal ventilator support is
required.Thefollowingcriteriashouldgenerallybemetbeforeextubation:
Minimalventilatorsupport:FIO2≤40%,PEEP5cmH2OtomaintainSpO2>90%.
Arterial blood gas: pH and PaCO2 should be at the patient’s baseline; particularly important for
patientswithchronicCO2retention.
Ventilation requirement: Minute ventilation should be <10 L/min and respiratory rate <30
breaths/min.
Mentalstatus:Patientshouldbeawake,alert,andcooperative.
Secretions: Secretions should be thin, scant in amount, and easily suctioned; patient should not
requiresuctioningmorefrequentlythanevery4hoursbeforeextubation.
Strength:Patientshouldhavestrongcoughandbeabletoliftheadoffthebedandholditinflexion
for>5seconds.
Breathingtrial:PatientshouldbeabletogeneratespontaneousVT>5mL/kgIBW.
Rapidshallowbreathingindex(RSBI):RSBIshouldbe≤105.Definedasratioofrespiratoryrate
toVTinliters(f/VT).RSBI>105accuratelypredictsweaningfailure,butRSBI≤105islessaccurate
atpredictingweaningsuccess.
33
Patency of airway: In patients with concern for laryngeal edema (e.g., angioedema, traumatic
intubation),cuffleakshouldbecheckedbeforeextubation.Absenceofcuffleakshouldgenerally
precludeextubation,andpatientsshouldbetreatedwithIVcorticosteroidsfor12–24hoursbefore
extubation.
34
Some patientsfelttobe readytoextubatebased onall objectivecriteria will still failextubation.
Failureratesashighas23.5%havebeenreported.
35
Weaningstrategies:Sedationinterruptionandbreathingtrialsfor30–120minutesshouldbedone
dailyandis themostimportantpredictor oftimely liberationfrom mechanical ventilation.36Weaning
strategiesincludethefollowing:
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PSV:Notime-triggeredbreaths,butpatientremainsconnectedtotheventilator.PEEPisusuallyat5
cmH2O,withlowlevelsofpressuresupport(5–10cmH2O)duringspontaneousbreathing.
T-piece/spontaneousbreathingtrial:Patientisremovedfromtheventilatorbutremainsintubated.
Endotracheal tube is connected to a heated, humidified circuit with minimal or no supplemental
oxygen.End-tidalCO2monitoringmaybeusedforadditionalsafety.
SIMV:Usedmostfrequentlyinsurgicalandneurosurgicalpatients.Setrespiratoryrateisgradually
decreasedoverhourstodaysuntilpatientisprimarilybreathingspontaneously.
SIMVhasthepoorestweaning outcomesofall techniques.However,neitherT-piece norPSVhas
proventobemorepredictiveofsuccessfulextubation.
37
Managementfollowingextubation:Patientsneedtobecloselymonitoredfollowingextubation.Good
airwayclearanceandoxygenationdecreasetheriskofreintubation.
Extubation to NPPV: In patients with COPD who are intubated for acute respiratory failure,
extubation to NPPV is associated with a reduction in mortality and health care–associated
pneumonia.38 More generally, in patients with chronic hypercapnic respiratory failure, two trials
have found that the use of NPPV reduces rates of reintubation following extubation.
39,40
Similar
benefitofNPPVhasnotbeendemonstratedinotheretiologiesofrespiratoryfailure.
Extubation to HFNC: The use of HFNC may also have a beneficial role in the prevention of
postextubationrespiratoryfailureinselectlow-riskpatients.Whenpatientswererandomlyassigned
toHFNCversusconventional oxygentherapyafterextubation,patients whoreceived HFNCwere
lesslikelytobeintubatedwithin48–72hours.
41,42
OtherstudieshaveshownHFNCtobenoninferior
whencomparedwithNPPVinpreventingreintubation.
43
Failure to wean: Defined as inability to liberate from mechanical ventilation 48–72 hours after
resolutionofunderlyingdiseaseprocess.Factorsthatshouldbeconsideredincludethefollowing:
Endotrachealtubeswithsmallerinnerdiameterincreaseairwayresistanceandmaymakebreathing
trialsmoredifficult.
Useofneuromuscularblockadeisassociatedwithprolongedweakness,particularlywhenusedwith
corticosteroids.
44
Critical illness myopathy and polyneuropathy places the patient at risk for recurrent respiratory
failure.
Psychiatric illnesses (delirium, anxiety, PTSD, etc.) may interfere with SBTs and other standard
weaningprotocols.
Acid–basedisturbancesmaymakeliberationfrommechanicalventilationdifficult.
Non–anion gap metabolic acidosis causes compensatory increase in minute ventilation
(respiratoryalkalosis)tonormalizepH,whichcanleadtotachypneaandrespiratoryfatigueupon
extubation.
Metabolic alkalosis causes blunting of ventilatory drive and decrease in minute ventilation
(respiratoryacidosis)tomaintainnormalpH,whichcanleadtohypercapniauponextubation.
Shock
GENERALPRINCIPLES
Aprocessinwhichbloodflowandoxygendeliverytotissuesarederanged,leadingtotissuehypoxia
andresultantcompromiseofcellularmetabolicactivityandorganfunction.
Maingoaloftherapyisrapidcardiovascularresuscitationtoreestablishtissueperfusion.
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Definitivetreatmentrequiresreversalofunderlyingprocesses.
ClassificationsofShock
HemodynamicpatternsassociatedwiththedifferentshockstatesarelistedinTable8-5.
TABLE8-5
HEMODYNAMICPATTERNSASSOCIATEDWITHSPECIFICSHOCKSTATES
TypeofShock CI SVR PVR SvO
2
RAP RVP PAP PAOP
Cardiogenic ↓ ↑ N ↓ ↑ ↑ ↑ ↑
Hypovolemic ↓ ↑ N ↓ ↓ ↓ ↓ ↓
Distributive N−↑ ↓ N N−↑ N−↓ N−↓ N−↓ N−↓
Obstructive
a
↓ ↑−N ↑ N−↓ ↑ ↑ ↑ N−↓
a
EqualizationofRAP,PAOP,diastolicPAP,anddiastolicRVPestablishesadiagnosisofcardiactamponade.
CI,cardiacindex;N,normal;PAOP,pulmonaryarteryocclusionpressure;PAP,pulmonaryarterypressure;PVR,pulmonary
vascularresistance;RAP,rightatrialpressure;RVP,rightventricularpressure;SvO2,mixedvenousoxygensaturation;SVR,
systemicvascularresistance.
Distributive:Shockcausedbymassivevasodilationandimpaireddistributionofbloodflow,resulting
intissuehypoxia. Usuallyassociated with hyperdynamic cardiac function,unless cardiac functionis
somehowimpaired(seelaterdiscussionofcardiogenicshock).
Primaryetiologiesaresepticshockandanaphylacticshock.Septicshockismostcommonlyseenin
medicalICUsandwillbefurtherdiscussedinthenextsection.AnaphylaxisisdiscussedinChapter
11,AllergyandImmunology.Otherlesscommontypesincludeneurogenicshockandadrenalshock.
Hemodynamicparameters will generally demonstrate increased cardiac output (CO), decreased
systemic vascular resistance (SVR) due to vasodilation, and elevated central venous oxygen
saturation(ScvO2)duetoineffectiveoxygenextractionbytissue.
Primarygoalsoftherapy
Volume resuscitation: Owing to massive peripheral vasodilation, patients have a functionally
decreased oxygen-carrying capacity, requiring volume resuscitation. IV crystalloid fluids are
primarilyused.
Treatmentofunderlyinginfection:Inadequateinitialantimicrobialtherapyisanindependentrisk
factor for in-hospital mortality inpatients with septic shock, so timely, effective antimicrobial
therapyisacornerstoneoftreatment.
Removaloftheoffendingagentinanaphylacticshock.
Cardiovascularsupportwithvasoactive agents (e.g.,norepinephrine).Vasoactiveagentswillbe
discussedinmoredetailinalatersection.
Hypovolemic: Shock causedbya decreaseineffectiveintravascular volumeanddecreased oxygencarryingcapacity.
Primaryetiologiesarehemorrhagic(e.g.,trauma,gastrointestinalbleeding)orfluiddepletion(e.g.,
diarrhea,vomiting).
Hemodynamic parameters will generally demonstrate a decreased CO, increased SVR, and
decreasedScvO2duetoincreasedoxygenextractionbyperipheraltissue.
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Primarygoalsoftherapy
Volumeresuscitation:IVbloodproductandcrystalloidareusedforresuscitationofhemorrhagic
andfluiddepletionshock,respectively,withgoalmeanarterialpressure(MAP)of60–65mmHg.
Overresuscitation may be detrimental in hemorrhagic shock and patients without significant
comorbiditiesmaytoleratelowerhemoglobinlevels(7g/dL)thanpreviouslybelieved.
Definitive treatment of underlying etiology of volume loss: For hemorrhagic shock, surgical
interventionmaybenecessary.
Obstructive: Shock caused by obstruction of the heart or great vessels, resulting in decreased left
ventricularfillingandcardiovascularcollapse.
Primaryetiologiesarepulmonaryembolism,cardiactamponade,andtensionpneumothorax.
Hemodynamic parameters will generally demonstrate decreased CO,normal to increased SVR,
andnormaltodecreasedScvO2.
Primarygoalsoftherapy
Supportive: Although patientsarepreloaddependent,excessive fluidadministrationcanleadto
rightventricularoverloadandimpairmentofLVfilling,therebyworseningshock.
Definitive therapy involves relieving the obstruction (e.g., thoracostomy in the case of a
pneumothorax,andpericardiocentesisintamponade).
Inacarefullyselectedgroup ofpatients,thrombolytictherapymaybebeneficialinpatientswith
pulmonaryemboli.
Cardiogenic: Shock caused by left ventricular systolic failure, resulting in decreased CO and
subsequentinsufficientoxygendistribution.
Primaryetiologiesaremyocardialinfarction,acutemitralregurgitation,andmyocarditis.
HemodynamicparameterswilldemonstratedecreasedCO,increasedSVR,anddecreasedScvO2.
Primarygoalsoftherapy
Mitigation of pulmonary edema: NPPV or endotracheal intubation with mechanical ventilation
reduces afterload, thereby encouraging forward flow, as well as preload. Additionally, the
applicationofpositive pressuretothealveolar spacecausespulmonaryedemafluidtomove to
theinterstitialspace.
Careful fluid management: Adequate preload to optimize ventricular function is important, but
volumeoverloadwillworsenrespiratorystatus,socarefulfluidmanagementisnecessary.Volume
removal (whether via diuresis or hemodialysis) is often a critical component of early
management.
Definitive therapy for underlying cardiac disease: In the event of myocardial infarction,
percutaneousrevascularizationshouldbeperformedinatimelyfashion.
Supportive:InotropicagentssuchasdobutaminemaybeusedtoaugmentCO.Otherinotropesare
discussed in “Pharmacologic Therapies.” Mechanical circulatory assist devices, including left
ventricularassistdevicesandintra-aorticballoonpumps,maybenecessaryinpatientswhodonot
respondtomedicaltherapy.
SepticShock
Definitionofsepsis:Sepsisisdefinedasalife-threateningorgandysfunctioncausedbydysregulation
ofthehostresponsetoaninfection.
Sepsis was previously identified based on the presence of at least two systemic inflammatory
responsesyndrome(SIRS)criteria:
Tachypnea:Respiratoryrate>20breaths/minorPaCO2<32mmHg
Whitebloodcellcount<4000cells/μLor>12,000cells/μL
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Tachycardia:Pulse>90bpm
Hypo-orhyperthermia:Temperature>38°Cor<36°C
The new sepsis guidelines now identify organ dysregulation in sepsis as an increase in the
SequentialOrganFailureAssessment(SOFA)scoreof≥2.
45
Septic shock is a subset of sepsis identified by persistent hypotension requiring vasopressors to
maintaina meanarterial bloodpressure≥65 mmafteradequatevolume resuscitation.Mortalityin
thesepatientsis 40%.
Management of septic shock: Management of septic shock involves early aggressive volume
resuscitationandattemptingtoachievehemodynamicstabilityquickly.
46
Volumeresuscitation:Patientsshouldbegintoreceiveatleast30mL/kgIBWIVcrystalloidfluid
withinthefirsthourofpresentation.47Smalleramountsoffluidmaybeneededifthereisconcomitant
heartfailureorpulmonaryedema,whereasadditionalvolumemayberequiredifthepatientremains
volumeresponsiveaftertheinitial30mL/kgbolus.Parameterstodeterminevolumeresponsiveness
(discussed in “Hemodynamic Measurements”) should be closely monitored during volume
resuscitationtopreventvolumeoverload.
A recentRCTfoundthatbalancedcrystalloids (i.e.,lactatedRinger solution)maybeassociated
withlowerratesofrenaldysfunction andevenimprovedmortalitywhenusedascomparedwith
normalsaline.
48
Severaltrials havenot foundsignificantbenefitinalbuminadministration whencompared with
crystalloidinsepticpatients.
49
Cardiovascular support: Vasoactive medications may be necessary if volume resuscitation is
insufficienttomaintainMAP≥65mmHg.Norepinephrinehasbecomethefirst-lineagentafterit
was demonstrated that dopamine had more adverse events.50 Vasopressin is frequently used as a
second-line agent. Mechanisms of action and other agents are discussed in “Pharmacologic
Therapies.”
Timely, effective antimicrobial administration:Delaysinstarting appropriateantimicrobialsare
associated with increased mortality.51 The Surviving Sepsis Guidelines recommend starting
antibioticsimmediatelyafterobtainingbloodcultures,ifpossible.
47
Sourcecontrol:Ifaspecificanatomicalsourceofinfectionisidentified(e.g.,necrotizingsofttissue
infection),interventionforsourcecontrolshouldbeperformedassoonasreasonablypossible.
52
Earlygoal-directedtherapy:Protocol formanagementofthefirst6hoursofsepsisproposed by
Rivers et al. in2001.46 Widely adapted in practice before recent multicenter, prospective, RCTs
calleditseffectivenessintoquestion.
53,54
However,thesestudieswerelimitedbypracticechangesin
controlgroup(Figure8-3).
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Figure 8-3 Early goal-directed therapy protocol.(Adapted from Rivers E, Nguyen B, Havstad S, et al. Early goal-
directedtherapyinthetreatmentofseveresepsisandsepticshock.NEnglJMed.2001;345:1368-1377.)
*Although included in the original early goal-directed therapy protocol, more recent trials have demonstrated a trend
towardincreasedharminpatientswhoreceivemoretransfusions;currentSurvivingSepsisGuidelinesdonotrecommend
transfusingtoachieveHctof30%.CVP,central venouspressure;Hct,hematocrit;IBW,idealbodyweight;MAP,mean
arterialpressure;ScvO2,centralvenousoxygensaturation.
Lactateclearance:Lactateclearanceisassociatedwithimprovedmortalityinsepticpatients.55The
most recentSurvivingSepsis Guidelinesrecommendtargeting resuscitationtonormalizelactatein
patientswithelevatedlactatelevels.
47
Procalcitonin(PCT): PCTis a biomarker that may aid in diagnosing sepsis, assessing treatment
response, and determining antibiotic duration. An elevated PCT >0.5 ng/mL is suggestive of a
bacterial infectionwhile a PCT <0.1 ng/mL makes bacterial infection less likely.56 Some studies
have shownthatuse of PCTmay reduce the unnecessaryusage of antibiotics.57 However, caution
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mustbeused,asalowPCTdoesnotexcludethepossibilityofaseverebacterialinfection.
PharmacologicTherapies
VASOCONSTRICTIVEANDINOTROPICAGENTS
Norepinephrine:Causespotentvasoconstrictionviaα1-andβ1-adrenergicactivity. Preferredagentin
septicshock.
Vasopressin: Causes vasoconstriction via three different G-peptide receptors. Primarily used as an
adjuncttonorepinephrine.Weakevidencethatitmayhavemortalitybenefitovernorepinephrineinless
severesepticshock(definedasrequiringtreatmentwithnorepinephrine5–14μg/mintomaintainMAP
≥65mmHg).
58
Epinephrine:Hasinotropicandvasoconstrictivepropertiesinadose-dependentfashionowingtoα1-
andβ-adrenergicactivity.Atlowdoses(≤0.05μg/kg/min),itincreasesCOandslightlyreducesSVR
owingto predominant β activity. At higher doses (>0.05 μg/kg/min), vasoconstriction predominates
owingtoincreasedα1activity.Preferred agent foranaphylactic shock,andisalso frequentlyusedin
cardiogenicshock.
Phenylephrine: Selective α1-receptor agonist causing vasoconstriction of larger arterioles. Few
studiessupportingitsuseinsepticshock.
AngiotensinII:RecentstudieshaveinvestigatedangiotensinIIwhichengagesthe renin–angiotensin–
aldosteronesystem.ThesestudiesshowedthatangiotensinIIincreasedbloodpressureinpatientswith
vasodilatoryshock.
59
Dobutamine:Inotropicagentthatreducesafterloadandincreasesstrokevolumeandheartrateviaβ1-
agonistactivity.Goodagentforcardiogenicshockbutincreasesriskofcardiacarrhythmias.
Dopamine:Hasinotropic,vasodilatory, andvasoconstrictive properties inadose-dependentfashion
duetoactiononperipheralα1-receptors,cardiacβ1-receptors,andrenalandsplanchnicdopaminergic
receptors.Atdoses<5μg/kg/min,primarilybehavesasavasodilator,increasingrenalbloodflow.At
dosesof5–10μg/kg/min,behavesasaninotrope.Atdoses>10μg/kg/min,behavesasavasopressor.
Isassociatedwithahigherrateofcardiacarrhythmiasthannorepinephrine.
50
Milrinone: Phosphodiesterase IIIinhibitor thathaspositive inotropic effect,causingincrease inCO.
Also causes systemic vasodilation, which decreases afterload, making it an alternative option for
cardiogenicshock.
Regardingvenous access, low-dose norepinephrine, phenylephrine,and epinephrine may be infused
peripherally for a limited period of time. However, central access is preferred as medication
extravasationcanleadtolocalischemia.
Ifextravasationoccurs,phentolamine(anα-antagonist)canbeinjectedintotheareaofextravasation
toreduceischemicinjury.
PeripheraladministrationofvasopressinandangiotensinIIisnotrecommended.
ADJUNCTIVETHERAPIES
Corticosteroids:Relativeadrenalinsufficiencymaycontributetorefractoryhypotensionduringseptic
shock. Datado notsupportthe useofcorticosteroids inmild septicshock. However,corticosteroids
shouldbeconsideredonanindividualbasisinpatientswithmoresevereshock,particularlyinpatients
chronically on steroids. Generally, hydrocortisone 200–300 mg daily divided on a q6–8h basis is
given.Previoustrialshaveshownfasterresolutionofshockwhenadministeringhydrocortisone,butno
difference in mortality.
60,61
Another recent trial showed a benefit in 90-day mortality when
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hydrocortisone (50 mg every 6 hours) and fludricortisone (50 µg daily) were administered in
conjunction.
62
Sodiumbicarbonate: No evidence supports the use of bicarbonate therapy in lactic acidemia from
sepsis with a pH≥7.15. Effectofbicarbonateon hemodynamics andvasopressor requirementswith
moresevereacidemiaisunknown,butbicarbonateisoftenrecommendedinpatientswithseverelactic
acidemia(pH<7.1)whoarehemodynamicallyunstable.
Methylene blue: Selective guanylate cyclase inhibitor, thereby mitigating nitric oxide–mediated
vasodilation.Observationalstudieshavedemonstratedbeneficialeffectsonhemodynamicparameters,
buteffectsonmorbidityandmortalityareunknown.
63
HemodynamicMeasurements
AlthoughCVP,MAP,andSvO2/ScvO2areusedastherapeuticendpointsintreatingshock,thereis
evidencethattheseparametersdonotreflectintravascularvolume.Thereisagrowingbodyofevidence
thatdynamicparameters,includingpulsepressurevariationandinferiorvenacava(IVC)diameters,may
betterreflectintravascularvolume,butitisunclearthattheuseoftheseleadstoimprovedoutcomes.
Staticparameters
CVP:Anapproximationofrightatrialpressureand,therefore,preload.Shouldbemeasuredfroman
internal jugular or subclavian venous catheter because readings from femoral catheters are
influenced byintra-abdominal pressuresandthusinaccurate.Thereis a poorrelationshipbetween
CVPandblood volume,64butlow values (<4mmHg) should generallylead to fluidresuscitation
withcarefulmonitoring.
65
ScvO2/SvO2: ScvO2 is a surrogate that is often used to reflect SvO2, which is thepercentage of
oxygenboundtohemoglobininbloodreturningtotherightsideoftheheart.ScvO2ismeasuredfrom
an internal jugular or subclavian venous catheter, while a true SvO2 must be measured with a
pulmonary artery catheter (PAC). Normal values are 65%–75%. A high value often represents
decreasedoxygenconsumption(commonlyseeninmitochondrialdysfunctionwithsepsis),whereas
low values indicate inadequate oxygen delivery (oftenduetolow COstates such as cardiogenic
shock).PreviousguidelinesrecommendedtargetinganScvO2>70%withdobutamineadministration
ifneeded,thoughmorerecenttrialshaveshownthatusinglactateclearanceasaresuscitationgoalis
noninferior.
66
PACs:APACcatheterprovidesdirectmeasurementsofpressuresintherightatrium,rightventricle,
andpulmonaryartery,aswellasapulmonarycapillarywedgepressure.Previouslycommonlyused
inthemanagementofsepticshockandARDSbutdidnotaffectmortalityormorbidity.
67
Dynamicparameters
EsophagealDoppler:ADopplerprobeisplacedinto theesophagusandrotatedtomeasureblood
flow through the descending aorta. System can be used to calculate CO and stroke volume, and
correlates well with CO as measured by PAC.68 Predicts volume responsiveness in critically ill
ventilatedpatientswithoutspontaneousbreathing.
69
Pulse pressure variation (ΔPp): Requires arterial line placement. Calculated as the difference
betweenmaximalandminimalsystolicbloodpressuresmeasuredoveronerespiratorycycledivided
by the mean of those values. ΔPp of 13% was an accurate predictor of fluid responsiveness in
mechanicallyventilatedpatientswithoutspontaneousbreathing.
70
IVCdistensibilityindex(dIVC):Calculatedasthe differencebetweenmaximal andminimal IVC
diametermeasuredoveronerespiratorycycledividedbytheminimalIVCdiameter.dIVCof18%
discriminatedbetweenvolumerespondersandnonresponderswith90%sensitivityandspecificityin
mechanically ventilated patients without spontaneous breathing in one study,71 but more recent
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studieshaveshownthismethodtobeapoorpredictoroffluidresponsiveness.
72
Thoracicbioreactance: Anoninvasive device is applied tothe chest andmeasures bioreactance
acrossthethoraxusingsensorpadsplacedonapatient’sthoraxsurroundingtheirheart.Bloodflow
(which is predominately in the aorta in the thorax) causes phase shifts in impedance, which is
detectedbythesensors.From thesemeasurements,strokevolumeandCOcanbeestimated.There
are conflicting data on the ability of thoracic bioreactance devices to reliably determine fluid
responsiveness.
73,74
CriticalCareUltrasound
Theuseofbedsideultrasonographyhasgreatlyexpandedrecentlyandisrapidlybecomingstandardof
careinICUs.Coursesincriticalcareultrasonographyarebecomingmorereadilyavailableandare
necessaryforcompleteproficiency.Thissectionisintendedtoserveasanoverviewofbasicconcepts
only.Criticalcareultrasoundshouldbeusedasanadjuncttootherclinicaldata.
Basicconcepts:Airandcalcifiedstructurestransmitsoundwavespoorly.Free-flowingfluidstransmit
soundwaveswell.
Basicdefinitions
Echogenicity:Theabilityofanobjecttoreflectsoundwaves.
Hyperechoic: Structures that reflectsound waves well;shows as white on ultrasound (e.g.,bone,
pleura,lung).
Hypoechoic: Structures that reflect sound waves poorly; shows as gray on ultrasound. Deeper
structuresarealsomorehypoechoicowingtoattenuationwithdistance(e.g.,lymphnodes,adipose
tissue,muscle).
Anechoic:Containingstructures thatallowsoundwaves topass throughfreely;showsasblackon
ultrasound(e.g.,bloodvessels,transudativepleuraleffusion).
Ultrasoundtofacilitatevascularaccess:MoredetailedinstructionsareavailableintheWashington
Manual of CriticalCare, Section XIX.Use of ultrasound to guide central venous access results in
increasedsuccessandreducedcomplicationrates.
Location: Ultrasound guidance is most commonly used for internal jugular and femoral venous
access.
Beforestartingtheprocedure:Bothinternaljugularandfemoralveinsshouldbescannedtoevaluate
foraberrantanatomyorvenousthrombosis.
Afterapplyingthesterilefield:Theprobeispositionedsothattheneedleisvisualizedfortheentire
durationofaccessingthevessel.
During theprocedure:Followinginsertionoftheguidewire, the lengthofthevessel is scannedto
ensurethattheguidewiredidnotinadvertentlyenteranyadjacentarteries.
Aftertheprocedure:Lungultrasoundcanbeusedtoruleoutapneumothorax.
Cardiacultrasound:Includesfivestandardviews,reviewedbelow.Usesbodytransducer.Intendedto
facilitateassessment ofvolumeresponsiveness,globalleftandrightventricularsystolicfunction,and
valvularfunction.
Parasternal long-axis view: Probe is placed adjacent to the sternum in the left third to fifth
intercostal spacewiththeorientationmarkerpointingtoward thepatient’srightshoulder.Theright
ventricularoutflowtract,leftventricularcavity,ascendingaorta,mitralvalve,andleftatriumshould
bevisualized.Assessesforpericardialeffusion,leftandrightventriculardysfunction,andvalvular
pathologies.
Parasternalshort-axisview:Proberemainsadjacenttothesternumintheleftthirdtofifthintercostal
space,butorientationmarkerisrotated90degreesclockwisetopointatthepatient’sleftshoulder.
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Cross-sectionalviewoftheleftandrightventriclesatthelevel ofthe papillarymusclesshouldbe
visualized.Assessesforpericardialeffusionandleftandrightventriculardysfunction.
Apicalfour-chamberview:Probeisplacedbetweenthemidclavicularandmidaxillarylinesofthe
leftlateralchestbetweenthefifthandseventhintercostalspaces,underneaththeleftnipple,withthe
orientation marker pointed at 3 o’clock. The left and right ventricles and atria, as well as the
tricuspid and mitral valves, should be visualized. Assesses left and right ventricular size and
function.SeeFigure8-4.
Figure 8-4 Cardiac ultrasound.Left (A): normal apical four-chamber view. A, apex; RV, right ventricle; RA, right
atrium; LV, left ventricle; LA, left atrium. Right (B): demonstrates same view in a patient with right ventricular
hypertrophyanddilation.
Subcostal long-axis view: Probeis placed below thexiphoid process withthe orientationmarker
pointed at 3 o’clock. The left and right ventricles and atria should be visualized. Assesses for
pericardialeffusionandleftandrightventriculardysfunction.Maybeusedforrapidassessmentof
cardiacfunctionduringperformanceofcardiopulmonaryresuscitation.
IVClongitudinalview:Proberemainsbelowthexiphoidprocess,butorientationmarkerisrotated
90 degrees counterclockwise to point at 12 o’clock. IVC in the longitudinal axis should be
visualized.AssessesIVCdiameterduringtherespiratorycycletodeterminevolumeresponsiveness.
Thoracicultrasound:Includesfourstandardpositions,performedbilaterally.Usesthebodytransducer
on theabdominal setting toexaminelung parenchyma;vascular transducermay be usedfordetailed
examinationofthepleura. Intended to facilitatethe diagnosis of pleural effusion,pulmonaryedema,
pulmonaryconsolidation,andpneumothorax.Alsousedtoguideasafethoracentesis.
Probeplacement:Bedsidelungultrasoundinemergency(BLUE)sprotocol,intendedforimmediate
diagnosisofacute respiratoryfailure,definesfourareasforinvestigation.75Theorientationmarker
shouldbepointedtowardthepatient’shead.
UpperBLUEpoint:Midclavicularline,secondintercostalspace
LowerBLUEpoint:Anterioraxillaryline,fourthorfifthintercostalspace
Phrenicpoint:Midaxillaryline,sixthorseventhintercostalspace;locationofthediaphragm
Posterolateral alveolar and/or pleural syndrome point: Posterior to the posterior axillary line,
fourthorfifthintercostalspace
Anatomic landmarks and ultrasound appearance: Knowledge of the normal sonographic
appearanceofthoracicanatomyisparamounttoidentifyingkeystructures.
https://t.me/med1917
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