upmc critical care - aast
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Exemplary Care Cutting-edge Research World-class Education
UPMC Critical Care
www.ccm.pitt.edu
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Shock and Monitoring
Samuel A. Tisherman, MD, FACS, FCCMProfessorDepartments of CCM and SurgeryUniversity of Pittsburgh
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Shock
Inadequate DO2
“Dysoxia”
Anaerobic metabolism Lactic acidosis
Activation of inflammatory cascades
Organ system dysfunction
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ShockNormal cardiovascular system
Pathophysiology of shock
Categories of shock
Resuscitation
Monitoring
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Key components of CV systemIntravascular volume
Cardiac outputPreloadHeart rateContractilityAfterload
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Key components of CV system
Resistance circuit –arterioles
Distribution of organ flow
CapillariesLeakObstruction to flowShunts
Venous capacitance vessels
Vary venous return
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Organ blood flowMost dependent upon mean arterial pressure (MAP)
AutoregulationMaintained during large variations of MAP60-130 mmHgCan be impaired - hypertension
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Autoregulation
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Supply and demandO2 delivery
HemoglobinSaturationCardiac output
O2 demand
VO2 = DO2 x ERO2
ER = extraction ratio
20-60%
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O2 supply dependency
Oxygen delivery
Oxy
gen
cons
umpt
ion
CriticalDO2
CriticalDO2
DysoxiaLactic acidosis
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Cytopathic HypoxiaSepsis
Normal oxygen deliveryImpaired mitochondrial O2 utilization
MediatorsInflammatory cytokinesInhibition of pyruvate dehydrogenaseInhibition of cytochrome a,a3 by NOIrreversible inhibition of one or more mitochondrial respiratory complexes by peroxynitritePoly(ADP-ribose) polymerase-1
Reperfusion Injury
ATPXanthine
Dehydrogenase
Hypoxanthine XanthineOxidase
O2
Oxygen radical formationLipid mediator release
Endothelial cell dysfunctionNeutrophil chemotaxisMicrovascular changes
Tissue injury
Ischemia
Reperfusion
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It’s not the fall that gets you….
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Organ failure
OrganDamage
IschemicInjury
Inflammatory mediators(TNF, NO, free radicals)
Reperfusioninjury
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HyperdynamicLow SVR (wide PP)
HypotensionHypodynamic
Low CO (narrow PP)
Pulmonary edema?Distributive shock
SepsisNeurogenic shock
Adrenal insufficiencyLiver failureAnaphylaxis Medications
No Yes
Cardiogenic shockMI
Valvular dzHypovolemiaHemorrhageDehydration
JVD?
No Yes
RV failureObstructive
PETamponade
PTX
Classifications of shock
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Hemorrhagic shockMost common cause of hypotension in trauma patients
Initial fluid should be crystalloid
TransfusionHypotensive after 2 L crystalloid (ATLS)Earlier for severe shock
Uncontrolled hemorrhageStop hemorrhageLimited fluid resuscitation
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Cardiogenic shockResuscitation simultaneous with revascularization
Patients may need higher than normal filling pressures (poor LV compliance)
Inotropes may worsen ischemia
Pacing may be helpful for relative bradycardia
Intra-aortic balloon pump improves coronary perfusion and decreases afterload
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Pulmonary embolismRisk factors
Hypercoagulability, stasis, trauma
PresentationRespiratoryCardiovascular
DiagnosisCT angio, VQ, echo, angio, d-dimer
ManagementAnticoagulation, thrombolytic, embolectomyPrevent the next one -?filter
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Cardiac tamponadePentrating trauma more common than blunt
Beck’s triad (hypotension, distant heart sounds, JVD) obscured by hypovolemia
High index of suspicion
Diagnose: echo or pericardial window
Treatment:Need sternotomy or thoracotomy (trauma)Pericardiocentesis (non-trauma)
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Septic shockDecreased preload
Hypovolemia (capillary leak)Increased venous capacitance
Vasodilatation
Cardiac dysfunctionVentricular dilatationDecreased ejection fraction
Cytopathic hypoxia
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Endstage shock
Cardiacdecompensation
Vasomotordysfunction
Irreversible shockTerminal hypodynamic state
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Initial management
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Initial managementResuscitation
Ventilation?intubation early
InfusionBolus to effect?bloodClear lactate
Pump therapyInotropic supportAfterload reduction
VasodilatationVasopressor support
Definitive therapyStop bleedingCirculatory assistAntibiotics and drainage/debridement
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Monitoring
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CVPOnly elevated in disease
RV dysfunctionPulmonary hypertensionLV dysfunctionTamponadeHyperinflationIntravascular volume expansion
Poor correlation with volume responsiveness
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PAOP and Preload
Muscle
LVEDV
LVEDP
LAP
PAOP
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CVP and PAOP
Kumar, et al. CCM, 2004.
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Functional Hemodynamic Monitoring
2-3 heart beats later
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Resp variation in pulse pressure
Michard and Teboul. Crit care, 2000. Limitations: spontaneous breathing, arrhythmias.
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Passive Leg Raising
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Passive Leg Raising
Monnet, et al. CCM, 2012.
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Preload EchoDistensibility index
Max-min DIVC x 100%Min DIVC
Collapsibility indexMax-min DIVC x 100%Max DIVC
Resp variability indexΔDIVC = Max-min DIVC x 100%
Mean DIVC
Feissel, et al. Intensive Care Med, 2004.
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Mixed venous oxygen - SvO2
Decrease SvO2Decrease DO2
Hb, O2 sat, cardiac outputIncrease O2 demands
Fever, sepsis, exerciseNormal >65%Critical value ~40%
Resuscitation endpoint for sepsis and cardiogenic shock
Sepsis -> maldistribution of blood flowSvO2 normal with tissue dysoxia still present
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Oxidative MetabolismGlucosePyruvate Lactate
Acetyl CoA
NADH/FADH2Electron transport chain
ADP 34 ATPO2 H2O
2 ATP Citric acidCycle
Mitochondria
2 ATP
Remember 2:38
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Base DeficitDefinition
Amount of base needed to normalize pH with normal PCO2
LimitationsAdministration of bicarbonateAlcohol intoxicationHyperchloremic metabolic acidosisSeizuresPre-existing acidosis
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LactateExcess production
Anaerobic metabolismInitial level and time to clearance useful
Decreased metabolism (liver, kidney)
Washout during reperfusion
SepsisIncrease flux of alanine from muscleDecreased PDH activityDecreased hepatic clearanceDysfunctional mitochondrial respiration
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Near Infrared Spectroscopy
LocationMuscleStomachBowelLiver
MeasurementsPO2PCO2pHO2 saturation of hemoglobinTissue oxyhemoglobin coupling to cytochrome a,a3 redox
Mitochondrial O2
HyperdynamicLow SVR (wide PP)
HypotensionHypodynamic
Low CO (narrow PP)
Pulmonary edema?Distributive shock
SepsisNeurogenic shock
Adrenal insufficiencyLiver failureAnaphylaxis Medications
No Yes
Cardiogenic shockMI
Valvular dzHypovolemiaHemorrhageDehydration
JVD?
No Yes
RV failureObstructive
PETamponade
PTX
FluidsBlood
Hemostasis
FluidsInotropes
Specific Tx
InotropesIABP
Revascularize
FluidsVasopressors
EGDTxTreat cause
Base deficitLactate SvO2
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www.ccm.pitt.edu