shock nga b. pham, md, faap critical care medicine children’s healthcare of atlanta egleston2006
TRANSCRIPT
SHOCK SHOCK
NGA B. PHAM, MD, FAAPNGA B. PHAM, MD, FAAP
CRITICAL CARE MEDICINECRITICAL CARE MEDICINE
CHILDREN’S HEALTHCARE OF ATLANTACHILDREN’S HEALTHCARE OF ATLANTA
EGLESTONEGLESTON
20062006
ObjectivesObjectives
Review basic physiologic aspects of Review basic physiologic aspects of shockshock
Define shock and its different Define shock and its different categoriescategories
Describe management of shockDescribe management of shock
What is Shock?What is Shock?Pathophysiology of shockPathophysiology of shock
OxygenOxygen
Demand > SupplyDemand > Supply
Definition of ShockDefinition of Shock
Inadequate tissue perfusion to meet Inadequate tissue perfusion to meet tissue demandstissue demands
Usually result of inadequate blood Usually result of inadequate blood flow and/or oxygen deliveryflow and/or oxygen delivery
Shock is not a blood pressure Shock is not a blood pressure diagnosisdiagnosis
Determinants of Oxygen DeliveryDeterminants of Oxygen Delivery
OxygenOxygenDelivery = Content x Cardiac Delivery = Content x Cardiac
outputoutput
Determinants of Oxygen DeliveryDeterminants of Oxygen Delivery
Oxygen content = 1.34 (Hgb x SaO2) + Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x 0.003)(PaO2 x 0.003)
SaO2: Oxygen saturationSaO2: Oxygen saturation Hgb: Hemoglobin concentrationHgb: Hemoglobin concentration PaO2: partial pressure Oxygen in plasmaPaO2: partial pressure Oxygen in plasma
To improve Oxygen contentTo improve Oxygen content Increase Hemoglobin concentrationIncrease Hemoglobin concentration Increase saturationIncrease saturation
Determinants of Oxygen DeliveryDeterminants of Oxygen Delivery
Cardiac outputCardiac output C.O. = Heart rate x stroke volumeC.O. = Heart rate x stroke volume
To improve Cardiac outputTo improve Cardiac output Increase Heart rateIncrease Heart rate Increase Stroke VolumeIncrease Stroke Volume
Preload – volume of blood in the ventriclePreload – volume of blood in the ventricle Afterload – resistance to contractionAfterload – resistance to contraction Contractility – force appliedContractility – force applied
Secondary Organ DysfunctionSecondary Organ Dysfunction
Respiratory failureRespiratory failure TachypneaTachypnea Decreased complianceDecreased compliance
Pulm edema, pulm infiltrate, etc.Pulm edema, pulm infiltrate, etc. Increased resistanceIncreased resistance Diaphragm fatigueDiaphragm fatigue
Central vs peripheralCentral vs peripheral Demand >> supplyDemand >> supply Inadequate O2 deliveryInadequate O2 delivery
Secondary Organ DysfunctionSecondary Organ Dysfunction
CNS – altered mental statusCNS – altered mental status Renal insufficiency – pre-renalRenal insufficiency – pre-renal Coagulation abnormalities – DICCoagulation abnormalities – DIC Hepatic/GI dysfunction – bowel Hepatic/GI dysfunction – bowel
ischemiaischemia Endocrine – Calcium, hypo-Endocrine – Calcium, hypo-
adrenalism, vasopressinadrenalism, vasopressin
Classification of ShockClassification of Shock
Hypovolemic Shock (#1 cause world Hypovolemic Shock (#1 cause world wide)wide) Dehydration, hemorrhagicDehydration, hemorrhagic
Cardiogenic ShockCardiogenic Shock Pump failure, obstructive, L-R shuntPump failure, obstructive, L-R shunt
Distributive ShockDistributive Shock NeurogenicNeurogenic AnaphylaxisAnaphylaxis
Septic Shock – All of the aboveSeptic Shock – All of the above
Classification of ShockClassification of Shock
CompensatedCompensated Organ perfusion is maintainedOrgan perfusion is maintained
UncompensatedUncompensated Circulatory failure with end organ Circulatory failure with end organ
dysfunctiondysfunction
IrreverisbleIrreverisble Irreparable loss of essential organsIrreparable loss of essential organs
Mechanical Requirements for Mechanical Requirements for Adequate Tissue PerfusionAdequate Tissue Perfusion
FluidFluid PumpPump VesselsVessels FlowFlow
Hypovolemic ShockHypovolemic Shock
#1 cause of death world wide#1 cause of death world wide GastroenteritisGastroenteritis Hemorrhagic – Trauma, GI bleedHemorrhagic – Trauma, GI bleed
Diagnosis of Hypovolemic ShockDiagnosis of Hypovolemic Shock
EarlyEarly Increase HRIncrease HR Decrease perfusionDecrease perfusion Normal BP, decrease pulse pressureNormal BP, decrease pulse pressure
LateLate Sign increase HRSign increase HR Sign decrease perfusion Sign decrease perfusion Decrease BPDecrease BP End organ dysfunctionEnd organ dysfunction
Pathophysiology of Pathophysiology of Hypovolemic ShockHypovolemic Shock
Decrease intravascular volumeDecrease intravascular volume Compensation – increase Compensation – increase
endogenous catecholaminesendogenous catecholamines Increase HR – increase C.O., O2 deliveryIncrease HR – increase C.O., O2 delivery Increase SVR – increase BP (esp Increase SVR – increase BP (esp
diastolic)diastolic) Compensation for <15% dehydrationCompensation for <15% dehydration
Cardiogenic ShockCardiogenic Shock
Pump failure/malfunctionPump failure/malfunction
(decreased contractility)(decreased contractility)
Cardiogenic ShockCardiogenic Shock
Electrical FailureElectrical Failure ArrhythmiasArrhythmias
Mechanical failureMechanical failure CardiomyopathyCardiomyopathy Metabolic – acidosisMetabolic – acidosis AnatomicAnatomic Hypoxia/ischemiaHypoxia/ischemia ObstructionObstruction
Cardiogenic ShockCardiogenic ShockSymptomsSymptoms
TachycardiaTachycardia TachypneaTachypnea Respiratory distressRespiratory distress Mental status changeMental status change Cool extremitiesCool extremities Poor perfusionPoor perfusion Signs of dehydrationSigns of dehydration
Cardiogenic ShockCardiogenic ShockObstruction of FlowObstruction of Flow
CausesCauses Pericardial tamponadePericardial tamponade Pulmonary embolismPulmonary embolism Pulmonary hypertensionPulmonary hypertension
Cardiogenic ShockCardiogenic ShockObstruction of FlowObstruction of Flow
Cardiac tamponadeCardiac tamponade CausesCauses
PericarditisPericarditis Post-traumaticPost-traumatic Post-cardiac surgeryPost-cardiac surgery Complication of central line placementComplication of central line placement
RecognitionRecognition TachycardiaTachycardia Low C.O., narrow pulse pressure (inc. diastole)Low C.O., narrow pulse pressure (inc. diastole) Inc. CVP, JVDInc. CVP, JVD PULSUS PARADOXUS (>10mmHg)PULSUS PARADOXUS (>10mmHg) Muffled heart sounds (??rub)Muffled heart sounds (??rub) NO RALESNO RALES
Distributive ShockDistributive Shock
Abnormal vessel toneAbnormal vessel tone
(decreased afterload)(decreased afterload)
Distributive ShockDistributive Shock
Vasodilitation Vasodilitation Venous PoolingVenous Pooling
Decreased Decreased AfterloadAfterload
Maldistribution of regional blood flowMaldistribution of regional blood flow
Distributive ShockDistributive Shock
Neurogenic or Anaphylactic ShockNeurogenic or Anaphylactic Shock Diminished or absent sympathetic Diminished or absent sympathetic
tonetone Reduce peripheral vascular toneReduce peripheral vascular tone Peripheral pooling of blood volumePeripheral pooling of blood volume Inadequate venous returnInadequate venous return Decreased perfusion, acidosis, Decreased perfusion, acidosis,
hypotensionhypotension
Septic ShockSeptic Shock
Terminology in SepsisTerminology in Sepsis Infection = response to micro organismInfection = response to micro organism Bacteremia = bug in bloodBacteremia = bug in blood Systemic Inflammatory Response Systemic Inflammatory Response
Syndrome (SIRS)Syndrome (SIRS) T>38, <36T>38, <36 Increase HRIncrease HR Increase RR, paCO2<32Increase RR, paCO2<32 WBC>12,000, <4,000, >10% bandsWBC>12,000, <4,000, >10% bands
Septic ShockSeptic Shock
Terminology in SepsisTerminology in Sepsis Sepsis = SIRS as response to a known Sepsis = SIRS as response to a known
infectioninfection Severe sepsis = Sepsis + organ Severe sepsis = Sepsis + organ
dysfunctiondysfunction Septic Shock = Sepsis + inadequate Septic Shock = Sepsis + inadequate
oxygen deliveryoxygen delivery Multiple Organ Dysfunction Syndrome Multiple Organ Dysfunction Syndrome
(MODS) – organ dysfunction that requires (MODS) – organ dysfunction that requires interventionintervention
Septic ShockSeptic Shock
Components of Septic shockComponents of Septic shock Decreased volumeDecreased volume Decreased pump functionDecreased pump function Abnormal vessel toneAbnormal vessel tone
Septic ShockSeptic Shock
Therapy for Caridovascular SupportTherapy for Caridovascular Support
PreloadPreload VolumeVolume
ContractilityContractility InotropesInotropes
AfterloadAfterload VasodilatorsVasodilators
Septic ShockSeptic Shock
EtiologiesEtiologies Inflammatory: too much, too littleInflammatory: too much, too little Coagulation pathway: DIC-bleeding, Coagulation pathway: DIC-bleeding,
pro-coagulant, microthombosispro-coagulant, microthombosis Multiple organ system failureMultiple organ system failure
Recognition of Septic ShockRecognition of Septic Shock
Early – Early – warm shock warm shock – similar to – similar to neurogenic shockneurogenic shock
Late – Late – Cold shock Cold shock – similar to – similar to cardiogenic shockcardiogenic shock
Diagnosis of Septic ShockDiagnosis of Septic Shock
Establish presence of infectionEstablish presence of infection Inc. HR, normal or dec. BP & Inc. HR, normal or dec. BP &
perfusionperfusion Latic acidosisLatic acidosis Muti-organ dysfunctionMuti-organ dysfunction
Early vs Late Septic ShockEarly vs Late Septic Shock
EarlyEarly LateLate
Heart rateHeart rate TachycardiaTachycardia Tachycardia/Tachycardia/
bradycardiabradycardia
Blood Blood pressurepressure
NormalNormal decreaseddecreased
PeripheralPeripheral
PerfusionPerfusionWarm/coolWarm/cool
Dec./inc. Dec./inc. pulsespulses
CoolCool
Dec. pulsesDec. pulses
Early vs Late Septic ShockEarly vs Late Septic Shock
EarlyEarly LateLate
End-organ: End-organ: skinskin
Dec. cap refillDec. cap refill Very dec. capVery dec. cap
RefillRefill
BrainBrain Irritable, Irritable, restlessrestless
Lethargic, Lethargic, unresponsiveunresponsive
KidneysKidneys OliguriaOliguria Oliguria, Oliguria, anuriaanuria
Treatment Strategies in Treatment Strategies in ShockShock
Principles of ResuscitationPrinciples of Resuscitation
Increase Oxygen Delivery\Increase Oxygen Delivery\ Increase Oxygen contentIncrease Oxygen content Increase Cardiac outputIncrease Cardiac output Increase blood pressureIncrease blood pressure
Decrease DemandDecrease Demand Sedation/analgesiaSedation/analgesia IntubationIntubation
Initial Treatment in ShockInitial Treatment in Shock
AAirwayirway Supplemental oxygen, intubationSupplemental oxygen, intubation
Carefull with cardiovascular collapse post intubation Carefull with cardiovascular collapse post intubation due to positive thoracic pressure decrease venous due to positive thoracic pressure decrease venous returnreturn
BBreathingreathing CCirculationirculation
Intravenous access – go early, go IOIntravenous access – go early, go IO Volume expansion (40cc/kg NS, repeat prn)Volume expansion (40cc/kg NS, repeat prn)
Carefull with cardiogenic shock (5cc/kg then reassess)Carefull with cardiogenic shock (5cc/kg then reassess) Optimize cardiac function, oxygenationOptimize cardiac function, oxygenation
Restoration of CirculationRestoration of CirculationVolumeVolume
Fluids, fluids, fluidsFluids, fluids, fluidsCrystalloids vs ColloidsCrystalloids vs Colloids
Restoration of CirculationRestoration of CirculationVolumeVolume
CrystalloidsCrystalloids NS is the fluid of choice, availabilityNS is the fluid of choice, availability Rapid redistribution out of intravascular Rapid redistribution out of intravascular
space – capillary leakspace – capillary leak
Restoration of CirculationRestoration of CirculationVolumeVolume
Colloids: albumin, bloodColloids: albumin, blood AlbuminAlbumin
Worsening of edema due to cap leak in early Worsening of edema due to cap leak in early sepsissepsis
BloodBlood Great volume expandersGreat volume expanders Side effects: with massive transfusion >1.5 Side effects: with massive transfusion >1.5
blood volumesblood volumes Risk of infectionRisk of infection Dilutional thrombocytopenia and factors V & VIIIDilutional thrombocytopenia and factors V & VIII Calcium binding hemodynamic instability (citrate)Calcium binding hemodynamic instability (citrate)
Restoration of CirculationRestoration of CirculationVolume – Fluid ChoicesVolume – Fluid Choices
Based on:Based on: Type of deficitType of deficit Urgency of repletionUrgency of repletion Pathophysiology of shockPathophysiology of shock
Restoration of CirculationRestoration of CirculationVolume – Fluid ChoicesVolume – Fluid Choices
Crystalloids for initial resuscitationCrystalloids for initial resuscitation Colloids/PRBC’s to replace blood lossColloids/PRBC’s to replace blood loss
Treatment of ShockTreatment of ShockCardiac SupportCardiac Support
AlphaAlpha DopamineDopamine BetaBeta
EpinephrineEpinephrine
NorepinephrineNorepinephrine DobutamineDobutamine
NeosynephrineNeosynephrine
InotropesInotropes
AgentAgent Site of ActionSite of Action DoseDose
Mcg/kg/minMcg/kg/minEffectsEffects
DopamineDopamine DopaminergicDopaminergic
BetaBeta
Alpha > BetaAlpha > Beta
1-31-3
5-105-10
11-2011-20
Renal vasodilationRenal vasodilation
Inotrope/vasoconstrictionInotrope/vasoconstriction
Increase perip. Vasc. resistanceIncrease perip. Vasc. resistance
DobutamineDobutamine Beta 1 & 2Beta 1 & 2 1-201-20 InotropeInotrope
VasodilationVasodilation
EpineprhineEpineprhine Beta > alphaBeta > alpha 0.05 – 1.00.05 – 1.0 Inotrope, vasoconstrictionInotrope, vasoconstriction
TachycardiaTachycardia
NorepinephriNorepinephrinene
Alpha > betaAlpha > beta 0.05 – 1.00.05 – 1.0 Profound vasoconstrictionProfound vasoconstriction
inotropeinotrope
NitroprussideNitroprusside VasodilatorVasodilator
(art > venous)(art > venous)0.5 – 1.00.5 – 1.0 VasodilationVasodilation
MilranoneMilranone Phosphodiesterase Phosphodiesterase inhibitorinhibitor
0.5 – 0.750.5 – 0.75 InotropeInotrope
vasodilationvasodilation
““New” Therapies in Septic ShockNew” Therapies in Septic Shock
VasopressinVasopressin SteroidsSteroids Activated protein C (Xigris) in Septic Activated protein C (Xigris) in Septic
ShockShock
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockVasopressinVasopressin
Unclear mechanism of actionUnclear mechanism of action Bridging vascular instability in high Bridging vascular instability in high
exogenous catecholamines exogenous catecholamines requirement septic shock, therefore requirement septic shock, therefore decrease side effects of toxic dosage decrease side effects of toxic dosage of catecholaminesof catecholamines
Also shows greater blood flow Also shows greater blood flow diversion from non-vital to vital diversion from non-vital to vital organsorgans
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockVasopressinVasopressin
Dosage 0.01 – 0.04U/min up to Dosage 0.01 – 0.04U/min up to 0.08U/min0.08U/min
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockSteroidsSteroids
Hypo-adrenalism: abnormal Hypo-adrenalism: abnormal hypothalamus-pituitary-adrenal axishypothalamus-pituitary-adrenal axis
At risk of adrenal insufficiency – in the At risk of adrenal insufficiency – in the presence of catecholamine presence of catecholamine requirementrequirement Fluid refractory shockFluid refractory shock Normal BP, cold shockNormal BP, cold shock Low BP, cold shockLow BP, cold shock
Dosage – stress doseDosage – stress dose Hydrocortisone 150 mg/m2 ivpHydrocortisone 150 mg/m2 ivp
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockSteroidsSteroids
Glucocorticoid function – immune Glucocorticoid function – immune responseresponse
Fall in circulating lymphocytesFall in circulating lymphocytes Inhibits neutrophils migration to the Inhibits neutrophils migration to the
inflammatory sitesinflammatory sites Inhibits macrophages secretionInhibits macrophages secretion Promotes eosinophilic apoptosisPromotes eosinophilic apoptosis Modulates cytokines production Modulates cytokines production
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockSteroidsSteroids
Glucocorticoid function – CardiovascularGlucocorticoid function – Cardiovascular Modulate vascular reactivity to Modulate vascular reactivity to
angiotensin II and to catecholamines -angiotensin II and to catecholamines -Not fully understood mechanismNot fully understood mechanism
Modulate vascular permeability and Modulate vascular permeability and production of NO and other production of NO and other vasodilator factorvasodilator factor
INCREASE IN BLOOD PRESSUREINCREASE IN BLOOD PRESSURE
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockSteroidsSteroids
Glucocorticoid production in stressGlucocorticoid production in stress Maintain homeostasisMaintain homeostasis Normalize vascular reactivityNormalize vascular reactivity Modulate inflammatory responseModulate inflammatory response
New” “ Therapies in Septic ShockNew” “ Therapies in Septic ShockActivated Protein C (Xigris)Activated Protein C (Xigris)
Recombinant Human Activated Protein Recombinant Human Activated Protein CC Prevent DIC cascade with antithrombotic Prevent DIC cascade with antithrombotic
activity by inhibiting factors Va & VIIIaactivity by inhibiting factors Va & VIIIa May exerts anti-inflammatory effects by May exerts anti-inflammatory effects by
inhibiting TNF and by blocking leukocytes inhibiting TNF and by blocking leukocytes adhesionsadhesions
Side effectsSide effects BleedingBleeding Pediatric trial terminated early (03/04) due Pediatric trial terminated early (03/04) due
to no benefit to known risk of bleedingto no benefit to known risk of bleeding