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ShockShock
Eric Kaiser M.D.Eric Kaiser M.D.Rosen’s Chapter 4Rosen’s Chapter 4
9-7-069-7-06
Slides by:Slides by:
Scott Gunderson D.O.Scott Gunderson D.O.
ShockShock
““Transition between life and death”Transition between life and death”
Failure to oxygenate & nourish the body Failure to oxygenate & nourish the body adequatelyadequately
Mortality > 20%Mortality > 20%
PathophysiologyPathophysiology&&
BiochemistryBiochemistry
PathophysiologyPathophysiology
Shock affects mitochondria firstShock affects mitochondria first
Without oxygen mitochondria convert fuels Without oxygen mitochondria convert fuels to lactate →to lactate → lactic acid lactic acid
Failure of the krebs cycleFailure of the krebs cycle Oxygen is the final electron accepter to form Oxygen is the final electron accepter to form
waterwater
Lactic AcidLactic Acid
Early shockEarly shock Skeletal muscle and splanchnic organs 1Skeletal muscle and splanchnic organs 1stst
affectedaffected Lactic acid productionLactic acid production
ResuscitationResuscitation Pyruvate delivery from glycolysis can Pyruvate delivery from glycolysis can
overwhelm krebs cycleoverwhelm krebs cycle
Systemic ResponseSystemic Response
DecreasedDecreased vascular wall tension increases vascular wall tension increases sympathetic stimulation (blocked in sepsis)sympathetic stimulation (blocked in sepsis) Increased epi, norepi, corticosteroids, renin, Increased epi, norepi, corticosteroids, renin,
and glucagonand glucagon Increased glycogenolysis and lipolysisIncreased glycogenolysis and lipolysis
Increased glucose and FFA’s to TCA can Increased glucose and FFA’s to TCA can overwhelm itoverwhelm it
Immune ResponseImmune Response
Neutrophil and macrophage activation due Neutrophil and macrophage activation due to hypoxiato hypoxia Enzymatic organ damageEnzymatic organ damage Capillary plugs causing microischemiaCapillary plugs causing microischemia TNF and Interleukins releasedTNF and Interleukins released
Cardiac PhysiologyCardiac Physiology
Contraction created by CaContraction created by Ca++++, ATP/CP, and , ATP/CP, and troponin Ctroponin C
Calcium inflow determines strength of Calcium inflow determines strength of contractioncontraction
Inotropics increase CaInotropics increase Ca++++ release in the release in the sarcoplasmic reticulum via sarcoplasmic reticulum via ββ-receptors or -receptors or cAMPcAMP
Cardiac PhysiologyCardiac Physiology
ATP/CP supply almost entirely from ATP/CP supply almost entirely from oxidative phosphorylation by mitochondriaoxidative phosphorylation by mitochondria
Complete turnover of ATP/CP every 5-10 Complete turnover of ATP/CP every 5-10 beatsbeats
Cardiac PhysiologyCardiac Physiology
Gregg PhenomenonGregg Phenomenon Contractile strength decreases with Contractile strength decreases with
decreased coronary perfusiondecreased coronary perfusion
Decreased coronary perfusion in shockDecreased coronary perfusion in shock
Decreased workload due to lower SVRDecreased workload due to lower SVR
Very minimal cardiac ischemia even in Very minimal cardiac ischemia even in severe shocksevere shock
Cardiac PhysiologyCardiac Physiology
Inflammatory actions of TNFInflammatory actions of TNFαα, , Interleukins, and NO decrease contractilityInterleukins, and NO decrease contractility
Acidosis can decrease contractility but Acidosis can decrease contractility but effect is minimaleffect is minimal
Clinical Features & Clinical Features & ManagementManagement
Clinical FeaturesClinical Features
Frequently no obvious etiologyFrequently no obvious etiology
Rapid recognitionRapid recognition H&P, ill appearance, diaphoresisH&P, ill appearance, diaphoresis HR and BP not reliableHR and BP not reliable HR/SBP ratio better indicatorHR/SBP ratio better indicator
Normal is less than 0.8Normal is less than 0.8 Urine output is great, but takes timeUrine output is great, but takes time
Normal >1.0 ml/kg/hrNormal >1.0 ml/kg/hr Lactic acid or base deficitLactic acid or base deficit
Shock Shock ClassificationClassification
Rapid, but Rapid, but detailed H&P detailed H&P to direct to direct therapytherapy
Flow diagramFlow diagram Figure 4-4 in Figure 4-4 in
Rosen’sRosen’s
Clinical DataClinical Data
CXR – infection, contusionsCXR – infection, contusionsEKG – ischemiaEKG – ischemiaGlucoseGlucoseCBC – anemia, leukocytosisCBC – anemia, leukocytosisElectrolytes – dehydration, GI bleed, Electrolytes – dehydration, GI bleed, acidosisacidosisABG – base deficit, acidosisABG – base deficit, acidosisUA – dehydrationUA – dehydration
ManagementManagement
IV, OIV, O22, monitor, monitor
BP readings every 2-5 minutesBP readings every 2-5 minutes Remember BP reading often underestimates Remember BP reading often underestimates
the level of shock until severethe level of shock until severe
Urine outputUrine output >1 cc/kg/min>1 cc/kg/min
ManagementManagement
IV accessIV access Peripheral vs. CentralPeripheral vs. Central
Most patients OK with one large bore or two Most patients OK with one large bore or two smaller bore peripheral IV’ssmaller bore peripheral IV’s
CVP pressure may be required for patient with CVP pressure may be required for patient with cardiac failure or renal failurecardiac failure or renal failure
Indwelling catheters should be used unless Indwelling catheters should be used unless hospital policy states against it in the EDhospital policy states against it in the ED
Volume ReplacementVolume Replacement
When is the tank full?When is the tank full? Goal CVP slightly elevated of 10-15 cm HGoal CVP slightly elevated of 10-15 cm H22OO Must correlate CVP with SBP, urine output, Must correlate CVP with SBP, urine output,
and lactate levels to adequately assess and lactate levels to adequately assess perfusionperfusion
VentilationVentilation
Rapid sequence intubation preferredRapid sequence intubation preferred Ketamine or etomidate are good choices due Ketamine or etomidate are good choices due
to minimal cardiovascular depressionto minimal cardiovascular depression Intubation protects aspiration, decreases Intubation protects aspiration, decreases
breathing workload, and initial treatment for breathing workload, and initial treatment for acidemiaacidemia
High negative pressures in bronchospasm or High negative pressures in bronchospasm or ARDS can decrease LVEF and positive ARDS can decrease LVEF and positive pressure removes thispressure removes this
AcidosisAcidosis
Acidosis is a negative inotropeAcidosis is a negative inotrope
No evidence supports using bicarbonate No evidence supports using bicarbonate for treatmentfor treatment
Treat with improved ventilation and mild Treat with improved ventilation and mild hyperventilationhyperventilation
THAM (tris[hydroxymethl]-aminomethane) THAM (tris[hydroxymethl]-aminomethane) may be used IV for acidosis reversalmay be used IV for acidosis reversal
Optimal HemoglobinOptimal Hemoglobin
Hemoglobin carries oxygenHemoglobin carries oxygen
High hematocrits increase viscosity and High hematocrits increase viscosity and cardiac workloadcardiac workload
Optimal balance is a hemoglobin of 10-12 Optimal balance is a hemoglobin of 10-12 gm%gm%
Goal-Directed TherapyGoal-Directed Therapy
Goal directed therapy is the practice of Goal directed therapy is the practice of resuscitating to a defined physiologic endpointresuscitating to a defined physiologic endpoint Wedge pressures – measures left ventricular filling Wedge pressures – measures left ventricular filling
pressures – controversial risk/benefitpressures – controversial risk/benefit Lactate clearing index – decrease in arterial lactate by Lactate clearing index – decrease in arterial lactate by
50% in 1 hour and continued efforts until lactate < 2 50% in 1 hour and continued efforts until lactate < 2 mMmM
GI tonography – permeable balloon in stomach or GI tonography – permeable balloon in stomach or rectum measuring pH to estimate perfusionrectum measuring pH to estimate perfusion
Questionable data supportingQuestionable data supporting
Specific Causes & Specific Causes & TreatmentTreatment
Hemorrhagic ShockHemorrhagic Shock
Rapid reduction in blood volumeRapid reduction in blood volume
Heart rate and blood pressure responses Heart rate and blood pressure responses can be variablecan be variable
No firm conclusion can be made by simply No firm conclusion can be made by simply HR and BP readingsHR and BP readings
Hemorrhagic ShockHemorrhagic Shock General Progression General Progression
Increased heart rate
Narrowed pulse pressure
Shunting from noncritical organs
Decreased cardiac fillingleading to decreased CO
Decreased SBP
Hemorrhagic ShockHemorrhagic Shock
Decreased perfusion to splanchnic organs Decreased perfusion to splanchnic organs precedes lower BPprecedes lower BP Lactic acid productionLactic acid production Base deficitBase deficit
Normal base deficit is greater than -2 mEq/LNormal base deficit is greater than -2 mEq/L
After 1/3 of blood volume lost hypotension After 1/3 of blood volume lost hypotension occursoccursAcidemia occurs about then as patient Acidemia occurs about then as patient cannot create enough respiratory cannot create enough respiratory compensation for the lactic acid compensation for the lactic acid
Hemorrhagic ShockHemorrhagic Shock
Organ injury in resuscitationOrgan injury in resuscitation Release of activated neutrophils & Release of activated neutrophils &
inflammatory cytokinesinflammatory cytokines Distorted balance of vasodilatation vs. Distorted balance of vasodilatation vs.
vasoconstrictionvasoconstriction May lead to ARDS, acute tubular necrosis, & May lead to ARDS, acute tubular necrosis, &
centrilobular ischemic liver damagecentrilobular ischemic liver damage
Consensus DefinitionConsensus Definition
Hemorrhagic Shock – 3 classificationsHemorrhagic Shock – 3 classifications Simple hemorrhageSimple hemorrhage
Bleeding with normal vital signs and base deficitBleeding with normal vital signs and base deficit Hemorrhage with hypoperfusionHemorrhage with hypoperfusion
Bleeding with base deficit < -5 mmol or persistent HR >100Bleeding with base deficit < -5 mmol or persistent HR >100 Hemorrhagic shockHemorrhagic shock
Bleeding with 4 or more of belowBleeding with 4 or more of below Ill appearance or mental statusIll appearance or mental status HR >100HR >100 RR >22 or PaCO2 <32RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hrUrine output < 0.5 cc/kg/hr Hypotension > 20 minutesHypotension > 20 minutes
Hemorrhagic Shock TreatmentHemorrhagic Shock Treatment
Several liters of crystalloids in adultsSeveral liters of crystalloids in adults
Three 20 cc/kg boluses in childrenThree 20 cc/kg boluses in children
If still in shock after bolus start PRBC’s at If still in shock after bolus start PRBC’s at 5-10 cc/kg5-10 cc/kg
Blood substitutes possibly in future but not Blood substitutes possibly in future but not currently advantageouscurrently advantageous
Hemorrhagic Shock TreatmentHemorrhagic Shock Treatment
Controlling hemorrhage is still always the Controlling hemorrhage is still always the cornerstone of treatmentcornerstone of treatment
Immediate surgery if hemorrhage cannot Immediate surgery if hemorrhage cannot be controlledbe controlled
In very rare cases inotropics may be In very rare cases inotropics may be beneficialbeneficial
Septic ShockSeptic Shock
Any microbe may cause, but gram Any microbe may cause, but gram negative most commonnegative most commonLipopolysaccharide is a key mediatorLipopolysaccharide is a key mediator1/3 of cases no organism is identified1/3 of cases no organism is identifiedHigher causes recently of gram positive Higher causes recently of gram positive due todue to Hospitalized patientsHospitalized patients ImmunocompromisedImmunocompromised Indwelling cathetersIndwelling catheters Increasing drug resistanceIncreasing drug resistance
Septic ShockSeptic Shock
3 major effects3 major effects HypovolemiaHypovolemia
Relative due to increased venous capacitanceRelative due to increased venous capacitance
Absolute due to GI loss, diaphoresis, tachypneaAbsolute due to GI loss, diaphoresis, tachypnea Cardiovascular depressionCardiovascular depression
Depression due to inflammatory mediatorsDepression due to inflammatory mediators Systemic inflammationSystemic inflammation
Capillary leak causing ARDS in up to 40%Capillary leak causing ARDS in up to 40%
Consensus DefinitionConsensus Definition
SIRSSIRS Two or more of the followingTwo or more of the following
Temperature > 38 C or <36 CTemperature > 38 C or <36 C
Heart rate > 90Heart rate > 90
Respiratory rate > 20 resp/min or PaCO2 <32Respiratory rate > 20 resp/min or PaCO2 <32
WBC > 12,000, < 4,000, or >10% bandsWBC > 12,000, < 4,000, or >10% bands
Septic ShockSeptic Shock Severe sepsis with hypotension unresponsive to fluid Severe sepsis with hypotension unresponsive to fluid
resuscitation and perfusion abnormalitiesresuscitation and perfusion abnormalities
Septic Shock TreatmentSeptic Shock Treatment
Ventilatory supportVentilatory support Decrease respiratory workload and correct Decrease respiratory workload and correct
hypoxiahypoxia
FluidsFluids Increase ventricular filingIncrease ventricular filing 20-25 cc/kg crystalloids followed by 5-10 20-25 cc/kg crystalloids followed by 5-10
cc/kg colloidscc/kg colloids
BloodBlood Used to keep Hct at 30-35% if neededUsed to keep Hct at 30-35% if needed
Septic Shock TreatmentSeptic Shock Treatment
AntibioticsAntibiotics If focus identifiedIf focus identified
Use clinical experience Use clinical experience
If no focus identifiedIf no focus identifiedSemisynthetic PCN with Semisynthetic PCN with ββ-lactamase inhibitor with -lactamase inhibitor with an aminoglycoside and vancomycinan aminoglycoside and vancomycin
Imipenem-cilastatin good monotherapy choiceImipenem-cilastatin good monotherapy choice
Antifungal in immunocompromisedAntifungal in immunocompromised
Septic Shock TreatmentSeptic Shock Treatment
VasopressorsVasopressors DopamineDopamine
Most common first line agent and a bad ideaMost common first line agent and a bad ideaRemove from you armamentariumRemove from you armamentarium
NorepinephrineNorepinephrineStart 0.5-1 µg/min and titrate to responseStart 0.5-1 µg/min and titrate to responseExcellent first choice; well studiedExcellent first choice; well studied
DobutamineDobutamineStart Start 5 5 µg/kg/minµg/kg/minHypotension unresponsive to vasopressors and Hypotension unresponsive to vasopressors and IVF.IVF.
Cardiogenic ShockCardiogenic Shock
Pump failurePump failure
Results when more than 40% of Results when more than 40% of myocardium damagedmyocardium damaged
Similar circulatory and metabolic changes Similar circulatory and metabolic changes to hemorrhagic shockto hemorrhagic shock
May also be due to a PEMay also be due to a PE
Consensus DefinitionsConsensus Definitions
CardiogenicCardiogenic Cardiac failureCardiac failure
Evidence of impaired cardiac outflow including Evidence of impaired cardiac outflow including dyspnea, tachycardia, rales, edema, or cyanosisdyspnea, tachycardia, rales, edema, or cyanosis
Cardiogenic shockCardiogenic shockCardiac failure plus four of below criteriaCardiac failure plus four of below criteria
Ill appearance or mental statusIll appearance or mental status HR >100HR >100 RR >22 or PaCO2 <32RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hrUrine output < 0.5 cc/kg/hr Hypotension > 20 minutesHypotension > 20 minutes
Cardiogenic Shock TreatmentCardiogenic Shock Treatment
Ventilatory supportVentilatory support Often needed in pulmonary edema or if Often needed in pulmonary edema or if
respiratory failure imminentrespiratory failure imminent
Avoid barbiturates, morphine, propofol and Avoid barbiturates, morphine, propofol and benzodiazepinesbenzodiazepines
Negative inotropic effectsNegative inotropic effects
Fentanyl, ketamine and etomidate much better Fentanyl, ketamine and etomidate much better choiceschoices
Cardiogenic Shock TreatmentCardiogenic Shock Treatment
Ionotropics/vasopressorsIonotropics/vasopressors Dobutamine and Milrinone are agents of Dobutamine and Milrinone are agents of
choicechoice Amrinone (Replaced by Milrinone)Amrinone (Replaced by Milrinone) MilrinoneMilrinone
Similar to amrinoneSimilar to amrinone
Load at 50 µg/kg (Consider half loading dose)Load at 50 µg/kg (Consider half loading dose)
Infuse at 0.37Infuse at 0.375 - 0.75 5 - 0.75 µg/kg/minµg/kg/min
Be prepared for hypotensionBe prepared for hypotension
Cardiogenic Shock TreatmentCardiogenic Shock Treatment
Intraaortic balloon pumpIntraaortic balloon pump When all pharmacologic therapy is failingWhen all pharmacologic therapy is failing
Requires appropriate facility and ICU/CCURequires appropriate facility and ICU/CCU
Improves cardiac output by 30%Improves cardiac output by 30%
Cardiogenic Shock TreatmentCardiogenic Shock Treatment
Myocardial infarction causing cardiogenic Myocardial infarction causing cardiogenic shockshock Management not significantly different than Management not significantly different than
another MI accept additional managementanother MI accept additional managementVentilatory support as neededVentilatory support as needed
Treat dysrhythmiasTreat dysrhythmias
Inotropic supportInotropic support
AspirinAspirin
HeparinHeparin
PTCA vs. thrombolyticsPTCA vs. thrombolytics
Cardiogenic Shock TreatmentCardiogenic Shock Treatment
Pulmonary EmbolismPulmonary Embolism Ventilatory supportVentilatory support IV fluidsIV fluids NorepinephrineNorepinephrine Thrombolytics (systemic vs. intra-arterial)Thrombolytics (systemic vs. intra-arterial) Possis catheterPossis catheter Surgical embolectomy at few centersSurgical embolectomy at few centers
Anaphylactic ShockAnaphylactic Shock
IgE mediated response to an allergenIgE mediated response to an allergen
Mast cells release histamineMast cells release histamine
Histamine causes Histamine causes Smooth muscle relaxationSmooth muscle relaxation
Bronchial contractionBronchial contraction
Capillary leakCapillary leak
Anaphylactic Shock TreatmentAnaphylactic Shock Treatment
EpinephrineEpinephrine 1 cc of 1:10,000 IV infused slowly and watch 1 cc of 1:10,000 IV infused slowly and watch
responseresponse 5 mg in 500 cc NS at 10 cc/hr thereafter5 mg in 500 cc NS at 10 cc/hr thereafter
May titrate to responseMay titrate to response Use even with coronary artery disease if Use even with coronary artery disease if
hypotensivehypotensive
Anaphylactic Shock TreatmentAnaphylactic Shock TreatmentCorticosteroidsCorticosteroids Decrease immune responseDecrease immune response Methylprednisolone 125mg IVMethylprednisolone 125mg IV Hydrocortisone 5-10 mg/kg IVHydrocortisone 5-10 mg/kg IV
AntihistaminesAntihistamines Diphenhydramine 0.5 mg/kg IVDiphenhydramine 0.5 mg/kg IV Cimetidine 2-5 mg/kg IVCimetidine 2-5 mg/kg IV FamotidineFamotidine
Intubation if neededIntubation if needed
Neurogenic ShockNeurogenic Shock
CNS cord lesions above T1CNS cord lesions above T1 Heart gets unopposed vagal simulationHeart gets unopposed vagal simulation Bradycardia and hypotensionBradycardia and hypotension
AtropineAtropine First line therapyFirst line therapy
Neurogenic Shock TreatmentNeurogenic Shock Treatment
Volume expansionVolume expansion Confirm by CVP and BPConfirm by CVP and BP
VasopressorsVasopressors EphedrineEphedrine
10 mg IV bolus good for 3-4 hours10 mg IV bolus good for 3-4 hours PhenylephrinePhenylephrine
100-180 100-180 µg/min IV until stableµg/min IV until stable
SummarySummary
Early recognition of shock and early Early recognition of shock and early treatment is keytreatment is key
Do not rely solely on a HR and BP to Do not rely solely on a HR and BP to determine their statusdetermine their status
Aggressive and goal directed therapy have Aggressive and goal directed therapy have proven to decrease mortalityproven to decrease mortality
ReferencesReferences
Jones, Alan E., & Kline, Jeffrey A. (2006). “Shock.” In Marx, Jones, Alan E., & Kline, Jeffrey A. (2006). “Shock.” In Marx, John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). Rosen's Rosen's Emergency Medicine: Concepts and Clinical PracticeEmergency Medicine: Concepts and Clinical Practice, 6th ed., , 6th ed., Pg. 41-56.Pg. 41-56. Mosby. Mosby.