Shock Eric Kaiser M.D. Rosen’s Chapter 4 9-7-06 Slides by: Scott Gunderson D.O

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


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


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


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


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


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


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


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


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


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%


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


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.

Documents

Shock Eric Kaiser M.D. Rosen’s Chapter 4 9-7-06 Slides by: Scott Gunderson D.O