ShockEric Kaiser M.D.Rosens Chapter 49-7-06

Slides by:Scott Gunderson D.O.

ShockTransition between life and death

Failure to oxygenate & nourish the body adequately

Mortality > 20%

Pathophysiology&Biochemistry

PathophysiologyShock affects mitochondria first

Without oxygen mitochondria convert fuels to lactate lactic acid

Failure of the krebs cycleOxygen is the final electron accepter to form water

Lactic AcidEarly shockSkeletal muscle and splanchnic organs 1st affectedLactic acid production

ResuscitationPyruvate delivery from glycolysis can overwhelm krebs cycle

Systemic ResponseDecreased vascular wall tension increases sympathetic stimulation (blocked in sepsis)Increased epi, norepi, corticosteroids, renin, and glucagonIncreased glycogenolysis and lipolysis

Increased glucose and FFAs to TCA can overwhelm it

Immune ResponseNeutrophil and macrophage activation due to hypoxiaEnzymatic organ damageCapillary plugs causing microischemiaTNF and Interleukins released

Cardiac PhysiologyContraction created by Ca++, ATP/CP, and troponin C

Calcium inflow determines strength of contraction

Inotropics increase Ca++ release in the sarcoplasmic reticulum via -receptors or cAMP

Cardiac PhysiologyATP/CP supply almost entirely from oxidative phosphorylation by mitochondria

Complete turnover of ATP/CP every 5-10 beats

Cardiac PhysiologyGregg PhenomenonContractile strength decreases with decreased coronary perfusionDecreased coronary perfusion in shockDecreased workload due to lower SVRVery minimal cardiac ischemia even in severe shock

Cardiac PhysiologyInflammatory actions of TNF, Interleukins, and NO decrease contractility

Acidosis can decrease contractility but effect is minimal

Clinical Features & Management

Clinical FeaturesFrequently no obvious etiologyRapid recognitionH&P, ill appearance, diaphoresisHR and BP not reliableHR/SBP ratio better indicatorNormal is less than 0.8Urine output is great, but takes timeNormal >1.0 ml/kg/hrLactic acid or base deficit

Shock ClassificationRapid, but detailed H&P to direct therapy

Flow diagramFigure 4-4 in Rosens

Clinical Data

CXR infection, contusionsEKG ischemiaGlucoseCBC anemia, leukocytosisElectrolytes dehydration, GI bleed, acidosisABG base deficit, acidosisUA dehydration

ManagementIV, O2, monitorBP readings every 2-5 minutesRemember BP reading often underestimates the level of shock until severe

Urine output>1 cc/kg/min

ManagementIV accessPeripheral vs. CentralMost patients OK with one large bore or two smaller bore peripheral IVsCVP pressure may be required for patient with cardiac failure or renal failureIndwelling catheters should be used unless hospital policy states against it in the ED

Volume ReplacementWhen is the tank full?Goal CVP slightly elevated of 10-15 cm H2OMust correlate CVP with SBP, urine output, and lactate levels to adequately assess perfusion

VentilationRapid sequence intubation preferredKetamine or etomidate are good choices due to minimal cardiovascular depressionIntubation protects aspiration, decreases breathing workload, and initial treatment for acidemiaHigh negative pressures in bronchospasm or ARDS can decrease LVEF and positive pressure removes this

AcidosisAcidosis is a negative inotropeNo evidence supports using bicarbonate for treatmentTreat with improved ventilation and mild hyperventilationTHAM (tris[hydroxymethl]-aminomethane) may be used IV for acidosis reversal

Optimal HemoglobinHemoglobin carries oxygen

High hematocrits increase viscosity and cardiac workload

Optimal balance is a hemoglobin of 10-12 gm%

Goal-Directed TherapyGoal directed therapy is the practice of resuscitating to a defined physiologic endpointWedge pressures measures left ventricular filling pressures controversial risk/benefitLactate clearing index decrease in arterial lactate by 50% in 1 hour and continued efforts until lactate < 2 mMGI tonography permeable balloon in stomach or rectum measuring pH to estimate perfusionQuestionable data supporting

Specific Causes & Treatment

Hemorrhagic ShockRapid reduction in blood volume

Heart rate and blood pressure responses can be variable

No firm conclusion can be made by simply HR and BP readings

Hemorrhagic Shock General Progression

Hemorrhagic ShockDecreased perfusion to splanchnic organs precedes lower BPLactic acid productionBase deficitNormal base deficit is greater than -2 mEq/LAfter 1/3 of blood volume lost hypotension occursAcidemia occurs about then as patient cannot create enough respiratory compensation for the lactic acid

Hemorrhagic ShockOrgan injury in resuscitationRelease of activated neutrophils & inflammatory cytokinesDistorted balance of vasodilatation vs. vasoconstrictionMay lead to ARDS, acute tubular necrosis, & centrilobular ischemic liver damage

Consensus DefinitionHemorrhagic Shock 3 classificationsSimple hemorrhageBleeding with normal vital signs and base deficitHemorrhage with hypoperfusionBleeding with base deficit < -5 mmol or persistent HR >100Hemorrhagic shockBleeding with 4 or more of belowIll appearance or mental statusHR >100RR >22 or PaCO2 4Urine output < 0.5 cc/kg/hrHypotension > 20 minutes

Hemorrhagic Shock TreatmentSeveral liters of crystalloids in adults

Three 20 cc/kg boluses in children

If still in shock after bolus start PRBCs at 5-10 cc/kg

Blood substitutes possibly in future but not currently advantageous

Hemorrhagic Shock TreatmentControlling hemorrhage is still always the cornerstone of treatment

Immediate surgery if hemorrhage cannot be controlled

In very rare cases inotropics may be beneficial

Septic ShockAny microbe may cause, but gram negative most commonLipopolysaccharide is a key mediator1/3 of cases no organism is identifiedHigher causes recently of gram positive due toHospitalized patientsImmunocompromisedIndwelling cathetersIncreasing drug resistance

Septic Shock3 major effectsHypovolemiaRelative due to increased venous capacitanceAbsolute due to GI loss, diaphoresis, tachypneaCardiovascular depressionDepression due to inflammatory mediatorsSystemic inflammationCapillary leak causing ARDS in up to 40%

Consensus DefinitionSIRSTwo or more of the followingTemperature > 38 C or 90Respiratory rate > 20 resp/min or PaCO2 12,000, < 4,000, or >10% bands

Septic ShockSevere sepsis with hypotension unresponsive to fluid resuscitation and perfusion abnormalities

Septic Shock TreatmentVentilatory supportDecrease respiratory workload and correct hypoxiaFluidsIncrease ventricular filing20-25 cc/kg crystalloids followed by 5-10 cc/kg colloidsBloodUsed to keep Hct at 30-35% if needed

Septic Shock TreatmentAntibioticsIf focus identifiedUse clinical experience

If no focus identifiedSemisynthetic PCN with -lactamase inhibitor with an aminoglycoside and vancomycinImipenem-cilastatin good monotherapy choiceAntifungal in immunocompromised

Septic Shock TreatmentVasopressorsDopamineMost common first line agent and a bad ideaRemove from you armamentariumNorepinephrineStart 0.5-1 g/min and titrate to responseExcellent first choice; well studiedDobutamineStart 5 g/kg/minHypotension unresponsive to vasopressors and IVF.

Cardiogenic ShockPump failureResults when more than 40% of myocardium damagedSimilar circulatory and metabolic changes to hemorrhagic shockMay also be due to a PE

Consensus DefinitionsCardiogenicCardiac failureEvidence of impaired cardiac outflow including dyspnea, tachycardia, rales, edema, or cyanosisCardiogenic shockCardiac failure plus four of below criteriaIll appearance or mental statusHR >100RR >22 or PaCO2 4Urine output < 0.5 cc/kg/hrHypotension > 20 minutes

Cardiogenic Shock TreatmentVentilatory supportOften needed in pulmonary edema or if respiratory failure imminent

Avoid barbiturates, morphine, propofol and benzodiazepinesNegative inotropic effectsFentanyl, ketamine and etomidate much better choices

Cardiogenic Shock TreatmentIonotropics/vasopressorsDobutamine and Milrinone are agents of choiceAmrinone (Replaced by Milrinone)MilrinoneSimilar to amrinoneLoad at 50 g/kg (Consider half loading dose)Infuse at 0.375 - 0.75 g/kg/minBe prepared for hypotension

Cardiogenic Shock TreatmentIntraaortic balloon pumpWhen all pharmacologic therapy is failing

Requires appropriate facility and ICU/CCU

Improves cardiac output by 30%

Cardiogenic Shock TreatmentMyocardial infarction causing cardiogenic shockManagement not significantly different than another MI accept additional managementVentilatory support as neededTreat dysrhythmiasInotropic supportAspirinHeparinPTCA vs. thrombolytics

Cardiogenic Shock TreatmentPulmonary EmbolismVentilatory supportIV fluidsNorepinephrineThrombolytics (systemic vs. intra-arterial)Possis catheterSurgical embolectomy at few centers

Anaphylactic ShockIgE mediated response to an allergenMast cells release histamineHistamine causes Smooth muscle relaxationBronchial contractionCapillary leak

Anaphylactic Shock TreatmentEpinephrine1 cc of 1:10,000 IV infused slowly and watch response5 mg in 500 cc NS at 10 cc/hr thereafterMay titrate to responseUse even with coronary artery disease if hypotensive

Anaphylactic Shock TreatmentCorticosteroidsDecrease immune responseMethylprednisolone 125mg IVHydrocortisone 5-10 mg/kg IV

AntihistaminesDiphenhydramine 0.5 mg/kg IVCimetidine 2-5 mg/kg IVFamotidine

Intubation if needed

Neurogenic ShockCNS cord lesions above T1Heart gets unopposed vagal simulationBradycardia and hypotension

AtropineFirst line therapy

Neurogenic Shock TreatmentVolume expansionConfirm by CVP and BP

VasopressorsEphedrine10 mg IV bolus good for 3-4 hoursPhenylephrine100-180 g/min IV until stable

SummaryEarly recognition of shock and early treatment is key

Do not rely solely on a HR and BP to determine their status

Aggressive and goal directed therapy have proven to decrease mortality

ReferencesJones, Alan E., & Kline, Jeffrey A. (2006). Shock. In Marx, John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Pg. 41-56. Mosby.