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Cardiogenic ShockCardiogenic Shock

Dr M. DurandDr M. Durand

Anesthesia Department IIAnesthesia Department II

CHU GrenobleCHU Grenoble

IntroductionIntroduction

Heart failure: hypotension.Heart failure: hypotension. Periferic signs of shockPeriferic signs of shock oliguriaoliguria Altered consciousnessAltered consciousness

Dyspneea – See massive PAO.Dyspneea – See massive PAO.

Lactate level elevation.Lactate level elevation.

EtiologyEtiology Most frequent:Most frequent: Myocardic infarctionMyocardic infarction

Obstructive causes:Obstructive causes: TamponadeTamponade Pulmonary embolysmPulmonary embolysm

Other causes:Other causes: MyocardiopathyMyocardiopathy Severe myocarditisSevere myocarditis

Valvulopathy :Valvulopathy : IA => EI, dissectionIA => EI, dissection IMIM RARA

Post CECPost CEC

PhysiopathologyPhysiopathology

Cardiac performance determinants Cardiac performance determinants PreloadPreload PostloadPostload ContractilityContractility Cardiac frequenceCardiac frequence

Preload determinantsPreload determinants

Diastola diminuationDiastola diminuation Acceleration of cardiac rateAcceleration of cardiac rate Loss of atrial contractionLoss of atrial contraction

Extraparietal pressure augumentation: Extraparietal pressure augumentation: tamponadetamponade PEPPEP

Compliance issues:Compliance issues: ischemicischemic Hypertrophic cardiomiopathyHypertrophic cardiomiopathy

Diastolic and sistolic cardiac inssuficienceDiastolic and sistolic cardiac inssuficience

Sistolic :Sistolic : Ventricular contraction alterationVentricular contraction alteration

DiastolicDiastolic Abnormal ventricular filling:Abnormal ventricular filling:

Decreased distensibility – ventricular fibrosisDecreased distensibility – ventricular fibrosis LV wall thickening.LV wall thickening.

causes : miocardic hypertrophy/ischemy.causes : miocardic hypertrophy/ischemy.

Right heart failureRight heart failure

Right ventriculeRight ventricule Very sensible at postloadVery sensible at postload

cardiac output maintained up to a systolic pressure of 40 cardiac output maintained up to a systolic pressure of 40 mmHgmmHg

Less sensitive to preloadLess sensitive to preload Expands easily because of it’s thinnessExpands easily because of it’s thinness It’s expansion may limit LV fillingIt’s expansion may limit LV filling Systo-diastolic perfusionSysto-diastolic perfusion

Spontanious respirationSpontanious respiration

Bronchial edema => increase resistance to gas Bronchial edema => increase resistance to gas flow => increased inspiratory depressionflow => increased inspiratory depression

Increased venous returnIncreased venous return Increase in the transparietal gradient of the LV Increase in the transparietal gradient of the LV

=> disconfort in the systolic ejection of LV.=> disconfort in the systolic ejection of LV.

Ventilation InteractionsVentilation Interactions In spontanious ventilation:In spontanious ventilation:

inspiration increases the venous return and therefore the inspiration increases the venous return and therefore the rate of RVrate of RV

TheThe increase in lung volume increases lung resistance increase in lung volume increases lung resistance In assisted ventilation:In assisted ventilation:

Increased intrathoracic pressureIncreased intrathoracic pressure Decreases venous returnDecreases venous return Increases postload of the RVIncreases postload of the RV

Increase in pulmonary volumeIncrease in pulmonary volume Increases vascular resistence of the lungsIncreases vascular resistence of the lungs

VG Interactions / Mechanical VentilationVG Interactions / Mechanical Ventilation

The increased intrathoracic pressure decreases venous The increased intrathoracic pressure decreases venous return and therefore preloads VGreturn and therefore preloads VG

the increased intrathoracic pressure reduces afterload the increased intrathoracic pressure reduces afterload by decreasing LV - transmural LV pressureby decreasing LV - transmural LV pressure

Decrease in the systolic stress of VGDecrease in the systolic stress of VG the increase in intrathoracic pressure by PEEP the increase in intrathoracic pressure by PEEP

increases these effectsincreases these effects

Hemodynamic tableHemodynamic table

Cardiogenic shock

Septic shock

DC PA

PVC PAPO DO2 ErO2

Fundamental anomalies in shock statesFundamental anomalies in shock states

Cardiac debit decreaseCardiac debit decrease Oxygen transportation decreaseOxygen transportation decrease

DO2 decreaseDO2 decrease Increase in extractionIncrease in extraction

Absence of inflammatory syndromeAbsence of inflammatory syndrome Secondary appearance of an inflammatory Secondary appearance of an inflammatory

syndromesyndrome Especially in post CPBEspecially in post CPB

Monitoring : the Swan GanzMonitoring : the Swan Ganz

Monitoring of cardiac output and filling pressuresMonitoring of cardiac output and filling pressures Approximation PAOP => POG => LVEDP => Approximation PAOP => POG => LVEDP =>

ventricular volumeventricular volume Error causes:Error causes:

PEP, decreased LV compliancePEP, decreased LV compliance Pulmonary embolysmPulmonary embolysm Mitral pathology, IAMitral pathology, IA Respiration interferenceRespiration interference

PAOP - guiding filling valuePAOP - guiding filling value

If PAOP <12 => filling is usefullIf PAOP <12 => filling is usefull If PAOP is between 12 and 18:If PAOP is between 12 and 18:

In the abscence of pulmonary edema => fillIn the abscence of pulmonary edema => fill In case of pulmonary edema => do not fillIn case of pulmonary edema => do not fill

If PAOP is over 18 => probably no fillingIf PAOP is over 18 => probably no filling Variation of PAOP and cardiac output should be Variation of PAOP and cardiac output should be

monitored during filling.monitored during filling.

Evaluation for echocardiographyEvaluation for echocardiography

Measurement of right and left ventricular surfacesMeasurement of right and left ventricular surfaces A A surface of the LV <7 cm2/m2 is in favor of surface of the LV <7 cm2/m2 is in favor of

hypovolemiahypovolemia evolution of the surface of the LV during fillingevolution of the surface of the LV during filling surface of the RV, risk of expansionsurface of the RV, risk of expansion

Swan Ganz and/or EcocardiographySwan Ganz and/or Ecocardiography

During filling with 3L of crystaloids:During filling with 3L of crystaloids: parallel increase in the surface and measured parallel increase in the surface and measured

pressurespressures Systolic volume increaseSystolic volume increase

End of filling process:End of filling process: increased filling pressures without increasing increased filling pressures without increasing

the ventricular surfacethe ventricular surface

Study of variation in blood pressure during Study of variation in blood pressure during mechanical ventilationmechanical ventilation

P

VNormal Function

Abnormal Function

Medication TreatmentMedication Treatment

1 2

Isoprenaline +++ +++ 0 0

Dopexamine 0 ++ 0 +

Dobutamine +++ + 0 0

Dopamine ++ + ++ +++

Adrenalin +++ +++ +++ 0

Noradrenalin ++ 0 +++ 0

TreatmentTreatment HemodynamicHemodynamic

FillingFilling OxigenationOxigenation Pain treatmentPain treatment

EthiologicalEthiological Thrombolysis is uneffectiveThrombolysis is uneffective Thrombolysis and counterpulsationThrombolysis and counterpulsation Percutaneous dilationPercutaneous dilation Emergency coronary surgeryEmergency coronary surgery Search for an VSD or IMSearch for an VSD or IM

Drug treatmentsDrug treatments

Phosphodiesterase inhibitors:Phosphodiesterase inhibitors: Positive inotropePositive inotrope Peripheric vassodilutantPeripheric vassodilutant They most be used:They most be used:

With caution when blood pressure is borderlineWith caution when blood pressure is borderline Not to be used when PA is already lowNot to be used when PA is already low

Diuretic and vassodilutant treatmentsDiuretic and vassodilutant treatments

Vasodilators increase cardiac output by decreasing Vasodilators increase cardiac output by decreasing afterloadafterload

Vasodilators have a limited role in acute Vasodilators have a limited role in acute : : Risk of aggravating hypotensionRisk of aggravating hypotension

Only the nitro-derivates are sometimes used:Only the nitro-derivates are sometimes used: low dose: vassodilutant => decreased venous returnlow dose: vassodilutant => decreased venous return High dose: arterial vasodilationHigh dose: arterial vasodilation

Diuretics should not be used in acute cardiogenic shock Diuretics should not be used in acute cardiogenic shock outside of the PAO.outside of the PAO.

Volemic expansionVolemic expansion

The existence of hypovolemia is not exceptional The existence of hypovolemia is not exceptional in cardiogenic shock:in cardiogenic shock: Administrated treatments:Administrated treatments:

sedationsedation diureticsdiuretics nitrosnitros

Prudent volemic expansionPrudent volemic expansion

Mechanical treatments - VentilationMechanical treatments - Ventilation

Hemodynamic effects:Hemodynamic effects: Decrease in the VA preloadDecrease in the VA preload Decrease in LV afterloadDecrease in LV afterload

Respiratory effects:Respiratory effects: Hypoxemy correctionHypoxemy correction Acidosis correctionAcidosis correction

Decrease in oxygen consumptionDecrease in oxygen consumption Respiratory work decreaseRespiratory work decrease sedationsedation

Non-invasive ventilationNon-invasive ventilation

The non-invasive ventilation allows:The non-invasive ventilation allows: Rapid correction of hypoxemia with shunt Rapid correction of hypoxemia with shunt

reductionreduction A decrease in respiratory frequence and A decrease in respiratory frequence and

therefore a decrease in respiratory workloadtherefore a decrease in respiratory workload Reduces the need for intubation during severe Reduces the need for intubation during severe

PAOPAO Most often: CPAP, PEP from 7.5 to 10 cmH2O.Most often: CPAP, PEP from 7.5 to 10 cmH2O.

Mechanical treatment: intra-aortic Mechanical treatment: intra-aortic counterpulsationcounterpulsation

Diastolic swelling of intra-aortic balloon: Diastolic swelling of intra-aortic balloon:

an increase in diastolic blood pressure => an increase in diastolic blood pressure => improved perfusion VGimproved perfusion VG

a decrease in blood pressure in late diastole => a decrease in blood pressure in late diastole => facilitates the left ventricular ejectionfacilitates the left ventricular ejection

Counterpulsation mechanismCounterpulsation mechanismIncreased diastolic pressure

Assisted tele-diastolic pressureNon-assisted tele-diastolic pressure

Non-assisted sistolic pressure

Assisted sistolic pressure

TreatmentTreatment

Etiological :Etiological : Tamponade => evacuation of the effusionTamponade => evacuation of the effusion Rhytm problemsRhytm problems

ACFAACFA BradycardiaBradycardia

Pulmonary embolismPulmonary embolism ValvulopathiesValvulopathies IDMIDM

LV infarctusLV infarctus

Shock complicating 10% of IDMShock complicating 10% of IDM Mortality remains very highMortality remains very high Installation of an ischemic vicious circleInstallation of an ischemic vicious circle

Hypotension

Perfusion pressure decrease

Ischemic aggravation

LVEDP increase

Sympathetic stim.

Mechanical complications of MIMechanical complications of MI

Mitral inssuficienceMitral inssuficience Pillar disruption or disfunctionPillar disruption or disfunction

CIVCIV Secondary painSecondary pain EcocardiographyEcocardiography SurgerySurgery

LV ruptureLV rupture 3/5° day3/5° day

RV infarctionRV infarction

Very rareVery rare Most often associated with a posterior/inferior Most often associated with a posterior/inferior

myocardial infarctionmyocardial infarction Low-speed + increase in CVP + no sign of Low-speed + increase in CVP + no sign of

respiratory signsrespiratory signs Treatment :Treatment :

FillingFilling InotropesInotropes IABPIABP SEASEA

MyocarditisMyocarditis

State of shock in a viral contextState of shock in a viral context Diffuse alteration of systolic function on Diffuse alteration of systolic function on

echocardiographyechocardiography TTT :TTT :

SymptomaticSymptomatic Corticoides +- ImmunosupressorsCorticoides +- Immunosupressors Circulatory assistenceCirculatory assistence

Frequent recoveryFrequent recovery

Cardiogenic shock of aortic stenosisCardiogenic shock of aortic stenosis

Rao => LV hypertrophy, and late dilationRao => LV hypertrophy, and late dilation On examination: breath mitigated by the low flowOn examination: breath mitigated by the low flow At echocardiography: gdt decreased by low-speed => At echocardiography: gdt decreased by low-speed =>

Area MeasurementArea Measurement Dangers of drug treatments:Dangers of drug treatments:

VD => decreased preload => lower ESR and lower BP VD => decreased preload => lower ESR and lower BP => myocardial ischemia=> myocardial ischemia

-antagonists poorly supported-antagonists poorly supported Counterpulsation awaiting surgeryCounterpulsation awaiting surgery

Cardiogenic shock from acute aortic Cardiogenic shock from acute aortic insufficiencyinsufficiency

Etiology: endocarditis, aortic dissectionEtiology: endocarditis, aortic dissection Clinical :Clinical :

Somewhat increased P differentialSomewhat increased P differential WheezingWheezing PTDVG > POGPTDVG > POG

Dg => echocardiographyDg => echocardiography

TamponadeTamponade

Pericardial effusion => increased pressure => Pericardial effusion => increased pressure => discomfort fillingdiscomfort filling

Dg :Dg : KT : egalisation of POD/PAPD/POGKT : egalisation of POD/PAPD/POG EchocardiographyEchocardiography

EffusionEffusion Signs of tamponadeSigns of tamponade

TreatmentTreatment Effusion evacuationEffusion evacuation Attention at anesthesy/ventilationAttention at anesthesy/ventilation

ConclusionsConclusions

Cardiogenic shockCardiogenic shock requires diagnosis and etiologic treatment requires diagnosis and etiologic treatment

whenever possiblewhenever possible treatment is not limited to dobutaminetreatment is not limited to dobutamine a complete hemodynamic assessment is a complete hemodynamic assessment is

necessary in case of failure of initial treatmentnecessary in case of failure of initial treatment

BibliographyBibliography

Choc cardiogénique : Encycl Med Chir, Choc cardiogénique : Encycl Med Chir, Anesthésie-Réanimation, 36-840-c-10, 1999, M Anesthésie-Réanimation, 36-840-c-10, 1999, M Shaller, P Eckert, D Tagan, LausanneShaller, P Eckert, D Tagan, Lausanne

Choc Cardiogénique : Anesthésie Réanimation Choc Cardiogénique : Anesthésie Réanimation Chirurgicale K SamiiChirurgicale K Samii

Infarctus aiguë du myocarde avec sus-décalage du Infarctus aiguë du myocarde avec sus-décalage du segment ST : 48°heures Encycl Med Chir, segment ST : 48°heures Encycl Med Chir, Anesthésie-Réanimation 36-725 F10Anesthésie-Réanimation 36-725 F10