Cardiogenic Shock

NITASHA SARSWAT, MDCARDIOLOGY FELLOW

Cardiogenic Shock

Types of Shock

Distributive/Septic Shock: variable cardiac output, decreased SVR

Hypovolemic Shock: decreased effective circulating volume

Obstructive Shock: circulatory failure caused by physical obstruction, e.g. cardiac tamponade or pulmonary embolism

Cardiogenic Shock: decreased cardiac output, pump failure

Definition of Cardiogenic Shock

• Inadequate tissue perfusion resulting from cardiac dysfunction

• Clinical definition: decreased CO and tissue hypoxia in the presence of adequate intravascular volume

• Hemodynamic definition: Sustained SBP<90 mm Hg, CI <2.2 L/min/m2, PCWP > 15 mm Hg

• Subset of severe LV failure patients who have non-hypotensive cardiogenic shock: peripheral hypoperfusion with preserved BP

Definition of Cardiogenic Shock

SBP < 90 mm Hg for at least 1 hour that is not responsive to fluid administration alone

Secondary to cardiac dysfunction

Associated with signs of hypoperfusion or a CI < 2.2 L/min/m2 and a PAWP > 15 mmg Hg

Pathophysiology of CS: Downward Spiral

How to identify Cardiogenic Shock

HistoryPhysical ExamEKGChest xrayEchocardiogramSwan-Ganz Catheter

History: Who gets Cardiogenic Shock?

• Acute MI Pump failure Mechanical complications: VSD, Papillary septal

rupture, free wall rupture and cardiac tamponade Right ventricular infarction

• Other conditions End-stage cardiomyopathy Myocarditis Myocardial contusion Prolonged cardiopulmonary bypass Septic shock with myocardial depression Valvular disease: AS, AR, MS, MR

History: Who gets Cardiogenic Shock?

Congestion at Rest

LowPerfusionat Rest

No

No Yes

Yes

Warm & Dry5%

Warm & Wet70%

Cold & Wet20%

Cold & Dry5%

Signs of congestion Orthopnea/PND JVD Ascites Edema Rales (not always)

Evidence of low perfusion Narrow pulse pressure Altered mental status Low serum sodium

Cool extremities Hypotension with ACE inhibitor Renal insufficiency

Stevenson LW. Eur J Heart Fail. 1999;1:251

Physical Exam: Hemodynamic Profiles in Heart Failure

Physical Exam

CO Cold extremities, distant pulses, acidosis, SvO2. Try to figure out whether a decrease in CO is due to hypovolemia or due to pump failure.

Pump Failure Distended neck veins, S3, cold extremities Preload (CVP)Flat or absent neck veins, tachycardia. Preload (CVP) jugular vein distention, enlarged veins elsewhere SVRBP and mental state may be NORMAL.

Findings: Cold extremities, distant pulses SVRHypotension is likely. Patient may be warm with full pulses if CO

is normal or elevated.

Other valuable studies: Spot Echo exam of the heart: addresses tamponade, CHF, ischemia,

hypovolemia O2 saturation from CVP line or PICC line: provides indirect but

meaningful estimates of the adequacy of DO2, cardiac function.

EKG

If STEMI, degree and severity of EKG should agree with severity of clinical condition

If ST elevations in precordial leads -> likely anterior MI -> LV pump failure is likely cause

If inferior STEMI -> need marked ST elevations with reciprocal ST depressions on EKG. Check RV leads. If no reciprocal changes or RV infarct, think mechanical problems such as papillary muscle rupture

Normal EKG (especially with arrhythmias): think myocarditis

Echocardiogram

• Overall and regional systolic function• Mechanical causes of shock

• Papillary muscle rupture• Acute VSD• Free wall rupture

• Degree of mitral regurgitation• Right ventricular infarction• Other causes of shock (tamponade, PE,

valvular stenosis)

Right Heart Catheterization

If no right heart catheterization is performed:PE, CXR and TTE must clearly demonstrate systemic hypoperfusion, low CO and elevation of LA pressure/PA pressure /RA pressure

If the above is not clear, perform right heart catheterization

Right Heart Catheterization

• Exclude volume depletion, RV infarction, mechanical complications

• Optimize therapy• CO to guide use of inotropic agents

• Filling pressures to guide use of vasopressors and vasodilators

• Titration to minimum dosage required to achieve therapeutic goals and minimize increases in oxygen demand and arrhythmogenic potential

Therapy/Treatment

ACC Guidelines

Vasopressors and Inotropes

Diuretics

Cardiac Catheterization

Intra-aortic balloon pumps (IABPs)

Left Ventricular Assist Devices (LVADs)

Therapy/Treatment: ACC Guidelines

Class I1. Intra-aortic balloon counterpulsation is recommended for STEMI

patients when cardiogenic shock is not quickly reversed with pharmacological therapy. The IABP is a stabilizing measure for angiography and prompt revascularization. (Level of Evidence: B)

2. Intra-arterial monitoring is recommended for the management of STEMI patients with cardiogenic shock. (Level of Evidence: C)

3. Early revascularization, either PCI or CABG, is recommended for patients less than 75 years old with ST elevation or LBBB who develop shock within 36 hours of MI and who are suitable for revascularization that can be performed within 18 hours of shock unless further support is futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: A)

Therapy/Treatment: ACC Guidelines

4. Fibrinolytic therapy should be administered to STEMI patients with cardiogenic shock who are unsuitable for further invasive care and do not have contraindications to fibrinolysis. (Level of Evidence: B)

5. Echocardiography should be used to evaluate mechanical complications unless these are assessed by invasive measures. (Level of Evidence: C)


Goal: optimize perfusion while minimizing toxicity

Close monitoring of mixed venous saturation

Invasive hemodynamic monitoring (arterial line, cardiac output monitoring) to guide therapy

Inotropes: shift Frank-starling curve to a higher plateau (increased contractility)

Low output syndrome without shock: start with an inotrope such as dobutamine

Low output syndrome with shock: start with dopamine or norepinephrine



Dobutamine: B1 and B2, inotropic but also causes peripheral vasodilation Good for non-hypotensive cardiogenic shock Start with 5 ug/kg/min, don’t go higher than 20

ug/kg/minDopamine: inotrope and vasopressor in

hypotensive cardiogenic shock Up to 3 ug/kg/min – vasodilation and increase blood

flow to tissue beds, but no good evidence for “renal-dose dopamine”

Start at 5 ug/kg/min up to 15 ug/kg/min. Good inotropic and chronotropic effect at doses between 3 and 10 ug/kg/min (B1)

Mild peripheral vasoconstriction beyond 10 ug/kg/min (A1)


Norepinephrine: primarily vasoconstrictor, mild inotrope Increases SBP/DBP and pulse pressure Increases coronary flow Start 0.01 to 3 ug/kg/min Good for severe shock with profound hypotension

Epinephrine: B1/2 effects at low doses, A1 effects at higher doses Increases coronary blood flow (increases time in

diastole) Prolonged exposure -> myocyte damage


Milrinone: phosphodiesterase inhibitor, decreases rate of intracellcular cAMP degradation -> increases cytosolic calcium Increases cardiac contractility at expense of increase

myocardial oxygen consumption More vasodilation than dobutamine Can be combined with dobutamine to increases

inotropy Start bolus 25 ug/kg (if pt is not hypotensive) over 10-

20 min then 0.25-0.75 ug/kg/min May be proarrythmic, questionable in setting of acute

MI


Vasopressin: causes vasoconstriction, glyconeogenesis, platelet aggregation and ACTH release Neutral or depressant effect on cardiac output Dose-dependent increase in PVR with resultant

increase in reflexive vagal tone Increases vascular sensitivity to norepinephrine Good for norepinephrine-resistant shock

Diuretics

Mainstay of therapy to treat pulmonary edema and augment urine output

No good data regarding optimal diuretic protocol or whether diuretics improve outcome in renal failure

Lower doses of lasix are needed to maintain urine output when continuous infusions are used Start at 5 mg/hr, can increase up to 20 mg/hr

Cardiac Catheterization in Cardiogenic Shock

ACC Guidelines: emergent coronary revascularization is the standard of care for CS due to pump failure (acute MI and shock)

Most often demonstrates multi-vessel disease: Left main disease 23% 3-vessel disease 64% 2-vessel disease 22% 1-vessel disease 14%

Compensatory hyperkinesis: favorable prognostic factor

Diastole

Inflation

Systole

Intra-Aortic Balloon Counterpulsation

Standby Counterpulsation

Arterial Pressure

SMH #619 2008

Deflation Inflation

Intra-Aortic Balloon Counterpulsation

Reduces afterload and augments diastolic perfusion pressure

Beneficial effects occur without increase in oxygen demand

No improvement in blood flow distal to critical coronary stenosis

No improvement in survival when used alone

May be essential support mechanism to allow for definitive therapy

StandardPercutaneous

Tandem Heart Complete support Transseptal puncture Need good RV function

Impella Complete support Easy to insert Also need good RV function

Left ventricular assist devices

Left Ventricular Assist Devices (LVADs)

Components of the Left Ventricular Assist

Device. The inflow cannula is inserted into the

apex of the left ventricle, and the outflow

cannula is anastomosed to the ascending aorta.

Blood returns from the lungs to the left side of

the heart and exits through the left ventricular

apex and across an inflow valve into the

prosthetic pumping chamber. Blood is then

actively pumped through an outflow valve into

the ascending aorta. The pumping chamber is

placed within the abdominal wall or peritoneal

cavity. A percutaneous drive line carries the

electrical cable and air vent to the battery

packs (only the pack on the right side is shown)

and electronic controls, which are worn on a

shoulder holster and belt, respectively.

Tandem Heart™

Continuous flowRemoves oxygenated

blood from LA via trans-septal catheter placed through femoral vein

Returns blood via femoral artery

Shown to ↓ LAP and PCWP ↓ MVO2

↑ MAP, CO

Impella

Continuous flowInserted into LV

through AVBlood returns to

descending aortaNot yet approved

in US

Outcomes in Cardiogenic Shock

In-hospital mortality rate: 50-60% for all age groupsMechanical complications: even higher rates of

mortality Ventricular septal rupture -> highest mortality (87% in SHOCK

Registry)RV infarction: SHOCK – mortality unexpectedly high,

similar to LV failure shock despite younger age, lower rate of anterior MI and higher prevalence of single vessel disease

In hospital survival of diabetic patients in SHOCK was only marginally lower than non-diabetic patients

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Cardiogenic Shock