Medical Information

Cardiogenic Shock

Cardiogenic Shock
June 26, 2006

Henry L. Green, FACC, FACP

Incidence

7% of patients with myocardial infarction.

Commonest cause of death in myocardial infarction.

Most common with ST elevation myocardial infarctions.

Only 10-15% present initially with shock, offering an opportunity to prevent it by reperfusion therapy, such as primary percutaneous intervention.

Management

Support measures

Used to help stabilize patient prior to and during revascularization to prevent end organ damage

Vasopressors

Dopamine or norepinephrine, depending on degree of hypotension at minimum dose required

Dobutamine alone or with dopamine may be combined if hypoperfusion is not accompanied by

frank hypotension.

Intraortic balloon pump – if possible, apply before transfer

Mechanical ventilation

Monitor ECG

Emergency drugs and defibrillator

Temporary pacemaker at hand

Lowering core temperature to 33° C may be helpful

Left ventricular assist device

Revascularization

Angioplasty or bypass grafting associated with better outcomes than intensive medical therapy. (Mortality about 30% with revascularization, 75% with medical therapy in GUSTO-I trial)

Should be done as early as possible, but there is no absolute time window.

Invasive treatment usually reserved for patients younger than 75 years. However, in selected patients (“physiologically younger”), invasive treatment is not always ruled out. Consider comorbidities, duration of shock, coronary anatomy, recency of MI.

Repair of mechanical defects

Septal rupture, mitral regurgitation

Specific forms of cardiogenic shock

Extensive myocardial infarction

Accounts for majority of patients with cardiogenic shock

Myocardial rupture

Incidence

3% of patients, commoner in elderly women, hypertensives, and those with poor collaterals

Usually no prior infarct.

Usually 1-4 days after onset, but can be up to 3 weeks

Acute rupture is usually rapidly fatal

Subacute rupture with pseudoaneurysm formation

Nausea, hypotension, pericardial pain

Jugular venous distention, pulsus paradoxicus, pericardial rub and new to-and-fro murmur may be found.

Symptoms

Angina, pleuritic pr pericardial pain

Syncope, hypotension

Arrhythmias

Nausea, restlessness, hypotension

Physical examination

Jugular venous distention (29%)

Pulsus paradoxicus (47%)

Electromechanical dissociation

Cardiogenic shock

Sudden death

Echocardiogram

Pericardial effusion with high-acoustic echoes (blood clot) -- not always visualized

Direct visualization of tear

Signs of tamponade

Right heart catheterization

Ventriculography insensitive

Signs of tamponade not always present

Treatment

Pericardiocentesis may temporarily relieve tamponade if present

Prompt surgery

Ventricular septal rupture

Incidence

Up to 4% of myocardial infarctions, usually 3-7 days after onset but may be earlier

Risk factors: hypertension, advanced age, female sex, absence of prior angina or MI

May occur with anterior, inferior or posterior infarcts, more often with anterior infarcts

Results in a large left to right shunt. This may decrease as left ventricle fails.

20% are associated with severe mitral regurgitation

Symptoms

Chest pain, dyspnea, symptoms of low output and shock

Physical examination

Pansystolic murmur, usually lower left sternal border

Usually loud, sometimes with thrill. With shock, murmur may be hard to identify

Often right and left ventricular gallops (S3). Pulmonic second sound accentuated

Right and left ventricular failure

Cardiogenic shock

Echocardiogram

Ventricular septal rupture

Left to right shunt

Right ventricular overload

Right heart catheterization

Increase in oxygen saturation from right atrium to right ventricle

Large V waves

Treatment

Medical

Intraortic balloon pump

Afterload reduction, nitroprusside

Diuretics

Usually inotropic agents

Oxygen (mask, CPAP, BIPAP or intubation)

Surgery

Usually required and best done early

Closure of defect and reconstruction of ventricle

Coronary artery bypass grafting

Prognosis

Roughly 50% mortality. Of those who survive surgery, 5-year survival is 70%

Acute severe mitral regurgitation

Incidence

Usually 2-7 days after the infarct

Usually with inferior infarcts (posteromedial papillary muscle has single artery, anterior muscle , has dual supply.)

Often due to papillary muscle dysfunction, less often papillary muscle rupture

Symptoms

Abrupt onset of shortness of breath, pulmonary edema; hypotension

Physical examination

Pansystolic murmur, usually apex.

May or may not be loud, rarely with a thrill

Variable signs of right ventricular overload

Severe pulmonary edema

Cardiogenic shock

Echocardiogram

Hypercontractile left ventricle

Torn papillary muscle or chordae tendineae

Flail mitral leaflet

Severe mitral regurgitation

Right heart catheterization

No increase in oxygen saturation from right atrium to right ventricle

Large V waves

Very high pulmonary capillary wedge pressure

Treatment

Medical therapy is generally a bridge to surgery

Vasodilators (e.g. sodium nitroprusside)

Intraortic balloon pump

Surgery

Mitral valve replacement or repair

Coronary bypass

Right ventricular infarction

Incidence

Occurs in nearly 50% of inferior infarcts

Physical examination

Hypotension, clear lungs and jugular venous distention (also found in pericardial tamponade, constrictive pericarditis, restrictive cardiomyopathy and large pulmonary embolus)

Unexpected drop in BP on administration of nitroglycerine

Kussmaul sign in presence of inferior infarct strongly suggests right ventricular infarction

ECG:

ST elevation in right precordial leads, especially V4r. May persist only 10-12 hours

Echocardiogram:

Increased right ventricular dimension

Treatment:

Avoid nitroglycerine

IV saline

Atrioventricular pacing if high grade AV block

Dobutamine

Intraortic balloon pump

Revascularization

Systolic anterior motion of anterior leaflet of mitral valve causing left ventricular outflow tract obstruction

Believed to be due to compensatory hyperkinesis of non-infarcted myocardium

Clinical

Systolic murmur

Hypotension

Echocardiogram:

Systolic motion of anterior mitral leaflet

Left ventricular outflow gradient

Treatment:

Avoid afterload reducing agents, vasodilators and inotropes

Beta blockers presumably to reduce hyperkinesis

Alpha agonists increase systemic vascular resistance and left ventricular volume

Postoperative course of patients operated on for septal rupture or severe mitral regurgitation is stormy, complicated by

Cardiogenic shock

Metabolic acidosis

Acute renal failure

Coagulopathy

Catabolic state

Deconditioning

Multiorgan failure

Malnutrition

Outcome

30 day mortality 47% with invasive treatment, 56% with conservative treatment

In those who survived 30 days, 85% were alive at 1 year. 83% of the survivors were in NYHA Class I or II at 1 year.

References

Reviews in Cardiovascular Medicine 2003 4:131

Heart 2002, 88:531

Haley JH, Sinak LJ, Tajik AJ, Ommen SR, Oh JK. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock. Mayo Clin

Proc. 1999;74:901-906.

Topol, Textbook of Cardiovascular Medicine, 2^nd ed.

Braunwald, Heart Disease, 6^th ed.

posted by Henry Green, MD, FACC, FACP @ 12:52 PM