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Cardiogenic Shock: 53
Etiopathogenesis & Clinical Recognition

Arrythmias: Cardiac output can be severely compro- rupture and 8% had shock due to other causes. In this
mised in instances of atrial tachyarrythmias (atrial registry, 75% developed cardiogenic shock within 24
flutter/ fibrillation with fast venticular rate), ventricu- hours of presentation. (5)
lar tachyarrythmias (ventricular tachycardia, ventric- Stages Of Shock: Shock is a continuum of physio-
ular fibrillation) and extreme bradyarrythmias (com- logical stages beginning with the triggering event
plete heart blocks with slow escape rhythms).
followed by the compensatory mechanisms and the
Mechanical: Acute severe mitral regurgitation due to effects of decreased perfusion and culminating in
papillary muscle rupture (secondary to MI), acute aor- death. (6)
tic regurgitation due to aortic dissection or acute val- Compensated Shock: Systolic blood pressure is
vular rupture (infective endocarditis) can lead to car- maintained within the normal range. However tissue
diogenic shock. Ventricular septal rupture or ruptured oxygen delivery is maintained by tachycardia and
left ventricular free wall can occur as consequence peripheral tissue vasoconstriction. Cardiac contrac-
to myocardial infarction and can lead to cardiogenic tility cannot improve in cardiogenic shock. Patients
shock.
in chronic heart failure remain in the compensated
Obstructive form of cardiogenic shock: Intracardiac stage. These patients are compensated by means of
obstruction like severe mitral stenosis or aortic ste- their own body’s homeostatic mechanisms in addi-
nosis leading to cardiogenic shock is usually due to tion to the anti heart failure drug treatment.
underlying hypovolemia or arrhythmias rather than Decompensated shock: This stage is reached rapidly
the critical obstruction per se.
in cardiogenic shock as the inciting stimulus primarily
Extra-cardiac causes of cardiogenic shock affects the myocardium. The patient develops symp-
are usually due to: toms related to increased filling pressures in the
heart. Later the signs and symptoms of decreased
1. Pulmonary vascular: Hemodynamically signifi- organ perfusion set in.
cant pulmonary embolism, severe pulmonary hy-
pertension lead to acute rise in right ventricular Irreversible shock: Progressive end-organ dysfunc-
pressures which eventually fails to accommodate tion leads irreversible organ damage, death and is
to the high pressures and thus leads to acute termed ‘multi-organ failure’.
right myocardial failure. Acute right ventricular
failure leads to interventricular interdependence Pathogenesis Of Cardiogenic Shock: (Fig 1)
and impaired filling of the left heart. Acute cardiogenic pump failure is responsible for
acute heart failure. Whereas, in patients with chronic
2. Mechanical: The primary abnormality is de-
creased preload to the left heart due to severe heart failure there is either deterioration in myocardi-
volume loss, tension pneumothorax, pericardial al functions or failure of compensatory mechanisms
tamponade, constrictive pericarditis or abdominal that leads directly to the stage of decompensation.
compartment syndrome. Cardiogenic shock is unique because signs and
symptoms are due to both backward and forward
Combined etiologies in shock: Few scenarios like the failure of the myocardial pump. Unlike in the other
following involve more than one mechanism contrib- types of shock wherein the improvement in cardiac
uting to shock other than the cardiac component: contractility and increase in stroke volume serves as
a primary compensatory response to maintain tissue
1. Septic shock with myocardial depression and
stunning perfusion, cardiogenic shock results in rapid fall of
hypotension due to loss of functional myocardium.
2. Neurogenic shock with myocardial stunning Peripheral tissue perfusion is maintained initially by
3. Hypovolemia contributing to shock along with peripheral vasoconstriction and increase in heart rate.
the cardiac pump failure Failure of these compensatory mechanisms leads
rapidly to the stage of hypotension and a vicious
4. Cardiac tamponade causing obstruction in addi- cycle sets in. This is compounded by hypoxemia
(7)
tion to primary pump failure caused by the pulmonary alveolar congestion.
In the SHOCK trial registry of 1160 patients with car- Backward failure of the myocardial pump leads to
diogenic shock, 74.5% of patients had predominant increase in the left ventricular diastolic pressures.
left ventricular failure, 8.3% had acute mitral regur- This increases the left atrial pressures. The increase
gitation, 4.6% had ventricular rupture, 3.4% had right in the pressures within the chambers of the heart is
ventricular failure, 1.7% had tamponade or myocardial

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