Clinical Features and Pathogenesis of Cardiogenic Shock

In this article, we will discuss the Clinical Features and Pathogenesis of Cardiogenic Shock. So, let’s get started.

Clinical Features and Pathogenesis

Irrespective of the cause of cardiogenic shock, it is characterized by a vicious circle of severe myocardial (systolic and diastolic) dysfunction. Systolic dysfunction results in fall in cardiac output, BP and thereby coronary perfusion pressure falls. Hypotension, oliguria, confusion or altered mental state, tachypnea, tachycardia and cold, clammy extremities are the manifestations of low output state or acute circulatory failure. Diastolic dysfunction on the other side of cycle causes a rise in CVP, left ventricular end-diastolic pressure, rise in PCWP, pulmonary congestion and edema, leading to hypoxia which further worsens the myocardial ischemia. Breathlessness, orthopnea, PND, cyanosis, cough, hemoptysis, hypoxia, perspiration and inspiratory crackles at the bases of the lungs, S3 and S4 gallops are features of acute pulmonary edema.

A systemic inflammatory response syndrome (SIRS) may accompany large infarction and shock. Inflammatory cytokines and excess nitric oxide may contribute to genesis of cardiogenic shock. Severe acidosis (lactic acidosis) reduces the efficacy of catecholamines and provoke arrhythmias. A Swan-Ganz catheter can be used to measure the pulmonary artery wedge pressure which is >18 mmHg.

Untreated or refractory shock leads to multiple organ dysfunction, e.g. heart, brain, lungs, kidney and liver.

Older patients mostly females, prior MI, diabetes and extensive anterior MI (EF<30%) are at increased risk of cardiogenic shock.

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