Cardiogenic shock occurs when decreased carbon dioxide leads to inadequate tissue perfusion and initiation of the shock syndrome. Cardiogenic shock may occur following a myocardial infarction when a large area of the muscles of the heart becoming ischemic, necrotic and hypokinetic (ineffective contractions of the heart).
Cardiogenic shock usually occurs as a result of the end-stage process of chronic heart failure, cardiac tamponade, pulmonary embolism, cardiomyopathy and cardiac dysrythmias. This condition is severely life-threatening with a high mortality rate which can result in death in a matter of minutes unless proper life-saving measures and prompt medical management is provided for. Just like hypovolemic shock, this type of shock is specific and affects the cardiac circulation in general which cuts off adequate circulation due to a rupture of one of the coronary arteries leading to massive blood loss within the cardiac circulation.
Pathophysiology of cardiogenic shock
The signs and symptoms of cardiogenic shock reflect the circular nature of the pathophysiology of heart failure. The degree of shock is relatively proportional to the extent of left ventricular dysfunction. The cardiac muscles lose its contractility power leading to a marked reduction in its ability to contract and pump oxygen within the cardiac and pulmonary circulation. The decreased carbon dioxide in turn reduces arterial blood pressure and tissue perfusion in the vital organs such as the brain, heart, lungs and kidneys. Flow to the coronary arteries is greatly reduced resulting in decreased oxygen supply to the myocardium which increases ischemia and further reduces the heart’s ability to pump blood to the general circulation. Furthermore the insufficiency to empty the ventricle during each contraction leads to increase in pulmonary pressure, pulmonary congestion and pulmonary edema further worsening episodes of hypoxia causing ischemia to the body’s vital organs.
Clinical manifestations of cardiogenic shock
The classic signs of cardiogenic shock are those of tissue hypoperfusion and result from heart failure and the overall state of shock. They normally include cerebral hypoxia (restlessness, confusion, agitation), low blood pressure, rapid and weak pulse, cold clammy skin, increased respiration cycles, respiratory crackles, increased heart rate (over 100 beats per minute) and decreased urinary output. Initially, arterial blood gas analysis may show respiratory alkalosis during the acute phase of the shock experience. Dysrhythmias are also very common ECG findings which are primarily a result of myocardial ischemia.
General management of cardiogenic shock
The most important approach in treating cardiogenic shock is to correct the underlying problem, reduce any additional demand on the heart. Major dysrythmias are best treated first because they may have caused
or contributed to the state of shock. If the patient has hypovolemia, diuresis is indicated. Moreover, diuretics and renal replacement therapies have also been widely used to reduce the circulating blood volume to alleviate and relieve the workload of the heart . The patient is placed on strict bed rest to conserve energy. If the patient has hypoxemia, oxygen administration is increased (often under positive pressure) when regular pressure is insufficient to meet tissue demands. Furthermore, intubation and sedation may be necessary to maintain efficient delivery of oxygen to the individual experiencing cardiogenic shock.