What is Cardiogenic Shock?
Cardiogenic shock is a condition of diminished cardiac output that severely impairs tissue perfusion. It's sometimes called pump failure. Cardiogenic shock can occur as a serious complication in nearly 15% of all patients who are hospitalized with acute myocardial infarction (MI). It typically affects patients whose area of infarction involves 40% or more of left ventricular muscle mass; in such patients, mortality may exceed 85%.
Causes of Cardiogenic Shock
Shock occurs whenever the heart is unable to pump enough blood for the needs of the body. Cardiogenic shock can be caused by disorders of the heart muscle, the valves, or the heart's electrical conduction system.
Other causes include myocarditis and depression of myocardial contractility after cardiac arrest and prolonged cardiac surgery. Mechanical abnormalities of the ventricle, such as acute mitral or aortic insufficiency or an acutely acquired ventricular septal defect or ventricular aneurysm, may also result in cardiogenic shock.
Signs & Symptoms of Cardiogenic Shock
The symptoms of cardiogenic shock include a weak and rapid pulse, rapid breathing, anxiety, cold hands and feet, fatigue, weakness, loss of ability to concentrate, confusion, agitation, profuse sweating, and decreased urine output. The skin is pale or moist, and cool to the touch.
Pulmonary artery pressure monitoring reveals increased pulmonary artery pressure (PAP) and pulmonary artery wedge pressure (PAWP), reflecting an increase in left ventricular enddiastolic pressure (preload) and heightened resistance to left ventricular emptying (afterload) caused by ineffective pumping and increased peripheral vascular resistance. Thermodilution catheterization reveals a reduced cardiac index (less than 1.8 L/ minute/ml).
Invasive arterial pressure monitoring shows systolic arterial pressure less than 80 mm Hg caused by impaired ventricular ejection.
Arterial blood gas analysis may show metabolic and respiratory acidosis and hypoxia.
Electrocardiography demonstrates possible evidence of acute MI, ischemia, or ventricular aneurysm.
Serum enzyme measurements display elevated levels of creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase, and alanine aminotransferase, which point to MI or ischemia and suggest heart failure or shock. CK and LDH isoenzyme levels may confirm acute Ml.
Cardiac catheterization - This procedure provides movie-type x-rays of the arteries that send blood to your heart. It also measures blood pressure within the heart. A slender tube called a catheter is threaded through an artery in the arm or groin and up into the coronary arteries. The procedure is also referred to as coronary angiography.
Treatment aims to enhance cardiovascular status by increasing cardiac output, improving myocardial perfusion, and decreasing cardiac workload with combinations of cardiovascular drugs and mechanical-assist techniques l.V. drugs may include dopamine, a vasopressor that increases cardiac output, blood pressure, and renal blood flow; amrinone or dobutamine, inotropic agents that increase myocardial contractility; and norepinephrine, when a more potent vasoconstrictor is necessary. Nitroprusside, a vasodilator, may be used with a vasopressor to further improve cardiac output by decreasing peripheral vascular resistance (afterload) and reducing left ventricular end-diastolic pressure (pre-load). The patient's blood pressure must be adequate to support nitroprusside therapy and must be monitored closely.
Treatment may also include the intraaortic balloon pump (lABP), a mechanicalassist device that at tempts to improve coronary artery perfusion and decrease cardiac workload. The inflatable balloon pump is inserted through the femoral artery into the descending thoracic aorta. The balloon inflates during diastole to increase coronary artery perfusion pressure and deflates before systole (before the aortic valve opens) to reduce resistance to ejection (afterload) and. therefore, lessen cardiac workload. Improved ventricular ejection, which significantly improves cardiac output, and a subsequent vasodilation in the peripheral vessels lead to lower preload volume.
When drug therapy and IABP insertion fail, a ventricular assist device may be used.
The risk may be reduced by prompt, aggressive treatment of related disorders.
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