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Cardiogenic Shock

Sometimes called pump failure, cardiogenic shock is a condition of diminished cardiac output that severely impairs tissue perfusion. It reflects severe left-sided heart failure and occurs as a serious complication in nearly 15% of all patients hospitalized with acute myocardial infarction (AMI).

Cardiogenic shock typically affects patients whose area of infarction exceeds 40% of muscle mass; in such patients, the fatality rate may exceed 85%. Most patients with cardiogcnlc shock die within 24 hours of onset. The Prognosis for those who survive is extremely poor.

Causes

Cardiogenic shock can spring from disorders of the heart muscle, the heart valves, or the heart's electrical conduction system. Some 5 to 15 percent of patients hospitalized for heart attacks develop the condition. It may also stem from other cardiac problems, such as heart failure, cardiomyopathy (an inflammation of the heart muscle), rupture of the heart, irregular heartbeats (arrhythmias), and valve disorders

Signs and symptoms

• Chest pain
• Skin may feel cool to touch
• Skin color pale or mottled
• Palpitations
• Profuse sweating
• Rapid and deep respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis.
• Fatigue due to hyperventilation and hypoxia.

Diagnosis

• Auscultation detects gallop rhythm, faint heart sounds and, possibly, if the shock results from rupture of the ventricular septum or papillary muscles, a holosystolic murmur.
• Pulmonary artery pressure monitoring reveals increased pulmonary artery pressure (pAP) and increased pulmonary artery wedge pressure (PAWP), reflecting a rise in left ventricular end-diastolic pressure (preloads) and increased resistance to left ventricular emptying (after load) resulting from ineffective pumping and increased peripheral vascular resistance. Thermodilution technique measures decreased cardiac output.
• Invasive arterial pressure monitoring shows hypotension from impaired ventricular ejection.
• Arterial blood gas (ABG) levels may show metabolic acidosis and hypoxia.
• Electrocardiography may reveal evidence of AMI, myocardial ischemia, or ventricular aneurysm.
• Enzyme levels show elevated creatine kinase (CK-MB, troponin Tor troponin I), lactate dehydrogenase (LD), aspartate aminotransferase, and alanine aminotransferase, which point to MI or myocardial ischemia and suggest heart failure or shock. CK-MB and LD isoenzyme values may confirm AMI.
• Echocardiography (color flow Doppler) shows left ventricular function, valvular disease, aneurysmal dilation, and ventricular septal defects.

Additional tests determine other conditions that can lead to pump dysfunction and failure, such as cardiac arrhythmias, cardiac tamponade, papillary muscle infarct or rupture, ventricular septal rupture, pulmonary embolus, venous pooling (associated with venodilators and continuous intermittent positive-pressure breathing), and hypovolemia.

Treatment

Cardiogenic shock is a medical emergency! Treatment requires hospitalization. The goal of treatment is to save the patient's life and treat the underlying cause of shock. Treatment combines various cardiovascular drugs and mechanical-assist techniques.

Cardiovascular drugs

Drug therapy may include LV. dopamine, a vasopressor that increases cardiac output, blood pressure, and renal blood flow, and LV. amrinone or dobutamine, inotropic agents that increase myocardial contractility. When a more potent vasoconstrictor is necessary, norepinephrine is used.

I.V. 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 (preload). However, the patient's blood pressure must be adequate to support nitroprusside therapy and must be monitored closely.

Mechanical-assist techniques

The intra-aortic balloon pump (IABP) is a mechanical-assist device that attempts to improve coronary artery perfusion and decrease cardiac workload. The inflatable balloon pump is surgically inserted through the femoral artery into the descending thoracic aorta.

Once in place, 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 vasculature lead to lower preload volume.

When drug therapy and IABP inser­tion fail, treatment may require an experimental device - the ventricular assist pump or the artificial heart.

Surgery: In many cases, surgery may be needed to repair the cause of the damage.

Prevention

• Once you've recovered, exercise daily. Regular exercise strengthens the heart.
• Get at least seven hours of sleep each night and nap during the day if you feel tired.
• Quit smoking
• To ease emotional stress, allow frequent rest periods, and provide for as much privacy as possible.
• Learn to control stress by adopting new ways to relax such as deep breathing exercises, muscle relaxing techniques, meditation, or yoga.
• Maintaining a healthy weight.
• Having regular check ups.