Cardiogenic shock

Cardiogenic shock: Excerpt from Handbook of Diseases

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 an 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 cardiogenic shock die within 24 hours of onset. The prognosis for those who survive is extremely poor.

Causes

Cardiogenic shock can result from any condition that causes significant left ventricular dysfunction with reduced cardiac output, such as an MI (most common), myocardial ischemia, papillary muscle dysfunction, end-stage cardiomyopathy and other cardiomyopathies (viral, toxic), cardiac arrest, ventricular arrhythmias (fibrillation, tachycardia), cardial amyloidosis, and myocardial degeneration.

Compensatory mechanisms

Regardless of the underlying cause, left ventricular dysfunction sets into motion a series of compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function.

As cardiac output falls in patients with left ventricular dysfunction, aortic and carotid baroreceptors initiate sympathetic nervous responses. These responses, in turn, increase heart rate, left ventricular filling pressure, and peripheral resistance to flow to enhance venous return to the heart.

These compensatory responses initially stabilize the patient’s condition but later cause deterioration with rising oxygen demands of the already compromised myocardium. The result? A vicious circle of low cardiac output, sympathetic compensation, myocardial ischemia, and even lower cardiac output.

Signs and symptoms

Cardiogenic shock produces signs and symptoms of poor tissue perfusion: cold, pale, clammy skin; a drop in systolic blood pressure to 30 mm Hg below baseline or a sustained reading below 80 mm Hg not attributable to medication; tachycardia; rapid, shallow respirations; oliguria (less than 20 ml of urine/hour); restlessness, mental confusion and obtundation; narrowing pulse pressure; and cyanosis.

Although many of these signs and symptoms also occur in patients with heart failure and other shock syndromes, they’re usually more profound in those with cardiogenic shock.

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 (preload) and increased resistance to left ventricular emptying (afterload) 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 an AMI, myocardial ischemia, or ventricular aneurysm.

❑ Enzyme levels show elevated creatine kinase (CK-MB, troponin T, or troponin I), lactate dehydrogenase (LD), aspartate aminotransferase, and alanine aminotransferase, which point to an MI or myocardial ischemia and suggest heart failure or shock. CK-MB and LD isoenzyme levels may confirm an AMI.

❑ Echocardiography (color-flow Doppler) shows left ventricular function, valvular disease, aneurysmal dilation, and ventricular septal defects.

Additional tests help identify 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

The aim of treatment is to enhance cardiovascular status by increasing cardiac output, improving myocardial perfusion, and decreasing cardiac workload. Treatment combines various cardiovascular drugs and mechanical-assist techniques.

Cardiovascular drugs

Drug therapy may include I.V. dopamine and a norepinephrine vasopressor to increase cardiac output, blood pressure, and renal blood flow, as well as I.V. amrinone or dobutamine to increase myocardial contractility. Furosemide is used to decrease pulmonary congestion.

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 decrease 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.

UNDER STUDY: Immediate reperfusion is an invasive intervention that shows some promise for patients with cardiogenic shock. An emergency left-sided heart catheterization is performed. If the patient has a treatable lesion, either an immediate percutaneous transluminal coronary angioplasty or a coronary artery bypass graft is performed.

Special considerations

❑ At the first sign of cardiogenic shock, check the patient’s blood pressure and heart rate.

Clinical tip  If the patient is hypotensive or is having difficulty breathing, ensure a patent I.V. line and a patent airway, and provide oxygen to promote tissue oxygenation.

❑ Monitor ABG levels to measure oxygenation and detect acidosis from poor tissue perfusion. Increase oxygen flow as indicated by ABG measurements. Check complete blood count and electrolyte levels.

❑ After diagnosis, monitor cardiac rhythm continuously. Frequently assess skin color and temperature and other vital signs. Watch for a drop in systolic blood pressure to less than 80 mm Hg (usually further compromising cardiac output).

❑ Insert an indwelling urinary catheter to measure output. Watch for an output below 30 ml/hour.

❑ Using a pulmonary artery catheter, closely monitor PAP, PAWP, and cardiac output. High PAWP indicates heart failure and requires an immediate response.

❑ When a patient is on an IABP, reposition him often and perform passive range-of-motion exercises to prevent skin breakdown. However, don’t flex the patient’s “ballooned” leg at the hip because this may displace or fracture the catheter.

❑ Assess pedal pulses and skin temperature and color to make sure circulation to the leg is adequate. Check the dressing on the insertion site frequently for bleeding, and change it according to your facility’s policy.

❑ Check the insertion site for hematoma or signs of infection, and culture any drainage.

❑ After the patient’s condition becomes hemodynamically stable, gradually reduce the frequency of balloon inflation to wean him from the IABP. During weaning, carefully monitor changes, chest pain, and other signs and symptoms of recurring cardiac ischemia and shock.

❑ Provide psychological support. The patient and his family may be anxious about the intensive care unit, IABP, and other tubes and devices, so offer reassurance.

Book Source Details

• Book Title: Handbook of Diseases
• Author(s): Springhouse
• Year of Publication: 2003
• Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5

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