Which of the following occurs as a compensatory mechanism for decreased cardiac output?

Epidemiology

The predominant cause of cardiogenic shock (Fig. 99-1) is left ventricular failure secondary to an extensive acute myocardial infarction (MI) or cumulative loss of myocardial function in a patient with previous MI. However, any cause of severe left ventricular (LV) or right ventricular (RV) dysfunction can lead to cardiogenic shock, including fulminant myocarditis (Chapter 54), end-stage cardiomyopathy (Chapter 54), a mechanical complication of an acute MI (Chapter 64), or prolonged cardiopulmonary bypass (Table 99-2).1b Stress-induced (takotsubo) cardiomyopathy may also present with cardiogenic shock (Chapter 54). Acute valvular regurgitation from endocarditis (Chapter 67) or chordal rupture (Chapter 66) can lead to shock, as can physiologic stress in the setting of severe valvular stenosis. Cardiac tamponade (Chapter 68) and massive pulmonary embolism (Chapter 74) with acute RV failure can cause shock without pulmonary edema. An important consideration is that some cardiogenic shock may have an iatrogenic component because of medications that exacerbate hypotension. Early diagnosis of impending shock and identification of patients at high risk for development of shock is essential, both to speed intervention and to avoid therapies that may worsen hemodynamics.

After a decline over the past two decades, the incidence of cardiogenic shock complicating acute MI appears to be increasing for unclear reasons. However, the mortality associated with cardiogenic shock continues to fall as effective early treatment and more widespread adoption of early revascularization have improved outcomes.1

Only about 25% of patients who develop cardiogenic shock are in shock when they initially present to the hospital; in the others, shock usually evolves over several hours. Patients with early and late shock show similar demographic, historical, clinical, and hemodynamic characteristics.

Risk factors for the development of cardiogenic shock in MI parallel those for LV dysfunction and the severity of coronary artery disease (CAD). Patient characteristics include older age, anterior MI, diabetes, hypertension, multivessel CAD, previous MI, and peripheral vascular or cerebrovascular disease. Clinical risk factors include decreased ejection fraction, larger infarctions, and lack of compensatory hyperkinesis in myocardial territories remote from the infarction. Clinical harbingers of impending shock include the degree ofhypotension and tachycardia at hospital presentation. The factors that predict mortality after cardiogenic shock reflect the severity of the acute insult as well as comorbid conditions.

Coronary angiography most often demonstrates multivessel CAD, with left main stenosis in 30% of patients and three-vessel coronary disease in 60%. Multivessel CAD may help explain failure to develop compensatory hyperkinesis in remote myocardial segments.

Myocardial Pathology

Cardiogenic shock is characterized by systolic and diastolic myocardial dysfunction.15,25 Progressive myocardial necrosis has been observed consistently in clinical and pathologic studies of patients with cardiogenic shock.15,26 Patients who develop shock after admission often have evidence of infarct extension, which can result from reocclusion of a transiently patent infarct artery, propagation of intracoronary thrombus, or a combination of decreased coronary perfusion pressure and increased myocardial oxygen demand.17,18 Myocytes at the border zone of an infarction are more susceptible to additional ischemic episodes; these adjacent segments are at particular risk.27 Mechanical infarct expansion, which is seen most dramatically after extensive anterior MI, also can contribute to late development of cardiogenic shock.17,28

Ischemia remote from the infarct zone may be particularly important in producing systolic dysfunction in patients with cardiogenic shock.22,29 Patients with cardiogenic shock usually have multivessel coronary artery disease,2,15 with limited vasodilator reserve, impaired autoregulation, and consequent pressure-dependent coronary flow in several perfusion territories.30 Hypotension and metabolic derangements have the potential to impair the contractility of noninfarcted myocardium in patients with shock.31 This can limit hyperkinesis of uninvolved segments, a compensatory mechanism typically seen early after MI.22,29

Myocardial diastolic function also is impaired in patients with cardiogenic shock. Myocardial ischemia causes decreased compliance, increasing the left ventricular filling pressure at a given end-diastolic volume.32,33 Compensatory increases in left ventricular volumes to maintain stroke volume increase filling pressures further. Elevation of left ventricular pressures can lead to pulmonary edema and hypoxemia (see Fig. 23-1).

In addition to abnormalities in myocardial performance, valvular abnormalities can contribute to increased pulmonary congestion. Papillary muscle dysfunction caused by ischemia is common and can lead to substantial increases in left atrial pressure; the degree of mitral regurgitation may be lessened by afterload reduction. This mechanism is distinct from complete rupture of the papillary muscle, a mechanical complication that manifests dramatically, with pulmonary edema and cardiogenic shock.

469.1

Cardiogenic Shock

Cardiogenic shock may be caused by (1) severe cardiac dysfunction before or after cardiac surgery, (2) septicemia, (3) severe burns, (4) anaphylaxis, (5) cardiomyopathy, (6) myocarditis, (7) myocardial infarction or stunning, and (8) acute central nervous system (CNS) disorders. It is characterized by low cardiac output and results in inadequate tissue perfusion (seeChapter 88).

Treatment is aimed at reinstitution of adequate cardiac output to prevent the untoward effects of prolonged ischemia on vital organs, as well as management of the underlying cause. Under normal physiologic conditions, cardiac output is increased as a result of sympathetic stimulation, which increases both contractility and heart rate. If contractility is depressed, cardiac output may be improved by increasing heart rate, increasing ventricular filling pressure (preload) through the Frank-Starling mechanism, or by decreasing systemic vascular resistance (afterload). Optimal filling pressure is variable and depends on a number of extracardiac factors, including ventilatory support and intraabdominal pressure. The increased pressure necessary to fill a relatively noncompliant ventricle should also be considered, particularly after open heart surgery, or in patients with restrictive or hypertrophic cardiomyopathies. If carefully administered incremental fluid does not result in improved cardiac output, abnormal myocardial contractility or an abnormally high afterload, or both, must be implicated as the cause of the low cardiac output. Although an increase in heart ratemay improve cardiac output, an excessive increase in heart rate may reduce cardiac output because of decreased time for diastolic filling. Additionally, high heart rates will increase myocardial oxygen demand, which may be counterproductive in a state of limited tissue oxygen supply.

Myocardial contractility usually improves when treatment of the basic cause of shock is instituted, hypoxia is eliminated, and acidosis is corrected. β-Adrenergic agonists such as dopamine, epinephrine, and dobutamine improve cardiac contractility, increase heart rate, and ultimately increase cardiac output. However, some of these agents also have α-adrenergic effects, which cause peripheral vasoconstriction and increase afterload, so careful consideration of the balance of these effects in an individual patient is important. The use of cardiac glycosides to treat acute low cardiac output states should be avoided.

Patients in cardiogenic shock may have a marked increase in systemic vascular resistance (SVR) resulting in high afterload and poor peripheral perfusion. If the increased SVR is persistent and the administration of positive inotropic agents alone does not improve tissue perfusion, the use of afterload-reducing agents may be appropriate, such as nitroprusside or milrinone in combination with a β-adrenergic agonist. Milrinone, a phosphodiesterase inhibitor (see earlier), is also a positive inotropic agent, and combined with a β-adrenergic agonist, it works synergistically to increase levels of myocardial cyclic adenosine monophosphate.

1 Define cardiogenic shock

Cardiogenic shock is a state of end-organ hypoperfusion due to cardiac failure and the inability of the cardiovascular system to provide adequate blood flow to the extremities and vital organs. In general patients with cardiogenic shock manifest persistent hypotension (systolic blood pressure less than 80 to 90 mm Hg or a mean arterial pressure 30 mm Hg below baseline), with a severe reduction in cardiac index (less than 1.8 L/min per m2) in the presence of adequate or elevated filling pressure (left ventricular [LV] end-diastolic pressure above 18 mm Hg or right ventricular (RV) end-diastolic pressure above 10 to 15 mm Hg).

Cardiogenic Shock

Cardiogenic shock is defined as an SBP less than 90 mm Hg for longer than 1 hour that is (1) not responsive to fluid administration alone, (2) secondary to cardiac dysfunction, or (3) associated with signs of hypoperfusion or cardiac index less than 2.2 L/min per m2 and pulmonary capillary wedge pressure greater than 18 mm Hg. It occurs in fewer than 10% of STEMI patients (2.4% in 1986 GISSI-1 trial; 6.5% in Germany ALKK-PCI registry as reported in 2013).

Almost 75% to 80% of cases of cardiogenic shock are due to severe LV systolic dysfunction; right ventricular infarction, mechanical complications from ventricular septal rupture, acute mitral regurgitation, and free wall rupture leading to tamponade account for the rest. Other uncommon causes of non-cardiogenic shock after STEMI are bleeding, systemic inflammatory response syndrome, infection, bowel ischemia, or iatrogenic (such as due to medication).

Cardiogenic shock due to mechanical complications after STEMI occurs in a bimodal fashion, with most cases occurringwithin 24 hours. Risk factors for mechanical complication include female gender, old age, and late or no reperfusion in the infarcted territory. An early echocardiogram is extremely helpful to delineate the etiology of cardiogenic shock to guide subsequent definitive treatment. Cardiogenic shock carries a high in-hospital mortality, approaching 50%, and is higher in patients older than 75 years. These high-mortality patients require immediate stabilization to prevent end-stage organ damage followed by emergency coronary angiography and revascularization (Table 4).

Epidemiology

Summary in the Context of Patient Perspectives for Personalizing Medicine

Commonly, fatalities in cardiogenic shock range between 50% and higher based on constitution and age. If the hospital or clinical setting allows for elections between Western medicine alone or combination therapy of Chinese and Western medicine, then injection treatment with Chinese medicine can provide favorable results.

In the case of combination therapy, patients can be weaned off Western medicine treatment. The patient’s condition can be stabilized while introducing Chinese medicine decoctions for preparing for patient discharge back to regular life. As early as possible during treatment, encourage the patient to organize diet and lifestyle modifications to address all disease conditions which contribute to cardiovascular disease.

8 What is the most common cause of cardiogenic shock?

Acute MI remains the leading cause of cardiogenic shock in the United States. In fact, despite the decline in its incidence with progressive use of timely primary PCI, cardiogenic shock still occurs in 5% to 8% of hospitalized patients with ST-segment-elevation myocardial infarction (STEMI). Unlike what is commonly believed, cardiogenic shock may also occur in up to 2% to 3% of patients with non–ST-segment-elevation myocardial infarction (NSTEMI). Overall, 40,000 to 50,000 cases of cardiogenic shock occur annually in the United States.

I. CAUSES

Acute myocardial infarction is the most common cause of cardiogenic shock. Other causes of cardiogenic shock are given in Table 1. The complete occlusion of a coronary artery by a clot causes death of an area of heart muscle that is supplied by that blood vessel and its branches. If a very large area of heart muscle is involved, the general pumping capability of the heart is severely compromised. Because dead myocardium cannot contract, blood cannot be effectively ejected out of the left ventricle into the aorta [see Fig. 1 in the chapter Anatomy of the Heart and Circulation). Blood is held up in the lungs and fluid accumulates in air sacs causing pulmonary edema which results in severe shortness of breath. Because blood cannot be ejected from the heart, the blood pressure falls drastically. When more than 40% of the heart muscle is involved, cardiogenic shock often occurs.

Cardiogenic Shock

Cardiogenic shock occurs when there is decreased cardiac output caused by pump failure. The main causes are listed in Box 37-2. In general, excluding patients with congenital heart disease, cardiogenic shock is much less common inchildren than in adults because of the relatively low incidence of coronary artery disease and congestive heart failure in the pediatric population. Cardiogenic shock should be strongly considered when there is no history of fluid losses, the physical examination reveals hepatomegaly or rales, the chest radiograph demonstrates cardiomegaly, and there is no clinical improvement despite oxygenation and volume expansion.

Management of cardiogenic shock should focus on correcting arrhythmias if present, improving preload and cardiac contractility, and reducing afterload. The workload of the heart can be minimized by the achievement of normothermia, correction of anemia if present, and sedation, intubation, and mechanical ventilation if necessary.

Although cardiogenic shock is uncommon as the primary cause of shock in children, it may be a late manifestation of other forms of shock.