AIPGMEE 2015

The type of congestive heart failure that occurs in association with beriberi is most accurately characterized as:
(a) Low-output left ventricular failure
(b) High-output left ventricular failure
(c) Low-output right ventricular failure
(d) High-output right ventricular failure

Forms of Ventricular Dysfunction

Heart failure may be described in various ways: systolic or diastolic, acute or chronic, left sided or right sided, high output or low output. Early in the course of heart failure, the various categories may have different clinical and therapeutic implications. Ultimately, however, all forms of heart failure are characterized by high ventricular end-diastolic pressure because of altered ventricular function and neurohormonal regulation.

Systolic and Diastolic Heart Failure

Decreased ventricular systolic wall motion reflects systolic dysfunction, whereas diastolic dysfunction is characterized by abnormal ventricular relaxation and reduced compliance. There are differences in both myocardial architecture and function in systolic and diastolic heart failure, but clinical signs and symptoms cannot reliably differentiate between these two entities.

Systolic Heart Failure

Causes of systolic heart failure include coronary artery disease, dilated cardiomyopathy, chronic pressure overload (aortic stenosis and chronic hypertension), and chronic volume overload (regurgitant valvular lesions and high-output cardiac failure). Coronary disease typically results in regional defects in ventricular contraction, which may become global over time, whereas all other causes of systolic heart failure produce global ventricular dysfunction. Ventricular dysrhythmias are common in patients with LV dysfunction. Patients with left bundle branch block and systolic heart failure are at high risk of sudden death.

A decreased ejection fraction, the hallmark of chronic LV systolic dysfunction, is closely related to the increase in the diastolic volume of the LV (Figure 6-1). Measuring the LV ejection fraction via echocardiography, radionuclide imaging, or ventriculography provides the quantification necessary to document the severity of ventricular systolic dysfunction.

FIGURE6-1 

Left ventricular dysfunction, regardless of cause, results in progressive remodeling of the ventricular chamber leading to dilation and a low ejection fraction. Cardiac dysrhythmias, progressive cardiac failure, and premature death are likely. Noncardiac factors such as neurohormonal stimulation, vasoconstriction, and renal sodium retention may be stimulated by left ventricular dysfunction and ultimately contribute to remodeling of the left ventricle and to the symptoms (dyspnea, fatigue, edema) considered characteristic of the clinical syndrome of congestive heart failure. 

(Adapted from Cohn JN. The management of chronic heart failure. N Engl J Med. 1996;335:490-498. Copyright 1996 Massachusetts Medical Society. All rights reserved.)

Diastolic Heart Failure

Symptomatic heart failure in patients with normal or near-normal LV systolic function is most likely due to diastolic dysfunction. However, diastolic heart failure may co-exist with systolic heart failure. The prevalence of diastolic heart failure is age dependent, increasing from less than 15% in patients younger than 45 years of age to 35% in those between the ages of 50 and 70 to more than 50% in patients older than 70 years. Diastolic heart failure can be classified into four stages. Class I is characterized by an abnormal LV relaxation pattern with normal left atrial pressure. Classes II, III, and IV are characterized by abnormal relaxation as well as reduced LV compliance resulting in an increase in LV end-diastolic pressure (LVEDP). As a compensatory mechanism, the pressure in the left atrium increases so that LV filling can occur despite the increase in LVEDP. Factors that predispose to decreased ventricular distensibility include myocardial edema, fibrosis, hypertrophy, aging, and pressure overload. Ischemic heart disease, long-standing essential hypertension, and progressive aortic stenosis are the most common causes of diastolic heart failure. In contrast to systolic heart failure, diastolic heart failure affects women more than men. Hospitalization and mortality rates are similar in patients with systolic and with diastolic heart failure. The major differences between systolic and diastolic heart failure are presented in Table 6-1.

TABLE6-1 Characteristics of patients with diastolic heart failure and patients with systolic heart failure

Characteristic	Diastolic heart failure	Systolic heart failure
Age	Frequently elderly	Typically 50-70 yr
Sex	Frequently female	More often male
Left ventricular ejection fraction	Preserved, ≥40%	Depressed, ≤40%
Left ventricular cavity size	Usually normal, often with concentric left ventricular hypertrophy	Usually dilated
Chest radiograph	Congestion ± cardiomegaly	Congestion and cardiomegaly
Gallop rhythm present	Fourth heart sound	Third heart sound
Hypertension	+++	++
Diabetes mellitus	+++	++
Previous myocardial infarction	+	+++
Obesity	+++	+
Chronic lung disease	++	0
Sleep apnea	++	++
Dialysis	++	0
Atrial fibrillation	+ Usually paroxysmal	+ Usually persistent
+, Occasionally associated with; ++, often associated with; +++, usually associated with; 0, no association.

Acute and Chronic Heart Failure

Acute heart failure is defined as a change in the signs and symptoms of heart failure requiring emergency therapy. Chronic heart failure is present in patients with long-standing cardiac disease. Typically, chronic heart failure is accompanied by venous congestion, but blood pressure is maintained. In acute heart failure due to a sudden decrease in cardiac output, systemic hypotension is typically present without signs of peripheral edema. Acute heart failure encompasses three clinical entities: (1) worsening chronic heart failure, (2) new-onset heart failure (such as that caused by cardiac valve rupture, large myocardial infarction, or severe hypertensive crisis), and (3) terminal heart failure that is refractory to therapy.

Left-Sided and Right-Sided Heart Failure

Increased ventricular pressures and subsequent fluid accumulation upstream from the affected ventricle produce the clinical signs and symptoms of heart failure. In left-sided heart failure, high LVEDP promotes pulmonary venous congestion. The patient complains of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, which can evolve into pulmonary edema. Right-sided heart failure causes systemic venous congestion. Peripheral edema and congestive hepatomegaly are the most prominent clinical manifestations. Right-sided heart failure may be caused by pulmonary hypertension or right ventricular myocardial infarction, but the most common cause is left-sided heart failure.

Low-Output and High-Output Heart Failure

The normal cardiac index varies between 2.2 and 3.5 L/min/m². It may be difficult to diagnose low-output heart failure, because a patient may have a cardiac index that is nearly normal in the resting state but shows an inadequate response to stress or exercise. The most common causes of low-output heart failure are coronary artery disease, cardiomyopathy, hypertension, valvular disease, and pericardial disease.

Causes of high cardiac output include anemia, pregnancy, arteriovenous fistulas, severe hyperthyroidism, beriberi, and Paget’s disease. The ventricles fail not only due to the increased hemodynamic burden, but also due to direct myocardial toxicity (thyrotoxicosis and beriberi) or due to myocardial anoxia caused by severe and prolonged anemia.