1 What is heart failure?

Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema. Some patients have exercise intolerance but little evidence of fluid retention, whereas others complain primarily of edema and report few symptoms of dyspnea or fatigue. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term heart failure is preferred over the older term congestive heart failure.

2 Name the causes of heart failure

The most common causes of HF in the United States are coronary artery disease, systemic hypertension, dilated cardiomyopathy, and valvular heart disease (Table 34-1).

TABLE 34-1 Causes of Heart Failure Conditions

Mechanical abnormalities

Pressure overload

Aortic stenosis, systemic hypertension, pulmonary hypertension

Volume overload

Valvular regurgitation, anemia, thyrotoxicosis, circulatory shunts

Restriction of ventricular filling

Mitral stenosis, constrictive pericarditis, left ventricular hypertrophy

Myocardial disease

Primary

Hypertrophic, restrictive, or dilated cardiomyopathies

3 Describe the classification of heart failure

Stage A: Patients with coronary artery disease, hypertension, or diabetes mellitus who do not yet demonstrate impaired left ventricular (LV) function, LV hypertrophy, or geometric chamber distortion

Stage B: Patients who are asymptomatic but demonstrate LV hypertrophy, geometric chamber distortion, and/or impaired LV systolic or diastolic function

Stage C: Patients with current or past symptoms of HF associated with underlying structural heart disease

Stage D: Patients with HF refractory to medical therapy that might be eligible for specialized advanced treatment strategies such as mechanical circulatory support, procedures to facilitate fluid removal, continuous inotropic infusions, cardiac transplantation, or end-of-life care.

This classification system recognizes that there are established risk factors and structural prerequisites for the development of HF (stages A and B) and that therapeutic interventions introduced even before the appearance of LV dysfunction or symptoms can reduce the morbidity and mortality of HF.

4 How is the severity of heart failure classified?

Typically the status of patients with heart failure can be classified on the basis of symptoms, impairment of lifestyle, or severity of cardiac dysfunction. The New York Heart Association (NYHA) classification is used to assess symptomatic limitations of heart failure and response to therapy:

Class I: Ordinary physical activity does not cause symptoms. Dyspnea occurs with strenuous or prolonged exertion at work or with recreation.

Class II: Ordinary physical activity results in symptoms. Dyspnea is occurring while walking or climbing stairs rapidly or walking uphill. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace results in symptoms.

Class III: Less than ordinary activity results in symptoms. Dyspnea occurs with walking one to two blocks on the level or climbing one flight of stairs at a normal pace.

Class IV: Dyspnea occurs at low level of physical activity or at rest.

The NYHA classification describes the functional status of patients with stages C or D heart failure. The severity of symptoms characteristically fluctuates even in the absence of changes in medications, and changes in medications can have either favorable or adverse effects on functional capacity in the absence of measurable changes in ventricular function. Some patients may demonstrate remarkable recovery associated with improvement in structural and functional abnormalities. Usually sustained improvement is associated with drug therapy, and that therapy should be continued indefinitely.

5 What major alterations in the heart occur in patients with heart failure?

LV dysfunction begins with some injury to, or stress on, the myocardium and is generally a progressive process. The principal manifestation of such progression is a change in the geometry and structure of the left ventricle such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. Specific patterns of ventricular remodeling occur in response to the imposed augmentation in workload. With pressure overload, the increased wall tension during systole initiates parallel addition of new myofibrils, causing wall thickening and concentric hypertrophy. With volume overload the wall tension increases during diastole, initiating series addition of new sarcomeres, resulting in chamber enlargement and eccentric hypertrophy. Ventricular dilation allows the chamber to eject an adequate stroke volume with less muscle shortening, but wall stress is increased as described by the Laplace relationship:

where P = intracavity pressure, R = the radius of the chamber, and h = the thickness of the chamber wall.

Increasing wall tension requires higher oxygen demand for the same performance. Myocardial hypertrophy with increasing wall thickness allows the heart to overcome pressure overload with decreased wall tension.

6 What is the Frank-Starling law?

The Frank-Starling law states that the force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched. In a clinical situation, when increased quantities of blood flow into the heart (increasing preload), the walls of the heart stretch. The cardiac muscle then contracts with increased force and, within limits, empties the expanded chambers with increasing stroke volume. There is an optimal sarcomere length and thus an optimal fiber length from which the most forceful contraction occurs. The left ventricle normally operates at an LV end-diastolic volume with less than optimal fiber lengths. The clinical implication of this is that stroke volume increases with increasing preload until the optimal fiber length of the myocardium is reached. Increasing the preload further causes a decrease in stroke volume.

7 How is cardiac output calculated? What is a normal cardiac output and index?

Cardiac output (CO) is the amount of blood that the heart can pump during 1 minute. The main determinants of CO:

where CO = arterial pressure/ total peripheral resistance, SV = stroke volume and HR = heart rate.

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34: Heart Failure