Heart Failure

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Heart failure (also termed congestive heart failure) is a complex of signs and symptoms that occurs when the heart fails to pump an adequate cardiac output.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

TABLE 14-11 Drugs Used in the Treatment of Hypertension

1. Diuretics: These drugs increase urinary excretion of sodium and water (Chapter 16). They tend to decrease cardiac output with little or no change in total peripheral resistance.

2. Beta-adrenergic receptor blockers: These drugs exert their antihypertensive effects mainly by reducing cardiac output.

3. Calcium channel blockers: These drugs reduce the entry of calcium into vascular smooth-muscle cells, causing them to contract less strongly. This lowers total peripheral resistance. (Surprisingly, it has been found that despite their effectiveness in lowering blood pressure, at least some of these drugs may significantly increase the risk of a heart attack. Accordingly their use as therapy for hypertension is presently under intensive review.)

4. Angiotensin-converting enzyme (ACE) inhibitors: As will be described in Chapter 16, the final step in the formation of angiotensin II, a vasoconstrictor, is mediated by an enzyme called angiotensin-converting enzyme. Drugs that block this enzyme therefore reduce the concentration of angiotensin II in plasma, which causes arteriolar vasodilation, lowering total peripheral resistance. The same effect can be achieved with drugs that block the receptors for angiotensin II. A reduction in plasma angiotensin II or blockage of its receptors is also protective against the development of heart-wall changes that lead to heart failure (see next section in text).

5. Drugs that antagonize one or more components of the sympathetic nervous system: The major effect of these drugs is to reduce sympathetic mediated stimulation of arteriolar smooth muscle and, thereby, reduce total peripheral resistance. Examples are drugs that inhibit the brain centers that mediate the sympathetic outflow to arterioles, and drugs that block alpha-adrenergic receptors on the arterioles.

This may happen for many reasons; two examples are pumping against a chronically elevated arterial pressure in hypertension, and structural damage due to decreased coronary blood flow. It has become standard practice to separate persons with heart failure into two categories: (1) those with diastolic dysfunction (problems with ventricular filling) and (2) those with systolic dysfunction (problems with ventricular ejection). Many persons with heart failure, however, have elements of both categories.

In diastolic dysfunction the wall of the ventricle has reduced compliance; that is, it is abnormally stiff and, therefore, has a reduced ability to fill adequately at normal diastolic filling pressures. The result is a reduced end-diastolic volume (even though the end-diastolic pressure in the stiff ventricle may be quite high) and, therefore, a reduced stroke volume by the Frank-Starling mechanism. Note that in pure diastolic dysfunction, ventricular compliance is decreased but ventricular contractility is normal.

There are several situations that lead ultimately to decreased ventricular compliance, but by far the most common is the existence of systemic hypertension. As noted in the previous section, the left ventricle, pumping chronically against an elevated arterial pressure, hypertrophies. The structural and biochemical changes associated with this hypertrophy make the ventricle stiff and less able to expand.

In contrast to diastolic dysfunction, systolic dysfunction results from myocardial damage due, for example, to a heart attack (see below) and is characterized by a decrease in cardiac contractility—a lower stroke volume at any given end-diastolic volume. This is manifested as a decrease in ejection fraction and, as illustrated in Figure 14-68, a downward shift of the ventricular function curve. The affected ventricle does not hypertrophy.

Ventricular Function Curve

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End-diastolic ventricular volume (ml)

FIGURE 14-68

Relationship between end-diastolic ventricular volume and stroke volume in a normal heart and one with heart failure due to systolic dysfunction (decreased contractility). The normal curve is that shown previously in Figure 14-29. With decreased contractility, the ventricular function curve is displaced downward; that is, there is a lower stroke volume at any given end-diastolic volume. Fluid retention causes an increase in end-diastolic volume and restores stroke volume toward normal by the Frank-Starling mechanism. Note that this compensation occurs even though contractility—the basic defect—has not been altered by the fluid retention.

0 100 200 500

End-diastolic ventricular volume (ml)

FIGURE 14-68

Relationship between end-diastolic ventricular volume and stroke volume in a normal heart and one with heart failure due to systolic dysfunction (decreased contractility). The normal curve is that shown previously in Figure 14-29. With decreased contractility, the ventricular function curve is displaced downward; that is, there is a lower stroke volume at any given end-diastolic volume. Fluid retention causes an increase in end-diastolic volume and restores stroke volume toward normal by the Frank-Starling mechanism. Note that this compensation occurs even though contractility—the basic defect—has not been altered by the fluid retention.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

TABLE 14-12 Drugs Used in the Treatment of Heart Failure

1. Diuretics: Drugs that increase urinary excretion of sodium and water (Chapter 16). These drugs eliminate the excessive fluid accumulation contributing to edema and/or worsening myocardial function.

2. Cardiac inotropic drugs: Drugs (like digitalis) that increase ventricular contractility by increasing cytosolic calcium concentration in the myocardial cell (see Chapter 6 for mechanism). The use of these drugs is presently controversial, however, since although they clearly improve the symptoms of heart failure, they do not prolong life and, in some studies, seem to have shortened it.

3. Vasodilator drugs: Drugs that lower total peripheral resistance and hence the arterial blood pressure (afterload) against which the failing heart must pump. Some inhibit a component of the sympathetic nervous pathway to the arterioles, whereas others [angiotensin-converting enzyme (ACE) inhibitors] block the formation of angiotensin II (see Chapter 16). In addition, the ACE inhibitors prevent or reverse the maladaptive remodeling of the myocardium that is mediated by the elevated plasma concentration of angiotensin II existing in heart failure.

4. Beta-adrenergic receptor blockers: Drugs that block the major adrenergic receptors in the myocardium. The mechanism by which this action improves heart failure is unknown (indeed, you might have predicted that such an action, by blocking sympathetically induced increases in cardiac contractility, would be counterproductive). One hypothesis is as follows: Excess sympathetic stimulation of the heart reflexly produced by the decreased cardiac output of heart failure may cause an excessive elevation of cytosolic calcium concentration, which would lead to cell apoptosis and necrosis; beta-adrenergic receptor blockers would prevent this.

The reduced cardiac output of heart failure, regardless of whether it is due to diastolic or systolic dysfunction, triggers the arterial baroreceptor reflexes. In this situation these reflexes are elicited more than usual because, for unknown reasons, there is a decreased sensitivity of the afferent baroreceptor receptors. In other words, the baroreceptors discharge less rapidly than normal at any given mean or pulsatile arterial pressure, and the brain "interprets" this decreased discharge as a larger-than-usual fall in pressure. The results of the reflexes are (1) heart rate is increased through increased sympathetic and decreased parasympathetic discharge to the heart, and (2) total peripheral resistance is increased by increased sympathetic discharge to systemic arterioles as well as by increased plasma concentrations of the two major hormonal vasoconstrictors—angiotensin II and vasopressin.

The reflex increases in heart rate and total peripheral resistance are initially beneficial in restoring cardiac output and arterial pressure just as if the changes in these parameters had been triggered by hemorrhage.

Maintained chronically throughout the period of cardiac failure, the baroreceptor reflexes also bring about fluid retention and an expansion—often mas-sive—of the extracellular volume. This is because, as described in Chapter 16, the neuroendocrine efferent components of the reflexes cause the kidneys to reduce their excretion of sodium and water. The retained fluid then causes expansion of the extracellular volume. Since the plasma volume is part of the extracellular fluid volume, plasma volume also increases. This in turn increases venous pressure, venous return, and end-diastolic ventricular volume, which tends to restore stroke volume toward normal by the Frank-Starling mechanism (Figure 14-68). Thus, fluid retention is also, at least initially, an adaptive response to the decreased cardiac output.

However, problems emerge as the fluid retention progresses. For one thing, when a ventricle with systolic dysfunction (as opposed to a normal ventricle) becomes very distended with blood, its force of contraction actually decreases and the situation worsens. Second, the fluid retention, with its accompanying elevation in venous pressure, causes edema—accumulation of interstitial fluid. Why does an increased venous pressure cause edema? The capillaries, of course, drain via venules into the veins, and so when venous pressure increases, the capillary pressure also increases and causes increased filtration of fluid out of the capillaries into the interstitial fluid. Thus, most of the fluid retained by the kidneys ends up as extra interstitial fluid rather than extra plasma. Swelling of the legs and feet is usually prominent, but the engorgement occurs elsewhere as well.

Most important in this regard, failure of the left ventricle—whether due to diastolic or systolic dysfunction—leads to pulmonary edema, which is the accumulation of fluid in the interstitial spaces of the lung or in the air spaces themselves. This impairs gas exchange. The reason for such accumulation is that the left ventricle temporarily fails to pump blood to the same extent as the right ventricle, and so the volume of blood in all the pulmonary vessels increases. The resulting engorgement of pulmonary capillaries raises the capillary pressure above its normally very low value, causing increased filtration out of the capillaries.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

TABLE 14-13 Major Causes of Edema

Physiological Event

Cause of Edema

Increased arterial pressure secondary to increased cardiac output*

Increased capillary pressure, leading to increased filtration

Local arteriolar dilation, as in exercise or inflammation

Increased capillary pressure, leading to increased filtration

Increased venous pressure, as in heart failure or venous obstruction

Increased capillary pressure, leading to increased filtration

Decreased plasma protein concentration, as in liver disease (decreased protein production), kidney disease (loss of protein in the urine), or protein malnutrition

Decreased force for osmotic absorption across capillary. Therefore, net filtration is increased.

Increased interstitial-fluid protein concentration resulting from increased capillary permeability to protein (as in inflammation)

Decreased force for osmotic absorption across capillary. Therefore, net filtration is increased.

Obstruction of lymphatic vessels, as in infection by filaria roundworms (elephantiasis)

Fluid filtered from the blood capillaries into the interstitial compartment is not carried away. Protein also accumulates in the interstitial fluid.

*In contrast, if arterial pressure is elevated because of increased total peripheral resistance, edema may not occur; the capillary pressure may not be elevated because the increased arteriolar resistance will prevent most of that increase in pressure from reaching the capillaries.

*In contrast, if arterial pressure is elevated because of increased total peripheral resistance, edema may not occur; the capillary pressure may not be elevated because the increased arteriolar resistance will prevent most of that increase in pressure from reaching the capillaries.

This situation usually worsens at night: During the day, because of the patient's upright posture, fluid accumulates in the legs; then the fluid is slowly absorbed back into the capillaries when the patient lies down at night, thus expanding the plasma volume and precipitating an attack of pulmonary edema.

Another component of the reflex response to heart failure that is at first beneficial but ultimately becomes maladaptive is the increase in total peripheral resistance, mediated by the sympathetic nerves to arterioles and by angiotensin II and vasopressin. By chronically maintaining the arterial blood pressure against which the failing heart must pump, more work must be expended by the failing heart.

One obvious treatment for heart failure is to correct, if possible, the precipitating cause (for example, hypertension). In addition, the various drugs available for treatment are summarized in Table 14-12. Finally, although cardiac transplantation is often the treatment of choice, the paucity of donor hearts, the high costs, and the challenges of postsurgical care render it a feasible option for only a very small number of patients.

In closing this section, it should be emphasized that there are causes of edema other than heart failure and the lymphatic malfunction described earlier. They are all understandable as imbalances in the Starling forces and are listed in Table 14-13.

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