Heart failure preload increase

It is this reduction in preload that, in some cases, is beneficial to patients experiencing heart failure or hypertension. Unlike a healthy heart, a failing heart is unable to pump all of the blood returned to it. Instead, the blood dams up and overfills the chambers of the heart. This results in congestion and increased pressures in the heart and venous system and the formation of peripheral edema. Because the failing heart is operating on the flat portion of a depressed cardiac function curve (see Figure 14.2), treatment with diuretics will relieve the congestion and edema, but have little effect on stroke volume and cardiac output. 

Therapy of congestive heart failure. By lowering peripheral resistance, diuretics aid the heart in ejecting blood (reduction in afterload, pp. 132, 306) cardiac output and exercise tolerance are increased. Due to the increased excretion of fluid, EEV and venous return decrease (reduction in preload, p. 306). Symptoms of venous congestion, such as ankle edema and hepatic enlargement, subside. The drugs principally used are thiazides (possibly combined with K+-sparing diuretics) and loop diuretics. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

These potent diuretic agents interact with almost the entire nephron, including Henle s loop (Fig. 7). Their primary effect is probably the inhibition of the active reabsorption of chloride ions, which then leads to the enhanced excretion of sodium ions and water. Plasma volume is reduced as a result of these effects, whereas in the long-term both cardiac preload and afterload will diminish. The metabolic side-effects of the loop diuretics are globally the same as those of the thiazides, with some incidental differences. Plasma renin activity increases by loop diuretic treatment and it can be well imagined that this effect is noxious in the long-term management of heart failure. The loop diuretics provoke a clearly... 

The primary direct result of an effective dose of nitroglycerin is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. Pulmonary vascular pressures and heart size are significantly reduced. In the absence of heart failure,... 

Furosemide Loop diuretic Decreases NaCI and KCI reabsorption in thick ascending limb of the loop of Henle in the nephron (see Chapter 15) Increased excretion of salt and water reduces cardiac preload and afterload reduces pulmonary and peripheral edema Acute and chronic heart failure severe hypertension edematous conditions Oral and IV duration 2-4 h Toxicity Hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy... 

In addition to these traditional vasodilators, nesir-itide (Natrecor) was developed as a newer method for producing arterial and venous dilation in people with heart failure.58 This substance was derived from human B-type natriuretic peptide (BNP) using recombinant DNA techniques. BNP is a naturally occurring substance that is released from the ventricles when the heart is subjected to increased blood volume and pressure.12 This substance dilates peripheral arteries and veins, thus reducing cardiac afterload and preload, respectively. Hence, nesiritide can be administered intravenously to reduce cardiac workload in certain patients with severe or acute heart failure.12,58... 

Clinical benefits and effects on mortality and hospitalization Whether used alone or in combination, hydralazine and isosorbide dinitrate decrease the preload and afterload, decrease mitral regurgitation, improve cardiac output, increase exercise capacity, modestly increase LVEF and prolong survival in patients with HF (63,64). V-Heart Failure Trial (HeFT) II (64) showed that enalapril had a major benefit on survival when compared with the combination of hydralazine-isosorbide dinitrate with enalapril in patients with predominantly NYHA class ll-lll. The African Americans in Heart Failure Trial (A-HeFT) (65) showed a beneficial effect of adding vasodilator therapy to African-American patients already treated with ACE inhibitors, (3 blockers, and spironolactone. There are no results with the same strategy in other patient groups. 

Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing venous capacitance arterial dilators reduce systemic arteriolar resistance and decrease afterload. Nitrates (see p. 175) are commonly employed venous dilators for patients with congestive heart failure. If the patient is intolerant of ACE inhibitors, the combination of hydralazine and isosorbide dinitrate is most commonly used. Amlodipine and felodipine (see p. 188) have less negative inotropic effect than other calcium channel blockers, and seem to decrease sympathetic nervous activity. 

Heart failure is a progressive disorder that begins with myo- cardial injury. In response to the injury, a number of compensatory responses are activated in an attempt to maintain adequate cardiac output, including the sympathetic nervous system, increased preload, vasoconstriction, and ventricular hypertrophy/remodeling. These compensatory mechanisms are responsible for the symptoms of heart failure and contribute to disease progression. 

In addition to causing symptoms of congestion, augmentation of preload in the heart failure patient will increase afterload because increasing the radius of the ventricle elevates wall tension. Because the failing ventricle is highly afterload-dependent, increases in performance augmented by preload at times may be offset by the attendant increase in afterload. Additionally, the effects of increased preload on force of contraction and afterload will increase myocardial... 

Heart failure is due to defects in cardiac contractility (the vigor of heart muscle), leading to inadequate cardiac output. Signs and symptoms include decreased exercise tolerance and muscle fatigue, coupled with the results of compensatory responses (neural and humoral) evoked by decreases in mean BP. Increased SANS activity leads to tachycardia, increased arteriolar tone T afterload, 4- output, 4 renal perfusion), and increased venous tone (T preload, T fiber stretch). Activation of the renin-angiotensin system results in edema, dyspnea, and pulmonary congestion. Intrinsic compensation results in myocardial hypertrophy. These effects are summarized in Figure IH-4-1. 

Drugs used to combat heart failure include those that decrease preload (e.g diuretics, ACE inhibitors, AT-1 receptor antagonists, and vasodilators), those that decrease afterload (e.g., ACE inhibitors, AT-1 receptor antagonists, and vasodilators), and those that increase cardiac contractibility (e.g., digitalis, beta agonists, and bipyridines). 

In heart failure, contractility is decreased, filling is increased, and ejection fraction is decreased. Thus, desirable changes include lowering afterload (to increase ejection fraction), lowering preload (to decrease filling), lowering of fluid volume, and increasing cardiac contractility. 

In patients with elevated systemic vascular resistance and normal-to-elevated systemic blood pressure, afterload reduction with nitroprusside is logical it should be emphasized that nitroprus-side also increases venous capacitance, thereby also decreasing preload. In the context of myocardial dysfunction, afterload reduction will typically lead to improved forward cardiac output. Nitroprusside may also be effective when the systemic vascular resistance is elevated and systemic blood pressure is reduced the caveat in this more complex hemodynamic setting is that the load reduction produced by nitroprusside must be counterbalanced by an increase in stroke volume. This derivative increase in stroke volume may not occur in the patient with advanced heart failure rather, the result will be a further reduction in mean arterial pressure and the potential risk of peripheral organ hypoperfusion. An alternative approach would be the use of an inotropic-dilator drug such as milrinone, which will provide both preload and afterload reduction its concurrent positive inotropic effect may offset the reduction in mean arterial pressure that can occur from vasodilation alone. 

Figure 4.1 Sites of action for drugs used to treat heart failure. Drugs that work in the hmrt enhance myocardial contractility, whereas drugs that work at other sites reduce preload or afterload. Diuretics do so by decreasing blood volume. Vasodilators increase the space provided for the blood (thus reducing pressure). Angiotensin convertin enzyme (ACE) inhibitors inhibit the synthesis of the vasoconstricting substance, angiotensin II, by blocking ACE in the lungs, where it is produced. ACE inhibitors also reduce aldosterone secretion, which leads to water loss and subsequent blood vdume reduction.

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