Management of Heart Failure

8 Management of Heart Failure

5. How is a diagnosis of left-sided CHF made?

The clinical signs of left-sided heart failure and primary respiratory tract disease are superficially similar. Because aggressive diuretic therapy can be lifesaving in CHF but harmful in the setting of respiratory tract disease, an accurate diagnosis is essential. A noninvasive diagnosis of left-sided CHF can be made radiographically; left atrial enlargement in the presence of pulmonary opacities compatible with edema is diagnostic (Fig. 8-1). Sometimes, the fragile clinical status of the animal is an impediment to careful radiographic examination and the risk-benefit ratio is in favor of empirical therapy. In these cases, a careful assessment of the history and physical examination findings is essential. Before empirical therapy, it is important to determine that a diagnosis of acute CHF is at least plausible.

A long history of cough and dyspnea suggests that primary respiratory tract disease is at least partly responsible for the clinical signs, because animals with overt CHF are unlikely to survive for months without treatment.

Heart failure results from heart disease; therefore it is important to consider whether it is likely that the animal has a cardiac disorder that could reasonably result in heart failure. The most common acquired heart diseases that result in left-sided CHF in dogs are dilated cardiomyopathy and degenerative mitral valve disease; the former most commonly affects middle aged, large-breed dogs, whereas the latter affects elderly, small-breed dogs. If CHF is present in an elderly small-breed dog, the murmur is usually loud. Conversely, it is extremely unlikely for an elderly small-breed dog to develop CHF in the absence of a murmur; in these cases, signs such as cough and dyspnea are almost always the result of respiratory tract disease. Dogs with dilated cardiomyopathy may have relatively subtle auscultatory findings. In these instances, a soft murmur or a gallop rhythm may have great clinical importance.

9. How is preload manipulated in acute or decompensated CHF?

Preload is the force that distends the ventricle at end-diastole. It is approximated in the living animal by end-diastolic ventricular pressure or volume. Although end-diastolic left ventricular pressure can be estimated through the measurement of the pulmonary capillary wedge pressure, this is not routinely measured in small animals. However, the concept of preload and its pharmacologic manipulation is theoretically useful.

Cardiogenic pulmonary edema results when high mean atrial pressures are communicated to the pulmonary veins and capillaries. Diuretics cause animals to produce large volumes of urine; the administration of a powerful diuretic such as furosemide rapidly decreases intravascular volume and, therefore, preload. The consequent decrease in left atrial pressure alters the Starling forces at the level of the pulmonary capillary and facilitates the reabsorption of edema fluid.

Furosemide is a high-ceiling loop diuretic appropriate for use in the setting of fulminant CHF. Published furosemide doses vary widely and to a large extent the dose and dosing interval are dictated by clinical response. Intravenous doses in the range of 2 to 7 mg/kg in dogs are reasonable when faced with animals with fulminant CHF. The intravenous route is generally preferred when it can be obtained without imposing undue stress on the animal. Other diuretics such as the thiazides, spironolactone, and amiloride may have a role in the management of animals with chronic CHF; however, they have a weaker diuretic effect than does furosemide and see little use in the treatment of fulminant CHF.

13. How is afterload manipulated in systolic failure?

Resistance is the quantity that determines the amount of blood that flows through a vascular bed when subject to a given pressure. In a sense, resistance is a measure of how difficult it is to force blood through the vessels. Resistance is dependent on a number of factors, but the most important of these is vessel diameter because this factor is subject to physiologic influences and manipulation by vasodilating drugs.

Vascular resistance is an important determinant of blood pressure and therefore afterload. However, afterload is best approximated by wall stress, which is related not only to blood pressure, but also to ventricular diameter and wall thickness. If ventricular dilation is not offset by hypertrophy, afterload is increased even if blood pressure is normal. This is the case in animals with dilated cardiomyopathy; the dilated, thin-walled ventricle functions at a mechanical disadvantage because afterload is high even if blood pressure is normal.

In CHF, increases in adrenergic tone and vasoactive hormones such as angiotensin II result in vasoconstriction. In the short term, this has the favorable effect of maintaining systemic blood pressure when cardiac output is low. However, in animals with dilated, thin-walled ventricles, systolic wall stress (afterload) is elevated; this increase in afterload comes at the price of an increase in myocardial oxygen demand. When systolic myocardial failure is present, there is a mismatch between contractility and afterload. Judicious vasodilation reduces afterload, which permits an increase in stroke volume. When mitral valve regurgitation is the cause of CHF, there is an analogous mismatch between vascular resistance and the resistance imposed by the regurgitant orifice; the compensatory increase in vascular resistance is a factor that limits stroke volume.

Vasodilators are not indicated in systolic failure because systemic hypertension is present; rather, they are effective because they decrease vascular resistance and allow stroke volume to increase. The favorable effect of vasodilation is one of degree; excessive vasodilation results in hypotension in animals with systolic failure as it does in normal individuals.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Management of Heart Failure

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