The medical management of animals with CHF is aimed at reversing or controlling the deleterious effects of the underlying disease.
These effects may include pulmonary congestion and edema, cardiac arrhythmias, reduced cardiac output, and excessive vasoconstriction. In severely affected cases, specific medications may be needed to control each of these complications.

Diet. When CHF is present, a sodium-restricted diet is recommended. This is most easily accomplished by feeding a prescription-type pet food. Recipes are available to those who resist prescription diets and prefer to formulate diets at home. A list of sodium free snacks is also helpful for owners. In large animals cases, access to salt blocks should be prevented.

Diuretics. Diuretics are the mainstay therapy in the management of animals with pulmonary edema. Of the several types of diuretics available (loop diuretics, thiazides, potassium-sparing), the loop diuretics such as furosemide are most commonly used. Furosemide is a potent diuretic which inhibits the resorption of sodium, potassium, chloride, and hydrogen ion from the ascending limb of the loop of Henle - as these ions are excreted, water follows. The dose and frequency of furosemide required is dependent upon the severity of pulmonary edema present and the degree of respiratory distress. In severe, life-threatening cases, furosemide should be administered intravenously (IV) and at relatively high dosages - 4-6 mg/kg. When administered IV, furosemide’s onset of action is 5 minutes, the peak effect occurs at 30 minutes, and effects wane at 2 hours. Once CHF patients have been stabilized, furosemide is usually continued orally at maintenance dosages - 0.5 to 1.0 mg/kg SID - BID. In managing chronic cases, the clinician should find the lowest dose of furosemide that will control pulmonary edema and its attendant clinical signs including cough and respiratory distress. Side effects of furosemide may include volume depletion and prerenal azotemia, hypokalemia, and metabolic alkalosis (renal loss of hydrogen).

Vasodilators. As discussed above, vasoconstriction is an important compensatory mechanism which occurs when cardiac output is compromised. Although beneficial in short-term situations, sustained vasoconstriction in the setting of chronic heart disease becomes maladaptive and actually hastens the development of clinical signs and cardiac failure. A major advance in congestive heart failure therapy has been the finding that blunting excessive vasoconstriction with vasodilators results in significant increases in quality of life and survival times. In veterinary medicine, the angiotensin-converting enzyme inhibitor, enalapril has been extensively studied and is approved for use in the dog in the United States. The addition of enalapril to conventional therapy in dogs with chronic congestive heart failure resulted in a significant decrease in clinical signs and a 92% increase in survival time. The use of vasodilators, such as enalapril, have become a very important part of our treatment strategy in animals with heart disease.

Angiotensin-converting enzyme (ACE) inhibitors are indicated in the treatment of mild to severe left-sided CHF in the dog. By reducing vasoconstriction and excessive systemic vascular resistance, ACE inhibitors improve cardiac output and reduce regurgitant fraction when mitral insufficiency is present. Enalapril’s efficacy was documented in a recent multicenter study involving 211 dogs with congestive heart failure. The addition of enalapril to conventional therapy resulted in an improvement in heart failure scores, a decrease in heart rate, frequency of cough, and degree of pulmonary edema. Side effects occurred with equal frequency in the placebo treated group, the most common being anorexia or inappetance, vomiting, and azotemia (28.7% of enalapril treated dogs, 25.9% of placebo treated dogs). Hypotension is rare (1.1%) are typically occurs when aggressive ACE inhibition is initiated in a volume depleted animal. Clinically, the most significant concern is the development of azotemia secondary to reduced renal perfusion. Although the risk is low, it is recommended to ascertain renal function prior to starting ACE inhibitor therapy. It is also advisable to decrease the diuretic dose by approximately 25%, and to monitor the BUN and creatinine 5-7 days after initiating ACE inhibitor therapy. If azotemia develops or worsens, it is recommended to decrease the diuretic dose. If azotemia persists despite diuretic dose adjustment, the frequency of enalapril administration should be decreased to once daily rather than BID. It is prudent to monitor renal function (BUN and Cr) periodically in older animals receiving enalapril and a diuretic. Enalapril should be initiated at 0.5 mg/kg once daily. The dose may be increased to 0.5 mg/kg BID if there is an inadequate response. Other ACE inhibitors used in veterinary medicine, but not approved include captopril (0.5 to 1.0 mg TID) and benazepril (0.25 mg/kg SID). Unlike enalapril and captopril, benazepril is hepatically excreted and may be useful in animals with heart failure and renal insufficiency.

Although enalapril and captopril are most commonly used, there are other vasodilators available. Hydralazine directly dilates arterioles presumably by increasing vasodilatory prostaglandins (PGI2). It is specific for arteriolar vasodilation and has little effect on venous tone. Hydralazine has been shown to be effective in decreasing pulmonary capillary wedge pressure (similar to left atrial pressure) and increasing cardiac index. Hypotension and tachycardia are common side effects, and it is recommended that animals be hospitalized and carefully monitored (blood pressure, electrocardiography) when instituting therapy. Considering hydralazine’s potential for serious side effects along with the safety and efficacy of ACE inhibitors, it is not surprising that the use of hydralazine has significantly declined recently. The cost is significantly lower than ACE inhibitors, and it may be the drug of choice when there are strict financial limitations. The initial dose is 1 mg/kg PO, to be increased in 1 mg/kg increments, up to 3 mg/kg depending on therapeutic response. The effective dose is then administered twice daily. Hypotension mandates a 24 hour discontinuation of the drug, followed by a 50% decrease in the dose. Persistent tachycardia should prompt a reduction in the dose, occasionally digoxin or a ß-blocker are required to control the rate. In a significant proportion of cases, recurrent vomiting and diarrhea necessitate discontinuation of this drug. Nitroglycerin is a useful venodilator in the setting of acute pulmonary edema. Through increasing venous capacitance, preload is decreased and blood volume is essentially shifted from the thorax to the abdomen. One major advantage is that nitroglycerin can be applied to the skin as it is transcutaneously absorbed. Thus, the administration can be performed without causing stress to the animal. The dose of 2% nitroglycerin ointment is 0.3 - 0.6 cm/kg, applied every 4-6 hours.
Gloves should be worn by the person applying the ointment and care should be taken to avoid contact with the ointment once it has been applied. The previous dose should be removed prior to administering subsequent applications. Side effects are infrequent - excessive use may result in hypotension, lethargy, and vomiting. Tolerance may occur with chronic use, therefore nitroglycerin-free periods should be planned every day or two. Sodium nitroprusside can also be used in the setting acute congestive heart failure as it causes rapid vasodilation. Unlike nitroglycerin, sodium nitroprusside is a balanced vasodilator, causing dilatation of both arterioles and veins. The result is a decrease in systemic vascular resistance and preload, and an increase in cardiac output. As the half-life is very short, this drug must be administered as a constant rate infusion. In addition, its potential to cause systemic hypotension warrants careful blood pressure monitoring during the infusion. It is common practice to administer sodium nitroprusside in conjunction with an infusion of dobutamine, a positive inotropic agent. Dobutamine further increases cardiac output and mitigates the hypotensive effects of sodium nitroprusside. The initial infusion rate of nitroprusside should be 1 µg/kg/min, with increases in 1 µg/kg/min increments every 5 minutes until the mean arterial pressure is approximately 70 mmHg. It is uncommon to exceed 5.0-7.0  µg/kg/min. If systemic hypotension occurs, the infusion should immediately be stopped. Due to the short half-life, blood pressure will increase once the infusion has been stopped, and the infusion can be reinitiated at a lower rate.

Positive inotropic agents. These agents increase cardiac contractility and are indicated when myocardial function, specifically contractility, is impaired. Dilated cardiomyopathy and chronic, advanced degenerative valve disease are two common indications in small animal practice. The digitalis glycosides are the most often used positive inotropic agents. Digoxin and digitoxin increase the intracellular concentration of calcium causing a modest increase in cardiac contractility. Digoxin is the most commonly used digitalis glycoside, and is available in tablet, elixir, and intravenous form. When administered orally in dogs, 4-5 days of treatment are required to achieve stabile blood levels, therefore oral digitalization is ineffective in the acute setting of myocardial failure. The dose of digoxin in the dog is 0.005 - 0.010 mg.kg PO BID. For large breed dogs, dosing digoxin at 0.22 mg/m2 is recommended to reduce the frequency of side effects. Rapid digitalization results in toxicity and is not recommended. Digoxin is renally excreted, therefore it should be used with caution in animals with renal insufficiency, if at all. Digitoxin would be the preferred digitalis glycoside in this setting as it is metabolized by the liver.

Side effects of digitalis are common as there is a narrow therapeutic index. Common side effects include depression, anorexia, vomiting, diarrhea, and cardiac arrhythmias. Serious toxicity can usually be avoided by following these guidelines: a) determine renal function prior to initiating digitalis therapy - lower the dose or use digitoxin if renal insufficiency is present; b) do not make dramatic changes in the animal’s diet when starting digitalis - this may interfere with appetite, which is monitored as an indicator of toxicity; c) client communication is essential - the owner should call if any signs of toxicity develop. A reduction in the dose or temporary discontinuation of the drug when side effects are first noted will prevent the occurrence of serious side effects. It is advisable to obtain a serum digitalis level after two weeks of therapy - this will ensure that the drug is appropriately dosed. To perform a digitalis level, obtain a serum sample 8 hours after the last dose has been administered. For most laboratories, the normal range is 1.0 to 2.5 ng/ml. Alter the dose accordingly if the level is outside the reference range. Electrolyte abnormalities, particularly hypokalemia, increase the risk of digitalis toxicity.

Dobutamine is a synthetic catecholamine which primarily stimulates ß1-adrenergic receptors. Through stimulation of these receptors, dobutamine mediates an increase in cardiac contractility. Its positive inotropic effects are much greater than that of the digitalis glycosides. Dobutamine must be administered as a constant rate infusion preferably by an infusion pump. Dobutamine is diluted with 5% dextrose and administered at 5 to 15 ug/kg/min. The major indication in veterinary medicine is severe myocardial failure secondary to dilated cardiomyopathy, although it may be used in dogs with degenerative valve disease and concurrent myocardial failure. Dobutamine can cause cardiac arrhythmias - therefore ECG monitoring is critical during the infusion. If cardiac arrhythmias worsen during the infusion, the rate of administration should be decreased or the infusion stopped. Dobutamine also increases conduction of the AV node, therefore if atrial fibrillation is present, the ventricular response may increase excessively. For this reason, it is recommended that dogs with atrial fibrillation be adequately digitalized prior to receiving a dobutamine infusion.
Although plasma dobutamine levels decrease rapidly 3 minutes after the infusion, beneficial effects often persist for weeks - this effect has resulted in the expression "dobutamine holiday" where congestive heart failure patients spend 1-2 days in the hospital to receive a dobutamine drip every month or so.

Non-drug therapy. L-carnitine deficiency has been documented in a family of boxers with dilated cardiomyopathy and supplementation resulted in an improvement in cardiac contractility. This compound plays a pivotal role in fatty acid metabolism and myocardial energy production. The incidence of L-carnitine deficiency in the general population of dogs with dilated cardiomyopathy has not been determined. The cost of this compound, along with the fact that an endomyocardial biopsy is required to document deficiency, have prevented widespread supplementation of L-carnitine. Supplementation with coenzyme Q10 has resulted in rather dramatic increases in cardiac contractility in humans with dilated cardiomyopathy, receiving conventional therapy. Coenzyme Q10 is a member of the electron transport chain and is essential in myocardial energy production. Clinical trials examining the efficacy of coenzyme Q10 in the dog are underway.