Basic Approach to Management of CHF

The goals of heart failure therapy are different for the short term/ acutely decompensated patient versus a long term /more stable patient, and are different depending on the stage of disease. Recently the American Heart Association has published new guidelines on staging heart failure, and this scheme is applicable to dogs and cats with heart disease.

In the short-term, optimizing hemodynamic function is vital (lowering atrial pressures, improving cardiac output) whereas modulation of neurohormonal activation must be considered in the long-term. Reversal of ventricular remodeling is desirable, though difficult to achieve. Prevention of sudden death is also desirable, and may be even harder to achieve.

Stage B: Heart Disease, No Congestive Heart Failure

Mitral valve disease (MVD) is generally not treated until clinical signs develop. Dilated cardiomyopathy (DCM) may be diagnosed in the asymptomatic phase, and it may be worth starting treatment to attempt to minimize progression, although there are few reports of any benefit in dogs.

ACE inhibitors are beneficial in human patients with early LV dysfunction. Beta-blockers may be helpful in slowing progression of myocardial disease, but must be used with great caution as they can cause dogs to develop signs of CHF.

Stage C: Heart Disease, Past or Present Congestive Heart Failure

Acute, Severe Congestive Heart Failure

It is relatively common for dogs to present with severe pulmonary edema and low-output signs, particularly with DCM. Short term goals are to improve oxygenation and tissue perfusion without critically compromising renal function.

Improve Oxygenation

Administer O₂: Give in a stress-free manner. Dogs with DCM may be too large for an oxygen cage, so 'flow-by' oxygen or an oxygen tent over the head can be used during initial assessment and treatment. Masks are often resented. Nasal oxygen is better for longer-term support (over subsequent hours), but must be humidified.

Sedation: Consider giving an opiate such as butorphanol (0.25mg/kg IM) if the dog is distressed IV furosemide: initial dose can be high (4mg/kg) but subsequent doses being smaller but given frequently (1-2mg/kg every 30-60 mins until respiratory rate decreased)

Venodilator therapy: Nitroglycerin is easy to use, but much less potent than intravenous sodium nitroprusside. Nitroprusside is a potent arteriodilator as well as venodilator, so usually must be given with a positive inotrope to maintain arterial pressures in acutely decompensated DCM patients. Pimobendan and ACE inhibitors both have venodilating effects which may help lower filling pressures, but with ACE inhibitors the increased risk of hypotension mandates that great care should be taken in acutely decompensated patients, and they are better avoided on initial presentation. If there is a significant pleural effusion present, this should be drained.

Increase Cardiac Output

Mainly important when arterial blood pressure is low, and can be achieved by optimizing heart rate and rhythm (e.g., by converting ventricular tachycardia to sinus rhythm), with positive inotropes or with arteriodilators. Dobutamine is the traditional positive inotrope for hemodynamic rescue in DCM, and the dose can be adjusted to effect as a constant rate infusion. The dose is usually started at 2.5mcg/kg/min (or less) and titrated up until heart rate increases or arrhythmias are seen. The animal is then maintained on the highest dose that does not result in these side-effects. The constant rate infusion is not continued for more than 48 hours, and animals should be weaned off gradually. Pimobendan may result in positive inotropic effects within a few hours when given orally, is much easier to use then dobutamine, and may be more appropriate for MVD dogs.

Mild-Moderate CHF

Dogs will sometimes present with milder signs of congestive heart failure (mildly increased respiratory effort or cough, exercise intolerance rather than weakness, or inappetence). These cases can be treated as out-patients with oral medications. The following recommendations also apply to home therapy of acutely decompensated patients following stabilization. The aims of home therapy are to eliminate abnormal fluid retention, modulate neurohormonal activation, and optimize hemodynamic function.

Eliminate Abnormal Fluid Retention

Furosemide (1-5 mg/kg q8-12h PO) is the mainstay of treatment to eliminate pulmonary oedema, ascites and pleural effusion. Dosing should be increased until ALL abnormal fluid accumulation is eliminated, or until unacceptable azotaemia develops. Generally all other medications are given at standard doses initially, and the furosemide is titrated to effect. An ACE inhibitor is usually added at the start of treatment for out-patients, or just before discharge from the hospital for previously decompensated patients. There is little evidence for choosing one ACE inhibitor over another. Although excess salt intake should be avoided, low salt diets are often not very palatable for acute CHF patients.

Modulate Neurohormonal Activation

ACE inhibitor: In addition to helping with sodium and water retention, ACE inhibition will result in beneficial vasodilatory effects, and potentially helpful myocardial effects.

Spironolactone: (1-2 mg/kg q12-24h) spironolactone may be added early on to help counteract the renin-angiotensin-aldosterone system. Doses used tend to be lower than the ranges published in pre-ACE inhibitor times.

Digoxin: (0.0025mg/kg q12h PO) digoxin is given as much for its effects on baroreceptor sensitivity and resulting decrease of sympathetic outflow as for its positive inotropic effect. It is certainly indicated for DCM patients with atrial fibrillation, although more caution should be exercised in the presence of ventricular arrhythmias. A loading dose is not usually given, and the target trough serum levels are lower than previously (0.8-1.2 ng/ml).

Optimize Hemodynamic Function

Pimobendan: (0.1-0.3 mg/kg q12h PO) Pimobendan should be given to improve cardiac output and reduce filling pressures. It may also have beneficial effects by reducing cytokine activation.

Optimize heart rate and rhythm: In atrial fibrillation, digoxin may be insufficient to control ventricular response. Diltiazem or a beta-blocker can be considered as additional therapy, although ideally all congestive signs should first be eliminated. Use of a beta-blocker in this context should be cautious (see above). If ventricular arrhythmias are present, these are more likely to be associated with a risk of sudden death than adversely affecting hemodynamics. If a decision is made to treat these, options include mexiletine, sotalol, or a beta-blocker. Again, care should be taken with the introduction of beta-blockers and doses should be slowly titrated upwards.

Stage D: Chronic Refractory CHF

Some patients will have persistent clinical signs of congestive failure, despite treatment. Some of these patients will have become refractory to frusemide therapy, or may just have suffered progression of the underlying disease.

In addition to the home therapy outlined above, further management options include:

 Subcutaneous furosemide injections (in addition to oral frusemide)

 Adding other classes of diuretics: increase dose of spironolactone (monitor for hyperkalemia), thiazides (use caution when adding thiazides--increased risk of azotemia, hypokalemia and hyponatremia)

 Aggressive dietary sodium restriction