Congestive Heart Failure: Approaches to Care

Congestive heart failure (CHF) is a clinical syndrome commonly encountered in small animal practice. Although there are a multitude of underlying cardiac diseases that can predispose patients to heart failure, the development of CHF represents a final common pathway resulting from insufficient cardiac function.

The primary mechanism for the development of CHF is a cascade of neurohormonal responses involving the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) that promotes sodium and water retention, increases in sympathetic tone, and peripheral vasoconstriction. The short-term benefit associated with these changes involves the preservation of adequate perfusion to tissues, chiefly by improving cardiac output and maintaining blood pressure. However, long-term consequences of neurohormonal activation and other mechanical changes lead to elevation of venous pressures resulting in signs of congestion (pulmonary edema, pleural effusion, and ascites). Additionally, neurohormonal activation increases cardiac workload and damages myocardial cells, contributing to progressive cardiac dysfunction.

As the progression of CHF continues, pulmonary edema (or other fluid retention) can cause intractable clinical signs, leading directly to the death of the patient or indirect death (owner-elected euthanasia). In some cases, the ability to maintain normal cardiac output declines, leading to signs of low output failure. In these patients, adequate blood pressure cannot be maintained, resulting in cardiogenic shock, multiple organ dysfunction, and death.

Many drugs are available for the treatment of CHF, but not all drugs are required in every case. While it is true that no 2 cases are identical, most patients with CHF can be categorized into 1 of several categories. These divisions are intended to assist the general practitioner in deciding which therapy may be most appropriate in a given situation; they are not intended to serve as comprehensive guidelines (see Table). In addition, the following recommendations reflect the author's preferences.

Presence/history of cardiogenic pulmonary edema; ascites in patients with degenerative valve disease; dog/cat with undetermined etiology

• Furosemide: 2 to 4 mg/kg (dog), 1 to 2 mg/kg (cat) Q 6 to 24 H as a starting dose; eventual doses will depend on individual response. The lowest possible dose should always be used.
• ACE inhibitors (eg, enalapril, benazepril): 0.5 mg/kg Q 12 to 24 H

As determined by reduced FS % on echocardiography

• Furosemide
• ACE inhibitors
• Digoxin: 0.003 to 0.005 mg/kg Q 12 to 24 H (Note: Beware of relative contraindications for digoxin, see Table) 
• +/- Spironolactone: 1 to 2 mg/kg Q 12 to 24 H

• Furosemide
• ACE inhibitors
• Spironolactone
• +/- Digoxin
• +/- Hydrochlorothiazide: 2 to 4 mg/kg Q 12 to 24 H; beware of significant electrolyte changes when used with other diuretics

• Furosemide
• ACE inhibitors
• Digoxin
• +/- Diltiazem (for heart rate control): 0.5 to 2 mg/kg Q 8 H (dogs) or extended-release diltiazem (Dilacor; Watson Pharmaceuticals, www.watson.com) 15 to 30 mg Q 24 H (cats)

Recently, a new drug called pimobendan (Vetmedin; Boehringer Ingelheim) has received approval by the FDA for use in the U.S. Pimobendan has been shown to improve clinical signs of heart failure in dogs, and is now considered a mainstay of therapy when treating heart failure either from degenerative valve disease or dilated cardiomyopathy. Its major mechanism of action is increasing cardiac contractility by inhibiting phosphodiesterase and sensitizing cardiac myofilaments to calcium.

The delay in approving pimobendan for use in animals stems from human trials that identified a tendency toward sudden death in patients receiving the drug. While there are no large scale trials in dogs to evaluate for adverse effects, there is no anecdotal evidence of an increase in arrhythmias or sudden death in dogs. In fact, the use of pimobendan has received an overwhelmingly positive clinical response, making it an important new drug in the treatment of CHF. Given residual concerns for its long-term safety, particularly in patients with only mild heart disease, the author recommends that pimobendan only be used in patients with congestive heart failure, and in conjunction with furosemide and ACE inhibitors. Consultation with a cardiologist prior to using this new medication is strongly recommended.

One of the most important times to consider referral is at the time of initial diagnosis. The clinical signs of CHF (coughing, increased respiratory rate and effort, exercise intolerance, weakness) are all nonspecific and can be related to any number of other disease conditions. Thoracic radiographs are used to document the presence of pulmonary edema, but interpretation can be confounded by the presence of concurrent respiratory disease. Early referral of a patient with suspected CHF to a cardiologist can help solidify a diagnosis and ensure appropriate therapeutic recommendations. Referral can also be considered when a patient becomes refractory to therapy that was initially effective. Patients are also commonly referred for intensive monitoring and support during acute decompensation.

If a client does not want to see a specialist, a cardiologist can be consulted by phone to discuss diagnostic and therapeutic decisions. As mentioned previously, the treatment of CHF can be either straightforward or complex, depending on the disease state and the presence of any complications. Some cases can be adequately managed by furosemide and ACE inhibitors, whereas more complicated cases may require a multitude of cardiac medications (see Table). Remember that phone consultations, while not ideal, may provide an avenue to effectively initiate and maintain treatment of CHF.

Referring a patient should always start with a phone call. Communication between a general practitioner and a cardiologist prior to the appointment facilitates the referral process. Discussing necessary diagnostics, identifying which tests might be performed locally, and preparing the specialist for any particular issues with either the patient or client can help minimize common difficulties. In addition, sending all pertinent information and recent diagnostics (laboratory results, ECGs, chest radiographs, etc) either with the client or prior to the appointment is also very useful.

Setting client expectations, avoiding redundant diagnostics, and establishing a relationship with the cardiologist are fundamental priorities and make the referral process more rewarding for everyone involved. Once a patient has been referred, follow-up evaluation can usually be managed locally, with reevaluation by the cardiologist when follow-up echocardiography is indicated.