Philip R. Fox, DVM, DACVIM, DECVIM-CA (Cardiology), DACVECC
Outpatient therapy can often be successful when financial constraints preclude generating a large database or permitting hospitalization.
A thorough history is paramount. Clinical signs are ultimately associated with acute pulmonary edema due to mitral regurgitation or occasionally DCM, and are caused by elevated left ventricular filling pressures which result in pulmonary edema. Respiratory distress is acute, generally less than 24 hours. If signs are intermittent and suddenly worse, then acute exacerbation of respiratory disease - not CHF - should be suspected. A chest radiograph should be performed to confirm CHF if the diagnosis is in question.
Treatment goals include 1) rapid resolution of pulmonary edema through preload and afterload reduction; 2) patient stabilization; and 3) avoidance of acute renal injury. Many cases of first-time acute CHF with limited client funds can be managed if the pet can be treated for 4–6 hours in your hospital, as follows:
Preload reduction: Firstly, give an IV bolus of furosemide (2 to 4 mg per kg). Ideally, this should be done via quick IV catheter placement.
Obtain blood for serum creatinine and electrolytes and for PCV/TS, if possible.
Afterload reduction: Secondly, give hydralazine, 0.75 mg per os.
Inodilator administration: Thirdly, administer pimobendan, 0.5 mg/kg per os.
Measure systolic BP: This is very helpful to guide further therapies.
Ancillary tests: Record an ECG if tachycardic or arrhythmic. Tap chest if severe effusion.
Repeat steps 1, 2, 4, 5 hourly until respiratory rate and effort and lung crackles substantially diminish (or skip one or more treatments if hypotension occurs).
Most dogs respond markedly within 4–6 hours and can be discharged on cardiac medications, to return for reevaluation the next day.
Rationale and Further Therapies
Furosemide produces brisk and rapid diuresis and natriuresis. Repeated boluses are given, as needed. Nonresponsiveness associated with escalating diuretic dose is usually associated with poor outcome. Aggressive use of loop diuretics can decrease renal perfusion and promote renal dysfunction (acute kidney injury) and electrolyte abnormalities including hypokalemia and hypochloremia. Pimobendan should be administered, 0.5 mg/kg TID for the first day, then reduced to 0.3 mg per kilogram q 12 h. Administration of an ACE inhibitor (enalapril, 0.5 mg/kg q 12 h) may help blunt neurohumoral activation, but should be used with caution if renal failure is present, and is generally started on the second or third day. Addition of spironolactone (1 mg/kg q 12–24 h) has gained popularity for its action to block actions of aldosterone. Patients with atrial fibrillation generally present with rapid ventricular heart rates. Resting ventricular response to atrial fibrillation > 160 beats per minute can substantially reduce cardiac filling and function, and efforts should be directed to reduce this heart rate. Calcium channel-blocking agents such as diltiazem hydrochloride (0.5–1.5 mg/kg q 8 h) or Dilacor (1.5–4 mg/kg q 12 h) are first-line agents to reduce the ventricular response to atrial fibrillation. Digoxin (0.0025–0.005 mg/kg q 12 h) with a target concentration 8 hours post pill of 0.8–1.5 ng/ml, may be added for cases of persistent rapid atrial fibrillation, if renal function is normal. Electrically or hemodynamically unstable ventricular arrhythmia is managed by lidocaine (2–8 mg/kg using 2 mg/kg IV boluses, followed by 40–80 mcg/kg/min CRI). It is important to monitor systemic blood pressure, renal function, electrolyte status, and ECG.