Given the incidence of collapsing trachea and COPD in small-breed dogs, combination therapy is often necessary to optimize
palliation of chronic cough in dogs with chronic valvular disease. Cardiogenic causes for progressive dyspnea and tachypnea
without significant cough is typically associated with pulmonary edema, pulmonary hypertension (especially in dogs with chronic
valvular disease), and/or severe ascites leading to limited excursion of the diaphragm. Pleural effusion is rarely severe
enough to cause dyspnea or tachypnea in dogs with heart failure and even right heart failure.
Cough and dyspnea or tachypnea due to refractory pulmonary edema can be confirmed with thoracic radiographs. Refractory pulmonary
edema should be managed through optimal reduction in plasma volume to achieve euvolemia. Renal function (BUN, creatinine),
systemic blood pressure and hydration status (PCV, TS) should be evaluated and taken into consideration during formulation
of a treatment plan. Strategies employed to regain euvolemia may include increased diuresis, venodilation, maximal inhibition
of the renin angiotensin aldosterone system (RAAS), dietary sodium restriction, and tolerable afterload reduction inotropic
In dogs receiving submaximal doses of furosemide, the dose and/or dosing frequency can be increased. Maximal chronic oral
doses for furosemide are 4-5 mg/kg PO TID. In dogs receiving maximal oral doses, the route of administration could be changed
to subcutaneous injections for one or all daily doses. Alternatively, a rescue diuretic could be added, such as hydrochlorothiazide.
When hydrochlorothiazide is added to chronic furosemide therapy (with or without spironolactone), diuresis and potential side-effects
of diuresis (hypovolemia leading to azotemia, electrolyte abnormalities especially hypokalemia) are potentiated due to sequential
nephron blockade. Thus, to minimize unwanted side effects when a thiazide diuretic is initiated, the furosemide dose is decreased
by approximately 50 percent and potassium supplementation is initiated. Typically, the furosemide dose is reduced from 4-5
mg/kg PO TID to 3-3.5 mg/kg BID or 2-2.5 mg/kg TID, spironolactone is left at the same dose, and hydrochlorothiazide is initiated
at 2 mg/kg BID. Over time, as the need for diuresis increases, the furosemide dose is then titrated up.
Venodilation using agents like topical nitroglycerine have no use in the chronic setting. In animals receiving sub-maximal
doses of ACEI, additional RAAS inhibition may be achieved by increasing the dose of enalapril or benazepril to 0.5-0.6 mg/kg
If spironolactone was not already part of the treatment plan, it could be added at this time at a dose between 0.5-2 mg/kg
BID. Its beneficial effects in this setting are likely related to its RAAS blockade, not diuresis. Dietary sodium restriction
may be useful if tolerated. Homemade sodium-restricted diets often are more palatable.
Finally, in normotensive animals additional afterload reduction may reduce filling pressures and thus reduce pulmonary edema.
When adding pure afterload reducers such as amlodipine (0.005-1.0 mg/kg PO SID to BID) or hydralazine (0.25-2 mg/kg PO BID)
to a background of ACEI and pimobendan, starting doses should be very low and re-evaluation of blood pressure, heart rate
and renal parameters should be frequent (every three to five days) during up-titration.
Finally, a combination of additional inotrope and afterload reduction may be recruited by increasing the frequency of pimobendan
to TID from BID.
When possible, multiple therapeutic changes should not be done concurrently but rather one or two changes made at a time.
Response should be evaluated to guide additional alterations.
Dyspnea and tachypnea due to pulmonary hypertension can be presumed in dogs whose degree of dyspnea is worse than expected
based on severity of radiographic infiltrates. Pulmonary hypertension can frequently be confirmed with a Doppler echo- cardiogram.
Many dogs with advanced chronic valvular disease develop secondary pulmonary hypertension and the requi- site clinical signs
such as respiratory embarrassment, exercise intolerance and collapse with exercise. Regardless of the cause of the pulmonary
hypertension, animals with dyspnea due to pulmonary hypertension may benefit from increasing the dose of pimobendan from BID
to TID and adding sildenafil (1-3 mg/kg BID). Short-term oxygen support may be needed while starting the new medications.
Ascites contributing to dyspnea and tachypnea should be removed in total if possible via abdominocentesis, and then diuretics
should be used to minimize the speed of recurrence.
Intermittent abdominocentesis often is required and well tolerated in the management of chronic right heart failure. If the
animal is eating and the frequency of abdominocentesis is not more than once every 10-14 days, typically albumin levels will
remain in the normal range. The clinical goal is to use diuretics to limit the frequency of abdominocentesis to every four
to six weeks.