Page 156 - Small Animal Internal Medicine, 6th Edition

128 PART I Cardiovascular System Disorders

increasing adverse events compared to placebo in dogs with trations measured to avoid toxicity (see Chapter 3, p. 70, and
stage B2 CMVD. Current evidence suggests that initiat- Table 3.3).
VetBooks.ir ing ACEI therapy at stage B2 does not significantly delay resolve. During chronic, compensated disease, however, mild
No exercise should be allowed until signs of CHF fully
CHF onset in most dogs. Nevertheless, some controversy
remains and, especially for dogs with advanced CMVD
exercise is best avoided. At-home monitoring is important
and severe left heart enlargement, an ACEI might provide to moderate regular activity can be beneficial. Strenuous
some benefit toward delaying CHF. In any case, for dogs because decompensation can occur unexpectedly. A persis-
with systemic hypertension, ACE inhibition is recom- tent increase in resting respiratory rate (RRR) can signal
mended as first-line therapy to moderate BP. Regular (mild early decompensation with pulmonary edema. If decom-
to moderate) exercise should be maintained as tolerated. pensated CHF develops, therapy is intensified or adjusted
Strenuous exercise that provokes shortness of breath or as needed while searching for any complicating factors that
excessive fatigue is to be avoided. Gradual transition to a may need to be addressed. Box 6.2 lists strategies for modify-
diet moderately reduced in salt, but also well balanced and ing or intensifying CHF therapy. Dogs with a persistent dry
with adequate protein content, is recommended. Although cough from primary airway disease or mainstem bronchus
some experimental studies found a possible myocardial compression, and no pulmonary edema, might require anti-
protective effect from β-blocker therapy, clinical β-blocker tussive therapy (e.g., hydrocodone bitartrate [0.25 mg/kg PO
therapy trials in dogs with stage B2 MVD have not q4-12h] or butorphanol [0.5 mg/kg PO q6-12h]).
delayed CHF onset. Therefore routine β-blocker use is not
recommended. MILD TO MODERATE SIGNS OF CHF
Early signs of decompensation usually include persistent
increases in RRR at home, shortness of breath, increased
CHF ONSET IN CMVD (STAGE C) respiratory effort or excessive panting, or decreased willing-
ness to exercise. A new or increased cough also might be
The onset of congestive signs appears gradually in some noted. The history and physical examination, thoracic radio-
dogs, but in others fulminant pulmonary edema or episodes graphs, NT-proBNP, and/or echocardiography can help the
of syncope can develop rapidly. Therapy should be guided by clinician differentiate CHF from other causes. BP measure-
clinical status and whether any complicating factors are ment and routine laboratory tests can be useful for identify-
present. Medical therapy is the mainstay for dogs that have ing other complications.
experienced decompensated CHF. Although surgical valve The individual patient’s clinical signs and response to
repair or replacement is sometimes an option and might be therapy guide the aggressiveness of CHF therapy. Furose-
available at some referral centers, treatment for most dogs is mide is instituted when clinical signs and radiographic evi-
solely medical. Clinical compensation (no congestive signs) dence of pulmonary edema first appear. Higher and more
for months to years can be possible with appropriate therapy, frequent doses are indicated for more severe edema. When
although frequent reevaluation and medication adjustment the signs of failure are controlled, the dose and frequency of
become necessary as the disease progresses. Intermittent epi- furosemide gradually are reduced to find the lowest effective
sodes of decompensation (congestive signs) are common in levels for long-term therapy in that patient. Although furo-
dogs on long-term heart failure therapy; often these can be semide alone might be prescribed initially as a therapeutic
successfully managed. trial in some cases (see later in this chapter), for chronic
Furosemide, pimobendan, and an ACEI comprise the heart failure treatment furosemide monotherapy is not rec-
standard, so-called “triple therapy” for dogs that have ommended and does not meet standard of care.
developed CHF. However, spironolactone often is added to Mild clinical signs with pulmonary venous congestion
these three other medications for chronic CHF, so perhaps and/or only mild pulmonary edema on radiographs often
“quadruple therapy” is a more apt description. Pimoben- responds well to PO furosemide (e.g., 1-2 mg/kg q12h), an
dan usually is well tolerated and, when compared directly ACEI given q24h, and pimobendan at standard dose (see
to an ACEI, has greater benefit for long-term heart failure Table 3.3, p. 64). A diet moderately reduced in salt is recom-
management. Generally, an ACEI and pimobendan are used mended. If the client can restrict activity at home, the patient
together for CHF management, although whether their ben- might be more comfortable there. No exercise should be
efits are additive is unclear. Pimobendan and ACEIs both allowed until the next reevaluation, usually in 5 to 7 days
can reduce LA pressure. Spironolactone may reduce the risk unless problems arise sooner. Then, if all CHF signs have
of cardiac death or euthanasia because of CHF in dogs with resolved, mild (to moderate) activity can be slowly reintro-
CMVD. Some dogs can develop serum electrolyte distur- duced. Recheck exams should assess clinical status, BP, renal
bances or azotemia while on spironolactone, so checking for function, and serum electrolytes; depending on clinical find-
these 1 to 2 weeks after initiating therapy and periodically ings and case progression, repeat thoracic radiographs, ECG,
thereafter is recommended. If for some reason pimobendan NT-proBNP, and echocardiogram might be appropriate
cannot be used, digoxin could be added instead, especially as well.
in advanced disease or for management of atrial tachyar- Some dogs show signs suggesting early CHF; without
rhythmias. Conservative doses are used and serum concen- clear radiographic evidence for pulmonary edema, however,