Page 854 - Cote clinical veterinary advisor dogs and cats 4th

Heart Failure, Chronic 411

with HF generally require lower initial HF due to valvular disease. The evidence ○ When azotemia is encountered in patients
doses: 0.5-2 mg/kg PO q 12-24h. that pimobendan decreases mortality rates receiving furosemide and ACE inhibitors,
VetBooks.ir nature of the HF state generally requires ○ Adverse effects associated with the provided the patient is free of congestive Diseases and Disorders
among Doberman pinschers with stage C
○ Furosemide is used first, but the progressive
furosemide is first decreased by 50%,
HF due to DCM is strong.
signs. If the creatinine does not decrease,
adjustment of doses. If clinical signs
suggest diuretic resistance or electrolyte
derangements are documented, other administration of pimobendan are appar- diuretic therapy is discontinued, provided
ently uncommon, although there is some
congestive signs are not evident. Only if
diuretics such as hydrochlorothiazide evidence that the drug may harm patients this is unsuccessful is the ACE inhibitor
2-4 mg/kg PO q 12h or spironolactone with mild subclinical valvular disease. Use discontinued.
1-2 mg/kg PO q 12h (dog) can be added. of this drug should be reserved for dogs ○ There are unfortunately few alternatives
Doing so allows for synergistic diuretic with stage C mitral valve degeneration and for patients that develop clinical signs spe-
action; different diuretics act in different for dogs with stage B2 mitral valve degen- cifically due to azotemia when congestive
parts of the nephron, which may minimize eration that meet the inclusion criteria of signs are present concurrently; this may
the negative effects of long-term (weeks or the EPIC clinical trial (see inclusion criteria reflect medically intractable HF. However,
more) administration of high doses of a under Prevention below). A proarrhythmic caution must be exercised because over-
single diuretic (e.g., > 3-4 mg/kg q 8-12h effect is possible but appears uncommon, interpretation of radiographs or abnormal
of furosemide). if it even exists in dogs. lung sounds (e.g., pulmonary rales/crackles
○ For patients with advanced disease and • Spironolactone 1-2 mg/kg PO q 12h (dog) due to interstitial lung fibrosis, not edema)
refractory HF, the use of torsemide ○ In chronic HF, excess aldosterone may can lead to inappropriately high diuretic
0.1-0.2 mg/kg q 12-24h can be considered contribute to the development of myo- doses, volume depletion, and azotemia.
as an alternative to furosemide. cardial fibrosis.
○ Diuretic dose should be determined by ○ Spironolactone is an aldosterone antago- Recommended Monitoring
clinical response; the optimal dose is the nist, which may limit the detrimental • Serum urea, creatinine, and electrolytes
lowest one that eliminates congestive effects of hyperaldosteronemia; careful • When applicable, serum digoxin concentra-
signs. monitoring of electrolytes is advised. tion
○ Excessive diuretic administration may ○ Minimal diuretic efficacy as monotherapy • A resting, at-home respiratory rate in excess of
decrease renal perfusion, create electrolyte in the dog 35 breaths/min is associated with pulmonary
imbalances, and contribute to potentially ○ Severe facial dermatitis was identified in edema in dogs treated for chronic HF.
harmful neuroendocrine activation. 30% of Maine coon cats receiving spi-
○ Most patients require lifelong diuretic ronolactone, and caution should therefore PROGNOSIS & OUTCOME
administration; progression of the be used in cats.
underlying disorder generally necessitates • Cautious addition of amlodipine Despite a favorable initial response, HF is gener-
increases in furosemide dose and/or the 0.0625-0.25 mg/kg PO q 24h (dog), ally associated with a poor long-term prognosis
use of additional diuretics. 0.125 mg/kg-0.25 mg/kg PO q 24h (cat) unless the causative disorder is curable. With
○ Furosemide administration sometimes can to conventional therapy can be considered current medical therapy, survival of 6 months or
be tapered or temporarily discontinued in for patients with refractory HF caused by more is a reasonable expectation, but longevity
cats with HCM. systolic dysfunction or for those in which SH is determined by numerous factors, including
• ACE inhibitors partially blunt the effects of complicates the clinical presentation. Blood the causative disease.
RAAS activation and reduce afterload. pressure monitoring is essential (p. 1065).
○ ACE inhibition has proven benefits for • Beta-blockers (BBs): despite experimental PEARLS & CONSIDERATIONS
patients with chronic HF caused by evidence to support the use of BBs in dogs
systolic dysfunction. Preliminary evidence with DCM or advanced mitral/tricuspid Comments
suggests a benefit for patients with chronic valve disease a benefit has not been supported • When the causative disorder is not curable,
HF caused by diastolic dysfunction by clinical experience. These medications chronic HF is a progressive and terminal
(e.g., cats with HF caused by HCM or must be added very carefully for dogs and syndrome. Attempts to identify a correctable
restrictive/unclassified cardiomyopathy). cats with chronic HF. cause are therefore important. Some patients
○ Of the ACE inhibitors, veterinary experi- ○ BBs are never started before a patient’s with DCM respond to supplementation with
ence is greatest with enalapril 0.5 mg/kg PO pulmonary edema has resolved. nutraceuticals such as taurine and L-carnitine.
q 12-24h (dog), benazepril 0.25-0.5 mg/ • Moderate dietary sodium restriction gener- • For sodium content of dog and cat foods, see
kg PO q 24h (dog), 0.5-1 mg/kg PO q ally is indicated. If palatable to the patient, http://vet.tufts.edu/heartsmart/diet/reduced
24h (cat), and ramipril 0.125 mg/kg low-sodium diets may reduce diuretic _sodium_diet.html.
PO q 24h (dog), 0.5 mg/kg PO q 24h requirements.
(cat). Prevention
• Digoxin Nutrition/Diet • In patients with clinically silent DCM,
2
○ 0.22 mg/m PO q 12h (dog); 0.03125 mg/ Moderate sodium restriction, adequate protein the onset of HF may be delayed by
CAT PO q 48h and energy content, and palatability are the administration of cardiac medications
○ Important in management of patients with important attributes of an optimal diet for (p. 263).
supraventricular tachycardia, in particular HF patients. ○ A clinical trial has provided evidence
atrial fibrillation. that administration of pimobendan to
• Pimobendan 0.1-0.3 mg/kg PO q 12h Possible Complications Doberman pinschers with subclinical
administered when stomach is empty is a • The cardiorenal syndrome, a decrease in renal echocardiographic evidence of DCM
phosphodiesterase inhibitor that acts as an function in patients with cardiac dysfunction, delays the onset of stage C HF.
inodilator. It is indicated for the treatment reflects the complex cardiovascular-renal • Recently published data provided evidence
of dogs that have developed advanced stage interactions characteristic of HF. Azotemia is that pimobendan, relative to placebo,
B2 or stage C HF due to valvular disease or associated with declining cardiac performance delays the onset of pulmonary edema in
DCM. and diuretic administration, but the cause canine patients with radiographically and
○ Pimobendan decreased mortality rates of azotemia in HF is multifactorial and has echocardiographically demonstrated cardiac
compared with benazepril in patients with been incompletely defined. enlargement resulting from subclinical

www.ExpertConsult.com