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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

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