Page 164 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 163

2–4 mcg/kg/min is started, and rapid up-titration can Often cats with life-threatening heart failure necessi-
be done. Effects may occur within 5 minutes of starting tating aggressive diuretic dosages are dehydrated and
the nitroprusside. Because pulmonary capillary wedge have prerenal azotemia as well as electrolyte depletions
pressure is not measurable by noninvasive methods, a (sodium, chloride, potassium, and calcium). During the
target is to decrease systolic blood pressure by 10– aggressive diuretic stage, once to twice a day renal panels
20 mm Hg, depending on the baseline blood pressure. (consisting of BUN, creatinine, and electrolytes) and
Nitroprusside should not be used in cats with low- PCV/TS may be considered to follow the degree of azo-
normal to low blood pressure (systolic BP <110 mm Hg) temia. Mild to moderate azotemia (BUN <60 mg/dl
because it would exacerbate low output heart failure [21 mmol/l], creatinine <2.5 mg/dl [220 mmol/l]) is
and create a more severe complication than the conges- expected and is typically tolerated without requiring
tive heart failure. fluids or a change in therapy. Concurrent use of furose-
Positive inotropic therapy with dobutamine (3–6 mcg/ mide and intravenous fluids for routine treatment of
kg/min IV CRI) or pimobendan (0.25 mg/kg PO q 12 h) heart failure is ineffective and counterproductive. Fluid Cardiomyopathies
can be used for cats with “burnt-out” HCM that have administration is reserved for cats that develop severe
significant concentric hypertrophy and also systolic prerenal azotemia that requires temporary discontinua-
myocardial failure, which is identified by echocardiogra- tion of furosemide and careful fluid administration
phy as thick ventricular walls and moderate to severely (1/4–1/2 maintenance rate intravenously of 0.45% NaCl
decreased myocardial contractility. This phenomenon is supplemented with potassium if indicated, or 50–75 ml
rare and usually represents a terminal stage of the disease of subcutaneous fluids). Chronic concurrent diuretic
associated with a grave prognosis. Cats are often critically and fluid administration, since they are counterproduc-
ill and appear disoriented, recumbent, weak, dyspneic, tive, should rather be handled with reduction of one and
and have systemic hypotension. These cases are best abolition of the other: a cat that is thought to need high-
managed in the critical care setting, and consultation dose diuretics and “a small dose of fluids to protect the
with a criticalist or cardiologist is recommended. In cats kidneys” in fact is receiving two treatments that negate
with HCM that have normal myocardial function but each other. An appropriate approach would be to admin-
systemic hypotension not caused by hypovolemia, dopa- ister a lower dose of diuretics and no fluids (same result).
mine is a preferable choice over dobutamine. Pimobendan The analogy is administering hydromorphone for seda-
should not be given to cats with severe HCM and signifi- tion and concurrently to give naloxone (the reversal
cant SAM of the mitral valve, since it may worsen the agent) to protect against respiratory center depression,
severity of the left ventricular outflow tract obstruction which is not as logical as simply administering a lower
and increase pressure overload to the already hypertro- dose of hydromorphone alone. Titration and monitor-
phied left ventricle. Pimobendan is a controversial ing are essential because overzealous fluid administra-
therapy for cats with refractory heart failure secondary to tion can result in the return of congestive heart failure.
advanced HCM with systolic dysfunction, but it may be See Chapter 24. Mild to moderate hypokalemia is also
considered for refractory therapy since SAM often is less expected during aggressive diuresis and often improves
of a component of the disease in this group of cats. These as diuretic therapy is tapered. Potassium supplementa-
are cats who continue to accumulate cardiogenic pleural tion with potassium gluconate may be considered in
effusion or pulmonary edema despite high or maximal hospitalized cats when the potassium concentration is
furosemide doses. Pimobendan has been anectodally ≤3 mEq/l. An ACE inhibitor should be withheld during
used in cats but not extensively researched for potential the acute diuresis stage of heart failure treatment,
adverse effects in cats, and it is not licensed for use in cats. because it may greatly exacerbate azotemia in the dehy-
Adverse side effects may be uncommon (5/161 cats, 3% drated animal. Ideally, an ACE inhibitor is started after
in a retrospective, uncontrolled survey) and may include rechecking the cat several days to a week after initial
vocalization, agitation, anorexia, vomiting, and consti- heart failure treatment, after a new baseline renal panel
pation (MacGregor et al. 2010). In cats with myocardial is done with the cat receiving furosemide.
failure that have been chronically maintained on ateno- Repeat radiographs may be taken during the course of
lol, the dose should be decreased and possibly weaned acute therapy, usually 1–2 days after starting furosemide,
off. However, empirically weaning all HCM cats that to assess for remaining amount of pulmonary edema and
decompensate off beta blockers is not necessary, unless help guide the dose of oral furosemide for home care.
heart failure becomes intractable. Reduction in the aten- Another option is to monitor resting respiratory rate and
olol dose may be pertinent in cats on chronic beta blocker respiratory effort for normalization as evidence of reso-
therapy that have relative bradycardia of <160 bpm in the lution of pulmonary edema. Depending on the amount
face of active heart failure. of dehydration, azotemia, and residual fluid, cats may be