Page 289 - Feline Cardiology

296 Section G: Congestive Heart Failure

heart failure patients may be caused by concurrent cat is eating and drinking. Fluid therapy is reserved for
intrinsic renal disease as well as “vasomotor nephropa- cats with moderate to severe azotemia (BUN > 60 mg/dl
thy,” a reversible and secondary cause of azotemia. [21 mmol/l], and creatinine >2.5 mg/dl [220 mmol/l]) if
Factors involved with vasomotor neuropathy include baseline values were normal) that are simultaneously
poor cardiac output and reduced renal perfusion, symptomatic for dehydration including anorexia and
increased renal venous pressure (if right heart pressures lethargy. Half-maintenance rate of intravenous fluids
are increased), neurohormonal activation, high dose with half-strength saline (0.45% NaCl, 2.5% dextrose)
loop diuretic therapy, or excessive vasodilator therapy. can be used in cats requiring careful rescue from their
Vasomotor nephropathy is often termed cardio-renal dehydration and moderate to severe azotemia.
syndrome and is found in approximately 20–30% of Administration of subcutaneous fluids (50–75 ml) is
human patients treated for acute heart failure (Nohria another option for cats that are not severely symptom-
et al. 2008. Progressive azotemia is one of the most atic for their dehydration and moderate to severe azote-
important factors in early cardiovascular mortality in mia. However, concurrent administration of fluids and
people and is also associated with severity of heart diuretics is counterproductive for routine treatment of
failure and diuretic use in dogs treated for heart failure heart failure. In such patients, the clinician must decide
(Gheorghiade and Pang 2009; Boswood and Murphy whether the patient’s intravascular volume needs to be
expanded (e.g., from overt dehydration) or reduced
2006; Nicolle et al. 2007). Chronic kidney disease is also
Congestive Heart Failure 15 years of age or older (Lulich 1992). Acute renal failure edema); it is not possible to do both. Most cats with
common in aged cats, with a prevalence of 30% in cats
(e.g., from excessive fluid retention, such as pulmonary
concurrent azotemia and heart disease have one of the
may be caused by renal thrombosis in cats suffering
two problems that is clinically predominant, and treat-
from arterial thromboembolism. Persistent severe hypo-
ment is aimed at it. For example, a veterinarian who
tension and a volume underloaded state causes renal
ischemia and potentially irreversible renal failure. Often,
a combination of intrinsic renal disease and secondary
patient is receiving diuretics, may achieve the same goal
simply by reducing the diuretic and giving no fluids. A
factors involved with the cardiorenal syndrome contrib- wants to treat a patient with injectable fluids, but the
ute to a decline in glomerular filtration rate and renal majority of azotemic patients do not require rescue with
function in cats treated for heart failure. A comprehen- fluids postdiuretic therapy. See Chapter 24.
sive assessment of baseline renal status (i.e., urinalysis,
serum chemistry at minimum) is needed to identify Electrolyte Abnormalities
patients with a higher risk for decline in renal function Hyponatremia, hypochloremia, and hypokalemia are
during heart failure treatment. Patients with known common electrolyte derangements seen during aggres-
renal dysfunction may be treated with more cautious sive diuretic therapy but are less common in cats receiv-
diuretics and careful monitoring of renal values (q 12– ing low to moderate doses of oral furosemide. Loop
24 hr) during acute treatment, as well as 5–7 days post- diuretics exert marked natriuresis and nonosmotic
discharge. Improvement in cardiac output may help release of antidiuretic hormone triggered by renal hypo-
increase renal perfusion and can be done with dobuta- perfusion. Hyponatremia rarely requires specific therapy
mine or pimobendan in cats with hypotension or myo- with hypertonic saline, but it may indicate the need for
cardial failure. Pimobendan increases cardiac output reduction of diuretic dose if it is moderate or severe.
and improves renal blood flow, may help reduce the Mild to moderate hypokalemia is a common abnormal-
need for high dose loop diuretic therapy, and can be ity during aggressive parenteral furosemide administra-
used in cats with myocardial failure or progressive/ tion to cats with acute heart failure. Supplementation is
refractory heart failure (controversial in HCM, to be usually instituted if there is severe hypokalemia
+
avoided at this time in cats with moderate or severe (K < 3 mEq/l) or severe ventricular arrhythmia (and
+
SAM). ACE inhibitors are usually postponed during the K < 4 mEq/l). Potassium may be supplemented acutely
acute diuresis phase and started once the patient is home in hospitalized patients with potassium chloride CRI
and eating/drinking. In patients with azotemia, lower (0.05–0.5 mEq/kg/hr). The low end of the dose (0.05–
doses of ACE inhibitors should be started first and may 0.1 mEq/kg/min) is an hourly maintenance dose, whereas
be up-titrated based on renal values (see Chapter 24). 0.5 mEq/kg/min is the highest dose that is reserved for
Mild to moderate azotemia (BUN <60 mg/dl patients with severe symptomatic hypokalemia
[21 mmol/l], creatinine <2.5 mg/dl [220 mmol/l]) is rel- (DeFrancesco 2008). Frequent monitoring of electro-
atively common during aggressive diuresis for acute lytes every 6–12 hours is needed, especially in cats receiv-
heart failure. Usually the azotemia improves during ing middle to high doses. Oral potassium gluconate
chronic lower dose furosemide therapy, as long as the (2 mEq PO q 12 h, titrating upward as necessary) may be