Myocardial stimulants
Pimobendan 
- Positive inotrope, vasodilator, platelet aggregation inhibitor (Ca sensitizer, PDE III and V inhibitor).
- Not licensed in cats.
- No evidence based medicine in cats.
- In cases with endstage heart failure , when systolic dysfunction is present.
Dobutamine
- Beta-adrenergic stimulating agent (beta1>beta2>alpha) , potent inotropic effects (acts on beta-1 receptors in cardiac muscle); minimal effect on heart-rate or systemic vascular resistance (beta2-stimulatory effect might lead to hypotension).
- In cases of uncontrolled heart failure, cardiogenic shock.
- As continuous rate infusion 2 µg/kg/min.
- After stabilization long-term improvement possible.
Diuretics
- To reduce edema in heart failure, hepatic disease, cerebral edema, hypoproteinemia, inflammation, and trauma .
- Most promote sodium excretion, reducing volume of extracellular fluid (ECF).
- Reduce hypertension .
- Prolonged therapy may → excessive loss of potassium and magnesium in urine → hypokalemia → increased susceptibility to toxicity from cardiac glycosides and arrhythmias and impair carbohydrate metabolism: can supplement with potassium , or potassium sparing agents, diuretic should be combined with angiotension-converting enzyme (ACE) inhibitors .
- Depleted ECF without loss of bicarbonate ions may → metabolic alkalosis.
- Excessive use may → hypovolemia, reduced cardiac output → reduced renal blood flow and glomerular filtration rate → compromise renal function.
- Classified according to site of action.
- Loop diuretics are more potent than distally acting diuretics but greater risk of potassium loss; should be used with ACEi and can be used with a distally active potassium-sparing diuretic.
Loop diuretics
- Most potent group - rapid onset, short duration.
- Block sodium/potassium/chloride resorption in ascending loop of Henle.
- Excessive doses can → hypovolemia and decompensated renal function ( → pre-renal azotemia ).
- Because so potent, effective when urine delivery is poor, ie in renal impairment.
- Increase magnesium excretion, and may cause severe potassium loss; hypomagnesemia potentiates the cardiac effects of hypokalemia.
- May potentiate ototoxic effects of aminoglycoside antibacterials.
- Furosemide - if IV → cause also venodilation, drug of choice as initial treatment for pulmonary edema.
Thiazides
- Inhibit sodium resorption in early distal tubule - proximal to site of aldosterone-stimulated sodium and potassium exchange → delivery of increased amounts of sodium to the area → greater potassium loss → may need potassium suppplementation.
- Reduce the formation of oxalate uroliths by increasing urinary calcium excretion.
- To treat cardiac or hypoproteinemic edema.
- Can be added to loop diuretic in refractory congestive heart failure (to achieve sequential nephrone blockade).
- Diabetes insipidus to reduce polyuria.
- Often combined with other diuretics.
- If already on loop diuretic metronimical dosing (q2-3 days recommended).
- Bendrofluazide *.
- Chlorothiazide * .
- Hydrochlorothiazide * . Frequently combined preparations, eg with amiloride.
Potassium sparing diuretics
- Act in late distal tubule, lessen sodium reabsorption and thereby indirectly reduce loss of potassium.
- Weak diuretics on their own, usually combined with more potent diuretics, and can enhance therapeutic effects in resistant edema.
- Reduce magnesium loss.
- Avoid use in conditions predisposing to hyperkalemia, eg renal failure, metabolic acidosis, diabetes mellitus.
- Avoid combination with beta-adrenoceptor blocking drugs (impair cellular uptake of potassium), however usually combined with potassium loosing diuretic, therefore, rarely of concern.
- Amiloride hydrochloride * - drug of choice for combination with thiazides; effective when no aldosterone excess (does not antagonize aldosterone specifically).
- Spironolactone * - competitively antagonizes aldosterone; self-limiting action, as increase in hyperkalemia → increased aldosterone secretion → competition. Next to diuretic effect used as anti-remodelling agent, opposes harmful effects of aldosterone (increased myocardial fibrosis, arrhythmias, reduction of nitric oxide release). In Maine Coone cats with HCM , no reduction of left ventricular mass was detected, but possible occurrence of ulcerative skin disease.
Sources
Publications
Refereed papers
- Recent references from PubMed .
- MacDonald K A et al (2008) The effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy. JVIM 22 (2), 335-341 PubMed .
- Stokol T et al (2008) Hypercoagulability in cats with cardiomyopathy. JVIM 22 , 546-552 PubMed .
- Brown S et al (2007) Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. ACVIM consensus statement. JVIM 21 , 542-558 PubMed .
- MacDonald K A et al (2007) The effect of ramipril on left ventricular mass, myocardial fibrosis, diastolic function and plasma neurohormones in Maine Coon cats with familial hypertrophic cardiomyopathy without heart failure. JVIM 20 , 1093-1105.
- Oyama M et al (2003) Effect of ACE inhibition on dynamic left ventricular outflow tract obstruction in cats with hypertrophic obstructive cardiomyopathy. JVIM 17 .
- Akkerdaas L C et al (1998) An alternative premedication and induction regime for cats with a decreased cardiovascular reserve. Vet Q 20 (Suppl 1), 108.
