Felis ISSN 2398-2950

Therapeutics: cardiovascular system

Contributor(s): Serena Brownlie, Sonja Fonfara, Phil Fox, Claire Targett

Myocardial stimulants

Pimobendan  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   Heart: congestive heart failure  , when systolic dysfunction is present.

Dobutamine

  • Beta-adrenergic stimulating agent (beta1>beta2>alpha)   Dobutamine  , 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   Therapeutics: diuretics  .
  • Most promote sodium excretion, reducing volume of extracellular fluid (ECF).
  • Reduce hypertension   Hypertension  .
  • Prolonged therapy may   →   excessive loss of potassium and magnesium in urine   →   hypokalemia   Hypokalemia      →   increased susceptibility to toxicity from cardiac glycosides and arrhythmias and impair carbohydrate metabolism: can supplement with potassium   Potassium chloride / gluconate  , or potassium sparing agents, diuretic should be combined with angiotension-converting enzyme (ACE) inhibitors   ACE inhibitors: overview  .
  • 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   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   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   Diabetes insipidus  to reduce polyuria.
  • Often combined with other diuretics.
  • If already on loop diuretic metronimical dosing (q2-3 days recommended).
  • Bendrofluazide*.
  • Chlorothiazide*   Chlorothiazide  .
  • Hydrochlorothiazide*   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*   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   Heart: hypertrophic cardiomyopathy  , no reduction of left ventricular mass was detected, but possible occurrence of ulcerative skin disease.

Vasodilators

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Drugs for tachyarrhythmias

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Adrenoceptor stimulants

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Anticoagulants

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Further Reading

Publications

Refereed papers
  • Recent references fromPubMed.
  • 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. JVIM22(2), 335-341PubMed.
  • Stokol T et al(2008)Hypercoagulability in cats with cardiomyopathy. JVIM22, 546-552PubMed.
  • Brown S et al(2007)Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. ACVIM consensus statement. JVIM21, 542-558PubMed.
  • 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. JVIM20, 1093-1105.
  • Oyama M et al(2003)Effect of ACE inhibition on dynamic left ventricular outflow tract obstruction in cats with hypertrophic obstructive cardiomyopathy. JVIM17.
  • Akkerdaas L C et al(1998)An alternative premedication and induction regime for cats with a decreased cardiovascular reserve. Vet Q20(Suppl 1), 108.


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