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When To & Not To Use Inotropes (Pimobendan, Dobutamine & Digoxin)
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Inotropic therapy, other than digoxin, has fallen largely into disfavor amongst human cardiologists because they do not prolong life, may worsen arrhythmias and/or increase heart rate, can be given only intravenously, and newer therapies have replaced them. Dobutamine, dopamine, and amrinone can be used intravenously in cases of myocardial failure to rescue phase IV dogs. Digoxin, on the other hand, continues to be used because it is the only positive (although only weakly so) inotrope that is orally available, slows heart rate, and normalizes baroreceptor function. In addition, the RADIANCE and DIG trials in humans showed patients in heart failure denied digoxin had worsening of signs, quality of life, exercise tolerance and hemodynamic status. Digoxin is exquisitely indicated in heart failure with myocardial failure, accompanied by SVT. A sound theoretical argument for digoxin can be made in dogs with heart failure, normal sinus rhythm and maintained myocardial function, only if the owners cannot afford pimobendan. However discretion must be used in these dogs as other drugs will control signs with less danger of toxicity. Therefore in some dogs (e.g. 4 pound Pomeranian with mitral regurgitation), the owner, inherent appetite, renal function, and severity of signs must be considered. In general, digoxin should be instituted in 1) late phase II with myocardial failure; 2) phase III (at same time as diuretic) in dogs without myocardial failure (MR); 3) or in any dog with atrial fibrillation and a rapid ventricular response.
Pimobendan, a newer phosphodiesterase 3 inhibiting inotrope, better termed an inodilator (inotrope and mixed vasodilator), has dramatically altered the way we manage heart failure. This drug, currently being used widely at 0.2-0.6 mg/kg divided BID (given 1 hour before feeding) is thought to work, in part, by sensitizing the troponin C complex to calcium. The aforementioned association between postive inotropes and sudden death has not been recognized with pimobendan, probably because there is less or no increase in intracellular calcium and because of its arteriolar dilating capacity, which unloads the ventricles. Pimobendan is additionally a positive lusitropic agent, improves appetite by reducing inflammatory mediators, and lowers pulmonary artery pressure in pulmonary hypertension. A prospective study by Fuentes, et al. […]
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