Pediatric Cardiac Tumors Medication
- Author: Edwin Rodriguez-Cruz, MD; Chief Editor: P Syamasundar Rao, MD more...
Focus medical treatment of a patient with a cardiac neoplasm on symptoms and possible complications resulting from primary disease. Two of the more common complications of patients with heart tumors are development of arrhythmias and congestive heart failure (CHF).
CHF management includes diuretics and afterload reduction. Severe cases with hemodynamic compromise may require intravenous inotropes, afterload reduction, vasodilators, and anticoagulation. Arrhythmias vary; thus, specific antiarrhythmics should be chosen.
These agents may improve left ventricular function by inhibiting the Na+/K+ -ATPase activity that results in increased myocardial contraction. This leads to sodium accumulation within the myocyte that stimulates the sodium calcium exchange pump. Increased intracellular calcium increases the force of contraction while producing antiarrhythmic effects on cardiac muscle.
Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system.
Hypoperfusion of kidneys causes retention of sodium and water, producing peripheral and pulmonary edema. Diuretics decrease intravascular volume overload. They promote excretion of water and electrolytes by the kidneys and are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites. Pay special attention to patients with a combination of CHF and outflow obstruction because a decrement in cardiac output caused by a decrease in cardiac preload produced by diuretics may further compromise patients' conditions.
Loop diuretic that increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. DOC in pediatric patients.
Thiazide diuretic. If given with furosemide, may decrease the hypercalciuria produced by furosemide.
Potassium-sparing diuretic. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Angiotensin converting enzyme inhibitors
ACE inhibitors are beneficial in all stages of chronic heart failure. Pharmacologic effects result in a decrease in systemic vascular resistance, reducing blood pressure, preload, and afterload. Dyspnea and exercise tolerance are improved. Blood pressure is determined by cardiac output and systemic resistance. When systemic resistance is decreased with afterload reduction, myocardial shortening and stroke volume improve; thus, cardiac output can be maintained at a lower heart rate with lower myocardial oxygen demand. ACE inhibitors decrease production of angiotensin II, a potent vasoconstrictor. As with the diuretics, pay special attention when administering to patients with outflow tract obstruction, since afterload is decreased.
Used to reduce afterload. Prevents conversion of Angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adrenergic agonist agents (inotropes)
These agents improve the hemodynamic status by increasing myocardial contractility and heart rate, resulting in increased cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.
Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses.
After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses < 20 mcg/kg/min.
Stimulates beta1-adrenergic receptors. Has less alpha1 stimulation than dopamine, producing less increase in systemic vascular resistance.
Cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitors
Inotropic effect occurs by inhibiting cAMP phosphodiesterase that increases cellular levels of cAMP. It does not affect the sodium-potassium pump like digitalis. Vasodilatory activity is related to direct relaxation effect on vascular smooth muscle.
Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine; may exacerbate myocardial ischemia.
Bipyridine positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines.
These agents alter the electrophysiologic mechanisms responsible for arrhythmia.
Class I-A antiarrhythmic used for PVCs. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in the threshold for excitation and by inhibition of ectopic pacemaker activity.
Class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Could be used IV/ET/IO.
Class II antiarrhythmic, nonselective, beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. May be used to treat supraventricular as well as ventricular tachyarrhythmias.
Currently under investigation for use in children. It has class II (ie, beta-blocking effects) and class III action potential prolongation properties. Less negative inotropic effect than class II antiarrhythmics.
Calcium channel blocker. Elicits negative inotropic effect. Can diminish PVCs associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AV node, verapamil can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardias (PSVT).
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