Pediatric Nonviral Myocarditis Medication
- Author: Stuart Berger, MD; Chief Editor: P Syamasundar Rao, MD more...
Medical therapy for CHF includes the use of inotropic agents, afterload reducing agents, diuretics, beta blockers, and anticoagulants. Antiarrhythmic agents may also be required if secondary rhythm disturbances erupt. Drugs used in the treatment of patients with myocarditis include the following:
These agents are used to increase cardiac contractility. Positive inotropic agents increase the force of contraction of the myocardium and are used to treat acute and chronic CHF. Some may also increase or decrease the heart rate (ie, positive or negative chronotropic agents), provide vasodilatation, or improve myocardial relaxation. These additional properties influence the choice of drug for specific circumstances.
Dopamine stimulates adrenergic and dopaminergic receptors. Its 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 the dose by 1-4 mcg/kg/min every 10-30 minutes until the optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses of less than 20 mcg/kg/min.
Epinephrine has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It directly acts on cardiac muscle, increasing myocardial systolic contractions. Digoxin's indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
These agents promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention have resulted in edema or ascites. These agents cause preload reduction through diuresis.
Furosemide is the mainstay of diuresis (reducing preload) in acute CHF. It increases the excretion of water by interfering with the chloride-binding cotransport system, resulting in the inhibition of sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
These agents reduce systemic vascular resistance and increase systemic blood flow resulting from CHF. They cause vasodilation, resulting in afterload reduction.
Nitroprusside is a potent vasodilating agent and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate.
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Useful in chronic CHF and in transition to oral agents from IV agents. The dosage range is wide and can be titrated to effect.
These agents are used to prevent recurrent or ongoing thromboembolic occlusion. They are recommended in patients with severe left ventricular dysfunction and/or in patients with documented left heart thrombus.
Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) in the range of 2-2.5.
Enoxaparin is a low ̶ molecular-weight derivative of heparin. It is used to prevent deep venous thrombosis (DVT), which may lead to pulmonary embolism in patients undergoing surgery who are at risk for thromboembolic complications. Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it preferentially increases the inhibition of factor Xa.
Probable mechanisms that underlie the therapeutic benefits of aspirin include inhibition of platelet aggregation.
Aspirin inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2. In the absence of thrombus in the heart, and with moderate left ventricular dysfunction, aspirin may be indicated at an antiplatelet dosage.
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