eMedicine Specialties > Emergency Medicine > Cardiovascular
Mitral Stenosis: Treatment & Medication
Updated: Aug 22, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- Prehospital care is appropriate for acute pulmonary edema or arrhythmia secondary to mitral stenosis.
- Oxygen administration is always indicated for symptomatic patients.
- In patients with significant acute dyspnea, appropriately trained personnel may administer agents that promote afterload reduction such as nitrates or ACE inhibitors.
- Clinically significant arrhythmias such as atrial fibrillation with rapid ventricular response should be corrected according to local protocols.
- Medications appropriate for use by prehospital personnel vary according to local protocol but may include diltiazem, amiodarone, esmolol, or metoprolol.
- Grossly unstable patients with atrial fibrillation with rapid ventricular response should receive synchronized DC cardioversion.
Emergency Department Care
The goal is to control symptoms, to prevent or retard disease progression, and to treat complications.
- Treatment of congestive heart failure
- Medications to consider include nitroglycerin, ACE inhibitors, and diuretics.
- Patients with severe mitral stenosis should maintain an upright posture and avoid strenuous physical activity.
- Sodium intake should be restricted, and maintenance doses of oral diuretics should be continued.
- The data on beta-blockers are conflicting; beta-blockade may be useful for patients with exertional symptoms if the symptoms occur primarily at high heart rates.
- Prevent or retard disease. Primary and/or secondary prophylaxis against streptococci/endocarditis should be administered.
- Penicillin is indicated whenever streptococcal infection is suspected in a patient with known rheumatic disease.
- Management of atrial fibrillation
- Much of the dyspnea related to mitral stenosis is rate related. Control of atrial fibrillation with rapid ventricular response may be considered with any of the following agents:
- Metoprolol
- Esmolol
- Diltiazem
- Digoxin
- If the patient is unstable and immediate cardioversion is indicated (synchronized 100 J, 200 J, 300 J, then 360 J monophasic, or biphasic equivalent, with prior sedation), then heparin should be administered before, during, and after cardioversion. Otherwise, electrical or chemical cardioversion should be performed after 3 weeks of warfarin anticoagulation.
- Anticoagulation is necessary in patients who are unable to maintain normal sinus rhythm.
- Anticoagulation may also be beneficial for patients with normal sinus rhythm with a prior embolic event or a left atrial dimension greater than 55 mm Hg noted by echocardiography.
- Much of the dyspnea related to mitral stenosis is rate related. Control of atrial fibrillation with rapid ventricular response may be considered with any of the following agents:
Consultations
- Cardiologist and/or cardiac thoracic surgeon
- Known or suspected cases of mitral stenosis with hemodynamic instability, arrhythmia, or embolization
- Cases involving a new onset or progression of symptoms
Medication
The goal of medical therapy is to control the rapid ventricular rate and to prevent thrombus formation and embolization. Conversion of atrial fibrillation to sinus rhythm may also decrease symptoms.
Antiarrhythmics
These agents alter the electrophysiologic mechanisms that are responsible for arrhythmia.
Amiodarone (Cordarone)
Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.
Has low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.
Adult
120 mg IV over 10 min follow by IV infusion Maintenance dosing: 400 mg PO tid for 1-3 wk until desired effect achieved then followed by weekly reductions (goal of lowest dose with desired therapeutic benefit)
Maintenance for AF: 200 mg/d PO
Pediatric
5 mg/kg IV over 5-60 min, then 5-15 mcg/kg/min infusion
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by macrolide antibiotics, ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong QT interval; coadministration may increase myopathy/rhabdomyolysis risk; associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs that prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk
Documented hypersensitivity; neonates; complete AV block; intraventricular conduction defects
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Known to cause serious (and at times fatal) toxicities including pulmonary and liver toxicities; may cause prolonged proarrhythmic effects; may cause optic neuritis/neuropathy or hypothyroidism or hyperthyroidism; CNS and GI toxicity may occur and typically dissipates with dose reduction
Esmolol (Brevibloc)
Ultra–short-acting that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared with placebo. Can be discontinued abruptly if necessary.
May be used with class I antiarrhythmics if digoxin therapy does not abort atrial arrhythmia. Administer in patients needing prompt slowing of ventricular rate in response to atrial flutter or fibrillation and who are most likely to become hemodynamically unstable if left without treatment or in those waiting for the start of the therapeutic effects of digoxin (average, 10 h). Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
Adult
Loading dose: 100-500 mcg/kg IV infused over 1 min
Maintenance dose: 25-200 mcg/kg/min IV continuous infusion (gradually titrated upward in increments of 25-50 mcg/kg/min q5-10min); not to exceed 300 mg/kg/min because safety of higher dosages is unknown
Pediatric
Administer as in adults
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, cardiogenic shock, and AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely
Digoxin (Lanoxin)
Cardiac glycoside that has direct inotropic effects in addition to indirect effects on the cardiovascular system. Effects on myocardium involve a direct action on the cardiac muscle that increases myocardial systolic contractions as well as indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Adult
0.25 mg IV; up to 1 mg loading dose followed by a maintenance dose of 0.125-0.25 mg qd
Pediatric
<2 years: Not established
2-5 years: 30-40 mcg/kg PO
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
IV doses are 80% of PO doses; maintenance doses are 25-35% of PO doses
Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis
Beta-adrenergic blockers
These drugs inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
Metoprolol (Lopressor)
Selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.
Adult
5 mg IV; repeat in 10 min; not to exceed 15 mg
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; COPD; cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
Calcium channel blockers
In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
Diltiazem (Cardizem CD, Cardizem SR, Tiazac, Dilacor)
During the depolarization, inhibits the calcium ion from entering the slow channels or the voltage-sensitive areas of the vascular smooth muscle and myocardium.
Adult
0.25 mg/kg IV over 2 min
Rebolus after 15 min prn with 0.35 mg/kg IV
Pediatric
Not established
May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers may increase cardiac depression; cimetidine may increase diltiazem levels
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur
Anticoagulants
These agents inhibit thrombogenesis.
Heparin
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin. Low molecular weight heparin probably is as effective but awaits the results from clinical studies.
Adult
80U/kg IV initially, followed by a maintenance infusion of 18 U/kg/h IV; target aPTT is 50-70 s
Pediatric
75U/kg IV initially, followed by a maintenance infusion of 15-25 U/kg/h IV; increase dose by 2-4 U/kg/h q6-8h prn, using aPTT results or anti-factor Xa levels
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity
Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock; monitor for bleeding in peptic ulcer disease, menstruation, increased capillary permeability, and when giving IM injections
Warfarin (Coumadin)
Inhibits vitamin K–dependent clotting factors II, VII, IX, and X and anticoagulant proteins C and S. Anticoagulation effect occurs 24 h after drug administration, but peak effect may happen 72-96 h later. Antidotes are vitamin K and FFP.
Adult
5-15 mg PO qd for 2-5 d, adjust to desired INR or PT; 2-10 mg/d PO qd maintenance
Adjust dose to maintain INR of 2.5-3.5 or PT of 1.5-2 times baseline
Pediatric
0.1 mg/kg/d PO qd, adjust to desired INR or PT; 0.05-0.34 mg/kg/d PO qd maintenance
Adjust dose to maintain INR of 2.5-3.5 or PT of 1.5-2 times baseline
Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects of warfarin include oral antibiotics, capecitabine, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac
Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis; caution when initiating or discontinuing enteral feeding or vitamin supplement containing vitamin K (adjust dose)
More on Mitral Stenosis |
| Overview: Mitral Stenosis |
| Differential Diagnoses & Workup: Mitral Stenosis |
 Treatment & Medication: Mitral Stenosis |
| Follow-up: Mitral Stenosis |
| Multimedia: Mitral Stenosis |
| References |
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References
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Further Reading
Keywords
mitral stenosis, mitral valve, MS, stenotic mitral valve, rheumatic fever, rheumatic heart disease, mitral valve replacement
