eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies
Cardiomyopathy, Cocaine: Treatment & Medication
Updated: Mar 24, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- Treatment of hypertension
- Patients who present with hypertension may require no treatment except monitoring and occasional use of benzodiazepines for sedation.
- Hypertension, however, may be more severe, and patients may require treatment for hypertensive crisis. This should include intravenous vasodilators and, occasionally, diuretics.
- Nitroglycerin is particularly useful if evidence of myocardial ischemia is present.
- If sympathetic blockers are needed (arrhythmia or ischemia), beta-blockers should not be used as the sole agents because this may lead to unopposed alpha activity and may worsen hypertension.
- An alpha-blocker or ganglionic blocker may be used in conjunction with beta-blockers.
- Myocardial ischemia
- Chest pain is a common presentation in patients who use cocaine, and this may be secondary to either myocardial ischemia or chest wall pain syndromes of other etiologies. An ECG evaluation is required in all such cases to aid in differentiating these possibilities.
- If myocardial ischemia without ST segment elevation is present, the patient should receive nitroglycerin, preferably intravenously. Narcotics also may be helpful if relief cannot be obtained with nitroglycerin.
- If an ST elevation is present, prompt cardiac catheterization should be performed. If that is not available, thrombolytic therapy should be considered. However, special care must be taken to exclude aortic dissection and intracranial bleeding, both of which are associated with cocaine use.
- Treatment of congestive heart failure
- Treatment consists of the standard treatment for congestive heart failure, ie, diuretics and vasodilators as tolerated.
- If shock is present, inotropic agents and vasopressors are indicated.
- If evidence of ongoing ischemia is present, aggressive use of agents directed at relieving vasospasm (nitrates and calcium channel blocking drugs) are indicated. Endotracheal intubation may be necessary.
- If arrhythmias are present and are felt to be compromising the clinical situation, they should be treated aggressively. The use of beta-blocking drugs as single agents is contraindicated.
- Treatment of cocaine addiction
- In most of the reported cases, patients have shown significant improvement following the cessation of cocaine use.
- In some cases, patients have returned to normal cardiac function, but recurrence is reported if the patient relapses into cocaine use.
- Efforts to assist the patient with their drug addiction should be a part of every treatment plan.
For related information, see the Medscape CME course New Statement on Cocaine-Associated MI Urges Caution With Beta Blockers, Emphasizes Kicking the Habit.
Consultations
- Consultation with a cardiologist is advisable. These patients may be critically ill, requiring the use of sophisticated monitoring and intensive pressor support. Cardiac catheterization may be necessary.
- Consultation with a psychiatrist also is advisable for assistance with drug abuse treatment issues. Hospitalization for detoxification may be necessary, particularly if other drugs also are being abused. Outpatient treatment of drug dependence is strongly advised. Abstinence is mandatory.
Medication
Acute presentation may include congestive heart failure, pulmonary edema, or cardiogenic shock. Diuretic therapy is initiated. Vasodilators (nitroglycerin) can be added to treat pulmonary edema secondary to cardiac decompensation. Vasoconstrictors and inotropic agents are added for shock or evidence of hypoperfusion; low-dose dopamine also may be added to increase renal perfusion. Diuretics and vasodilators are the drugs of choice for long-term management.
Diuretics
The initial drop in cardiac output produced by diuresis causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels and peripheral vascular resistance falls below its pretreatment baseline.
Furosemide (Lasix)
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.
Dose must be individualized to the patient. When treating infants, titrate with increments of 1 mg/kg/dose until satisfactory effect is achieved. Provides primary diuretic therapy PO/IV in CHF. Also used as maintenance therapy in CHF.
Adult
40-200 mg IV; then 40-120 mg PO
Larger dose may be required in severe cases
Pediatric
Not established; suggested dosing for infants is to titrate in increments of 1 mg/kg/dose PO/IV until satisfactory effect is achieved
Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently
Documented hypersensitivity; severe electrolyte abnormalities; significant intravascular volume contraction
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Close medical supervision and dose evaluation are required to prevent fluid and electrolyte imbalance; may cause excessive dehydration during ascent, but no reports of deleterious effects; observe for blood dyscrasias and liver or kidney damage; loop diuretics may increase urinary excretion of magnesium and calcium; perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Nitrates
These agents are effective vasodilators.
Nitroglycerin (Minitran, Nitrogard, Nitrol, Nitrolingual, Nitrostat, Nitro-Dur)
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in blood pressure. DOC in acute cardiogenic pulmonary edema unresponsive to diuretic therapy.
Adult
IV: 5-200 mcg/min titrated to response
Topically: 0.5-2 in of 4% ointment q6-8h
SL: 200-500 mcg (1/400-1/150 grains) q5min
Also available as topical patches
Pediatric
Not established
Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)
Documented hypersensitivity; severe anemia, shock, postural hypotension, head trauma closed-angle glaucoma, or cerebral hemorrhage
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 coronary artery disease and low systolic blood pressure
Vasopressors
Diminish blood flow through vasoconstriction.
Dopamine (Intropin)
Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dose-dependent. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced by higher doses.
Useful for support of BP and renal function. 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.
Adult
1-5 mcg/kg/min IV increases renal blood flow, improving urine output
5-10 mcg/kg/min IV increases cardiac output, with both inotropic and chronotropic effects
10-20 mcg/kg/min IV with continuous monitoring and dose adjustment for BP support
Pediatric
Not established
Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine
Documented hypersensitivity; pheochromocytoma or ventricular fibrillation
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
Monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure closely during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia
Cardiac inotropics agents
Inotropic agents increase cardiac output.
Dobutamine (Dobutrex)
Useful in presence of cardiogenic shock with low cardiac output. May be useful when used with dopamine in renal doses.
Adult
2-20 mcg/kg/min IV increases cardiac output with little effect on heart rate or SVR
Pediatric
Not established
Beta-adrenergic blockers antagonize effects; general anesthetics may increase toxicity
Documented hypersensitivity; idiopathic hypertropic subaortic stenosis; ongoing myocardial ischemia; agents increase myocardial oxygen demand
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Following myocardial infarction, use with extreme caution; hypovolemic state should be corrected before using this drug
Angiotensin-converting enzyme inhibitors
Improve cardiac output by decreasing afterload.
Lisinopril (Prinivil, Zesteril)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
5-10 mg/d PO qd; start 2.5 mg PO qd; max 40 mg PO qd
Pediatric
Not established
NSAIDs may reduce hypotensive effects of lisinopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases lisinopril levels; probenecid may increase lisinopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics
Documented hypersensitivity
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
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe congestive heart failure
Captopril (Capoten)
Oldest and most completely studied ACE inhibitor. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Adult
6.5-25 mg PO tid/qid (other ACE inhibitors have a more convenient dosing schedule)
Pediatric
Not established
NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics
Documented hypersensitivity; hypotension; renal artery stenosis
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
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe congestive heart failure; hyperkalemia may occur
Calcium channel blockers
In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
Diltiazem (Cardizem)
Effective in controlling tachyarrhythmias associated with cocaine use. Slows AV nodal conduction time and prolongs AV nodal refractory period, which may convert SVT or slow the rate in atrial fibrillation. Also has vasodilator activity but may be less potent than other agents.
Adult
0.25 mg/kg IV bolus for acute SVT; if ineffective, give 0.35 mg/kg IV; may follow with 5-10 mg/h IV infused over 24 h
Maintenance: 180-360 mg PO qd
Pediatric
Not established
May increase carbamazepine, digoxin, and cyclosporine 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 levels
Documented hypersensitivity; hypotension; WPW syndrome or a wide-complex tachycardia; sick sinus syndrome; acute MI; pulmonary congestion; second/third-degree heart block
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
More on Cardiomyopathy, Cocaine |
| Overview: Cardiomyopathy, Cocaine |
| Differential Diagnoses & Workup: Cardiomyopathy, Cocaine |
 Treatment & Medication: Cardiomyopathy, Cocaine |
| Follow-up: Cardiomyopathy, Cocaine |
| References |
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References
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Further Reading
Keywords
cocaine cardiomyopathy, cocaine myocarditis, cocaine-induced heart failure, chronic cardiomyopathy, cocaine abuse, cocaine addiction
