eMedicine Specialties > Emergency Medicine > Cardiovascular

Cardiomyopathy, Dilated: Treatment & Medication

Author: Uche A Blackstock, MD, Staff Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate
Coauthor(s): Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Sep 30, 2008

Treatment

Prehospital Care

In cases of severe acute failure, EMS personnel may initiate treatment with oxygen, nitrates, and furosemide en route to the hospital. Cardiac monitoring, continuous pulse oximetry, and ECG may also be performed by units with advanced life support (ALS) certification. Further ventilatory support or even intubation may be indicated if the patient is in extremis.

Emergency Department Care

Treatment of dilated cardiomyopathy is essentially the same as treatment of CHF and pulmonary edema; however, obtaining a thorough history from patients with dilated cardiomyopathy helps determine etiology.

  • When beginning treatment, administer oxygen, initiate continuous pulse oximetry and cardiac monitoring, and obtain intravenous access.
  • Mainstays of medical therapy are preload reduction, afterload reduction, diuresis, and airway support.
  • In patients with severe refractory pulmonary edema, a trial of continuous positive airway pressure (CPAP) or bimodal positive airway pressure (BiPAP) may obviate the need for intubation.

Consultations

Consult an internist, an intensivist, or a cardiologist as indicated for admission when a patient has been diagnosed with dilated cardiomyopathy for the first time or for continued inpatient treatment or monitoring. Emergent consultation with a cardiologist may also be indicated for echocardiography in the ED. 

Medication

Goals of treatment include symptom relief, improved cardiac output, shortened hospital stay, fewer ED visits, reversal of injury process, and decreased mortality.

In 1994, Baker et al reviewed the incidence of thromboembolism in patients with heart failure due to left ventricular systolic dysfunction and found no clinical evidence to support the use of anticoagulants in those patients who were in sinus rhythm.6 Therefore, restrict the use of anticoagulants to those patients in atrial fibrillation, with artificial valves, or with known mural thrombus.

In cases of dilated cardiomyopathy secondary to myocarditis, corticosteroids have been suggested to be helpful in decreasing inflammation; however, the Multicenter Myocarditis Treatment Trial showed no benefit in the use of corticosteroids and azathioprine for treatment of biopsy-proven inflammation in dilated cardiomyopathy.7 Some smaller uncontrolled studies have shown benefit, but these results have not been confirmed with a controlled study.

Highlights from pertinent literature also are included below.

Angiotensin-converting enzyme (ACE) inhibitors

When treating dilated cardiomyopathy, use ACE inhibitors first. The Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) group in 1987 showed that the addition of enalapril to the conventional treatment of CHF yielded a 31% reduction in mortality rate at 1 year.8 A similar study by Studies of Left Ventricular Dysfunction (SOLVD) investigators in 1991 revealed a 16% risk reduction.9 Losartan, an angiotensin receptor blocker, also has been effective in decreasing mortality rates. 


Enalapril (Vasotec)

Competitive inhibitor of angiotensin-converting enzymes. Reduces angiotensin II levels, causing decrease in aldosterone secretion.

Adult

1.25 mg IV q6h

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; diuretics may enhance hypotensive effects

Documented hypersensitivity; pregnancy; renal insufficiency; history of angioedema or ACE inhibitor allergy; hypotension

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF; may cause hypotension

Cardiac glycosides

Foxglove and its derivatives are the oldest treatment of heart failure, but they still have a place in medicine despite recent advances in other drug categories. In 1990, Jaeschke et al did a meta-analysis of 7 double-blind, placebo-controlled trials.10 The analysis revealed that 1 in 9 patients with CHF showed significant clinical benefit from treatment with digoxin. Note that this was an improvement of symptoms, not a reduction in mortality.

The Digitalis Investigation Group trial demonstrated that digoxin decreases heart failure hospitalizations but has no effect on long-term survival.11

Although little controversy exists as to the benefit of digoxin in patients with symptomatic left ventricular dysfunction and concomitant atrial fibrillation, the debate continues over its role in patients with normal sinus rhythm.


Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Causes direct action on cardiac muscle, resulting in increased myocardial systolic contractions. Causes indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Adult

0.125-0.25 mg IV q6h for 2 doses, then qd for maintenance

Pediatric

8-50 mcg/kg IV, based on age and ideal body weight

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; ventricular fibrillation; SA or AV node disease; accessory AV pathway (eg, Wolff-Parkinson-White syndrome); idiopathic hypertrophic subaortic stenosis; hypokalemia (K+ <2); signs of digitalis toxicity

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

Impaired renal function prolongs renal half-life; hypokalemia, hypomagnesemia, and hypercalcemia may cause toxicity; hypokalemia may reduce positive inotropic effect; 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; in patients with acute MI, may precipitate arrhythmias and heart failure

Loop diuretics

Loop diuretics are necessary adjuncts in the medical therapy for heart failure when symptoms are due to sodium and water retention. They are the mainstay of diuretic therapy because they produce significantly more natruresis than other diuretics, particularly in the setting of decreased glomerular rate. They provide symptomatic relief without prolonging life or altering disease course.

Despite clear indications for loop diuretics in the reduction of volume overload, controversy exists regarding their use in acute decompensated failure. No large prospective trial has examined diuretics in acute decompensated heart failure.

Loop diuretics have a tendency to cause hypokalemia and hypomagnesemia; therefore, monitor electrolyte levels and replace as necessary.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system. This interference results from inhibition of sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Adult

20-160 mg IV q6h until desired diuresis achieved

Pediatric

2 mg/kg PO q6h until desired diuresis 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); may enhance anticoagulant activity of warfarin; may increased plasma levels and toxicity of lithium

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

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

Observe for blood dyscrasias and liver or kidney damage; may increase urinary excretion of magnesium and calcium; perform frequent determinations of serum electrolytes, CO2, glucose, creatinine, uric acid, calcium, and BUN during first few months of therapy and periodically thereafter

Beta-blockers

The most recent and promising research has yielded great reductions in mortality rates when beta-blockers are added to outpatient management of CHF. In 1993, the Metoprolol in Dilated Cardiomyopathy (MDC) study compared patients who had experienced heart failure and were treated with metoprolol in addition to conventional therapies with those who were treated solely with conventional therapies.12 The study revealed a 34% reduction in primary endpoints (ie, need for heart transplant, death) in those who were treated with metoprolol in addition to conventional therapies.

In 1996, the US Carvedilol Study showed a 65% reduction in mortality in patients with heart failure treated with carvedilol.13 Carvedilol acts in 3 ways: as a beta-blocker, an alpha-blocker, and an antioxidant.

The Metoprolol CR/XL Randomized Intervention Trial in CHF (MERIT-HF), the largest trial ever completed using a beta-blocker in heart failure, was performed in 13 European countries and the United States.14 The results were announced in 1999. MERIT-HF was a randomized, double-blind trial that compared the effects of extended-release metoprolol (metoprolol-XL) with the effects of a placebo on survival and other outcome measures (eg, sudden death, hospitalization for heart failure, quality of life). The trial, which began in 1997 and was scheduled to continue until 2000, closed prematurely following an interim analysis that identified a highly positive effect of metoprolol-XL on all causes of mortality.

A statistically significant 34% reduction in relative risk for total mortality at 1 year was observed; mortality rates were 7.2% in the metoprolol-XL group and 11% in the placebo group (P =0.0062;). Results at the time of study termination also revealed a 38% reduction in cardiovascular mortality, a 41% reduction in sudden death, and a 49% reduction in CHF mortality.14


Metoprolol (Lopressor)

Selective beta-1 adrenergic receptor blocker that decreases automaticity of contractions.

Adult

5 mg IV q5min for 3 doses; if tolerated, may give 100 mg PO qd
Carefully monitor BP, heart rate, and ECG during IV administration

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 may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, or contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Documented hypersensitivity; hypotension; bradycardia; AV/SA node disease; cardiogenic shock; overt cardiac failure

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 drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG


Carvedilol (Coreg)

Antiadrenergic beta-blocker shown to be of benefit in patients with heart failure. Some evidence suggests it is even more beneficial than metoprolol.

Adult

6.25-50 mg PO bid as tolerated (maximum of 75 mg/d if <85 kg, 100 mg/d if >85 kg)

Pediatric

Not established

Carvedilol significantly interacts with cytochrome p450 system and most drugs eliminated by this mechanism; notably, may increase digoxin levels by as much as 14%
Cimetidine increases level of carvedilol; rifampin decreases serum carvedilol levels

Documented hypersensitivity; hypotension; bradycardia; AV/SA node disease; cardiogenic shock; overt cardiac failure

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 drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG

Vasodilators

In 1986, the VA Cooperative Study revealed a 36% reduction in mortality risk in patients treated with preload and afterload reducers (ie, isosorbide dinitrate, hydralazine) in addition to conventional heart failure medications.15

Preload reduction with venodilators is thought to be helpful in acute decompensated heart failure by reducing congestions and minimizing cardiac oxygen demand. Afterload reduction is also thought to be helpful in some patients with acute decompensated heart failure by decreasing myocardial oxygen demand and improving forward flow.

Intravenous nitrate therapy resulted in acute improvement of dyspnea in 2 randomized trials. Similarly, morphine acts as a venodilator, and it central suppresses symptoms of breathlessness; however, no rigorous studies of morphine have been performed in acute decompensated heart failure. Sublingual nitroglycerin spray, nitropaste, and IV nitroglycerin also have been advocated in the treatment of pulmonary edema secondary to CHF.


Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Adult

10-20 mg/dose IV q4-6h prn; may increase to 40 mg/dose; change to PO therapy as soon as possible

Pediatric

0.1-0.2 mg/kg IV q4-6h prn; not to exceed 20 mg or 1.7-3.5 mg/kg/d divided in 4-6 doses

MAOIs and beta-blockers may increase toxicity; effects may be decreased by indomethacin

Documented hypersensitivity; mitral valve rheumatic heart disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Implicated in MI; use caution in patients with suspected coronary artery disease


Nitroglycerin (Nitro-Bid)

Relaxes vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing decrease in BP.

Adult

Injection: 10-20 mcg/min IV continuous infusion
Nitrospray: 0.4 mg (single spray), which is equivalent to single 1/150 SL; may repeat doses q3-5min as hemodynamics permit; not to exceed 1.2 mg
Nitropaste: Apply 1-2 inches of ointment to chest wall

Pediatric

0.1-1 mcg/kg/min IV continuous infusion

Aspirin may increase serum concentrations; concurrent calcium-channel blockers may cause marked symptomatic orthostatic hypotension (adjust dosage of either agent prn)

Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; 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

Coronary artery disease; low systolic BP


Isosorbide dinitrate and hydralazine (BiDil)

Fixed-dose combination of isosorbide dinitrate (20 mg/tab), a vasodilator with effects on both arteries and veins, and hydralazine (37.5 mg/tab), a predominantly arterial vasodilator. Indicated for heart failure in blacks, based in part on results from the African American Heart Failure Trial. Two previous trials in general population of patients with severe heart failure found no benefit but suggested benefit in black patients. Compared with placebo, blacks showed 43% reduction in mortality rate, 39% decrease in hospitalization rate, and decrease in symptoms from heart failure.16

Adult

1 tab PO tid; may titrate upward, not to exceed 2 tab tid

Pediatric

Not established

Hydralazine may increase propranolol, metoprolol, and lisinopril AUC and Cmax; isosorbide dinitrate may cause additive vasodilating effects with other vasodilators (eg, sildenafil [Viagra], vardenafil [Levitra]), especially when coadministered with alcohol

Documented hypersensitivity; allergy to organic nitrates

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

May cause symptomatic hypotension even with small doses; careful hemodynamic monitoring required if administered in patients with acute MI
Hydralazine: May cause SLE-like symptoms, including glomerulonephritis, tachycardia, hypotension, and peripheral neuritis (pyridoxine therapy may be required)
Isosorbide dinitrate: If hypotension exists, may aggravate angina associated with hypertrophic cardiomyopathy

Potassium-sparing diuretics

Spironolactone acts as an aldosterone receptor blocker and, with concomitant use of ACE inhibitors, helps break the cycle of sodium retention and fluid overload via the renin-aldosterone axis.

In September 1999, Pitt et al published the results of their spironolactone trial. They found that adding 12.5-25 mg of spironolactone per day to a standard treatment regimen for CHF (ie, ACE inhibitor, furosemide, digoxin) yielded a 35% reduction in hospitalization, significant improvements in New York Heart Association (NYHA) functional class, and a 30% reduction in risk of death.17


Spironolactone (Aldactone)

Used in management of edema resulting from excessive aldosterone excretion. Competes for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

Adult

12.5-25 mg PO qd

Pediatric

1.5-3.5 mg/kg/d PO in divided doses q6-24h

May increase half-life of digoxin; may decrease effect of anticoagulants; potassium and other potassium-sparing diuretics may increase toxicity

Documented hypersensitivity; anuria; renal failure; hypotension; hyperkalemia

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Renal or hepatic impairment

More on Cardiomyopathy, Dilated

Overview: Cardiomyopathy, Dilated
Differential Diagnoses & Workup: Cardiomyopathy, Dilated
Treatment & Medication: Cardiomyopathy, Dilated
Follow-up: Cardiomyopathy, Dilated
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

dilated cardiomyopathy, cardiomyopathy, disease of the myocardium, heart disease, low cardiac output, cardiac failure, heart failure, congestive heart disease, CHD, congestive heart failure, CHF, contractile dysfunction, ventricular chamber enlargement, systolic dysfunction, ventricular arrhythmias, supraventricular arrhythmias, conduction system abnormalities, thromboembolism, sudden death

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Contributor Information and Disclosures

Author

Uche A Blackstock, MD, Staff Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate
Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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