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Congestive Heart Failure and Pulmonary Edema

Author Information and Disclosures

Contents

Treatment and Medication

Treatment

Prehospital Care:

  • Prehospital notification by emergency medical services (EMS) personnel should alert ED staff of a patient presenting with signs and symptoms of CHF and pulmonary edema. They should receive on-line medical advice for patients with high-risk presentations.
  • Begin treatment with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask.
  • Utilize cardiac monitoring and continuous pulse oximetry.
  • Obtain intravenous access, as well as a prehospital ECG, if available.
  • Provide nitroglycerin sublingual or spray for active chest pain in the patient without severe hypotension and IV furosemide.

Emergency Department Care:

  • Begin ED treatment of a patient presenting with signs and symptoms of CHF and pulmonary edema with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask. Utilize cardiac monitoring and continuous pulse oximetry. Obtain IV access.
  • To reduce venous return, elevate the head of the bed. Patients may be most comfortable in a sitting position with their legs dangling over the side of the bed, which allows for reduced venous return and decreased preload.
  • Therapy generally starts with nitrates and diuretics if patients are hemodynamically stable. Many other treatment modalities may play some role in acute management.
  • If possible, treat the underlying cause as well, if identified. This is particularly necessary for patients with known diastolic dysfunction who respond best to reductions in blood pressure, rather than to diuretics, nitrates, and inotropic agents. Serum BNP levels may be very useful in the setting of undifferentiated dyspnea, or in the future may be useful to gauge therapeutic success.
  • Eliminate contributing factors when possible.
  • Restrict fluid and sodium.
  • Consider other treatment modalities, including nesiritide. Nesiritide may be useful in lieu of nitroglycerin in patients with moderate respiratory distress, particularly if the patient will not tolerate noninvasive ventilation or in the patient who cannot have nitroglycerin by protocol (ie, in an observation unit).
    • Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP)—Recent data comparing nasal CPAP therapy and facemask ventilation therapy have demonstrated decreased need for intubation rates when these modalities are used. In patients with severe CHF treated with CPAP, however, no significant difference was found in short-term mortality rates and length of hospital stay. Although BiPAP therapy may improve ventilation and vital signs more rapidly then CPAP, a higher incidence of MI associated with BiPAP has been reported. BiPAP and CPAP are contraindicated in the presence of acute facial trauma, the absence of an intact airway, and in patients with an altered mental status or who are uncooperative.
    • Alternating tourniquets, formerly a mainstay of therapy, have been used to decrease preload. Their use has been supplanted by newer therapies such as intravenous nitroglycerin and nitroprusside.
    • Phlebotomy with removal of 500 mL of blood or via plasmapheresis is another former mainstay of therapy used to decrease preload. Its use has been supplanted by newer therapies such as intravenous nitroglycerin and nitroprusside.

Consultations:

  • Cardiology
  • Critical care services
  • Cardiothoracic surgery for possible heart valve surgery or transplantation

Medication

The goal of pharmacotherapy is to achieve a PCWP of 15-18 mm Hg and a cardiac index >2.2 L/min/m2, while maintaining adequate blood pressure and perfusion to essential organs. These goals may need to be modified for some patients.

Use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase prevalence of recurrent CHF with chronic use. Conflicting evidence currently exists both in favor of and against the use of calcium channel blockers in the acute setting; at this time limit their acute use to patients with diastolic dysfunction and heart failure, a condition not easily determined in the emergency department.

Angiotensin converting enzyme (ACE) inhibitors, such as SL captopril or IV enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation. Haude compared 25 mg of SL captopril with 0.8 mg of sublingual nitroglycerin in 24 patients with class III and class IV CHF and found that captopril induces a more sustained and more pronounced improvement in hemodynamics. Annane gave 1 mg of IV enalapril to 20 patients presenting with acute class III and class IV CHF over 2 hours and demonstrated rapid hemodynamic improvement with no significant adverse effects on cardiac output or hepatosplanchnic measurements.

Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Since the information on this subject is still controversial and limited to small studies, the routine use of ACE inhibitors cannot be recommended at this time. ACE inhibitors remain a promising area in need of further study.

Beta-blockers, possibly by restoring beta-1 receptor activity or via prevention of catecholamine activity, appear to be cardioprotective in patients with depressed left ventricular function. The US Carvedilol Heart Failure study group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35% or less. Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. The role of beta-blockers in the acute setting, however, is currently unclear; limit use until hemodynamic studies indicate that further deterioration will not occur.

Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach is often used, particularly as both may cause bronchospasm. Aerosolized beta-2 agonists, which are the more selective of beta-agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function. Terbutaline has been shown to be successful in this setting, as well as albuterol, isoetharine, and bitolterol.

Limit roles of theophylline and aminophylline in the acute setting. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects. Nevertheless, they can exacerbate dysrhythmias (eg, multifocal atrial tachycardia [MAT], ischemia) by increasing cardiac work.

Steroids, IV or PO, have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension. Inhaled steroids, because of their lack of systemic side effects, may be a reasonable option in this confusing patient presentation; however, given their delayed onset of action, they remain an area in need of further study.

Please see the chapter on Asthma for dosing schedules.

Drug Category: Diuretics First-line therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium chloride reabsorption in the ascending loop of Henle.

Furosemide (Lasix) -- Administer loop diuretics IV, since this allows for both superior potency and higher peak concentration despite increased incidence of side effects, particularly ototoxicity.
Adult DoseA reasonable approach for furosemide might be as follows:
10-20 mg IV for patients symptomatic with CHF not already using diuretics
40-80 mg IV for patients already using diuretics
80-120 mg IV for patients whose symptoms are refractory to the initial dose after 1 h of its administration
Higher doses and more rapid redosing may be appropriate for the patient in severe distress
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, hepatic coma, anuria, severe electrolyte depletion
Interactions 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
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsPerform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Metolazone (Mykrox, Zaroxolyn) -- Both chlorothiazide and metolazone have been used as adjunctive therapy in patients initially refractory to furosemide. Chlorothiazide, however, at doses of 250-500 mg IV, decreases GFR with CHF and, thus, is less potent and causes a greater loss of potassium. Conversely, metolazone has been demonstrated to be synergistic with loop diuretics in treating refractory patients.
Adult Dose5-10 mg PO before redosing with furosemide
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, hepatic coma, encephalopathy, anuria
InteractionsThiazides may decrease effect of anticoagulants, sulfonylureas, and gout treatments; anticholinergics and amphotericin B may increase toxicity of thiazides; effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, or methenamine; when administered concurrently, thiazides increase toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants
Pregnancy B - Usually safe but benefits must outweigh the risks.
PrecautionsCaution in hepatic or renal disease, diabetes mellitus, gout, or lupus erythematosus
 

Drug Category: Nitrates --Reduce myocardial oxygen demand by lowering preload and afterload.

In severely hypertensive patients, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, due to thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside, IV nitroglycerin is still the therapy of choice for afterload reduction.

Nitroglycerin (Nitro-Bid, Nitrol, Nitrostat) -- SL nitroglycerin and nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg.
Similar to SL, nitrospray's onset is 1-3 min with a half-life of 5 min. Applicability of nitrospray may be easier, and storage is up to 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients given nitrospray with pulmonary edema in an ICU setting.
Topical nitrate therapy is reasonable in a patient presenting with class I to II CHF. However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred since it is easier to monitor hemodynamics and absorption, particularly in the diaphoretic patient.
Oral nitrates, due to delayed absorption, have little role in the acute presentations of CHF.
Adult DoseNitrospray: single spray (0.4 mg) equivalent to a single 1/150 SL; may repeat q3-5min as hemodynamics permit, up to a maximum of 1.2 mg
Ointment: Apply 1-2 inches of nitropaste to chest wall
Injection: start at 20 mcg/min IV and rate to effect in 5-10 mcg increments q3-5min
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, severe anemia, shock, postural hypotension, head trauma, closed-angle glaucoma, cerebral hemorrhage
InteractionsAspirin 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)
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsExercise caution with coronary artery disease and low systolic blood pressure.
Nitroprusside sodium (Nitropress) -- Produces vasodilation and increases inotropic activity of the heart. At higher dosages may exacerbate myocardial ischemia by increasing heart rate. Easily titratable.
Adult Dose10-15 mcg/min IV and titrate to effective dose range of 30-50 mcg/min and a systolic blood pressure of at least 90 mm Hg
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, subaortic stenosis, optic atrophy, tobacco amblyopia, idiopathic hypertrophic, atrial fibrillation or flutter
InteractionsPatients receiving other hypertensive therapy may be more sensitive to sodium nitroprusside
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsCaution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has the ability to lower blood pressure and thus should be used only in those patients with mean arterial pressures >70 mm Hg
 

Drug Category: Analgesics --Morphine IV is an excellent adjunct in acute therapy. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload. Also causes arterial dilatation, which reduces systemic vascular resistance (SVR) and increases cardiac output. Narcan also can reverse the effects of morphine. However, some evidence indicates that morphine use in acute pulmonary edema may increase the intubation rate.

Morphine sulfate (Duramorph, Astramorph, MS Contin) -- DOC for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated until desired effect is obtained.
Adult Dose2-5 mg IV and repeated q10-15min unless respiratory rate is <20 breaths/min or systolic blood pressure is <100 mm Hg
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, hypotension, potentially compromised airway with uncertain rapid airway control, respiratory depression, nausea, emesis, constipation, urinary retention
InteractionsPhenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsCaution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
 

Drug Category: Inotropic agents --Principal inotropic agents include dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In the hypotensive patient presenting with CHF, dopamine and dobutamine are agents usually used. Inamrinone or milrinone inhibits phosphodiesterase, resulting in an increase of intracellular cyclic AMP and alteration in calcium transport. As a result, they increase cardiac contractility and reduce vascular tone by vasodilatation.

Dopexamine is a new synthetic catecholamine with beta-2 and dopaminergic properties causing vasodilation and increased inotropism but with tachycardia as well. Ultimately may have a role as an emergent inotropic agent, but dobutamine is probably the current agent of choice.

Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished efficacy at times of increased sympathetic tone. Thus, has little, if any, benefit in the patient presenting concomitantly with atrial fibrillation and rapid ventricular response. Limit use of digoxin to chronic CHF in which its role has been well established.

These agents augment both coronary and renal blood flow.

Dopamine (Intropin) -- Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation is produced by higher doses.
Positive inotropic agent at 2-10 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg cause vasoconstriction, which increases afterload.
Adult Dose5 mcg/kg/min IV and increase at 5 mcg/kg/min increments to a 20 mcg/kg/min dose
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity, pheochromocytoma, ventricular fibrillation
InteractionsPhenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsMonitor closely urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during the 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
Dobutamine (Dobutrex) -- Produces vasodilation and increases inotropic state. At higher dosages may cause increased heart rate, thus exacerbating myocardial ischemia. Strong inotropic agent with minimal chronotropic effect and no vasoconstriction.
Adult DoseStarting dose: 2.5 mcg/kg/min IV; generally therapeutic in the range of 10-40 mcg/kg/min
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter
InteractionsBeta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsFollowing a myocardial infarction use with extreme caution; hypovolemic state should be corrected before using this drug
 

Drug Category: Human B-type natriuretic peptides --Growing data suggest that Human B-type natriuretic peptides such as Nesiritide may be effective in reducing pulmonary capillary wedge pressure and improving dyspnea in patients with acutely decompensated congestive heart failure. Nesiritide serves as a second messenger to dilate veins and arteries.

Nesiritide (Natrecor) -- Recombinant DNA form of human B-type natriuretic peptides (hBNP), which dilate veins and arteries.
Human BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. Reduces pulmonary capillary wedge pressure and improves dyspnea in patients with acutely decompensated congestive heart failure.
Adult Dose2 mcg/kg IV bolus over 60 s; follow by 0.01 mcg/kg/min continuous infusion; bolus volume (mL) = 0.33 X patient weight (kg); infusion flow rate of bolus (mL/h) = 0.1 X patient wt (kg)
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; systolic blood pressure <90 mm Hg; patients suspected of having, or known to have, low cardiac filling pressures, significant valvular stenosis, restrictive or obstructive cardiomyopathy, constrictive pericarditis, pericardial tamponade, conditions in which cardiac output is dependent upon venous return
InteractionsConcurrent administration with ACE inhibitors and other vasodilators may cause hypotension
Pregnancy C - Safety for use during pregnancy has not been established.
PrecautionsDo not initiate at dose higher than recommended; may affect renal function in patients whose renal function may depend on activity of renin-angiotensin-aldosterone system; may cause hypotension (administer in settings where blood pressure can be monitored closely); discontinue drug if hypotension develops; ventricular tachycardia, non-sustained VT, headache, abdominal pain, back pain, insomnia, anxiety, angina pectoris, nausea, and vomiting may occur
 
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Bibliography

  1. Andersson B, Waagstein F: Spectrum and outcome of congestive heart failure in a hospitalized population. Am Heart J 1993 Sep; 126(3 Pt 1): 632-40[Medline].
  2. Annane D, Bellissant E, Pussard E: Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation 1996 Sep 15; 94(6): 1316-24[Medline].
  3. Chen JT: Radiographic diagnosis of heart failure. Heart Dis Stroke 1992 Mar-Apr; 1(2): 58-63[Medline].
  4. Clinical Quality Improvement Network Investigators: Mortality risk and patterns of practice in 4606 acute care patients with congestive heart failure. The relative importance of age, sex, and medical therapy. Arch Intern Med 1996 Aug 12-26; 156(15): 1669-73[Medline].
  5. Collins SP, Lindsell CJ, Storrow AB: Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann Emerg Med 2006 Jan; 47(1): 13-8[Medline].
  6. Collins SP, Hinckley WR, Storrow AB: Critical review and recommendations for nesiritide use in the emergency department. J Emerg Med 2005 Oct; 29(3): 317-29[Medline].
  7. Connors AF, Speroff T, Dawson NV: The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996 Sep 18; 276(11): 889-97[Medline].
  8. Edwards JD, Grant PT, Plunkett P, Nightingale P: The haemodynamic effects of sublingual nitroglycerin spray in severe left ventricular failure. Intensive Care Med 1989; 15(4): 247-9[Medline].
  9. Goldstein RE, Boccuzzi SJ, Cruess D: Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. The Adverse Experience Committee; and the Multicenter Diltiazem Postinfarction Research Group. Circulation 1991 Jan; 83(1): 52-60[Medline].
  10. Gordon HS, Harper DL, Rosenthal GE: Racial variation in predicted and observed in-hospital death. A regional analysis. JAMA 1996 Nov 27; 276(20): 1639-44[Medline].
  11. Hamilton RJ, Carter WA, Gallagher EJ: Rapid improvement of acute pulmonary edema with sublingual captopril. Acad Emerg Med 1996 Mar; 3(3): 205-12[Medline].
  12. Harlan WR, Oberman A, Grimm R, Rosati RA: Chronic congestive heart failure in coronary artery disease: clinical criteria. Ann Intern Med 1977 Feb; 86(2): 133-8[Medline].
  13. Kannel WB, Pinsky JL: Trends in cardiac failure incidence and causes of three decades in the Framingham study. J Am Coll Cardiol 1991; 17: 87A.
  14. Kiyingi A, Field MJ, Pawsey CC: Metalozone in treatment of severe refractory congestive cardiac failure. Lancet 1990; 335: 29-31[Medline].
  15. Kostuk W, Barr JW, Simon AL: Correlations between the chest film and hemodynamics in acute myocardial infarction. Circulation 1973; 48: 624-632[Medline].
  16. Lin M, Yang YF, Chiang HT: Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up. Chest 1995 May; 107(5): 1379-86[Medline].
  17. Maisel AS, Krishnaswamy P, Nowak RM, et al: Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002 Jul 18; 347(3): 161-7[Medline].
  18. Massie BM: Congestive heart failure: Current controversies and future prospects. Am J Cardiol 1990.
  19. McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002 Jul 23; 106(4): 416-22[Medline].
  20. Mehta S, Jay GD, Woolard RH: Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med 1997 Apr; 25(4): 620-8[Medline].
  21. Melandri G, Semprini F, Branzi A: Comparative haemodynamic effects of transdermal vs intravenous nitroglycerin in acute myocardial infarction with elevated pulmonary artery wedge pressure. Eur Heart J 1990 Jul; 11(7): 649-55[Medline].
  22. Mueller C, Scholer A, Laule-Kilian K, et al: Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004 Feb 12; 350(7): 647-54[Medline].
  23. Mueller C, Laule-Kilian K, Frana B, et al: Use of B-type natriuretic peptide in the management of acute dyspnea in patients with pulmonary disease. Am Heart J 2006 Feb; 151(2): 471-7[Medline].
  24. Mueller C, Frana B, Rodriguez D, et al: Emergency diagnosis of congestive heart failure: impact of signs and symptoms. Can J Cardiol 2005 Sep; 21(11): 921-4[Medline].
  25. Parmley WW: Pathophysiology and current therapy of congestive heart failure. J Am Coll Cardiol 1989 Mar 15; 13(4): 771-85[Medline].
  26. Peacock, et al: Prospective randomized outcomes study of acutely decompensated CHF treated initially in outpatients with Natrecor (PROACTION). J Am Coll Cardiol 2003; 4 (Suppl A): 336A.
  27. Polese A, Fiorentini C, Olivari MT: Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema. Am J Med 1979 May; 66(5): 825-30[Medline].
  28. Wright SP, Doughty RN, Pearl A, et al: Plasma amino-terminal pro-brain natriuretic peptide and accuracy of heart-failure diagnosis in primary care: a randomized, controlled trial. J Am Coll Cardiol 2003 Nov 19; 42(10): 1793-800[Medline].

Synonyms And Related Keywords

CHF, pulmonary edema, ventricular failure, forward ventricular failure, backward ventricular failure, systolic dysfunction, diastolic dysfunction, dyspnea, beta natriuretic peptide, BNP, orthopnea, paroxysmal nocturnal dyspnea, PND, cardiomyopathy, valvular heart disease, hypertension, peripheral edema, jugular venous distention, tachycardia, coronary artery disease, congenital heart disease, myocarditis, infectious endocarditis, pulmonary embolus, hyperthyroidism

Author Information and Disclosures

Author: Shamai Grossman, MD, MS, Assistant Professor, Department of Emergency Medicine, Harvard Medical School; Director, The Clinical Decision Unit and Cardiac Emergency Center, Beth Israel Deaconess Medical Center

Coauthor(s): David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Vice-Chair, Department of Emergency Medicine, Massachusetts General Hospital

Shamai Grossman, MD, MS, is a member of the following medical societies: American College of Emergency Physicians

Editor Information

Editor(s): William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Consulting Staff, Department of Emergency Medicine, Bellevue Hospital Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Barry Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, and Professor of Anatomy and Neurobiology, Research Director, Department of Emergency Medicine, University of Arkansas for Medical Sciences

 
 
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