Cardiogenic Pulmonary Edema Medication

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Henry H Ooi, MD, MRCPI  more...
Updated: Dec 28, 2015

Medication Summary

Loop diuretics have long been the cornerstone of cardiogenic pulmonary edema (CPE) treatment, with furosemide being the most commonly used of these drugs. Premedication with drugs that decrease preload (eg, nitroglycerin [NTG]) and afterload (eg, angiotensin-converting enzyme [ACE] inhibitors) before the administration of loop diuretics can prevent adverse hemodynamic changes.

Nesiritide is recombinant human brain-type natriuretic peptide (BNP); it reduces pulmonary capillary wedge pressure (PCWP), pulmonary artery pressure, RA pressure, and systemic vascular resistance while increasing the cardiac index and stroke volume index. Therapy with nesiritide has decreased plasma renin, aldosterone, norepinephrine, and endothelin-1 levels and reduced ventricular ectopy and ventricular tachycardia. Heart-rate variability also improves with nesiritide. However, owing to the lack of positive outcomes data (ASCEND-HF) from the use of nesiritide, nesiritide cannot be recommended for routine use in the broad population of patients with acute heart failure.

Inotropic support is usually used following unsuccessful attempts at preload and afterload reduction or when hypotension precludes the use of these strategies. The 2 main classes of inotropic agents that are available are catecholamine agents and phosphodiesterase inhibitors (PDIs).


Preload Reducers

Class Summary

Reduced pulmonary venous return decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli. Preload reducers include NTG (eg, Deponit, Minitran, Nitro-Bid IV, Nitro-Bid ointment, Nitrodisc, Nitro-Dur, Nitrogard, Nitroglyn, Nitrol, Nitrolingual, Nitrong, Nitrostat, Transdermal-NTG, Transderm-Nitro, Tridil) and furosemide (eg, Lasix).

Nitroglycerin IV (Nitro-Bid, Minitran, Nitrostat)


NTG is the drug of choice (DOC) for patients who are not hypotensive. It provides excellent and reliable preload reduction, and high dosages provide mild afterload reduction. NTG has rapid onset and offset (both within minutes), allowing for rapid clinical effects and rapid discontinuation of effects in adverse reactions.

Furosemide (Lasix)


Furosemide is the most commonly used loop diuretic. It increases the excretion of water by interfering with the chloride-binding cotransport system, inhibiting sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Furosemide reduces preload by diuresis in 20-60 minutes. It may contribute to hastened preload reduction with a direct vasoactive mechanism, but this is controversial.

As many as 50% of patients with CPE have total-body euvolemia. Although furosemide is generally administered to all patients with CPE, it is probably most useful in patients with total-body fluid overload.

The oral form of furosemide has a relatively slow onset of action and, therefore, is generally not appropriate in CPE.


Afterload Reducers

Class Summary

Reduced systemic vascular resistance increases cardiac output and improves renal perfusion, allowing for diuresis.



Captopril prevents the conversion of angiotensin I to angiotensin II. It is a potent vasodilator that lowers aldosterone secretion. It is an option in patients who are unable to tolerate NTG (eg, concurrent use of sildenafil). Hemodynamic (improved afterload and cardiac output) and subjective (decreased dyspnea) improvements occur in 10-15 minutes. Although captopril is not specifically formulated for sublingual (SL) use, the tablet can be wetted before it is placed under the patient's tongue to achieve the desired effect.

Enalapril (Vasotec)


Enalapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion. The use of IV captopril to treat decompensated heart failure and pulmonary edema not been studied as well as SL captopril has.

In 1993, Varriale evaluated patients with severe CHF and mitral regurgitation; he observed improved preload, afterload, cardiac output, and magnitude of regurgitation. In 1996, Annane evaluated patients with acute CPE and found improvements in preload and afterload. There was no demonstrated effect on cardiac output. Both studies showed an excellent safety profile.

Nitroprusside (Nitropress)


Nitroprusside is a potent, direct smooth muscle–relaxing agent that primarily reduces afterload but can mildly reduce preload. It improves cardiac output but can precipitously decrease blood pressure. Intra-arterial blood pressure monitoring is strongly recommended. Nitroprusside is excellent for use in critically ill patients because of its rapid onset and offset of action (within 1-2 min). It is excellent for use against pulmonary edema associated with severe hypertension that is unresponsive to other agents.


Inotropic Agents

Class Summary

These agents produce vasodilation and increase the inotropic state. At high dosages, they may increase the patient's heart rate, exacerbating myocardial ischemia. Conversely, phosphodiesterase enzyme inhibitors or bipyridine-positive inotropic agents have little chronotropic activity. They differ from digitalis glycosides and catecholamines in their mechanism of action.



Dobutamine is a synthetic catecholamine that mainly has beta1-receptor activity but also has some beta2- and alpha-receptor activity. It is commonly used in CPE and mild hypotension (systolic blood pressure 90-100 mm Hg). Dobutamine has a combination of beneficial hemodynamic effects (eg, positive inotropism, decreased afterload due to mild vasodilation, increased cardiac output).



Dopamine is a naturally occurring catecholamine that acts as a precursor to norepinephrine. It stimulates adrenergic and dopaminergic receptors. Dopamine's hemodynamic effect is dose dependent. A low dose is associated with dilation in renal and splanchnic vasculature, enhancing diuresis. Moderate doses enhance cardiac contractility and heart rate. High doses increase afterload due to peripheral vasoconstriction. The use of dopamine in CPE is generally reserved for patients with moderate hypotension (eg, systolic blood pressure 70-90 mm Hg). Moderate to high doses are usually used.

Norepinephrine (Levophed)


Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, increasing myocardial contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload; it may decrease cardiac output and increase myocardial oxygen demand and cardiac ischemia. This agent is generally reserved for patients with severe hypotension (eg, systolic blood pressure < 70 mm Hg) or hypotension unresponsive to other medication.



Milrinone is a positive inotropic agent and vasodilator. It reduces afterload and preload and increases cardiac output. In several comparisons, milrinone improved preload, afterload, and cardiac output more than dobutamine, without significantly increased myocardial oxygen consumption.

Contributor Information and Disclosures

Ali A Sovari, MD, FACP Fellow in Clinical Cardiac Electrophysiology, Cedars Sinai Medical Center/Heart Institute

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Physician Scientists Association, American Physiological Society, Biophysical Society, Heart Rhythm Society, Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.


Abraham G Kocheril, MD, FACC, FACP, FHRS Professor of Medicine, University of Illinois College of Medicine

Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology, Central Society for Clinical and Translational Research, Heart Failure Society of America, Cardiac Electrophysiology Society, American College of Physicians, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP Associate Professor of Medicine, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Ronald Reagan UCLA Medical Center

Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.


Amal Mattu, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Program, Department of Surgery, Division of Emergency Medicine, University of Maryland School of Medicine

Amal Mattu, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine.

Disclosure: Nothing to disclose.

Ari M Perkins, MD, Consulting Staff, Department of Emergency Medicine, Greenwich Hospital

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

  1. Komiya K, Ishii H, Murakami J, et al. Comparison of chest computed tomography features in the acute phase of cardiogenic pulmonary edema and acute respiratory distress syndrome on arrival at the emergency department. J Thorac Imaging. 2013 Sep. 28 (5):322-8. [Medline].

  2. Ray P, Arthaud M, Birolleau S, et al. Comparison of brain natriuretic peptide and probrain natriuretic peptide in the diagnosis of cardiogenic pulmonary edema in patients aged 65 and older. J Am Geriatr Soc. 2005 Apr. 53(4):643-8. [Medline].

  3. Pfisterer M, Buser P, Rickli H, Gutmann M, Erne P, Rickenbacher P, et al. BNP-guided vs symptom-guided heart failure therapy: the Trial of Intensified vs Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIME-CHF) randomized trial. JAMA. 2009 Jan 28. 301 (4):383-92. [Medline].

  4. McCullough PA, Nowak RM, McCord J, Hollander JE, Herrmann HC, Steg PG, 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].

  5. Wang F, Wu Y, Tang L, Zhu W, Chen F, Xu T, et al. Brain natriuretic peptide for prediction of mortality in patients with sepsis: a systematic review and meta-analysis. Crit Care. 2012 May 6. 16 (3):R74. [Medline].

  6. Al Deeb M, Barbic S, Featherstone R, Dankoff J, Barbic D. Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Acad Emerg Med. 2014 Aug. 21(8):843-852. [Medline].

  7. Wang XT, Liu DW, Zhang HM, Chai WZ. Integrated cardiopulmonary sonography: a useful tool for assessment of acute pulmonary edema in the intensive care unit. J Ultrasound Med. 2014 Jul. 33(7):1231-9. [Medline].

  8. Rogoza K, Kosiak W. Usefulness of lung ultrasound in diagnosing causes of exacerbation in patients with chronic dyspnea. Pneumonol Alergol Pol. 2015 Dec 21. [Medline].

  9. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. Oct., 2005. 294(5):1625-33. [Medline].

  10. L'Her E, Duquesne F, Girou E, et al. Noninvasive continuous positive airway pressure in elderly cardiogenic pulmonary edema patients. Intensive Care Med. 2004 May. 30(5):882-8. [Medline].

  11. Mehta S, Nava S. Mask ventilation and cardiogenic pulmonary edema: another brick in the wall. Intensive Care Med. 2005 Jun. 31(6):757-9. [Medline].

  12. Lazzeri C, Gensini GF, Picariello C, et al. Acidemia in severe acute cardiogenic pulmonary edema treated with noninvasive pressure support ventilation: a single-center experience. J Cardiovasc Med (Hagerstown). 2015 Sep. 16 (9):610-5. [Medline].

  13. Weitz G, Struck J, Zonak A, Balnus S, Perras B, Dodt C. Prehospital noninvasive pressure support ventilation for acute cardiogenic pulmonary edema. Eur J Emerg Med. 2007 Oct. 14(5):276-9. [Medline].

  14. Frontin P, Bounes V, Houze-Cerfon CH, et al. Continuous positive airway pressure for cardiogenic pulmonary edema: a randomized study. Am J Emerg Med. 2011 Sep. 29(7):775-81. [Medline].

  15. Willmore A, Dionne R, Maloney J, Ouston E, Stiell I. Effectiveness and safety of a prehospital program of continuous positive airway pressure (CPAP) in an urban setting. CJEM. 2015 Nov. 17 (6):609-16. [Medline].

  16. Newby D. Efficacy of non-invasive ventilation in patients with acute cardiogenic pulmonary oedema: The 3CPO trial. Presented at the ESC meeting. Sept 2007. [Full Text].

  17. Pirracchio R, Resche Rigon M, Mebazaa A, Zannad F, Alla F, Chevret S. Continuous positive airway pressure (CPAP) may not reduce short-term mortality in cardiogenic pulmonary edema: a propensity-based analysis. J Card Fail. 2013 Feb. 19 (2):108-16. [Medline].

  18. 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].

  19. Bauer JB, Randazzo MA. Nesiritide for outpatient treatment of heart failure. Am J Health Syst Pharm. 2005. 15;62(24):2639-2642.

  20. Cheng JW, Merl MY, Nguyen HM. Effect of nesiritide on renal function: a retrospective review. Curr Med Res Opin. 2005 Nov. 21(11):1857-63. [Medline].

  21. Scroggins N, Edwards M, Delgado R 3rd. Increased cost effectiveness with nesiritide vs. milrinone or dobutamine in the treatment of acute decompensated heart failure. Congest Heart Fail. 2005 Nov-Dec. 11(6):311-4. [Medline].

  22. Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. 2005 Apr 20. 293 (15):1900-5. [Medline].

  23. O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med. 2011 Jul 7. 365(1):32-43. [Medline].

  24. Maggioni AP, Latini R, Carson PE, et al. Valsartan reduces the incidence of atrial fibrillation in patients with heart failure: results from the Valsartan Heart Failure Trial (Val-HeFT). Am Heart J. Mar, 2005. 149(3):548-57. [Medline].

  25. Ducharme A, Swedberg K, Pfeffer MA, et al. Prevention of atrial fibrillation in patients with symptomatic chronic heart failure by candesartan in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program. Am Heart J. Jul, 2006. 152(1):86-92. [Medline].

  26. Felker GM, Benza RL, Chandler AB, Leimberger JD, Cuffe MS, Califf RM, et al. Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study. J Am Coll Cardiol. 2003 Mar 19. 41 (6):997-1003. [Medline].

  27. Earl GL, Fitzpatrick JT. Levosimendan: a novel inotropic agent for treatment of acute, decompensated heart failure. Ann Pharmacother. 2005 Nov. 39(11):1888-96. [Medline].

  28. Follath F, Franco F, Cardoso JS. European experience on the practical use of levosimendan in patients with acute heart failure syndromes. Am J Cardiol. 2005 Sep 19. 96(6A):80G-5G. [Medline].

  29. Parissis JT, Filippatos G, Farmakis D, Adamopoulos S, Paraskevaidis I, Kremastinos D. Levosimendan for the treatment of acute heart failure syndromes. Expert Opin Pharmacother. 2005 Dec. 6(15):2741-51. [Medline].

  30. Mebazaa A, Nieminen MS, Packer M, et al. Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE Randomized Trial. JAMA. May, 2007. 297(17):1883-91. [Medline].

  31. Gheorghiade M, Konstam MA, Burnett JC Jr, et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA. Mar, 2007. 297(12):1332-43. [Medline].

  32. Konstam MA, Gheorghiade M, Burnett JC Jr, et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA. Mar, 2007. 297(12):1319-31. [Medline].

  33. Costanzo MR, Guglin ME, Saltzberg MT, et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. Feb, 2007. 49(6):675-83. [Medline].

  34. Bart BA, Goldsmith SR, Lee KL, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012 Dec 13. 367 (24):2296-304. [Medline].

  35. McCullough PA, Duc P, Omland T, et al. B-type natriuretic peptide and renal function in the diagnosis of heart failure: an analysis from the Breathing Not Properly Multinational Study. Am J Kidney Dis. 2003 Mar. 41 (3):571-9. [Medline].

  36. Chioncel O, Ambrosy AP, Bubenek S, Filipescu D, Vinereanu D, Petris A, et al. Epidemiology, pathophysiology, and in-hospital management of pulmonary edema: data from the Romanian Acute Heart Failure Syndromes registry. J Cardiovasc Med (Hagerstown). 2016 Feb. 17 (2):92-104. [Medline].

  37. Brusasco C, Corradi F, De Ferrari A, Ball L, Kacmarek RM, Pelosi P. CPAP devices for emergency prehospital use: a bench study. Respir Care. 2015 Dec. 60 (12):1777-85. [Medline].

Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.
Radiograph shows acute pulmonary edema in a patient known to have ischemic cardiomyopathy. Findings are Kerley B lines (1mm thick and 1cm long) in the lower lobes and Kerley A lines in the upper lobes.
Radiograph demonstrates cardiomegaly, bilateral pleural effusions, and alveolar opacities in a patient with pulmonary edema.
Radiograph shows interstitial pulmonary edema, cardiomegaly, and left pleural effusion presenting at an earlier stage of pulmonary edema.
Lateral chest radiograph shows prominent interstitial edema and pleural effusions.
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