Modern Management of Cardiogenic Pulmonary Edema

https://doi.org/10.1016/j.emc.2005.07.005Get rights and content

Section snippets

Pathophysiology

CPE results from leakage of fluid from the pulmonary capillaries and venules into the alveolar space as a result of increased hydrostatic pressure. When the pulmonary capillary hydrostatic pressure exceeds pulmonary interstitial pressure, fluid transudates into the pulmonary alveoli and interstitium [2]. Hydrostatic pressure rises when the left ventricle (LV) is unable to effectively handle its pulmonary venous return [4]. Once fluid begins to build up in the pulmonary interstitium, a vicious

Etiologies

There are five major causes of CPE in clinical practice (Box 1). The most common cause is an acute exacerbation of chronic LV failure. Chronic LV failure usually is the result of congestive heart failure (CHF) or a cardiomyopathy. An acute exacerbation of chronic LV failure can occur because of medication or dietary noncompliance (eg, discontinuation of diuretic medications, excessive salt intake, and so forth) or from acute cardiac ischemia.

Patients without a prior history of chronic LV

Emergency department evaluation

Traditionally, the diagnosis of CPE in the ED has been based on history, physical examination, and chest radiography. Most patients presenting with CPE have a prior history of CHF. Most report the onset of dyspnea on exertion progressing to dyspnea at rest, orthopnea, peripheral edema, and paroxysmal nocturnal dyspnea. The progression of symptoms before ED presentation may take hours to days; however, an episode of acute ischemia or acute valvular dysfunction may cause symptoms to progress much

Emergency department management

Initial management of patients who experience CPE should focus on the “ABCs” of resuscitation. Large bore intravenous (IV) lines should be in place to administer needed medications. Patients should be placed in an upright sitting position attached to a cardiac monitor and pulse oximetry. Supplemental oxygen should be provided by way of a facemask with fraction of inspired oxygen of 1.0. If the patient remains persistently hypoxic despite the supplemental oxygen, or if the patient develops

Preload reduction

The first goal in pharmacologic treatment of CPE is preload reduction. Preload reduction reduces right heart and pulmonary venous return and, therefore, right-heart filling pressures and pulmonary capillary hydrostatic pressures, resulting in early symptomatic improvements in dyspnea. The typical medications used for preload reduction are nitroglycerin, morphine sulfate, and loop diuretics. More recently, a recombinant form of beta-natriuretic peptide known as nesiritide has been used for

Noninvasive positive pressure ventilation

NPPV has been used successfully in patients who present with CPE and has gained popularity amongst acute care physicians. There are two types of NPPV, continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP). In CPAP, the patient breaths against a continuous flow of positive airway pressure. In BiPAP, the patient receives additional positive pressure during inspiration. As a result, higher pressures can be applied during inspiration and lower pressures during

Assisted circulation

Placement of an intra-aortic balloon pump (IABP) can be a life-saving intervention in patients who experience CS. Shock in these patients is usually the result of a large AMI or acute valvular disorder. The IABP serves as a temporizing measure while preparations for more definitive therapies are made. IABP counterpulsation provides blood pressure support while also providing improvements in coronary diastolic perfusion, afterload, and cardiac output. Definitive therapy for the patient who

Disposition

Although patients who experience mild CHF decompensations that are attributable to dietary indiscretions (excessive salt intake) or medication noncompliance can receive diuretics in the ED for symptomatic improvement and be discharged, patients who present with pulmonary edema should be admitted to a cardiac-monitored bed. Patients who require mechanical ventilation, experience acute valvular dysfunction, require inotropic support, and present with evidence of acute cardiac ischemia/infarction

Summary

CPE is a life-threatening condition associated with an in-hospital mortality rate of 15% to 20%. To minimize morbidity and mortality, physicians must be able to promptly diagnose and treat these patients. The use of BNP testing is associated with improvements in diagnostic ability beyond physical assessment and chest radiography. Treatment should focus on fluid redistribution through preload and afterload reduction rather than simply diuresis. The most effective and safest preload-reducing

First page preview

First page preview
Click to open first page preview

References (118)

  • G.I. Nelson et al.

    Haemodynamic advantages of isosorbide dinitrate over frusemide in acute heart-failure following myocardial infarction

    Lancet

    (1983)
  • D. Northridge

    Frusemide or nitrates for acute heart failure?

    Lancet

    (1996)
  • G. Cotter et al.

    Randomized trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema

    Lancet

    (1998)
  • P.A. Kraus et al.

    Acute preload effects of furosemide

    Chest

    (1990)
  • A. Sacchetti et al.

    Effect of ED management on ICU use in acute pulmonary edema

    Am J Emerg Med

    (1999)
  • W.D. Bussmann et al.

    Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema

    Am J Cardiol

    (1978)
  • H.L. Haber et al.

    Bolus intravenous nitroglycerin predominantly reduces afterload in patients with severe congestive heart failure

    J Am Coll Cardiol

    (1993)
  • A. Sacchetti et al.

    Effect of ED management on ICU use in acute pulmonary edema

    Am J Emerg Med

    (1999)
  • M. Gammage

    Treatment of acute pulmonary oedema: diuresis or vasodilatation?

    Lancet

    (1998)
  • J. Figueras et al.

    Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema

    Am J Cardiol

    (1979)
  • R.J. Henning et al.

    Effect of afterload reduction on plasma volume during acute heart failure

    Am J Cardiol

    (1978)
  • T.L. Biddle et al.

    Effect of furosemide on haemodynamic and lung water in acute pulmonary edema secondary to myocardial infarction

    Am J Cardiol

    (1979)
  • S.K. Mukherjee et al.

    Mechanisms of hemodynamic actions of furosemide: differentiation of vascular and renal effects on blood pressure in functionally anephric hypertensive patients

    Am Heart J

    (1981)
  • P. Pickkers et al.

    Direct vasoactivity of frusemide

    Lancet

    (1996)
  • L. Gehm et al.

    Pulmonary edema in the renal failure patient

    Am J Emerg Med

    (1989)
  • R.E. Schmieder et al.

    Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis

    Am J Kidney Dis

    (1987)
  • S.H. Kubo et al.

    Identification of normal neurohormonal activity in mild congestive heart failure and stimulating effect of upright posture and diuretics

    Am J Cardiol

    (1987)
  • R.M. Mills et al.

    Sustained hemodynamic effects of an infusion of nesiritide (human b-type natriuretic peptide) in heart failure: a randomized, double-blind, placebo-controlled clinical trial. Natrecor Study Group

    J Am Coll Cardiol

    (1999)
  • U. Elkayam et al.

    Comparison of effects of left ventricular filling pressure of intravenous nesiritide and high-dose nitroglycerin in patients with decompensated heart failure

    Am J Cardiol

    (2004)
  • M. Haude et al.

    Sublingual administration of captopril versus nitroglycerin in patients with severe congestive heart failure

    Int J Cardiol

    (1990)
  • K. Langes et al.

    Efficacy and safety of intravenous captopril in congestive heart failure

    Curr Ther Res

    (1993)
  • A. Sacchetti et al.

    ED management of acute congestive heart failure in renal dialysis patients

    Am J Emerg Med

    (1993)
  • G.M. Felker et al.

    Between Scylla and Charybdis: the choice of inotropic agent for decompensated heart failure

    Am Heart J

    (2001)
  • R.M. Gagnon et al.

    Combined hemodynamic effects of dobutamine and IV nitroglycerin in congestive heart failure

    Chest

    (1980)
  • J.B. Shipley et al.

    Milrinone: basic and clinical pharmacology and acute and chronic management

    Am J Med Sci

    (1996)
  • R. Grose et al.

    Systemic and coronary effects of intravenous milrinone and dobutamine in congestive heart failure

    J Am Coll Cardiol

    (1986)
  • G. Mager et al.

    Phosphodiesterase III inhibition or adrenoreceptor stimulation: milrinone as an alternative to dobutamine in the treatment of severe heart failure

    Am Heart J

    (1991)
  • M.H. Yamani et al.

    Comparison of dobutamine-based and milrinone-based therapy for advanced decompensated congestive heart failure: hemodynamic efficacy, clinical outcome, and economic impact

    Am Heart J

    (2001)
  • J.L. Anderson et al.

    Occurrence of ventricular arrhythmias in patients receiving acute and chronic infusions of milrinone

    Am Heart J

    (1986)
  • M.S. Nieminen et al.

    Hemodynamic and neurohumoral effects of continuous infusion of levosimendan in patients with congestive heart failure

    J Am Coll Cardiol

    (2000)
  • F. Follath et al.

    Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (the LIDO study): a randomized double-blind trial

    Lancet

    (2002)
  • D.M. Baratz et al.

    Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure

    Chest

    (1992)
  • A. Mattu

    Cardiogenic pulmonary edema

    Current Opinion in Cardiovascular, Pulmonary, and Renal Investigational Drugs

    (2000)
  • A. Mattu et al.

    Pulmonary edema, cardiogenic

    eMedicine Journal

    (2002)
  • A. Chait et al.

    The bedside chest radiograph in the evaluation of incipient heart failure

    Radiology

    (1972)
  • W. Kostuk et al.

    Correlation between the chest film and hemodynamics in acute myocardial infarction

    Circulation

    (1973)
  • J.T. Chen

    Radiographic diagnosis of heart failure

    Heart Dis Stroke

    (1992)
  • R.G. Badgett et al.

    Can the clinical examination diagnose left-sided heart failure in adults?

    JAMA

    (1997)
  • P.A. McCullough et al.

    Uncovering heart failure in patients with a history of pulmonary disease: rationale for the early use of B-type natriuretic peptide in the emergency department

    Acad Emerg Med

    (2003)
  • G.R. Pesola

    The use of B-type natriuretic peptide (BNP) to distinguish heart failure from lung disease in patients presenting with dyspnea to the emergency department

    Acad Emerg Med

    (2003)
  • Cited by (33)

    • Clinical Mimics: An Emergency Medicine–Focused Review of Asthma Mimics

      2017, Journal of Emergency Medicine
      Citation Excerpt :

      The patient may provide a history of orthopnea or paroxysmal nocturnal dyspnea. Treatment of “flash” pulmonary edema usually involves venodilators and positive pressure ventilation, and therapy must be tailored to the individual patient (for example, the degree of volume overload or lack thereof, evidence of an ischemic cardiac cause, etc.) (7,8). Diuretics can be added after appropriate venodilation in patients with flash pulmonary edema.

    • Morphine in the treatment of acute pulmonary oedema - Why?

      2016, International Journal of Cardiology
      Citation Excerpt :

      The third drug, morphine, has been used due to its anticipated anxiolytic and vasodilatory properties. During the last decade, a discussion about the benefits and especially the risks accompanying the use of morphine in cases of pulmonary oedema has been raised [1,4,8–11]. In a retrospective study from 2008 based on the ADHERE registry, morphine given in acute decompensated heart failure was an independent predictor of increased hospital mortality, with an odds ratio of 4.8 (95% CI: 4.52–5.18, p < 0.001) [2].

    • Congestive Heart Failure

      2015, Emergency Medicine Clinics of North America
    • Postoperative Intensive Care Management in Adults

      2015, Transplantation of the Liver: Third Edition
    View all citing articles on Scopus
    View full text