eMedicine Specialties > Emergency Medicine > Cardiovascular

Congestive Heart Failure and Pulmonary Edema

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, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Jan 14, 2010

Introduction

Background

Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to adequately maintain the circulation of blood. The most severe manifestation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.

CHF can be categorized as forward or backward ventricular failure. Backward failure is secondary to elevated systemic venous pressure, whereas left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. Furthermore, heart failure can be subdivided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a dilated left ventricle with impaired contractility, whereas diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

The radiograph below shows signs of congestive heart failure.

Chest radiograph shows signs of congestive heart ...

Chest radiograph shows signs of congestive heart failure (CHF).

Chest radiograph shows signs of congestive heart ...

Chest radiograph shows signs of congestive heart failure (CHF).


The New York Heart Association's functional classification of CHF is one of the most useful. Class I describes a patient who is not limited with normal physical activity by symptoms. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activity.

Pathophysiology

Congestive heart failure (CHF) is summarized best as an imbalance in Starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium.

Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary capillary pressure (about 7-12 mm Hg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry.

Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. However, when the capacity of lymphatic drainage is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema.

Etiologies of pulmonary edema may be placed in the following 6 categories:

  1. Pulmonary edema secondary to altered capillary permeability: Acute respiratory distress syndrome (ARDS), infectious causes, inhaled toxins, circulating exogenous toxins, vasoactive substances, disseminated intravascular coagulopathy (DIC), immunologic processes reactions, uremia, near drowning, and other aspirations
  2. Pulmonary edema secondary to increased pulmonary capillary pressure: Cardiac causes and noncardiac causes, including pulmonary venous thrombosis, stenosis or veno-occlusive disease, and volume overload
  3. Pulmonary edema secondary to decreased oncotic pressure found with hypoalbuminemia
  4. Pulmonary edema secondary to lymphatic insufficiency
  5. Pulmonary edema secondary to large negative pleural pressure with increased end expiratory volume
  6. Pulmonary edema secondary to mixed or unknown mechanisms including high altitude pulmonary edema (HAPE), neurogenic pulmonary edema, heroin or other overdoses, pulmonary embolism, eclampsia, postcardioversion, postanesthetic, postextubation, and post–cardiopulmonary bypass

This article is limited to cardiac causes of pulmonary edema and congestive heart failure (CHF) and its relevant emergency care.

Frequency

United States

More than 3 million people have congestive heart failure (CHF), and more than 400,000 new patients present yearly. The prevalence rate of CHF is 1-2%.

Mortality/Morbidity

  • Approximately 30-40% of patients with congestive heart failure (CHF) are hospitalized every year. CHF is the leading diagnosis-related group (DRG) among hospitalized patients older than 65 years. The 5-year mortality rate after diagnosis was reported in 1971 as 60% in men and 45% in women. In 1991, data from the Framingham heart study showed the 5-year mortality rate for CHF essentially remaining unchanged, with a median survival of 3.2 years for males and 5.4 years for females. This may be secondary to an aging US population with declining mortality due to other diseases.
  • The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths. After auditing data on 4606 patients hospitalized with CHF between 1992-1993, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes.
  • Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality rate.

Race

  • Blacks are 1.5 times more likely to die of CHF than whites are. Nevertheless, black patients appear to have similar or lower in-hospital mortality rates than white patients.

Sex

  • Prevalence is greater in males than in females in patients aged 40-75 years.
  • No sex predilection is noted among patients older than 75 years.

Age

  • Prevalence of CHF increases with increasing age and affects about 10% of the population older than 75 years.

Clinical

History

  • Anxiety
  • Dyspnea at rest
  • Dyspnea upon exertion: This has been found to be the most sensitive symptom reported, yet the specificity for dyspnea is less than 60%.
  • Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms are observed; however, the sensitivity for orthopnea and PND is only 20-30%.
  • Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF).
  • Edema
  • Nonspecific symptoms
    • Weakness
    • Lightheadedness
    • Abdominal pain
    • Malaise
    • Wheezing
    • Nausea
  • Past medical history
    • Cardiomyopathy
    • Valvular heart disease
    • Alcohol use
    • Hypertension
    • Angina
    • Prior myocardial infarction
    • Familial heart disease

Physical

  • Findings such as peripheral edema, jugular venous distention, and tachycardia are highly predictive of congestive heart failure (CHF). Overall specificity of physical examination has been reported at 90%; however, this same study reported a sensitivity of only 10-30%.
  • Tachypnea, using accessory muscles of respiration, has been observed.
  • Hypertension may be present.
  • Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV] function) may be observed.
  • The skin may be diaphoretic or cold, gray, and cyanotic.
  • Jugular venous distention (JVD) is frequently present.
  • Wheezing or rales may be heard on lung auscultation.
  • Apical impulse is frequently laterally displaced.
  • Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S3 or S4).
  • Lower extremity edema may also be noted, especially in the subacute process.

Causes

  • Various cardiac diseases cause congestive heart failure (CHF) and pulmonary edema.
  • The most common cause of heart failure is coronary artery disease, which is secondary to loss of left ventricular muscle, ongoing ischemia, or decreased diastolic ventricular compliance.
  • Other disease processes include hypertension, valvular heart disease, congenital heart disease, other cardiomyopathies, myocarditis, and infectious endocarditis.
  • CHF is often precipitated by cardiac ischemia or dysrhythmias, cardiac or extracardiac infection, pulmonary embolus, physical or environmental stresses, changes or noncompliance with medical therapy, dietary indiscretion, or iatrogenic volume overload.
  • One also must consider systemic processes such as pregnancy and hyperthyroidism as precipitants of CHF.

More on Congestive Heart Failure and Pulmonary Edema

Overview: Congestive Heart Failure and Pulmonary Edema
Differential Diagnoses & Workup: Congestive Heart Failure and Pulmonary Edema
Treatment & Medication: Congestive Heart Failure and Pulmonary Edema
Follow-up: Congestive Heart Failure and Pulmonary Edema
Multimedia: Congestive Heart Failure and Pulmonary Edema
References

References

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Further Reading

Keywords

congestive heart failure, CHF, weak heart, pulmonary edema, fluid retention, low blood flow, ventricular failure, forward ventricular failure, backward ventricular failure, systolic dysfunction, diastolic dysfunction, dyspnea, beta natriuretic peptide, BNP, blood circulation, treatment, 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, acute respiratory deficiency syndrome, ARDS, disseminated intravascular coagulopathy, DIC

uremia, pulmonary venous thrombosis, stenosis, veno-occlusive disease, high altitude pulmonary edema, HAPE, neurogenic pulmonary edema, cardiomyopathy, coronary artery disease, ischemia, hyperthyroidism

Contributor 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
Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, 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

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

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

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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