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Congestive Heart Failure and Pulmonary Edema

Authors: Shamai Grossman, MD, MSAuthor Information and Disclosures

Editors: William K Chiang, MD; Francisco Talavera, PharmD, PhD; Gary Setnik, MD; John Halamka, MD; Barry Brenner, MD, PhD, FACEPEditor Information

Last Updated: May 11, 2006

Synonyms and related keywords ›

Overview

Introduction

Background: Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to maintain the circulation of blood adequately. 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, while 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, while diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

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: 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. When the capacity of lymphatic drainage is exceeded, however, 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-includes acute respiratory deficiency 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-comprises 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 chapter is limited to cardiac causes of pulmonary edema and CHF and its relevant emergency care.

Frequency:

  • In the US: More than 3 million people have CHF, and more than 400,000 new patients present yearly. Prevalence of CHF is 1-2% of the general population.

Mortality/Morbidity:

  • Approximately 30-40% of patients with 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:

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

Sex:

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

Age:

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

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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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