Excerpt from Congestive Heart Failure and Pulmonary Edema

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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 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. 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 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: 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

United States

More than 3 million people have 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 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.

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