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Congestive Heart Fail u re

Ta rlan Hedayati, MD

Negean Afifi, DO

Key Points

• A normal ejection fraction does not exclude congestive

heart failure (CHF), as CHF can occur secondary to either

systolic or diastolic dysfunction.

• Nitroglycerin is the initial treatment of choice because

it reduces both preload and afterload and rapidly

improves patient symptoms.

INTRODUCTION

Congestive heart failure ( CHF) is the leading cause of hospitalizations in the United States in patients older than 65 years.

Once symptomatic, up to 35% of patients will die within

2 years of the diagnosis, and more than 60% will succumb

within 6 years. The annual costs of treatment are more than

$27 billion and will only increase given the aging population.

Heart failure occurs when the myocardium is unable to

provide sufficient cardiac output to meet the metabolic

demands of the body. As the myocardium can no longer

keep up with the return of venous blood, pulmonary and

systemic vascular congestion occurs. Common causes of

CHF include myocardial infarction, valvulopathies, cardio ­

myopathies, and chronic uncontrolled hypertension.

Based on the underlying pathophysiology, heart failure

can be divided into systolic and diastolic s ubtypes. Systolic

heart failure develops when a direct myocardial injury

impairs normal cardiac contractility causing a secondary

decline in ejection fraction (eg, myocardial infarction).

Diastolic heart failure develops when impaired cardiac

compliance limits ventricular filling (preload) causing a

consequent drop in overall cardiac output ( eg, left ventricular hypertrophy).

In acute decompensated CHF, the global decrease in

cardiac output forces a compensatory increase in systemic

57

• Consider acute coronary syndrome as the primary

precipitant of CHF.

• CHF associated with cardiogenic shock maintains a

very high mortality rate despite appropriate medical

management.

vascular resistance (SVR) to maintain vital organ perfusion. This increase in SVR is actually counterproductive

and causes a further reduction in cardiac output as the

already compromised myocardium now faces an ever

higher afterload. The downward spiral continues as myo ­

cardial oxygen demand increases because of the increased

ventricular workload, resulting in further compromise of

the myocardium. Consequent elevations in left atrial and

ventricular pressures eventually beget pulmonary edema

and respiratory distress.