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Congestive heart failure (CHF) AND PULMONARY EDEMACongestive 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. 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. Physical:
Prehospital Care:
Use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase prevalence of recurrent CHF with chronic use. Conflicting evidence currently exists both in favor of and against the use of calcium channel blockers in the acute setting; at this time limit their acute use to patients with diastolic dysfunction and heart failure, a condition not easily determined in the emergency department. Angiotensin converting enzyme (ACE) inhibitors, such as SL captopril or IV enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation. Haude compared 25 mg of SL captopril with 0.8 mg of sublingual nitroglycerin in 24 patients with class III and class IV CHF and found that captopril induces a more sustained and more pronounced improvement in hemodynamics. Annane gave 1 mg of IV enalapril to 20 patients presenting with acute class III and class IV CHF over 2 hours and demonstrated rapid hemodynamic improvement with no significant adverse effects on cardiac output or hepatosplanchnic measurements. Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Since the information on this subject is still controversial and limited to small studies, the routine use of ACE inhibitors cannot be recommended at this time. ACE inhibitors remain a promising area in need of further study. Beta-blockers, possibly by restoring beta-1 receptor activity or via prevention of catecholamine activity, appear to be cardioprotective in patients with depressed left ventricular function. The US Carvedilol Heart Failure study group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35% or less. Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. The role of beta-blockers in the acute setting, however, is currently unclear; limit use until hemodynamic studies indicate that further deterioration will not occur. Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach is often used, particularly as both may cause bronchospasm. Aerosolized beta-2 agonists, which are the more selective of beta-agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function. Terbutaline has been shown to be successful in this setting, as well as albuterol, isoetharine, and bitolterol. Limit roles of theophylline and aminophylline in the acute setting. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects. Nevertheless, they can exacerbate dysrhythmias (eg, multifocal atrial tachycardia [MAT], ischemia) by increasing cardiac work. Date: 2015-01-12; view: 979
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