CRT & RRT Exam Secrets Study Guide

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Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged frothy sputum. Diagnosis is clinical and by chest x-ray. Treatment is with O2, IV nitrates, diuretics, and sometimes morphine and short-term IV positive inotropes, endotracheal intubation, and mechanical ventilation.

If LV filling pressure increases suddenly, plasma fluid moves rapidly from pulmonary capillaries into interstitial spaces and alveoli, causing pulmonary edema. Although precipitating causes vary by age and country, about ½ of cases result from acute coronary ischemia; some from decompensation of significant underlying HF, including diastolic dysfunction HF due to hypertension; and the rest from arrhythmia, an acute valvular disorder, or acute volume overload often due to IV fluids. Drug or dietary nonadherence is often involved.

Symptoms and Signs

Patients present with extreme dyspnea, restlessness, and anxiety with a sense of suffocation. Cough producing blood-tinged sputum, pallor, cyanosis, and marked diaphoresis are common; some patients froth at the mouth. Frank hemoptysis is uncommon. The pulse is rapid and low volume, and BP is variable. Marked hypertension indicates significant cardiac reserve; hypotension with systolic BP < 100 mg Hg is ominous. Inspiratory fine crackles are widely dispersed anteriorly and posteriorly over both lung fields. Marked wheezing (cardiac asthma) may occur. Noisy respiratory efforts often make cardiac auscultation difficult; a summation gallop—merger of S3 and S4)—may be present. Signs of RV failure (eg, neck vein distention, peripheral edema) may be present.

Diagnosis

Chest x-ray
Serum BNP
ECG, cardiac markers, and other tests for etiology as needed

A COPD exacerbation can mimic pulmonary edema due to LV failure or even that due to biventricular failure if cor pulmonale is present. Pulmonary edema may be the presenting symptom in patients without a history of cardiac disorders, but COPD patients with such severe symptoms usually have a history of COPD, although they may be too dyspneic to relate it.

A chest x-ray, done immediately, is usually diagnostic, showing marked interstitial edema. Bedside measurement of serum BNP levels (elevated in pulmonary edema; normal in COPD exacerbation) is helpful if the diagnosis is in doubt. ECG, pulse oximetry, and blood tests (cardiac markers, electrolytes, BUN, creatinine, and, for severely ill patients, ABGs) are done. An echocardiogram may be helpful to determine the cause of the pulmonary edema (eg, MI, valvular dysfunction, hypertensive heart disease, dilated cardiomyopathy) and may influence the choice of therapies. Hypoxemia can be severe. CO2 retention is a late, ominous sign of secondary hypoventilation.

Treatment

O2
Furosemide
Nitrates
Morphine
Ventilatory assistance as needed
Cause treated

Initial treatment includes 100% O2 by nonrebreather mask; upright position; furosemide 0.5 to 1.0 mg/kg IV; nitroglycerin 0.4 mg sublingually q 5 min, followed by an IV drip at 10 to 20 μg/min, titrated upward at 10 μg/min q 5 min as needed to a maximum 300 μg/min if systolic BP is > 100 mm Hg; and morphine 1 to 5 mg IV once or twice. If hypoxia is significant, noninvasive ventilatory assistance with bilevel positive airway pressure (BiPAP) is helpful, but if CO2 retention is present or the patient is obtunded, tracheal intubation and assisted ventilation are required.

Specific additional treatment depends on etiology: thrombolysis or direct percutaneous coronary angioplasty with or without a stent for acute MI or another acute coronary syndrome; a vasodilator for severe hypertension; direct-current cardioversion for supraventricular or ventricular tachycardia; and an IV β-blocker, IV digoxin, or cautious use of an IV Ca channel blocker to slow the ventricular rate for rapid atrial fibrillation (cardioversion is preferred). Other treatments, such as IV BNP (nesiritide) and new inotropic drugs (levosimendan), remain under study to elucidate safety profiles and efficacy. Because fluid status before onset of pulmonary edema is usually normal in patients with acute MI, diuretics are less useful than in patients with chronic HF and may precipitate hypotension. If systolic BP falls < 100 mm Hg or shock develops, IV dobutamine and an intra-aortic balloon pump (counterpulsation) may be required.

Once patients are stabilized, long-term HF treatment is as described above.

Last full review/revision March 2008 by J. Malcolm O. Arnold, MD

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