(See also Heart Failure)
If left ventricular (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 one half of cases result from acute coronary ischemia; some from decompensation of significant underlying heart failure (HF), including HF with preserved ejection fraction (HFpEF) 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.
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 blood pressure (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 3rd (S3) and 4th (S4) heart sounds—may be present. Signs of right ventricular (RV) failure (eg, neck vein distention, peripheral edema) may be present.
A COPD (chronic obstructive pulmonary disease) 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/NT-proBNP 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 [blood urea nitrogen], creatinine and, for severely ill patients, arterial blood gas [ABG] measurements) are done.
Echocardiography may be helpful to determine the cause of the pulmonary edema (eg, myocardial infarction, valvular dysfunction, hypertensive heart disease, dilated cardiomyopathy) and may influence the choice of therapies.
Hypoxemia can be severe. Carbon dioxide retention is a late, ominous sign of secondary hypoventilation.
Initial treatment includes identifying the cause; 100% oxygen by nonrebreather mask; upright position; furosemide 0.5 to 1.0 mg/kg IV or by continuous infusion 5 to 10 mg/hour; nitroglycerin 0.4 mg sublingually every 5 minutes, followed by an IV drip at 10 to 20 mcg/minute, titrated upward at 10 mcg/minute every 5 minutes as needed to a maximum 300 mcg/minute if systolic BP is > 100 mm Hg. Morphine, 1 to 5 mg IV once or twice, has long been used to reduce severe anxiety and the work of breathing but is decreasingly used (except in palliative care) due to observational studies suggesting a poorer outcome with its use. Noninvasive ventilatory assistance with bilevel positive airway pressure (BiPAP) is helpful if hypoxia is significant. If carbon dioxide retention is present or the patient is obtunded, tracheal intubation and mechanical ventilation are required.
Specific additional treatment depends on etiology:
For acute myocardial infarction or another acute coronary syndrome, thrombolysis or direct percutaneous coronary angioplasty with or without stent placement
For severe hypertension, an IV vasodilator
For supraventricular or ventricular tachycardia, direct-current cardioversion
For rapid atrial fibrillation, cardioversion is preferred. To slow the ventricular rate, an IV beta-blocker, IV digoxin, or cautious use of an IV calcium channel blocker
In patients with acute MI, fluid status before onset of pulmonary edema is usually normal, so diuretics are less useful than in patients with acute decompensation of chronic heart failure 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.
Some newer drugs, such as IV BNP (nesiritide), and calcium-sensitizing inotropic drugs (levosimendan, pimobendan), vesnarinone, and ibopamine, may have initial beneficial effects but do not appear to improve outcomes compared to standard therapy, and mortality may be increased. Serelaxin, a recombinant form of the human pregnancy hormone relaxin-2, has been tried but benefits were not shown in a large international randomized study. Omecamtiv mecarbil, an oral cardiac myosin activator, is being evaluated for ability to reduce morbidity and mortality in patients currently or recently hospitalized with decompensated heart failure.
Once patients are stabilized, long-term HF treatment is begun.
Acute pulmonary edema can result from acute coronary ischemia, decompensation of underlying heart failure, arrhythmia, an acute valvular disorder, or acute volume overload.
Patients have severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged frothy sputum.
Clinical examination and chest x-ray are usually sufficient for diagnosis; ECG, cardiac markers, and sometimes echocardiography are done to identify cause.
Treat the cause and give oxygen and IV furosemide and/or nitrates as needed; try noninvasive ventilatory assistance initially but use tracheal intubation and assisted ventilation if necessary.