Chapter 22. Congestive Heart Failure and Acute Pulmonary Edema

Acute pulmonary edema is one of the most critical presentations of the many clinical effects of heart failure. The most common precipitating factors of heart failure are atrial fibrillation, acute myocardial infarction or ischemia, discontinuation of medications (diuretics), increased sodium load, drugs that impair myocardial function, and physical overexertion.

Patients with acute pulmonary edema usually present with symptoms of left ventricular heart failure, severe respiratory distress, frothy pink or white sputum, moist pulmonary rales, and a third heart sound (S3) or fourth heart sound (S4). Patients frequently are tachycardic and hypertensive. Cardiac dysrhythmias, such as atrial fibrillation or premature ventricular contractions, are common. There may be a history of exertional dyspnea, paroxysmal nocturnal dyspnea, or orthopnea. Patients with right ventricular heart failure have dependent edema of the extremities and may have jugular venous distention, hepatic enlargement, and a hepatojugular reflex. The traditional distinction between right and left heart failure does not have great bearing on ED management, as volume overload and respiratory distress will be approached in the same manner. However, consideration must be given to patients in whom there is a suspicion of valvular pathology or acute right ventricular infarction.

The diagnosis of acute pulmonary edema is made with clinical findings and the chest x-ray. The severity of illness may dictate need for a portable (anterior-posterior) chest x-ray be taken. Additional tests that assist inmanagement include an electrocardiogram, serum electrolytes, serum urea nitrogen, creatinine, complete blood cell count, arterial or venous blood gas, B-type natriuretic peptide, and cardiac markers (eg, troponin). The diagnosis of right-side heart failure is made clinically. In left-side heart failure, the chest x-ray will show enlargement of the cardiac silhouette.

In the differential diagnosis, consider the common causes of acute respiratory distress: asthma, chronic obstructive pulmonary disease, pneumonia, pulmonary embolus, allergic reactions, and other causes of respiratory failure. Also in the differential are other causes of noncardiogenic pulmonary edema, such as drug-related alveolar capillary damage or acute respiratory distress syndrome.

The treatment of patients in acute pulmonary edema includes oxygen, preload reducers, diuretics, afterload reducers, and inotropic agents.

1. Oxygen therapy, up to 100% delivered by non-rebreather mask should be administered to achieve an oxygen saturation of at least 95% by pulse oximetry.

2. If hypoxia persists despite oxygen therapy, or if the patient is showing signs of respiratory distress (eg, tripod stature, accessory muscle use, inability to speak), continuous positive airway pressure (CPAP) or biphasic positive airway pressure (BiPAP) should be applied.

3. Immediate intubation is indicated for unconscious or visibly tiring patients.

4. Nitroglycerin 0.4 milligram should be administered sublingually (may be repeated every 1 to 5 min). If the patient does not respond, or if the electrocardiogram shows ischemia, nitroglycerin 0.4 microgram/kilogram/min should be initiated as an intravenous drip and titrated rapidly to BP and symptom reduction.

5. After nitrates, an intravenous diuretic can be administrated, such as furosemide 40 to 80 milligrams intravenously, bumetanide 0.5 to 1 milligram intravenously, or torsemide 10 milligrams intravenously. Electrolytes (especially serum potassium) should be monitored.

6. Transient hypotension may develop after nitroglycerin is started. This may be due to marked clinical improvement, and should improve with decreasing the dose or cessation of nitroglycerin. If hypotension persists, initiate a fluid bolus (250 to 1000 cc) and be suspicious of a right ventricular infarction, valvular pathology (severe aortic stenosis), hypovolemia, or recent use of medications for erectile dysfunction.

7. For patients with resistant hypertension or those who are not responding well to nitroglycerin, nitroprusside may be used, starting at 0.3 microgram/kilogram/min and titrated.

8. For hypotensive patients or patients in need of additional inotropic support, see Chapter 19 “Cardiogenic Shock,” for management.

9. Coexisting dysrhythmias (see Chapter 2) or electrolyte disturbances (see Chapter 4) should be treated, and those therapies that impair the inotropic state of the heart should be avoided.

Acute mitral valve or aortic valve regurgitation should be considered, especially if the heart is of normal size, because the patient may need emergency surgery. Until excluded, acute myocardial infarction should be considered as the cause of pulmonary edema exacerbation. Because the initial electrocardiogram may fail to demonstrate ischemic changes, repeat electrocardiograms are indicated for those patients with initially normal tracings, who fail to improve.

Morphine can be given (2 to 5 milligrams intravenously) and repeated as needed for pain control. Its use is controversial, however, and may cause respiratory depression. For anuric (dialysis) patients, sorbitol and phlebotomy may have some benefit; however, dialysis is the treatment of choice in these patients who prove resistant to nitrates.

Patients with acute pulmonary edema may require admission to the intensive care unit for ongoing invasive hemodynamic monitoring. In the presence of new dysrhythmias, uncontrolled hypertension, or suspected myocardial infarction, the patient should be admitted to a telemetry bed for evaluation and optimization of drug therapy.

Long-term treatment of congestive heart failure includes dietary salt reduction, chronic use of diuretics such as furosemide, afterload reducers such as angiotensin-converting enzyme inhibitors, β-blockers, or digoxin. Patients with an exacerbation of chronic congestive heart failure without chest pain or complicating factors who respond to diuretics may be discharged home if close follow-up is arranged.