Introduction
Essentials of Diagnosis

• Acute onset or worsening of dyspnea at rest.
• Tachycardia, diaphoresis, cyanosis.
• Pulmonary rales, rhonchi; expiratory wheezing.
• X-ray shows interstitial and alveolar edema with or without cardiomegaly.
• Arterial hypoxemia.

General Considerations
Typical causes of acute cardiogenic pulmonary edema include acute myocardial infarction or severe ischemia, exacerbation of chronic heart failure, acute volume overload of the left ventricle (valvular regurgitation), and mitral stenosis. By far the most common presentation in developed countries is one of acute or subacute deterioration of chronic heart failure, precipitated by discontinuation of medications, excessive salt intake, myocardial ischemia, tachyarrhythmias (especially rapid atrial fibrillation), or intercurrent infection. Often in the latter group, there is preceding volume overload with worsening edema and progressive shortness of breath for which earlier intervention can usually avoid the need for hospital admission.

 

Clinical Findings
Acute pulmonary edema presents with a characteristic clinical picture of severe dyspnea, the production of pink, frothy sputum, and diaphoresis and cyanosis. Rales are present in all lung fields, as are generalized wheezing and rhonchi. Pulmonary edema may appear acutely or subacutely in the setting of chronic heart failure or may be the first manifestation of cardiac disease, usually acute myocardial infarction, which may be painful or silent. Less severe decompensations usually present with dyspnea at rest and rales and other evidence of fluid retention but without severe hypoxia.

A number of noncardiac conditions can also produce pulmonary edema. This occurs either because of imbalance in the Starling forces (either a decrease in plasma proteins or an increase in pulmonary venous pressure) or a functional or anatomic abnormality of the alveolar-capillary membrane. Causes include intravenous narcotics, increased intracerebral pressure, high altitude, sepsis, several medications, inhaled toxins, transfusion reactions, shock, and disseminated intravascular coagulation. These are distinguished from cardiogenic pulmonary edema by the clinical setting, the history, and the physical examination. Conversely, in most patients with cardiogenic pulmonary edema, an underlying cardiac abnormality can usually be detected clinically or by the ECG, chest x-ray, or echocardiogram.

The chest radiograph reveals signs of pulmonary vascular redistribution, blurriness of vascular outlines, increased interstitial markings, and, characteristically, the butterfly pattern of distribution of alveolar edema. The heart may be enlarged or normal in size depending on whether heart failure was previously present. Assessment of cardiac function by echocardiography is important, since a substantial proportion of patients have normal ejection fractions with elevated atrial pressures due to diastolic dysfunction. In cardiogenic pulmonary edema, the PCWP is invariably elevated, usually over 25 mm Hg. In noncardiogenic pulmonary edema, the wedge pressure may be normal or even low.

Treatment
In full-blown pulmonary edema, the patient should be placed in a sitting position with legs dangling over the side of the bed; this facilitates respiration and reduces venous return. Oxygen is delivered by mask to obtain an arterial PO₂ greater than 60 mm Hg. Noninvasive pressure support ventilation may improve oxygenation and prevent severe CO₂ retention while pharmacologic interventions take effect. However, if respiratory distress remains severe, Endotracheal intubation and mechanical ventilation may be necessary.

Morphine is highly effective in pulmonary edema and may be helpful in less severe decompensations when the patient is uncomfortable. The initial dosage is 2-8 mg intravenously (subcutaneous administration is effective in milder cases) and may be repeated after 2-4 hours. Morphine increases venous capacitance, lowering left atrial pressure, and relieves anxiety, which can reduce the efficiency of ventilation. However, morphine may lead to CO₂ retention by reducing the ventilatory drive. It should be avoided in patients with narcotic-induced pulmonary edema, who may improve with narcotic antagonists, and in those with neurogenic pulmonary edema.

Intravenous diuretic therapy (furosemide, 40 mg, or bumetanide, 1 mg - or higher doses if the patient has been receiving chronic diuretic therapy) is usually indicated even if the patient has not exhibited prior fluid retention. These agents produce venodilation prior to the onset of diuresis.

Nitrate therapy accelerates clinical improvement by reducing both blood pressure and left ventricular filling pressures. Sublingual nitroglycerin or isosorbide dinitrate, topical nitroglycerin, or intravenous nitrates will ameliorate dyspnea rapidly prior to the onset of diuresis, and these agents are particularly valuable in patients with accompanying hypertension. Intravenous nesiritide (recombinant BNP), when given as a bolus followed by an infusion, improves dyspnea more rapidly than intravenous nitroglycerin, though this may reflect the cautious way in which nitroglycerin is up-titrated by many practitioners. This agent, as well as nitrates, may precipitate hypotension, especially since these agents are used in combination with multiple drugs that lower blood pressure. In patients with low-output states - particularly when hypotension is present - positive inotropic agents are indicated. These approaches to treatment have been discussed previously.

Bronchospasm may occur in response to pulmonary edema and may itself exacerbate hypoxemia and dyspnea. Treatment with inhaled ß-adrenergic agonists or intravenous aminophylline may be helpful, but both may also provoke tachycardia and supraventricular arrhythmias.

In most cases, pulmonary edema responds rapidly to therapy. When the patient has improved, the cause or precipitating factor should be ascertained. In patients without prior heart failure, evaluation should include echocardiography and in many cases cardiac catheterization and coronary angiography. Patients with acute decompensation of chronic heart failure should be treated to achieve a euvolemic state and have their medical regimen optimized. Generally, an oral diuretic and an ACE inhibitor should be initiated, with efficacy and tolerability confirmed prior to discharge. In selected patients, early but careful initiation of ß-blockers in low doses should be considered.

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Jain P et al: Current medical treatment for the exacerbation of chronic heart failure resulting in hospitalization. Am Heart J 2003;145(2 Suppl):S3.

Young JB et al: Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA 2002;287:1531.