ESSENTIALS OF DIAGNOSIS
Acute onset or worsening of dyspnea at rest.
Tachycardia, diaphoresis, cyanosis.
Pulmonary rales, rhonchi; expiratory wheezing.
Radiograph shows interstitial and alveolar edema with or without cardiomegaly.
Typical causes of acute cardiogenic pulmonary edema include acute MI or severe ischemia, exacerbation of chronic heart failure, acute severe hypertension, acute kidney injury, acute volume overload of the LV (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.
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 (see AUDIO 10–22). 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 MI, which may be painful or silent. Less severe decompensations usually present with dyspnea at rest, rales, and other evidence of fluid retention but without severe hypoxia.
Noncardiac causes of pulmonary edema include intravenous opioids, increased intracerebral pressure, high altitude, sepsis, medications, inhaled toxins, transfusion reactions, shock, and disseminated intravascular coagulation. These are distinguished from cardiogenic pulmonary edema by the clinical setting, history, and physical examination. Conversely, in most patients with cardiogenic pulmonary edema, an underlying cardiac abnormality can usually be detected clinically or by ECG, chest radiograph, 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 (see eFigure 10–1 and eFigure 10–2). 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 has normal EFs with elevated atrial pressures due to diastolic dysfunction. In cardiogenic pulmonary edema, BNP is elevated, and the PCWP is invariably elevated, usually over 25 mm Hg. In noncardiogenic pulmonary edema, the wedge pressure may be normal or even low.
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 ...