Clinical and physiologic studies in pulmonary thromboembolism ∗

Abstract

The clinical and physiologic studies of 72 patients with pulmonary thromboembolism were analyzed in detail. Pulmonary emboli occurred most frequently in the setting of some chronic condition, such as heart disease, previous pulmonary embolism, or chronic obstructive pulmonary disease. Coronary disease was most common, followed by mitral disease. The incidence of chronic bronchitis and emphysema can be expected to rise. The four most often encountered symptoms were: dyspnea in all patients, cough and pleural pain in about two thirds, and hemoptysis in slightly more than one third. Nonspecific physical findings were most frequent: loud P 2, tachypnea, rales and tachycardia. More specific findings of embolism, such as pleural friction rub and chest splinting, occurred in less than a fifth of the patients. Phlebitis was present in only a third. No specific laboratory test is presently available, but determination of enzyme levels (LDH, SGOT) were useful in suggesting the presence of pulmonary embolism. Over half of the patients had the characteristic elevated level of serum lactic dehydrogenase (LDH) and a normal level of serum glutamic oxalacetic transaminase (SGOT). However, negative studies do not exclude embolism. The most frequent biochemical triad consisted of elevated LDH and normal SGOT and bilirubin. Bilirubin elevation generally signaled the presence of complicating congestive failure. The white cell count in uncomplicated embolism was less than 15,000/mm. 3 Ventilatory derangements included hyperventilation, pulmonary restriction, bronchoconstriction and diminished diffusing capacity. Impairment of oxygenation was observed in almost all patients. Two thirds showed evidence of venous admixture, and other contributing factors responsible for hypoxemia were diffusion defects and diminished ventilation-perfusion ratios. Virtually all patients with pO 2 levels less than 60 mm. Hg showed evidence of venous admixture. Pulmonary hypertension was observed in varying degrees in 80 per cent of the patients. Almost all patients with mean pulmonary artery pressures above 30 mm. Hg and all those with pressures above 40 had hemodynamic evidence of right heart failure. About two-thirds of the patients showed a diminished cardiac index, increased arteriovenous oxygen extraction, and elevated right ventricular end-diastolic pressure when these combined determinations were made. Fifty-eight per cent of the patients were initially correctly diagnosed. The others had various nonspecific symptoms and signs attributed to congestive failure, pneumonia, myocardial infarction or chronic pulmonary disease. In each instance, a diagnostic protocol was useful in heightening suspicion of pulmonary emboli. The final decision was based on the results of lung scanning, selective pulmonary angiography, or both.