Pulmonary vascular changes following air embolism in the dog.

The effect of an intravenous injection of air in a dose of 1 ml/kg body weight was determined in 15 healthy mongrel dogs. In 4 control dogs the mean pulmonary artery pressure rose to 2-3 times the resting values at 30 seconds, and carbon monoxide diffusing capacity and pulmonary capillary blood volume decreased by half. In the animals pretreated either with heparin or with methysergide (antiserotonin group) the results were the same as in the control animals. In the vagotomized dogs, the rise in pulmonary artery pressure was not significant, and the decrease in pulmonary capillary blood volume was of lesser magnitude and shorter duration than in the control and the antiserotonin dogs. It is concluded that the intravenous injection of air in supine dogs causes a transient obstruction of small pulmonary arteries. Evidence is presented to implicate a vagal mechanism in both main aspects of the response, namely the pulmonary artery pressure rise, and the partial obstruction of the pulmonary capillary bed. These studies offer additional explanation of the symptoms of respiratory distress observed in rapid decompression.     

Cost-effectiveness of primary and secondary prevention of fatal pulmonary embolism in high-risk surgical patients.

Because death due to pulmonary embolism is relatively rare following general surgery, many question the need for prophylaxis. In addition, there has been reluctance to apply new interventions whose cost-effectiveness has not been adequately evaluated. A cost-effectiveness analysis based on over 1000 high-risk patients undergoing abdominothoracic surgery, with effectiveness measured in terms of numbers of deaths from pulmonary embolism averted, has shown subcutaneous administration of heparin in low doses starting 2 hours before the operation to be the most cost-effective of several active approaches to prophylaxis. It averted seven of the eight deaths expected without active prophylaxis per 1000 such patients and cost half as much as the traditional approach of intervening only when venous thromboembolism becomes clinically apparent. Intravenous administration of dextran, although effective, was expensive, and leg scanning with iodine-125-labelled fibrinogen was extremely expensive. Intermittent pneumatic compression of the legs was inexpensive, but, as with leg scanning, its effectiveness has not been determined in randomized trials.     

Pulmonary embolism associated with hemolymphangioma of lower extremity.

We present a case of major pulmonary embolization from a hemolymphangiomatous malformation of the loin and lower extremity. Treatment was with a low-dose infusion of urokinase for a short period directly into the pulmonary artery, and dramatic clinical improvement was noted. Prolonged maintenance therapy was with a low dose of heparin.     

Pulmonary vascular pressure-flow characteristics in canine pulmonary embolism

We tested the hypothesis that, in canine embolic pulmonary hypertension, upstream transmission of increased left atrial pressure (LAP) is inversely related to the level of the pressure intercept (PI) obtained by extrapolation from the linear pulmonary vascular pressure-flow (P-Q) plot. P-Q coordinates were obtained by varying Q through systemic fistulas. Seven group 1 dogs were embolized with autologous blood clot to produce marked pulmonary hypertension and mean pulmonary arterial pressure (PAP), and PI increased from 15 to 41 mmHg (P less than 0.001) and from 8.8 to 31 mmHg (P less than 0.001), respectively. Before and after embolization we assessed effects of increased LAP, produced by inflation of a left atrial balloon, on PAP at constant Q. Embolization depressed the mean slope of this relationship from 0.78 to 0.16 (P less than 0.001). Subsequently, six group 2 dogs were embolized to produce moderate pulmonary hypertension with a mean PI of 22 mmHg. This value was significantly less than PI in group 1 (P less than 0.01). After embolization, the slope of the PAP-LAP relationship was greater in group 2 than group 1: 0.47 vs. 0.16 (P less than 0.01). We conclude that the upstream transmission of left atrial pressure is inversely related to PI and that marked embolic pulmonary hypertension produces an effective vascular waterfall.     

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Clinical observations have indicated that patients who are in shock and who have coexisting acidosis respond relatively poorly to sympathomimetic amines. In experiments with dogs, it was found that, in the presence of acidosis, the pressor action of epinephrine, norepinephrine and metaraminol was considerably reduced. The effect on cardiac rhythm was also considerably lessened after the pH value of the blood had been lowered. In view of these observations in animals, six human patients with profound shock and acidosis were studied. All had a considerably lessened pressor response to vasopressor agents; then, after elevation of the blood pH by intravenous infusion of a 1-molar solution of sodium lactate, responsiveness was restored. These observations emphasize the desirability of close observation of the acid-base status, and early treatment of acidosis, as an important aspect in the management of patients with shock.