Alveolar Gas Exchange in Clinical Pulmonary Embolism

Ed, Robin; Ce, Forkner; Pa, Bromberg; Croteau,; Dm, Travis

doi:10.1056/nejm196002112620604

Cited by 89 publications

(26 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Closure of the terminal airways, if relatively more extensive than obstruction of the vessels, may result in the perfusion of nonventilated alveoli with consequent venous admixture. This explanation is consistent with the inability of 100 per cent oxygen to abolish venous admixture (8,9), and appears to be supported by the partial correlation between QE and CL (Figure 5).…”

Section: Methodssupporting

confidence: 80%

“…Robin (8) and Julian (44), and their associates, observed an increased alveolar dead space based on a widened alveolar-arterial Pco2 difference in pulmonary embolism. In view of the gross mechanical nonhomogeneity of the lung after embolism, alveolar sampling is invalid.…”

Section: Methodsmentioning

confidence: 99%

“…A fall in the pulmonary diffusing capacity for oxygen was assumed by Williams (7) to be due to a reduction in the area of the alveolocapillary membrane. Venous admixture was not abolished, however, by breathing 100 per cent oxygen (8,9), and it also occurred after the intravenous injection of oxygen itself (10). This prompted the conclusion that arterial hypoxia was caused by the opening of pulmonary arteriovenous anastomoses (9).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Cardiorespiratory Effects of Experimental Lung Embolism*

Halmagyi¹,

Colebatch²

1961

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Methodssupporting

confidence: 80%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Cardiorespiratory Effects of Experimental Lung Embolism*

Halmagyi¹,

Colebatch²

1961

J. Clin. Invest.

View full text Add to dashboard Cite

“…Another aspect of this study was concerned with the mechanisms responsible for arterial hypoxemia, a common finding in experimental as well as clinical pulmonary thromboembolization. Various mechanisms have been proposed to explain this finding: alveolar hypoventilation, a decrease in lung diffusing capacity (22), abnormally rapid passage of blood through a pulmonary capillary bed decreased in volume, ventilation-perfusion abnormalities, localized right-toleft shunts, and atelectasis.…”

Section: Methodsmentioning

confidence: 99%

Ventilation-perfusion abnormalities in experimental pulmonary embolism.

Levy¹,

Stein²,

Totten³

et al. 1965

J. Clin. Invest.

View full text Add to dashboard Cite

The changes in pulmonary function that occur as a result of experimental pulmonary vascular occlusion have been intensively investigated. The techniques employed for producing pulmonary vascular occlusion have included balloon occlusion (1-3) and the injection of particulate matter (4) into the pulmonary artery. The results of such studies are not directly comparable to clinical pulmonary thromboembolism, where vascular occlusion is produced by autogenous thrombi. It might be anticipated, a priori, that substantial differences would occur because of the different physicochemical nature of the embolic material and the different pattern of embolization. In the present studies the effects of autogenous thromboemboli on ventilation-perfusion relationships, pulmonary gas exchange, pulmonary mechanics, and the ultrastructure of the lung are described.Two questions related to pulmonary thromboembolism are of particular interest. First is the problem of redistribution of ventilation after embolization. Several investigators have described a shift of pulmonary ventilation away from nonperfused lung segments after balloon occlusion of a pulmonary artery (1,5,6). We have developed a technique to evaluate whether redistribution of ventilation occurs after autogenous pulmonary thromboembolism. Second is the evaluation of the mechanisms resulting in arterial hypoxemia after autogenous pulmonary thromboembolism.* Submitted for publication December 22, 1964; accepted July 1, 1965. This work was supported in part by grants HE-05059 and HE-05317 from the National Institutes of Health and in part by a grant from the Tuberculosis League of Pittsburgh. MethodsSixty-five healthy, mongrel dogs ranging in weight from 9 to 26 kg were studied. The animals were anesthetized with either pentobarbital, thiopental sodium, or chloralose by intravenous administration and intubated with an endotracheal tube. Thirty-four dogs were studied during spontaneous ventilation (spontaneous ventilation dogs, SVD), and in 31 dogs spontaneous ventilation was abolished by either d-tubocurarine or succinylcholine administered intravenously, and ventilation was then maintained with an Etsten bellows pump set to deliver a constant tidal volume at a constant frequency (controlled ventilation dogs, CVD). The total amount of barbiturate administered was such as previously observed to maintain adequate anesthesia in nonparalyzed animals. Autogenous thrombi were produced and released into the pulmonary circulation as previously described (7).The following measurements were made before and within 30 minutes after embolization in the SVD and CVD while they were breathing room air. Minute ventilation (VE) was measured by standard techniques. Femoral arterial blood was analyzed for oxygen content and capacity, and C02 content by the technique of Van Slyke and Neill (8). Arterial pH was measured with a glass electrode at 37°C. Plasma C02 content was derived with the correction factors of Van Slyke and Sendroy from the whole blood CO2 content, the arterial hematocrit,...

show abstract

“…(c) Patients with recurrent emboli are not separated from those with a single episode of embolization (7). (d) Postoperative patients, who may have other causes for hypoxemia, are included (13). (e) The diagnosis frequently is made only on clinical grounds, and the extent of embolic occlusion is seldom assessed.…”

Section: Introductionmentioning

confidence: 99%

Hypoxemia in pulmonary embolism, a clinical study

Wilson¹,

Pierce²,

Johnson³

et al. 1971

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis.When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.

show abstract

Alveolar Gas Exchange in Clinical Pulmonary Embolism

Cited by 89 publications

References 10 publications

Cardiorespiratory Effects of Experimental Lung Embolism*

Cardiorespiratory Effects of Experimental Lung Embolism*

Ventilation-perfusion abnormalities in experimental pulmonary embolism.

Hypoxemia in pulmonary embolism, a clinical study

Contact Info

Product

Resources

About