Gas exchange after pulmonary thromboemoblization in dogs.

Abstract

SUMMARY Gas exchange following experimental pulmonary thromboembolization was studied with an inert gas elimination technique in 17 dogs. Pulmonary arterial, systemic arterial, and expired gas concentrations of six gases infused intravenously were measured before embolization and 5,10,15,30,60, and 120 minutes after embolization. Distributions of ventilation-perfusion (VA/Q) ratios were derived from the measured concentrations. In all dogs, embolization caused an increase in blood flow and ventilation to VA/Q ratios less than 1. There were no lung units with VA/Q ratios between 10 and 100 before embolization, but, in two-thirds of the dogs, such regions developed after embolization. Ventilation to unperfused lung showed a transient increase of 2-6%. Radioisotope studies of lobes removed post-mortem indicated that thromboemboli rarely caused complete abolition of lobar blood flow. Pulmonary embolization did not cause arteriovenous shunts to appear. The hypoxemia caused by embolization could be accounted for by the changes in VA/Q distributions. Over the 2-hour period after embolization, lung function improved as the distributions partially returned toward the preembolization patterns.THE HYPOXEMIA that follows pulmonary embolization with various substances has been well documented in humans and in experimental animals. The proposed mechanisms for the hypoxemia in pulmonary embolization include right-to-left shunting, 1 " 8 diffusion impairment, 9 -10 and ventilation-perfusion ( V A / Q ) inequality. 1 ' 3 ' "• 1 2Using a recently described method, 13 it is possible to measure the distribution of VA/Q ratios together with shunt and ventilation to unperfused lung. The method requires simultaneous measurement of pulmonary arterial, systemic arterial, and mixed expired gas concentrations of six inert gases infused intravenously. The results can be used to determine the relative contributions to arterial hypoxemia by shunt and V A / Q inequality. Using this method, we studied the gas exchange abnormalities occurring in pulmonary thromboembolization of a moderate degree in dogs. Methods Grouping of DogsThe 19 mongrel dogs (20-30 kg) utilized in this study were divided into three groups. In 12 dogs (group A) thromboemboli were formed in a segment of inferior vena cava. In five subsequent dogs (group B) the thromboemboli were formed in polyethylene tubing and then released into the inferior vena cava. In two dogs (group C) no emboli were formed, but a cuff was inflated around the left pulmonary artery to accomplish complete obstruction of blood flow. The purpose of studying the latter group was to test the sensitivity of the inert gas elimination

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

“…The obliteration of a large portion of the pulmonary vascular bed results in increased blood flow through the remaining pulmonary capillaries. The VA/Q ratios ofthe perfused units thus fall (20). Although it is unlikely that this would lead to units with VA/( ratios as low as 0.01 or below, these units could result from a combination of increased blood flow and airway obstruction.…”

“…result of decreased transit time of blood through a reduced pulmonary capillary bed with resulting failure of alveolar-end capillary equilibration (18). Recently, VA/Q inequality and intrapulmonary shunt have been implicated as causes for the hypoxemia (19)(20)(21). A low cardiac output state with resulting reduction of mixed venous saturation has also been reported (22), but its impact on arterial hypoxemia has not been evaluated.…”

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

“…Site A, the COX-1/2 enzyme, was inhibited with ketorolac, and site B, the thromboxane synthase enzyme, was inhibited with furegrelate. Figure 1 shows that one could rationalize that proximal inhibition at the COX-1/2 enzyme might result in decreased substrate that is available to produce vasodilatory prostaglandins (PGI 2 and PGE 2 ), resulting in worsened pulmonary hypertension (34) and ventilation-perfusion relationships (7,33). Also, the location of COX-1/2 suggests that COX-1/2 inhibition might cause arachidonate to be shunted toward the lipoxygenase pathway, resulting in increased synthesis of vasoconstrictive and bronchoconstrictive leukotrienes (28, 38).…”

Perfusion Lung Scintigraphy for the Diagnosis of Pulmonary Embolism: A Reappraisal and Review of the Prospective Investigative Study of Acute Pulmonary Embolism Diagnosis Methods

“…The V/Q mismatch criterion to diagnose PE is at variance with several studies [33][34][35][36][37] in which the authors showed that ventilation is shifted away from embolized lung regions. 38 The concept that dead space ventilation is not significantly increased in the course of PE 38 was widely held in respiratory pathophysiology before the V/Q scanning approach was developed as it was asserted by Julius H. Comroe, Jr, who, in 1966, 39 foresaw that: "[T]he decrease in wasted ventilation (ventilation to unperfused or poorly perfused lung) helps the patient but hinders the physician in diagnosis."…”