The Mechanisms of Abnormal Gas Exchange in Acute Massive Pulmonary Embolism^1,2

Abstract

Hypoxemia usually accompanies acute pulmonary embolism in humans, but its mechanism remains poorly understood. We studied 2 patients with acute, massive pulmonary embolism (APE) documented by pulmonary angiography. Both patients had a markedly increased alveolar-arterial oxygen difference (AaPO2). The technique of multiple inert gas elimination was used to determine the distribution of ventilation-perfusion ratios (VA/Q). An increase in VA/Q inequality was found in both patients, but this increased inequality was caused entirely by an increase in the ventilation of lung units with high VA/Q ratio. No blood flow was found perfusing lung units with a VA/Q ratio of less than 1.0. Both patients, however, had a large amount of blood flow (20 and 39% of the cardiac output) perfusing unventilated lung units (shunt), and the percent of minute ventilation to unperfused lung units as well as the VD/VT determined from the Bohr equation were increased. We conclude that in these 2 patients with APE, VA/Q inequality did not play a major role in their hypoxemia and that the widened AaPO2 is explained by the large shunts that were found.

Embolia pulmonar quase fatal, um modelo experimental

“…While right-left shunt was the factor described by Wilson et al [17] and D'Alonzo et al [18], inadequacy of V A /Q was also the factor attributed by Manier et al [19] and Huet et al [20].…”

Guidelines for the Diagnosis, Treatment and Prevention of Pulmonary Thromboembolism and Deep Vein Thrombosis (JCS 2009) - Digest Version -

“…68 Oxygen therapy should be initiated for patients with an partial pressure of arterial oxygen (PaO2) of ≤60 Torr (mmHg) (or a peripheral oxygen saturation [SpO2] of ≤90%).…”

Prognostic Value of Arterial/Alveolar Oxygen Tension Ratio (a/APO2) in Acute Pulmonary Embolism

“…8,9 An increased area of pulmonary artery obstruction destabilizes normal distribution of ventilation perfusion and increases shunt. The lung regions exhibit alveolar dead space with high ventilation/perfusion ratios and shunting because of perfusion of atelectatic areas.…”