Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Abstract

Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/ perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin-mediated vasoconstriction also persisted at significant level during the early phase. More than 30 years ago, Eugene Robin commented on the problems of diagnosing acute pulmonary thromboembolism (APTE) by referring the physicians' attitudes to the emperor's vanity in Hans Christian Andersen's fable. 1,2 Although significant advances have occurred over the years, 3-5 some aspects of its pathophysiology remain puzzling. 6 This report provides an updated review of the literature, published mostly from 1980 onward, specifically addressing the mechanisms of hypoxemia and pulmonary hypertension (PH) after APTE. The emphasis is on the elucidation of the underlying pathophysiological principles and bringing them to the bedside, rather than on presenting meta-analysis or clinical trials. It also allows for occasional personal perspectives but has excluded recent works at the molecular level. GAS EXCHANGE IN APTEHypoxemia is a common and nonspecific feature of APTE. 7,8 It remains mysterious because the patient's arterial oxygen tension (PaO 2 ) is often unpredictable and correlates poorly with embolic load. [9][10][11] It is also associated with very different V/Q (ventilation/perfusion ratio) patterns measured by the multiple inert gas elimination technique (MIGET) among similar subjects 12 or in the same subject over time. 12,13 The roles of anatomical shunts may be important among a minority of patients but are questionable in the rest. These variations in gas exchange are clinically relevant in a negative way, because blood gas results do not contribute to defining pretest probabilities in the interpretation of nuclear scans. 1,14,15 The major purpose of this communication is to discuss the key factors that determine the degree of hypoxemia after APTE and their relevance to 5 commonly asked questions:1. Why do patients with APTE present with such a wide range of hypoxemia? 2. Why do many patients with APTE have relatively clear chest X-rays while severely hypoxic? 3. Can patients with significant APTE present with relatively normal PaO 2 ? 4. Why does hypoxemia worsen when cardiac output is increased? 5. Why do some patients with APTE have pulmonary infarcts and the others do not?

Pulmonary artery hemodynamics are associated with duration of nocturnal desaturation but not apnea-hypopnea index

“…We believe that the most likely explanation entails heterogeneity in ventilation/perfusion (V/Q) relationships throughout the different regions of the lung, with low V/Q ratio lung units existing in some areas 14,15 and high V/Q relationships in others. 16 Under these circumstances, positional changes in blood flow distribution during sleep may lead to increased flow through low V/Q lung regions and subsequent hypoxia while supine. We found that T90 was associated with markers of PH severity (mPAP and PVR).…”

Retrograde lung perfusion in the treatment of massive pulmonary embolism. A randomised porcine study

“…Even if a greater number of pigs had shown a significant lower number of atelectasis in the group with retrograde perfusion, this may indicate the worsening of microatelectasis because of the one hour of no flow in the pulmonary vessels in the antegrade group, thus suggesting it as a beneficial effect of retrograde perfusion. It has been debated that a PE in itself may provoke atelectasis as a way of helping to restore the disequilibrium in the ventilation-perfusion ratio in the lungs, most likely mediated by a low CO 2 in the obstructed vessels in the lungs [11][12][13]. Further research is needed to verify this hypothesis.…”

Budd-Chiari Like Syndrome in a Dog: Hematology, Biochemistry, Histopathology and CT Scan Angiography Findings

“…The respiratory distress could be caused by pulmonary artery thrombosis and mild pulmonary edema. Adult respiratory distress syndrome (ARDS), or non-cardiogenic pulmonary oedema and hypoxia could be associated with pulmonary thromboembolism [29]. Furthermore there is a possibility of Hepatopulmonary syndrome (HPS) in this patient.…”