The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

Tsang, John Y. C.; Lamm, Wayne J. E.; Neradilek, Blažej; Polissar, Nayak L.; Hlastala, Michael P.

doi:10.4137/ccrpm.s773

Cited by 1 publication

(3 citation statements)

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“…Others showed similar results using fluid and other vasopressors 18 . A recent study also confirmed that when Qt was increased intermittently by dobutamine after APTE, PaO 2 did not improve and sometimes worsened 36 . Upon further analysis, this variation of hypoxemia at higher Qt was mostly accounted for by the interplay between the beneficial effect of higher PvO 2 on PaO 2 and the deleterious effect of worsening V‐Q mismatch, caused by the maldistribution of regional Q, as demonstrated by the FMS data 36 …”

Section: Mechanisms Of Hypoxemia Following Aptementioning

confidence: 65%

“…18 A recent study also confirmed that when Qt was increased intermittently by dobutamine after APTE, PaO 2 did not improve and sometimes worsened. 36 Upon further analysis, this variation of hypoxemia at higher Qt was mostly accounted for by the interplay between the beneficial effect of higher PvO 2 on PaO 2 and the deleterious effect of worsening V-Q mismatch, caused by the maldistribution of regional Q, as demonstrated by the FMS data. 36 Earlier reports have shown that during severe shock following acute pulmonary embolism, the degree of hypoxemia did not reflect the severity of embolic obstruction.…”

Section: Gas Exchange In Aptementioning

confidence: 99%

“…36 Upon further analysis, this variation of hypoxemia at higher Qt was mostly accounted for by the interplay between the beneficial effect of higher PvO 2 on PaO 2 and the deleterious effect of worsening V-Q mismatch, caused by the maldistribution of regional Q, as demonstrated by the FMS data. 36 Earlier reports have shown that during severe shock following acute pulmonary embolism, the degree of hypoxemia did not reflect the severity of embolic obstruction. 37 To interpret these data in another way, when pulmonary blood flow becomes dangerously low, there is simply insufficient Q to create more low-V/Q units, and patient's blood gases may look less life-threatening than expected.…”

Section: Gas Exchange In Aptementioning

confidence: 99%

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

Tsang

Hogg

2014

Pulm. circ.

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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?

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Section: Mechanisms Of Hypoxemia Following Aptementioning

confidence: 65%