Influence of Cardiac Output on Oxygen Exchange in Acute Pulmonary Embolism

Manier, G.; Castaing, Y.

doi:10.1164/ajrccm/145.1.130

Cited by 72 publications

(49 citation statements)

References 2 publications

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“…The pattern of distribution of either ventilation or perfusion, however, depends largely on cardiac output. (13) When such patients continue to have normal cardiac output, blood flow redistribution can result in the formation of areas of low ventilation or perfusion within the lung zone unaffected by thromboembolism. This means that there is an overperfusion of non-embolised regions, which in turn leads to hypoxaemia.…”

Section: Discussionmentioning

confidence: 99%

“…The factor observed to play an extremely important role in hypoxaemia in patients with APE is reduced mixed venous oxygen tension, which is a direct consequence of low cardiac output. (13,14) Although decreased cardiac output plays an important role in hypoxaemia, hypoxaemia can occur regardless of changes in cardiac output. Indeed, patients with massive pulmonary embolisms can present with severe hypoxaemia even if their cardiac output and blood pressure are normal.…”

Section: Discussionmentioning

confidence: 99%

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Severe hypoxaemia can predict unfavourable clinical outcomes in individuals with pulmonary embolism aged over 40 years

Souza¹,

Resende²,

Rodrigues³

2014

smedj

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INTRODUCTION Acute pulmonary embolism (APE) is an urgent clinical condition that can progress in a wide variety of ways. Therefore, we sought to develop an easy-to-apply algorithm, to be based on readily available clinical indicators, effective in predicting unfavourable outcomes. METHODSThis was a retrospective cohort study based on systematically collected data in a database. The study included 102 patients with APE who were admitted to a tertiary care hospital. The following outcomes were defined as unfavourable: shock, the need for mechanical ventilation, the use of thrombolytics, and death. Logistic regression analysis was used to explore variables significantly associated with outcome and to calculate post-test probabilities. RESULTSThe prevalence of unfavourable outcomes was 25.5% (26 of the 102 patients with APE). The risk of an unfavourable outcome was reduced to 7.0% for patients with APE who were aged ≤ 40 years. In patients with APE who were aged > 40 years, the presence of hypoxaemia (i.e. peripheral oxygen saturation < 90%) alone increased the risk of an unfavourable outcome to 57.0%. A recent history of trauma and the presence of pre-existing lung or heart disease were significantly associated with unfavourable outcomes. The inclusion of those variables in the logistic regression model increased the post-test risk of an unfavourable outcome to 65.0%-86.0%. CONCLUSIONAdvanced age (i.e. > 40 years), the presence of hypoxaemia, a recent history of trauma and the presence of pre-existing lung or heart disease are risk factors for unfavourable outcome in patients with APE.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Severe hypoxaemia can predict unfavourable clinical outcomes in individuals with pulmonary embolism aged over 40 years

Souza¹,

Resende²,

Rodrigues³

2014

smedj

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“…Jardin et al 1979). Several previous investigators, who pioneered in this area using the MIGET method, found inconsistent relationship between arterial oxygenation and cardiac output but did not have a more detailed explanation (Manier et al 1992). In the present study, we specifi cally studied the mechanisms on how regional pulmonary blood fl ow was distributed inside the embolized lung when the cardiac output was intermittently altered, in an attempt to elucidate the underlying pathophysiology.…”

Section: Discussionmentioning

confidence: 93%

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

Tsang

Lamm

Neradilek³

et al. 2008

Clinical medicine. Circulatory, respiratory and pulmonary medic

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Previous studies reported that the degree of hypoxemia following acute pulmonary thromboembolism (APTE) was highly variable and that its mechanism was mainly due to the creation of many high and low ventilation/perfusion (V/Q) units, as a result of the heterogeneous regional blood fl ow (Q) caused by embolic obstruction. We studied the effect of changing cardiac output (Q t ) on gas exchange after APTE in 5 embolized piglets (23 ± 3 Kg), using Dobutamine intermittently at approximately 20 µg/kg/min for 120 minutes. The distribution of ventilation (V) and perfusion (Q) at various times was mapped using fl uorescent microspheres in 941 ± 60 lung regions. After APTE, increase in Q t by Dobutamine improved venous oxygen tension (PvO 2 ) but arterial PaO 2 did not change consistently. On the other hand, cluster analysis showed that the V/Q ratio of most lung regions was lowered due to increases in Q at the same time. We concluded that the effect of changing cardiac output on gas exchange following APTE was affected by the simultaneous and varying balance between the changing V/Q mismatch and the concomitantly changing PvO 2 , which might explain the unpredictability of PaO 2 in the clinical setting.

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“…25,35,98 Some suggested that this inverse correlation was due to the abolition of hypoxic pulmonary vasoconstriction due to the concomitant higher PvO 2 . 99 As it turns out, the answer lies mostly in the heterogeneity of regional blood flow.…”

Section: Why Does Hypoxemia Worsen When Qt Is Increased?mentioning

confidence: 99%

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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Influence of Cardiac Output on Oxygen Exchange in Acute Pulmonary Embolism

Cited by 72 publications

References 2 publications

Severe hypoxaemia can predict unfavourable clinical outcomes in individuals with pulmonary embolism aged over 40 years

Severe hypoxaemia can predict unfavourable clinical outcomes in individuals with pulmonary embolism aged over 40 years

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

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

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