Hypoxemia in pulmonary embolism, a clinical study

Wilson, James E.; Pierce, Alan K.; Johnson, Robert L.; Winga, Edward R.; Harrell, William R.; Curry, George C.; Mullins, C. Buddie

doi:10.1172/jci106516

Cited by 68 publications

(31 citation statements)

References 38 publications

(36 reference statements)

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“…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].…”

Section: Discussionmentioning

confidence: 90%

Embolia pulmonar quase fatal, um modelo experimental

Pereira¹,

Moreira²,

Paschoal³

et al. 2011

Rev Bras Cir Cardiovasc

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Embolia pulmonar quase fatal, um modelo experimental: variáveis hemodinâmicas, gasométricas e capnográficasNear-fatal pulmonary embolism in an experimental model: hemodynamic, gasometric and capnographic variables Abstract Introduction: Experimental studies on pulmonary embolism (PE) are usually performed under mechanical ventilation. Most patients with suspicion of PE enter the Emergency Services in spontaneous breathing and environmental air. Thus, under these conditions, measurements of hemodynamic, gasometric and capnographic variables contribute largely to a more specific comprehension of cardiopulmonary and gasometric alterations in the acute phase of the disease. Studies which evaluated animals under conditions are lacking.Objective: This study aimed to submit animals under spontaneous ventilation and without supplemental oxygen to PE.Methods: PE was induced in six pigs using autologous blood clots, and cardiorespiratory and gasometric records were performed before and after PE. The values of "near fatal" mean pulmonary arterial pressure (MPAP) were previously determined.Results Conclusion: In this model, the near fatal MPAP was from 2 to 2.5 times the basal MPAP; and the capnographic variables, associated with arterial and venous gasometry, showed effective in discriminating an acute obstructive profile.Descriptors: Pulmonary embolism. Hypertension, pulmonary. Capnography. Models, animal. Swine. ResumoIntrodução: Estudos experimentais de embolia pulmonar (EP) são habitualmente realizados sob ventilação mecânica. A maioria dos pacientes com suspeita de EP adentra os Serviços de Emergência em respiração espontânea e em ar ambiente. Assim, medidas das variáveis hemodinâmicas, gasométricas e capnográficas, nessas condições, em muito Universitária "Zeferino Vaz"

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“…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].…”

Section: Discussionmentioning

confidence: 90%

Embolia pulmonar quase fatal, um modelo experimental

Pereira¹,

Moreira²,

Paschoal³

et al. 2011

Rev Bras Cir Cardiovasc

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“…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.…”

Section: Resultsmentioning

confidence: 99%

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

Dantzker¹,

Bower²

1979

J. Clin. Invest.

130

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A B S T R A C T We have examined the mechanisiis of abnormal gas exchange in seven patients with chroniic obliteration of the pulmonary vascular bed secondary to recurrent pulmonary emboli or idiopathic pulmonary hypertension. All ofthe patients had a widened alveolararterial oxygen gradient and four were significantly hypoxemic with arterial partial pressures of oxygen <80 torr. Using the technique of multiple inert gas elimination, we found that ventilation-perfusion (VA/Q) relationships were only minimally abnormlal w\ith a imiean of 10% (range, 2-19%) of cardiac output perfusing abnormal units. These units consisted of shunt ancd units with VA/0 ratios <0.1. In addition, the dead space was found to be normal in each patient. There was no evidence for diffusion impairment, and the widenied alveolar-arterial oxygen gradient was completely explained by VA/Q inequality. Significanit hypoxemila occurred only when VA/Q inequality was combined with a low mixed venous oxygen content.

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“…Thus, the interactions of so many independent and sometimes confl icting variables, such as the different cardiovascular response or PvO 2 , the varying locations or the sizes of the emboli, which could divert fl ows in erratic ways, could render the subsequent PaO 2 almost impossible to predict. These factors might therefore explain the relatively poor correlation between the PaO 2 and the embolic load among many patients with APTE (Wilson et al 1971). In this latter clinical study, cardiac index among patients was found to vary greatly.…”

Section: Discussionmentioning

confidence: 71%

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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Hypoxemia in pulmonary embolism, a clinical study

Cited by 68 publications

References 38 publications

Embolia pulmonar quase fatal, um modelo experimental

Embolia pulmonar quase fatal, um modelo experimental

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

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

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