Alterations in Gas Exchange Following Pulmonary Thromboembolism

Dantzker, David R.; Bower, James S.

doi:10.1378/chest.81.4.495

Cited by 52 publications

(26 citation statements)

References 22 publications

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“…Pulmonary embolism profoundly affects the matching of ventilation and perfusion in the lung [7]. A number of different approaches to measurement of gas exchange abnormalities, such as the physiological dead space fraction [2,3,8,9], the arterial-end tidal CO 2 gradient [2,3,8,10,11] and the alveolararterial oxygen gradient [12][13][14] have been evaluated as possible means of diagnosing PE.…”

Section: Discussionmentioning

confidence: 99%

Diagnosis of pulmonary embolism by measurement of alveolar dead space

Olsson

Jonson²,

Wollmer

1998

Journal of Internal Medicine

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Section: Discussionmentioning

confidence: 99%

Diagnosis of pulmonary embolism by measurement of alveolar dead space

Olsson

Jonson²,

Wollmer

1998

Journal of Internal Medicine

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“…The complex abnormalities in gas exchange that occur are multiple, but the literature remains unassertive to elucidate the underlying mechanisms (1)(2)(3)(4)(5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…Analysis of the mechanisms involved in the genesis of this severe hypoxemia in humans with PE is difficult because of the multiple variables associated, including car-diopulmonary disease (8,9). Dantzker and Bower (8) stated that this difficulty exists even in experimental situations because of differences in species, the specific experimental circumstances, as well as the size, composition and quantity of the embolized material utilized, which may influence results in each individual model (11).…”

Section: Introductionmentioning

confidence: 99%

“…Dantzker and Bower (8) stated that this difficulty exists even in experimental situations because of differences in species, the specific experimental circumstances, as well as the size, composition and quantity of the embolized material utilized, which may influence results in each individual model (11).…”

Section: Introductionmentioning

confidence: 99%

“…These include low-partial oxygen pressure in mixed venous blood (P v O 2 ), the mismatch between ventilation and perfusion, the intrapulmonary shunt, the diffusion limitation, and the severity of the embolism, impairing the identification of the real cause of hypoxemia (8,9). Recently, the mechanisms responsible for gas exchange have been investigated with the use of the multiple inert gas elimination technique (9).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms underlying gas exchange alterations in an experimental model of pulmonary embolism

Ferreira¹,

Terzi²,

Paschoal³

et al. 2006

Braz J Med Biol Res

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The aim of the present study was to determine the ventilation/perfusion ratio that contributes to hypoxemia in pulmonary embolism by analyzing blood gases and volumetric capnography in a model of experimental acute pulmonary embolism. Pulmonary embolization with autologous blood clots was induced in seven pigs weighing 24.00 ± 0.6 kg, anesthetized and mechanically ventilated. Significant changes occurred from baseline to 20 min after embolization, such as reduction in oxygen partial pressures in arterial blood (from 87.71 ± 8.64 to 39.14 ± 6.77 mmHg) and alveolar air (from 92.97 ± 2.14 to 63.91 ± 8.27 mmHg). The effective alveolar ventilation exhibited a significant reduction (from 199.62 ± 42.01 to 84.34 ± 44.13 mL) consistent with the fall in alveolar gas volume that effectively participated in gas exchange. The relation between the alveolar ventilation that effectively participated in gas exchange and cardiac output (V A eff/Q ratio) also presented a significant reduction after embolization (from 0.96 ± 0.34 to 0.33 ± 0.17 fraction). The carbon dioxide partial pressure increased significantly in arterial blood (from 37.51 ± 1.71 to 60.76 ± 6.62 mmHg), but decreased significantly in exhaled air at the end of the respiratory cycle (from 35.57 ± 1.22 to 23.15 ± 8.24 mmHg). Exhaled air at the end of the respiratory cycle returned to baseline values 40 min after embolism. The arterial to alveolar carbon dioxide gradient increased significantly (from 1.94 ± 1.36 to 37.61 ± 12.79 mmHg), as also did the calculated alveolar (from 56.38 ± 22.47 to 178.09 ± 37.46 mL) and physiological (from 0.37 ± 0.05 to 0.75 ± 0.10 fraction) dead spaces. Based on our data, we conclude that the severe arterial hypoxemia observed in this experimental model may be attributed to the reduction of the V A eff/Q ratio. We were also able to demonstrate that V A eff/Q progressively improves after embolization, a fact attributed to the alveolar ventilation redistribution induced by hypocapnic bronchoconstriction. Correspondence

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