The pathologic physiology of pulmonary embolism. A physiologic discussion of the vascular reactions following pulmonary arterial obstruction by emboli of varying size

Nelson, James; Smith, John R. Lindsay

doi:10.1016/0002-8703(59)90114-0

Cited by 32 publications

(9 citation statements)

References 67 publications

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“…Not unexpectedly, pulmonary arterial pressure and pulmonary vascular resistance did not increase after the inflation of the pulmonary catheter, underlining, in our large animal model, the high reserve capacity of pulmonary arterial vessels. 26 Nevertheless, other researchers in a similar setting have found a significant increase in pulmonary arterial pressure, likely due to a greater region of vascular occlusion. 27 Of note, in pathologic conditions the filling of the balloon of the pulmonary artery catheter might, in rare cases, increase pulmonary vascular resistance to a level leading to right heart failure and hemodynamic collapse.…”

Section: Physiologic Effects Of Pulmonary Artery Occlusionmentioning

confidence: 90%

Short-term Physiologic Consequences of Regional Pulmonary Vascular Occlusion in Pigs

Länger

Castagna²,

Brusatori³

et al. 2019

Anesthesiology

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Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Acute unilateral pulmonary arterial occlusion causes ventilation–perfusion mismatch of the affected lung area. A diversion of ventilation from nonperfused to perfused lung areas, limiting the increase in dead space, has been described. The hypothesis was that the occlusion of a distal branch of the pulmonary artery would cause local redistribution of ventilation and changes in regional lung densitometry as assessed with quantitative computed tomography. Methods In eight healthy, anesthetized pigs (18.5 ± 3.8 kg) ventilated with constant ventilatory settings, respiratory mechanics, arterial blood gases, and quantitative computed tomography scans were recorded at baseline and 30 min after the inflation of the balloon of a pulmonary artery catheter. Regional (left vs. right lung and perfused vs. nonperfused area) quantitative computed tomography was performed. Results The balloon always occluded a branch of the left pulmonary artery perfusing approximately 30% of lung tissue. Physiologic dead space increased (0.37 ± 0.17 vs. 0.43 ± 0.17, P = 0.005), causing an increase in Paco2 (39.8 [35.2 to 43.0] vs. 41.8 [37.5 to 47.1] mmHg, P = 0.008) and reduction in pH (7.46 [7.42 to 7.50] vs. 7.42 [7.38 to 7.47], P = 0.008). Respiratory system compliance was reduced (24.4 ± 4.2 vs. 22.8 ± 4.8 ml · cm H2O−1, P = 0.028), and the reduction was more pronounced in the left hemithorax. Quantitative analysis of the nonperfused lung area revealed a significant reduction in lung density (−436 [−490 to −401] vs. −478 [−543 to −474] Hounsfield units, P = 0.016), due to a reduction in lung tissue (90 ± 23 vs. 81 ± 22 g, P < 0.001) and an increase in air volume (70 ± 22 vs. 82 ± 26 ml, P = 0.022). Conclusions Regional pulmonary vascular occlusion is associated with a diversion of ventilation from nonperfused to perfused lung areas. This compensatory mechanism effectively limits ventilation perfusion mismatch. Quantitative computed tomography documented acute changes in lung densitometry after pulmonary vascular occlusion. In particular, the nonperfused lung area showed an increase in air volume and reduction in tissue mass, resulting in a decreased lung density.

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Section: Physiologic Effects Of Pulmonary Artery Occlusionmentioning

confidence: 90%

Short-term Physiologic Consequences of Regional Pulmonary Vascular Occlusion in Pigs

Länger

Castagna²,

Brusatori³

et al. 2019

Anesthesiology

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“…[73032] Inert occlusion studies have demonstrated that more than half of the lung (~60-70%) may be occluded before PH is reached. [6833] The model is representative of an inert (nonhematogenous) obstruction—given that no vasoconstriction is included in the model—and, given the slightly higher than average baseline PAP, predicts a level of occlusion very similar to these measurements.…”

Section: Resultsmentioning

confidence: 99%

Blood Flow Redistribution and Ventilation‐Perfusion Mismatch During Embolic Pulmonary Arterial Occlusion

2011

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Acute pulmonary embolism causes redistribution of blood in the lung, which impairs ventilation/perfusion matching and gas exchange and can elevate pulmonary arterial pressure (PAP) by increasing pulmonary vascular resistance (PVR). An anatomically-based multi-scale model of the human pulmonary circulation was used to simulate pre- and post-occlusion flow, to study blood flow redistribution in the presence of an embolus, and to evaluate whether reduction in perfused vascular bed is sufficient to increase PAP to hypertensive levels, or whether other vasoconstrictive mechanisms are necessary. A model of oxygen transfer from air to blood was included to assess the impact of vascular occlusion on oxygen exchange. Emboli of 5, 7, and 10 mm radius were introduced to occlude increasing proportions of the vasculature. Blood flow redistribution was calculated after arterial occlusion, giving predictions of PAP, PVR, flow redistribution, and micro-circulatory flow dynamics. Because of the large flow reserve capacity (via both capillary recruitment and distension), approximately 55% of the vasculature was occluded before PAP reached clinically significant levels indicative of hypertension. In contrast, model predictions showed that even relatively low levels of occlusion could cause localized oxygen deficit. Flow preferentially redistributed to gravitationally non-dependent regions regardless of occlusion location, due to the greater potential for capillary recruitment in this region. Red blood cell transit times decreased below the minimum time for oxygen saturation (<0.25 s) and capillary pressures became high enough to initiate cell damage (which may result in edema) only after ~80% of the lung was occluded.

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“…Since blood platelets normally contain serotonin which is released by the processes of clotting it seems possible that some, at least, of the physiological effects of pulmonary embolism may be due to the action of serotonin or of a substance liberated by serotonin (Nelson and Smith, 1959). Smith and Smith (1955) found that in cats anaesthetized with chloralose serotonin produced effects similar to those produced by fragmented blood clot.…”

Section: Discussionmentioning

confidence: 99%

Serotonin and embolization by small blood clots in dogs.

Marshall¹

1966

Thorax

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The pathologic physiology of pulmonary embolism. A physiologic discussion of the vascular reactions following pulmonary arterial obstruction by emboli of varying size

Cited by 32 publications

References 67 publications

Short-term Physiologic Consequences of Regional Pulmonary Vascular Occlusion in Pigs

Short-term Physiologic Consequences of Regional Pulmonary Vascular Occlusion in Pigs

Blood Flow Redistribution and Ventilation‐Perfusion Mismatch During Embolic Pulmonary Arterial Occlusion

Serotonin and embolization by small blood clots in dogs.

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