Transpulmonary passage of venous air emboli

Butler, Bruce D; Hills, B. A.

doi:10.1152/jappl.1985.59.2.543

Cited by 209 publications

(112 citation statements)

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“…The alteration in the resistance of the lung vessels and the mismatch between ventilation and perfusion cause intrapulmonary right-to-left shunting and increased alveolar dead space leading to decreased gas exchange [267], arrhythmia [268], pulmonary hypertension [268], right ventricular strain [269] and arterial AE related to shunting [270].…”

Section: Pathophysiologymentioning

confidence: 99%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

Eur Respir J

162

127

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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than ''simple'' mechanical obstruction after embolisation of vascular thrombi. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung.NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE.Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.

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Section: Pathophysiologymentioning

confidence: 99%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

Eur Respir J

162

127

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“…This mechanism was demonstrated in animals as well as in humans. [12][13][14] Considering the large volume of air entering the venous system, the occurrence of cardiac arrest in this patient was most likely attributable to acute cor pulmonale and possibly an arterial/coronary air embolism by flooding of the pulmonary air filter and not by the subcutaneous emphysema alone.…”

Section: Discussionmentioning

confidence: 83%

Ventilation-Induced Massive Lethal Air Embolism and Subcutaneous Emphysema in a Patient With a Lung Cavern

Verelst¹,

Verbrugghe²,

Lammens³

et al. 2014

Respir Care

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The simultaneous occurrence of subcutaneous emphysema and intravascular air due to an air embolism is a rare condition. Here, we report a patient with COPD who developed a severe episode of hemoptysis due to rupture of a previously undiagnosed lung cavern. Intubation and ventilation led to the development of both massive subcutaneous emphysema and a massive air embolism, resulting from aspiration of air through a torn pulmonary vessel in the cavern. The dramatic amount of intravenous air and subsequent conduction along the venous system to the right heart and pulmonary trunk caused major hemodynamic compromise and ultimately death. The degree of subcutaneous emphysema, especially the massive venous air embolism, was unprecedented.

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“…The pulmonary circuit in healthy individuals can filter small volumes without consequences to pulmonary vascular pressure. 20 A significant amount of venous air emboli entering the pulmonary capillaries may cause functional obstruction of the microvasculature in the form of a precapillary block and may lead to increased pulmonary vascular resistance, sustained pulmonary hypertension, and increased peripheral resistance. 21,22 While the property of turbulent flow should not be neglected, when taking Hagen-Poiseuille's equation dV ¼ pr 4 8llP into account, an increase in vessel diameter would decrease driving pressure needed to maintain flow.…”

Section: Discussionmentioning

confidence: 99%