Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass

Macnaughton, Peter; Braude, S.; Hunter, David N.; Denison, D M; Evans, Timothy W.

doi:10.1097/00003246-199209000-00016

Cited by 97 publications

(35 citation statements)

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“…Therefore, in order to assess the effects of one-lung ventilation and operative procedure on gaseous exchange, the rebreathing method was utilized. The values measured were in agreement with those obtained in anaesthetized patients undergoing coronary artery bypass surgery [29]. Mean KCO fell in patients undergoing pneumonectomy and more markedly in all those undergoing lobectomy, but was not significantly different perioperatively in the biopsy or wedge resection group.…”

Section: Discussionsupporting

confidence: 86%

Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection

Williams

Quinlan²,

Goldstraw³

et al. 1998

Eur Respir J

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Lung injury is a potential complication of lung resection and has been termed postpneumonectomy pulmonary oedema (PPO) [1,2]. In its extreme form, PPO represents one cause of the acute respiratory distress syndrome (ARDS) and the less severe acute lung injury (ALI) [3]. PPO complicates 4-7% of pneumonectomies and 1-7% of lobectomies, with an associated mortality of 50-100% [4][5][6][7], and therefore represents a significant operative complication. Predicting patients at risk of developing PPO has proved difficult. Age, the side of lung resection [5], the volume of fluid infused perioperatively [1,8], and preoperative lung function have all been proposed as possible predictive factors, but with little statistical support. The pathophysiology of PPO is uncertain, although the use of fresh frozen plasma, mechanical ventilatory support [9] and the extent of mediastinal lymphatic dissection [10] may be contributory factors.Ischaemia-reperfusion (I-R) injury may also contribute to PPO, in that operative ischaemia may lead to lung damage, but on reperfusion injury is increased owing to the formation of reactive oxygen species (ROS) [11,12], possibly secondary to neutrophil recruitment and activation in the lung [13,14]. I-R-mediated damage is known to occur following rapid re-expansion of a collapsed lung, after removal of thrombus in massive pulmonary embolus and following lung transplantation. Furthermore, evidence of ROS-mediated oxidative damage has been found in patients with ARDS precipitated by a wide variety of serious medical and surgical conditions [15,16].The primary aim of this investigation was therefore to seek evidence of oxidative damage and lung injury in patients undergoing routine thoracic surgery involving onelung ventilation. During lobectomy, the relevant lung may be partly or completely collapsed, potentially suffering I-R-mediated injury on re-expansion. During pneumonectomy or open lung biopsy, the lung is less frequently manipulated in this fashion. To evaluate the possible connection between evidence of ROS activation, clinically detectable lung injury and the type of surgical resection, patients undergoing pneumonectomy, lobectomy and lesser resections (wedge, segmentectomy or open lung biopsy with a low risk) were investigated. Methods Study subjectsPatients over 18 yrs of age scheduled to undergo elective thoracic surgery and providing informed consent were Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection. E.A. Williams, G.J. Quinlan, P. Goldstraw, J.W.W. Gothard, T.W. Evans. ©ERS Journals Ltd 1998. ABSTRACT: Postpneumonectomy pulmonary oedema (PPO) complicates a significant number of thoracic surgical procedures involving lung resection and in its extreme form is indistinguishable from the acute respiratory distress syndrome. This study investigated the possibility that ischaemia-reperfusion (I-R) injury contributes to PPO via the production of damaging reactive oxygen species.In a prospective, observational, comparative study, patients undergoing...

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Section: Discussionsupporting

confidence: 86%

Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection

Williams

Quinlan²,

Goldstraw³

et al. 1998

Eur Respir J

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“…This may reflect the fact that our patients had good pre-operative lung function and were post-surgical, requiring only a relatively short period of assisted ventilation; in Jones' study only 50% of patients were post-surgical. MacNaughton et al [4], found a positive correlation between postoperative hypoxaemia and length of cardiopulmonary bypass time, a finding the present study failed to confirm. Although MacNaughton's group concluded that the postoperative hypoxaemia in their patients was due to loss of lung volume, we could not demonstrate that CPAP applied after 5 h of IPPV was beneficial, possibly because most of the lost lung volume is regained during this period of assisted ventilation.…”

Section: Discussioncontrasting

confidence: 85%

“…Due to the type of ventilator available in our Intensive Care Unit (Blease Manley), patients receive postoperative ventilatory support in the form of intermittent positive pressure ventilation for 4-8 h until cardiovascular stability is established and are then transferred to a fully spontaneous mode of breathing prior to extubation. While these intubated patients are breathing spontaneously, the addition of continuous positive airway pressure (CPAP) may theoretically improve lung functional residual capacity and thus reduce venti1ation:perfusion mismatch, since cardiopulmonary bypass can result in a deterioration in lung function characterised by loss of lung volume and an increase in alveolar-arterial oxygen difference [4]. Additionally, in patients with raised pulmonary artery wedge pressure, the use of CPAP may produce an increase in cardiac index that may secondarily improve oxygenation [S].…”

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confidence: 99%

The role of continuous positive airway pressure during weaning from mechanical ventilation in cardiac surgical patients

Bailey¹,

Jones²,

Kelleher³

1995

Anaesthesia

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“…It has been suggested that neutrophil activation during extracorporeal circulation and during lung reperfusion leads to a significant release of inflammatory mediators [24][25][26] with a consequential increase in pulmonary vascular permeability and endothelial cell damage [27,28], both possibly reflected in an increase in plasma SPB and RAGE levels. Furthermore, the required mechanical ventilation, although time-limited, might represent per se a cause of acute lung injury [12].…”

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confidence: 99%

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

et al. 2010

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Surfactant derived protein B (SPB) and plasma receptor for advanced glycation end products (RAGE) have been proposed as markers of lung injury. The former is produced specifically by pneumocytes while RAGE production is present in several body tissues. Cardiopulmonary bypass (CPB) generates a transient lung injury. We measured SPB and RAGE in plasma before surgery and after CPB, as well as 24 h and 48 h later.We analysed plasma samples from 20 subjects scheduled for elective coronary artery bypass grafting. We performed a quantitative analysis of plasma levels of RAGE and SPB mature form (8 kDa) by ELISA and a semi-quantitative analysis of SPB immature form (,40 kDa) by Western blotting.Surgery procedures were uneventful. After CPB RAGE median (75th-25th interquartile difference) increased from 633 (539)

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Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass

Cited by 97 publications

References 0 publications

Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection

Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection

The role of continuous positive airway pressure during weaning from mechanical ventilation in cardiac surgical patients

Surfactant protein B and RAGE increases in the plasma during cardiopulmonary bypass: a pilot study

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