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Development of atelectasis and arterial to end-tidal PCO2-difference in a porcine model of pneumoperitoneum
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
Department of Anaesthesiology and Intensive Care Medicine, Otto-von-Guericke-University Magdeburg, Germany.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
2009 (English)In: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 103, no 2, 298-303 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Intraperitoneal insufflation of carbon dioxide (CO2) may promote collapse of dependent lung regions. The present study was undertaken to study the effects of CO2-pneumoperitoneum (CO2-PP) on atelectasis formation, arterial oxygenation, and arterial to end-tidal PCO2-gradient (Pa-E'(CO2)). METHODS: Fifteen anaesthetized pigs [mean body weight 28 (SD 2) kg] were studied. Spiral computed tomography (CT) scans were obtained for analysis of lung tissue density. In Group 1 (n=5) mechanical ventilation (V(T)=10 ml kg (-1), FI(O2)=0.5) was applied, in Group 2 (n=5) FI(O2) was increased for 30 min to 1.0 and in Group 3 (n=5) negative airway pressure was applied for 20 s in order to enhance development of atelectasis. Cardiopulmonary and CT data were obtained before, 10, and 90 min after induction of CO2-PP at an abdominal pressure of 12 mmHg. RESULTS: Before CO2-PP, in Group 1 non-aerated tissue on CT scans was 1 (1)%, in Group 2 3 (2)% (P<0.05, compared with Group 1), and in Group 3 7 (3)% (P<0.05, compared with Group 1 and Group 2). CO2-PP significantly increased atelectasis in all groups. PaO2/FI(O2) fell and venous admixture ('shunt') increased in proportion to atelectasis during anaesthesia but CO2-PP had a varying effect on PaO2/FI(O2) and shunt. Thus, no correlation was seen between atelectasis and PaO2/FI(O2) or shunt when all data before and during CO2-PP were pooled. Pa-E'(CO2), on the other hand correlated strongly with the amount of atelectasis (r2=0.92). CONCLUSIONS: Development of atelectasis during anaesthesia and PP may be estimated by an increased Pa-E'(CO2).

Place, publisher, year, edition, pages
2009. Vol. 103, no 2, 298-303 p.
Keyword [en]
lung, atelectasis, measurement techniques, computed tomography, model, pig, partial pressure, Pa-Pe'(CO2) ratio, Surgery, laparoscopy
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-113070DOI: 10.1093/bja/aep102ISI: 000268107800023PubMedID: 19443420OAI: oai:DiVA.org:uu-113070DiVA: diva2:289529
Available from: 2010-01-25 Created: 2010-01-25 Last updated: 2017-12-12Bibliographically approved
In thesis
1. The Effect of CO2-Pneumoperitoneum on Ventilation Perfusion Distribution of the Lung
Open this publication in new window or tab >>The Effect of CO2-Pneumoperitoneum on Ventilation Perfusion Distribution of the Lung
2011 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Laparoscopic operations are a common and popular way for abdominal procedures. They are usually performed by insufflation of carbon dioxide (CO2) into the abdominal cavity. However, insufflation of CO2 may interfere with cardiac and circulatory as well as respiratory functions. The CO2-pneumoperitoneum (PP) may cause hypercarbia and acidosis. The direct effects of CO2 and acidosis lead to decreased cardiac contractility, sensitization of the myocardium to arrhythmogenic effects of catecholamines and systemic vasodilatation. There may even be long-lasting post-operative effects on breathing control.

The pneumoperitoneum may also cause several respiratory changes, e.g. decreased functional residual capacity (FRC) and vital capacity (VC), formation of atelectasis, reduced respiratory compliance and increased airway pressure. Still, arterial oxygenation is mostly maintained or even improved during PP.

In view of the apparently contradictory results in respiratory mechanics and gas exchange, the present studies were performed to evaluate respiratory changes on gas exchange and ventilation-perfusion distributions during PP in a porcine model. It was demonstrated that atelectasis during anaesthesia and PP may be estimated by an increased arterial to endtidal PCO2-gradient (study I). Perfusion was redistributed away from dorsal, collapsed lung regions when PP was established. This resulted in a better ventilation-perfusion match (study II). Increasing abdominal pressure shifted blood flow more and more away from collapsed lung tissue, decreased pulmonary shunt and improved oxygenation from 8 to 16 mmHg PP, despite an increase of atelectasis formation (study III). CO2-PP enhanced the shift of blood flow towards better ventilated parts of the lung compared to Air-PP. Moreover, sodium natriumprusside worsened the ventilation-perfusion match even more and blunted the effects previously seen with carbon dioxide. CO2 should therefore be the mediator of enhancing HPV during PP.

In conclusion, pneumoperitoneum with CO2 causes atelectasis with elimination of ventilation in the dependent lung regions. However, an efficient shift of blood flow away from collapsed, non-ventilated regions results in a better ventilation-perfusion matching and better oxygenation of blood than without PP. A prerequisite for the beneficial effect is the use of carbon dioxide for the abdominal inflation, since it enhances HPV.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2011. 58 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 662
Keyword
lung, atelectasis; computed tomography; multiple inert gas elimination technique; model, pig; Pa–ECO2 ratio; surgery, laparoscopy; lung, blood flow; single photon emission computed tomography; ventilation/perfusion distribution; gas exchange; hypoxic pulmonary vasoconstriction
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-149746 (URN)978-91-554-8045-5 (ISBN)
Public defence
2011-05-11, Enghoff Salen, Akademiska Hospital, Entrance 30, Uppsala, 13:15 (English)
Opponent
Supervisors
Available from: 2011-04-20 Created: 2011-03-22 Last updated: 2011-05-05Bibliographically approved

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