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Effect of increased intra-abdominal pressure (IAP) on lung function in a sepsis model
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
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 Surgical Sciences, Anaesthesiology and Intensive Care.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
(English)Manuscript (preprint) (Other academic)
Abstract [en]

We have previously shown that mechanical ventilation with positive pressure increases abdominal edema formation and causes an increase in intra-abdominal pressure (IAP) in a sepsis-like porcine model. In this study we investigated, in the same animal model effects of increase in IAP on the cardiovascular and respiratory system. Twelve pigs of Swedish country breed with a mean weight 28 kg were anesthetized and mechanically ventilated. Six animals received a continuous infusion of endotoxin and the other six served as controls. Catheters were inserted for vascular pressure recordings and cardiac output was measured by thermo-dilution. In both groups IAP was temporarily elevated to 20 mmHg by insufflation of CO2 into the abdominal cavity. Endotoxin infusion caused significant increases in pulmonary artery and central venous pressures and increase in shunt with fall in PaO2. Respiratory compliance was reduced. IAP elevation by CO2 insufflation increased these pressures as well as shunt further and caused additional decrease in compliance. Deflation of the abdomen returned vascular pressures to pre-insufflation but shunt remained increased and PaO2 was still reduced as was compliance. In control animals similar but smaller changes were seen on increase in IAP but with deflation not only vascular pressures but also shunt and PaO2 returned to normal. This suggests that in the sepsis-like condition, increased IAP causes persisting deterioration of lung function even when IAP has been normalized. We propose this to be caused by lung collapse that remains, at least for some time, after deflation.

Keyword [en]
intra-abdominal pressure, IAP, pneumoperitoneum, shunt, MIGET, sepsis
National Category
Anesthesiology and Intensive Care Physiology
Research subject
Anaesthesiology and Intensive Care; Clinical Physiology
Identifiers
URN: urn:nbn:se:uu:diva-207402OAI: oai:DiVA.org:uu-207402DiVA: diva2:648017
Available from: 2013-09-13 Created: 2013-09-13 Last updated: 2014-01-23
In thesis
1. Effect of Ventilatory Support on Abdominal Fluid Balance in a Sepsis Model
Open this publication in new window or tab >>Effect of Ventilatory Support on Abdominal Fluid Balance in a Sepsis Model
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

In patients affected by acute respiratory failure or acute respiratory distress syndrome (ARDS) the leading cause of death is failure of different vital organs other than the lungs, so called multiple organ dysfunction syndrome (MODS). The abdominal organs have a crucial role in the pathogenesis of this syndrome.

There is a lack of knowledge regarding the mechanisms by which mechanical ventilation can affect the abdominal compartment. One hypothesis is that mechanical ventilation can interfere with abdominal fluid balance causing edema and inflammation.

We addressed the question whether different levels of ventilatory support (mechanical ventilation with different levels of positive end-expiratory pressure, PEEP, and spontaneous breathing with or without PEEP) can influence abdominal edema and inflammation in both healthy and endotoxin-exposed animals.

The effect on lymphatic drainage from the abdomen exerted by different degrees of ventilatory support was evaluated (paper I). We demonstrated that endotoxin increases abdominal lymph production, that PEEP and mechanical ventilation increase lymph production but also impede lymphatic drainage; spontaneous breathing improves lymphatic drainage from the abdomen.

By adapting a non-invasive nuclear medicine imaging technique and validating it (paper II), we have been able to evaluate extravascular fluid accumulation (edema formation) in the abdomen over time (paper III) demonstrating that edema increases during endotoxemia, mimicking a sepsis-like condition, and that spontaneous breathing, compared to mechanical ventilation, reduces extravascular fluid. Pro-inflammatory cytokines TNF-α and IL-6 in intestinal biopsies are reduced during spontaneous breathing compared to mechanical ventilation.

Abdominal edema results in increased intra-abdominal pressure (IAP): in paper IV we analyzed the effect of increased intra-abdominal pressure on the respiratory system. Pulmonary shunt fraction increased with high IAP both in healthy and LPS animals, resulting in decreased level of oxygenation. These changes are only partially reversible by reducing IAP.

In conclusion, mechanical ventilation is a life-saving tool but the possible side effect at the extra-pulmonary level should be considered, and the introduction of some degree of spontaneous breathing when clinically possible is a suggested choice.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2013. 35 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 941
Keyword
mechanical ventilation, lymph flow, spontaneous breathing, positive end-expiratory pressure, PEEP, abdominal edema, inflammation, intra-abdominal pressure, IAP
National Category
Anesthesiology and Intensive Care Physiology
Research subject
Anaesthesiology and Intensive Care; Clinical Physiology
Identifiers
urn:nbn:se:uu:diva-207218 (URN)978-91-554-8787-4 (ISBN)
Public defence
2013-12-09, Enghoffsalen, Entrance 50, University Hospital, Uppsala, 13:15 (English)
Opponent
Supervisors
Funder
Swedish Heart Lung FoundationSwedish Research Council, 5315
Available from: 2013-11-15 Created: 2013-09-10 Last updated: 2014-01-23

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