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Evidence for negative effects of elevated intra-abdominal pressure on pulmonary mechanics and oxidative stress.

ABSTRACT: To compare the effects of pneumoperitoneum on lung mechanics, end-tidal CO2 (ETCO2), arterial blood gases (ABG), and oxidative stress markers in blood and bronchoalveolar lavage fluid (BALF) during laparoscopic cholecystectomy (LC) by using lung-protective ventilation strategy.Forty-six patients undergoing LC and abdominal wall hernia (AWH) surgery were assigned into 2 groups. Measurements and blood samples were obtained before, during pneumoperitoneum, and at the end of surgery. BALF samples were obtained after anesthesia induction and at the end of surgery.Peak inspiratory pressure, ETCO2, and pCO2 values at the 30th minute were significantly increased, while there was a significant decrease in dynamic lung compliance, pH, and pO2 values in LC group. In BALF samples, total oxidant status (TOS), arylesterase, paraoxonase, and malondialdehyde levels were significantly increased; the glutathione peroxidase levels were significantly decreased in LC group. The serum levels of TOS and paraoxonase were significantly higher at the end of surgery in LC group. In addition, arylesterase level in the 30th minute was increased compared to baseline. Serum paraoxonase level at the end of surgery was significantly increased when compared to AWH group.Our study showed negative effects of pneumoperitoneum in both lung and systemic levels despite lung-protective ventilation strategy.

SUBMITTER: Davarcı I

PROVIDER: S-EPMC4320804 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Project description:BackgroundThe intra-abdominal pressure (IAP) is an important clinical parameter that can significantly change during respiration. Currently, IAP is recorded at end-expiration (IAPee), while continuous IAP changes during respiration (?IAP) are ignored. Herein, a novel concept of considering continuous IAP changes during respiration is presented.MethodsBased on the geometric mean of the IAP waveform (MIAP), a mathematical model was developed for calculating respiratory-integrated MIAP (i.e. MIAPri=IAPee+i??IAP), where 'i' is the decimal fraction of the inspiratory time, and where ?IAP can be calculated as the difference between the IAP at end-inspiration (IAPei) minus IAPee. The effect of various parameters on IAPee and MIAPri was evaluated with a mathematical model and validated afterwards in six mechanically ventilated patients. The MIAP of the patients was also calculated using a CiMON monitor (Pulsion Medical Systems, Munich, Germany). Several other parameters were recorded and used for comparison.ResultsThe human study confirmed the mathematical modelling, showing that MIAPri correlates well with MIAP (R2 = 0.99); MIAPri was significantly higher than IAPee under all conditions that were used to examine the effects of changes in IAPee, the inspiratory/expiratory (I:E) ratio, and ?IAP (P <0.001). Univariate Pearson regression analysis showed significant correlations between MIAPri and IAPei (R = 0.99), IAPee (R = 0.99), and ?IAP (R = 0.78) (P <0.001); multivariate regression analysis confirmed that IAPee (mainly affected by the level of positive end-expiratory pressure, PEEP), ?IAP, and the I:E ratio are independent variables (P <0.001) determining MIAP. According to the results of a regression analysis, MIAP can also be calculated asMIAP=-0.3+IAPee+0.4??IAP+0.5?IE.ConclusionsWe believe that the novel concept of MIAP is a better representation of IAP (especially in mechanically ventilated patients) because MIAP takes into account the IAP changes during respiration. The MIAP can be estimated by the MIAPri equation. Since MIAPri is almost always greater than the classic IAP, this may have implications on end-organ function during intra-abdominal hypertension. Further clinical studies are necessary to evaluate the physiological effects of MIAP.

Project description:The effects of a moderately elevated intra-abdominal pressure (IAP) on lung mechanics in acute respiratory distress syndrome (ARDS) have still not been fully analyzed. Moreover, the optimal positive end-expiratory pressure (PEEP) in elevated IAP and ARDS is unclear. In this paper, 18 pigs under general anesthesia received a double hit lung injury. After saline lung lavage and 2 h of injurious mechanical ventilation to induce an acute lung injury (ALI), an intra-abdominal balloon was filled until an IAP of 10 mmHg was generated. Animals were randomly assigned to one of three groups (group A = PEEP 5, B = PEEP 10 and C = PEEP 15 cmH2O) and ventilated for 6 h. We measured end-expiratory lung volume (EELV) per kg bodyweight, driving pressure (ΔP), transpulmonary pressure (ΔPL), static lung compliance (Cstat), oxygenation (P/F ratio) and cardiac index (CI). In group A, we found increases in ΔP (22 ± 1 vs. 28 ± 2 cmH2O; p = 0.006) and ΔPL (16 ± 1 vs. 22 ± 2 cmH2O; p = 0.007), with no change in EELV/kg (15 ± 1 vs. 14 ± 1 mL/kg) when comparing hours 0 and 6. In group B, there was no change in ΔP (26 ± 2 vs. 25 ± 2 cmH2O), ΔPL (19 ± 2 vs. 18 ± 2 cmH2O), Cstat (21 ± 3 vs. 21 ± 2 cmH2O/mL) or EELV/kg (12 ± 2 vs. 13 ± 3 mL/kg). ΔP and ΔPL were significantly lower after 6 h when comparing between group C and A (21 ± 1 vs. 28 ± 2 cmH2O; p = 0.020) and (14 ± 1 vs. 22 ± 2 cmH2O; p = 0.013)). The EELV/kg increased over time in group C (13 ± 1 vs. 19 ± 2 mL/kg; p = 0.034). The P/F ratio increased in all groups over time. CI decreased in groups B and C. The global lung injury score did not significantly differ between groups (A: 0.25 ± 0.05, B: 0.21 ± 0.02, C: 0.22 ± 0.03). In this model of ALI, elevated IAP, ΔP and ΔPL increased further over time in the group with a PEEP of 5 cmH2O applied over 6 h. This was not the case in the groups with a PEEP of 10 and 15 cmH2O. Although ΔP and ΔPL were significantly lower after 6 hours in group C compared to group A, we could not show significant differences in histological lung injury score.

Project description:IntroductionIntra-abdominal hypertension (IAH) causes atelectasis, reduces lung volumes and increases respiratory system elastance. Positive end-expiratory pressure (PEEP) in the setting of IAH and healthy lungs improves lung volumes but not oxygenation. However, critically ill patients with IAH often suffer from acute lung injury (ALI). This study, therefore, examined the respiratory and cardiac effects of positive end-expiratory pressure in an animal model of IAH, with sick lungs.MethodsNine pigs were anesthetized and ventilated (48 +/- 6 kg). Lung injury was induced with oleic acid. Three levels of intra-abdominal pressure (baseline, 18, and 22 mmHg) were randomly generated. At each level of intra-abdominal pressure, three levels of PEEP were randomly applied: baseline (5 cmH2O), moderate (0.5 × intra-abdominal pressure), and high (1.0 × intra-abdominal pressure). We measured end-expiratory lung volumes, arterial oxygen levels, respiratory mechanics, and cardiac output 10 minutes after each new IAP and PEEP setting.ResultsAt baseline PEEP, IAH (22 mmHg) decreased oxygen levels (-55%, P <0.001) and end-expiratory lung volumes (-45%, P = 0.007). At IAP of 22 mmHg, moderate and high PEEP increased oxygen levels (+60%, P = 0.04 and +162%, P <0.001) and end-expiratory lung volume (+44%, P = 0.02 and +279%, P <0.001) and high PEEP reduced cardiac output (-30%, P = 0.04). Shunt and dead-space fraction inversely correlated with oxygen levels and end-expiratory lung volumes. In the presence of IAH, lung, chest wall and respiratory system elastance increased. Subsequently, PEEP decreased respiratory system elastance by decreasing chest wall elastance.ConclusionsIn a porcine sick lung model of IAH, PEEP matched to intra-abdominal pressure led to increased lung volumes and oxygenation and decreased chest wall elastance shunt and dead-space fraction. High PEEP decreased cardiac output. The study shows that lung injury influences the effects of IAH and PEEP on oxygenation and respiratory mechanics. Our findings support the application of PEEP in the setting of acute lung injury and IAH.

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Evidence for negative effects of elevated intra-abdominal pressure on pulmonary mechanics and oxidative stress.

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