The respiratory pressure-abdominal volume curve in a porcine model

Background: Increasing intra-abdominal volume (IAV) can lead to intra-abdominal hypertension (IAH) or abdominal compartment syndrome. Both are associated with raised morbidity and mortality. IAH can increase airway pressures and impair ventilation. The relationship between increasing IAV and airway pressures is not known. We therefore assessed the effect of increasing IAV on airway and intra-abdominal pressures (IAP). Methods: Seven pigs (41.4 +/−8.5 kg) received standardized anesthesia and mechanical ventilation. A latex balloon inserted in the peritoneal cavity was inflated in 1-L increments until IAP exceeded 40 cmH2O. Peak airway pressure (pPAW), respiratory compliance, and IAP (bladder pressure) were measured. Abdominal compliance was calculated. Different equations were tested that best described the measured pressure-volume curves. Results: An exponential equation best described the measured pressure-volume curves. Raising IAV increased pPAW and IAP in an exponential manner. Increases in IAP were associated with parallel increases in pPAW with an approximate 40% transmission of IAP to pPAW. The higher the IAP, the greater IAV effected pPAW and IAP. Conclusions: The exponential nature of the effect of IAV on pPAW and IAP implies that, in the presence of high grades of IAH, small reductions in IAV can lead to significant reductions in airway and abdominal pressures. Conversely, in the presence of normal IAP levels, large increases in IAV may not affect airway and abdominal pressures

Commonly applied positive end-expiratory pressures do not prevent functional residual capacity decline in the setting of intra-abdominal hypertension: a pig model

Introduction Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. The optimal ventilation strategy remains unclear in these patients. We examined the effect of positive end-expiratory pressures (PEEP) on functional residual capacity (FRC) and oxygen delivery in a pig model of intra-abdominal hypertension. Methods Thirteen adult pigs received standardised anaesthesia and ventilation. We randomised three levels of intra-abdominal pressure (3 mmHg (baseline), 18 mmHg, and 26 mmHg) and four commonly applied levels of PEEP (5, 8, 12 and 15 cmH2O). Intra-abdominal pressures were generated by inflating an intra-abdominal balloon. We measured intra-abdominal (bladder) pressure, functional residual capacity, cardiac output, haemoglobin and oxygen saturation, and calculated oxygen delivery. Results Raised intra-abdominal pressure decreased FRC but did not change cardiac output. PEEP increased FRC at baseline intra-abdominal pressure. The decline in FRC with raised intra-abdominal pressure was partly reversed by PEEP at 18 mmHg intra-abdominal pressure and not at all at 26 mmHg intra-abdominal pressure. PEEP significantly decreased cardiac output and oxygen delivery at baseline and at 26 mmHg intra-abdominal pressure but not at 18 mmHg intra-abdominal pressure. Conclusions In a pig model of intra-abdominal hypertension, PEEP up to 15 cmH2O did not prevent the FRC decline caused by intra-abdominal hypertension and was associated with reduced oxygen delivery as a consequence of reduced cardiac output. This implies that PEEP levels inferior to the corresponding intra-abdominal pressures cannot be recommended to prevent FRC decline in the setting of intra-abdominal hypertension

Matching positive end-expiratory pressure to intra-abdominal pressure prevents end-expiratory lung volume decline in a pig model of intra-abdominal hypertension

Objective: Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. In a previous experimental study, positive end-expiratory pressures of up to 15 cm H2O did not prevent end-expiratory lung volume decline caused by intra-abdominal hypertension. Therefore, we examined the effect of matching positive end-expiratory pressure to the intra-abdominal pressure on cardio-respiratory parameters. Design: Experimental pig model of intra-abdominal hypertension. Setting: Large animal facility, University of Western Australia. Subjects: Nine anesthetized, nonparalyzed, and ventilated pigs (48 ± 7 kg). Interventions: Four levels of intra-abdominal pressure (baseline, 12, 18, and 22 mm Hg) were generated in a randomized order by inflating an intra-abdominal balloon. At each level of intra-abdominal pressure, three levels of positive end-expiratory pressure were randomly applied with varying degrees of matching the corresponding intra-abdominal pressure: baseline positive end-expiratory pressure (= 5 cm H2O), moderate positive end-expiratory pressure (= half intra-abdominal pressure in cm H2O + 5 cm H2O), and high positive end-expiratory pressure (= intra-abdominal pressure in cm H2O). Measurements: We measured end-expiratory lung volume, arterial oxygen levels, respiratory mechanics, and cardiac output 5 mins after each new intra-abdominal pressure and positive end-expiratory pressure setting. Main Results: Intra-abdominal hypertension decreased end-expiratory lung volume and PaO2 (−49% [p \u3c .001] and −8% [p \u3c .05], respectively, at 22 mm Hg intra-abdominal pressure compared with baseline intra-abdominal pressure) but did not change cardiac output (p = .5). At each level of intra-abdominal pressure, moderate positive end-expiratory pressure increased end-expiratory lung volume (+119% [p \u3c .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) while minimally decreasing cardiac output (−8%, p \u3c .05). High positive end-expiratory pressure further increased end-expiratory lung volume (+233% [p \u3c .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) but led to a greater decrease in cardiac output (−26%, p \u3c .05). Neither moderate nor high positive end-expiratory pressure improved PaO2 (p = .7). Intra-abdominal hypertension decreased end-expiratory transpulmonary pressure but did not alter end-inspiratory transpulmonary pressure. Intra-abdominal hypertension decreased total respiratory compliance through a decrease in chest wall compliance. Positive end-expiratory pressure decreased the respiratory compliance by reducing lung compliance. Conclusions: In a pig model of intra-abdominal hypertension, positive end-expiratory pressure matched to intra-abdominal pressure led to a preservation of end-expiratory lung volume, but did not improve arterial oxygen tension and caused a reduction in cardiac output. Therefore, we do not recommend routine application of positive end-expiratory pressure matched to intra-abdominal pressure to prevent intra-abdominal pressure–induced end-expiratory lung volume decline in healthy lungs

Additional file 2: Table S1. of The respiratory pressure—abdominal volume curve in a porcine model

Equation parameters of intra-abdominal and airway pressure-volume curves. (DOCX 55 kb

Additional file 1: Figure S1. of The respiratory pressure—abdominal volume curve in a porcine model

Intra-abdominal pressure (IAP) in centimeter of water in function of increasing additional intra-abdominal volume (IAV) in liters. Example of one pig showing measured IAP values (crosses), calculated IAP values using Venegas equation (dotted curve) and exponential equation (dashed curve). Venegas equation: V = a + [b/(1 + e −(P − c)/d )] [12], V represents additional IAV, P represents absolute IAP, and a, b, c, and d represents fitting parameters. Exponential equation: V = v + k × Ln (P − p) where V represents additional IAV, P represents absolute IAP, and v, k, p represents fitting parameters. (TIF 384 kb

Additional file 3: Figure S3. of The respiratory pressure—abdominal volume curve in a porcine model

Pressure-volume curves showing intra-abdominal pressure in centimeter of water at the initial PEEP level of 5 cmH2O (dashed curve) and the subsequent PEEP level of 15 cmH2O (solid curve) in function of increasing additional intra-abdominal volume in liters. (TIF 445 kb