Assessment of changes in intra-abdominal pressure and cardiac output induced by liver compression in healthy anesthetized spontaneously breathing dogs

Abstract

Objective: Liver compression (LC) has been proposed to predict fluid responsiveness in human pediatric patients. Because the evaluation of fluid responsiveness through LC depends on the mechanism of increased intra-abdominal pressure (IAP), understanding the impact of LC on IAP, cardiac output (CO), and respiratory parameters is essential. Thus, this study aimed to investigate the effects of LC on these parameters.

Methods: The present study used six healthy beagles. All dogs were anesthetized with isoflurane and allowed to breathe spontaneously in dorsal recumbency. After instrumentation, LC was performed at four different pressures in a sequential, non-randomized manner: (1) 10 mmHg, approximately half of the minimum value within the range; (2) 22 mmHg, a commonly used pressure within the range; (3) 44 mmHg, twice the pressure of the minimum value within the range; and (4) 60 mmHg, twice the pressure of the maximum value within the range. At each pressure, CO via transthoracic echocardiography, IAP, and cardiorespiratory parameters were measured before, during, and after LC.

Results: Overall, our results showed that the IAP was significantly increased at all pressures during LC (P < 0.001), yielding a linear correlation between LC pressure and IAP (P < 0.001; r² = 0.89). The maximum IAP during LC was 7 mmHg, and intra-abdominal hypertension was not induced. LC at 22 mmHg significantly increased the IAP by 1.7 mmHg, but did not significantly alter the CO or respiratory parameters.

Conclusions: This is the first study to evaluate the effects of LC on IAP, CO, and respiratory parameters in healthy, anesthetized, and spontaneously breathing dogs. Our findings indicate that applying LC with a commonly used pressure may have a low risk of inducing intra-abdominal hypertension and related complications. Further studies are required to explore the use of LC in various clinical settings.

Fig 1. Transthoracic echocardiographic measurements of mitral valve diameter and velocity time integral in left apical four-chamber view of healthy, anesthetized, and spontaneously breathing dogs.

Fig 2. Timeline of the study design and data collection for evaluating the effects of liver compression (LC) on intra-abdominal pressure (IAP), cardiac output (CO), and respiratory parameters in healthy, anesthetized, and spontaneously breathing dogs.

Following anesthetic induction and instrumentation, the dogs were allowed 10 min to stabilize cardiorespiratory variables. Data were collected at three time points: immediately before LC (pre-LC); during the application of pressure to the mid-abdomen for 1 min (LC); and 5 min after the release of pressure (post-LC). A 5-min stabilization period was provided between changes in LC pressure.

Fig 3. Effect of various liver compression (LC) pressures on intra-abdominal pressure (IAP) at the three time points (pre-LC, immediately before LC; LC, during the application of pressure to the mid-abdomen for 1 min; post-LC, 5 min after the release of pressure) in healthy, anesthetized, and spontaneously breathing dogs.

*Significant difference from 10 mmHg at the same time point (P < 0.05). ^†Significant difference from 22 mmHg at the same time point (P < 0.05). ^§Significant difference from pre-LC within the same stage (P < 0.05). ^¶Significant difference from LC within the same stage (P < 0.05).

Fig 4. Correlation between liver compression (LC) pressures ranging from 10–60 mmHg and intra-abdominal pressure (IAP) in healthy, anesthetized, and spontaneously breathing dogs.

*Significant difference from 10 mmHg at the same time point (P < 0.05). ^†Significant difference from 22 mmHg at the same time point (P < 0.05). ^§Significant difference from pre-LC within the same stage (P < 0.05). ^¶Significant difference from LC within the same stage (P < 0.05).