Background: The intrathoracic pressure regulator (ITPR) was created to improve hemodynamics by generating continuous negative airway pressure between positive pressure ventilations to enhance cardiac preload in apnoeic animals. In normovolemic and hypovolemic pigs, we tested the hypothesis that continuous negative intrathoracic pressure set at -5 or -10 mmHg, interrupted only for intermittent positive pressure ventilations, would decrease intracranial (ICP) and right atrial (RAP) pressure, and increase mean arterial pressure (MAP). Methods: Twelve pigs were anesthetized with propofol and ventilated with a bag. The ITPR was used to vary baseline endotracheal pressures (ETPs) for 5 min periods in the following sequence: 0, -5, 0, -10, 0 mmHg under normovolemic conditions. Six pigs were bled 50% (32.5 ± mL/kg) of their estimated blood volume and the airway pressure sequence was repeated. Six other pigs were bled 35% (22.75 ± mL/kg) of their estimated blood volume and the same airway pressure sequence was repeated. Intracranial, aortic, right atrial pressures, arterial blood gases, end tidal CO2 (ETCO2), were measured. ANOVA was used for statistical analysis. Linear regression analysis was performed for ETP and ICP. Results: Mean arterial and vital organ perfusion pressures were significantly improved and RA pressure significantly decreased with the use of the ITPR; the effect was greater with the more negative ETPs and lower circulating blood volume. The change of ICP was linearly related to the ETP and blood loss: ΔICP = [1.22 - 0.84(1 - %blood loss/100)] × ETP, r2 = 0.88 (in mmHg), p < 0.001. There were no adverse device effects and there was a significant increase of ETCO2 with the use of ITPR. Conclusion: The ITPR decreased RAP and ICP significantly and improved mean arterial and cerebral and coronary perfusion pressures without affecting acid base balance severely. The decrease in ICP was directly proportional to the reduction in intrathoracic pressure. The effects were more pronounced in severe hypovolemic and hypotensive states with more negative ETP pressure.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Sep 2006|
Bibliographical noteFunding Information:
Yannopoulos Demetris was supported by an American Heart Association Postdoctoral Fellowship Grant: 0425714Z. This work was support by a United States Defense Department Small Business Innovation Research Grant # W81XWH-04-C-0022.
- Circulatory and respiratory physiology
- Intrathoracic pressure