Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs

Demetris Yannopoulos, Anja Metzger, Scott McKnite, Vinay Nadkarni, Tom P. Aufderheide, Ahamed Idris, David Dries, David G. Benditt, Keith G. Lurie

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

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 languageEnglish (US)
Pages (from-to)445-453
Number of pages9
JournalResuscitation
Volume70
Issue number3
DOIs
StatePublished - Sep 2006

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Hypovolemia
Swine
Perfusion
Pressure
Blood Volume
Atrial Pressure
Cerebrovascular Circulation
Intermittent Positive-Pressure Ventilation
Acid-Base Equilibrium
Positive-Pressure Respiration

Keywords

  • Circulatory and respiratory physiology
  • Hemorrhage
  • Intrathoracic pressure
  • Resuscitation
  • Shock

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Nursing(all)

Cite this

Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs. / Yannopoulos, Demetris; Metzger, Anja; McKnite, Scott; Nadkarni, Vinay; Aufderheide, Tom P.; Idris, Ahamed; Dries, David; Benditt, David G.; Lurie, Keith G.

In: Resuscitation, Vol. 70, No. 3, 09.2006, p. 445-453.

Research output: Contribution to journalArticle

Yannopoulos, D, Metzger, A, McKnite, S, Nadkarni, V, Aufderheide, TP, Idris, A, Dries, D, Benditt, DG & Lurie, KG 2006, 'Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs', Resuscitation, vol. 70, no. 3, pp. 445-453. https://doi.org/10.1016/j.resuscitation.2006.02.005
Yannopoulos, Demetris ; Metzger, Anja ; McKnite, Scott ; Nadkarni, Vinay ; Aufderheide, Tom P. ; Idris, Ahamed ; Dries, David ; Benditt, David G. ; Lurie, Keith G. / Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs. In: Resuscitation. 2006 ; Vol. 70, No. 3. pp. 445-453.
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AU - Yannopoulos, Demetris

AU - Metzger, Anja

AU - McKnite, Scott

AU - Nadkarni, Vinay

AU - Aufderheide, Tom P.

AU - Idris, Ahamed

AU - Dries, David

AU - Benditt, David G.

AU - Lurie, Keith G.

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N2 - 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.

AB - 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.

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