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Keith G Lurie - One of the best experts on this subject based on the ideXlab platform.
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intrathoracic pressure regulation improves 24 hour survival in a porcine model of hypovolemic shock
Anesthesia & Analgesia, 2007Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Keith G LurieAbstract:BACKGROUND: The intrathoracic pressure regulator (ITPR) plus positive pressure ventilation (PPV) has been shown to improve coronary and cerebral perfusion pressures during hypovolemia by improving mean arterial blood pressure and by decreasing right atrial and intracranial pressures. We hypothesized that application of intermittent negative intrathoracic pressure in a pig model of severe hypovolemic hypotension would increase 24-h neurological intact survival rates. METHODS: Eighteen isoflurane-anesthetized pigs were bled 55% of their estimated blood volume and were then prospectively randomized to either ITPR treatment with -8 mm Hg endotracheal pressure plus PPV or only PPV alone for 90 min. All survivors were reinfused with their own blood. Arterial blood gases, end-tidal CO2, and aortic pressures were monitored for the 90 min and neurological evaluation was performed at 12 and 24 h after reinfusion. RESULTS: ITPR plus PPV treatment for 90 min prevented the progression of metabolic acidosis and significantly improved mean arterial blood pressure (mean over 90 min, 55 +/- 3 vs 35 +/- 2.4 mm Hg, P < 0.001) when compared with controls. Twenty-four hour survival significantly improved with use of the ITPR when compared with untreated controls: 9/9 (100%) vs 1/9 (11%), P < 0.01. CONCLUSIONS: Use of the ITPR plus PPV for 90 min significantly increased arterial blood pressure and 24 h neurologically intact survival rates compared with controls treated with PPV alone.
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intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs
Resuscitation, 2006Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, David G Benditt, Vinay Nadkarni, Tom P Aufderheide, Ahamed H Idris, David Dries, Keith G LurieAbstract:Summary 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 −10mmHg, 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 5min periods in the following sequence: 0, −5, 0, −10, 0mmHg 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 CO 2 (ETCO 2 ), 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, r 2 =0.88 (in mmHg), p 2 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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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Vinay M Nadkarni, Anu Rao, Kurt Kruger, David G Benditt, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vac...
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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Kurt Kruger, David G Benditt, Vinay Nadkarni, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. Methods and Results— In protocol 1, 20 pigs (weight, 30±0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of IT...
Dennis E Bulman - One of the best experts on this subject based on the ideXlab platform.
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missense mutations in ITPR1 cause autosomal dominant congenital nonprogressive spinocerebellar ataxia
Orphanet Journal of Rare Diseases, 2012Co-Authors: Lijia Huang, Jodi Warman Chardon, Melissa T Carter, Kathie L Friend, Tracy Dudding, Stuart Douglas, Peter W. Schofield, Jeremy Schwartzentruber, Dennis E BulmanAbstract:Background: Congenital nonprogressive spinocerebellar ataxia is characterized by early gross motor delay, hypotonia, gait ataxia, mild dysarthria and dysmetria. The clinical presentation remains fairly stable and may be associated with cerebellar atrophy. To date, only a few families with autosomal dominant congenital nonprogressive spinocerebellar ataxia have been reported. Linkage to 3pter was demonstrated in one large Australian family and this locus was designated spinocerebellar ataxia type 29. The objective of this study is to describe an unreported Canadian family with autosomal dominant congenital nonprogressive spinocerebellar ataxia and to identify the underlying genetic causes in this family and the original Australian family. Methods and Results: Exome sequencing was performed for the Australian family, resulting in the identification of a heterozygous mutation in the ITPR1 gene. For the Canadian family, genotyping with microsatellite markers and Sanger sequencing of ITPR1 gene were performed; a heterozygous missense mutation in ITPR1 was identified. Conclusions: ITPR1 encodes inositol 1,4,5-trisphosphate receptor, type 1, a ligand-gated ion channel that mediates calcium release from the endoplasmic reticulum. Deletions of ITPR1 are known to cause spinocerebellar ataxia type 15, a distinct and very slowly progressive form of cerebellar ataxia with onset in adulthood. Our study demonstrates for the first time that, in addition to spinocerebellar ataxia type 15, alteration of ITPR1 function can cause a distinct congenital nonprogressive ataxia; highlighting important clinical heterogeneity associated with the ITPR1 gene and a significant role of the ITPR1-related pathway in the development and maintenance of the normal functions of the cerebellum.
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Missense mutations in ITPR1 cause autosomal dominant congenital nonprogressive spinocerebellar ataxia
Orphanet journal of rare diseases, 2012Co-Authors: Lijia Huang, Jodi Warman Chardon, Melissa T Carter, Kathie L Friend, Tracy Dudding, Stuart Douglas, Peter W. Schofield, Jeremy Schwartzentruber, Ruobing Zou, Dennis E BulmanAbstract:Congenital nonprogressive spinocerebellar ataxia is characterized by early gross motor delay, hypotonia, gait ataxia, mild dysarthria and dysmetria. The clinical presentation remains fairly stable and may be associated with cerebellar atrophy. To date, only a few families with autosomal dominant congenital nonprogressive spinocerebellar ataxia have been reported. Linkage to 3pter was demonstrated in one large Australian family and this locus was designated spinocerebellar ataxia type 29. The objective of this study is to describe an unreported Canadian family with autosomal dominant congenital nonprogressive spinocerebellar ataxia and to identify the underlying genetic causes in this family and the original Australian family. Exome sequencing was performed for the Australian family, resulting in the identification of a heterozygous mutation in the ITPR1 gene. For the Canadian family, genotyping with microsatellite markers and Sanger sequencing of ITPR1 gene were performed; a heterozygous missense mutation in ITPR1 was identified. ITPR1 encodes inositol 1,4,5-trisphosphate receptor, type 1, a ligand-gated ion channel that mediates calcium release from the endoplasmic reticulum. Deletions of ITPR1 are known to cause spinocerebellar ataxia type 15, a distinct and very slowly progressive form of cerebellar ataxia with onset in adulthood. Our study demonstrates for the first time that, in addition to spinocerebellar ataxia type 15, alteration of ITPR1 function can cause a distinct congenital nonprogressive ataxia; highlighting important clinical heterogeneity associated with the ITPR1 gene and a significant role of the ITPR1-related pathway in the development and maintenance of the normal functions of the cerebellum.
Demetris Yannopoulos - One of the best experts on this subject based on the ideXlab platform.
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intrathoracic pressure regulation improves 24 hour survival in a porcine model of hypovolemic shock
Anesthesia & Analgesia, 2007Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Keith G LurieAbstract:BACKGROUND: The intrathoracic pressure regulator (ITPR) plus positive pressure ventilation (PPV) has been shown to improve coronary and cerebral perfusion pressures during hypovolemia by improving mean arterial blood pressure and by decreasing right atrial and intracranial pressures. We hypothesized that application of intermittent negative intrathoracic pressure in a pig model of severe hypovolemic hypotension would increase 24-h neurological intact survival rates. METHODS: Eighteen isoflurane-anesthetized pigs were bled 55% of their estimated blood volume and were then prospectively randomized to either ITPR treatment with -8 mm Hg endotracheal pressure plus PPV or only PPV alone for 90 min. All survivors were reinfused with their own blood. Arterial blood gases, end-tidal CO2, and aortic pressures were monitored for the 90 min and neurological evaluation was performed at 12 and 24 h after reinfusion. RESULTS: ITPR plus PPV treatment for 90 min prevented the progression of metabolic acidosis and significantly improved mean arterial blood pressure (mean over 90 min, 55 +/- 3 vs 35 +/- 2.4 mm Hg, P < 0.001) when compared with controls. Twenty-four hour survival significantly improved with use of the ITPR when compared with untreated controls: 9/9 (100%) vs 1/9 (11%), P < 0.01. CONCLUSIONS: Use of the ITPR plus PPV for 90 min significantly increased arterial blood pressure and 24 h neurologically intact survival rates compared with controls treated with PPV alone.
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intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs
Resuscitation, 2006Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, David G Benditt, Vinay Nadkarni, Tom P Aufderheide, Ahamed H Idris, David Dries, Keith G LurieAbstract:Summary 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 −10mmHg, 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 5min periods in the following sequence: 0, −5, 0, −10, 0mmHg 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 CO 2 (ETCO 2 ), 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, r 2 =0.88 (in mmHg), p 2 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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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Vinay M Nadkarni, Anu Rao, Kurt Kruger, David G Benditt, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vac...
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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Kurt Kruger, David G Benditt, Vinay Nadkarni, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. Methods and Results— In protocol 1, 20 pigs (weight, 30±0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of IT...
Anja Metzger - One of the best experts on this subject based on the ideXlab platform.
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intrathoracic pressure regulation improves 24 hour survival in a porcine model of hypovolemic shock
Anesthesia & Analgesia, 2007Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Keith G LurieAbstract:BACKGROUND: The intrathoracic pressure regulator (ITPR) plus positive pressure ventilation (PPV) has been shown to improve coronary and cerebral perfusion pressures during hypovolemia by improving mean arterial blood pressure and by decreasing right atrial and intracranial pressures. We hypothesized that application of intermittent negative intrathoracic pressure in a pig model of severe hypovolemic hypotension would increase 24-h neurological intact survival rates. METHODS: Eighteen isoflurane-anesthetized pigs were bled 55% of their estimated blood volume and were then prospectively randomized to either ITPR treatment with -8 mm Hg endotracheal pressure plus PPV or only PPV alone for 90 min. All survivors were reinfused with their own blood. Arterial blood gases, end-tidal CO2, and aortic pressures were monitored for the 90 min and neurological evaluation was performed at 12 and 24 h after reinfusion. RESULTS: ITPR plus PPV treatment for 90 min prevented the progression of metabolic acidosis and significantly improved mean arterial blood pressure (mean over 90 min, 55 +/- 3 vs 35 +/- 2.4 mm Hg, P < 0.001) when compared with controls. Twenty-four hour survival significantly improved with use of the ITPR when compared with untreated controls: 9/9 (100%) vs 1/9 (11%), P < 0.01. CONCLUSIONS: Use of the ITPR plus PPV for 90 min significantly increased arterial blood pressure and 24 h neurologically intact survival rates compared with controls treated with PPV alone.
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intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs
Resuscitation, 2006Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, David G Benditt, Vinay Nadkarni, Tom P Aufderheide, Ahamed H Idris, David Dries, Keith G LurieAbstract:Summary 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 −10mmHg, 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 5min periods in the following sequence: 0, −5, 0, −10, 0mmHg 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 CO 2 (ETCO 2 ), 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, r 2 =0.88 (in mmHg), p 2 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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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Vinay M Nadkarni, Anu Rao, Kurt Kruger, David G Benditt, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vac...
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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Kurt Kruger, David G Benditt, Vinay Nadkarni, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. Methods and Results— In protocol 1, 20 pigs (weight, 30±0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of IT...
Scott Mcknite - One of the best experts on this subject based on the ideXlab platform.
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intrathoracic pressure regulation improves 24 hour survival in a porcine model of hypovolemic shock
Anesthesia & Analgesia, 2007Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Keith G LurieAbstract:BACKGROUND: The intrathoracic pressure regulator (ITPR) plus positive pressure ventilation (PPV) has been shown to improve coronary and cerebral perfusion pressures during hypovolemia by improving mean arterial blood pressure and by decreasing right atrial and intracranial pressures. We hypothesized that application of intermittent negative intrathoracic pressure in a pig model of severe hypovolemic hypotension would increase 24-h neurological intact survival rates. METHODS: Eighteen isoflurane-anesthetized pigs were bled 55% of their estimated blood volume and were then prospectively randomized to either ITPR treatment with -8 mm Hg endotracheal pressure plus PPV or only PPV alone for 90 min. All survivors were reinfused with their own blood. Arterial blood gases, end-tidal CO2, and aortic pressures were monitored for the 90 min and neurological evaluation was performed at 12 and 24 h after reinfusion. RESULTS: ITPR plus PPV treatment for 90 min prevented the progression of metabolic acidosis and significantly improved mean arterial blood pressure (mean over 90 min, 55 +/- 3 vs 35 +/- 2.4 mm Hg, P < 0.001) when compared with controls. Twenty-four hour survival significantly improved with use of the ITPR when compared with untreated controls: 9/9 (100%) vs 1/9 (11%), P < 0.01. CONCLUSIONS: Use of the ITPR plus PPV for 90 min significantly increased arterial blood pressure and 24 h neurologically intact survival rates compared with controls treated with PPV alone.
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intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs
Resuscitation, 2006Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, David G Benditt, Vinay Nadkarni, Tom P Aufderheide, Ahamed H Idris, David Dries, Keith G LurieAbstract:Summary 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 −10mmHg, 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 5min periods in the following sequence: 0, −5, 0, −10, 0mmHg 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 CO 2 (ETCO 2 ), 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, r 2 =0.88 (in mmHg), p 2 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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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Vinay M Nadkarni, Anu Rao, Kurt Kruger, David G Benditt, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vac...
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intrathoracic pressure regulator during continuous chest compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest
Circulation, 2005Co-Authors: Demetris Yannopoulos, Scott Mcknite, Anja Metzger, Kurt Kruger, David G Benditt, Vinay Nadkarni, Keith G LurieAbstract:Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled −10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. Methods and Results— In protocol 1, 20 pigs (weight, 30±0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of IT...
