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Keith G Lurie - One of the best experts on this subject based on the ideXlab platform.
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effect of regulating airway pressure on intrathoracic pressure and vital Organ Perfusion pressure during cardiopulmonary resuscitation a non randomized interventional cross over study
Scandinavian Journal of Trauma Resuscitation and Emergency Medicine, 2015Co-Authors: Scott Mcknite, Demetris Yannopoulos, Anja Metzger, Younghoon Kwon, Guillaume Debaty, Laura Puertas, Jennifer Rees, Keith G LurieAbstract:The objective of this investigation was to evaluate changes in intrathoracic pressure (Ppl), airway pressure (Paw) and vital Organ Perfusion pressures during standard and intrathoracic pressure regulation (IPR)-assisted cardiopulmonary resuscitation (CPR). Multiple CPR interventions were assessed, including newer ones based upon IPR, a therapy that enhances negative intrathoracic pressure after each positive pressure breath. Eight anesthetized pigs underwent 4 min of untreated ventricular fibrillation followed by 2 min each of sequential interventions: (1) conventional standard CPR (STD), (2) automated active compression decompression (ACD) CPR, (3) ACD+ an impedance threshold device (ITD) CPR or (4) ACD+ an intrathoracic pressure regulator (ITPR) CPR, the latter two representing IPR-based CPR therapies. Intrapleural (Ppl), airway (Paw), right atrial, intracranial, and aortic pressures, along with carotid blood flow and end tidal CO2, were measured and compared during each CPR intervention. The lowest mean and decompression phase Ppl were observed with IPR-based therapies [Ppl mean (mean ± SE): STD (0.8 ± 1.1 mmHg); ACD (−1.6 ± 1.6); ACD-ITD (−3.7 ± 1.5, p < 0.05 vs. both STD and ACD); ACD-ITPR (−7.0 ± 1.9, p < 0.05 vs. both STD and ACD)] [Ppl decompression (mean ± SE): STD (−6.3 ± 2.2); ACD (−13.0 ± 3.8); ACD-ITD −16.9 ± 3.6, p < 0.05 vs. both STD and ACD); ACD-ITPR −18.7 ± 3.5, p < 0.05 vs. both STD and ACD)]. Interventions with the lower mean or decompression phase Ppl also demonstrated lower Paw and were associated with higher vital Organ Perfusion pressures. IPR-based CPR methods, specifically ACD-ITPR, yielded the most pronounced reduction in both Ppl and Paw and resulted in the most favorable augmentation of hemodynamics during CPR.
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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, 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...
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vasopressin improves survival after cardiac arrest in hypovolemic shock
Anesthesia & Analgesia, 2000Co-Authors: Wolfgang G Voelckel, Scott Mcknite, Keith G Lurie, Karl H Lindner, Todd M Zielinski, Anette C Krismer, Volker WenzelAbstract:UNLABELLED: Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital Organ Perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), and 2 (0-48) mL. 100 g(-1). min(-1), respectively; and after vasopressin 96 (12-161), and 44 (16-105) mL. 100 g(-1). min(-1), respectively (P: or =55 min (P: < 0. 01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital Organ Perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted. IMPLICATIONS: The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital Organ Perfusion and prolonged survival in an animal model of suspended infusion therapy.
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active compression decompression cpr improves vital Organ Perfusion in a dog model of ventricular fibrillation
Resuscitation, 1995Co-Authors: Mark W Chang, Keith G Lurie, Paul Coffeen, Jeffrey J Shultz, Robert J Bache, Carl W WhiteAbstract:Objectives This study was designed to assess whether a new method of cardiopulmonary resuscitation (CPR), termed active compression-decompression CPR, or ACD-CPR, improves Organ Perfusion when compared with standard (S) CPR in a dog model of ventricular fibrillation. Background ACD-CPR has recently been shown to improve hemodynamic and respiratory parameters during cardiac arrest when compared with standard CPR. However, to our knowledge, the effects of ACD-CPR on tissue Perfusion have not been investigated. Methods Ventricular fibrillation was induced in eight anesthetized, intubated animals. ACD-CPR and standard CPR were each performed twice in alternating order. All interventions were preceded by 1 min of ventricular fibrillation, in which no CPR was performed, and consisted of 6 min of CPR with either technique during which tissue Perfusion was measured. Compressions were performed at 80/min with a 50 percent duty cycle and 175 to 200 N downward force applied to the chest wall for both techniques. Epinephrine was administered at the beginning of each 6-min CPR interval. Hemodynamic monitoring of aortic and right atrial pressure was performed continuously and myocardial, cerebral, and renal blood flows were measured using the radiolabeled microsphere technique at baseline and during all interventions. Results Baseline Organ Perfusion and hemodynamics were similar for all dogs. Baseline left ventricular, brain, and renal blood flows were 62.0±5.5, 14.1±2.1, and 476.3±55.5 ml/min/100 g, respectively (mean±SEM). Compared with standard CPR, ACD-CPR resulted in higher global left ventricular (22.5±6.2 vs 14.1±4.0 ml/min/100 g, p Conclusions We conclude that ACD-CPR improves tissue Perfusion and systemic hemodynamics compared with standard CPR.
Demetris Yannopoulos - One of the best experts on this subject based on the ideXlab platform.
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effect of regulating airway pressure on intrathoracic pressure and vital Organ Perfusion pressure during cardiopulmonary resuscitation a non randomized interventional cross over study
Scandinavian Journal of Trauma Resuscitation and Emergency Medicine, 2015Co-Authors: Scott Mcknite, Demetris Yannopoulos, Anja Metzger, Younghoon Kwon, Guillaume Debaty, Laura Puertas, Jennifer Rees, Keith G LurieAbstract:The objective of this investigation was to evaluate changes in intrathoracic pressure (Ppl), airway pressure (Paw) and vital Organ Perfusion pressures during standard and intrathoracic pressure regulation (IPR)-assisted cardiopulmonary resuscitation (CPR). Multiple CPR interventions were assessed, including newer ones based upon IPR, a therapy that enhances negative intrathoracic pressure after each positive pressure breath. Eight anesthetized pigs underwent 4 min of untreated ventricular fibrillation followed by 2 min each of sequential interventions: (1) conventional standard CPR (STD), (2) automated active compression decompression (ACD) CPR, (3) ACD+ an impedance threshold device (ITD) CPR or (4) ACD+ an intrathoracic pressure regulator (ITPR) CPR, the latter two representing IPR-based CPR therapies. Intrapleural (Ppl), airway (Paw), right atrial, intracranial, and aortic pressures, along with carotid blood flow and end tidal CO2, were measured and compared during each CPR intervention. The lowest mean and decompression phase Ppl were observed with IPR-based therapies [Ppl mean (mean ± SE): STD (0.8 ± 1.1 mmHg); ACD (−1.6 ± 1.6); ACD-ITD (−3.7 ± 1.5, p < 0.05 vs. both STD and ACD); ACD-ITPR (−7.0 ± 1.9, p < 0.05 vs. both STD and ACD)] [Ppl decompression (mean ± SE): STD (−6.3 ± 2.2); ACD (−13.0 ± 3.8); ACD-ITD −16.9 ± 3.6, p < 0.05 vs. both STD and ACD); ACD-ITPR −18.7 ± 3.5, p < 0.05 vs. both STD and ACD)]. Interventions with the lower mean or decompression phase Ppl also demonstrated lower Paw and were associated with higher vital Organ Perfusion pressures. IPR-based CPR methods, specifically ACD-ITPR, yielded the most pronounced reduction in both Ppl and Paw and resulted in the most favorable augmentation of hemodynamics during CPR.
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sodium nitroprusside enhanced cardiopulmonary resuscitation snpecpr improves vital Organ Perfusion pressures and carotid blood flow in a porcine model of cardiac arrest
Resuscitation, 2012Co-Authors: Jason C Schultz, Scott Mcknite, Nicolas Segal, James Kolbeck, Emily Caldwell, Demetris YannopoulosAbstract:Purpose of the study To describe a new method of CPR that optimizes vital Organ Perfusion pressures and carotid blood flow. We tested the hypothesis that a combination of high dose sodium nitroprusside (SNP) as well as non-invasive devices and techniques known independently to enhance circulation would significantly improve carotid blood flow (CBF) and return of spontaneous circulation (ROSC) rates in a porcine model of cardiac arrest.
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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, 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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effect of regulating airway pressure on intrathoracic pressure and vital Organ Perfusion pressure during cardiopulmonary resuscitation a non randomized interventional cross over study
Scandinavian Journal of Trauma Resuscitation and Emergency Medicine, 2015Co-Authors: Scott Mcknite, Demetris Yannopoulos, Anja Metzger, Younghoon Kwon, Guillaume Debaty, Laura Puertas, Jennifer Rees, Keith G LurieAbstract:The objective of this investigation was to evaluate changes in intrathoracic pressure (Ppl), airway pressure (Paw) and vital Organ Perfusion pressures during standard and intrathoracic pressure regulation (IPR)-assisted cardiopulmonary resuscitation (CPR). Multiple CPR interventions were assessed, including newer ones based upon IPR, a therapy that enhances negative intrathoracic pressure after each positive pressure breath. Eight anesthetized pigs underwent 4 min of untreated ventricular fibrillation followed by 2 min each of sequential interventions: (1) conventional standard CPR (STD), (2) automated active compression decompression (ACD) CPR, (3) ACD+ an impedance threshold device (ITD) CPR or (4) ACD+ an intrathoracic pressure regulator (ITPR) CPR, the latter two representing IPR-based CPR therapies. Intrapleural (Ppl), airway (Paw), right atrial, intracranial, and aortic pressures, along with carotid blood flow and end tidal CO2, were measured and compared during each CPR intervention. The lowest mean and decompression phase Ppl were observed with IPR-based therapies [Ppl mean (mean ± SE): STD (0.8 ± 1.1 mmHg); ACD (−1.6 ± 1.6); ACD-ITD (−3.7 ± 1.5, p < 0.05 vs. both STD and ACD); ACD-ITPR (−7.0 ± 1.9, p < 0.05 vs. both STD and ACD)] [Ppl decompression (mean ± SE): STD (−6.3 ± 2.2); ACD (−13.0 ± 3.8); ACD-ITD −16.9 ± 3.6, p < 0.05 vs. both STD and ACD); ACD-ITPR −18.7 ± 3.5, p < 0.05 vs. both STD and ACD)]. Interventions with the lower mean or decompression phase Ppl also demonstrated lower Paw and were associated with higher vital Organ Perfusion pressures. IPR-based CPR methods, specifically ACD-ITPR, yielded the most pronounced reduction in both Ppl and Paw and resulted in the most favorable augmentation of hemodynamics during CPR.
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sodium nitroprusside enhanced cardiopulmonary resuscitation snpecpr improves vital Organ Perfusion pressures and carotid blood flow in a porcine model of cardiac arrest
Resuscitation, 2012Co-Authors: Jason C Schultz, Scott Mcknite, Nicolas Segal, James Kolbeck, Emily Caldwell, Demetris YannopoulosAbstract:Purpose of the study To describe a new method of CPR that optimizes vital Organ Perfusion pressures and carotid blood flow. We tested the hypothesis that a combination of high dose sodium nitroprusside (SNP) as well as non-invasive devices and techniques known independently to enhance circulation would significantly improve carotid blood flow (CBF) and return of spontaneous circulation (ROSC) rates in a porcine model of cardiac arrest.
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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, 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...
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vasopressin improves survival after cardiac arrest in hypovolemic shock
Anesthesia & Analgesia, 2000Co-Authors: Wolfgang G Voelckel, Scott Mcknite, Keith G Lurie, Karl H Lindner, Todd M Zielinski, Anette C Krismer, Volker WenzelAbstract:UNLABELLED: Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital Organ Perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), and 2 (0-48) mL. 100 g(-1). min(-1), respectively; and after vasopressin 96 (12-161), and 44 (16-105) mL. 100 g(-1). min(-1), respectively (P: or =55 min (P: < 0. 01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital Organ Perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted. IMPLICATIONS: The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital Organ Perfusion and prolonged survival in an animal model of suspended infusion therapy.
Anja Metzger - One of the best experts on this subject based on the ideXlab platform.
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effect of regulating airway pressure on intrathoracic pressure and vital Organ Perfusion pressure during cardiopulmonary resuscitation a non randomized interventional cross over study
Scandinavian Journal of Trauma Resuscitation and Emergency Medicine, 2015Co-Authors: Scott Mcknite, Demetris Yannopoulos, Anja Metzger, Younghoon Kwon, Guillaume Debaty, Laura Puertas, Jennifer Rees, Keith G LurieAbstract:The objective of this investigation was to evaluate changes in intrathoracic pressure (Ppl), airway pressure (Paw) and vital Organ Perfusion pressures during standard and intrathoracic pressure regulation (IPR)-assisted cardiopulmonary resuscitation (CPR). Multiple CPR interventions were assessed, including newer ones based upon IPR, a therapy that enhances negative intrathoracic pressure after each positive pressure breath. Eight anesthetized pigs underwent 4 min of untreated ventricular fibrillation followed by 2 min each of sequential interventions: (1) conventional standard CPR (STD), (2) automated active compression decompression (ACD) CPR, (3) ACD+ an impedance threshold device (ITD) CPR or (4) ACD+ an intrathoracic pressure regulator (ITPR) CPR, the latter two representing IPR-based CPR therapies. Intrapleural (Ppl), airway (Paw), right atrial, intracranial, and aortic pressures, along with carotid blood flow and end tidal CO2, were measured and compared during each CPR intervention. The lowest mean and decompression phase Ppl were observed with IPR-based therapies [Ppl mean (mean ± SE): STD (0.8 ± 1.1 mmHg); ACD (−1.6 ± 1.6); ACD-ITD (−3.7 ± 1.5, p < 0.05 vs. both STD and ACD); ACD-ITPR (−7.0 ± 1.9, p < 0.05 vs. both STD and ACD)] [Ppl decompression (mean ± SE): STD (−6.3 ± 2.2); ACD (−13.0 ± 3.8); ACD-ITD −16.9 ± 3.6, p < 0.05 vs. both STD and ACD); ACD-ITPR −18.7 ± 3.5, p < 0.05 vs. both STD and ACD)]. Interventions with the lower mean or decompression phase Ppl also demonstrated lower Paw and were associated with higher vital Organ Perfusion pressures. IPR-based CPR methods, specifically ACD-ITPR, yielded the most pronounced reduction in both Ppl and Paw and resulted in the most favorable augmentation of hemodynamics during CPR.
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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, 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...
Elazer R Edelman - One of the best experts on this subject based on the ideXlab platform.
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multilayer flow modulator enhances vital Organ Perfusion in patients with type b aortic dissection
American Journal of Physiology-heart and Circulatory Physiology, 2018Co-Authors: Farhad Rikhtegar Nezami, Lambros S Athanasiou, Junedh M Amrute, Elazer R EdelmanAbstract:The majority of aortic dissection modeling efforts have focused on the maintenance of physiological flow using minimally invasive placed grafts. The multilayer flow modulator is a complex mesh cons...