Resuscitation 85 (2014) 683–688
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Experimental paper
Miniaturized mechanical chest compressor improves calculated cerebral perfusion pressure without compromising intracranial pressure during cardiopulmonary resuscitation in a porcine model of cardiac arrest夽 Jiefeng Xu a,d , Xianwen Hu a , Zhengfei Yang a , Xiaobo Wu a , Joe Bisera a,b , Shijie Sun a,b , Wanchun Tang a,b,c,∗ a
Weil Institute of Critical Care Medicine, Rancho Mirage, CA, United States Keck School of Medicine of the University of Southern California, Los Angeles, CA, United States c Department of Emergency Medicine, School of Medicine of the University of California, San Diego, CA, United States d Department of Emergency Medicine, Yuyao People’s Hospital, Medical School of Ningbo University, Ningbo, China b
a r t i c l e
i n f o
Article history: Received 18 July 2013 Received in revised form 6 January 2014 Accepted 10 January 2014 Keywords: Cardiopulmonary resuscitation Cardiac arrest Hemodynamics Cerebral perfusion pressure Intracranial pressure Miniaturized chest compressor
a b s t r a c t Objective: One of the major goals of cardiopulmonary resuscitation (CPR) is to provide adequate oxygen delivery to the brain for minimizing cerebral injury resulted from cardiac arrest. The optimal chest compression during CPR should effectively improve brain perfusion without compromising intracranial pressure (ICP). Our previous study has demonstrated that the miniaturized mechanical chest compressor improved hemodynamic efficacy and the success of CPR. In the present study, we investigated the effects of the miniaturized chest compressor (MCC) on calculated cerebral perfusion pressure (CerPP) and ICP. Methods: Ventricular fibrillation was electrically induced and untreated for 7 min in 13 male domestic pigs weighing 39 ± 3 kg. The animals were randomized to receive mechanical chest compression with the MCC (n = 7), or the Thumper device (n = 6). CPR was performed for 5 min before defibrillation attempt by a single 150 J shock. At 2.5 min of CPR, the epinephrine at a dose of 20 g/kg was administered. Additional epinephrine was administered at an interval of 3 min thereafter. If resuscitation was not successful, CPR was resumed for an additional 2 min prior to the next defibrillation until successful resuscitation or for a total of 15 min. Post-resuscitated animals were observed for 2 h. Results: Significantly greater intrathoracic positive and negative pressures during compression and decompression phases of CPR were observed with the MCC when compared with the Thumper device. The MCC produced significantly greater coronary perfusion pressure and end-tidal carbon dioxide. There were no statistically significant differences in systolic and mean ICP between the two groups; however, both of the measurements were slightly greater in the MCC treated animals. Interestingly, the diastolic ICP was significantly lower in the MCC group, which was closely related to the significantly lower negative intrathoracic pressure in the animals that received the MCC. Most important, systolic, diastolic and mean calculated CerPP were all significantly greater in the animals receiving the MCC. Conclusions: In the present study, mechanical chest compression with the MCC significantly improved calculated CerPP but did not compromise ICP during CPR. It may provide a safe and effective chest compression during CPR. Protocol number: P1205. © 2014 Elsevier Ireland Ltd. All rights reserved.
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at http://dx.doi.org/10.1016/j.resuscitation.2014.01.014. ∗ Corresponding author at: Weil Institute of Critical Care Medicine, 35100 Bob Hope Drive, Rancho Mirage, CA 92270, United States. E-mail addresses: [email protected] (J. Xu), [email protected] (X. Hu), [email protected] (Z. Yang), Mike [email protected] (X. Wu), [email protected] (J. Bisera), [email protected] (S. Sun), [email protected] (W. Tang). 0300-9572/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.resuscitation.2014.01.014
684
J. Xu et al. / Resuscitation 85 (2014) 683–688
1. Introduction The primary goal of cardiopulmonary resuscitation (CPR) is to establish the critical levels of blood flow to the heart and brain until spontaneous circulation is restored. High-quality chest compression has been recognized as the key determinant for the success of resuscitation. The latest guidelines emphasize that chest compression should be performed with adequate rate and depth, complete chest recoil and minimized pauses.1 Conventional manual CPR is simple, quick, inexpensive and always available; however, even chest compression provided by trained or experienced rescuers often fails to meet the requirements of guidelines.2,3 In the specific clinical setting such as transferring the patients or vehicular transportation, the quality of manual chest compression is difficult to maintain.4 Mechanical chest compression delivers more consistent and reliable chest compression, eliminates the elements of rescuer fatigue and compression interruption and could potentially overcome the limitations of manual chest compression. Recent clinical studies have demonstrated that the mechanical devices were beneficial to provide continuous chest compression with minimizing no-chest compression intervals during ambulance transportation and interventional coronary catheterization.5,6 The cerebral blood flow is closely related to cerebral perfusion pressure (CerPP), which is defined as the difference between mean aortic pressure (MAP) and intracranial pressure (ICP). During the compression phase of CPR, increased intrathoracic pressure is usually accompanied with both increases in MAP and ICP. The increases in intrathoracic pressure may cause a greater increase in ICP than MAP which result in a decrease in CerPP.7 In the present study, we investigated the effects of a recently developed miniaturized mechanical chest compressor (MCC) on calculated CerPP and ICP in a porcine model of cardiac arrest (CA). We hypothesized that mechanical chest compression with the MCC would improve calculated CerPP but would not compromise ICP during CPR.
2. Materials and methods All animals received humane care in compliance with the “Principles of Laboratory Animal Care” formulated by the National Society for Medical Research and the Guide for the Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (8th edition. Washington, DC, National Academies Press, 2011). The protocol was approved by the Institutional Animal Care and Use Committee of the Weil Institute of Critical Care Medicine.
2.1. Animal preparation Thirteen male domestic pigs weighing 39 ± 3 kg were fasted overnight with the exception of free access to water. Anesthesia was initiated by intramuscular injection of ketamine (20 mg/kg) and completed by an ear vein injection of sodium pentobarbital (30 mg/kg). An additional dose of sodium pentobarbital (8 mg/kg) was injected at hourly intervals to maintain anesthesia. A cuffed endotracheal tube was advanced into the trachea. The animals were mechanically ventilated with a volume controlled ventilator (Model MA-1, Puritan Bennett Inc., Carlsbad, CA) with a tidal volume of 15 ml/kg, peak flow of 40 l/min and FiO2 of 0.21. Endtidal carbon dioxide (ETCO2 ) was continuously monitored with an infrared capnometer (Model NPB-70, Nellcor Puritan Bennett Inc., Pleasanton, CA). Respiratory frequency was adjusted to maintain ETCO2 between 35 and 40 mm Hg. The conventional lead II electrocardiogram was continuously monitored by applying three
adhesive electrodes to the shaved skin of the right upper and left upper-and-lower limbs. For the measurement of ICP, a burr hole of 3 mm in diameter was drilled in the midst between the left eyebrow and the posterior bony prominence. A 5 F transducer-tipped Millar catheter (Model SPC-450S, Millar Instruments Inc., Houston, TX) was inserted 2 cm into the parietal lobe and then reflected ICP continuously. The catheter was firmly fixed with bolts and sutures around the skull. For the measurement of aortic pressure and the collection of blood samples, a fluid-filled 8 F catheter (Model 6523, USCI, C.R. Bard Inc., Salt Lake City, UT) was advanced from the right femoral artery into the thoracic aorta. For the measurements of right atrial pressure and core (blood) temperature, a 7 F pentalumen, thermodilutiontipped catheter (Abbott Critical Care # 41216, Chicago, IL) was advanced from the right femoral vein into the right atrium. Both catheters were flushed intermittently with saline containing 5 IU bovine heparin per ml. For inducing ventricular fibrillation (VF), a 5 F pacing catheter (EP Technologies Inc., Mountain View, CA) was advanced from the right subclavian vein into the right ventricle. For the measurement of intrathoracic pressure, another 5 F Millar catheter was advanced from the incisor teeth into the esophagus for a distance of 35 cm. The position of all catheters was confirmed by characteristic pressure morphology and with fluoroscopy. In addition, the depth of chest compression during CPR was measured by a linear potentiometer. The piston of the compressor was positioned in the midline at the level of the fifth interspace. Blood temperature was maintained at 37.5 ± 0.5 ◦ C with the aid of a cooling/warm blanket throughout the entire experiment. 2.2. Experimental procedures Fifteen minutes prior to inducing VF, baseline measurements were obtained. The animals were randomized by the Sealed Envelope Method to receive mechanical chest compression with the MCC (Resuscitation International Inc., Scottsdale, AZ) (n = 7) or the Thumper device (Model 1004, Michigan Instruments Inc., Grand Rapids, MI) (n = 6). VF was induced by 1 mA alternating current through the 5 F pacing catheter, delivered to the right ventricular endocardium. Mechanical ventilation was discontinued after onset of VF. Prior to initiating the resuscitation protocol, the pacing catheter was withdrawn to avoid heart injury during chest compression. After 7 min of untreated VF, CPR was started. Both the MCC and Thumper devices were programmed to provide an equal compression-relaxation interval of 50% duty cycle and the same compression rate of 100 compressions per minute. The initial compression depth of the MCC and Thumper devices was adjusted to achieve a threshold coronary perfusion pressure (CorPP) of above 12 mm Hg in 1 min. Coincident with the start of precordial compression, the animals were mechanically ventilated with a tidal volume of 15 ml/kg, FiO2 of 1.0 and a rate of 10 breaths per minute. After 2.5 min of CPR, the first bolus of epinephrine at a dose of 20 g/kg was administered. After 5 min of CPR, defibrillation was attempted with a single 150-J biphasic waveform electrical shock delivered between the conventional right infraclavicular electrode and the apical electrode with a Heartstart XL defibrillator (Philips Medical System Inc., Andover, MA). If an organized rhythm with a MAP of above 50 mm Hg persisted for an interval of 5 min or more, the animal was regarded as return of spontaneous circulation (ROSC). With failure to achieve ROSC, chest compression and ventilation were immediately resumed for 2 min prior to another defibrillation. The protocol was repeated until successful resuscitation or for a total of 15 min. Additional doses of epinephrine were administered at an interval of 3 min after the first bolus injection. After successful resuscitation, the animals were observed for 2 h. If a recurrent VF occurred after ROSC, a 150-J electrical shock was attempted. Mechanical ventilation was continued with FiO2 of 1.0 for 30 min,
J. Xu et al. / Resuscitation 85 (2014) 683–688 Table 1 Baseline characteristics.
Table 2 Cardiopulmonary resuscitation outcomes. MCC
Body weight (kg) Heart rate (beats min−1 ) MAP (mm Hg) End-tidal CO2 (mm Hg) SICP (mm Hg) MICP (mm Hg) DICP (mm Hg) SCerPP (mm Hg) MCerPP (mm Hg) DCerPP (mm Hg) Arterial lactate (mmol L−1 )
685
38.1 114 107 39.9 18.7 17.2 16.5 107 90 81 0.9
Thumper ± ± ± ± ± ± ± ± ± ± ±
1.9 8 6 1.7 1.4 1.7 2.1 5 5 6 0.1
39.2 118 109 39.7 18.6 17.5 16.9 108 92 83 0.9
± ± ± ± ± ± ± ± ± ± ±
3.5 9 6 0.5 1.2 1.2 1.3 5 6 7 0.2
p 0.49 0.47 0.49 0.79 0.96 0.75 0.67 0.60 0.51 0.53 0.43
MCC, miniaturized chest compressor; MAP, mean aortic pressure; SICP, systolic intracranial pressure; DICP, diastolic ICP; MICP, mean ICP; SCerPP, systolic cerebral perfusion pressure; DCerPP, diastolic CerPP; MCerPP, mean CerPP. Values are presented as mean ± SD. p < 0.05 was considered significant.
0.5 for the second 30 min and 0.21 thereafter. At the end of the 2 h post-resuscitation, the animals were then euthanized with an intravenous injection of 150 mg/kg sodium pentobarbital. A necropsy was routinely performed for documentation of possible injuries to the bony thorax and thoracic and abdominal viscera resulting from the surgical or CPR intervention or the presence of obfuscating diseases. 2.3. Measurements Aortic and right atrial pressures, ICP, electrocardiogram and ETCO2 values were continuously recorded on a PC-based dataacquisition system supported by WINDAQ software (DATAQ, Akron, OH). Baseline and post-resuscitation MAP were calculated as (systolic aortic pressure (SAP) + 2× diastolic aortic pressure (DAP))/3. During CPR, MAP was calculated as (SAP + DAP)/2 due to the 50% duty cycle. CorPP was calculated as the difference between decompression diastolic aortic and time-coincident right atrial pressures. CerPP was calculated by the following three ways: (1) maximum SAP minus coincident ICP; (2) end-diastolic aortic pressure minus diastolic ICP; (3) MAP minus mean ICP.8 Intrathoracic pressure and compression depth were measured in real time during CPR. Aortic blood pH, PCO2 , PO2 , hemoglobin and lactate concentrations were measured at baseline and hourly after resuscitation on 200 L aliquots of blood with a Stat Profile pHOx Plus L analyzer (Model PHOXplusL; Nova Biomedical Corporation, Waltham, MA).
ROSC Duration of CPR (min) Number of shocks to ROSC Epinephrine dosage (mg) Incidence of recurrent VF Chest compression depth (cm) Rib fracture (n)
MCC
Thumper
p
7/7 5.1 ± 0.4 1.0 ± 0.0 0.86 ± 0.26 1.4 ± 2.3 3.8 ± 0.5 1.1 ± 1.1
5/6 7.0 ± 4.0 2.0 ± 2.0 1.46 ± 1.37 9.2 ± 8.7 5.7 ± 0.6 3.5 ± 1.5
0.46 0.24 0.21 0.28 0.04
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Experimental paper
Miniaturized mechanical chest compressor improves calculated cerebral perfusion pressure without compromising intracranial pressure during cardiopulmonary resuscitation in a porcine model of cardiac arrest夽 Jiefeng Xu a,d , Xianwen Hu a , Zhengfei Yang a , Xiaobo Wu a , Joe Bisera a,b , Shijie Sun a,b , Wanchun Tang a,b,c,∗ a
Weil Institute of Critical Care Medicine, Rancho Mirage, CA, United States Keck School of Medicine of the University of Southern California, Los Angeles, CA, United States c Department of Emergency Medicine, School of Medicine of the University of California, San Diego, CA, United States d Department of Emergency Medicine, Yuyao People’s Hospital, Medical School of Ningbo University, Ningbo, China b
a r t i c l e
i n f o
Article history: Received 18 July 2013 Received in revised form 6 January 2014 Accepted 10 January 2014 Keywords: Cardiopulmonary resuscitation Cardiac arrest Hemodynamics Cerebral perfusion pressure Intracranial pressure Miniaturized chest compressor
a b s t r a c t Objective: One of the major goals of cardiopulmonary resuscitation (CPR) is to provide adequate oxygen delivery to the brain for minimizing cerebral injury resulted from cardiac arrest. The optimal chest compression during CPR should effectively improve brain perfusion without compromising intracranial pressure (ICP). Our previous study has demonstrated that the miniaturized mechanical chest compressor improved hemodynamic efficacy and the success of CPR. In the present study, we investigated the effects of the miniaturized chest compressor (MCC) on calculated cerebral perfusion pressure (CerPP) and ICP. Methods: Ventricular fibrillation was electrically induced and untreated for 7 min in 13 male domestic pigs weighing 39 ± 3 kg. The animals were randomized to receive mechanical chest compression with the MCC (n = 7), or the Thumper device (n = 6). CPR was performed for 5 min before defibrillation attempt by a single 150 J shock. At 2.5 min of CPR, the epinephrine at a dose of 20 g/kg was administered. Additional epinephrine was administered at an interval of 3 min thereafter. If resuscitation was not successful, CPR was resumed for an additional 2 min prior to the next defibrillation until successful resuscitation or for a total of 15 min. Post-resuscitated animals were observed for 2 h. Results: Significantly greater intrathoracic positive and negative pressures during compression and decompression phases of CPR were observed with the MCC when compared with the Thumper device. The MCC produced significantly greater coronary perfusion pressure and end-tidal carbon dioxide. There were no statistically significant differences in systolic and mean ICP between the two groups; however, both of the measurements were slightly greater in the MCC treated animals. Interestingly, the diastolic ICP was significantly lower in the MCC group, which was closely related to the significantly lower negative intrathoracic pressure in the animals that received the MCC. Most important, systolic, diastolic and mean calculated CerPP were all significantly greater in the animals receiving the MCC. Conclusions: In the present study, mechanical chest compression with the MCC significantly improved calculated CerPP but did not compromise ICP during CPR. It may provide a safe and effective chest compression during CPR. Protocol number: P1205. © 2014 Elsevier Ireland Ltd. All rights reserved.
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at http://dx.doi.org/10.1016/j.resuscitation.2014.01.014. ∗ Corresponding author at: Weil Institute of Critical Care Medicine, 35100 Bob Hope Drive, Rancho Mirage, CA 92270, United States. E-mail addresses: [email protected] (J. Xu), [email protected] (X. Hu), [email protected] (Z. Yang), Mike [email protected] (X. Wu), [email protected] (J. Bisera), [email protected] (S. Sun), [email protected] (W. Tang). 0300-9572/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.resuscitation.2014.01.014
684
J. Xu et al. / Resuscitation 85 (2014) 683–688
1. Introduction The primary goal of cardiopulmonary resuscitation (CPR) is to establish the critical levels of blood flow to the heart and brain until spontaneous circulation is restored. High-quality chest compression has been recognized as the key determinant for the success of resuscitation. The latest guidelines emphasize that chest compression should be performed with adequate rate and depth, complete chest recoil and minimized pauses.1 Conventional manual CPR is simple, quick, inexpensive and always available; however, even chest compression provided by trained or experienced rescuers often fails to meet the requirements of guidelines.2,3 In the specific clinical setting such as transferring the patients or vehicular transportation, the quality of manual chest compression is difficult to maintain.4 Mechanical chest compression delivers more consistent and reliable chest compression, eliminates the elements of rescuer fatigue and compression interruption and could potentially overcome the limitations of manual chest compression. Recent clinical studies have demonstrated that the mechanical devices were beneficial to provide continuous chest compression with minimizing no-chest compression intervals during ambulance transportation and interventional coronary catheterization.5,6 The cerebral blood flow is closely related to cerebral perfusion pressure (CerPP), which is defined as the difference between mean aortic pressure (MAP) and intracranial pressure (ICP). During the compression phase of CPR, increased intrathoracic pressure is usually accompanied with both increases in MAP and ICP. The increases in intrathoracic pressure may cause a greater increase in ICP than MAP which result in a decrease in CerPP.7 In the present study, we investigated the effects of a recently developed miniaturized mechanical chest compressor (MCC) on calculated CerPP and ICP in a porcine model of cardiac arrest (CA). We hypothesized that mechanical chest compression with the MCC would improve calculated CerPP but would not compromise ICP during CPR.
2. Materials and methods All animals received humane care in compliance with the “Principles of Laboratory Animal Care” formulated by the National Society for Medical Research and the Guide for the Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (8th edition. Washington, DC, National Academies Press, 2011). The protocol was approved by the Institutional Animal Care and Use Committee of the Weil Institute of Critical Care Medicine.
2.1. Animal preparation Thirteen male domestic pigs weighing 39 ± 3 kg were fasted overnight with the exception of free access to water. Anesthesia was initiated by intramuscular injection of ketamine (20 mg/kg) and completed by an ear vein injection of sodium pentobarbital (30 mg/kg). An additional dose of sodium pentobarbital (8 mg/kg) was injected at hourly intervals to maintain anesthesia. A cuffed endotracheal tube was advanced into the trachea. The animals were mechanically ventilated with a volume controlled ventilator (Model MA-1, Puritan Bennett Inc., Carlsbad, CA) with a tidal volume of 15 ml/kg, peak flow of 40 l/min and FiO2 of 0.21. Endtidal carbon dioxide (ETCO2 ) was continuously monitored with an infrared capnometer (Model NPB-70, Nellcor Puritan Bennett Inc., Pleasanton, CA). Respiratory frequency was adjusted to maintain ETCO2 between 35 and 40 mm Hg. The conventional lead II electrocardiogram was continuously monitored by applying three
adhesive electrodes to the shaved skin of the right upper and left upper-and-lower limbs. For the measurement of ICP, a burr hole of 3 mm in diameter was drilled in the midst between the left eyebrow and the posterior bony prominence. A 5 F transducer-tipped Millar catheter (Model SPC-450S, Millar Instruments Inc., Houston, TX) was inserted 2 cm into the parietal lobe and then reflected ICP continuously. The catheter was firmly fixed with bolts and sutures around the skull. For the measurement of aortic pressure and the collection of blood samples, a fluid-filled 8 F catheter (Model 6523, USCI, C.R. Bard Inc., Salt Lake City, UT) was advanced from the right femoral artery into the thoracic aorta. For the measurements of right atrial pressure and core (blood) temperature, a 7 F pentalumen, thermodilutiontipped catheter (Abbott Critical Care # 41216, Chicago, IL) was advanced from the right femoral vein into the right atrium. Both catheters were flushed intermittently with saline containing 5 IU bovine heparin per ml. For inducing ventricular fibrillation (VF), a 5 F pacing catheter (EP Technologies Inc., Mountain View, CA) was advanced from the right subclavian vein into the right ventricle. For the measurement of intrathoracic pressure, another 5 F Millar catheter was advanced from the incisor teeth into the esophagus for a distance of 35 cm. The position of all catheters was confirmed by characteristic pressure morphology and with fluoroscopy. In addition, the depth of chest compression during CPR was measured by a linear potentiometer. The piston of the compressor was positioned in the midline at the level of the fifth interspace. Blood temperature was maintained at 37.5 ± 0.5 ◦ C with the aid of a cooling/warm blanket throughout the entire experiment. 2.2. Experimental procedures Fifteen minutes prior to inducing VF, baseline measurements were obtained. The animals were randomized by the Sealed Envelope Method to receive mechanical chest compression with the MCC (Resuscitation International Inc., Scottsdale, AZ) (n = 7) or the Thumper device (Model 1004, Michigan Instruments Inc., Grand Rapids, MI) (n = 6). VF was induced by 1 mA alternating current through the 5 F pacing catheter, delivered to the right ventricular endocardium. Mechanical ventilation was discontinued after onset of VF. Prior to initiating the resuscitation protocol, the pacing catheter was withdrawn to avoid heart injury during chest compression. After 7 min of untreated VF, CPR was started. Both the MCC and Thumper devices were programmed to provide an equal compression-relaxation interval of 50% duty cycle and the same compression rate of 100 compressions per minute. The initial compression depth of the MCC and Thumper devices was adjusted to achieve a threshold coronary perfusion pressure (CorPP) of above 12 mm Hg in 1 min. Coincident with the start of precordial compression, the animals were mechanically ventilated with a tidal volume of 15 ml/kg, FiO2 of 1.0 and a rate of 10 breaths per minute. After 2.5 min of CPR, the first bolus of epinephrine at a dose of 20 g/kg was administered. After 5 min of CPR, defibrillation was attempted with a single 150-J biphasic waveform electrical shock delivered between the conventional right infraclavicular electrode and the apical electrode with a Heartstart XL defibrillator (Philips Medical System Inc., Andover, MA). If an organized rhythm with a MAP of above 50 mm Hg persisted for an interval of 5 min or more, the animal was regarded as return of spontaneous circulation (ROSC). With failure to achieve ROSC, chest compression and ventilation were immediately resumed for 2 min prior to another defibrillation. The protocol was repeated until successful resuscitation or for a total of 15 min. Additional doses of epinephrine were administered at an interval of 3 min after the first bolus injection. After successful resuscitation, the animals were observed for 2 h. If a recurrent VF occurred after ROSC, a 150-J electrical shock was attempted. Mechanical ventilation was continued with FiO2 of 1.0 for 30 min,
J. Xu et al. / Resuscitation 85 (2014) 683–688 Table 1 Baseline characteristics.
Table 2 Cardiopulmonary resuscitation outcomes. MCC
Body weight (kg) Heart rate (beats min−1 ) MAP (mm Hg) End-tidal CO2 (mm Hg) SICP (mm Hg) MICP (mm Hg) DICP (mm Hg) SCerPP (mm Hg) MCerPP (mm Hg) DCerPP (mm Hg) Arterial lactate (mmol L−1 )
685
38.1 114 107 39.9 18.7 17.2 16.5 107 90 81 0.9
Thumper ± ± ± ± ± ± ± ± ± ± ±
1.9 8 6 1.7 1.4 1.7 2.1 5 5 6 0.1
39.2 118 109 39.7 18.6 17.5 16.9 108 92 83 0.9
± ± ± ± ± ± ± ± ± ± ±
3.5 9 6 0.5 1.2 1.2 1.3 5 6 7 0.2
p 0.49 0.47 0.49 0.79 0.96 0.75 0.67 0.60 0.51 0.53 0.43
MCC, miniaturized chest compressor; MAP, mean aortic pressure; SICP, systolic intracranial pressure; DICP, diastolic ICP; MICP, mean ICP; SCerPP, systolic cerebral perfusion pressure; DCerPP, diastolic CerPP; MCerPP, mean CerPP. Values are presented as mean ± SD. p < 0.05 was considered significant.
0.5 for the second 30 min and 0.21 thereafter. At the end of the 2 h post-resuscitation, the animals were then euthanized with an intravenous injection of 150 mg/kg sodium pentobarbital. A necropsy was routinely performed for documentation of possible injuries to the bony thorax and thoracic and abdominal viscera resulting from the surgical or CPR intervention or the presence of obfuscating diseases. 2.3. Measurements Aortic and right atrial pressures, ICP, electrocardiogram and ETCO2 values were continuously recorded on a PC-based dataacquisition system supported by WINDAQ software (DATAQ, Akron, OH). Baseline and post-resuscitation MAP were calculated as (systolic aortic pressure (SAP) + 2× diastolic aortic pressure (DAP))/3. During CPR, MAP was calculated as (SAP + DAP)/2 due to the 50% duty cycle. CorPP was calculated as the difference between decompression diastolic aortic and time-coincident right atrial pressures. CerPP was calculated by the following three ways: (1) maximum SAP minus coincident ICP; (2) end-diastolic aortic pressure minus diastolic ICP; (3) MAP minus mean ICP.8 Intrathoracic pressure and compression depth were measured in real time during CPR. Aortic blood pH, PCO2 , PO2 , hemoglobin and lactate concentrations were measured at baseline and hourly after resuscitation on 200 L aliquots of blood with a Stat Profile pHOx Plus L analyzer (Model PHOXplusL; Nova Biomedical Corporation, Waltham, MA).
ROSC Duration of CPR (min) Number of shocks to ROSC Epinephrine dosage (mg) Incidence of recurrent VF Chest compression depth (cm) Rib fracture (n)
MCC
Thumper
p
7/7 5.1 ± 0.4 1.0 ± 0.0 0.86 ± 0.26 1.4 ± 2.3 3.8 ± 0.5 1.1 ± 1.1
5/6 7.0 ± 4.0 2.0 ± 2.0 1.46 ± 1.37 9.2 ± 8.7 5.7 ± 0.6 3.5 ± 1.5
0.46 0.24 0.21 0.28 0.04
