Johanna C Moore1, Joe Holley2, Nicolas Segal3, Michael C Lick4, José Labarère5, Ralph J Frascone6, Kenneth W Dodd7, Aaron E Robinson7, Charles Lick8, Lauren Klein7, Andrew Ashton9, Angela McArthur9, Adamantios Tsangaris10, Anna Makaretz11, Mike Makaretz12, Guillaume Debaty13, Paul E Pepe14, Keith G Lurie15. 1. Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN, USA; Minneapolis Medical Research Foundation, Minneapolis, MN, USA. Electronic address: johanna.moore@hcmed.org. 2. Department of Emergency Medicine, University of Tennessee, Memphis, Medical Director, Memphis Fire Department and State of Tennessee, USA. 3. Department of Emergency Medicine, University of Minnesota, Minneapolis, MN, USA. 4. Minneapolis Medical Research Foundation, Minneapolis, MN, USA. 5. Quality of Care Unit, CIC 1406, INSERM, University Hospital of Grenoble Alps, Grenoble, France; University Grenoble Alps/CNRS/CHU de Grenoble Alpes/TIMC - IMAG UMR 5525, Grenoble, France. 6. Department of Emergency Medicine, Regions Hospital, St. Paul, MN, USA. 7. Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN, USA; Minneapolis Medical Research Foundation, Minneapolis, MN, USA. 8. Allina Health Emergency Medical Services, St. Paul, MN, USA. 9. Anatomy Bequest Program, University of Minnesota, Minneapolis, MN, USA. 10. Department of Medicine-Cardiovascular Division, University of Minnesota, Minneapolis, MN, USA. 11. Brown University School of Public Health, Providence, RI, USA. 12. Maine General Medical Center, Augusta, ME, USA. 13. University Grenoble Alps/CNRS/CHU de Grenoble Alpes/TIMC - IMAG UMR 5525, Grenoble, France. 14. Departments of Emergency Medicine, Internal Medicine, School of Public Health and Office of Health System Affairs, The University of Texas Southwestern Medical Center, Dallas, TX, USA. 15. Minneapolis Medical Research Foundation, Minneapolis, MN, USA; Department of Emergency Medicine, University of Minnesota, Minneapolis, MN, USA.
Abstract
AIM: The objectives were: 1) replicate key elements of Head Up (HUP) cardiopulmonary resuscitation (CPR) physiology in a traditional swine model of ventricular fibrillation (VF), 2) compare HUP CPR physiology in pig cadavers (PC) to the VF model 3) develop a new human cadaver (HC) CPR model, and 4) assess HUP CPR in HC. METHODS: Nine female pigs were intubated, and anesthetized. Venous, arterial, and intracranial access were obtained. After 6 min of VF, CPR was performed for 2 min epochs as follows: Standard (S)-CPR supine (SUP), Active compression decompression (ACD) CPR + impedance threshold device (ITD-16) CPR SUP, then ACD + ITD HUP CPR. The same sequence was performed in PC 3 h later. In 9 HC, similar vascular and intracranial access were obtained and CPR performed for 1 min epochs using the same sequence as above. RESULTS: The mean cerebral perfusion pressure (CerPP, mmHg) was 14.5 ± 6 for ACD + ITD SUP and 28.7 ± 10 for ACD + ITD HUP (p = .007) in VF, -3.6 ± 5 for ACD + ITD SUP and 7.8 ± 9 for ACD + ITD HUP (p = .007) in PC, and 1.3 ± 4 for ACD + ITD SUP and 11.3 ± 5 for ACD + ITD HUP (p = .007) in HC. Mean systolic and diastolic intracranial pressures (ICP) (mmHg) were significantly lower in the ACD + ITD HUP group versus the ACD + ITD SUP group in all three CPR models. CONCLUSION: HUP CPR decreased ICP while increasing CerPP in pigs in VF as well as in PC and HC CPR models. This first-time demonstration of HUP CPR physiology in humans provides important implications for future resuscitation research and treatment.
AIM: The objectives were: 1) replicate key elements of Head Up (HUP) cardiopulmonary resuscitation (CPR) physiology in a traditional swine model of ventricular fibrillation (VF), 2) compare HUP CPR physiology in pig cadavers (PC) to the VF model 3) develop a new human cadaver (HC) CPR model, and 4) assess HUP CPR in HC. METHODS: Nine female pigs were intubated, and anesthetized. Venous, arterial, and intracranial access were obtained. After 6 min of VF, CPR was performed for 2 min epochs as follows: Standard (S)-CPR supine (SUP), Active compression decompression (ACD) CPR + impedance threshold device (ITD-16) CPR SUP, then ACD + ITD HUP CPR. The same sequence was performed in PC 3 h later. In 9 HC, similar vascular and intracranial access were obtained and CPR performed for 1 min epochs using the same sequence as above. RESULTS: The mean cerebral perfusion pressure (CerPP, mmHg) was 14.5 ± 6 for ACD + ITD SUP and 28.7 ± 10 for ACD + ITD HUP (p = .007) in VF, -3.6 ± 5 for ACD + ITD SUP and 7.8 ± 9 for ACD + ITD HUP (p = .007) in PC, and 1.3 ± 4 for ACD + ITD SUP and 11.3 ± 5 for ACD + ITD HUP (p = .007) in HC. Mean systolic and diastolic intracranial pressures (ICP) (mmHg) were significantly lower in the ACD + ITD HUP group versus the ACD + ITD SUP group in all three CPR models. CONCLUSION: HUP CPR decreased ICP while increasing CerPP in pigs in VF as well as in PC and HC CPR models. This first-time demonstration of HUP CPR physiology in humans provides important implications for future resuscitation research and treatment.
Keywords:
Active compression decompression CPR; Cardiac arrest; Cardiopulmonary resuscitation; Cerebral perfusion; Head up CPR; Human cadaver; Impedance threshold device; Swine
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