Mohamad Hakam Tiba1, Brendan M McCracken2, Brandon C Cummings3, Carmen I Colmenero4, Chandler J Rygalski5, Cindy H Hsu6, Thomas H Sanderson7, Brahmajee K Nallamothu8, Robert W Neumar9, Kevin R Ward10. 1. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: tibam@med.umich.edu. 2. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: bmccrac@med.umich.edu. 3. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: cummingb@med.umich.edu. 4. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: cico@med.umich.edu. 5. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Molecular and Integrative Physiology, United States. Electronic address: rygalski.5@buckeyemail.osu.edu. 6. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States; University of Michigan, Department of Surgery. Electronic address: hcindy@med.umich.edu. 7. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Molecular and Integrative Physiology, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: thsand@med.umich.edu. 8. University of Michigan, Department of Internal Medicine, Division of Cardiology, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: bnallamo@med.umich.edu. 9. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: neumar@med.umich.edu. 10. University of Michigan, Department of Emergency Medicine, United States; University of Michigan, Department of Biomedical Engineering, United States; University of Michigan, Department of Michigan Center for Integrative Research in Critical Care, United States. Electronic address: keward@med.umich.edu.
Abstract
AIM: We examined the use of a Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) catheter during cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) to assess its effect on haemodynamics such as coronary perfusion pressure (CPP), common carotid artery blood flow (CCA-flow) and end-tidal CO2 (PetCO2) which are associated with increased return of spontaneous circulation (ROSC). METHODS: Six male swine were instrumented to measure CPP, CCA-Flow, and PetCO2. A 7Fr REBOA was advanced into zone-1 of the aorta through the femoral artery. Ventricular fibrillation was induced and untreated for 8 min. CPR (manual then mechanical) was initiated for 24 min. Continuous infusion of adrenaline (epinephrine) was started at minute-4 of CPR. The REBOA balloon was inflated at minute-16 for 3 min and then deflated/inflated every 3 min for 3 cycles. Animals were defibrillated up to 6 times after the final cycle. Animals achieving ROSC were monitored for 25 min. RESULTS: Data showed significant differences between balloon deflation and inflation periods for CPP, CCA-Flow, and PetCO2 (p < 0.0001) with an average difference (SD) of 13.7 (2.28) mmHg, 15.5 (14.12) mL min-1 and -4 (2.76) mmHg respectively. Three animals achieved ROSC and had significantly higher mean CPP (54 vs. 18 mmHg), CCA-Flow (262 vs. 135 mL min-1) and PetCO2 (16 vs. 8 mmHg) (p < 0.0001) throughout inflation periods than No-ROSC animals. Aortic histology did not reveal any significant changes produced by balloon inflation. CONCLUSION: REBOA significantly increased CPP and CCA-Flow in this model of prolonged CA. These increases may contribute to the ability to achieve ROSC.
AIM: We examined the use of a Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) catheter during cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) to assess its effect on haemodynamics such as coronary perfusion pressure (CPP), common carotid artery blood flow (CCA-flow) and end-tidal CO2 (PetCO2) which are associated with increased return of spontaneous circulation (ROSC). METHODS: Six male swine were instrumented to measure CPP, CCA-Flow, and PetCO2. A 7Fr REBOA was advanced into zone-1 of the aorta through the femoral artery. Ventricular fibrillation was induced and untreated for 8 min. CPR (manual then mechanical) was initiated for 24 min. Continuous infusion of adrenaline (epinephrine) was started at minute-4 of CPR. The REBOA balloon was inflated at minute-16 for 3 min and then deflated/inflated every 3 min for 3 cycles. Animals were defibrillated up to 6 times after the final cycle. Animals achieving ROSC were monitored for 25 min. RESULTS: Data showed significant differences between balloon deflation and inflation periods for CPP, CCA-Flow, and PetCO2 (p < 0.0001) with an average difference (SD) of 13.7 (2.28) mmHg, 15.5 (14.12) mL min-1 and -4 (2.76) mmHg respectively. Three animals achieved ROSC and had significantly higher mean CPP (54 vs. 18 mmHg), CCA-Flow (262 vs. 135 mL min-1) and PetCO2 (16 vs. 8 mmHg) (p < 0.0001) throughout inflation periods than No-ROSC animals. Aortic histology did not reveal any significant changes produced by balloon inflation. CONCLUSION: REBOA significantly increased CPP and CCA-Flow in this model of prolonged CA. These increases may contribute to the ability to achieve ROSC.
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