Cindy H Hsu1, Mohamad H Tiba2, André L Boehman3, Brendan M McCracken4, Danielle C Leander5, Stephanie C Francalancia6, Zachary Pickell7, Thomas H Sanderson8, Kevin R Ward9, Robert W Neumar10. 1. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Department of Surgery, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: hcindy@med.umich.edu. 2. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: tibam@med.umich.edu. 3. Department of Mechanical Engineering, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: boehman@umich.edu. 4. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: bmccrac@med.umich.edu. 5. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: danlean@umich.edu. 6. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: sfranc@umich.edu. 7. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; College of Literature Science and the Arts, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: zpickell@umich.edu. 8. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Department of Molecular and Integrative Physiology, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: thsand@med.umich.edu. 9. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Department of Biomedical Engineering, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: keward@med.umich.edu. 10. Department of Emergency Medicine, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA; Michigan Center for Integrative Research in Critical Care, University of Michigan Medical School, 2800 Plymouth Road, Ann Arbor, MI, 48109, USA. Electronic address: neumar@med.umich.edu.
Abstract
AIM: It remains unclear whether cardiac arrest (CA) resuscitation generates aerosols that can transmit respiratory pathogens. We hypothesize that chest compression and defibrillation generate aerosols that could contain the SARS-CoV-2 virus in a swine CA model. METHODS: To simulate witnessed CA with bystander-initiated cardiopulmonary resuscitation, 3 female non-intubated swine underwent 4 minutes of ventricular fibrillation without chest compression or defibrillation (no-flow) followed by ten 2-minute cycles of mechanical chest compression and defibrillation without ventilation. The diameter (0.3-10 µm) and quantity of aerosols generated during 45-second intervals of no-flow and chest compression before and after defibrillation were analyzed by a particle analyzer. Aerosols generated from the coughs of 4 healthy human subjects were also compared to aerosols generated by swine. RESULTS: There was no significant difference between the total aerosols generated during chest compression before defibrillation compared to no-flow. In contrast, chest compression after defibrillation generated significantly more aerosols than chest compression before defibrillation or no-flow (72.4 ± 41.6 × 104 vs 12.3 ± 8.3 × 104 vs 10.5 ± 11.2 × 104; p < 0.05), with a shift in particle size toward larger aerosols. Two consecutive human coughs generated 54.7 ± 33.9 × 104 aerosols with a size distribution smaller than post-defibrillation chest compression. CONCLUSIONS: Chest compressions alone did not cause significant aerosol generation in this swine model. However, increased aerosol generation was detected during chest compression immediately following defibrillation. Additional research is needed to elucidate the clinical significance and mechanisms by which aerosol generation during chest compression is modified by defibrillation.
AIM: It remains unclear whether cardiac arrest (CA) resuscitation generates aerosols that can transmit respiratory pathogens. We hypothesize that chest compression and defibrillation generate aerosols that could contain the SARS-CoV-2 virus in a swine CA model. METHODS: To simulate witnessed CA with bystander-initiated cardiopulmonary resuscitation, 3 female non-intubated swine underwent 4 minutes of ventricular fibrillation without chest compression or defibrillation (no-flow) followed by ten 2-minute cycles of mechanical chest compression and defibrillation without ventilation. The diameter (0.3-10 µm) and quantity of aerosols generated during 45-second intervals of no-flow and chest compression before and after defibrillation were analyzed by a particle analyzer. Aerosols generated from the coughs of 4 healthy human subjects were also compared to aerosols generated by swine. RESULTS: There was no significant difference between the total aerosols generated during chest compression before defibrillation compared to no-flow. In contrast, chest compression after defibrillation generated significantly more aerosols than chest compression before defibrillation or no-flow (72.4 ± 41.6 × 104 vs 12.3 ± 8.3 × 104 vs 10.5 ± 11.2 × 104; p < 0.05), with a shift in particle size toward larger aerosols. Two consecutive humancoughs generated 54.7 ± 33.9 × 104 aerosols with a size distribution smaller than post-defibrillation chest compression. CONCLUSIONS: Chest compressions alone did not cause significant aerosol generation in this swine model. However, increased aerosol generation was detected during chest compression immediately following defibrillation. Additional research is needed to elucidate the clinical significance and mechanisms by which aerosol generation during chest compression is modified by defibrillation.
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