Duty cycle of 33% increases cardiac output during cardiopulmonary resuscitation

PLoS One. 2020 Jan 28;15(1):e0228111. doi: 10.1371/journal.pone.0228111. eCollection 2020.

Abstract

Background: The aim of this study was to investigate whether 33% duty cycle increases end-tidal carbon dioxide (ETCO2) level, a surrogate measurement for cardiac output during cardiopulmonary resuscitation (CPR), compared with 50% duty cycle.

Methods: Six pigs were randomly assigned to the DC33 or DC50 group. After 3 min of induced ventricular fibrillation (VF), CPR was performed for 5 min with 33% duty cycle (DC33 group) or with 50% duty cycle (DC50 group) (phase I). Defibrillation was delivered until return of spontaneous circulation (ROSC) thereafter. After 30 min of stabilization, the animals were re-assigned to the opposite groups. VF was induced again, and CPR was performed (phase II). The primary outcome was ETCO2 during CPR, and the secondary outcomes were coronary perfusion pressure (CPP), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and right atrial pressure (RAP).

Results: Mean ETCO2 was higher in the DC33 group compared with the DC50 group (22.5 mmHg vs 21.5 mmHg, P = 0.018). In a linear mixed model, 33% duty cycle increased ETCO2 by 1.0 mmHg compared with 50% duty cycle (P < 0.001). ETCO2 increased over time in the DC33 group [0.6 mmHg/min] while ETCO2 decreased in the DC50 group [-0.6 mmHg/min] (P < 0.001). Duty cycle of 33% increased SAP (6.0 mmHg, P < 0.001), DAP (8.9 mmHg, P < 0.001) RAP (2.6 mmHg, P < 0.001) and CPP (4.7 mmHg, P < 0.001) compared with the duty cycle of 50%.

Conclusion: Duty cycle of 33% increased ETCO2, a surrogate measurement for cardiac output during CPR, compared with duty cycle of 50%. Moreover, ETCO2 increased over time during CPR with 33% duty cycle while ETCO2 decreased with 50% duty cycle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterial Pressure / physiology
  • Atrial Pressure / physiology
  • Capnography
  • Carbon Dioxide / analysis*
  • Carbon Dioxide / physiology
  • Cardiac Output / physiology*
  • Cardiopulmonary Resuscitation / methods*
  • Cerebrovascular Circulation / physiology
  • Disease Models, Animal
  • Male
  • Monitoring, Physiologic
  • Prospective Studies
  • Swine
  • Tidal Volume / physiology
  • Ventricular Fibrillation / physiopathology
  • Ventricular Fibrillation / therapy*
  • Ventricular Fibrillation / veterinary*

Substances

  • Carbon Dioxide

Grants and funding

This work was supported by Seoul National University Hospital (grant number 0420170380), and the grant was given to Gil Joon Suh.