The effect of compression duration on hemodynamics during mechanical high-impulse CPR

Acad Emerg Med. Sep-Oct 1994;1(5):430-7. doi: 10.1111/j.1553-2712.1994.tb02522.x.


Objective: To determine whether shorter compression durations combined with fixed increased compression velocity during mechanical high-impulse CPR (HI-CPR) improve resuscitation hemodynamics, compared with mechanical standard CPR (SCPR).

Methods: A porcine model of ventricular fibrillation was used, with each animal serving as its own control. Twelve anesthetized swine (20-25 kg each) were instrumented for hemodynamic monitoring. Ventricular fibrillation was induced and followed, after 3 minutes, by mechanical SCPR (50% duty cycle) for 10 minutes. Mechanical HI-CPR was then applied, with compression durations varied randomly at 2-minute intervals for 20% (COM20), 30% (COM30), and 40% (COM40) of the CPR cycle. A 2-minute mechanical SCPR control phase completed the experiment.

Results: Hemodynamic measurements were significantly better for COM20 and COM30 vs SCPR, including, respectively: mean arterial pressure (MAP), 45 +/- 8 and 43 +/- 7 vs 36 +/- 7 torr; coronary perfusion pressure (CPP), 21 +/- 6 and 21 +/- 8 vs 16 +/- 6 torr; and end-tidal CO2 (ETCO2), 7 +/- 2 and 6.6 +/- 2 vs 5 +/- 1.4 torr. MAP, CPP, and ETCO2 during COM40 were not significantly different from those during SCPR, and there was no difference between COM20 and COM30 for any hemodynamic parameter. Aortic flow velocity was significantly better in COM20, COM30, and COM40 vs SCPR: 2.3 +/- 0.7, 2.1 +/- 0.9, and 1.95 +/- 0.9 vs 1.3 +/- 0.5 cm/sec, respectively.

Conclusion: In a swine model of mechanical HI-CPR, shorter compression durations combined with fixed increased compression velocity significantly improve resuscitation hemodynamics, compared with those afforded by mechanical SCPR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiopulmonary Resuscitation / methods*
  • Hemodynamics
  • Swine
  • Time Factors
  • Ventricular Fibrillation / physiopathology
  • Ventricular Fibrillation / therapy*