Clinical observations suggest that the assumption of a linear relationship between chest compression pressure and cardiac output may be oversimplified. More complex behaviour may occur when the transmural pressure is large, changing the compliances and resistances in the intra-thoracic vasculature. A fundamental understanding of these compression induced phenomena is required for improving CPR. An extensively used, lumped element computer model (model I) of the circulation was upgraded and refined to include the intrathoracic vasculature (model II). After validation, model II was extended by adding variable compliances and resistances (model III) to the vascular structures. Successively, ranges of compression pressures, frequencies, duty cycles and compression pulse shapes were applied while controlling all other parameters. Cardiac output was then compared. The nonlinearities in compliance and resistance become important, limiting factors in cardiac output, starting in our experimental series at 70 mmHg peak compression pressure, and increasing with higher pressures. This effect is reproducible for sinusoidal and trapezoidal compression forms, resulting in lower cardiac output in all experiments at high compression pressures. Duty cycle and wait time are key parameters for cardiac output. Our data strongly indicate that vascular compliance, especially the ability of vessels to collapse (and potentially the cardiac chambers), can be a central factor in the limited output generated by chest compressions. Just pushing 'harder' or 'faster' is not always better, as an 'optimal' force and frequency may exist. Overly forceful compression can limit blood flow by restricting filling or depleting volume in the cardiac chambers and central great vessels.
|Publication status||Published - May 2011|
- Chest compressions
- Vascular collapse
- Cardiac output
- Duty cycle