This study was conducted to investigate the importance of the depth of chest compression in producing effective cardiopulmonary resuscitation (CPR) in animals, as indicated by cardiac output and mean arterial blood pressure. Cardiac output was measured by a modified indicator dilution technique in 8 anesthetized dogs, 6 to 12 kg body weight, during repeated 2-minute episodes of electrically induced ventricular fibrillation and CPR provided by a mechanical chest compressor and ventilator (Thumper ® ). Chest compression exceeding a threshold value (x0) between 1.5 and 3.0 cm was required in each animal to produce measurable cardiac output. In particular, cardiac output (CO) was linearly related to chest compression depth (x) by an expression of the form CO = a(x-x0) for x > x0, and CO = 0 for x  x0. The mean value of x0 was 2.3 cm. A similar threshold for measurable blood pressure was observed in 7 of the 8 dogs, with a mean value of 1.8 cm. For chest compression of 2.5 cm or greater, relatively modest increases in chest compression depth caused relatively large changes in cardiac output.

Davis, Robert W.; and Silver, Douglas I., "Cardiac output during cardiopulmonary resuscitation at various compression rates and durations" (1981) AbstractCardiac output during cardiopulmonary resuscitation (CPR) was measured by a modified indicator-dilution technique in 20 anesthetized dogs (6-12 kg) during repeated 1-to 2-min episodes of electrically induced ventricular fibrillation and CPR, produced by a mechanical chest compressor and ventilator. With compression rates from 20 to 140/min and compression durations (duty cycles) from 10 to 90% of cycle time, cardiac output (CO) was predicted by the equation:where CR is compression rate, DC is duty cycle, SVmax (19 ml) is the effective capacity of the pumping chamber, and kl (0.00207 min) and k2 (0.00707 min) are ejection and filling constants. This expression predicts maximal CO for DC = 0.40 and CR = 126/min as well as 90-100% of maximal CO for 0.3 < DC < 0.5 and 70 < CR < 150/min. Such mathematical analysis may prove useful in the optimization of CPR.

This study was conducted to determine the effects of high pressure interposed ventilations during cardiopulmonary resuscitation (CPR). Cardiac output was measured by a modified indicator dilution technique in eight anesthetized, intubated mongrel dogs. Positive pressure ventilations (12/min, 80% O 2 ) were interposed after every five chest compressions (performed at 62/min) by a mechanical chest compressor (Thumper ® ). On repeated trials in the same animal, ventilation pressures from 10-50 cm of H 2 O were tested in randomized sequence, while the technique of chest compression was held constant. Arterial blood gases immediately after resuscitation were monitored. Increasing ventilation pressure had surprisingly little effect on cardiac output during CPR, although blood gases were profoundly altered. For ventilation pressures of 10, 20, 30, 40, and 50 cm of H 2 O, producing mean tidal volumes 23, 38, 61, 83, and 94 ml/kg; cardiac output remained nearly constant, averaging 21, 25, 23, 26, and 24 ml/min/kg. Corresponding mean post-resuscitation pH was 7.24, 7.41, 7.51, 7.56, and 7.53; PCO 2 was 41, 26, 18, 16, and 15 torr. The post-resuscitation arterial oxygen tension was greater than 100 torr at all ventilation pressures except 10 cm of H 2 O. Interposed ventilations of pressure and volume more than adequate to prevent acidosis during CPR did not impair artificial cardiac output. If anything, cardiac output was slightly improved by more forceful ventilation.2