Cardiac output during cardiopulmonary resuscitation at various compression rates and durations

Cardiac 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 \u3c DC \u3c 0.5 and 70 \u3c CR \u3c 150/min. Such mathematical analysis may prove useful in the optimization of CPR

Effect of thoracic venting on arterial pressure, and flow during external cardiopulmonary resuscitation in animals

To test the hypothesis that fluctuations in global intrathoracic pressure are the dominant cause of blood flow during external cardiopulmonary resuscitation (CPR) the authors studied the effects of open pneumothorax on experimental CPR in 7 domestic pigs and 12 mongrel dogs. Similar studies were conducted independently at three laboratories and are reported jointly. All studies were conducted during electrically induced ventricular fibrillation and with standard CPR technique, including ventral-dorsal chest compression at 60/min, 0.5 sec compression duration, 1:5ventilation:compression ratio. During alternate periods of CPR, intrathoracic pressure was vented through bilateral chest tubes, placed to create open pneumothorax and partial collapse of the lungs. During this maneuver, global intrathoracic pressure fluctuations were greatly attenuated, but direct but direct cardiac compression and adequate ventilation continued. In the three laboratories, systolic/diastolic arterial pressures during CPR with thoracic venting (± SE) averaged 68 ± 4.2/28 ± 3.3, 60 ± 10/18 ± 4.5, and 66 ± 6.3/23 ± 1.5 mm Hg. These values are compared to 68 ± 4.4/27 ± 3.0, 67 ± 12/17 ± 6.1, and 56± 6.2/22 ± 1.9 mm Hg with the thorax intact. Carotid artery mean flow, measured with an in-line flowmeter, was 13.0 ± 2.2 ml/min vented vs. 13.4 ± 2.6 intact in 7 pigs; 11.4 ± 3.8 ml/min vented vs. 11.2 ± 3.7 intact in 5 dogs. Cardiac output, determined by indicator dilution, was 25 ± 4.3 ml/min/kg vented vs. 20 ± 4.3 intact in 7 dogs. Thoracic venting did not decrease blood pressures and flows during CPR, as would be predicted from the hypothesis that generalized intrathoracic pressure fluctuations are the dominant hemodynamic mechanism. The results are consistent with the classical notion that CPR works by compression of the heart between the sternum and the spine. This mechanism should not be discounted in future attempts to improve CPR

Effect of thoracic venting on arterial pressure, and flow during external cardiopulmonary resuscitation in animals

To test the hypothesis that fluctuations in global intrathoracic pressure are the dominant cause of blood flow during external cardiopulmonary resuscitation (CPR) the authors studied the effects of open pneumothorax on experimental CPR in 7 domestic pigs and 12 mongrel dogs. Similar studies were conducted independently at three laboratories and are reported jointly. All studies were conducted during electrically induced ventricular fibrillation and with standard CPR technique, including ventral-dorsal chest compression at 60/min, 0.5 sec compression duration, 1:5ventilation:compression ratio. During alternate periods of CPR, intrathoracic pressure was vented through bilateral chest tubes, placed to create open pneumothorax and partial collapse of the lungs. During this maneuver, global intrathoracic pressure fluctuations were greatly attenuated, but direct but direct cardiac compression and adequate ventilation continued. In the three laboratories, systolic/diastolic arterial pressures during CPR with thoracic venting (± SE) averaged 68 ± 4.2/28 ± 3.3, 60 ± 10/18 ± 4.5, and 66 ± 6.3/23 ± 1.5 mm Hg. These values are compared to 68 ± 4.4/27 ± 3.0, 67 ± 12/17 ± 6.1, and 56± 6.2/22 ± 1.9 mm Hg with the thorax intact. Carotid artery mean flow, measured with an in-line flowmeter, was 13.0 ± 2.2 ml/min vented vs. 13.4 ± 2.6 intact in 7 pigs; 11.4 ± 3.8 ml/min vented vs. 11.2 ± 3.7 intact in 5 dogs. Cardiac output, determined by indicator dilution, was 25 ± 4.3 ml/min/kg vented vs. 20 ± 4.3 intact in 7 dogs. Thoracic venting did not decrease blood pressures and flows during CPR, as would be predicted from the hypothesis that generalized intrathoracic pressure fluctuations are the dominant hemodynamic mechanism. The results are consistent with the classical notion that CPR works by compression of the heart between the sternum and the spine. This mechanism should not be discounted in future attempts to improve CPR