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

نویسندگان

  • C F Babbs
  • N Bircher
  • D E Burkett
  • H A Frissora
  • B C Hodgkin
  • P Safar
چکیده

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.

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عنوان ژورنال:
  • Critical care medicine

دوره 9 11  شماره 

صفحات  -

تاریخ انتشار 1981