Effect of pain and analgesia on compensatory reserve

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The measurement of the body’s capacity to compensate for reduced blood volume can be assessed with a compensatory reserve measurement (CRM). The CRM, which is calculated from changes in features of the arterial waveform, represents the integration of compensatory mechanisms during states of low tissue perfusion and oxygenation, such as hemorrhage. This study was designed to test the hypothesis that pain which activates compensatory mechanisms and analgesia that result in reduced blood pressure are associated with lower compensatory reserve. This study evaluated CRM in obstetric patients during labor as pain intensity increased from no pain to severe pain and compared CRM before and after epidural anesthesia.


CRM was calculated from a finger pulse oximeter placed on the patient’s index finger and connected to the DataOx monitor in healthy pregnant women (n = 20) before and during the active labor phase of childbirth.


As pain intensity, based on an 11-point scale (0, no pain; 10, worst pain), increased from 0 to 8.4 ± 0.9 (mean ± SD), CRM was not affected (81 ± 10% to 82 ± 13%). Before analgesia, CRM was 84 ± 10%. CRM at 10 minutes, 20 minutes, 30 minutes, 40 minutes, 50 minutes, and 60 minutes after analgesia was 82 ± 11%, 83 ± 14%, 83 ± 15%, 86 ± 12%, 89 ± 9%, and 87 ± 10%, respectively. There was a transient 2% reduction followed by a 5% increase in CRM from before to after epidural anesthesia (p = 0.048). Pain scores before and after analgesia were 7 ± 2 and 1 ± 1, respectively (p < 0.001).


These results indicate that pain and analgesia contribute minimally, but independently to the reduction in compensatory reserve associated with trauma and hemorrhage. As such, our findings suggest that analgesia can be safely administered on the battlefield while maintaining the maximal capacity of mechanisms to compensate for blood loss.


Diagnostic study, level II.

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