Postoperative analgesia by nicomorphine intramuscularly versus high thoracic epidural administration. Effects on ventilatory and airway occlusion pressure responses to CO2.
In this study the effects of nicomorphine, administered either intramuscularly or by high thoracic epidural route, on the ventilatory and airway occlusion pressure response to CO2 were investigated and compared. Twenty-four patients scheduled for thoracic surgery were allocated randomly to postoperative pain relief by i.m. nicomorphine or by high thoracic epidural nicomorphine. The ventilatory response to 5% carbon dioxide was measured in all patients: first 1 day before operation, secondly on the first day after surgery immediately before nicomorphine administration and finally after the administration, at the moment when no further rise in end-tidal PCO2 (PETCO2) was measured. Respiratory response was assessed in two ways, by measuring minute ventilation (VE) and mouth occlusion pressure (P0.1). There was a significant depression in ventilatory response to CO2 in the intramuscular group (P = 0.03) due to nicomorphine as assessed by the slope of VE vs PETCO2. No significant depression was found in the epidural group, irrespective of measurement of VE or P0.1. No significant shift of apnoeic threshold-PETCO2 was observed in either group.
D000698:Analgesia; D002245:Carbon Dioxide; D006801:Humans; D007268:Injections, Epidural; D007273:Injections, Intramuscular; D009022:Morphine Derivatives / Q000008:administration & dosage* / Q000627:therapeutic use; D009539:Nicotinic Acids / Q000008:administration & dosage / Q000627:therapeutic use; D010149:Postoperative Pain / Q000517:prevention & control*; D012119:Respiration / Q000187:drug effects; D012129:Respiratory Function Tests; D013903:Thoracic Surgery
D009022:Morphine Derivatives; D009539:Nicotinic Acids; D002245:Carbon Dioxide; C008549:nicomorphine