Craig B. Caldwell

Transcutaneous electrical nerve stimulation: an alternative approach to the management of postoperative pain.

HE MANAGEMENT of postoperative pain has T been and continues to be a significant problem in surgical practice in terms of both the additional stress it places on the patient’s physiologic reserves and the symptomatic discomfort it causes. It is well known by practitioners that pain is an individual experience and this fact is reflected in a wide variation in the incidence and severity of pain and in the need for analgesics. A number of factors including age, anesthetic technique, personality of the patient, previous experience, physical status, site of operation, and surgical management affect the incidence of postoperative pain (1, 2). In light of the problems associated with postoperative pain, various strategies for the management of pain have been proposed. The most commonly used method stresses the use of systemic analgesics, narcotics, and related drugs. Regional analgesia offers an attractive alternative to the use of narcotics and tranquilizers in that respiratory depression and sedation are avoided and the patient can be made pain free for extended periods using long-acting local anesthetics.

The Effect of Lidocaine on the Ventilatory Response to Carbon Dioxide

The authors determined the effect of intravenous lidocaine, both as a bolus and as an infusion, on the ventilatory response to CO2. Bolus injection of 1.5 mg/kg lidocaine caused a decrease in the slope of the CO2 ventilatory response curve from 2.66 ± 0.30 (x ± SEM) to 1.31 ± 0.44 1 · min-1 · mmHg-1 within 90 s; the effect was transient, with slope returning to 2.39 ± 0.83 1 · min-1 · mmHg-1 150 s after injection. The transient, subconvulsive lidocaine concentrations present during ventilatory depression (8.9 ± 2.0 μg/ml) may be sufficient to desensitize the medullary ventilatory control centers.Lidocaine infusion at the rate of 60 μg · kg-1 · min-1 (serum lidocaine concentrations of 3.5 ± 0.2 μg/ml) increased the slope of steady state CO2 response curves from 2.89 ± 0.29 to 4.17 ± 0.44 1 · min-1 · mmHg-1 (P < 0.05); with discontinuation of the infusion, slope returned to 3.18 ± 0.33 1 · min-1 · mmHg-1 (P < 0.05).The authors conclude that bolus injection of lidocaine transiently can depress ventilatory control, however, rapid redistribution of lidocaine makes this a transient phenomenon that can be treated with supplemental oxygen if necessary. The increased CO2 sensitivity observed during lidocaine infusion suggests that studies of ventilatory control in patients receiving conduction anesthetics must take into account the direct effect of absorbed anesthetics on ventilatory control.

Modification of lidocaine protein binding with CO2

Using new, specially designed ultrafiltration devices and an enzyme immunoassay technique, the authors determined the effect of carbon dioxide tension on the fractional binding of lidocaine to human plasma proteins. Identical samples of serum at therapeutic (2.2 μg.ml-1 ) and toxic (6.8 μg.ml-1 ) lidocaine concentrations were tonometered at 37° C to CO2 tensions between 0.13 and 10.7 kPa (1.0 to 80.5 mmHg). The fraction of unbound lidocaine increased linearly with increasing pCO2 (r = 0.93, p < 0.001). These changes help to explain the increased central nervous system toxicity of lidocaine associated with hypercarbia.RésuméAvec I’utilisation d’un nouvel appareil conçu pour ultrafiltration et une technique enzymatique d’immunoassay, les auteurs ont déterminé les ejfets du CO2 sur la liaison fractionnelle de la lidocaine aux protéines plas-matiques humaines. Des échantillons identiques de strum à des doses thérapeutiques (2.2 µg-ml-1) et toxiques (6.8 µg-ml-1) de lidocaïne ont été étudiés par tonométrie à 37° Cpour despCO2 variant de 0.13 à10.7kPa (1.0 à 80.5 mmHg). La fraction de lidocaine non Ueée a augmenté d’une faeon linéaire avec l’augmentation de la pCO2 (r = 0.93, p < 0.001). Ces changements aident à expliquer l’augmentation de la toxicité de la lidocaïne sur le système nerveux central quand elle est associée è l’hypercarbie.

The effect of lidocaine infusion on the ventilatory response to hypoxia.

The authors studied the effect of lidocaine infusion on the ventilatory response to isocapnic hypoxia in nine healthy male subjects. Lidocaine infusion (serum concentration 3.6 ± 0.1 μg/ml) was associated with a decrease in the shape factor, “A,” of the hypoxic ventilatory response in eight of our nine subjects (P < 0.02). Overall, “A” decreased from 419 ± 102 1·min−1·mmHg before lidocaine to 335 ± 77 1·min−1·mmHg during lidocaine infusion (&OV0335; ± SEM, N = 9). The authors conclude that despite significant intersubject variability, clinically useful serum lidocaine concentrations depress hypoxic ventilatory drive. Patients with carbon dioxide retention, whose resting ventilation depends on hypoxic drive, may be at risk of ventilatory failure when lidocaine is administered for arrhythmia control or regional anesthesia.

Intraoperative fluid management influences carbon dioxide production and respiratory quotient.

The authors studied the effects of glucose-containing versus non-glucose-containing solutions for intraoperative fluid management on CO2 production and respiratory quotient (RQ) during the first postoperative hour. Three groups of patients were studied. Patients in Group 1 received normal saline during the operation and first postoperative hour; patients in Groups 2 and 3 received 5% glucose in half normal saline during the operation. This solution was continued through the postoperative period for patients in Group 2, while patients in Group 3 were given normal saline postoperatively. All patients received 500–1000 ml during the first hour and 500 ml/h thereafter. During the first postoperative hour, CO2 production and O2 consumption were measured every 15 min.RQ was significantly higher in Group 2 (0.93 ± 0.01) than in Group 1 (0.77 ± 0.01) (&OV0335; ± SEM, P < 0.05). CO2 production was about 20% higher in Group 2 than in Group 1. There were no differences in O2 consumption between Groups 1 and 2. In Group 3, RQ decreased significantly (from 0.97 ± 0.04 to 0.87 ± 0.03) during the first postoperative hour but remained higher than in Group 1. The authors conclude that intraoperative administration of glucose-containing solutions increases RQ postoperatively; this effect can be reversed partially by changing to glucose-free solutions in the postanesthetic period.

Induction dose-response curves for midazolam and ketamine in premedicated ASA class III and IV patients.

Using probit analysis, dose-response curves for induction of anesthesia with midazolam or ketamine were constructed in ASA class III and IV patients premedicated with morphine, 0.1 mg/kg, and glycopyrrolate, 4 μg/kg. For ketamine, ED50 values for abolition of the response to verbal commands, eyelash stimulation, and painful stimulation were 0.9, 1.3, and 1.3 mg/kg, respectively; corresponding ED95 values were 1.6, 2.3, and 4.3 mg/kg, which are within the range of clinically recommended doses. For midazolam, ED50 values for verbal commands, eyelash stimulation, and painful stimulation were 0.19, 0.24, and 0.36 mg/kg, significantly greater than those previously reported for unpremedicated ASA class I and II patients. The corresponding ED45 values, 0.35, 0.43, and 1.04 mg/kg exceed previously reported values and are appreciably greater than the doses used in most previous studies of midazolam inductionMidazolam decreased systolic blood pressure slightly but significantly (from 138 ± 4 to 128 ± 4 mm Hg, · &OV0398; sem, P < 0.005), while diastolic blood pressure and heart rate remained unchanged. In contrast, ketamine increased systolic blood pressure (from 141 ± 4 to 164 ± 5 mm Hg, P < 0.005), diastolic blood pressure (from 71 ± 3 to 88 ± 4 mm Hg, P < 0.005), and heart rate (from 84 ± 2 to 102 ± 4 beats/min, P < 0.005). On the basis of these data, we conclude that in ASA class III and IV patients, midazolam induction allows for hemodynamic stability and avoids the significant tachycardia and hypertension associated with equipotent doses of ketamine