Neurohumorally induced cardiac dysrhythmias during nitrous oxide-oxygen-thiopental anesthesia.

Barbiturate, nitrous oxide, and oxygen are commonly used by the oral and maxillofacial surgeon to anesthetize the ambulatory oral surgery patient. The authors report three cases of ventricular dysrhythmia occurring from surgical stimulation during nitrous oxide-oxygen-thiopental anesthesia. These dysrhythmias were most likely mediated via direct neural stimulation of cardiac sympathetic nerves. Concomitant with adrenergic stimulation, a rise in the arterial plasma norepinephrine level was documented, along with an increase in the rate-pressure product. Immediate recognition and treatment of ventricular dysrhythmia is mandatory to preclude further serious cardiovascular complications or death.

Arterial plasma epinephrine concentrations and hemodynamic responses after dental injection of local anesthetic with epinephrine.

The effect of dental injection of local anesthetic on arterial plasma epinephrine concentrations and cardiovascular functions was assessed in patients having a maxillary third molar extracted. After three and five minutes, arterial plasma epinephrine concentrations were more than two times higher than baseline values in patients who were given an injection of a standard Carpule (1.8 ml) of 2% lidocaine with 1/100,000 epinephrine (18 micrograms). The heart rate and pressure-rate product increased slightly above baseline control values, and the mean arterial pressure declined slightly (P less than .05) after five minutes. Patients who received an injection of lidocaine alone had no significant change of plasma epinephrine or of the cardiovascular parameters measured. Although the hemodynamic responses to lidocaine plus epinephrine in these healthy young adults were small, the significant increase of systemic plasma epinephrine concentrations suggests that high-risk patients who receive this type of anesthesia should be monitored carefully.

Effect of spinal anesthesia on adrenergic tone and the neuroendocrine responses to surgical stress in humans.

In order to quantitate the effect of spinal anesthesia on adrenergic tone, plasma levels of norepinephrine (NE) and epinephrine (EPI) were measured by radioenzymatic assay in 24 patients were then compared to those of 10 patients receiving inhalation anesthesia (halothane-nitrous oxide). High thoracic dermatome spinal anesthesia caused suppression of both arterial plasma NE and EPI and a fall of mean arterial pressure (MAP); in contrast, no changes of NE, EPI, or MAP were observed in patients receiving low spinal anesthesia. Overall, there was a relationship between the sensory dermatome anesthesia level and changes of both plasma NE (r = 0.71, P less than 0.001) and EPI (r = 0.52,P less than 0.02). In the inhalation anesthesia group, plasma NE increased during the operation and plasma levels of NE, EPI, growth hormone, and cortisol were elevated during the postoperative recovery period. These neuroendocrine responses to surgical stress were not observed in patients receiving either low or high spinal anesthesia. Thus, the effect of spinal anesthesia on adrenergic tone depends on the cord level of anesthesia and can be quantitated by measurement of plasma catecholamines. The neuroendocrine responses to surgical stress were prevented in patients who received low spinal anesthesia and who had no suppression of efferent adrenergic tone. These findings indicate that neural afferents from the site of tissue injury, which were blocked by low spinal anesthesia, mediated both the adrenergic and the hormonal responses to surgical stress in the inhalation anesthesia group.

Relationship of impaired insulin secretion during surgical stress to anesthesia and catecholamine release.

Impaired insulin secretion has been observed during surgical stress in man. To determine the relationship between insulin secretion during anesthesia and surgical stress and plasma levels of norepinephrine (NE) and epinephrine (Epi), studies were performed in 16 patients before and during elective minor surgical procedures. In 8 patients studied during halothane inhalation anesthesia before operation, the acute insulin response (AIR) to glucose (5 g, IV) fell to 51 +/- 3% of the preanesthesia AIR (mean +/- SEM; P < 0.001). This inhibition of AIR appeared unrelated to increased adrenergic activity, since during anesthesia alone, plasma NE did not change significantly and plasma Epi fell from 94 +/- 11 to 34 +/- 10 pg/ml (P < 0.01). During the postoperative recovery period in these patients, after discontinuation of the anesthesia, the AIR to glucose was 50 +/- 5% of the preanesthesia baseline response (P < 0.001). At this time, both plasma NE and Epi were increased compared to preanesthesia levels [NE: 240 +/- 40 (preanesthesia) vs. 340 +/- 43 (postoperative); Epi: 219 +/- 43 (preanesthesia) vs. 94 +/- 11 (postoperative); both P < 0.05]. In eight patients undergoing similar operations during low spinal anesthesia, no inhibition of the AIR to glucose occurred, and plasma NE and Epi did not increase significantly during or after the operation. During the recovery period, there was a relationship between plasma Epi and the degree of inhibition of the AIR to glucose (r = 0.70; n = 11; P < 0.05). Thus, inhibition of insulin secretion during surgical stress may be mediated both by direct effect of the anesthesia used and by activation of the sympathetic nervous system.

Effects of anesthesia and surgical stress on insulin secretion in man.

Surgical stress with inhalation anesthesia is associated with increased circulating catecholamines, hyperglycemia, and impaired insulin secretion. These changes do not occur during surgical stress with spinal anesthesia, suggesting that they are neurally mediated due to pain initiated afferents from the site of tissue trauma. Inhalation anesthesia alone was found to suppress basal insulin levels and the insulin response to intravenous glucose with no significant increase in plasma norepinephrine and a decrease in plasma epinephrine. Thus, these changes in insulin secretion are not attributable to adrenergic mechanisms. In the postoperative period, however, suppressed insulin secretion was found to be correlated with elevated plasma epinephrine concentrations and may, therefore, be mediated by adrenergic mechanisms. Thus, these findings indicate that impaired insulin secretion during surgical stress may have two etiologies--one related to the type of anesthesia used and the other due to adrenomedullary stimulation due to pain.

Limb blood flow. The influence of temperature during halothane-nitrous oxide anesthesia.

Twenty adult patients were examined before anesthesia, during anesthesia, and at the end of surgery to determine the influence of body cooling on limb blood flow during prolonged halothane-nitrous oxide anesthesia. Measurements included temperature, mean arterial pressure, and leg blood flow. Cooling was prevented in ten patients by warmed anesthetic gases. The mean tympanic temperature at end of surgery was 37 degrees C for the warmed (W) and 35 degrees C for the unwarmed (UW) patients, a significant difference. The mean value for leg blood flow was significantly decreased in the UW patients (W = 5.0 vs UW = 3.1 mL/100 cc of tissue/min). These results indicate that body cooling during prolonged inhalation anesthesia was associated with a reduced limb blood flow. Therefore, pulmonary warming may be of potential benefit under similar conditions to help prevent intraoperative vascular complications.

Arterial-venous differences of plasma catecholamines in man.

To investigate the relationship between forearm venous levels of catecholamines and systemic levels, simultaneous arterial and forearm vein blood samples were obtained from 14 subjects undergoing elective dental procedures and assayed with a sensitive and specific radioenzymatic assay. Baseline venous levels of norepinephrine were greater than arterial levels (305 +/- 30 pg/ml versus 221 +/- 18; +/- SEM, p less than .005). Conversely, arterial epinephrine levels were higher than venous (132 +/- 17 pg/ml versus 80 +/- 10; p less than .005). There was a significant relationship between arterial and venous levels of both norepinephrine (r = .77, p less than .01) and epinephrine (r = .67, p less than .01). The arterial-venous epinephrine difference increased from the baseline value of 44 +/- 14 pg/ml to 108 +/- 16 (p less than .005) by 3 min after subcutaneous injection of epinephrine (18 microgram), but the arterial-venous difference returned to 65 +/- 24 by 5 min after injection (p = NS versus baseline). These findings indicate that under the conditions of this study, forearm tissues produced more norepinephrine than they removed, but removed more epinephrine than they produced. Baseline venous and arterial levels were related; when epinephrine production was augmented, there was a short time lag for the venous epinephrine increase.

Sequence of return of neurological function and criteria for safe ambulation following subarachnoid block (spinal anaesthetic).

Twenty-three adult men were studied during and after subarachnoid block anaesthesia for elective surgery. Measurements were obtained of mean arterial pressure and pulse, both supine and after standing for five minutes, core body (tympanic) and peripheral skin (toe) temperatures and blood flow in the leg. Time of measurements included one hour after the injection of tetracaine and after regression of the block. Results obtained indicate that the sequence of return of neurological activity following tetracaine subarachnoid block is sympathetic nervous system activity, pinprick sensation, somatic motor function followed by proprioception in the feet. This progression provides the basis for recommended criteria which indicate when it is safe for patients who have been subarachnoid block anaesthesia to become ambulatory. These criteria include: (1) return of pinprick sensation in the peri-anal area (sacral 4--5); (2) plantar flexion of the foot (while supine) at pre-anaesthetic levels of strength; and (3) return of proprioception in the big toe, always provided that the patient is not hypovolaemic or sedated.

Prevention of post-anaesthesia shivering.

This study involves ventilation of the lungs with warmed humidifed anaesthetic gases during prolonged elective abdominal operations. Tympanic, oesophageal and toe temperatures were compared bewteen twenty warmed and twenty un-warmed patients at various times during operation and recovery. Fifty per cent (10/20) unwarmed patients shivered in the recovery room, while none of the warmed patients shivered. Our data indicate that pulmonary ventilation with warm humidified anaesthetic gases provides heat transfer by the lungs, preventing hypothermia during operation and post -anaesthesia shivering is prevented by maintaining the patient normothermic in both the operating room and the recovery room.

Physiopathology and control of postoperative pain.

Potent systemic (narcotic) analgesics, when given in doses sufficient to produce ample pain relief, usually also produce mental and respiratory depression and, at times, circulatory impairment, that prolong postoperative morbidity. Complications due to morphine sulfate or meperidine hydrochloride can be minimized by titrating the patient's pain with small intravenous doses of narcotics (morphine sulfate, 2 to 3 mg, or meperidine hydrochloride, 15 to 25 mg) administered slowly at 15- to 20-minute intervals until the pain is relieved. On the third or fourth postoperative day, acetaminophen tablets usually suffice to provide relief of pain with little or no risk to patients. Continuous segmental epidural block or intercostal block, with or without splanchnic block, provide excellent pain relief that, in contrast to the narcotic, is complete. These are especially useful after operations on the chest or abdomen or the lower extremity. Regional analgesia is especially indicated in patients not adequately relieved from severe postoperative pain with narcotics, or when these drugs are contraindicated by advanced pulmonary, renal, or hepatic disease. Continuous caudal analgesia is also effective to completely releive severe postoperative pain in the lower limbs and perineum.

Early reversal of postoperative hypoxemia.

Peridural analgesia was combined with the respiratory-stimulant effect of doxapram for intermittent hyperinflation of the lungs to reverse early postoperative (PO) hypoxemia following inhalation anesthesia for upper abdominal operations. Twenty unpremedicated men undergoing upper abdominal operations were studied for 5 hours in the recovery room. Ten of these patients received doxapram plus peridural analgesia; the other 10, doxapram plus morphine analgesia. Rectal temperature, PaO2, PaCO2, respiratory rate, exhaled minute ventilation (VE), tidal volume (VT), and blood pressure and pulse were measured. The mean increase from control for VE was 9.6 L/min and for VT, 356 ml/breath during doxapram therapy for the morphine group. Corresponding values for the peridural group were 14.4 L/min for VE and 660 ml/breath for VT. Mean PaO2 for the morphine group decreased significantly from the corresponding preoperative value (p less than 0.005). Lack of significant change between preoperative and PO values for PaO2 for the peridural group would indicate that under the conditions of this study, early PO hypoxemia can be reversed by the combination of peridural analgesia with doxapram therapy.

Pethidine revisited: plasma concentrations and effects after intramuscular injection.

Plasma concentrations of pethidine following i.m. gluteal injection were measured in surgical patients and volunteers. The mean plasma concentrations tended to be higher in the patients than in the volunteers; this may be a result of a slower initial absorption rate. At least 80% of the dose was absorbed from the injection site over the 6-hr period of the study. Fluctuations in plasma pethidine concentration were observed, probably caused by variations in local and systemic blood flow. This effect was more noticeable in the patient group. In general, the time-course of subjective effects in volunteers could be related to maximum plasma pethidine concentrations. However, patients appeared to be less sensitive to these effects at similar plasma drug concentrations, possibly because of catecholamine-mediated stimulus, suggesting that plasma concentrations may be a poor guide to the clinical response in patient-volunteer comparison.

Meperidine kinetics in man. Intravenous injection in surgical patients and volunteers.

The plasma concentration-time profiles of meperidine following intravenous injection in surgical patients and volunteers were investigated by reference to a classical two-compartment open model. Physiologic characteristics of the subject and variables associated with the surgery and anesthesia were screened as determinants of the kinetic patterns observed. When meperidine administration preceded induction of anesthesia, induction was consistently followed by an increase in venous plasma concentrations that prevented classical kinetic analysis. To facilitate calculations in subsequent studies in patients, meperidine injections were made following induction of anesthesia. Type of anesthesia or premedication, patients' sex, or cigarette smoking did not appear to be important factors in this evaluation. Increasing alcohol consumption was associated with increasing volumes of distribution. Increasing age was associated with increasing fraction of drug unbound in plasma. These factors may relate directly to clinical observations that heavy alcohol consumers tend to be more refractory to central nervous system (CNS) depressants and that elderly patients are more susceptible to respiratory depression from narcotics.