J. Gilbert Stone

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent

In a non-double-blind, prospective, randomized study, the intraoperative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beat-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication-Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beat-adrenergic blocking agent had normal preoperative electroca rdiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a betaadrenergic blocking agent (P < 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untereated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beat-adrenergic blocking agent, given with premedication, can significantly reduce that risk.

Deliberate mild intraoperative hypothermia for craniotomy.

BackgroundDespite enthusiasm for the use of mild hypothermia during neurosurgical procedures, this therapy has not been evaluated systematically. This study examined the feasibility and safety of deliberate mild hypothermia and rewarming. MethodsThirty patients scheduled for craniotomy were assigned to either a normothermic or mildly hypothermic group. Tympanic membrane temperature was monitored at anesthetic induction, throughout the isoflurane-fentanyl-N2O-O2 anesthetic, and for 18 h postoperatively. Normothermic patients were warmed to 36.5–37.0°C after an initial temperature decrease, and hypothermic patients were cooled to 35°C. In the hypothermic group temperatures were allowed to drift to 34.5°C before rewarming was initiated. Water blankets and convective heating devices were used to cool and rewarm. ResultsThe minimum temperature achieved by the hypothermic group was 34.3 ± 0.4°C. Cooling occurred at a rate of 1.0 ± 0.4°C/h. Rewarming took place at a rate of 0.7 ± 0.6°C/h (range 0.1–1.8) in the hypothermic group. Hypothermia did not delay emergence from anesthesia (20 ± 15 min) compared with normothermia (15 ± 15 min, P = .45). Mean temperature upon intensive care unit admission was 35.8 ± 1.0°C for the hypothermic group and 37.1 ± 0.5°C for the normothermic group (P < 0.0001). The hypothermic patients had more postoperative shivering. From 8 to 18 h postoperatively the temperatures of the two groups were similar except for a slightly greater temperature in the hypothermic patients at 12 h (37.6 ± 0.5 vs. 37.3 ± 0.4°C, P = .029). ConclusionsAlthough deliberate mild hypothermia is easily achieved intraoperatively, complete rewarming may be difficult to attain during craniotomy with current methods. In addition to the need for determining whether deliberate mild hypothermia confers cerebral protection in humans, the potential risks of the therapy need to be further characterized.

Isolated Cerebral Hypothermia by Single Carotid Artery Perfusion of Extracorporeally Cooled Blood in Baboons

OBJECTIVE Hypothermia has been demonstrated to protect the brain from ischemic or traumatic injury. Previous efforts to induce cerebral hypothermia have relied on techniques requiring total body cooling that have resulted in serious cardiovascular derangements. A technique to selectively cool the brain, without systemic hypothermia, may have applications for the treatment of neurological disease. METHODS After induction of general anesthesia in 12 baboons, the right common carotid artery and ipsilateral femoral artery were each occlusively cannulated and joined to a centrifugal pump. In a closed-circuit system, blood was continually withdrawn from the femoral artery, cooled by water bath, and infused through the common carotid artery with its external branches occluded. Pump flow was varied so that right carotid pressure approximated systemic blood pressure. In six animals, perfusate was cooled to decrease right cerebral temperature to < 19 degrees C for 30 minutes. In six animals, right cerebral temperature was decreased to < 25 degrees C for 3 hours. In those six animals, 133Xe was injected into the right carotid artery before, during, and after hypothermia. Peak radioactivity and washout curves were recorded from bilateral cranial detectors. Systemic warming was accomplished by convective air and warm water blankets. Esophageal, rectal, and bilateral cerebral temperatures were continuously recorded. RESULTS In animals cooled to < 19 degrees C, right cerebral temperature decreased from 34 degrees C to 18.5 +/- 1.1 degrees C (mean +/- standard deviation), P < 0.01, in 26 +/- 13 minutes. Simultaneously, left cerebral temperature decreased to 20.7 +/- 1.6 degrees C. During 30 minutes of stable cerebral hypothermia, esophageal temperature decreased from 35.1 +/- 2.3 degrees C to 34.2 +/- 2.2 degrees C, P < 0.05. In animals cooled to < 25 degrees C, right cerebral temperature decreased from 34 degrees C to 24.5 +/- 0.6 degrees C in 12.0 +/- 6.0 minutes, P < 0.01. Simultaneously, left cerebral temperature decreased to 26.3 +/- 4.8 degrees C. After 3 hours of stable cerebral hypothermia, esophageal temperature was 34.4 +/- 0.5 degrees C, P < 0.05. Right hemispheric cerebral blood flow decreased during hypothermia (26 +/- 16 ml/min/100 g) compared to values before and after hypothermia (63 +/- 29 and 51 +/- 34 ml/min/100 g, respectively; P < 0.05). Furthermore, hypothermic perfusion resulted in a proportionally increased radioactivity peak detected in the left cerebral hemisphere after right carotid artery injection of 133Xe (0.8 +/- 0.2:1, left:right) compared to normothermia before and after hypothermia (0.3 +/- 2 and 0.3 +/- 1, respectively; P < 0.05). Normal heart rhythm, systemic arterial blood pressure, and arterial blood gas values were preserved during hypothermia in all animals. CONCLUSION Bilateral cerebral deep or moderate hypothermia can be induced by selective perfusion of a single internal carotid artery, with minimal systemic cooling and without cardiovascular instability. This global brain hypothermia results from profoundly altered collateral cerebral circulation during artificial hypothermic perfusion. This technique may have clinical applications for neurosurgery, stroke, or traumatic brain injury.

Pharmacokinetics and pharmacodynamics of rocuronium (Org 9426) in elderly surgical patients.

The effects of age on the pharmacokinetic and pharmacodynamic responses to rocuronium (Org 9426) were studied in 20 elderly (>70 yr) and 20 younger control patients (<60 yr) during N2O/O2, fentanyl anesthesia. The onset times were the same for both the elderly and younger control group, but the duration of action of rocuronium was significantly prolonged in the elderly patients. Elderly patients, when compared with the younger, also exhibited a significant decrease in plasma clearance (3.67 ± 1.0 vs 5.03 ± 1.5 mL·kg−1·min−1, mean ± SD) and volume of distribution (399 ± 122 vs 553 ± 279 mL/kg, mean ± SD). During the recovery phase of paralysis, no significant difference was seen in the log plasma concentration versus twitch tension response relationship between 20% and 80% paralysis in young and elderly patients receiving rocuronium. The differences in action of rocuronium between the elderly and younger groups can be fully explained by the observed differences in the distribution and elimination of rocuronium between the two groups. The decreased total body water and decreased liver mass which normally accompany aging are likely explanations for the pharmacokinetic changes found in the elderly in this study. We conclude that the action of rocuronium is prolonged in patients aged more than 70 yr because of decreased elimination of the drug.

Hypertension during anesthesia on discontinuation of sodium nitroprusside-induced hypotension.

The authors had observed that on intraoperative discontinuation of sodium nitroprusside being administered to induce hypotension, mean arterial pressure increased to above the pre-hypotension level. Twelve patients who received hypotensive anesthesia for surgical correction of cerebral aneurysms were studied to evaluate the role of the renin–angiotensin system in this phenomenon. In the awake state, mean arterial pressure was 100 ± 2 torr and plasma renin activity 3.0 ± 0.1 ng/ml/hr. Thirty minutes after the establishment of stable halothane–nitrous oxide anesthesia, mean arterial pressure decreased to 85 ± 1 torr and plasma renin activity increased to 4.4 ± 0.1 ng/ml/hr. No appreciable change in either occurred over the next two hours of operation. During sodium nitroprusside-induced hypotension, mean arterial pressure decreased to 49 ± 2 torr and plasma renin activity increased to 15.2 ± 0.2 ng/ml/hr. Thirty minutes after discontinuation of sodium nitroprusside administration, mean arterial pressure increased to 112 ± 2 torr, which was not only higher than the prehypotension level, but also significantly higher than that recorded in the awake state. Plasma renin activity at that time was 10.9 ± 0.1 ng/ml/hr. As the half-life of plasma renin is 15 min, the data suggest that the persistently increased plasma renin activity is probably responsible for the increase of arterial pressure following sodium nitroprusside-induced hypotension.

Direct Intraoperative Measurement of Human Brain Temperature

OBJECTIVE Because hypothermia enhances human tolerance for cerebral ischemia, profound hypothermia is induced in many centers so that the circulation can be arrested while clips are applied to high-risk giant cerebral aneurysms. Brain temperature is measured directly with an intracerebral probe that avoids the uncertainty of surrogate monitoring. However, when there is a large thermal gradient between brain temperature and that of the operating room, even direct measurements can sometimes be misleading. This study was undertaken to determine how deeply a thermal sensor must be embedded in the cerebral parenchyma to ensure that the ambient environment does not distort the measurement of brain temperature. METHODS Each of 39 normothermic patients had a thermocouple sensor inserted into a temporal lobe seizure focus just before its resection. Brain temperature was measured as the sensor was withdrawn in stages. RESULTS At both 3 and 2 cm beneath the cortical surface, the temperature of the brain was essentially the same. However, when the sensor was withdrawn to 1 cm, recorded temperature decreased from 35.7 +/- 0.9 to 34.3 +/- 1.4 degrees C (P < 0.001) and irrigation in the vicinity caused major thermal change. At shallower depths, even lower brain temperatures were recorded. No morbidity was attributable to the temperature measurements. CONCLUSION Direct intraoperative measurement of human brain temperature is feasible and safe, but accuracy requires that the temperature sensor be inserted at least 2 cm into the cerebral cortex.

Nocturnal oxygenation during patient-controlled analgesia.

UNLABELLED Patient-controlled analgesia (PCA) has become a standard modality for the management of postoperative pain, although anecdotal reports of excessive sedation and respiratory depression impugn its safety. To study the prevalence and severity of nocturnal hypoxemia, we measured arterial oxygen saturation (SpO2) continuously overnight in 32 postoperative patients who were receiving morphine via PCA. To evaluate the potential benefit of providing concurrent supplemental oxygen, the patients breathed oxygen-enriched air the night of surgery and room air the next night. Patients experienced more pain and consumed twice as much morphine the first night. However, breathing supplemental oxygen that night, the nocturnal mean SpO2 was 99%+/-1%, 94%+/-4% (P<0.001), and only four patients had periods of hemoglobin desaturation <90%. In contrast, breathing room air the subsequent night, the mean SpO2 was lower (94%+/-4%; P<0.001), and hypoxemia occurred more frequently and was more severe: 18 patients experienced episodes of SpO2 <90%, 7 patients experienced episodes of SpO2 <80%, and 3 patients experienced episodes of SpO2 <70%. One patient required resuscitation for profound bradypnea and cyanosis, but none suffered permanent sequelae. We conclude that when postoperative patients use PCA at night, hypoxemia can be substantial and oxygenation can be improved by providing supplemental oxygen. IMPLICATIONS Oxygen saturation was measured postoperatively in patients using morphine patient-controlled analgesia. Substantial nocturnal hypoxemia occurred in half of the patients while they breathed room air. The severity of the hypoxemia was reduced when patients received supplemental oxygen.

Pulmonary Shunting during Anesthesia with Deliberate Hypotension

Pulmonary shunling (&OV0422;t,/&OV0422;t, with FIO2 = 1) was measured in 18 anesthetized patients during deliberate hypotension. Hypotension was induced in 12 patients with sodium nitroprusside and light halothane anesthesia and in six others with deep halothane anesthesia and mechanical hyperventilation. Similar results were observed in the two groups. During the hypotensive period mean arterial pressure (MAP) was reduced to 49 ± 2 torr, a 37 per cent decrease from the control level after the onset of operation and a 40 per cent decrease compared with the recovery level during closure of the wound. &OV0422;t/&OV0422;t, however, remained unchanged throughout the study; 52 ± 0.9 per cent initially, 5.4 ± 0.8 per cent during hypotension, and 4.7 ± 0.5 per cent during recovery. It is concluded that pulmonary shunting need not develop during dliberate hypotension induced with either technique.

Ventilatory complications of carbon dioxide laser laryngeal surgery

STUDY OBJECTIVE To evaluate complications associated with ventilatory techniques accompanying endolaryngeal carbon dioxide laser surgery. DESIGN Retrospective survey of the Society of Academic Anesthesia Chairmen. SETTING Operating room at an urban medical center. PATIENTS Data from 15,701 patients were analyzed. MEASUREMENTS AND MAIN RESULTS Twenty-six percent of patients were ventilated with Venturi jet ventilation and the rest through an endotracheal tube. Reported complications were classified as ventilation related and ventilation unrelated, as well as by severity. A total of 49 complications occurred in the Venturi jet group (1.2%). Of these complications, 24 were ventilation related (0.58%) and 18 were serious or life threatening (0.43%). There were no deaths in this group. Ventilation through an endotracheal tube was associated with a lower frequency of overall complications (0.36%), ventilation-related complications (0.15%), serious or life-threatening complications (0.15%), and serious or life-threatening ventilation-related complications (0.11%) (p less than 0.001). However, there were eight airway fires in this latter group, one resulting in a fatality. CONCLUSIONS No clear choice of ventilatory technique is supported by this survey, but teamwork and experience give the best results.

Consequences of Electroencephalographic-suppressive Doses of Propofol in Conjunction with Deep Hypothermic Circulatory Arrest

Background Some patients who undergo cerebral aneurysm surgery require cardiopulmonary bypass and deep hypothermic circulatory arrest. During bypass, these patients often are given large doses of a supplemental anesthetic agent in the hope that additional cerebral protection will be provided. Pharmacologic brain protection, however, has been associated with undesirable side effects. These side effects were evaluated in patients who received large doses of propofol. Methods Thirteen neurosurgical patients underwent cardiopulmonary bypass and deep hypothermic circulatory arrest to facilitate clip application to a giant or otherwise high-risk cerebral aneurysm. Electroencephalographic burst suppression was established before bypass with an infusion of propofol, and the infusion was continued until the end of surgery. Hemodynamic and echocardiographic measurements were made before and during the prebypass propofol infusion and again after bypass. Emergence time also was determined. Results Prebypass propofol at 243 plus/minus 57 micro gram *symbol* kg sup -1 *symbol* min sup -1 decreased vascular resistance from 34 plus/minus 8 to 27 plus/minus 8 units without changing heart rate, arterial or filling pressures, cardiac index, stroke volume, or ejection fraction. Propofol blood concentration was 8 plus/minus 2 micro gram/ml. Myocardial wall motion appeared hyperdynamic at the end of cardiopulmonary bypass, and all patients were weaned therefrom without inotropic support. After bypass, vascular resistance decreased further, and cardiovascular performance was improved compared to baseline values. Nine of the 13 patients emerged from anesthesia and were able to follow commands at 3.1 plus/minus 1.4 h. Three others had strokes and a fourth had cerebral swelling. Conclusions Propofol infused at a rate sufficient to suppress the electroencephalogram does not depress the heart or excessively prolong emergence from anesthesia after cardiopulmonary bypass and deep hypothermic circulatory arrest.