Effect of chronic cocaine exposure on the hemodynamic response to vasopressors in sheep.

BACKGROUND: The purpose of this study was to determine how chronic cocaine exposure affects the hemodynamic response to epinephrine, dopamine, phenylephrine, and ephedrine in awake sheep. METHODS: The hemodynamic response to dopamine (10 microg/kg), phenylephrine (1.5 microg/kg), and ephedrine (0.15 mg/kg) boluses was determined at baseline before low-dosage cocaine exposure and again after 15 and 18 days of cocaine exposure. The hemodynamic response to epinephrine (0.15 microg/kg), phenylephrine (1.5 microg/kg), and ephedrine (0.15 mg/kg) was determined at baseline before high-dosage cocaine exposure and again after 15 and 18 days of cocaine exposure. RESULTS: Chronic cocaine exposure abolished the mean arterial pressure and heart rate responses to dopamine but did not alter the responses to epinephrine, phenylephrine, or ephedrine. CONCLUSION: In awake sheep, chronic cocaine exposure markedly impairs the hemodynamic response to dopamine but not to epinephrine, phenylephrine, or ephedrine.

Chronic cocaine administration does not modify haemodynamic responses to isoflurane anaesthesia in sheep.

PURPOSE: Cocaine use is epidemic in the developed world, resulting in numerous patients presenting for surgery and anaesthesia with a history of chronic cocaine exposure. The purpose of this study was to determine the effect of chronic cocaine exposure on the cardiovascular response to isoflurane general anaesthesia. METHODS: The changes in mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP) and systemic vascular resistance (SVR) with increasing concentration of isoflurane (1%, 1.7%, and 2.4% end tidal) were determined at baseline in six sheep. The animals then received a continuous cocaine infusion (0.2 mg.kg-1.hr-1) and twice daily cocaine boluses (4 mg.kg-1) for 17 days followed on day 18 by a cocaine binge consisting of eight cocaine boluses (4 mg.kg-1) administered at one hour intervals. The haemodynamic studies conducted at baseline prior to cocaine exposure were then repeated on days 15 and 18. RESULTS: Increasing concentrations of isoflurane produced the expected dose-dependent cardiovascular depression, but this was not altered by cocaine exposure. CONCLUSION: Although chronic cocaine exposure has been shown to increase isoflurane minimum alveolar concentration by 25% in sheep; chronic cocaine exposure does not result in tolerance of the cardiovascular depression produced by isoflurane.

Effect of chronic cocaine administration on the hemodynamic response to acute hemorrhage in awake and anesthetized sheep.

BACKGROUND: Although Cocaine use is common in trauma victims, little is known about how cocaine affects the cardiovascular response to trauma and associated blood loss. This study determined the effect of chronic cocaine use on the cardiovascular response to hemorrhage in awake and anesthetized sheep. METHODS: The hemodynamic and acid-base responses to graded hemorrhage were determined in awake and anesthetized sheep at baseline and after 15 and 18 days of chronic cocaine exposure. RESULTS: Chronic cocaine exposure resulted in a moderate paradoxical bradycardic response to hemorrhage in awake sheep, but did not otherwise alter the hemodynamic response to hemorrhage. In anesthetized animals, cocaine exposure impaired the ability to maintain mean arterial pressure and cardiac output during hemorrhage, and resulted in a marked paradoxical bradycardic response to hemorrhage. CONCLUSIONS: Chronic cocaine exposure did not have an important effect on the cardiovascular response to hemorrhage in awake sheep. However, in anesthetized sheep, chronic cocaine exposure diminished the compensatory cardiovascular response to graded hemorrhage.

Chronic cocaine administration reversibly increases isoflurane minimum alveolar concentration in sheep.

BACKGROUND: Significant numbers of patients are seen for surgery and anesthesia with a history of chronic cocaine use. However, little is known about how cocaine use influences anesthetic physiology and pharmacology. The purpose of this study was to investigate the effect of chronic cocaine exposure on the minimum alveolar concentration (MAC) of isoflurane in sheep. METHODS: Isoflurane MAC was determined at baseline in 12 sheep using a standard protocol. The animals were subsequently exposed to cocaine for 18 days. Cocaine exposure consisted of a continuous subcutaneous cocaine infusion at 0.2 mg.kg-1.h-1, twice daily 4-mg/kg intravenous boluses and repeated hourly 4 mg/kg cocaine boluses for 8 h on day 18. Minimum alveolar concentration determinations were repeated again on days 15, 18, and on day 28 after 10 days of cocaine abstinence. RESULTS: Compared to baseline MAC (1.53 +/- 0.12%) cocaine exposure significantly increased isoflurane MAC on days 15 (1.91 +/- 0.14%) and 18 (1.78 +/- 0.13%; P = .005). MAC decreased after discontinuation of cocaine and was not different from baseline on day 28 (1.67 +/- 0.11). CONCLUSIONS: In sheep, chronic cocaine exposure resulted in a reversible increase in isoflurane MAC. This finding contrasts with studies of other central nervous system stimulants, which have demonstrated a decrease in MAC after chronic drug exposure.

Hyperglycemia and neurological outcome in patients with head injury.

To examine the relationship between serum glucose and the outcome of patients suffering from head injury, the authors retrospectively reviewed the clinical course of 169 patients admitted for treatment to Harborview Medical Center (a regional trauma center). All patients underwent craniotomy for evacuation of intracranial hematoma and/or placement of a subarachnoid bolt for intracranial pressure monitoring under general anesthesia. Patients with a Glasgow Coma Scale (GCS) score of 8 or less had significantly higher serum glucose levels than patients with GCS scores of 12 to 15 (mean +/- standard error of the mean 192 +/- 7 mg/dl vs. 130 +/- 8 mg/dl or 10.7 +/- 0.4 mmol/liter vs. 7.2 +/- 0.4 mmol/liter) (p less than 0.0001). Patients who subsequently remained in a vegetative state or died had significantly higher glucose levels both on admission and postoperatively than patients who had good outcome or moderate disability (217 +/- 12 mg/dl vs. 167 +/- 6 mg/dl or 12.1 +/- 0.7 mmol/liter vs. 9.3 +/- 0.3 mmol/liter on admission, and 240 +/- 16 mg/dl vs. 156 +/- 5 mg/dl or 13.3 +/- 0.9 mmol/liter vs. 8.9 +/- 0.3 mmol/liter postoperatively) (p less than 0.0001). Among the more severely injured patients (GCS score less than or equal to 8), a serum glucose level greater than 200 mg/dl (11.1 mmol/liter) postoperatively is associated with a significantly worse outcome (p less than 0.01). The authors conclude that severely head-injured patients frequently develop hyperglycemia and the elevated serum glucose level may aggravate ischemic insults and worsen the neurological outcome in such patients.

Observer reliability in detecting surreptitious random occlusions of the monaural esophageal stethoscope.

The esophageal stethoscope is used often during anesthesia to monitor ventilation and cardiac function. Deficiencies in observer vigilance may limit the effectiveness of this monitoring instrument. The aim of this study was to determine how long it took for an observer to detect a surreptitiously occluded monaural esophageal stethoscope in the setting of clinical anesthesia. During routine anesthesia, where an esophageal stethoscope was in use, a computer-guided device would artificially, silently, and at random time intervals, occlude the stethoscope tubing. Personnel using the stethoscope noted when they perceived the absence of stethoscope sounds. We studied 320 stethoscope occlusions in 32 patients. The time between stethoscope occlusion and detection was 34 +/- 59 seconds (mean +/- SD). Eighty-seven percent of detections were made in less than 60 seconds. However, 13% of detections were delayed for more than 60 seconds, and 2.3% for more than 240 seconds. While anesthesia personnel using an esophageal stethoscope could detect most stethoscope occlusions, failure to appreciate such episodes occurred in a small but significant number of cases. This suggests that the esophageal stethoscope has some definite limitations as a continuous monitor and that other monitoring techniques, such as oximetry, capnography, and ventilator disconnect alarms, as well as visual/tactile inspection of the patient, should be used as well.

Anesthesia for trauma.

Trauma is the leading cause of death for persons aged 1 to 38 years. Successful management is facilitated by prehospital endotracheal intubation, transport to regional trauma centers, rapid resuscitation by an on-site team of trained physicians, timely operative intervention, and provision of care by well-prepared anesthesiologists familiar with the potential complications typical of traumatized patients. No particular anesthetic agent or technique is ideal. Causes for intraoperative hypotension include hypovolemia, hemopneumothorax, pericardial tamponade, an intracranial mass, acidosis, and hypothermia. The anesthesiologist should play an active role in all phases of trauma management, including provision of postoperative intensive care and pain relief.

A database system for abstract selection for a major anesthesia society meeting.

Until the present time, record keeping for abstract selection for major anesthesia meetings has been performed by manual methods - paper, pen, and typewriter. We describe the construction and implementation of a microcomputer based system to facilitate data recording, form-letter generation, and program construction. Based on MicroPro's WordStar, InfoStar, MailMerge series, the database has reduced the total effort required to construct the final program from 1.5 hours per abstract submitted for the 1984 meeting to 0.7 hours for the 1986 meeting. Problems encountered were mastery of the system by operating personnel, floppy disk overflow, and data loss of unknown etiology. The significant time savings attest to the value of the system.

Continuous transcutaneous PCO2 monitoring during epidural morphine analgesia.

We evaluated the transcutaneous PCO2 (PtcCO2) sensor as a ventilation monitor for patients receiving epidural morphine analgesia during interstitial radiation therapy for carcinoma of the cervix. The sensor was heated to 42 degrees C. Ten patients were monitored for 18 +/- 7 h after 2.9 +/- 0.5 mg of morphine was injected epidurally. Baseline respiratory rate (RR) and PtcCO2 were 21 +/- 3 breath/min and 37 +/- 8 torr, respectively. Peak PtcCO2 was 43 +/- 7 torr, corresponding to a RR of 19 +/- 3 breath/min. The increase of PtcCO2 from baseline was statistically significant. PtcCO2 peaked from 1 to 19 h after epidural morphine, and 90% of patients showed peak values between 11 PM and 4:30 AM. The prolonged monitoring caused no complications. Although there was no clinically significant respiratory depression in these patients, the PtcCO2 sensor may be a useful monitor of ventilation during epidural morphine administration.

Transcutaneous monitoring of oxygen tension during one-lung anesthesia.

Twenty adult patients were monitored with a transcutaneous oxygen tension sensor during one-lung ventilation. Anesthesia was maintained with enflurane-oxygen or isoflurane-oxygen. The transcutaneous oxygen tension values accurately followed the trend of arterial oxygen tension (r = 0.94, n = 96, transcutaneous oxygen tension = 4.8 + 0.78 X arterial oxygen tension). The transcutaneous oxygen tension values averaged 80% of the arterial oxygen tension values (transcutaneous oxygen tension index = transcutaneous oxygen tension/arterial oxygen tension = 0.80 +/- 0.18) (mean +/- standard deviation). When one-lung ventilation was initiated, there was a progressive drop in transcutaneous oxygen tension which reached a minimum of 19 +/- 10 minutes. The mean of the minimum transcutaneous oxygen tension and arterial oxygen tension values was 66 +/- 44 torr and 83 +/- 43 respectively. This resulted in a mean alveolar-arterial oxygen gradient of 515 +/- 152 torr during one-lung ventilation. In eight patients, the arterial oxygen tension fell below 60 torr, 45 +/- 9 torr. When two-lung ventilation was resumed, the transcutaneous oxygen tension and arterial oxygen tension values promptly rose to mean values of 342 +/- 121 torr and 411 +/- 103 torr, respectively in 9 +/- 3 minutes. The transcutaneous oxygen tension monitor provided a continuous assessment of the patient's oxygenation, gave early warning of potentially hazardous hypoxia, and permitted nearly real-time assessment of the efficacy of corrective therapies.

Perfluorocarbon infusion in bleeding patients refusing blood transfusions.

Six severely anemic surgical patients who refused blood products were treated with a perfluorochemical (PFC) emulsion (Fluosol-DA 20%). When these patients received high inspired oxygen concentrations, the emulsion resulted in moderate increases of arterial oxygen content but considerable increases of oxygen consumption, suggesting improved microcirculatory oxygen distribution. The mean +/- SD percentages of consumed oxygen transported by dissolved oxygen in PFC and PFC plus plasma emulsions were 22% +/- 5% and 60% +/- 12%, respectively. Several adverse clinical effects were seen, however, including transient decreases in leukocyte counts, hypotension, and abnormal hepatic and pulmonary function.