Long-duration low-flow sevoflurane and isoflurane effects on postoperative renal and hepatic function.

UNLABELLED: Sevoflurane degradation by carbon dioxide absorbents during low-flow anesthesia forms the haloalkene Compound A, which causes nephrotoxicity in rats. Numerous studies have shown no effects of Compound A formation on postoperative renal function after moderate-duration (3-4 h) low-flow sevoflurane; however, effects of longer exposures remain unresolved. We compared renal function after long-duration low-flow (<1 L/min) sevoflurane and isoflurane anesthesia in consenting surgical patients with normal renal function. To maximize degradant exposure, Baralyme was used, and anesthetic concentrations were maximized (no nitrous oxide and minimal opioids). Inspired and expired Compound A concentrations were quantified. Blood and urine were obtained for laboratory evaluation. Sevoflurane (n = 28) and isoflurane (n = 27) groups were similar with respect to age, sex, weight, ASA status, and anesthetic duration (9.1 +/- 3.0 and 8.2 +/- 3.0 h, mean +/- SD) and exposure (9.2 +/- 3.6 and 9.1 +/- 3.7 minimum alveolar anesthetic concentration hours). Maximum inspired Compound A was 25 +/- 9 ppm (range, 6-49 ppm), and exposure (area under the concentration-time curve) was 165 +/- 95 (35-428) ppm. h. There was no significant difference between anesthetic groups in 24- or 72-h serum creatinine, blood urea nitrogen, creatinine clearance, or 0- to 24-h or 48- to 72-h urinary protein or glucose excretion. Proteinuria and glucosuria were common in both groups. There was no correlation between Compound A exposure and any renal function measure. There was no difference between anesthetic groups in 24- or 72-h aspartate aminotransferase or alanine aminotransferase. These results show that the renal and hepatic effects of long-duration low-flow sevoflurane and isoflurane were similar. No evidence for low-flow sevoflurane nephrotoxicity was observed, even at high Compound A exposures as long as 17 h. Proteinuria and glucosuria were common and nonspecific postoperative findings. Long-duration low-flow sevoflurane seems as safe as long-duration low-flow isoflurane anesthesia. IMPLICATIONS: Postoperative renal function after long-duration low-flow sevoflurane (with Compound A exposures greater than those typically reported) and isoflurane anesthesia were not different, as assessed by serum creatinine, blood urea nitrogen, and urinary excretion of protein and glucose. This suggests that low-flow sevoflurane is as safe as low-flow isoflurane, even at long exposures.

Screen-based anesthesia simulation with debriefing improves performance in a mannequin-based anesthesia simulator.

BACKGROUND: Previous investigations have established the need for improved training for management of anesthetic emergencies. Training with inexpensive screen-based anesthesia simulators may prove to be helpful. PURPOSES: We measured the effectiveness of screen-based simulator training with debriefing on the response to simulated anesthetic critical incidents. METHODS: Thirty-one 1st-year clinical anesthesia residents were randomized into 2 groups. The intervention group handled 10 anesthetic emergencies using the screen-based anesthesia simulator program and received written feedback on their management, whereas the traditional (control) group was asked to study a handout covering the same 10 emergencies. All residents then were evaluated on their management of 4 standardized scenarios in a mannequin-based simulator using a quantitative scoring system. RESULTS: The average point score for the simulator-with-debriefing group was 52.6 +/- 9.9 out of 95 possible points. The traditional group average point score was 43.4 +/- 5.9, p = .004. CONCLUSIONS: Residents who managed anesthetic problems using a screen-based anesthesia simulator handled the emergencies in a mannequin-based anesthesia simulator better than residents who were asked to study a handout covering the same problems. Computer simulations with feedback are effective as a supplement to traditional residency training methods for the management of medical emergencies.

Autonomic and cardiovascular function in the geriatric patient.

The elderly patient is at an increased risk for hemodynamic instability during anesthesia. The underlying mechanisms are primarily a decrease in the beta-receptor response to stimulation, stiffening of the connective tissue throughout the cardiovascular system, and increased vascular resistance during surgical stress and an increased dependency on cardiac filling. Unfortunately, the ability to maintain a steady preload diminishes with age and in general, changes in blood volume are buffered less effectively. Anesthetic management requires closer monitoring of blood pressure and a greater emphasis on vasomotor tone than on fluid administration when treating hypotension.

Systolic blood pressure at end-expiration measured by the automated systolic pressure variation monitor is equivalent to systolic blood pressure during apnea.

OBJECTIVE: It is necessary to define a reference systolic arterial blood pressure (RP) to calculate delta-Up (dUp) and delta-Down (dDown) for systolic pressure variation. Most studies define the reference pressure as the average systolic blood pressure during a short period of apnea. We describe an automated systolic pressure variation monitor that measures airway pressure and defines the reference pressure as the systolic blood pressure at end-expiration. The present study compares the reference systolic blood pressure measured at end-expiration by the automated systolic pressure variation monitor and the reference systolic blood pressure measured during apnea to test whether the end-expiration value is an adequate substitute for the value during apnea. METHODS: After obtaining informed consent, 108 sets of measurements of systolic pressure variation (SPV) were made in 20 intubated, mechanically-ventilated, anesthetized patients by the automated SPV monitor and during apnea. Measurements were taken during periods of hemodynamic stability defined as three consecutive end-expiratory systolic blood pressures within four mmHg of each other. The three systolic pressures at end-expiration were averaged (RPmonitor). Immediately following these measurements, the ventilator was turned off and the systolic blood pressure was measured at 6, 8, 10 and 12 seconds of apnea. The reference pressure during apnea (RPapnea) was defined as the average of the systolic blood pressure at 8, 10 and 12 seconds of apnea. For each measurement set, RPmonitor and the systolic blood pressure at 6 seconds of apnea (SBP6) were compared to RPapnea using Bland-Altman analysis. RESULTS: Bland-Altman analysis for the difference between SBP6 and RPapnea yielded a small bias of -0.3 mmHg with standard deviation of 1.3, indicating that the systolic pressure tends to continue to increase slightly after 6 seconds of apnea. Results were similar for the difference between RPmonitor and RPapnea (-0.2 +/- 3.1 mmHg). CONCLUSIONS: dUp and dDown are calculated using the reference pressure. RPmonitor is an average of 0.2 mm Hg less than RPapnea, thus dUp calculated by the automated SPV monitor is an avenge of 0.2 mm Hg greater than dUp measured by the reference pressure during apnea and dDown is 0.2 mm Hg less. Since the bias of -0.2 mmHg is clinically insignificant, there is acceptable agreement between the reference pressure obtained during apnea and that obtained by the automated SPV monitor at end-expiration. The mean difference between RPmonitor and RPapnea is explained by the continued rise in systolic pressure during the period of apnea as demonstrated by the difference between SBP6 and RPapnea.

Use of a computerized advanced cardiac life support simulator improves retention of advanced cardiac life support guidelines better than a textbook review.

OBJECTIVE: To determine whether an advanced cardiac life support (ACLS) computer simulation program improves retention of ACLS guidelines more effectively than textbook review. DESIGN: Randomized, controlled trial. SETTING: Academic medical center. PARTICIPANTS: Forty-five anesthesia residents and faculty tested 10 to 11 months after ACLS provider course training. INTERVENTION: Participants were randomized and asked to prepare for a mock resuscitation (Mega Code) with either textbooks or a computerized ACLS simulation program. MAIN OUTCOME MEASURE: Performance on a standardized Mega Code examination that required application of supraventricular tachycardia, ventricular fibrillation, and second-degree Type II atrioventricular block algorithms. Mega Code sessions were administered by an instructor who was blinded as to the subject group. The sessions were videotaped and scored by two evaluators who also were blinded as to the subject group. RESULTS: Participants who used the ACLS simulation program scored significantly higher (mean 34.9 +/- 5.0 [SD] of 47 possible points) than participants who reviewed using a textbook (29.2 +/- 4.9); p < .001. Pass-fail rates for the algorithms were also higher for the group that reviewed with the simulator (mean 2.5 +/- 0.5 of 3 possible passes) than the group that used the textbook (1.6 +/- 1.0); p = .001. CONCLUSIONS: Use of a computerized ACLS simulation program improves retention of ACLS guidelines better than textbook review.

Epidural anesthesia and the thermoregulatory responses to hyperthermia--preliminary observations in volunteer subjects.

BACKGROUND: Clinical reports associate the use of epidural anesthesia with an increase in core temperature in women in labor. We tested the hypothesis that epidural anesthesia alters thermoregulatory responses to hyperthermia in human volunteers. METHODS: Each of four volunteers were studied on two days: Control and Anesthesia. On the Control day, the subject was warmed via the skin, and the core (esophageal) temperature threshold for sweating (detected on the forehead) was determined. The subject was then cooled until sweating stopped. The subject was warmed again, and a second sweating threshold was determined. The difference between the first and second sweating thresholds was noted. On the Anesthesia day, two sequential sweating threshold measurements were obtained in a similar fashion; however, a mid-thoracic level of epidural anesthesia was established before the second sweating threshold measurement. The first and second sweating threshold differences were compared between the two study days. The presence or absence of sweating on the thigh was noted during all four warming periods. RESULTS: Average skin temperatures were similar (about 37 degrees C) during all four sweating threshold measurements. On the Control day, the second sweating threshold value was always slightly less than the first (average difference (mean+/-SD): -0.18+/-0.14 degrees C). In contrast, on the Anesthesia day, the second sweating threshold value (determined with an epidural block) was always greater than the first (average difference: +0.37+/-0.16 degrees C). Epidural anesthesia, therefore, increased the sweating threshold by 0.55+/-0.27 degrees C. Epidural anesthesia blocked sweating in the thigh in two of the subjects. CONCLUSIONS: An epidural block alters the thermoregulatory responses to warming by increasing the threshold for thermoregulatory sweating and, in some cases, preventing leg sweating.

Myocardial ischemia and adverse cardiac outcomes in cardiac patients undergoing noncardiac surgery with sevoflurane and isoflurane. Sevoflurane Ischemia Study Group.

UNLABELLED: Sevoflurane is associated with less tachycardia and coronary vasodilation than isoflurane and thus might be associated with less myocardial ischemia. This multicenter study examined the incidence of myocardial ischemia and adverse cardiac outcomes in adults (40-87 yr) with cardiac disease having elective noncardiac surgery. Patients were randomized to receive either sevoflurane (S) (n = 106) or isoflurane (I) (n = 108) in conjunction with sodium thiopental, vecuronium, fentanyl, and 50%-70% N2O. Intraoperative hemodynamics were maintained within 20% of awake baseline with standard drugs. A Holter monitor was applied 3-24 h before surgery and maintained until 48 h after surgery. Electrocardiograms and blood samples for analysis of the MB isoenzyme fraction of creatine phosphokinase were obtained preoperatively and daily for 48 h postoperatively. Anesthetic exposure (1.79 +/- 0.15 [mean +/- SE] minimum alveolar concentration-hour) and duration of surgery (219 +/- 13 min) did not differ between groups. The incidence of ischemia in the pre-, intra- and postoperative periods, adverse cardiac outcomes (18% occurrence), intraoperative hemodynamic variations (+/-20% change from ward baseline), and administration of adjunct cardiovascular medications were similar between groups. In cardiac patients having noncardiac surgery, sevoflurane was comparable to isoflurane with respect to the incidence of intra- and postoperative myocardial ischemia and in the frequency of adverse cardiac outcomes. IMPLICATIONS: Surgical patients with heart disease are at risk of heart complications, some of which could be induced by an anesthetic. We compared the incidence of cardiac complications between patients receiving sevoflurane and isoflurane. We found that the frequency of additional heart problems in cardiac patients receiving sevoflurane was not different from that associated with isoflurane.

Effects of intrathecal opioid on extubation time, analgesia, and intensive care unit stay following coronary artery bypass grafting.

STUDY OBJECTIVE: To determine if intrathecal opioid decreases time to extubation after coronary artery bypass surgery without compromising postoperative analgesia. DESIGN: Prospective randomized trial. SETTING: Veterans Affairs Hospital. PATIENTS: 21 ASA physical status III and IV men scheduled for elective coronary bypass surgery, who had not received medications that would impair anticoagulation at the time of surgery. INTERVENTIONS: Patients were randomized to receive 10 micrograms/kg morphine and 25 micrograms fentanyl intrathecally preoperatively (n = 12) or no intrathecal opioid (n = 9). The latter group received 25 to 50 micrograms/kg fentanyl and 0.05 to 0.1 mg/kg midaxolam intraoperatively, whereas the intrathecal opioid group received intravenous (i.v.) fentanyl and midazolam only as needed. Both groups were administered i.v. morphine and midazolam postoperatively as needed by intensive care unit (ICU) personnel who were blinded to the treatment group. MEASUREMENTS AND MAIN RESULTS: For the first 24 hours postoperatively, pain levels (0 = none, to 10 = most severe) and sedation levels (1 = none, to 5 = unconscious) were measured hourly. The time to extubation and discharge from the ICU was recorded. ECG evidence of myocardial ischemia was noted. Pain scores were low for both groups (1.5), but the intrathecal opioid subjects exhibited less sedation than the high-dose fentanyl subjects [means +/- standard deviation (SD) of 2.3 +/- 0.4 vs. 2.8 +/- 0.5, p = 0.03]. Extubation time was 12 hours shorter in the intrathecal opioid group (2.9 +/- 5.3 vs. 14.7 +/- 6.8, p = 0.001). The five subjects with a one day ICU stay were all in the intrathecal opioid group (p = 0.04). The incidence of myocardial ischemia did not differ between the two groups. CONCLUSIONS: Intrathecal opioid can facilitate early extubation and discharge from the ICU without compromising analgesia or increasing myocardial ischemia.

Reduction in post-intubation respiratory resistance by isoflurane and albuterol.

PURPOSE: This study examined the bronchodilating effects of 0.6 MAC and 1.1 MAC isoflurane (ISF) on respiratory system resistance (Rrs) following tracheal intubation and determined whether albuterol supplements that effect. METHODS: Sixty-seven adult patients were anaesthetized with 2 micrograms.kg-1 fentanyl and 5 mg.kg-1 thiopentone and their tracheas intubated following administration of 1 mg.kg-1 succinylcholine. Respiratory system resistance was measured following intubation and the patients then randomized to receive either 1.1 MAC ISF in oxygen or 0.6 MAC ISF in 50% nitrous oxide and oxygen. Ten minutes later, Rrs was again measured. Patients were then further randomized to receive albuterol or a placebo using incremental doses of 2, 5, and 10 puffs (albuterol puff = 90 micrograms) delivered via a metered dose inhaler at ten minute intervals. RESULTS: Isoflurane at 1.1 MAC decreased post-intubation Rrs by 23 +/- 5% (mean +/- sem) whereas the decrease was only 7 +/- 5% for 0.6 MAC ISF (P < 0.01). Two puffs of albuterol resulted in a further decrease of 12 +/- 3% (mean +/- sem) in Rrs compared with a 2 +/- 4% decrease in the placebo groups (P < 0.05). Additional puffs of albuterol resulted in no further changes in Rrs. CONCLUSION: We conclude that following tracheal intubation the reduction in Rrs produced by ISF is highly concentration dependent. Albuterol results in a small further reduction in Rrs.

Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease.

Aging and disease may make the elderly patient with cardiac disease particularly susceptible to hypotension during spinal anesthesia. We studied 15 men, 59-80 y old, with histories of prior myocardial infarction (n = 9), congestive heart failure (n = 2), and/or stable myocardial ischemia (n = 11) given spinal anesthesia with 50 mg lidocaine in dextrose. Technetium-99m-labeled red blood cell imaging estimated left ventricular ejection fraction (EF) and changes in blood volume in the abdominal organs and legs. Arterial and pulmonary artery catheters provided hemodynamic measurements. Sensory block averaged T4 (range T1-10). Mean arterial pressure decreased 33% +/- 15% (SD) (P < 0.001), secondary to decreases in vascular resistance (SVR), -26% +/- 13% (P < 0.001) and cardiac output, -10% +/- 16% (P = 0.03). EF increased from 53% +/- 11% to 58% +/- 14% (P < 0.001) while left ventricular end-diastolic volume (LVEDV) decreased (-19% +/- 9%, P < 0.001). Blood volume increased in the legs (6% +/- 6%, P = 0.006), kidneys (10% +/- 9%, P < 0.001), and mesentery (7% +/- 5%, P 0.001) but not in the liver or spleen. Cardiac function was well maintained. We concluded that the primary mechanism of hypotension was a decrease in SVR, not cardiac output, despite the decrease in LVEDV.

The effect of isoflurane, halothane, sevoflurane, and thiopental/nitrous oxide on respiratory system resistance after tracheal intubation.

BACKGROUND: After tracheal intubation, lung resistance and therefore respiratory system resistance (R[rs]) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparing the efficacy of available agents. This study compared the bronchodilating efficacy of four anesthetic maintenance regimens: 1.1 minimum alveolar concentration (MAC) end-tidal sevoflurane, isoflurane or halothane, and thiopental/nitrous oxide. METHODS: Sixty-six patients underwent tracheal intubation after administration of 2 microg/kg fentanyl, 5 mg/kg thiopental, and 1 mg/kg succinylcholine. Vecuronium or pancuronium (0.1 mg/kg) was then given to ensure paralysis during the rest of the study. Postintubation R(rs) was measured using the isovolume technique. Maintenance anesthesia was then randomized to thiopental 0.25 mg x kg(-1) x min(-1) plus 50% nitrous oxide, or 1.1 MAC end-tidal isoflurane, halothane, or sevoflurane. The R(rs) was measured after 5 and 10 min of maintenance anesthesia. Data were expressed as means +/- SD. RESULTS: Maintenance with thiopental/nitrous oxide failed to decrease R(rs), whereas all three volatile anesthetics significantly decreased R(rs) at 5 min with little further improvement at 10 min. Sevoflurane decreased R(rs) more than either halothane or isoflurane (P < 0.05; 58 +/- 14% of the postintubation R(rs) vs. 69 +/- 20% and 75 +/- 13%, respectively). CONCLUSIONS: After tracheal intubation in persons without asthma, sevoflurane decreased R(rs) as much or more than isoflurane or halothane did during a 10-min exposure at 1.1 MAC.

Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation.

BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate.

The hemodynamic and renal effects of sevoflurane and isoflurane in patients with coronary artery disease and chronic hypertension. Sevoflurane Ischemia Study Group.

In patients without significant cardiovascular disease, the hemodynamic effects of sevoflurane and isoflurane are similar; however, the hemodynamic effects of sevoflurane in patients with hypertension and ischemic heart disease are unknown. To examine the effects of sevoflurane in comparison to isoflurane in this high-risk population, 214 patients scheduled for elective surgery were enrolled if they had evidence of ischemic heart disease or multiple risk factors for ischemic heart disease. Patients were randomly assigned to receive sevoflurane (n = 106) or isoflurane (n = 108) for anesthetic maintenance in conjunction with fentanyl and nitrous oxide in oxygen. Deviations in arterial blood pressure or heart rate of more than 20% from preinduction values that persisted after adjustment of the volatile anesthetic concentration were treated with intravenous phenylephrine, ephedrine, nitroglycerin, atropine, or esmolol as needed. Creatinine, blood urea nitrogen (BUN), and urine protein were measured before surgery, immediately after surgery, and 24 and 48 h postoperatively. For analysis, patients were divided into those with and those without the diagnosis of chronic hypertension. Heart rate and arterial blood pressure responses to sevoflurane and isoflurane were not different for the patients with or without chronic hypertension. Neither anesthetic was associated with a more frequent treatment for hemodynamic deviation. After surgery, creatinine and BUN decreased in both the sevoflurane and isoflurane groups without significant differences between groups. The incidence of post-operative proteinuria was similar in the sevoflurane and isoflurane groups. We conclude that hemodynamic stability in patients with hypertension and ischemic heart disease is similar with sevoflurane and isoflurane. No differences in renal function were observed between the sevoflurane and isoflurane groups.

The effect of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during mechanical and spontaneous ventilation.

In dogs and humans, the magnitude of the variation in systolic pressure (SPV) over the respiratory cycle during mechanical ventilation appears to be inversely related to intravascular volume. Also reported to correlate with changes in volume status is delta down, the difference between systolic pressure at end-expiration and the lowest value during the respiratory cycle. These variables were examined during graded hemorrhage in eight anesthetized, mechanically ventilated subjects, and seven awake, spontaneously breathing subjects. SPV and delta down were measured in sequence at baseline, after 500 mL blood removal, after 1000 mL (total) blood removal, after 500 mL hetastarch replacement, after 1000 mL (total) hetastarch replacement, and after 500 mL normal saline (NS). Repeated-measures analysis of variance was used to test the significance of the change in SPV and delta down among the interventions. During mechanical ventilation, each 500-mL hemorrhage significantly increased SPV and delta down, and each 500-mL hetastarch infusion significantly decreased SPV and delta down. After hetastarch, both SPV and delta down were smaller than at baseline and may explain why the infusion of NS caused nonsignificant reductions in SPV and delta down. A SPV of 5 mm Hg or less, or a delta down of 2 mm Hg or less appeared to indicate minimal intravascular volume depletion. During spontaneous ventilation, delta down could not be determined accurately in several subjects, and SPV did not change in the appropriate direction in all cases of hemorrhage and volume infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of prophylactic bronchodilator treatment on lung resistance after tracheal intubation.

BACKGROUND: After induction of anesthesia, lung resistance increases. We hypothesized that prophylactic bronchodilator treatment before tracheal intubation would result in a lower lung resistance after placement of the endotracheal tube. METHODS: Forty-two adult patients were randomized to receive one of three inhaled medications 1 h before surgery. All patients first underwent pulmonary function tests. Patients then received either inhaled albuterol (360 micrograms) (n = 12), inhaled ipratropium bromide (72 micrograms) (n = 15) or a placebo inhalation (n = 15). Two, 5, and 15 min after tracheal intubation, lung resistance was measured using the method of von Neergard and Wirtz. RESULTS: Patients who received either bronchodilator had significantly lower lung resistance after intubation than those receiving placebo. At 2 min, lung resistances were 12.7 +/- 1.4 cmH2O.l-1.s-1 (mean +/- SEM) for the placebo group, 6.4 +/- 3.1 cmH2O.l-1.s-1 for the ipratropium-treated group (P < 0.05 vs. placebo), and 7.2 +/- 0.8 cmH2O.l-1.s-1 for the albuterol-treated group (P < 0.05 vs. placebo). The differences in lung resistance persisted through the final measurement at 15 min. Three of fifteen placebo-treated patients developed audible wheezing whereas no patients developed wheezing in either bronchodilator-treated group (P < 0.05 by Fisher's exact test). Although smokers and nonsmokers in the placebo group developed similar resistances after intubation, bronchodilator treatment resulted in lower resistance in nonsmokers than in smokers (P < 0.05). CONCLUSIONS: Prophylactic treatment with either an inhaled beta 2-adrenergic agonist or an inhaled cholinergic antagonist produced lower lung resistance after intubation when compared with an inhaled placebo medication. The effect was more pronounced in nonsmokers than in smokers.

Maximal skin blood flow is decreased in elderly men.

When subjected to total body heating and exercise, skin blood flow does not increase as much in elderly as in young subjects. It is not known whether this age-related decline is due to the autonomic dysfunction that develops in the elderly or to changes at the level of the blood vessels of the skin. We used local heating of the forearm to quantify the intrinsic ability of the cutaneous vasculature to dilate in seven young men (avg age 31 yr) and seven elderly men (avg age 71 yr). A water spray was used to maintain a neutral skin temperature of 32-35 degrees C for > 10 min, followed by 60 min of a 42 degrees C skin temperature to induce maximal skin blood flow. Forearm blood flow was measured by venous occlusion plethysmography with a mercury-in-Silastic circumference gauge. At the neutral skin temperature, forearm blood flows in the elderly subjects were comparable to those in the young subjects: 3.0 +/- 0.5 vs. 2.8 +/- 1.0 ml.min-1 x 100 ml-1. During the last 10 min of heating, however, blood flows were much lower in the elderly than in the young subjects: 11.1 +/- 2.7 vs. 19.9 +/- 5.2 ml.min-1 x 100 ml-1 (P = 0.002). We conclude that aging results in a reduction of the maximal conductance of the cutaneous vasculature.

Calcium channel blockers do not enhance increases in plasma potassium after succinylcholine in humans.

STUDY OBJECTIVE: To determine whether chronic calcium channel blocker therapy exaggerates the rise in plasma potassium concentration ([K+]) after succinylcholine administration. DESIGN: Prospective clinical study. SETTING: University and Veterans Affairs hospitals. PATIENTS: 36 ASA physical status III and IV male patients: 21 patients taking chronic calcium channel blockers and 15 patients not receiving calcium channel blockers, all of whom were scheduled for inpatient surgical procedures with general anesthesia. INTERVENTIONS: In all patients, anesthesia was induced with high-dose opioids plus a sedative-hypnotic, and intubation was facilitated with 1 to 1.5 mg/kg succinylcholine without nondepolarizing neuromuscular blocker pretreatment. MEASUREMENTS AND MAIN RESULTS: Plasma [K+] was measured prior to induction and 1, 3, 5, 8, 11, and 15 minutes after succinylcholine was administered. A modest average peak rise of 0.5 mEq/L in plasma [K+] was observed, but there were no differences between patients who were or were not receiving calcium channel blockers. CONCLUSIONS: Patients receiving chronic calcium channel blocker therapy are at no greater risk of hyperkalemia after succinylcholine than those not taking such medications.

Syringe pumps for infusion of vasoactive drugs: mechanical idiosyncrasies and recommended operating procedures.

Syringe pumps for vasoactive infusions have the advantages of small size and weight, portability, and low cost of the disposable components. However, limited syringe capacity necessitates the use of high drug concentrations, and the accidental delivery of even a small volume of infusate could seriously alter the patient's hemodynamics. To determine the circumstances under which drug delivery might be delayed, or inadvertent boluses could be delivered into the manifold, two brands of commercially available clinical syringe pumps were connected to a stopcock manifold via small-bore tubing and a series of tests were performed. When the syringe pumps were operated at 3 mL/h against a closed stopcock, the pumps' occlusion alarms did not sound for 18-22 min, and when the stopcock subsequently was opened, 0.6-0.9 mL of infusate was delivered as a bolus. Elevating the syringe pump by 120 cm resulted in the delivery of up to 0.5 mL of infusate with the pump turned off. When a syringe pump operating at 6 mL/h was turned off, typically an additional 0.05 mL was delivered during the ensuing 2-3 min. Depending upon the method used to flush the tubing prior to use, delays in drug delivery of 2-3 min occurred at an infusion rate of 3 mL/h. These observations emphasize the need for careful equipment setup and proper use of the manifold stopcocks to avoid unintended drug administration or delay in drug administration.