Cardiovascular effects of sevoflurane, isoflurane, halothane, and fentanyl-midazolam in children with congenital heart disease: an echocardiographic study of myocardial contractility and hemodynamics

BACKGROUND: The cardiovascular effects of halogenated anesthetic agents in children with normal hearts have been studied, but data in children with cardiac disease are limited. This study compared the effects of halothane, isoflurane, sevoflurane, and fentanyl-midazolam on systemic and pulmonary hemodynamics and myocardial contractility in patients with congenital heart disease. METHODS: Fifty-four patients younger than age 14 scheduled to undergo congenital heart surgery were randomized to receive halothane, sevoflurane, isoflurane, or fentanyl-midazolam. Cardiovascular and echocardiographic data were recorded at baseline and at randomly ordered 1 and 1.5 minimum alveolar concentrations, or predicted equivalent fentanyl-midazolam plasma concentrations. The shortening fraction and ejection fraction (using the modified Simpson rule) were calculated. Cardiac index was assessed by the velocity-time integral method. RESULTS: Halothane caused a significant decrease in mean arterial pressure, ejection fraction, and cardiac index, preserving only heart rate at baseline levels. Fentanyl-midazolam in combination caused a significant decrease in cardiac index secondary to a decrease in heart rate; contractility was maintained. Sevoflurane maintained cardiac index and heart rate and had less profound hypotensive and negative inotropic effects than halothane. Isoflurane preserved both cardiac index and ejection fraction, had less suppression of mean arterial pressure than halothane, and increased heart rate. CONCLUSIONS: Isoflurane and sevoflurane preserved cardiac index, and isoflurane and fentanyl-midazolam preserved myocardial contractility at baseline levels in this group of patients with congenital heart disease. Halothane depressed cardiac index and myocardial contractility.     

Effects of sevoflurane, isoflurane, and halothane on regional myocardial blood flow in the ischemic canine heart

The effects of sevoflurane (Sev), isoflurane (Iso), and halothane (Hal) on coronary circulation were studied in 30 dogs with acute coronary arterial stenosis. Regional myocardial blood flow (rMBF) was measured by hydrogen clearance method. There was no significant difference between each anesthetic agent in heart rate, mean arterial pressure, and cardiac output under any anesthesia level. As the inspired concentration of each anesthetic is increased, rMBF decreased significantly and rMBF/rate-pressure-product (RPP) ratio increased in normal area. In Sev and Iso groups, rMBF/RPP ratios were higher than that in Hal group, suggesting luxury perfusion caused by Sev and Iso. In the ischemic area, rMBF was reduced depending on the inspired concentration of each anesthetic agent and transmural maldistribution of blood flow was not observed with any anesthetic agent. Nevertheless the ratio of rMBF in ischemic area to that of normal area was decreased in Sev and Iso groups, but not in Hal group. In this study, neither Sev nor Iso worsened regional myocardial ischemia. However, Sev-induced coronary vasodilation may cause regional myocardial ischemia by redistribution of flow under steal prone condition.     

Effects of sevoflurane and isoflurane on the ratio of cerebral blood flow/metabolic rate for oxygen in neurosurgery

Purpose. To examine the changes in cerebral blood flow (CBF) equivalent (CBF divided by cerebral metabolic rate for oxygen) during craniotomy under isoflurane and sevoflurane anesthesia in patients with intracranial disorders. Method. In 16 neurosurgical patients (8 anesthetized with isoflurane and 8 with sevoflurane), the CBF equivalent was measured while the end-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 minimum alveolar concentration (MAC) before surgery, and then 1.0 MAC during surgery, which lasted more than 4 h. Results. There was no significant difference in CBF equivalent at 0.5 MAC between the isoflurane (20 ± 4 ml blood/ml oxygen) and the sevoflurane (19 ± 4 ml blood/ml oxygen) groups. With increasing anesthetic depth from 0.5 to 1.0 MAC, the CBF equivalent significantly (P < 0.05) increased in both groups (22 ± 7 and 21 ± 5, respectively). At 1.0 MAC during operation, the CBF equivalent with both anesthetics was maintained with minimal fluctuation for 4 h. There were no significant differences in the average value of the CBF equivalent during a 4-h period at 1.0 MAC between the isoflurane (23 ± 5) and the sevoflurane (20 ± 4) groups. Conclusion. Deepening anesthesia from 0.5 to 1.0 MAC with isoflurane and sevoflurane produced a slight increase in the CBF equivalent. The CBF equivalent at 1.0 MAC was maintained with no difference between the two agents during 4 h of neurosurgery. Received: August 2, 1999 / Accepted: April 3, 2000     

Blood/gas partition coefficients of halothane,isoflurane and sevoflurane in horse blood

Background. Blood/gas partition coefficients (_b/g) for volatileagents in horse blood are reported for halothane but not forisoflurane and sevoflurane. We measured the _b/g of halothane,isoflurane and sevoflurane in the blood of fasted horses. Thecorrelation with age, weight and some haematological and biochemicalvariables was studied. The temperature correction factor forisoflurane solubility was calculated. Methods. Twenty-four horses were randomly allocated to halothane(n=8), isoflurane (n=8) or sevoflurane (n=8). Blood sampleswere taken after 10 h’ fasting. Calculation of _b/g wasbased on the measurement of anaesthetic partial pressures inblood at 37 °C, which was achieved with tonometer equilibrationand headspace gas chromatography. Results. Mean _b/g was 1.66 (SD 0.06) for halothane, 0.92 (0.04)for isoflurane, and 0.47 (0.03) for sevoflurane. The _b/g valueswere all significantly lower than in humans (P<0.001). Nocorrelation was found between _b/g and weight, age, haematocrit,plasma triglycerides, cholesterol or total bilirubin. The changein isoflurane solubility per 1 °C temperature increase was–2.63 (0.13)%. Conclusion. The _b/g values of halothane, isoflurane and sevofluranein fasted horses are significantly lower than those reportedin humans. The _b/g for halothane in this study agrees with valuesreported in the literature but a positive correlation with plasmatriglycerides could not be confirmed. Knowledge of _b/g can refinemodels of anaesthetic uptake. Br J Anaesth 2003; 91: 276–8     

The comparative cardiovascular effects of sevoflurane with halothane and isoflurane

Using closed chest dogs, the cardiovascular effects of sevoflurane were compared with those of halothane and isoflurane in equipotent doses of 1.0, 1.5, 2.0, 2.5 and 3.0 MAC. They were evaluated by the changes of arterial blood pressure, central venous pressure, pulmonary artery pressure, maximum rate of left ventricular pressure rise (LV dp/dt), cardiac output and coronary sinus blood flow. The suppression of left cardiac function by sevoflurane was less than that of halothane, but was greater than that of isoflurane. Heart rate, systemic vascular resistance with sevoflurane were slightly lower than that of isoflurance. The coronary sinus blood flows with sevoflurane and isoflurane were significantly (P < 0.05 at 1.0 MAC, P < 0.005 at 2.0 MAC) higher than halothane. There was no significant difference on coronary sinus flow between sevoflurane and isoflurane. The depth of anesthesia could be quickly changed by adjustment of inspired sevoflurane concentration in comparison with the other two anesthetics.(Kazama T, Ikeda K: The comparative cardiovascular effects of sevoflurane with halothane and isoflurane. J Anesth 2: 63–68, 1988)     

The effects of sevoflurane and halothane anesthesia on cerebral blood flow velocity in children

We compared cerebral blood flow velocity during anesthesia with sevoflurane and halothane in 23 children admitted for elective surgery (age, 0.4-9.7 yr; median age, 1.9 yr; ASA physical status I-II). Inhaled induction was performed in a randomized sequence with sevoflurane or halothane. Under steady-state conditions, cerebral blood flow velocity (systolic [V(s)], mean [V(mn)], and diastolic [VD]) were measured by a blinded investigator using transcranial pulsed Doppler ultrasonography. The anesthetic was then changed. CBFV measurements were repeated after washout of the first anesthetic and after steady-state of the second (equivalent minimal alveolar concentration to first anesthetic). The resistance index was calculated. VD and V(mn) were significantly lower during sevoflurane (V(mn) 1.35 m/s) than during halothane (V(mn) 1.50 m/s; P = 0.001), whereas V(s) was unchanged. The resistance index was lower during halothane (P < 0.001). Our results indicate lower vessel resistance and higher mean velocity during halothane than during sevoflurane. IMPLICATIONS: The mean cerebral blood flow velocity is significantly decreased in children during inhaled anesthesia with sevoflurane than during halothane. This might be relevant for the choice of anesthetic in children with risk of increased intracranial pressure, neurosurgery, or craniofacial osteotomies.     

Comparison of the cardiovascular effects of isoflurane and sevoflurane as measured by magnetic resonance imaging in children with congenital heart disease

STUDY OBJECTIVE: To compare the cardiovascular effects of isoflurane and sevoflurane at minimum alveolar concentration (MAC) = 1 in children with congenital heart disease using cardiac magnetic resonance imaging. DESIGN: Randomized, crossover, single-blinded study. SETTING: Tertiary-care teaching hospital. PATIENTS: 10 pediatric patients with congenital heart diseases scheduled to undergo cardiac magnetic resonance studies. INTERVENTIONS: Patients were randomized to receive either isoflurane or sevoflurane as the "first inhalation agent." After a period or more than 20 minutes, they were crossed over to receive the "second inhalation agent." MEASUREMENTS: Heart rate, mean arterial pressure (MAP), cardiac index, stroke volume index, and ejection fraction (EF) at one MAC for both agents were all recorded. MAIN RESULTS: Both isoflurane and sevoflurane caused a significant decrease in MAP from the baseline (P = 0.013). The mean values (+/-SD) of stroke volume (mL), cardiac index (L min(-1) m(-2)), and EF (%) for isoflurane versus sevoflurane were 21.5 (+/-9.2) versus 19.6 (+/-6.2), 4.1 (+/-1.2) versus 3.7 (+/-0.87), and 64.2 (+/-14.5) versus 62.5 (+/-13.8), respectively. CONCLUSION: Both isoflurane and sevoflurane were found to be comparable in terms of cardiovascular effects.     

Mivacurium infusion requirement and spontaneous recovery of neuromuscular transmission in children anaesthetized with nitrous oxide and fentanyl,halothane, isoflurane or sevoflurane

BACKGROUND: Forty children, aged 3-11 years, ASA I or II, were allocated at random to receive N2O/O2-fentanyl or 1 MAC halothane, isoflurane or sevoflurane-N2O/O2 anaesthesia. Mivacurium was used for muscle relaxation. METHODS: Electromyographic response of the adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using the Relaxograph (Datex, Helsinki, Finland). An intubating dose of mivacurium, 0.2 mg.kg-1 was given, and when T1 returned to 5%, muscle relaxation was maintained by continuous infusion of mivacurium, adjusted manually to maintain a stable 90-99% block. RESULTS: Halothane, isoflurane and sevoflurane groups had lower infusion requirements for mivacurium than the N2O-fentanyl group (P=0.000083). Mivacurium requirement was 18.8 +/- 6.8, 10.8 +/- 4.2, 6.9 +/- 3.9 and 9.6 +/- 5.6 microg.kg-1.min-1 for children receiving N2O/O2-fentanyl, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: Spontaneous recovery from T1=10% to TOF ratio=0.7 was insignificantly prolonged from 6.3 to 12.5 min in the fentanyl group to 7-16.5 min in children anaesthetized with inhalational anaesthetics.     

Direct vasodilation by sevoflurane, isoflurane, and halothane alters coronary flow reserve in the isolated rat heart

Direct vasodilation of coronary resistance vessels by anesthetics may reduce coronary flow reserve and interfere with myocardial flow-metabolism coupling. This study was performed to evaluate the potential for the halogenated anesthetic agents sevoflurane, isoflurane, and halothane to alter the regulation of coronary flow via a direct action on coronary resistance vessels. Coronary flow and flow reserve were measured in the quiescent isolated perfused rat heart at anesthetic concentrations between 0 and 3 x MAC. In order to minimize anesthetic-induced secondary changes in coronary resistance, constant coronary perfusion pressure was maintained; the left ventricular cavity was vented; and tetrodotoxin was used to achieve cardiac arrest. These conditions permitted the dissociation of direct anesthetic actions from indirect regulatory processes affecting coronary vascular resistance (CVR). Coronary flow reserve was defined as the difference between coronary flow prior to and during administration of a maximally vasodilating dose of adenosine. Each anesthetic significantly reduced the magnitude of both CVR and coronary flow reserve in a concentration-dependent manner. Sevoflurane reduced coronary flow reserve significantly less than did halothane and isoflurane. At high concentrations (3.0 x MAC), coronary flow reserve was abolished by halothane and was decreased to near zero by isoflurane; however, flow reserve was reduced only 48% from control by sevoflurane. This difference among anesthetics is explained primarily by variations in the magnitude of direct coronary vasodilation produced by each anesthetic, rather than by effects on maximal vasodilator capacity. These data show that sevoflurane's intrinsic vasodilator action on coronary resistance vessels differs substantially from that of halothane and isoflurane.     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.     

The influence of halothane, isoflurane and sevoflurane on rocuronium infusion in children

BACKGROUND: Rocuronium is a non-depolarizing neuromuscular blocking agent with intermediate duration of action and without significant cumulative properties, suitable for continuous infusion. This study was designed to determine the infusion requirements in children under nitrous oxide and fentanyl, halothane, isoflurane or sevoflurane anaesthesia. METHODS: Forty children, 3-11 years old, ASA physical status group I or II were studied. They were randomly allocated to receive fentanyl-nitrous oxide, 1 MAC halothane-nitrous oxide, 1 MAC isoflurane-nitrous oxide or 1 MAC sevoflurane-nitrous oxide anaesthesia. Rocuronium, 0.6 mg(-1) was used to facilitate endotracheal intubation. Electromyographic response of adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using Relaxograph (Datex, Helsinki, Finland). Once the first twitch response (T1) returned to 5%, muscle relaxation was maintained by continuous infusion of rocuronium, adjusted automatically in a closed-loop system to maintain a stable 90-99% T1 depression. The block was considered stable if it changed by no more than 2% over a 10-min observation period. RESULTS: Halothane, isoflurane and sevoflurane groups had ower infusion requirements than the fentanyl-nitrous oxide group (P<0.00075). Rocuronium requirement (mean +/- SD) at one hour from the commencement of anaesthesia was 16.7+/-2.3, 13.6+/-3.7, 13.1+/-5.1 and 8.4+/-1.6 microg x kg(-1) x min(-1) for children receiving fentanyl-nitrous oxide, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: The rocuronium infusion rate required to maintain stable 90-99% T1 depression was reduced by approximately 20% with halothane and isoflurane anaesthesia, and by 50% with evoflurane anaesthesia when compared to fentanyl-nitrous oxide anaesthesia. Significant patient-to-patient variability of infusion rate makes monitoring of neuromuscular transmission necessary.     

Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart

This study was designed to examine the effects of inhalationanaesthetics on function and metabolism in isolated ischaemicrat hearts. Four volatile anaesthetics in two different concentrations(1.0 to 1.5 MAC) were used before whole heart ischaemia wasinduced for 1 5 mm followed by reperfusion for 30 mm. The datawere compared with a control group in which inhalation anaestheticswere not used. Before ischaemia, volatile anaesthetics depressedventricular function. During reperfusion, ventricular functionand coronary flow in both halothane groups were significantlylower than those in the control group. Myocardial ATP concentrationsin the 1.0 MAC of enflurane and isoflurane groups were significantlyhigher than those in the control group. We conclude that halothanehad more depressant effects than the other anaesthetics andthat enflurane and isoflurane may enhance metabolic recoveryin the ischaemic working rat heart. (Br. J. Anaesth. 1995; 74:569–575)     

Arterial to inspired partial pressure ratio of halothane, isoflurane, sevoflurane and desflurane in rats

The inspired partial pressure of an anaesthetic is often used as an index of arterial partial pressure in small animal experiments. We have investigated the influence of anaesthetic solubility on the ratio of arterial to inspired partial pressure in 24 rats, allocated randomly to receive halothane, isoflurane or desflurane at four different inspired concentrations. The arterial partial pressure of the volatile agent was measured by two-stage headspace analysis using a gas chromatograph calibrated with the same gas used to calibrate the Datex Capnomac that measured the inspired concentration. Mean values of arterial to inspired ratio at the lowest concentrations were 0.60 (95% confidence intervals 0.50, 0.71) for 0.8% halothane, 0.54 (0.38, 0.69) for 0.8% isoflurane, 0.72 (0.59, 0.86) for 1.5% sevoflurane and 0.71 (0.54, 0.87) for 4% desflurane. Analysis of variance showed a significant effect of anaesthetic agent (P = 0.008) on the arterial to inspired ratio. Thus volatile anaesthetic agents do not demonstrate a fixed arterial to inspired ratio in rats.      

Concentration-dependent inotropic effects of halothane, isoflurane and sevoflurane on rat ventricular myocytes

We have described the concentration-dependent inotropic effects of halothane, isoflurane and sevoflurane on rat ventricular cells and investigated the role of the sarcoplasmic reticulum (SR) in these inotropic actions. Single ventricular myocytes, isolated from rat hearts, were stimulated electrically at 1 Hz and contractions recorded optically. Cells were exposed to a range of concentrations of halothane, isoflurane or sevoflurane for a period of 1 min to determine the concentration-dependency of their inotropic actions. For each anaesthetic, the peak negative inotropic action was determined early during an exposure, and sustained negative inotropic action was measured at steady-state just before wash-off. In some experiments, cells were equilibrated with ryanodine 1 microgramsmol litre-1 to investigate the role of the SR in these intropic effects. Halothane caused a concentration-dependent initial increase in contractions (to mean 130 (SEM 28)% at 10 mmol litre-1) followed by rapid onset of a negative inotropic effect (K0.5 0.34 mmol litre-1 for peak effect; K0.5 0.46 mmol litre-1 for sustained effect). Exposure to isoflurane induced a small potentiation of contractions in some cells, followed by a concentration-dependent decrease in contraction in all cells (K0.5 0.85 mmol litre-1 for peak effect; K0.5 1.92 mmol litre-1 for sustained effect); contractions recovered partially during a 1-min exposure. On wash-off, contractions were increased transiently above control. Sevoflurane caused a large initial decrease in contraction which then returned rapidly towards control (K0.5 0.2 mmol litre-1 for peak effect; K0.5 2.57 mmol litre-1 for sustained effect). In common with isoflurane, removal of sevoflurane caused a transient increase in contractions above control. After exposure to ryanodine, the positive inotropic effects of halothane and isoflurane did not occur, and recovery of contractions during exposure to isoflurane and sevoflurane was abolished as was the transient increase in contractions seen on wash-off, indicating that these effects were mediated via the SR. Halothane had the most potent sustained negative inotropic effect but there was little difference between the negative inotropic effects of isoflurane and sevoflurane at clinically relevant concentrations. At higher concentrations, sevoflurane caused a less potent negative inotropic effect than isoflurane. The SR plays a major role in the effects of all three anaesthetics. One possible mechanism underlying the initial potentiation of contraction by halothane (and isoflurane) may be sensitization of the Ca(2+)-induced Ca(2+)-release process of the SR.      

Comparison of the effects of sevoflurane, isoflurane and halothane on rat myocardium

The effects of sevoflurane on myocardial contraction and relaxation are poorly understood. Therefore, we studied the effects of equianaesthetic concentrations (0.5, 1, 1.5, 2 and 2.5 MAC) of sevoflurane, isoflurane and halothane on inotropic and lusitropic (myocardial relaxation) variables, and post-rest potentiation in rat left ventricular papillary muscles in vitro. Sevoflurane and isoflurane caused comparable concentration-dependent negative inotropic effects which were significantly lower than those induced by halothane (P < 0.05). Sevoflurane and isoflurane did not modify lusitropic variables under low or high load, whereas halothane showed a negative lusitropic effect at high concentrations. Halothane suppressed post-rest potentiation, whereas isoflurane and sevoflurane did not. Post-rest recovery was unaffected by halothane, isoflurane or sevoflurane at any concentration. Thus in rat myocardium, sevoflurane and isoflurane caused comparable negative inotropic effects, had no significant lusitropic effects and did not alter post-rest potentiation, suggesting that they did not significantly modify the functions of the sarcoplasmic reticulum.      

Effect of halothane, isoflurane and fentanyl on spectral components of heart rate variability

We have examined the effect of isoflurane, halothane and fentanylon heart rate variability (HRV) using power spectral analysis(PSA). Forty patients were allocated randomly to receive oneof four anaesthetic techniques. Anaesthesia was induced withpropofol 2 mg kg^–1 and all patients breathed a mixtureof 66% nitrous oxide in oxygen. Twenty of these spontaneouslybreathing patients received 1.5% isoflurane and 20 received0.75% halothane. Ten patients in each of these groups receivedfentanyl 1 µg kg^–1 before induction. PSA was performedon 5-min segments of beat-to-beat R-R interval data taken beforeand 5 min after induction. No significant difference was observedin time domain or spectral HRV measures between inhalation agents.Fentanyl was associated with significantly slower heart rates,although no difference was observed in the power spectrum ofthose receiving fentanyl. Analysis of pooled data from the 40subjects showed that mean heart rate was unchanged and heartrate SD was decreased, as were total and individual powers inthree frequency bands of the HRV spectrum (low 0.02–0.08Hz, mid 0.08–0.15 Hz and high 0.15–0.45 Hz). A significantdecrease in the ratio of high power to (low+mid) power indicateda shift towards sympatholysis with anaesthesia. However, a significantlygreater depression of mid frequency components in comparisonwith low or high frequencies suggests that anaesthesia selectivelydepressed components of the HRV mechanism, independent of ageneral effect on autonomic tone.     

Rapid inhalation induction in children: 8% sevoflurane compared with 5% halothane

Sevoflurane has a lower blood-gas solubility and a less pungent odour than halothane; this may allow more rapid induction of anaesthesia. In a randomized, blinded study, we compared the induction characteristics of maximum initial inspired concentration of 8% sevoflurane and 5% halothane using conventional vaporizers in children aged 3 months to 3 years. There was no statistically significant difference in induction times between the two groups: mean times to loss of consciousness were 1 min 12 s (SD 18 s, range 40 s-1 min 44 s) for sevoflurane and 1 min 16 s (SD 17 s, range 50 s-1 min 52 s) for halothane, although these times were shorter than in previous studies using a gradual increase in vapour concentration. A small number of complications were noted in both groups, although none interfered with induction of anaesthesia. Struggling scores were lower in the sevoflurane group than in the halothane group (chi-square for trends = 6.34, P < 0.02). A significant number (11 of 15) of parents of children in the sevoflurane group who had previous experience of halothane induction preferred sevoflurane (chi-square for trends = 4.03, P < 0.05). We conclude that with this technique, induction was rapid with both sevoflurane and halothane. Our assessment of patient struggling and parents' perceptions suggests that induction with sevoflurane was more pleasant than with halothane.      

Solubility of desflurane (I-653), sevoflurane, isoflurane, and halothane in human blood

The blood/gas partition coefficients for the new volatile anesthetic agent desflurane (I-653), sevoflurane, isoflurane, and halothane were determined, simultaneously, in 8 human volunteers to compare the solubilities of these agents in blood. The blood/gas partition coefficient for desflurane [0.49 +/- 0.03 (mean +/- SD)] was smallest, followed by sevoflurane (0.62 +/- 0.04), isoflurane (1.27 +/- 0.06), and halothane (2.46 +/- 0.09). Differences among the anesthetic agents were significant (P less than 0.001). The results of this study confirm that among these agents the solubility of desflurane in human blood is the smallest. The results suggest that the washin and washout of desflurane will be more rapid than that of sevoflurane, isoflurane, and halothane, and the washin and washout of sevoflurane will be more rapid than that of isoflurane and halothane.