The effects of sevoflurane and desflurane anesthesia on QTc interval and cardiac rhythm in children

BACKGROUND: Inhalational anesthetics may prolong QTc interval (QT interval corrected for heart rate) of the ECG and cause life-threatening arrythmias. The effects of desflurane on QTc interval and cardiac rhythm have not been reported previously in children. We assessed the effects of desflurane anesthesia on QTc interval and cardiac rhythm and compared them with sevoflurane anesthesia in children. METHODS: The study was performed on 20 children admitted for inguinal hernia repair, with normal QTc intervals. Anesthesia was induced with propofol and intubation was achieved with vecuronium. Anesthesia was maintained with 2% sevoflurane (group I, n = 11) or 6% desflurane (group II, n = 9) and 66% nitrous oxide in oxygen. Electrocardiogram recordings were obtained by Holter recorder. QTc intervals were measured at baseline, 5, 10, 15, and 30 min after inhalation. RESULTS: None of the patients had significant arrythmia with desflurane anesthesia. One patient in the sevoflurane group had single, bigemini and multiform ventricular extrasystoles. There was no statistically significant difference in the baseline QTc values of the groups. Desflurane significantly prolonged QTc interval 5 min after induction until 30 min of anesthesia compared with baseline values (P = 0.029), while no significant prolongation was observed with sevoflurane (P = 0.141). CONCLUSIONS: Use of 2% sevoflurane during maintenance of anesthesia does not significantly prolong QTc interval while 6% desflurane significantly prolonged QTc interval in children with normal QTc interval undergoing inguinal herniorrhaphy.     

The effect of inhalational anaesthetics on QTc interval

BACKGROUND AND OBJECTIVE: The aim of this study was to assess time dependent cumulative effects of three different inhalation anaesthetics on QTc interval during the maintenance of anaesthesia. METHOD: Seventy-five ASA I-II male patients undergoing inguinal herniorrhaphy were randomly allocated into three groups. No premedication was given. Anaesthesia was induced with thiopental and tracheal intubation was facilitated by vecuronium in all groups. Anaesthesia was maintained with 0.8% halothane (Group I) (n = 25), 1% isoflurane (Group II) (n = 25), or 2% sevoflurane (Group III) (n = 25) and 66% nitrous oxide in oxygen. Three lead electrocardiogram recordings were taken before induction, 2, 5, 10, 15, 30 and 45 min after induction and after extubation. Heart rate, systolic, diastolic, mean arterial pressure and SpO2 were recorded at the same time. Heart rate and corrected QT interval were evaluated by using Bazett's formula. Multivariate analysis of variance for repeated measures was used to determine intergroup and intragroup differences. RESULTS: There was no statistically significant difference in the baseline QTc values of the groups. There was no difference between QTc values with halothane and sevoflurane. There was a difference between QTc values with isoflurane and those with the other two inhalation anaesthetics (P < 0.05). Although QTc values in the isoflurane group were higher at all times, the critical value of 440 ms was not exceeded. CONCLUSION: We conclude that halothane 0.8%, isoflurane 1% and sevoflurane 2% do not prolong QTc interval.     

QTc interval and QTc dispersion during haemodiafiltration

BACKGROUND and AIM: Our aim was to evaluate QTc interval and QTc dispersion in 27 end-stage renal disease (ESRD) patients undergoing Acetate Free Biofiltration (AFB) in order to ascertain any correlations between the electrrocardiographic (ECG) parameters, serum Na+, K+, Ca++, Mg++ and intraerythrocytic Mg++ (Mg++e) concentrations. All measures were made at t0 (session beginning), t1 (first hour), t2 (second hour), t3 (third hour), and t4 (session end). RESULTS: Blood pressure, heart rate, bodyweight and total ultrafiltration in the three dialysis sessions were constant. A significant progressive increase occurred in serum Ca++ during the sessions, while there was a significant diminution in serum K+. The pattern for Mg++ concentrations in serum and erythrocytes differed: in serum it decreased, whereas Mg++e increased. At t4, the QTc interval was reduced to a significant extent with respect to the baseline value. QTc dispersion significantly increased at t1 without there being significant variations at other times with respect to t0. At t2, t3 and t4, values promptly returned to baseline levels. QTc had a negative correlation with serum Ca++ levels at t4. In contrast, an inverse correlation was found between QTc dispersion and serum K+ at t1. No other correlations could be found between any other electrolytes, QTc interval or QTc dispersion. CONCLUSION: In conclusion, the decrease observed in the QTc interval at the end of an AFB session was inversely related to serum Ca++ concentrations. Moreover, an increase in QTc dispersion occurred during the first hour of the session, and was negatively correlated with serum K+.     

Effect of anthracyclines and isoflurane on QTc interval

BackgroundAnaesthetics and anthracyclines can affect the QT interval of the electrocardiogram (ECG). This study investigated whether the use of isoflurane in anthracyclines pretreated patients may induce or augment the QT prolongation to an arrhythmogenic level.Materials and methodsFifty-four female patients with breast cancer scheduled for mastectomy were included in the study, 27 received anthracyclines based chemotherapy before surgery, whereas 27 did not. All patients received a standardized balanced anaesthetic in which 0.5% end tidal concentration of isoflurane was used. The QT and corrected QT intervals (QTc) were measured before anaesthesia, after 1, 5, 15, 30, 60 min, respectively, following intubation and during recovery from anaesthesia.ResultsStatistically significant QTc prolongation was observed in patients who received anthracycline chemotherapy even prior to the administration of anaesthesia. The comparison of QTc interval at different intervals of isoflurane anaesthesia also showed a statistically significant difference between the two groups namely anthracycline treated group (study group) versus control group.A sample size of 27 in each group was calculated in order to achieve a study power of 80% with type 1 error rate of 5%. For the purpose of calculation, values of QT and QTc interval (range, mean, standard deviation) from the study of Owczuk et al. were used. t-test and analysis of variance were employed using SPSS version 10. P < 0.05 was considered as statistically significant.ConclusionsAnthracycline chemotherapy can produce significant prolongation of QTc interval. In addition, use of 0.5% end tidal concentration of isoflurane can further augment the QTc interval significantly.     

Influence of autonomic neuropathy on QTc interval lengthening during hypoglycemia in type 1 diabetes

Hypoglycemia produces electrocardiographic QTc lengthening, a predictor of arrhythmia risk and sudden death. This results from both sympatho-adrenal activation and a lowered serum potassium. It has been suggested that cardiac autonomic neuropathy (CAN) might indicate those who are at particular risk. We tested this hypothesis in 28 adults with type 1 diabetes and 8 nondiabetic control subjects. After standard tests of autonomic function and baroreflex sensitivity (BRS) measurement, diabetic participants were divided into three groups: 1) CAN- with normal BRS (BRS+; n = 10), 2) CAN- with impaired BRS (BRS-; n = 9), and 3) CAN+ (n = 9). QTc was then measured during controlled hypoglycemia (2.5 mmol/l) using a hyperinsulinemic clamp. Mean (+/-SE) QTc lengthened from 377 +/- 9 ms (baseline) to a maximum during hypoglycemia of 439 +/- 13 ms in BRS+ subjects and from 378 +/- 5 to 439 +/- 10 ms in control subjects. Peak QTc tended to be lower in CAN+ (baseline, 383 +/- 6; maximum, 408 +/- 10) and BRS- groups (baseline, 380 +/- 8; maximum, 421 +/- 11; F = 1.7, P = 0.18). Peak epinephrine concentrations (nmol/l) were 3.1 +/- 0.8 (BRS+), 2.6 +/- 0.5 (BRS-), 1.4 +/- 0.3 (CAN+), and 5.7 +/- 0.8 (control subjects). These data do not indicate that those with CAN are at particular risk for abnormal cardiac repolarization during hypoglycemia. Indeed, they suggest that such patients may be relatively protected, perhaps as a result of attenuated sympatho-adrenal responses.     

The effects of sevoflurane, isoflurane and desflurane on QT interval of the ECG

BACKGROUND AND OBJECTIVE: To determine if there is any significant difference between the effects of desflurane, isoflurane and sevoflurane on the QT interval, QT dispersion, heart rate corrected QT interval and QTc dispersion of the electrocardiogram. METHODS: The study was conducted in a prospective, double blind and randomized manner in a teaching hospital. Ninety ASA I patients, aged 16-50 yr, undergoing general anaesthesia for noncardiac surgery were studied. RESULTS: There was no significant change in QT intervals during the study in any group (P > 0.05). QT dispersion in the sevoflurane group 49+/-14 ms vs. 37+/-10 ms; in the desflurane group 55+/-16 and 62+/-21 ms vs. 35+/-14 ms and in the isoflurane group 54+/-26 and 59+/-24 ms vs. 42+/-19 ms were significantly increased at 3 and 10 min after 1 MAC of steady end-tidal anaesthetic concentration compared with baseline values (P < 0.05). QTc values in the sevoflurane group were 444+/-24 and 435+/-2 1ms vs. 413+/-19 ms (P < 0.05), in the isoflurane group were 450+/-26 and 455+/-34 ms vs. 416+/-34 ms (P < 0.05), in the desflurane group were 450+/-26 and 455+/-34 ms vs. 416+/-34 ms (P < 0.05) at 3 and 10 min after reaching 1 MAC of anaesthetic concentration and significantly increased compared with baseline values. QTc dispersion increased significantly with sevoflurane 62+/-14 ms vs. 45+/-16 ms (P < 0.05); isoflurane 70+/-36 ms at 3 min and 75+/-36 ms at 10 min after reaching 1 MAC of anaesthetic concentration vs. 50+/-24 ms (P < 0.05); desflurane 67+/-25 ms at 3 min and 74+/-27 ms at 10 min after 1 MAC concentration vs. 41+/-22 ms (P < 0.05). CONCLUSION: Sevoflurane, isoflurane and desflurane all prolonged QTd, QTc and QTcd but there were no significant intergroup differences.     

Use of the QTc interval and QTc dispersion in patients on haemodialysis: assessment of reproducibility.

Sir, Cardiac arrhythmias, frequently encountered in haemodialysis(HD) patients [1], are one of the major causes of cardiac deathin end-stage renal disease (ESRD). Increased QT and QT dispersion(QTd) measurements on a surface electrocardiogram (ECG) haveshown to be a useful and reliable means for predicting susceptibilityto life threatening ventricular arrhythmias. QT interval, reflectingthe total ventricular recovery time, and QTd, a direct measureof regional heterogeneity of myocardial repolarization, areboth abnormally prolonged in ESRD [2]. Moreover, recently, theseelectrical markers were found to be independent predictors oftotal and cardiovascular mortality in both non-uraemic     

Effects of fentanyl pretreatment on the QTc interval during propofol induction

Prolongation of the corrected QT (QTc) interval is associated with various anaesthetic drugs. The QTc prolongation may become more exacerbated during laryngoscopy and intubation, which is possibly caused by sympathetic stimulation. The aim of this study was to investigate the effects of fentanyl on the QTc interval during propofol induction in healthy patients. The patients were randomly allocated to receive either fentanyl (n = 25) or saline (n = 25) before induction. The QTc interval was significantly prolonged immediately after intubation in control group compared to preceding values, but it did not change in the fentanyl group. The number of patients with the prolonged QTc interval exceeding 20 ms immediately after intubation compared to the baseline values was 14 in the control group and seven in the fentanyl group. In conclusion, pretreatment with fentanyl 2 microg x kg(-1) significantly attenuated QTc prolongation associated with laryngoscopy and tracheal intubation during propofol induction.     

The effect of bolus administration of remifentanil on QTc interval during induction of sevoflurane anaesthesia

Stimulation of the sympathetic nervous system associated with tracheal intubation causes corrected QT (QTc) interval prolongation. We postulated that the use of remifentanil during induction of anaesthesia might prevent this. Sixty unpremedicated, ASA grade 1 patients were selected and randomly allocated to receive either saline (group S), remifentanil 0.5 microg x kg(-1) (group R 0.5) or remifentanil 1.0 microg x kg(-1) (group R1.0) 1 min before laryngoscopy. The QTc interval was significantly prolonged immediately following intubation in group S and group R0.5, but it remained stable in group R1.0, compared with the QTc interval just before laryngoscopy. It is concluded that the administration of remifentanil 1.0 microg x kg(-1) before intubation can prevent the prolongation of the QTc interval associated with tracheal intubation during induction of anaesthesia with sevoflurane.     

Haemodialysis increases QTc interval but not QTc dispersion in ESRD patients without manifest cardiac disease

Sir, I read with interest the article by Covic and co-workers [1]showing that haemodialysis increases the QTc interval (mainlydue to rapid changes in electrolyte plasma concentrations),but not QTc dispersion in uraemic patients without manifest     

Effects of target concentration infusion of propofol and tracheal intubation on QTc interval

This study was designed to evaluate the effect of target controlled infusion of propofol on QTc interval and tracheal intubation. Twenty-five unpremedicated, ASA class I or II patients were selected and target concentration infusion of propofol at 5 microg x ml(-1) was used throughout the study. The QTc interval was measured before anaesthetic induction (baseline, T1), 10 min after propofol infusion (T2), immediately after tracheal intubation (T3), and 1 min after tracheal intubation (T4). The QTc interval increased significantly at 10 min after the propofol infusion started compared to baseline (p = 0.003). After tracheal intubation, the QTc interval was further increased when compared to that at T2 (p < 0.0001). The increased QTc interval was within normal limit and no patient had an arrhythmia. In conclusion, although statistically significant, the increase in QTc interval was too small to be clinically significant during propofol infusion. However, the combination of propofol and tracheal intubation must be used carefully in patients with prolonged QTc interval.     

Potassium removal increases the QTc interval dispersion during hemodialysis.

This study was planned to clarify the mechanism(s) by which hemodialysis increases the QTc dispersion, a marker of risk of ventricular arrhythmias. To this aim, 10 uremic patients, without any relevant heart diseases, underwent two different types of hemodialysis schedules. In the first, 1 h of isolated high rate ultrafiltration preceded the standard diffusive procedure. In the second, during the first hour of standard bicarbonate hemodialysis, the decrease of plasma potassium concentration was prevented by increasing K+ concentration in the dialysate, according to its pre dialysis plasma levels. During the high rate ultrafiltration period, together with ECG signs of increased sympathetic nervous system activity and catecholamines secretion, the QTc dispersion did not change significantly. Instead, an evident increment was observed 1 h after the start of the diffusive hemodialysis, then slowly progressing until the end of the dialysis and finally returning to the pre dialysis values within 2 h after the end of the session. To the contrary, the increase of the QTc dispersion was totally blunted during a standard hemodialysis procedure in absence of plasma K+ decrease, but appeared again when the K+ dialysate fluid concentration was restored to 2 mmol/l. This study provides evidence that the increase of QTc dispersion occurring on hemodialysis is mainly related to the diffusive process, more precisely to the K+ removal. This is one more reason to focus attention on K+ removal rate especially when hemodialysis treatment is given in uremics affected by cardiac diseases with high risk of arrhythmias.     

不同剂量艾司洛尔对气管插管诱发QT间期延长的影响

目的 评价不同剂量艾司洛尔对气管插管诱发QT间期延长的影响.方法 择期拟行腹腔镜下胆囊切除术患者60例,ASA分级Ⅰ或Ⅱ级,年龄20岁～60岁,用随机数字表法分为3组(每组20例):对照组(C组)、艾司洛尔1组(E1)、艾司洛尔2组(E2).E1组于麻醉诱导前5 min给予艾司洛尔0.3 mg/kg,后持续0.1 mg·kg-1·min-1输注;E2组麻醉诱导前5 min给予艾司洛尔0.3 mg/kg,后持续0.25 mg·kg-1·min-1输注;C组给予同容量的生理盐水.分别于给予艾司洛尔前(T0)、给予艾司洛尔后(T1)、给予依托咪酯后1 min(T2)、气管插管即刻(T3)、气管插管后30 s(T4)、2(T5)、4 min(T6)记录平均动脉压(MAP)、心率(HR),并描记心电图(ECG),比较3组患者的血压、HR、QT间期不同变化.结果 E1组和E2组在T1、T2、T4 QT间期分别为(382±11)、(380±6)、(406±13)ms和(379±13)、(370±11)、(400±7) ms.与C组比较,E1组和E2组在T1、T2、T4 QT间期显著缩短(P＜0.05),E1组和E2组之间差异无统计学意义(P＞0.05).结论 静脉诱导期间静脉注射0.3 mg/kg,后持续0.1 mg· kg-1·min-1输注艾司洛尔或者0.3 mg/kg后持续0.25 mg·kg-1·min-1输注艾司洛尔均可有效抑制气管插管诱发QT间期延长,有效抑制气管插管诱发的交感神经反射,但是0.3 mg/kg后持续0.25 mg· kg-1·min-1输注艾司洛尔更易导致低血压和心动过缓的发生.     

Renin-angiotensin polymorphisms and QTc interval prolongation in end-stage renal disease

BACKGROUND: Polymorphisms of renin-angiotensin system (RAS) genes in patients with end-stage renal disease (ESRD) on chronic hemodialysis may be associated with QTc interval prolongation, leading to fatal arrhythmias. The objective of this study was to determine (1) the prevalence of QTc prolongation in hemodialysis patients, and (2) the association of a prolonged QTc in these patients with RAS polymorphisms [angiotensin-converting enzyme-insertion/deletion (ACE-I/D), angiotensin type 1 receptor-A1166C (AT1R-A1166C), and angiotensinogen-M235T (AGT-M235T)]. METHODS: Twelve-lead electrocardiograms (ECGs), serum electrolytes (sodium, potassium, and calcium), and ACE and angiotensin II levels were obtained 10 to 12 hours after a hemodialysis session in 43 patients with ESRD on chronic hemodialysis [mean age (+/-SD), 55 +/- 14 years]. Using polymerase chain reaction (PCR), the presence of polymorphisms of the ACE-I/D, AT1R-A1166C, and AGT-M235T genes was determined from the buccal cells. A maximum QT interval in patients with sinus rhythm and normal QRS duration was corrected for heart rate using Hodges' formula. RESULTS: Fifty-eight percent of the patients had QTc interval prolongation (>440 msec). The ACE-DD genotype (P = 0.002) and the C allele of the AT1R-A1166C gene (P = 0.004), but not the AGT-M235T gene, contributed to QTc prolongation. CONCLUSION: Polymorphisms of ACE and AT1R genes additively contribute to QTc prolongation found in a great majority of ESRD patients. Therefore, ESRD patients with both or one of these polymorphisms may be at a higher risk for sudden cardiac death.     

The effect of esmolol on the QTc interval during induction of anaesthesia in patients with coronary artery disease

The aim of this study was to evaluate whether esmolol has an effect on QT interval during induction of anaesthesia using etomidate and fentanyl in patients with known coronary artery disease. Sixty patients were prospectively randomised to either a control group or the esmolol group. Esmolol was administered as a bolus 1 mg.kg⁻¹, followed by a continuous infusion at 250 μg.kg⁻¹min⁻¹. All patients received etomidate 0.3 mg.kg⁻¹ and fentanyl 15 μg.kg⁻¹. The ECG was recorded prior to induction of anaesthesia (T0), 5 min following the start of drug infusions (T1), 1 min following etomidate (T2), 3 min following vecuronium (T3), 30 s (T4), 2 min (T5) and 4 min (T6) after intubation. In the esmolol group, QTc interval was significantly shorter at T1, T2 and T4 compared to the control group (p < 0.05). In conclusion, QTc interval increased following tracheal intubation during induction of anaesthesia using etomidate and fentanyl. An infusion of Esmolol attenuated the QTc interval prolongation associated with tracheal intubation.     

艾司洛尔对老年冠心病患者气管插管QTc间期的影响

目的 评价艾司洛尔在麻醉诱导气管插管时对老年冠心病患者QTc间期的影响.方法 50例ASA Ⅱ级,年龄60～75岁择期全麻手术患者随机分为艾司洛尔组(E组)与对照组(C组).E组麻醉诱导前单次静脉缓慢注射艾司洛尔0.3 mg/kg后100 μg·kg-1·min-1持续输注至气管插管后4 mim;C组给予等容量生理盐水.记录给予艾司洛尔前(T0)、单次给予艾司洛尔或生理盐水后2 min(T1)、芬太尼与丙泊酚诱导后1 min(T2)、维库溴铵后3 min(插管前,T3)及插管后30 s(T4)、2 min(T5)与4 min(T6)QTc、MAP及HR变化.结果 T4～T6时QTc间期C组均长于T0时(P＜0.05),且C组明显长于E组(P＜0.01),其中QTc＞440 ms者C组显著多于E组(P＜0.05).结论 麻醉诱导气管插管期间老年冠心病患者QTc间期延长,而艾司洛尔可缩短与气管插管有关的QTc间期延长.     

Effects of halothane and quinidine on intracardiac conduction and QTc interval in pentobarbital-anesthetized dogs.

To confirm in vitro data that halothane and quinidine depressed cardiac conduction and prolonged action potential (AP) duration, the electrocardiogram and His bundle electrogram were recorded in dogs during basal pentobarbital anesthesia, after 1% halothane or quinidine (2.38 +/- 0.22 micrograms/mL serum concentration [mean +/- SEM]), or both. Purkinje fibers from a second dog were superfused with blood from the intact (support) dog, and APs were recorded. In the intact dogs, 1% halothane caused no changes in the electrocardiogram or His bundle electrogram. Quinidine prolonged QRS duration, QT interval, and rate-corrected QT (P < 0.05). Ventricular conduction (HS interval) slowed, and atrial effective refractory period increased (P < 0.05). Quinidine combined with halothane widened QRS, QT, and rate-corrected QT, prolonged the HS interval, and increased the vulnerability of the atrioventricular node to conduction block. Three of 20 dogs developed torsades de pointes-type ventricular tachycardia during simultaneous quinidine and halothane administration. In cross-superfused Purkinje fibers, the AP duration to 50% repolarization was shortened, and conduction time was prolonged by 1% halothane (both P < 0.05). Quinidine decreased AP amplitude, prolonged AP duration to 90% repolarization, and slowed conduction (P < 0.05). Quinidine combined with halothane decreased AP amplitude, and prolonged both AP duration to 90% repolarization and conduction (P < 0.05). When 1% halothane and therapeutic concentrations of quinidine are administered in dogs, depressed conduction and an acquired long QT syndrome with malignant ventricular arrhythmias may develop.