Effects of Practolol and Metoprolol on QT Interval, Heart Rate and Arterial Pressure during Induction of Anaesthesia

The effects of the selective β₁-adrenergic receptor blocking agents, practolol with intrinsic sympathetic activity (ISA) and metoprolol without ISA, were studied on QT interval, heart rate, arterial pressure and cardiac arrhythmias during the induction of anaesthesia in 142 adults. In the control group, the QT interval was statistically significantly prolonged after thiopental, and the most marked prolongation occurred after suxamethonium. Neither practolol nor metoprolol alone affected the QT interval. Practolol 100 μg/kg i.v., but not 40 or 150 μg/kg i.v., almost completely reduced the prolongation of the QT interval after suxamethonium. In all doses of 20, 30 and 40 μg/kg i.v. metoprolol statistically significantly and dose-dependently reduced the prolongation of the QT interval after thiopental, suxamethonium and laryngoscopy, but the prolongation of the QT interval after intubation still occurred. Practolol and metoprolol alone statistically significantly reduced heart rate, but did not prevent the increase of heart rate after thiopental. The effects on arterial pressure were minimal. Neither practolol nor metoprolol prevented the cardiovascular intubation response. Ventricular ectopic beats after intubation occurred in 20% of the patients in the control group and their incidence ranged from 20 to 27% in the groups pretreated with practolol or metoprolol 20 μg/kg. In the groups pretreated with metoprolol 30 or 40 μg/kg, ventricular ectopic beats occurred in 5% and 8%, respectively. It is concluded that the selective β₁-adrenergic receptor blocking agents practolol with ISA, and especially metoprolol without ISA, reduced the prolongation of the QT interval after suxamethonium. The results suggest that the prolongation of the QT interval after suxamethonium may be mediated by the stimulation of the sympathetic nervous system caused by suxamethonium.     

Perioperatives Monitoring des QT-Intervalls

The feasibility of routine perioperative monitoring of the QT interval is demonstrated for the first time in two patients suffering from acquired long QT syndrome. These cases demonstrate that automatic perioperative monitoring of the QT interval is simple and easy to achieve. Besides sufficient premedication, normalized electrolytes, a calm and quiet atmosphere, avoiding QT prolonging drugs and the possibility of immediate defibrillation, monitoring of the QT interval should be considered in the perioperative treatment of these cardiac risk patients.     

Idiopathic prolonged QT interval and QT dispersion: the effects of propofol during implantation of cardioverter-defibrillator

Local anaesthesia combined with conscious sedation is becoming a popular technique for implantation of cardioverter-defibrillator devices. Propofol was given to provide loss of consciousness during defibrillation shock administration, for induced ventricular fibrillation testing. Propofol was found to decrease QT interval and QT dispersion in two patients with idiopathic prolonged QT interval and QT dispersion. The findings of the procedure are reported.     

Torsade de pointes and long QT syndrome following major blood transfusion

We report a rare complication following transfusion of a large volume of blood in an adult patient. An electrophysiological disturbance of the cardiac cycle with prolongation of the QT interval developed, which was followed by recurrent episodes of torsade de pointes, a unique form of ventricular tachycardia. The most likely cause of this acquired long QT syndrome was hypomagnesaemia secondary to massive blood transfusion. Treatment with a magnesium infusion restored the QT interval to normal and temporary ventricular pacing prevented further ventricular arrhythmias.     

Sevoflurane-associated torsade de pointes in a patient with congenital long QT syndrome genotype 2

Although patients with congenital long QT syndrome (c-LQTS) are considered to be at high risk for anesthesia, few reports describe c-LQTS genotype-specific considerations for anesthesia. We describe a case of torsade de pointes (TdP) caused by sevoflurane in a patient with c-LQTS genotype 2 (LQT2). A 39-year-old woman diagnosed with c-LQTS was scheduled for an elective therapeutic abortion. Immediately after starting the operation, the patient developed TdP. Since pulseless ventricular tachycardia was sustained despite intravenous injection of lidocaine, defibrillation was performed. Analysis of the electrocardiogram revealed that the corrected QT interval before anesthesia was 530 ms and 2.0% sevoflurane markedly prolonged the corrected QT interval to 693 ms. Postoperative studies revealed a mutation in the KCNH2 gene. Anesthesiologists should note that patients with LQT2 could be more susceptible to volatile anesthetics than are those with other major genotypes. Genotype-specific management of anesthesia may reduce the risk of developing TdP during the perioperative period.     

Recovery from fatal ventricular fibrillation after immediate application of percutaneous cardiopulmonary support

We present a patient who recovered from refractory ventricular fibrillation after immediate application of percutaneous cardiopulmonary support (PCPS). On the postoperative day (POD) 3 after the Y-grafting surgery for abdominal aortic aneurysm, circulation collapsed due to sudden onset of ventricular fibrillation. Because ventricular fibrillation had persisted in spite of medical treatment and defibrillation, we established PCPS and his circulation recovered. Although an emergent coronary angiography revealed no new lesions, we performed an emergent percutaneous catheter intervention to deny the possibility that ischemic changes had contributed to the arrhythmia. Soon after percutaneous transluminal coronary angioplasty, we successfully weaned him from PCPS, and extubated his trachea on the POD 5 without any neurological deficits. On the POD 8, ventricular fibrillation occurred again and defibrillation was effective at this time. We suspected cardiac ischemia, prolonged QT interval, and electrical remodeling due to hypertrophic heart as possible causes of refractory ventricular fibrillation. Therefore, we performed percutaneous transluminal coronary angioplasty, terminated famotidine administration, maintained normal electrolytes level, started administration of beta-blocker, and implanted an cardioverter defibrillator. On the POD 16, he was discharged from the ICU with no neurological deficits.     

Increased prevalence of prolonged QT interval in males with primary or secondary hypogonadism: A pilot study

Symptoms and signs of male hypogonadism span all organ systems, including the cardiovascular apparatus. The electrocardiographic QT interval reflects cardiac ventricular repolarization and, if prolonged, increases the risk of malignant arrhythmias. QT interval duration is similar in boys and girls during childhood, but shortens in males after puberty and experimental studies suggest that testosterone is a major contributor to shortening of QT interval in men. The aim of the present pilot study was to assess the duration of ventricular repolarization in adult males with primary or secondary hypogonadism. Standard ECG recordings were performed in 26 men (mean age 39.2 ± 2.17 years) with pituitary or testicular hypogonadism and repeated in 15 patients during testosterone replacement. Twenty-six age-matched control men were also analysed. Measured QT intervals were corrected for heart rate according to Bazzett's formula (QTc = QT/√RR interval). The prevalence of prolonged QTc was considerably higher in hypogonadal patients (four of 26 men) than in control men (none, p  < 0.05) and in the general, healthy population (<2.5%). QTc interval normalized on hormone replacement therapy in the four patients presenting prolonged QTc in the hypogonadal state. Heart rate and left ventricular mass did not differ among the two groups and no known QT-prolonging factor was apparent in patients with abnormal QTc interval. In conclusion, a high number prolonged QT interval measurements was observed in hypogonadal men who may therefore be at increased risk for cardiac arrhythmias. This observation reveals an additional feature of male hypogonadism, which may benefit from testosterone replacement therapy.     

Increased Persistent Sodium Current Due to Decreased PI3K Signaling Contributes to QT Prolongation in the Diabetic Heart

Diabetes is an independent risk factor for sudden cardiac death and ventricular arrhythmia complications of acute coronary syndrome. Prolongation of the QT interval on the electrocardiogram is also a risk factor for arrhythmias and sudden death, and the increased prevalence of QT prolongation is an independent risk factor for cardiovascular death in diabetic patients. The pathophysiological mechanisms responsible for this lethal complication are poorly understood. Diabetes is associated with a reduction in phosphoinositide 3-kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including the persistent sodium current I_NaP. Here, we report a mechanism for diabetes-induced QT prolongation that involves an increase in I_NaP caused by defective PI3K signaling. Cardiac myocytes of mice with type 1 or type 2 diabetes exhibited an increase in APD that was reversed by expression of constitutively active PI3K or intracellular infusion of phosphatidylinositol 3,4,5-trisphosphate (PIP3), the second messenger produced by PI3K. The diabetic myocytes also showed an increase in I_NaP that was reversed by activated PI3K or PIP3. The increases in APD and I_NaP in myocytes translated into QT interval prolongation for both types of diabetic mice. The long QT interval of type 1 diabetic hearts was shortened by insulin treatment ex vivo, and this effect was blocked by a PI3K inhibitor. Treatment of both types of diabetic mouse hearts with an I_NaP blocker also shortened the QT interval. These results indicate that downregulation of cardiac PI3K signaling in diabetes prolongs the QT interval at least in part by causing an increase in I_NaP. This mechanism may explain why the diabetic population has an increased risk of life-threatening arrhythmias.Patients with diabetes are at increased risk of developing life-threatening cardiac arrhythmias, independent of other risk factors such as atherosclerosis and hypertension. Diabetes is an independent risk factor for sudden cardiac death, mortality after myocardial infarction, and major complications of acute coronary syndrome such as ventricular arrhythmias (1). However, pathophysiological mechanisms responsible for the increased risk of sudden cardiac death remain poorly understood, and consequently there has been relatively little progress in the prevention and treatment of this diabetes complication. QT interval prolongation on the electrocardiogram (ECG) is a well-established risk factor for lethal ventricular arrhythmias (2), and not only do diabetic patients have a greater prevalence of QT interval prolongation than control populations (3,4), but a prolonged QT interval corrected for heart rate (QTc) is an independent risk factor for cardiovascular death in diabetic people (5–7).The signaling defect that causes QT interval prolongation in diabetes has remained elusive. An interesting lead came from our recent demonstration that decreased cardiac phosphoinositide 3-kinase (PI3K) signaling results in QT interval prolongation and is responsible for the increased risk of long QT syndrome and lethal arrhythmias caused by some anticancer drugs (8). Our results raised the possibility that suppression of this signaling pathway might also play a role in QT interval prolongation associated with diabetes, where reduced production of or sensitivity to insulin results in decreased activation of PI3K and its downstream effector, Akt.Primary prolongation of the QT interval (i.e., that which is independent of an altered QRS complex on the ECG) results from lengthening of the action potential duration (APD) in individual cardiac myocytes. The APD is regulated by inward and outward ion currents, and our previous study demonstrated that PI3K signaling regulates both types. PI3K inhibition caused reductions in the L-type calcium current (I_CaL), the delayed rectifier potassium currents I_Kr and I_Ks, and the peak sodium current (I_Na), whereas it caused an increase in the persistent (late) sodium current (I_NaP) (8). In the current study, we used mouse models to investigate a possible connection between decreased cardiac PI3K signaling and the prolonged QT interval in diabetes. Whereas I_Kr and I_Ks play little or no role in regulating the APD in adult mouse myocytes (9,10), I_NaP has a major role, such that expression of gain-of-function mutant sodium channels that increase I_NaP prolongs the murine APD and QT interval (11,12). Therefore, we used I_NaP as a marker of PI3K effects on cardiac ion channels and asked whether an increase in I_NaP contributes to QT interval prolongation in these diabetic mouse models.     

QT dispersion in patients with end-stage renal failure and during hemodialysis.

Interlead variability of the QT interval in surface electrocardiogram (ECG), i.e., QT dispersion, reflects regional differences in ventricular recovery time, and it has been linked to the occurrence of malignant arrhythmias in different cardiac diseases. The purpose of the study was to assess the effect of hemodialysis on QT and corrected QT (QTc) interval and dispersion in chronic hemodialyzed patients. Data of 34 nondiabetic patients (male/female = 21/13; mean age, 54 +/- 15 yr) on chronic hemodialysis were studied. Polysulfone capillaries and bicarbonate dialysate containing (in mEq/L) 135 Na+, 2.0 K+, 1.5 Ca2+, and 1.0 Mg2+ were used. Simultaneous 12-lead ECG were recorded before and after hemodialysis in a standard setting. The QT intervals for each lead were measured manually on enlarged (x3) ECG by one observer using calipers. Each QT interval was corrected for patient heart rate: QTc = QT/square root of RR (in milliseconds [ms]). The average cycle intervals were 853 +/- 152 ms predialysis and 830 +/- 173 ms postdialysis; the difference was not significant. The maximal QT interval changed significantly from 449 +/- 43 to 469 +/- 41 ms (P < 0.01). The corrected maximal QT interval increased significantly from 482 +/- 42 to 519 +/- 33 ms (P < 0.01). The QT dispersion changed from 56 +/- 15 to 85 +/- 12 ms (P < 0.001) and the corrected QT interval dispersion from 62 +/- 18 to 95 +/- 17 ms (P < 0.001). During hemodialysis, the serum potassium and phosphate levels decreased from 5.5 +/- 0.8 to 3.9 +/- 0.5 (mM) and from 2.3 +/- 0.5 to 1.6 +/- 0.4 (mM), respectively, whereas calcium increased from 2.2 +/- 0.23 to 2.5 +/- 0.22 (mM). It is concluded that hemodialysis increases the QT and QTc interval and QT and QTc dispersion in patients with end-stage renal failure. Thus, it may be stated that the nonhomogeneity of regional ventricular repolarization increases during hemodialysis. Measurement of QT and QTc dispersion is a simple bedside method that can be used for analyzing ventricular repolarization during hemodialysis.     

Treatment of tachyarrhythmias in a patient with the long QT syndrome by autotransplantation of the heart and sinus node-triggered atrial pacing.

The case history of a 37-year-old woman with the long QT syndrome and drug-refractory paroxysmal ventricular tachyarrhythmias is reported. She was resuscitated eight times between 1980 and 1987. The duration of these attacks increased from a few minutes to 8 hours and the interval between them decreased from 2 years to 4 weeks. An autotransplantation was performed of the anatomically and hemodynamically normal heart. She has had normal QT intervals and has been free of tachyarrhythmias since the operation in June 1987. Because of a slow escape low atrial rhythm, she was treated with a dual-chamber pacemaker programmed in the VDD mode with a coupling interval of 15 msec. The pacemaker wires were connected to the nontransplanted atrial cuff ("atrial" wire) and the transplanted atrium ("ventricular" wire). The hemodynamic effect of the resultant sinus node-driven low atrial pacing was restoration of normal values. This is the first report of successful autotransplantation of the heart for ventricular tachyarrhythmias caused by the long QT syndrome.     

Effects of sevoflurane versus propofol on QT interval.

BACKGROUND: Prolongation of the QT interval is an alteration of the electrocardiogram (ECG) that may result in a potentially dangerous polymorphic ventricular tachycardia known as torsade de pointes. Michaloudis et al. investigated the effect of isoflurane and halothane on the QT interval in premedicated and non premedicated children, and in premedicated adults. Isoflurane significantly prolonged the QTc interval, in contrast to halothane, which shortened the QTc interval. The aim of the study was to evaluate the effect of sevoflurane on the QT interval in patients undergoing non-cardiac surgery. METHODS: One hundred and eighty patients classified as ASA physical status I-III were enrolled and 102 were excluded. Patients had been scheduled for elective non cardiac surgery. Exclusions criteria were: cardiovascular impairment or chronic obstructive lung disease, medication affecting QT interval, and an abnormal prolongation of the QTc interval (440 ms). The patients were then randomly allocated to one of two groups, one receiving sevoflurane anesthesia and the other receiving propofol anesthesia. In all patients, a 12 lead ECG was recorded before surgery, after intubation, after extubation. The investigators reading the ECG were blinded to the type of induction and anesthesia used. The following variables were recorded or calculated: heart rate, P-R interval, QRS interval, QT interval, QTc interval according to Bazett's formula, systolic, diastolic and mean blood pressure. RESULTS: The sevoflurane significantly prolongs the QT and the QTc interval, whereas the induction and total intravenous anesthesia with propofol significantly shortens the QT but not the QTc interval. CONCLUSIONS: The amount the sevoflurane-associated QT prolongation may possibly be of clinical significance in some patients presenting long QT syndrome, hypokalemia, or in presence of other agents or factors that lengthen QT.     

Flecainide attenuates rate adaptation of ventricular repolarization in guinea-pig heart

Objectives: Flecainide is class Ic antiarrhythmic agent that was found to increase the risk of sudden cardiac death. Arrhythmic responses to flecainide could be precipitated by exercise, suggesting a role played by inappropriate rate adaptation of ventricular repolarization. This study therefore examined flecainide effect on adaptation of the QT interval and ventricular action potential duration (APD) to abrupt reductions of the cardiac cycle length. Design: ECG and ventricular epicardial and endocardial monophasic APD were recorded in isolated, perfused guinea-pig heart preparations upon a sustained cardiac acceleration (rapid pacing for 30 s), and following a single perturbation of the cycle length evoked by extrasystolic stimulation. Results: Sustained increase in heart rate was associated with progressive bi-exponential shortening of the QT interval and APD. Flecainide prolonged ventricular repolarization, delayed its rate adaptation, and decreased the amplitude of QT interval and APD shortening upon rapid cardiac pacing. During extrasystolic stimulation, flecainide attenuated APD shortening in premature ventricular beats, with effect being greater upon using a longer basic drive cycle length (S₁-S₁=550 ms versus S₁-S₁=300 ms). Conclusions: Flecainide-induced arrhythmia may be partly accounted for by attenuated adaptation of ventricular repolarization to sudden changes in cardiac cycle length provoked by transient tachycardia or ectopic beats.     

Cardiac resynchronization therapy for management of congestive heart failure after repair of tetralogy of Fallot in an elderly patient

A 65-year-old woman underwent total correction of tetralogy of Fallot with closure of ventricular septal defect, right ventricular outflow patch, pulmonary valve replacement and tricuspid valve repair. Pacemaker implantation using epicardial electrodes was simultaneously needed because she had complete atrioventricular block. The postoperative course was excellent. Eighteen months postoperatively, she was admitted with severe congestive heart failure and frequent ventricular arrhythmia. Echocardiography and cardiac catheterization revealed depressed left ventricular function caused by conduction delay. Cardiac resynchronization therapy with a defibrillation system was effective for improvement of left ventricular function. Ventricular contractility rapidly recovered to normal, and the patient has been asymptomatic for two years since implantation.     

QT interval abnormalities: risk factors and perioperative management in long QT syndromes and Torsades de Pointes

Electrophysiological abnormalities of the QT interval of the standard electrocardiogram are not uncommon. Congenital long QT syndrome is due to mutations of several possible genes (genotype) that result in prolongation of the corrected QT interval (phenotype). Abnormalities of the QT interval can be acquired and are often drug-induced. Torsades de Pointes (TP) is an arrhythmia that is a result of aberrant repolarization/QT abnormalities. If not recognized and corrected quickly, QT interval abnormalities may precipitate potentially fatal ventricular dysrhythmias. The main mechanism responsible for the development of QT prolongation is blockade of the rapid component of the delayed rectifier potassium current (I _kr), encoded for by the human-ether-a-go-go-related gene (hERG). The objectives of this review were (1) to describe the electrical pathophysiology of QT interval abnormalities, (2) to differentiate congenital from acquired QT interval abnormalities, (3) to describe the currently known risk factors for QT interval abnormalities, (4) to identify current drug-induced causes of acquired QT interval abnormalities, and (5) to recommend immediate and effective management strategies to prevent unanticipated dysrhythmias and deaths from QT abnormalities in the perioperative period.     

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 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.     

Effects of antiarrhythmics and hypokalemia on the rate adaptation of cardiac repolarization

Objectives. In normal conditions, sudden heart rate acceleration provokes a rapid reduction in ventricular action potential duration (APD). The protracted APD rate adaptation favors early afterdepolarizations and precipitates arrhythmia. Nevertheless, it is uncertain as to whether the rate-dependent changes of ventricular repolarization can be adversely modified by arrhythmogenic drugs (quinidine and procainamide) and hypokalemia, in comparison to the agents with safe therapeutic profile, such as lidocaine. Design. The rate adaptation of QT interval and monophasic APD obtained from the left ventricular (LV) and the right ventricular (RV) epicardium was examined during rapid cardiac pacing applied in isolated, perfused guinea-pig heart preparations. Results. At baseline, an abrupt increase in cardiac activation rate was associated with a substantial reduction of the QT interval and ventricular APD in the first two cardiac cycles, which was followed by a gradual shortening of repolarization over subsequent pacing intervals. The time constants of the fast (τ_fast) and slow (τ_slow) components of the APD dynamics determined from a double exponential fit were longer in RV compared to LV chamber. Quinidine, procainamide, and hypokalemia prolonged ventricular repolarization and delayed the rate adaptation of the QT interval and APD in LV and RV, as evidenced by increased τ_fast and τ_slow values. In contrast, lidocaine had no effect on the dynamic changes of ventricular repolarization upon heart rate acceleration. Conclusions. The rate adaptation of ventricular repolarization is delayed by arrhythmogenic interventions, such as quinidine, procainamide, and hypokalemia, but not changed by lidocaine, a clinically safe antiarrhythmic agent.     

Prediction of successful defibrillation in human victims of out-of-hospital cardiac arrest: a retrospective electrocardiographic analysis

In the present study we sought to examine the efficacy of an electrocardiographic parameter, 'amplitude spectrum area' (AMSA), to predict the likelihood that any one electrical shock would restore a perfusing rhythm during cardiopulmonary resuscitation in human victims of out-of-hospital cardiac arrest. AMSA analysis is not invalidated by artefacts produced by chest compression and thus it can be performed during CPR, avoiding detrimental interruptions of chest compression and ventilation. We hypothesised that a threshold value of AMSA could be identified as an indicator of successful defibrillation in human victims of cardiac arrest. Analysis was performed on a database of electrocardiographic records, representing lead 2 equivalent recordings from automated external defibrillators including 210 defibrillation attempts from 90 victims of out-of-hospital cardiac arrest. A 4.1 second interval of ventricular fibrillation or ventricular tachycardia, recorded immediately preceding the delivery of the shock, was analysed using the AMSA algorithm. AMSA represents a numerical value based on the sum of the magnitude of the weighted frequency spectrum between two and 48 Hz. AMSA values were significantly greater in successful defibrillation (restoration of a perfusing rhythm), compared to unsuccessful defibrillation (P < 0.0001). An AMSA value of 12 mV-Hz was able to predict the success of each defibrillation attempt with a sensitivity of 0.91 and a specificity of 0.97. In conclusion, AMSA analysis represents a clinically applicable method, which provides a real-time prediction of the success of defibrillation attempts. AMSA may minimise the delivery of futile and detrimental electrical shocks, reducing thereby post-resuscitation myocardial injury.     

Total intravenous anesthesia for repositioning an implantable defibrillator in a patient with long QT syndrome

We report the case of a 27-year-old woman with congenital long QT syndrome (LQTS) who was scheduled for surgery to reposition an implantable defibrillator. Given the risk of sudden death due to fatal ventricular arrhythmia, the woman required implantation of a defibrillator with pacemaker capability. Combined anesthesia-analgesia was used in order to minimize the risk of ventricular arrhythmia caused by increased serum concentrations of catecholamines. When cardioversion, defibrillation and anti-tachycardia functions had been deactivated, anesthesia was induced with propofol, fentanyl and rocuronium. Anesthesia was maintained with an infusion of propofol and remifentanil. We describe the pathophysiology and treatment of LQTS and discuss anesthetic management for repositioning a defibrillator in a patient with congenital LQTS.     

Acquired long QT syndrome and elective anesthesia in children

We present the case of a child who had had a previous episode of torsades de pointes (TdP) and who was scheduled for elective surgery under general anesthesia. The pathophysiology of this condition and the anesthesia concerns are discussed. An 8-year-old male with a history of osteogenic sarcoma had undergone an uneventful limb salvage procedure 2 years earlier. During a subsequent admission to the hospital, he had had a cardiopulmonary arrest with complete recovery. Telemetry electrocardiogram (ECG) rhythm recordings obtained during the event showed TdP that degenerated into ventricular fibrillation, which then terminated spontaneously. On a subsequent ECG, the QTc interval was 694 ms. The prolonged QT interval was attributed to homeopathic use of cesium chloride supplements and the QT interval normalized after cesium was stopped. He presented for an elective procedure and, with an anesthetic plan that emphasized medications without known effect on the QT interval, had an uneventful perioperative course. The optimal anesthesia plan for patients with prolonged QT or those suspected to be at risk for prolongation of the QT interval has not been well described. Available evidence suggests that using total intravenous anesthesia with propofol may be the safest and was used uneventfully in this case. Additionally, this case emphasizes the need to inquire about the use of supplements and naturopathic medications, even in children, that may have life-threatening side effects or interactions with anesthetic agents.