Modulation of the Q-T Interval by the Autonomic Nervous System

Recent investigations have clarified some of the effects of the autonomic nervous system on duration and spatial distribution of the Q-T interval in humans. The use of atrial pacing to fix heart rate or 24-hour continuous electrocardiographic recording to develop a regression formula for individual patients has provided a means to interpret the effects of an intervention that alters both the heart rate and the Q-T interval. Drugs that affect Ihe autonomic nervous system can influence Q-T interval directly or by changing rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. For example, the Q-T interval during sinus rhythm or afrial pacing and the ventricular effective refractory period shorten after atropine plus propranolol, but corrected Q-T interval using Bazetf's formula does not change. No change occurs in the Q-T interval during sinus rhythm or atrial pacing, or in ventricular effective refractory period after administration of propranolol although corrected Q-T interval using Bazett's formula markedly shortens. Q-T interval during sinus rhythm and atrial pacing and ventricular effective refractory period decrease after atropine but correct Q-T interval lengthens. To define further the relationship of the autonomic nervous system on the duration of the Q-T interval we studied the effects of sleep. Fifteen patients receiving no drugs underwent 3–6 days of continuous electrocardiography recordings. The duration of the Q-T interval was longer during sleep in all 15 patients independent of heart rate change. This prolongation of the Q-T interval during sleep may reflect increased parasympathetic tone or decreased sympathetic tone on the ventricle. Further investigation of the relation of the autonomic nervous system to ventricular depolarization and repolarization may delineate some of Ihe trigger mechanisms for the development of lethal ventricular arrhythmias in humans.     

Sotalol poisoning associated with asystole

Sotalol overdose has special features because this beta-blocker has the potential to lenghten the Q-T interval and to initiate severe arrhythmias such as ventricular tachycardia or fibrillation. We describe the case of a 70-year-old woman who ingested 6.72 g sotalol with suicide attempt. Despite administration of activated charcoal, glucagon, atropine and isoprenaline, two episodes of asystole occurred, requiring cardiopulmonary resuscitation. Further treatment included ventricular pacing and dopamine. The patient recovered without neurologic nor cardiac sequelae.     

毒蕈中毒的心脏损害

本文分析了107例毒蕈中毒的心脏损害情况及对预后影响,指出毒蕈中毒的心电图异常出现率与肾功障碍程度及血钾浓度高低无明显关系,并提示毒蕈中毒引起心律失常者死亡率高,预后差,故对毒蕈中毒者不能忽视毒蕈对心脏的直接作用。     

探讨心脏电生理昼夜变异性与缺血性心脏病的关系

[目的]探讨心脏电生理改变,即Q -T间期变异昼夜规律及心率变异性与缺血性心脏病的关系。[方法]观察5 5例缺血性心脏病病人(观察组)和5 0例正常成人(对照组)的2 4h心脏电生理改变,监测0 6:0 1～2 2 :0 0和2 2 :0 1～0 6:0 0时段的动态心电图中Q -T间期、Q -T间期变异、Q -T/HR斜率的变化及昼夜规律。[结果]两组心率、Q -T间期、Q -T间期变异、Q -T/HR斜率均呈明显的昼夜规律,两组比较昼夜心率、Q -T间期无统计学意义(P >0 .0 5 ) ;但Q -T间期变异、Q -T/HR斜率有统计学意义(P <0 .0 5 )。[结论]Q -T间期变异、Q -T/HR斜率能反映心室水平的自主神经调节及心室肌本身的状态,对预测室性心律失常及猝死的发生具有重要的价值和临床意义。     

急性心肌梗死溶栓治疗对Q—T离散度和心率变异性的影响

目的：探讨急性心肌梗死溶栓治疗对Q-T离散度和心率变异性的影响。方法：观察急性心肌梗死发病6h内接受溶栓治疗的60例患者,按溶栓后冠脉有无再通分为再通组（36例）和未再通组（24例）,测定溶栓治疗前后Q-T离散度和溶栓治疗后的心率变异性（SDNN和RMSSD）。结果：溶栓前两组Q-T离散度无差异。溶栓后Q-T离散度再通组明显低于未再通组（P＜0.05),再通组明显大于未再通组（P＜0.05)。在再通组SDNN和RMSSD和Q-T离散度的下降值之间非常显著相关（Ps＜0.01,Pr＜0.02),而未再通组没有发现这种相关性（P＞0.05)。Lown氏分级3级以上室性心律失常溶栓前再通组与未再通组无显著性差异（P＞0.05),溶栓后再通组显著低于未再通组（P＜0.01)。结论：急性心肌梗死早期有效的溶栓治疗可缩短Q-T离散度,提高SDNN和RMSSD,改善心肌电稳定性和植物神经功能,并减少恶性室性心律失常的发生。心率变异和Q-T离散度的下降值之间有一定的相关性,两者结合可提高对恶生心律失常发生的预测价值,提高对溶栓疗效的判断。急性心肌梗死早期恶性心律失常和猝死的发生除了和Q-T离散度显著增大有关外,还有可能与心率变异（SDNN和RMSSD）的下降有关。     

Changes in Q-T and Q-aT Intervals at Rest and During Exercise With Different Modes of Cardiac Pacing

The influence of heart rate variation on the Q-T and Q-aT intervals (measured from the onset of the QRS to the end or the apex, respectively, of the T-wave) was studied both at rest and during exercise using different modes of pacing. The studies were made on 21 patients with high-degree atrioventricular block. In seven patients with programmable ventricular inhibited (VVI) pacemakers, an increase in pacing rate during rest produced significant shortening of both Q-T and Q-aT. During observations made at rest and during exercise in 14 patients with fixed rate VVI, atrial rate matched asynchronous (VVIm) or atrial triggered (VAT) pacing. Significant shortening of Q-T and Q-aT intervals occurred during exercise in all pacing modes, but was greatest with VVIm and VAT. The Q-T and Q-aT changes were almost parallel in all situations. For measurements made by two independent observers the coefficient of variation was lower for Q-aT than for Q-T (2.2 versus 2.5) and the correlation coefficient was higher (0.96 versus 0.93), indicating easier identification of Q-aT than of Q-T. This study indicated that changes in Q-T and in Q-aT are influenced by intrinsic factors in addition to the ventricular rate. Atrioventricular synchronization did not seem to influence these changes.     

Q-T interval dispersion in patients with coronary heart disease in various terms after angioplastic revascularization

According to epidemiological researches data, in 75-80% of coronary heart disease (CHD) cases, the cause of sudden death is ventricular rhythm disturbances. Degree of coronary arteries lesion plays an important role in development of these disturbances. Study of Q-T interval dispersion is one of prospective methods of noninvasive assessment of risk of occurrence of dangerous for life ventricular arrhythmias. The authors studied indices of Q-T interval end its parts dispersion in patients with coronary atherosclerosis, and also estimated influence of angioplastic myocardial revasculization on electrical instability markers during 6 months after intracoronary intervention. It was proved that coronary atherosclerosis in patients with CHD contributes to increase of degree of myocardial depolarization and repolarization nonhomogeneity. Value of Q-T interval and its parts dispersion does not depend on number of affected coronary arteries. Revascularization of myocardium contributes to reliable decrease of Q-T interval and its parts dispersion. More marked its decrease is registered in 6 months after transcutaneous intracoronary intervention. Development of restenosis is accompanied by increase of indices of Q-T interval and its parts dispersion.     

Heart block and prolonged Q-Tc interval following muscle relaxant reversal: a case report

Heart block and Q-Tc interval prolongation have been reported with several agents used in anesthesia, and the US Food and Drug Administration mandates evaluation of the Q-T interval with new drugs. Drug-induced Q-T interval prolongation may precipitate life-threatening arrhythmias, is considered a precursor for torsades de pointes, and may predict cardiovascular complications. In the patient described in this article, heart block occurred and the Q-Tc interval became prolonged after muscle relaxant reversal with neostigmine; both were considered to be related to the combination of agents used in the case, as well as to other predisposing factors such as morbid obesity. The agents used that affected cardiac conduction were neostigmine, desflurane, droperidol, dolasetron, and dexmedetomidine. Although the heart block was resolved after 2 doses of atropine, prolonged P-R and Q-Tc intervals persisted into the immediate postoperative period but returned to baseline within 4 hours. Clinical implications of this report include increasing awareness of the multitude of factors affecting Q-T interval prolongation during anesthesia.     

Polymorphous Ventricular Tachycardia Associated with a Marked Prolongation of the Q-T Interval Induced by Amiodarone

We report the case of a patient who developed a life-threatening polymorphous ventricular tachycardia (PVT) after six weeks of treatment with amiodarone. The Q-T interval was markedly prolonged at 0.86 second. The drug induction of PVT was strongly suggested by the fact that PVT resolved four days after withdrawal of amiodarone when the Q-T interval had shortened to 0.60 second; the arrhythmia has not recurred in the nine months of follow-up since then. Amiodarone, though a very effective antiarrhythmic agent, may induce serious PVT.     

Cocaine-induced torsades de pointes in idiopathic long Q-T syndrome.

Torsades de pointes is a ventricular tachycardia characterized by the QRS complexes of changing amplitude that appear to twist around an isoelectric line. It usually precipitates in the setting of underlying Q-T interval prolongation, which has both congenital and acquired causes. The common acquired causes of torsades precipitation are medications, electrolyte imbalance, and severe bradycardia. This report presents a case of torsades de pointes that was precipitated by substance abuse in a patient with idiopathic long Q-T syndrome and required several treatment modalities.     

Clinical effectiveness and potential hazards of combined kordaron and quinidine therapy of patients with atrial fibrillation]

Clinical efficacy of and potential risk for complications from combined cordarone+quinidine treatment were studied in 52 patients with atrial fibrillation (AF). Out of 32 patients with a persistent pattern of the disease the sinus rhythm was recovered in 28 (87.5%) of the patients; out of 20 patients with paroxysmal pattern of AF resistant to routine anti-arrhythmic treatment, the sinus rhythm was recovered in 14 (70%) patients. Almost 50% Q-T prolongation was recorded in one patient with paroxysmal AF. Despite the withdrawal of the medication, 4 hours later ventricular tachycardia of the "pirouette" type arose that 2-3 minutes later was followed by ventricular fibrillation with clinical death. After effective electric defibrillation in the presence of lidocaine treatment ventricular fibrillation repeated 7 times. A total of 32 cardiac defibrillations were performed for 6 hours. The normalization of the Q-T interval was observed on the fourth day only. The patient was discharged from the hospital in a satisfactory condition.     

滥用联邦止咳露糖浆致低钾性麻痹的临床分析

目的探讨滥用联邦止咳露糖浆诱发低钾性麻痹的原因及临床特点。方法对滥用联邦止咳露糖浆导致的低钾性麻痹16例的临床资料进行回顾性分析。结果本组联邦止咳露糖浆滥用时间3～30个月,发作前24 h内均有明确的大量饮用联邦止咳露糖浆史。所有病例均有四肢肌力迟缓性瘫痪,不能行走,近端重于远端,下肢重于上肢,且反复发作。腱反射正常或减退,无感觉障碍,病理征阴性,其中2例伴失眠、亢奋、一过性幻视等轻度精神症状,3例合并严重腹泻。16例血钾1.4～2.3 mmol/L;心肌酶检测肌酸激酶均稍高于正常值。心电图检查示U波、QT间期延长、ST段轻度下移等低钾性心电图改变。经补钾治疗后均恢复正常。结论滥用联邦止咳露糖浆可诱发低钾性麻痹,应引起医生及患者的重视。     

Circadian structure of cardiac rhythm in tachyarrhythmia

AIM: To determine clinical implication of changes in the structure of circadian cardiac rhythm in patients with tachyarrhythmia basing on estimation of the circadian index (CI). MATERIAL AND METHODS: 24-h Holter monitoring was conducted in 154 patients aged 4 to 18 years: 125--with supraventricular paroxysmal tachycardia, 13--with long Q-T interval, 16--with idiopathic ventricular tachycardia. CI was calculated as mean day heart rate (from 7.00 to 22.00)/mean night heart rate (from 23.00 to 6.00). RESULTS: Patients with long Q-T interval had less CI while those with supraventricular paroxysmal and idiopathic ventricular tachycardia had higher CI vs normal values. CI changes became more pronounced with growing disease severity. CONCLUSION: Cardiac arrhythmia with low CI is associated with progressive vegetative denervation while that with high CI occurs in increased cardiac sensitivity to sympathetic impacts.     

Cardiac arrest following myocardial infarction

In-hospital cardiac arrest secondary to ventricular dysrhythmias following acute myocardial infarction remains a serious concern for hospital staff. One cause associated with this life-threatening problem is hypokalemia, which leads to electrical instability in myocardial cells resulting in primary ventricular fibrillation. In this article, a case study is presented that illustrates the hospital course of a patient with severe hypokalemia who experienced ventricular fibrillation immediately following admission to the emergency department.     

Predictors of ventricular tachycardia in patients with mitral prolapse

128 patients with primary mitral prolapse and 72 healthy controls were examined using noninvasive methods. The analysis of the findings revealed predictors of electric myocardial unstability: reduced variability of cardiac rhythm, diastolic left ventricular dysfunction, late ventricular potentials and growing dispersion of the Q-T interval. Detection of mitral regurgitation correlates with development of ventricular arrhythmia.     

Recurrent ventricular fibrillation related to hypokalemia in early repolarization syndrome

We describe a case of early repolarization syndrome in which augmented J waves were documented during an electrical storm associated with hypokalemia. The patient was referred to our hospital for therapy to treat recurrent ventricular fibrillation (VF). The 12-lead electrocardiogram showed giant J waves associated with hypokalemia during multiple episodes of VF. Although antiarrhythmic agents or deep sedation were not effective for the VF, an intravenous supplementation of potassium completely suppressed the VF with a reduction in the J-wave amplitude. Our report discusses the possible relationship between hypokalemia and VF in early repolarization syndrome. (PACE 2012; 35:e234-e238).     

Extracorporeal Membrane Oxygenation for Hypokalemia and Refractory Ventricular Fibrillation Associated with Caffeine Intoxication

BackgroundCaffeine has been reported as a cause of cardiac arrest after massive overdose. Here, we report the case of a patient with caffeine intoxication, which can cause fatal dysrhythmias and severe hypokalemia. They were successfully treated with extracorporeal membrane oxygenation (ECMO).Case ReportA 43-year-old woman with a history of bipolar disorder presented to the emergency department after suicidal drug ingestion (caffeine and amitriptyline). Immediately after arrival, she experienced multiple episodes of ventricular fibrillation with severe hypokalemia requiring cardiopulmonary resuscitation and medical therapy. However, conventional treatment was not successful. We instituted ECMO early during resuscitation because prolonged hypokalemia refractory to aggressive potassium replacement precluded the use of antidysrhythmic medications for refractory circulatory compromise with ventricular fibrillation. The use of ECMO provided time to correct hypokalemia (19.3 g potassium) and reduce the caffeine level with hemodialysis. Although she had sustained cardiac arrest, she recovered fully and was discharged home.Why Should an Emergency Physician be Aware of This?Our case indicates the potential effectiveness of ECMO in severely poisoned patients with fatal dysrhythmias. ECMO could provide time for removal of toxic drugs and correction of electrolyte abnormalities.     

QT interval dispersion and autonomic modulation in subjects with anxiety

This study was designed to assess Q-T interval dispersion as a marker of electrical instability in subjects with anxiety. Recent observations have shown that the presence of anxiety symptoms increases the risk of sudden death. The Kawachi anxiety questionnaire identified 29 subjects (male/female ratio 13:16) who scored 0, 22 subjects (male/female ratio 14:8) who scored 1, and 37 subjects (male/female ratio 13:24) who scored 2 or more. In all subjects we measured electrocardiographic interlead QT dispersion and autonomic function through spectral analysis of R-R interval and blood pressure variabilities and left ventricular mass. Compared with subjects who scored 0, those reporting 2 or more symptoms showed increased heart rate-corrected QT dispersion (54.9+/-1.7 ms vs. 34.9+/-3.2 ms, P<.001), sympathetic modulation (normal logarithm low-frequency power/high-frequency power 0.59+/-0.1 vs. 0.12+/-0.04, P<.05), and left ventricular mass (120.7+/-3.5 g/m2 vs. 97.9+/-2.8 g/m2, P<.001). Probably because it augments sympathetic activity, anxiety causes left ventricular mass to increase and, like hypertension, increases heart rate-corrected Q-T interval dispersion. The consequent electrical instability could be the substrate responsible for inducing fatal ventricular arrhythmias.     

Ventricular Fibrillation After Intravenous Atropine in a Patient with Atrioventricular Block

A 69-year-old black woman with complete AV block developed ventricular fibrillation following an IV injection of 1 mg of atropine sulphate. After a successful DC countershock, the ECG showed a polymorphous ventricular tachycardia which subsided spontaneously. Cardiac catheterization revealed a small left ventricular diverticulum and normal coronary arteries. This seems to be the first reported case of atropine-induced ventricular fibrillation in a patient with complete AV block. The fact that this occurred without previous change of the ventricular rate suggests that the adverse action of atropine was mediated through a mere vagolytic effect at the ventricular level.     

Antagonism of deslanoside-induced cardiotoxicity by combined nicotinic and muscarinic blockade of autonomic ganglia.

The effect of ganglionic blockade on cardiotoxicity induced by deslanoside (25 mug/kg i.v. at 15-minute intervals) was evaluated in Dial-urethane anesthetized cats. Electrocardiogram, blood pressure and pre- and postganglionic cardiac sympathetic nerve recordings were monitored. When deslanoside was given to control animals, 150 +/- 8.2 and 179 +/- 11.9 mug/kg produced ventricular tachycardia and ventricular fibrillation, respectively. Pretreatment of cats with either hexamethonium or atropine alone did not influence the doses of deslanoside required to produce ventricular tachycardia or ventricular fibrillation. However, pretreatment with the combination of hexamethonium and atropine significantly increased the dose of deslanoside needed to produce ventricular tachycardia (181 +/- 12.3 mug/kg) and ventricular fibrillation (219 +/- 12.3 mug/kg). Furthermore, administration of atropine to hexamethonium-pretreated cats intoxicated with deslanoside decreased deslanoside-induced postganglionic nerve activity. These results indicate that blockade of both nicotinic and muscarinic ganglionic transmission is essential for a protective influence against cardiotoxicity induced by deslanoside.