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PubMed1995

A comparison of adenosine and verapamil for the treatment of supraventricular tachycardia in the prehospital setting.

STUDY OBJECTIVE: To compare the efficacy and base hospital physician use of adenosine with that of verapamil in the prehospital treatment of supraventricular tachycardia (SVT). DESIGN: A 12-month prospective chart review of adenosine administration and a 12-month retrospective chart review of verapamil administration. SETTING: A single-tier advanced life support emergency medical service system. PARTICIPANTS: Prehospital adult patients presenting with narrow-complex SVT. INTERVENTIONS: Field paramedics identified SVT. They then administered verapamil or adenosine under on-line physician medical control. Paramedics administered up to two i.v. doses of verapamil, 2.5 mg and 5 mg, or up to two i.v. doses of adenosine, 6 mg and 12 mg. They recorded ECG readings; blood pressure; pulse; respirations; and symptoms before, during, and after drug administration. RESULTS: During the verapamil period, paramedics identified 102 cases of SVT and administered verapamil to 17 patients. Review by a cardiologist revealed 6 of the 17 patients to have been in atrial fibrillation, atrial tachycardia, or sinus tachycardia. Of the remaining 11 patients, 7 (64%) converted from SVT to sinus rhythm. During the adenosine period, paramedics identified 89 cases of SVT, and they administered adenosine to 64 patients. Eight patients had no review because prehospital rhythm strips were lost. Of the remaining 56 patients, 24 were later determined to have been in atrial fibrillation, atrial tachycardia, sinus tachycardia, atrial flutter, or ventricular tachycardia. Of the remaining 32 patients who were in SVT, adenosine converted 25 (78%) to sinus rhythm. An important incidental finding was the misinterpretation of tachydysrhythmias in 30 of 73 patients by paramedics and base hospital physicians. CONCLUSION: Our study showed no difference in conversion rates between verapamil and adenosine. Base hospital physicians were more likely to order adenosine than verapamil. Paramedics and base hospital physicians often misinterpret tachydysrhythmias.

Adenosine↗
PubMed1982

Electrocardiograms and 13 year cardiovascular mortality in Busselton study.

In 2119 unselected Busselton subjects 40 to 79 years of age, the 13 year mortality from cardiovascular disease was significantly higher in those whose initial electrocardiogram showed Q and QS patterns, left axis deviation, ST depression, T wave depression, flat or biphasic T waves, atrial fibrillation or flutter, and ventricular extrasystoles. In angina-free subjects whose electrocardiographic codes occurred in isolation from any other electrocardiographic abnormality, ventricular extrasystoles were associated with significantly higher mortality from cardiovascular disease compared with controls.

Adult↗
PubMed1993

Amiodarone prophylaxis for tachycardias after coronary artery surgery: a randomised, double blind, placebo controlled trial.

BACKGROUND: Arrhythmias are a common cause of morbidity after cardiac surgery. This study assessed the efficacy of prophylactic amiodarone in reducing the incidence of atrial fibrillation or flutter and ventricular arrhythmias after coronary artery surgery. METHODS: A double blind, randomised, placebo controlled trial. 60 patients received a 24 hour intravenous infusion of amiodarone (15 mg/kg started after removal of the aortic cross clamp) followed by 200 mg orally three times daily for 5 days, and 60 patients received placebo. RESULTS: 6 patients (10%) in the amiodarone group and 14 (23%) in the placebo group needed treatment for arrhythmias (95% confidence interval (95% CI) for the difference between groups was 0 to 26%, p = 0.05). The incidence of supraventricular tachycardia detected clinically and requiring treatment was lower in the amiodarone group (8% amiodarone v 20% placebo, 95% CI 0 to 24%, p = 0.07). The incidence detected by 24 hour Holter monitoring was similar (17% amiodarone v 20% placebo). Untreated arrhythmias in the amiodarone group were either clinically benign and undetected (n = 3) or the ventricular response rate was slow (n = 2). Age > 60 years was a positive risk factor for the development of supraventricular tachycardia in the amiodarone group but not in the placebo group. Fewer patients had episodes of ventricular tachycardia or fibrillation recorded on Holter monitoring in the amiodarone group (15% amiodarone v 33% placebo, 95% CI 3 to 33%, p = 0.02). Bradycardia (78% amiodarone v 48% placebo, 95% CI 14% to 46%, p < 0.005) and pauses (7% amiodarone v 0% placebo) occurred in more amiodarone treated patients. Bradycardia warranted discontinuation of treatment in one patient treated with amiodarone. CONCLUSIONS: The incidence of clinically significant tachycardia was reduced by amiodarone. The ventricular response rate was slowed in supraventricular tachycardia, but the induction of bradycardia may preclude the routine use of amiodarone for prophylaxis.

Adult↗
PubMed2005

Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter.

The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were administered nicotine (5 mg.kg(-1).day(-1) sc) for 1 mo using osmotic minipumps. High-resolution epicardial (1,792 bipolar electrodes) and endocardial Halo catheters were used to map activation during induced atrial rhythms. Nicotine promoted inducible sustained AFL at a mean cycle length of 134 +/- 10 ms in all MI dogs (n = 6) requiring pacing and electrical shocks for termination. No AFL could be induced in MI dogs (n = 6), control (non-MI) dogs (n = 3) not exposed to nicotine, and dogs with no MI and exposed to nicotine (n = 3). Activation maps during AFL showed a single reentrant wavefront in the right atrium that rotated either clockwise (60%) or counterclockwise (40%) around the crista terminalis and through the isthmus. Ablation of the isthmus prevented the induction of AFL. Nicotine caused a significant (P < 0.01) but highly heterogeneous increase in atrial interstitial fibrosis (2- to 10-fold increase in left and right atria, respectively) in the MI group but only a 2-fold increase in the right atrium in the non-MI group. Nicotine also flattened (P < 0.05) the slope of the epicardial monophasic action potential duration (electrical restitution) curve of both atria in the MI but not in non-MI dogs. Two-dimensional simulation in an excitable matrix containing an isthmus and nicotine's restitutional and reduced gap junctional coupling (fibrosis) parameters replicated the experiments. Chronic nicotine in hearts with MI promotes AFL that closely resembles typical human AFL. Increased atrial interstitial fibrosis and flattened electrical restitution are important substrates for the AFL.

Animals↗
PubMedDate not supplied

[Conduction disturbances and cardiac arrhythmias in myotonic dystrophy--diagnosis and clinical significance in adult populations].

Myotonic dystrophy (DM) is the most frequent adult form of muscular dystrophy. The clinical presentation consists of both muscular and systemic involvement. One of the main causes of high mortality is sudden cardiac death due to tachyarrhythmias and conduction disturbances. The knowledge of cardiovascular complications is very important because of diagnostic and therapeutic possibilities. The main cardiological complications of DM are arrhythmias associated with the destruction of the conduction system. The main electrocardiographic changes (prolongation of the P-R interval, left anterior hemiblock, increased QRS duration) reflect destruction of the His-Purkinje system and may progress very rapidly, leading to death due to Stokes-Adams attacks. The most frequent tachyarrhythmias are atrial and ventricular extrasystoles, atrial flutter and fibrillation, as well as ventricular tachycardia, that can be a cause of sudden death. The mechanisms underlying ventricular arrhythmias are conduction disturbances, prolongation of the QT interval, impaired coronary reserve and autonomic function. A common type of tachycardia seen in patients with DM is that originating from the branches of the bundle of His (bundle-branch re-entry). Risk stratification (in respect of cardiological complications) is possible on the basis of electrophysiological studies, clinical symptoms and a family history. Invasive electrophysiological investigation and implantation of a pacemaker may be indicated in patients with electrocardiographic features of a significant disease of the conduction system. Multicentre clinical trials assessing the efficacy of this therapeutic strategy are underway.

Adult↗
PubMed2004

[Long-term outcome and cardiac arrhythmias in infants with right atrial isomerism].

OBJECTIVE: The investigators compared the outcome of infants and children having right atrial isomerism with normal pulmonary venous drainage to those with anomalous drainage and determined factors associated with poor outcome. They further determined the prevalence of symptomatic cardiac arrhythmia in these patients and its relation to long-term morbidity and mortality. METHODS: The authors made a retrospective review of management and outcome of 116 infants and children diagnosed to have right atrial isomerism between January 1980 and December 2000. The type, timing and precipitating factors of symptomatic cardiac arrhythmia that occurred in patients, among a cohort of 85 who had or are awaiting surgical interventions, were noted. RESULTS: The 116 patients presented at a median of 1 day (range 1 day to 3.7 years) with cyanosis in the majority (96%). No interventions were planned in 31 (27%) patients who all died. The early surgical mortality for pulmonary venous repair was 25% (2/8), Fontan procedure 26% (5/19), cavopulmonary shunting 8% (1/13) and systemic-pulmonary arterial shunt insertion 2% (1/53). Late mortality was related to infection (n = 10), sudden death of unknown aetiology (n = 7) and documented arrhythmia (n = 1). Patients with obstructed anomalous pulmonary venous drainage had poor survival (P < 0.001). The mean (SEM) survival estimates for those with normal pulmonary venous drainage at 1, 5, 10 and 15 years were 81 (5)%, 67 (7)%, 60 (8)% and 43 (12)%, respectively, similar to those of patients with non-obstructed anomalous drainage (P = 0.06). Independent risk factors for mortality included pulmonary venous obstruction (relative risk RR 3.8, P = 0.001) and a single ventricle (RR 2.9, P = 0.016). Symptomatic cardiac arrhythmia occurred in 15/85 (18%) patients; 11 of whom had supraventricular tachycardia, and 1 atrial tachycardia, 1 atrial flutter, 1 ventricular tachycardia and 1 congenital complete heart block. The arrhythmias occurred before surgery in 4, early after surgery in 5, and late after surgery in 6 patients. Freedom from arrhythmia at 1, 5, 10, 15 and 20 years was (93 +/- 3)%, (86 +/- 4)%, (80 +/- 6)%, (73 +/- 9)% and (48 +/- 15)%, respectively. Logistic regression failed to identify any risk factors for symptomatic arrhythmia. CONCLUSION: The long-term outcome of infants and children with right atrial isomerism, whether associated with normal or anomalous pulmonary venous drainage, remains unfavourable. Sepsis and sudden death are major causes of late mortality. While symptomatic cardiac arrhythmias are not uncommon. They do not seem to relate to the overall high mortality and occurrence of sudden death in this patient group. Nonetheless, detailed assessment and aggressive management of cardiac arrhythmias once they occur are warranted in light of the precarious single ventricular haemodynamics.

Arrhythmias, Cardiac↗
PubMedDate not supplied

[A case of acute poisoning by amiodarone].

The paper describes a 57-year-old female patient who took 5 g more amiodarone following its 5-year consumption to commit suicide. Three hours later she was taken to hospital. She showed a prolonged fall in blood pressure (BP). The normal values of BP were maintained by epinephrine infusion. In addition to a longer QT interval up to 500 ms, the ECG displayed a short-term episode of atrial flutter, single ventricular premature beats, Type I intermittent atrioventricular block. Sinus bradycardia was absent. Atropine was found to increase cardiac rhythm.

Acute Disease↗
PubMed1984

[Clinical and electrophysiologic findings in patients with syncope following myocardial infarct].

34 patients with syncope (median number of episodes 2) which remained unexplained after thorough medical and neurological evaluation underwent an intracardiac electrophysiological study with atrial and ventricular programmed stimulation. All patients had a history of well-documented myocardial infarction 24 months (median, 3-120) prior to the electrophysiological study. During programmed ventricular stimulation 6 patients had inducible ventricular fibrillation or flutter, and 10 patients had sustained ventricular tachycardia. In 14 patients non-sustained ventricular tachycardia was induced, whereas in only 4 patients 1 to 3 repetitive ventricular responses were induced. Therapy was instituted on the basis of electrophysiologic testing. During the follow-up of 8 months (median, 1-37) 27 patients had no recurrence of syncope. Syncope persisted and remained unexplained by the electrophysiological study in 3 patients. One patient had ventricular fibrillation and two died suddenly, two of these patients after having discontinued antiarrhythmic medication 2 weeks before. Another patient died of non-cardiac cause. It is concluded that 1) the results indicate a high ventricular vulnerability (88%) in patients with unexplained syncope after myocardial infarction, 2) the evaluation by electrophysiological studies may identify the potential mechanism for syncopes, 3) electrophysiological testing offers a rationale for specific prophylactic therapy.

Cardiac Complexes, Premature↗
PubMed1983

[Emergency treatment of arrhythmias in neonates and infants].

Emergency treatment of cardiac arrhythmias was required in 41 newborn and infants aged two days to 9 months (mean 77 days) from July 1977 until September 1981. Heart defects were present in 27 (65.8%). Invasive electrophysiological studies were performed in all patients. The different types of arrhythmias were: bradyarrhythmias in 9 (21.9%): bradycardia to cardiac arrest (5), congenital complete AV-block (3), postoperative complete AV-block (1). Tachyarrhythmias in 32 patients (78.1%): reentry through accessory connections (21), congenital atrial flutter (6), ventricular flutter/fibrillation (3), and AV-nodal tachycardia (2). Overdrive atrial or ventricular stimulation with a consecutive series of 15-20 impulses of 5-10 Volts abolished arrhythmic attacks in 22 patients including 4 in whom prior digitalization had no effect. In two other patients overdrive pacing achieved sinus rhythm only after i.v. Propafenon. In 4 further patients 36.2 to 63.8 mg/m2 i.v. Propafenon and in 4 other patients DC synchronized cardioversion with 1 to 3 Wsec/kg restored a normal heart rate. The 3 patients with congenital complete heart block died, one despite permanent pacing. Oral Propafenon therapy with 300 mg/m2 die in three divided doses following emergency therapy of tachyarrhythmias was discontinued in patients without arrhythmias after 1 year on drug therapy. There was no relapse after a mean follow-up period of 1.9 years. Only patients with congestive heart failure due to cardiac defects needed additional digitalisation. Thus, in our experience antiarrhythmic drug therapy with Propafenon was more effective in this age group than digitalization.

Arrhythmias, Cardiac↗
PubMed1994

[Arrhythmia and conduction defects in polymyositis].

The prevalence of cardiac complications of dermatomyositis and polymyositis is generally underestimated. The authors report the case of heart block as the presenting symptom of the disease, situated in the atrioventricular node. Initially paroxysmal, it eventually became permanent. It was associated with atrial (fibrillation and flutter) and ventricular hyperexcitability (ventricular tachycardia in runs). Myocardial biopsy provided histological proof of the cardiac disease and the definitive link between the nodal conduction defect and the polymyositis.

Adult↗
PubMed1994

[Non-pharmacological methods of treatment of tachycardia].

Anti-tachycardia drugs have the advantage of preventing recurrent arrhythmia in most cases but have the disadvantage of requiring long-term prescriptions and producing extra-cardiac and cardiac side effects. In addition, paradoxical arrhythmogenic effects sometimes occur. With the advent of radiofrequency catheter ablation and implantable defibrillators, a whole new range of indications for non-drug treatments suddenly became possible. Radiofrequency ablation is now a real alternative in cases of Wolff-Parkinson-White junctional tachycardia with intranodal re-entry and accessory pathways since the success rate is 95%. For atrial flutter and ventricular tachycardia, myocardial localizations of the causal lesions are more diffuse and the clinical success rate is lower. Consequently, since other arrhythmias may occur, ablative treatment is usually reserved for drug-resistant cases. An implantable defibrillator is the only treatment, with the exception of cases with an identifiable acute origin, for ventricular fibrillation. In many countries, defibrillators are also implanted for drug-resistant ventricular tachycardia.

Catheter Ablation↗
PubMedDate not supplied

The relationship between performance on computer-based clinical simulations and two written methods of evaluation: cognitive examination and self-evaluation of expertise.

The purpose of this study was to explore the relationship between computer-based clinical simulation performance and two commonly used methods of evaluation: cognitive examination and self-evaluation of expertise. The convenience sample of 68 critical care nurses completed the Basic Knowledge Assessment Tool for Critical Care (BKAT), a cardiovascular self-assessment tool (CST), and two computer-based clinical simulations requiring the management of myocardial infarction patients with tachydysrhythmias (atrial flutter and ventricular tachycardia). Simulation performance was measured by proficiency score and patient outcome (live/die). Proficiency on the atrial simulation was significantly correlated with knowledge as measured by the BKAT (r = 0.46, p 0.001) and with self-evaluation of clinical expertise (r = 0.32, p = 0.008). Atrial patient outcome was also significantly correlated with the BKAT (r = 0.28, p = 0.006) and the CST score (r = 0.22, p = 0.036). However, in the ventricular simulation only proficiency score and self-evaluation of expertise were significantly correlated (r = 0.24, p = 0.049). The modest relationships found in this study may indicate that, while clinical simulation performance is related to knowledge and self-evaluation of expertise, the constructs measured are not synonymous. This evidence provides support for the use of clinical simulations as an adjunct to other methods of evaluation.

Adult↗
PubMed1977

Interaction of quinidine and propranolol in experimental cardiac arrhythmias in the dog.

Quinidine, propranolol and their combination were studied in atrial fibrillation induced by the topical application of acetylcholine or aconitine, injury-stimulation-induced atrial flutter and ventricular ectopic tachycardia produced by coronary occlusion in the dog. The effect of combination of quinidine and propranolol was significantly greater than that of the individual drug in atrial arrhythmias but not in ventricular arrhythmias. The study provides experimental support for the combined clinical use of quinidine and propranolol in the treatment of atrial arrhythmias.

Acetylcholine↗
PubMed1996

[Clinical use of beta-blocker an as antiarrhythmic agent].

It has been reported that beta-blocker treatment reduces the incidence of sudden cardiac death after myocardial infarction, possibly due to antiischemic and antiarrhythmic effects. Beta adrenoceptor blocking drugs are administered, as an antiarrhythmic agent in patients with hyperthyroidism, atrial fibrillation, atrial flutter and ventricular tachyarrhythmias. Even low dose beta-blocker administration reduces the incidence of PVC's. Beta blockers are expected to decrease the ventricular rate of persistent tachyarrhythmias resulting from excessive cardiac sympathetic tone. Existence of denervated areas in myocardium in the cases of ventricular tachyarrhythmias may be shown in the cardiac scintigram as abnormal myocardial uptake of 123I-MIBG.

Adrenergic beta-Antagonists↗
PubMed1991

[Results of programmed ventricular stimulation in induced non-sustained polymorphic ventricular tachycardia and maintenance of stimulation].

Programmed ventricular stimulation risks inducing non-pathological ventricular fibrillo-flutter. The aim of this study was to determine if the induction of a non-sustained polymorphic ventricular tachycardia (over 5 intraventricular reentries) could prevent this incident. One hundred and thirty-three non-sustained polymorphic tachycardias were induced by 2 or 3 extrastimuli during 1450 programmed ventricular stimulation studies. Ventricular stimulation was continued and led to ventricular fibrillo-flutter in 46 cases (Group I); to induction of sustained ventricular tachycardia in 26 cases (Group II) or to no other arrhythmias excepting the non-sustained tachycardia in 61 cases (Group III). The duration of the salvo was similar in all 3 groups. The rate of the induced arrhythmia was significantly lower in Group II (234 vs 290/min). The essential difference between the three groups was the clinical context. Only patients in Group II had previously documented sustained ventricular tachycardia and only patients in Group III had no apparent underlying cardiac disease. These results suggest that the decision to stop programmed ventricular stimulation should be based on the clinical indications of the study. In patients with previously documented or probable sustained ventricular tachycardia, it would seem to be necessary to continue ventricular stimulation irrespective to the rate and duration of the induced non-sustained ventricular tachycardia.

Cardiac Pacing, Artificial↗
PubMed1978

Lidocaine-induced cardiac rate changes in atrial fibrillation and atrial flutter.

To assess atrial and ventricular rate changes after lidocaine injection, 18 atrial flutter patients and 35 atrial fibrillation patients were given intravenous lidocaine, mean dose 100 mg. Continuous electrocardiographic recording for 5 minutes before and at least 10 minutes after lidocaine injection was used to determine rate changes. The atrial flutter rate decreased after lidocaine in 17 of 18 patients (94 per cent), mean maximal decrease 27 beats/minute. The ventricular rate response in atrial flutter was variable but in three patients increased 21, 27, and 47 beats/minute respectively (P less than 0.001). In atrial fibrillation, the mean ventricular rate after rapid lidocaine injection increased six beats/minute (P less than 0.01). In three of 35 atrial fibrillation patients (9 per cent), the ventricular rate increase was greater than 20 beats/minute (P less than 0.001), and in two patients (6 per cent), the ventricular rate increase was associated with potentially serious clinical events. Lidocaine-induced ventricular rate increases are common in atrial flutter and fibrillation, particularly in patients who are also receiving quinidine.

Adult↗