Simple approach to an apparently chaotic arrhythmia.

Deciphering complex arrhythmias requires a strict, systematic approach. In a step-by-step analysis of an electrocardiogram recorded from a patient with severe metabolic disturbances, we present a few simple suggestions that may often be helpful in electrocardiographic interpretation.

Rate-dependent patterns of modulated ventricular parasystole.

The effects of ventricular pacing on the arrangement of ventricular parasystolic beats were studied in 14 patients. By analyzing the effects of various pacing rates and modalities, it was found that both rate and pattern of manifest parasystolic beats were intimately related to the rate and coupling interval of the paced rhythm. Our findings indicate that fixed coupling of ectopic beats is not incompatible with parasystole; modulated parasystole may manifest as fixed rate classic parasystole; a parasystolic pacemaker can be entrained by a wide range of driving rates both above and below the intrinsic rate of the parasystole; and with different driving rates, these rate-dependent patterns can be observed in the same patient. Our observations suggest that spontaneous or drug-induced changes in the heart rate can lead to major alterations in the frequency and patterns of ventricular parasystole.

A study of modulated ventricular parasystole by programmed stimulation.

To analyze the phase-dependent sensitivity of the parasystolic pacemaker to nonparasystolic beats, 11 patients with modulated ventricular parasystole were studied using the ventricular extrastimulus method. The intrinsic parasystolic cycle lengths ranged from 1,100 to 1,800 ms. Premature stimuli altered the duration of the parasystolic cycle lengths by amounts that depended on timing of the test impulses within the parasystolic cycles. Premature impulses delivered during the first part of the parasystolic cycles prolonged the parasystolic cycle lengths to 107 to 151% of the intrinsic parasystolic cycle lengths and impulses applied during the second part abbreviated them to 70 to 81% of the intrinsic parasystolic cycle lengths. In 10 patients the accelerating effects were of greater magnitude than the decelerating effects. Transition from the accelerating to slowing phases was progressive or unstable in 9 patients and abrupt in 2. Changes induced by individual stimuli were short-lived and the parasystolic pacemakers returned immediately to their original rates. In 1 patient the biphasic sensitivity of parasystole to premature stimuli was shown to sustain for 21 days.

Scope and limitations of a general unknown screening by gas chromatography-mass spectrometry in acute poisoning.

The gold standard for the diagnosis of acute poisoning is toxicological analysis. Because information on the incorporated toxic substance provided by the patient or his relatives is known from experience to be unreliable in about 40% of all intoxications, a screening procedure that covers most relevant drugs and toxicants is required rather than an analytical procedure optimized for the identification of a single class of substances. The special task for a general unknown screening procedure is to identify a toxic substance among endogenous or food-derived substances as well as environmental toxicants in a biological matrix on an emergency basis. Because the unknown toxic substance may vary considerably in its physicochemical properties and its concentration range, a universally applicable screening procedure is required. Although gas chromatography-mass spectrometry has been used for three decades, it still offers many unique advantages in terms of sensitivity, specificity, reliability, and coverage of a large number of toxic substances. Because the procedure has to be kept as simple and as short as possible, compromises have to be made with respect to extraction, derivatization, and mass-spectral techniques. The specimen of choice for a general unknown screening is-if available-urine. The standard mode of ionization is electron impact. The identification of unknown substances is highly challenging because, in our experience, previously unknown metabolites may be detected rather frequently in acute poisoning. Although an automated mass spectra library search considerably facilitates the identification process, expert knowledge on the identification of substances not included in the library as well as knowledge in clinical toxicology and metabolism is indispensable.

Underdrive suppression of the sinus rhythm in man.

This report demonstrates unusual responses of the sinus rhythm to atrial pacing. The sinus rhythm failed to become manifest when the heart was driven at a rate slower than the inherent sinus rate. Sinus rhythm returned only after termination of underdrive pacing with the recovery time longer than twice the cycle length of the control sinus rhythm. The largest difference between underdrive and sinus cycle lengths measured 600 msec. To the best of our knowledge, underdrive suppression of the sinus rhythm has not been previously reported in man.

Two-to-one sinoatrial block. Normalization by carotid massage.

In a clinical case of 2:1 sinoatrial block, carotid massage, paradoxically, released the sinoatrial block and doubled the manifest sinus rate. This resulted from a deceleration of the sinus discharge rate which allowed consecutive sinus impulses to traverse the sinoatrial junction.

Hemoperfusion in severe chlorprothixene overdose.

Two to twelve hours after suicidal ingestion of an estimated dose of 10 g chlorprothixene, a 31-year-old female was admitted to the emergency ward of the clinic with cardiorespiratory arrest. After successful resuscitation, the further clinical course was complicated by persistent ventricular extrasystoles and ventricular fibrillation which necessitated repeated defibrillation. Since the patient did not respond satisfactorily to supportive treatment, a combined hemoperfusion/hemodialysis was performed. Under extracorporeal detoxication, elimination of chlorprothixene from plasma was accompanied by substantial improvement of the patient's clinical condition, although only about 1.6% of the estimated dose had been removed. This case seems to indicate that evaluation of the therapeutic efficacy of hemoperfusion should not be based exclusively on the relation of the amount of the eliminated drug to total absorbed dose.

Atrioventricular junctional escape rhythm suppressed by verapamil: evidence suggesting abnormal automaticity.

A clinical case of atrioventricular junctional escape rhythm is reported with unusual responses to overdrive pacing, lidocaine, and verapamil which were suggestive of abnormal automaticity.

Failure of idioventricular suppression in man by overdrive pacing as well as lidocaine: the role of abnormal automaticity.

Five patients with third-degree atrioventricular block and an idioventricular escape rhythm who showed unusual responses to overdrive ventricular pacing and lidocaine are presented. In four cases, the idioventricular rhythm was not suppressed by overdrive; in one, the recovery time of the escape rhythm was shorter than the escape cycle length. Lidocaine did not affect the cycle lengths and recovery times of the idioventricular rhythms. These responses are characteristic of abnormal automaticity. The role of abnormal automaticity in human idioventricular escape rhythms has not been previously supported by these characteristic responses to overdrive pacing and lidocaine.

Gap in bundle-branch conduction elicited by programmed His bundle stimulation.

The gap phenomenon in right bundle-branch conduction was elicited during programmed stimulation of the His bundle. Premature beats with short and long coupling intervals showed undisturbed intraventricular conduction, while the premature beat with intermediate coupling interval blocked within the right bundle branch. The electrophysiologic mechanism of "supernormal" conduction of the earliest beats was conduction delay at a proximal site within the His bundle which allowed recovery of the right bundle branch. This study shows that programmed His bundle stimulation is a valuable method in analyzing conduction characteristics of the distal atrioventricular conduction system in cases where atrioventricular nodal refractoriness would preclude this by atrial stimulation.

Clinical course, therapy, outcome and analytical data in amitriptyline and combined amitriptyline/chlordiazepoxide overdose.

A total of 103 cases of amitriptyline (AT) overdose (group 1) and 81 cases of overdose with a fixed combination of AT and chlordiazepoxide (CDE) (group 2), treated at our Intensive Care Unit or reported to our Poison Information Center between 1985-1990, were evaluated with respect to clinical course, symptoms and outcome, as well as efficacy of therapy. The mean amount of AT was considerably higher in group 1 compared to group 2 (13 mg kg-1 vs 7.7 mg kg-1). The most frequent symptoms in both groups were impaired consciousness, anticholinergic symptoms, seizures, arrhythmia and hypotension. Respiratory insufficiency necessitated respirator therapy in 63 of the patients. Two patients in group 1 and one patient in group 2 did not survive. Therapy included primary detoxification by gastric lavage and repeated administration of activated charcoal. In four of eight patients with cardiac conduction disturbances, hypertonic sodium bicarbonate led to a significant reduction in QRS duration and AV interval. Physostigmine was effective in eight of 14 patients with pronounced anticholinergic symptoms. No effect was observed in the other six patients. Haemoperfusion, which was performed in five patients, led to rapid improvement of coma after initiation of therapy in four patients. The clinical efficacy of haemoperfusion in AT overdose despite the high volume of distribution of AT deserves further investigation. The rather high average overdose of AT implies that large package sizes of AT were available to the patients. A major step towards prevention of serious AT overdose would be the prescription of package sizes containing a total of less than 500 mg AT.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic disposition of ajmaline.

Urine was collected from six patients receiving a continuous infusion of 20 mg/h ajmaline. Pooled urine was extracted with and without enzymatic conjugate cleavage or hydrolysis with concentrated hydrochloric acid. The extracts were analyzed by gas chromatography/mass spectrometry. Ajmaline and its metabolites in urine were identified in the form of their acetylated derivatives. Twenty two different acetylated derivatives of ajmaline and its metabolites could be detected. Three of these derivatives were artifacts generated by acetylation and/or thermal decomposition. The major metabolic pathways were mono- and di-hydroxylation of the benzene ring with subsequent O-methylation, reduction of the C-21, oxidation of the C-17 and C-21-hydroxyl function, N-oxidation, and a combination of these metabolic steps. Ajmaline and its metabolites were mainly excreted in the form of their conjugates. Furthermore, the interference of sparteine, debrisoquine, quinidine, and nifedipine with ajmaline metabolism was studied with semiquantitative thin-layer chromatography. Ajmaline metabolism was inhibited by co-administration of sparteine or quinidine, but not by debrisoquine or nifedipine. Sparteine most likely competed with ajmaline metabolism. Quinidine probably bound competitively to ajmaline-metabolizing enzymes without being metabolized itself. Additionally, the metabolic ratio of hydroxyajmaline/ajmaline in urine was determined in 9 extensive metabolizers and one poor metabolizer of dextromethorphan. The poor metabolizer had a significantly reduced metabolic ratio of hydroxyajmaline/ajmaline, which indicates that ajmaline metabolism probably co-segregates with polymorphic sparteine/debrisoquine/dextromethorphan metabolism.

Chlormezanone plasma and blood levels in patients after single and repeated oral doses and after suicidal drug overdose.

Chlormezanone plasma concentrations were determined in 5 volunteers (group 1) after a single oral dose of 200 mg of chlormezanone with high performance liquid chromatography. A plasma elimination half-life of 23 +/- 2.3 h was calculated. The mean peak chlormezanone plasma level was 1.86 +/- 0.2 micrograms/ml, 1 h after ingestion. Additionally, chlormezanone plasma levels were determined after repeated oral doses of chlormezanone recommended for treatment of muscular spasms due to degenerative skeletal disease. After 5 days of repeated daily doses of 3 x 200 mg (group 2; 12 patients) or 3 x 400 mg (group 3; 10 patients) of chlormezanone, mean predose chlormezanone plasma levels were 12.0 +/- 2.0 micrograms/ml (group 2) and 22.7 +/- 4.0 micrograms/ml (group 3), respectively. Comparable plasma concentrations were determined after 10 days of repeated doses of 3 x 200 mg or 3 x 400 mg of chlormezanone in 3 patients from each of these 2 groups. In 7 patients of group 3, chlormezanone had to be discontinued on the 5th day due to increasing muscular weakness, ataxia and exercise-inducible tachycardia. After a loading dose of 800 mg and repeated doses of 3 x 200 mg chlormezanone to 5 patients (group 4), plasma levels of 6.5 +/- 2.1 micrograms/ml, 8.9 +/- 2.2 micrograms/ml, 12.7 +/- 2.0 micrograms/ml, and 10.4 +/- 2.4 micrograms/ml were determined after 2, 8, 16, and 36 h, respectively. Trace amounts of a degradation product of the acid-labile chlormezanone could be detected in plasma besides the unchanged drug after administration of repeated oral doses.(ABSTRACT TRUNCATED AT 250 WORDS)

[Adenosine-sensitive atrial tachycardia]. / Adenozin szenzitív pitvari tachycardia.

The authors describe a case of a 71 year old man who suffered from chronic lung disease and had atrial tachycardias. 18 mg adenosine terminated his paroxysmal supraventricular tachycardia. The Holter monitoring showed that the tachycardia began at the late diastole with normal PQ interval, suggesting that an ectopic atrial tachycardia was terminated. They propose that adenosine is a "new" drug for termination of some form of atrial tachycardia.

[Intermittent Romano-Ward syndrome]. / Intermittáló Romano-Ward-syndroma.

Two cases are described to have intermittent long QT syndrome. This type of long QT syndrome is not easy to recognize and the result could be fatal in case taking I/A type antiarrhythmic drugs. The first patient who was investigated had got "chinidin syncope" two years earlier, the second one had symptoms of syncope and dizziness for 3 months. The long QT syndrome was diagnosed in both cases by Holter monitoring. For these reason this paper underline the value of Holter monitoring as a diagnostic tool to establish the diagnosis of long QT syndrome. The monophasic action potential showed early after depolarisations in both cases.

[Ventricular tachycardia masquerading as supraventricular tachycardia]. / Supraventricularis tachycardiát utánzó kamrai tachycardia.

To distinguish supraventricular tachycardia with aberrancy from ventricular tachycardia is sometimes difficult. It seems to be easy to distinguish the two forms in patients with preexisting bundle branch block: if the QRS morphology during tachycardia is identical to those during at rest the tachycardia is supraventricular, if different, ventricular. We present two cases with preexisting bundle branch block and wide complex tachycardia whose QRS morphologies were almost same to those during normal rest rhythm. The atrioventricular dissociation and the response to adenosine and lidocaine strongly suggests ventricular tachycardia. In these cases ventricular tachycardia masqueraded as supraventricular tachycardia and the identical QRS morphology with the preexisting bundle branch block may suggest a misdiagnosis of supraventricular tachycardia.

[Clinical importance of monophasic action potential registration in long QT syndrome]. / Monofázisos akciós potenciál regisztrálás klinikai jelentösége hosszú QT-szindrómában.

For more than 30 years, the monophasic action potential has been used as an experimental tool for the study of myocardial repolarisation. With recent improvements in catheter design, the utility of the tool as a means to identify the bases for ventricular arrhythmias in humans has been greatly improved. Abnormalities of repolarisation leading to ventricular arrhythmia formation can be identified and specific pharmacological therapies may be evaluated. The pathomechanism of major arrhythmias (ventricular tachycardia, ventricular fibrillation) occurring in long QT syndrome (LQTS) is not yet fully elucidated. The authors have recorded the monophasic action potentials (MAP) of the right ventricle in three patients with LQTS and with previous episodes of major ventricular arrhythmias. The changes in MAP duration and after depolarisation in response to spontaneous arrhythmias, programmed electrostimulation, atrial pacing and isoproterenol treatment were studied. In all of the three patients the early afterdepolarisation was present, which in two cases exhibited pause-dependent features. Thus in these patients dual chamber pacemaker implantatious were performed. These were the first permanent recordings of MAP during electrophysiological examination in Hungary and also the first evidences that the early afterdepolarisation does play a pathogenic role in the development of idiopathic LQTS. Further evaluation of the technique by cardiac electro-physiologists may improve both the diagnosis and the treatment of ventricular arrhythmias dependent upon afterdepolarisation formation.

[Transient Q-waves in coronary disease]. / Tranziens Q-hullámok coronariabetegségben.

The authors discuss the transient ischemic Q waves in various situations. Five cases are presented. Two patients had exercise-induced Q waves, one patient had right bundle branche block-dependent Q waves, one patient had transient Q waves after thrombolytic therapy and one patient had transient Q waves caused by Prinzmetal angina. Profound ischemia may not result in necrosis but may cause myocardial stunning. Myocardial stunning may be accompanied by deranged electrophysiologic activity with transient loss of electromotive forces.

[The use of adenosine in the diagnosis and treatment of cardiac arrhythmias]. / Adenozin alkalmazása a szívritmuszavarok diagnosztikájában és kezelésében.

The authors investigated the effect of adenosine or ATP on narrow QRS tachycardia in 56 pts, 3 pts with wide QRS tachycardia 9 pts with suspected latent preexcitation and 10 pts with PVC suspected to be ventricular parasystole. After the bolus iv. administration of adenosine or ATP every SVT was stopped related to AV node (44 pts), but in the rest twelve related to atrial origin of SVT only one automatic atrial tachycardia could be stopped. From the 9 patient suspected to have concealed WPW 2 pts had delta wave during the effect of adenosine, and in four pts parasystole was demonstrated among the pts had varying coupling interval PVC. None of the pts who had wide QRS tachycardia was the tachycardia stopped, but in two cases the supraventricular origin--atrial flutter and tachycardia--was discovered. The authors emphasize the favourable effect of adenosine in narrow complex tachycardia and suggest that it can given safely in wide QRS tachycardia of unknown origin either. The diagnostic effect of adenosine can be used in sinus rhythm too if latent preexcitation or ventricular parasystole is suspected.

[Experience with a transvenous pacemaker-cardioconverter-defibrillator without subcutaneous patch]. / Transzvénás, subcutan patch nélküli pacemaker-cardioverter-defibrillátorokkal szerzett tapasztalataink.

Sudden cardiac death caused by malignant ventricular arrhythmias is one of the main causes of cardiovascular mortality. Implantation of cardioverter-defibrillators has resulted in the reduction of the incidence of sudden cardiac death caused by malignant ventricular arrhythmias from the yearly 10-30% to 1%. For the very first time in Hungary, the authors applied only transvenous lead configuration for automatic cardioverter defibrillators in three patients. The indications of the implantation were ventricular fibrillation in one case, ventricular tachycardias refractory to drug treatment in two cases. Ventricular arrhythmias were secondary to coronary heart disease in two patients, dilatative cardiomyopathy in one patient. Preoperative, intraoperative and postoperative electrophysiological studies were regularly taken. Using Biotronik Phylax 03 device with a right ventricular electrode and a superior vena cava electrode and without subcutaneous patch the intraoperative defibrillation thresholds were 6, 11 and 12 J respectively. The fractally iridium coating increases the surface of the electrodes that has a very good effect on defibrillation threshold. During a mean follow-up of six months the occurring spontaneous ventricular arrhythmias (1 ventricular fibrillation and 5 ventricular tachycardias) were terminated by Phylax 03 with cardioversion-defibrillation or overdrive stimulation. The authors' results of intraoperative testing and clinical experiences show that the Phylax 03 biphasic system due to low defibrillation thresholds without subcutaneous patch can safely be applied with only transvenous implant technique in patients with major ventricular arrhythmias to prevent sudden cardiac death and to terminate ventricular tachycardia.