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Results for “Accelerated Idioventricular Rhythm”

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PubMed1996

[When should we stop cardiopulmonary resuscitation in patients brought to the emergency room in cardiac arrest without pre-hospital care?].

PURPOSE: The decision of stopping cardiopulmonary resuscitation (CPR) in patients brought to emergency room in arrest remains a challenge. Such decision is even more difficult when someone is brought by bystanders, after an acute loss of consciousness without any out-of-hospital care. To evaluate the probability of survival of these patients we reviewed retrospectively charts in our institution, during a period of five years. METHODS: One hundred and one patients that fulfilled these characteristics came to our emergency in arrest. The time to arrival since symptoms started, cardiac rhythm at first electrocardiogram (EKG), age, gender, initial CPR success, late outcomes and previous diseases were obtained. Patients were divided in two groups regarding which cardiac rhythms they had at first EKG: A-patients arriving in asystole; and VF-patients arriving in ventricular fibrillation. To evaluate time to arrival, we arbitrarily choose 15 min as a reference point. RESULTS: In these 101 subjects the mean age was 62 +/- 13.7 years and 63 (62.3%) were men. Previous heart disease was documented in 74 [dilated cardiomyopathy in 22 (21.7%), coronary heart disease in 41 (40.6%), arterial hypertension in 25 (24.7%) and others in 6 (5.6%)]. In 66 episodes we were sure of the time patients spent before arrival (mean 2.5 +/- 11 min). Only in 63 subjects we had no doubts about the rhythm at entrance: VF in 37 (58.7%), A in 22 (34.9%) and an accelerated idioventricular rhythm (AIR) in four (6.3%). Time to arrival was 18.6 +/- 10.6 in VF vs 32.5 +/- 11.7 min in A (p = 0.012). Fourteen (13.8%) subjects resumed a supraventricular rhythm with systolic pressure > or = 90 mmHg after CPR and all of them were in VF (13) or AIR (one). Nine patients (8.9%) evolved in coma. Only five (4.9%) were discharged from the hospital without any neurological disturbance and their time to arrival ranged from one to 15 (9 +/- 5.8) min. CONCLUSION: Delayed arrival to the emergency room (> 15 min) associated with asystole were predictors of unsuccessful CPR, and both data are helpful in deciding when to stop CPR in subjects arriving at the emergency department with no out-of-hospital care.

Aged↗

PubMed2000

[Idioventricular rhythm in patients with acute myocardial infarction: an indicator of perfusion or ischemic symptom].

Episodes of idioventricular rhythm occur frequently during the first hours of myocardial infarction. In patients receiving thrombolytic therapy, idioventricular rhythms may be an indicator of successful reperfusion--called "reperfusion arrhythmia". The aim of our study was to assess an incidence of idioventricular rhythm and other ventricular arrhythmias and their relations to thrombolytic therapy and reperfusion in a relatively large group of patients with acute myocardial infarction (AMI). The study included 100 patients with AMI, divided into three groups: with anterior, inferior and inferior with right ventricle infarction. Sixty six patients were treated with thrombolysis. 24-hour Holter recordings were obtained in every patient and reperfusion was assessed clinically. Episodes of idioventricular rhythm and other ventricular arrhythmias were more frequent in the thrombolytic group but not in patients with clinically established reperfusion. The main conclusion from our study is, that accelerated idioventricular rhythm is not specific for reperfusion but rather for myocardial ischaemia. The higher incidence of the ventricular arrhythmias in the thrombolytic group partially depends of their earlier hospitalization, and time-dependent inclusion into treated group.

Adult↗

PubMed1991

[Evaluation of clinical criteria of coronary artery recanalization in acute myocardial infarction].

Clinical features of recanalization of infarct-related coronary artery during thrombolytic therapy or emergency PTCA and their correlation with immediate coronary angiography were analysed in 23 patients with acute myocardial infarction (AMI) to evaluate the predictive value of clinical criteria of reperfusion. The coronary angiography was performed before treatment and every 15 to 30 minutes during intravenous (rt-PA) or intracoronary (UK or SK) thrombolysis. Reperfusion was achieved in 16 cases by thrombolysis and in 4 cases by PTCA. The results revealed that in patients with reperfusion chest pain was relieved rapidly at least 70% in a period of 30 minutes, the ST segments fell by 50% or more from their elevated levels during a period of 30 minutes. Transient "paradoxical" increase of ST segment elevation followed by rapid falling was observed in 4 patients. This phenomenon was considered as a reliable marker of reperfusion. The changes in cardiac rhythm and conduction were noticed in 90% of the patients with reperfusion, among them accelerated idioventricular rhythm and disappearance of new-onset AVB and intraventricular conduction defects were useful bedside evidences of reperfusion, and transient significant sinus bradycardia or AVB with or without transient hypotension were useful markers of reperfusion in inferior myocardial infarction. When these clinical criteria were separately used as predictor of infarct-related coronary artery recanalization, the specificity was about 70% to 80%. Using the presence of all 3 criteria, the specificity and predictive value increased to 100% and the sensitivity was 70.6%. The time interval between onset of symptoms and peak CK and CK-MB were significantly shorter in patients with reperfusion than in those without persistent reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1982

Cardiac disorders in penicillin-induced anaphylaxis. Association with intravenous epinephrine therapy.

This report describes cardiac dysfunction in two patients experiencing penicillin-induced anaphylaxis. Telemetric monitoring of the patients' ECGs initially disclosed sinus rhythm. Immediately after intravenous (IV) injections of epinephrine chloride, ventricular premature beats and apparent accelerated idioventricular rhythm occurred in one patient and possible ventricular tachycardia occurred in the other. These observations demonstrate the value of ECG monitoring of patients during anaphylaxis and emphasize the potential hazards of administering epinephrine by the IV route in this clinical setting.

Adult↗

PubMed1976

Ventricular rhythms in acute myocardial infarction.

Ectopic ventricular activity in acute myocardial infarction is considered to be benign if it is slow and regular (accelerated idioventricular rhythm), but ominous when rapid (ventricular tachycardia). However, it has been observed in an increasing number of reports that these two types may coexist in the same patient, altering thereby the clinical significance of both. In the present study electrocardiograms were analyzed of 55 patients hospitalized for acute myocardial infarction, in whom idioventricular rhythm occurred. It was found that three major types of ventricular rhythms could be identified: a regular-stable rhythm, an irregularunstable one, and a third variant which was a combination of these two types. The stable ventricular rhythm was self limited and harmless. The unstable and combined types which were characterized by random coupling times and varying interbeat intervals, were frequently associated with re-entrant beats and fast ventricular rates and therefore a potentially ominous prognosis. It is suggested that the Ca++ dependent slow diastolic depolarization may be the mechanism responsible for the unstable ventricular rhythm, and the reasons for this assumption are discussed. A therapeutic approach based on the above considerations is described.

Acute Disease↗

PubMed1992

Ventricular arrhythmias in horses: 21 cases (1984-1989).

Ventricular premature depolarizations (VPD) were identified in 21 horses in which unexplained tachycardia or an arrhythmia was detected on auscultation. Horses were categorized into 3 groups on the basis of ECG findings. Seven horses had uniform isolated VPD (group 1); 7 horses had repetitive uniform VPD at a rate < 100 VPD/min (group 2); and 7 horses had either multiform VPD, R-on-T, or > or = 100 VPD/min (group 3). Concurrent systemic disease was identified in 12 horses, 7 of which had gastrointestinal tract disorders. Serum cardiac isoenzyme activities were high in 6 (2 from each group) of 13 horses in which they were measured. Serum electrolyte concentrations were normal in all but 1 of 11 horses in which they were measured. Antiarrhythmic drugs were given to 9 horses (all of which were in group 2 or group 3), 6 of which converted to sinus rhythm. Two horses that had R-on-T in the ECG died shortly after initiation of antiarrhythmic treatment. An accelerated idioventricular rhythm persisted in 1 horse for at least 8 months and failed to respond to antiarrhythmic drugs. Ventricular premature depolarizations resolved or decreased considerably in frequency in 11 horses without the administration of antiarrhythmic agents. Treatment in these horses included therapy for any underlying systemic disease, corticosteroids, nonsteroidal antiinflammatory drugs, or stall rest. The remaining horse was euthanatized several hours after hospitalization. Five horses died or were euthanatized either during hospitalization or several months after being discharged. Myocardial lesions were identified at necropsy in 2 horses.

Animals↗

PubMed2004

[Slow ventricular tachycardia presenting in the antenatal period].

The authors report two cases of slow ventricular tachycardia presenting in the antenatal period. One foetus had anasarca at 38 weeks' gestation. After birth, improved myocardial function contributed to the rapid resorption of the effusions. The other case was well tolerated in the foetal and neonatal periods. In both cases, Holter ECG recorded an intermittent ventricular arrhythmia with salvos of sustained ventricular tachycardia with a maximum rate of 185/min, only 10% higher than the underlying sinus rhythm, disappearing on acceleration of the sinus rhythm. The aetiological investigation was negative. Therapeutic abstention was supported by the spontaneously favourable outcome after 3 and 5 months. Slow ventricular tachycardia or accelerated idioventricular rhythms are usually considered to be benign but the case with foetal anasarca suggests that they should be carefully followed up in the neonatal period. In the absence of a consensus on management, therapeutic abstention implies regular cardiological examination until the arrhythmia has disappeared.

Female↗

PubMed1982

Method for evaluating the effects of antiarrhythmic drugs on ventricular tachycardias with different electrophysiologic characteristics and different mechanisms in the infarcted canine heart.

In a canine model of myocardial infarction caused by coronary occlusion and reperfusion, ventricular tachycardia occurs spontaneously at 24 hours and has many of the characteristics of an accelerated idioventricular rhythm. It cannot be induced by premature or rapid stimulation of the ventricles; overdrive pacing during this tachycardia usually causes some transient overdrive suppression but occasionally there is overdrive acceleration. We suggest that this arrhythmia is caused mainly by enhanced automaticity. Ventricular tachycardia also can be induced by premature or rapid ventricular pacing 3 to 5 days after infarction, but it does not occur spontaneously. It can be stopped by overdrive pacing, suggesting that it is caused by reentry. Electrocardiographic features are identical to chronic, recurrent sustained ventricular tachycardia in human patients. Because the arrhythmias occurring at different times probably result from different mechanisms this canine model is useful for comparing the actions of drugs on different kinds of arrhythmias. Lidocaine and procainamide generally abolished tachycardia 24 hours after infarction, but only procainamide abolished tachycardia 3 to 5 days after infarction. Isoproterenol accelerated tachycardia at both times. Verapamil did not abolish tachycardia 3 to 5 days after infarction.

Animals↗

PubMed1996

Accelerated ST-segment reduction after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) compared to urokinase.

Effects of therapy with urokinase (UK) and with recombinant tissue plasminogen activator (rtPA) were compared in patients with acute myocardial infarction (AMI). To achieve homogenous therapeutic conditions the comparison was restricted to patients having their first AMI and to cases of clinically successful thrombolytic therapy (defined by non-invasive criteria, such as a 50% decrease in elevated ST-segment in the worst load of a 12 lead ECG within 300 min after onset of thrombolytic therapy, complete pain resolution during thrombolytic therapy, and later confirmed by angiography 10 days after AMI). Effects of UK and rtPA on continuous multilead ST-segment analysis and cardiac proteins (creatine kinase and its isoenzyme CK-MB, aspartate transaminase and hydroxybutyrate dehydrogenase) were analyzed during 24 hours following onset of therapy. Continuous ST analysis showed a faster resolution of the elevated ST-segments after thrombolytic therapy with rtPA than with UK(p < 0.01). Accelerated idioventricular rhythms (p < 0.05) occurred sooner following rtPA than UK treatment. The wash-out of creatine kinase was increased (p < 0.01) after rtPA. Although both drugs induced comparable, angiographically controlled reperfusion, the results suggest that the process of reperfusion was accelerated during thrombolysis with rtPA compared to UK. Thrombolytic therapy of AMI with rtPA may hence improve myocardial salvage.

Adult↗

PubMedDate not supplied

Twenty-four-hour ambulatory electrocardiography in normal cats.

Twenty-four-hour ambulatory electrocardiograms were recorded in two age groups of 10 normal cats each: group 1 (1 to 4 years) and group 2 (8 to 14 years), with equal numbers of males and females in each group. Average heart rates over the 24-hour recording period ranged from 114 to 202 beats/minute (bpm). The mean 24-hour average rate did not differ between group 1 and group 2 (157.6 vs. 156.3+/-5.3 bpm, respectively); however, females (both groups combined) had higher average heart rates than males (166.8 vs. 147.1+/-5.3 bpm, respectively). Females also had a higher mean minimum heart rate than males (116.9 vs. 96.5+/-4.2 bpm, respectively); but there were no gender or age group differences in maximum heart rate. Results of hourly analyses of average, minimum, and maximum heart rates were similar. Mean heart rates rose from mid-afternoon to about 9:00 PM and were lowest just after midnight. Although regular sinus rhythm predominated, periods of sinus arrhythmia were evident in most cats, especially in early morning hours. Supraventricular extrasystoles were uncommon. Isolated ventricular extrasystoles occurred more frequently in group 2 cats; multiform configuration was observed in both groups. Repetitive ventricular extrasystoles, which usually consisted of occasional couplets, occurred more frequently in group 2 cats. One older cat had 2 short runs of ventricular tachycardia. Another older cat appeared to have a recurrent accelerated idioventricular rhythm.

Age Factors↗

PubMed1992

[R-R variability in acute anterior infarct after thrombolytic therapy].

PURPOSE: To analyse the effects of thrombolysis on the integrity of the autonomic nervous system, in patient with acute myocardial infarction (AMI) of the anterior wall, using the determination of the heart rate variability. METHODS: We prospectively evaluated the R-R variability of the 31 consecutive patients with anterior AMI submitted to coronary thrombolysis (25 males; mean age 59 +/- 14 years) from Holter tapes. An algorithm in a 286 computer program was used for heart rate variability (HRV). With this system, R-R variations during sinus rhythm and for a five consecutive minutes periods was determined. The results were expressed as the mean of the total determined periods; the standard deviation of the mean of all determined periods and the mean of the standard deviation. The reperfusion criteria was the early enzymatic rise of the CKMB activity levels (< or = 12 h) combined with a 50% or more reduction in the ST segment elevation within the first hour after thrombolytic therapy and the presence of an accelerated idioventricular rhythm at the same time. The reperfused group (group 1 = 16 patients) and non-reperfused group (group 2 = 15 patients) were compared in terms of R-R variability. RESULTS: Mean R-R: group 1 = 716 +/- 84 ms (540-820 ms); group 2 = 595 +/- 115 ms (390-870 ms)-p < 0.02. ms (34-92 ms); group 2 = 50 +/- 14 ms (23-77 ms)-p < 0.01. HRV 50 ms: group 1 = 2 patients; group 2 = 5 patients. Means SD of the R-R: group 1 = 44 +/- 14 ms (26-65 ms); group 2 = 39 +/- 17 ms (19-69 ms)-p: ns. CONCLUSION: Patients with anterior AMI and thrombolytic therapy demonstrate greater HRV; this finding suggested better integrity of the autonomic nervous system, with possible effects on prognosis.

Aged↗

PubMed1996

Ionic mechanisms of ischemia-related ventricular arrhythmias.

The aim of this review is the utmost simplification of the cellular electrophysiologic background of ischemia-related arrhythmias. In the acute and subacute phase of myocardial infarction, arrhythmias can be caused by an abnormal impulse generation, abnormal automaticity or triggered activity caused by early or delayed afterdepolarizations (EAD and DAD), or by abnormalities of impulse conduction (i.e., reentry). This paper addresses therapeutic intervention aimed at preventing the depolarization of "pathologic" slow fibers, counteracting the inward calcium (Ca) influx that takes place through the L-type channels (Ca antagonists), or hyperpolarizing the diastolic membrane action potential, increasing potassium (K) efflux (K-channel openers) in arrhythmias generated by an abnormal automaticity (ectopic tachycardias or accelerated idioventricular rhythms). If the cause enhanced impulse generation is related to triggered activity, and since both EAD and DAD are dependent on calcium currents that can appear during a delayed repolarization, the therapeutic options are to shorten the repolarization phase through K-channel openers or Ca antagonists, or to suppress the inward currents directly responsible for the afterdepolarization with Ca blockers. Magnesium seems to represent a reasonable choice, as it is able to shorten the action potential duration and to function as a Ca antagonist. Abnormalities of impulse conduction (re-entry) account for the remainder of arrhythmias that occur in the acute and subacute phase of ischemia and for most dysrhythmias that develop during the chronic phase. Reentrant circuits due to ischemia are usually Na channel-dependent. Drug choice will depend on the length of the excitable gap: in case of a short gap (ventricular fibrillation, polymorphic ventricular tachycardia, etc.), the refractory period has been identified as the most vulnerable parameter, and therefore a correct therapeutic approach will be based on drugs able to prolong the effective refractory period (K-channel blockers, such as class III antiarrhythmic drugs); on the other hand, for those arrhythmias characterized by a long excitable gap (most of the monomorphic ventricular tachycardias), the most appropriate therapeutic intervention consists of depressing ventricular excit-ability and conduction by use of sodium-channel blockers such as mexiletine and lidocaine. Compared with other class I antiarrhythmic agents, these drugs minimally affect refractoriness and exhibit a use-dependent effect and a voltage dependent action (i.e., more pronounced on the ischemic tissue because of its partial depolarization).

Animals↗

PubMed1983

Reperfusion arrhythmia: a marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction.

We studied the effects of coronary recanalization on arrhythmogenesis in patients undergoing intracoronary thrombolysis during the early hours of myocardial infarction. Catheterization, ventriculography, coronary angiography, and intracoronary streptokinase infusion were performed in 22 patients. Twenty-one of 22 had thrombotic total occlusion of the infarct-related transient thrombolysis with reocclusion by the end of the procedure. In 12 of these 17 patients, restoration of antegrade coronary flow was accompanied by transient arrhythmia. In these 12 patients coronary angiography within seconds of onset of arrhythmia showed vessel patency in a previously totally occluded coronary artery. Two additional patients developed arrhythmias during streptokinase infusion but after reperfusion had already been established. Accelerated idioventricular rhythm was most often noted. Sinus bradycardia and atrioventricular block with hypotension occurred during restoration of flow in arteries supplying the inferoposterior left ventricle. These arrhythmias may be useful noninvasive markers of successful reperfusion during thrombolytic therapy in acute myocardial infarction.

Adult↗

PubMed1986

Prophylactic tocainide or lidocaine in acute myocardial infarction.

Twenty-nine patients with acute myocardial infarction (AMI) were studied in a randomized double-blind trial of intravenous lidocaine and tocainide, followed by either oral tocainide or placebo without regard to previous therapy, for the prophylaxis of arrhythmias associated with acute infarction. No patient had symptomatic ventricular tachycardia or fibrillation, although 1 patient taking lidocaine was withdrawn from therapy because of breakthrough arrhythmias. One patient in each group died from mechanical complications of AMI. Tocainide was administered to 16 patients and lidocaine to 13. Seven of the 13 patients receiving lidocaine had ventricular tachycardia or accelerated idioventricular rhythm, compared with 2 of 16 receiving tocainide (p less than 0.05). Adverse effects were noted in 11 of the 13 patients receiving lidocaine and 6 of the 16 patients receiving tocainide. The infusions used provided therapeutic levels of lidocaine or tocainide and the transition to oral tocainide was accomplished safely with maintenance of therapeutic antiarrhythmic levels. Thus, tocainide appears to be at least as efficacious and may be safer than lidocaine for the prophylaxis of ventricular arrhythmias associated with AMI. The transition to oral tocainide is well tolerated and can be accomplished with minimal difficulty.

Administration, Oral↗

PubMed1987

Clinical types of proarrhythmic response to antiarrhythmic drugs.

The problem of drug-induced or drug-aggravated cardiac arrhythmias has been recognized for many years. Digitalis glycosides and class I, II, III, or IV antiarrhythmic drugs can cause severe sinus node dysfunction or atrioventricular block. Digitalis can cause a variety of supraventricular arrhythmias; atrial tachycardia with block and nonparoxysmal atrioventricular junctional tachycardia are the most characteristic. Recognition that class IA and class III antiarrhythmic drugs can aggravate arrhythmias or cause new arrhythmias in patients being treated for potentially malignant or malignant ventricular arrhythmias has intensified the interest in proarrhythmia in recent years. Several characteristic types of proarrhythmic response have been described. Torsades de pointes (multiform) ventricular tachycardia (VT) accompanied by prolongation of the QT interval can be caused by class IA and class III antiarrhythmic drugs as well as other drugs that bind to the membrane sodium channels of ventricular cells, for example, tricyclic antidepressants. Uniform VT in patients with malignant ventricular arrhythmias and poor left ventricular function is a characteristic proarrhythmic response to class IC antiarrhythmic drugs. Bidirectional VT or accelerated idioventricular rhythm are characteristic of digitalis toxicity. More difficult to establish as proarrhythmic responses are increased frequency of ventricular premature depolarizations and increased ease of inducing VT with programmed ventricular stimulation.

Anti-Arrhythmia Agents↗

PubMed1983

Acute cocaine poisoning. Importance of treating seizures and acidosis.

Cocaine poisoning has increased recently, and survival is rare because of its sudden onset and rapidly fatal course. A patient is described in whom cocaine poisoning developed. This condition was manifest by the findings of acute agitation, diaphoresis, and tachycardia, and was complicated by grand mal seizures, severe respiratory and metabolic acidosis, apnea, and accelerated idioventricular rhythm. After control of the seizures with diazepam and treatment of the acidosis with ventilation and bicarbonate, the ventricular dysrhythmia abated, and the patient made a quick recovery. Recently reported experiments suggest that seizures are a major determinant of lethality in cocaine poisoning. Treatment of the seizures is of prime importance, and correction of the acidosis can normalize cardiac rhythm and function in these critically ill patients.

Acidosis↗

PubMed1988

Protective effects of captopril against ischemia/reperfusion-induced ventricular arrhythmias in vitro and in vivo.

The effects of the converting enzyme inhibitor captopril on the susceptibility of the heart to ventricular arrhythmias following ischemia, both in vitro and in vivo, were studied. In isolated rat hearts, captopril, administered either before or at the end of ischemia, reduced ventricular fibrillation upon reperfusion after 15 minutes of local ischemia. Reduction of purine overflow, improvement in contractility, and increase in coronary blood flow occurred concomitantly. In vivo, a closed-chest pig model was used to determine the effects of captopril, administered at the end of ischemia and continued orally, on the susceptibility to ventricular arrhythmias during the chronic phase of myocardial infarction. Myocardial ischemia was induced by 60-minute inflation of a balloon catheter in the left anterior descending coronary artery. Upon reperfusion, an accelerated idioventricular rhythm occurred, both in 10 untreated and in 10 captopril-treated animals. Creatine kinase levels during the reperfusion period were significantly lower after captopril treatment. Two weeks after the short-term experiments, monomorphic ventricular tachycardia could be induced with programmed electrical stimulation in six of eight surviving untreated pigs. In contrast, in none of the six surviving captopril-treated animals was ventricular tachycardia inducible. Thus, early intervention with captopril during the development phase of myocardial infarction may have beneficial effects on the subsequent development of ventricular arrhythmias. Salvage of ischemic myocardium, improvement in ventricular function, beneficial effects on coronary flow, and decreased activity of the sympathetic nervous system may all contribute.

Animals↗

PubMed1990

Accuracy in clinical arrhythmia detection of a real-time Holter system (Oxford Medilog 4500).

The accuracy of a real-time analysis Holter system (Oxford Medilog 4500) in detecting ventricular and supraventricular arrhythmias was evaluated. Hand-counted data from randomly selected hours of 152 ECG monitorings of 152 patients were used as the control standard. Accuracy of the system was evaluated on 606 hours for premature ventricular complexes (PVC), PVC couplets and supraventricular extrasystoles (SVE), and on 1,789 hours for ventricular tachycardia (VT), accelerated idioventricular rhythm (AIVR), and supraventricular tachycardia (SVT). Sensitivity and positive predictive accuracy for the Oxford system were (1) 92.9% and 94.9% for PVC; (2) 90.1% and 87.8% for PVC couplets; (3) 98.1% and 56% for AIVR; (4) 80% and 82.3% for VT; (5) 88.6% and 56.5% for SVE, and (6) 43.7% and 60.2% for SVT. Furthermore, negative predictive accuracy, the ability to predict the total absence of an arrhythmic event in an hour, was determined. It was 91.7% for PVC, 99.5% for PVC couplets, 99.9% for AIVR, 99.7% for VT, 95% for SVE, and 98% for SVT. ventricular arrhythmias, whereas significant inaccuracies appear to exist in the analysis of supraventricular arrhythmias.

Algorithms↗