Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ventricular Flutter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed2001

Dofetilide: a new class III antiarrhythmic agent.

Dofetilide is a new, pure class III antiarrhythmic agent that prolongs the refractory period and action potential duration without having beta-blocking or calcium channel-blocking properties, making it unique among established class III agents. Dofetilide is effective in converting atrial and ventricular arrhythmias, and in maintaining sinus rhythm after cardioversion. Interestingly, it is more effective in converting atrial flutter than atrial fibrillation. It appears to be safe in patients with left ventricular dysfunction and postmyocardial infarction. In small studies, intravenous dofetilide was superior to flecainide, procainamide and amiodarone in converting atrial fibrillation and flutter. Dofetilide can be administered orally or intravenously with no significant effect on heart rate or blood pressure, but it can prolong QT interval and cause torsade de pointes in 3% to 4% of patients receiving it intravenously and in 0.8% to 1.5% of patients receiving it orally. So far, it is recommended that therapy be initiated in hospital under electrocardiogram monitoring for at least two days, with particular care to avoid torsade de pointes in high risk patients such as women, and those with bradycardia, hypokalemia, hypomagnesia and renal dysfunction. Studies have failed to show any extracardiac side effects.

Anti-Arrhythmia Agents↗
PubMed1996

Clinical improvement after revision in Fontan patients.

BACKGROUND: Arrhythmias, decreased exercise tolerance, or malabsorption will develop in a significant number of Fontan patients. Fontan revision consisting of creation of lateral atrial tunnel, reconnection of the Glenn shunt when present, or both appears to improve these patients. METHODS: Over a 34-month period, 9 patients underwent Fontan revision. The mean age was 11 +/- 5 years and the mean interval from Fontan operation to revision was 3 +/- 2 years. The reason for revision included marked impairment in exercise capacity, inability to go to school consistently, and chronic fatigue in 6 patients, 3 of whom also had serious atrial arrhythmias. Five of the 6 patients had a classic Glenn shunt. The mean right atrial pressure was greater than the pressure of the Glenn shunt (20 +/- 1.6 versus 17 +/- 0.8 mm Hg). Three of the 6 patients also showed a significant gradient between the right or left pulmonary artery wedge and ventricular end-diastolic pressure, indicating pulmonary vein obstruction from the bulging atrial septum or partitioning patch (13 +/- 3 versus 6.8 +/- 1 mm Hg). The remaining 3 patients had revision because of malabsorption (1), hepatomegaly and obstructed right pulmonary veins from bulging atrial septum (1), and tricuspid insufficiency (1). Fontan revision was accomplished with creation of a lateral atrial tunnel and Glenn reconnection in 6 patients, Glenn reconnection in 2, and creation of a lateral atrial tunnel in 1. Four patients had additional procedures. RESULTS: One patient died of Pseudomonas pneumonia. Early extubation, chest tube removal, and postoperative hospital discharge were accomplished in 8 patients (mean = 1.4 +/- 1, 2.8 +/- 1, and 8 +/- 3 days, respectively). One patient died 8 months postoperatively of brain damage after ventricular fibrillation from attempted cardioversion for atrial flutter. The remaining patients had marked improvement in exercise capacity with ability to consistently go to school, improvement in duration and tolerance to arrhythmias on less medication, and resolution of malabsorption up to 37 months postoperatively (mean, 20 +/- 12 months). CONCLUSIONS: We conclude that creation of lateral atrial tunnel with excision of a bulging atrial septum or atrial partitioning patch that causes pulmonary venous obstruction, reconnection of the Glenn shunt, which allows better distribution of flow based on the pulmonary vascular bed and resistance of each lung, or a combination of these procedures will improve Fontan patients.

Activities of Daily Living↗
PubMed2003

Arrhythmias in the intensive care patient.

PURPOSE OF REVIEW: Atrial fibrillation, atrial flutter, AV-nodal reentry tachycardia with rapid ventricular response, atrial ectopic tachycardia, and preexcitation syndromes combined with atrial fibrillation or ventricular tachyarrhythmias are typical arrhythmias in intensive care patients. Most frequently, the diagnosis of the underlying arrhythmia is possible from the physical examination, the response to maneuvers or drugs, and the 12-lead surface electrocardiogram. In all patients with unstable hemodynamics, immediate DC-cardioversion is indicated. Conversion of atrial fibrillation to sinus rhythm is possible using antiarrhythmic drugs. Amiodarone has a conversion rate in atrial fibrillation of up to 80%. However, caution in the use of short-term administration of intravenous amiodarone in critically ill patients with recent-onset atrial fibrillation is absolutely necessary, and the duration of therapy should not exceed 24 to 48 hours. Ibutilide represents a relatively new class III antiarrhythmic agent that has been reported to have conversion rates of 50% to 70%; it seems that ibutilide is even successful when intravenous amiodarone failed to convert atrial fibrillation. RECENT FINDINGS: Newer studies compared the outcome of patients with atrial fibrillation and rhythm- or rate-control. Data from these studies (AFFIRM, RACE) clearly showed that rhythm control is not superior to rate control for the prevention of death and morbidity from cardiovascular causes. Therefore, rate-control may be an appropriate therapy in patients with recurrent atrial fibrillation after DC-cardioversion. Acute therapy of atrial flutter in intensive care patients depends on the clinical presentation. Atrial flutter can most often be successfully cardioverted to sinus rhythm with energies less than 50 joules. Ibutilide trials showed efficacy rates of 38-76% for conversion of atrial flutter to sinus rhythm compared with conversion rates of 5-13% when intravenous flecainide, propafenone, or verapamil was administered. In addition, a high dose (2 mg) of ibutilide was more effective than sotalol (1.5 mg/kg) in conversion of atrial flutter to sinus rhythm (70% versus 19%). SUMMARY: There is general agreement that bystander first aid, defibrillation, and advanced life support is essential for neurologic outcome in patients after cardiac arrest due to ventricular tachyarrhythmias. The best survival rate from cardiac arrest can be achieved only when (1) recognition of early warning signs, (2) activation of the emergency medical services system, (3) basic cardiopulmonary resuscitation, (4) defibrillation, (5) management of the airway and ventilation, and (6) intravenous administration of medications occurs as rapidly as possible. Public access defibrillation, which places automatic external defibrillators in the hands of trained laypersons, seems to be an ideal approach in the treatment of ventricular fibrillation. The use of automatic external defibrillators by basic life support ambulance providers or first responder in early defibrillation programs has been associated with a significant increase in survival rates. Drugs such as lidocaine, procainamide, sotalol, amiodarone, or magnesium were recommended for treatment of ventricular tachyarrhythmias in intensive care patients. Amiodarone is a highly efficacious antiarrhythmic agent for many cardiac arrhythmias, ranging from atrial fibrillation to malignant ventricular tachyarrhythmias, and seems to be superior to other antiarrhythmic agents.

Aged↗
PubMed1978

Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter.

Electrophysiological studies were performed during sinus rhythm on 21 patients who had demonstrated the spontaneous occurrence of sustained atrial flutter. The purpose was to determine if atrial conduction disease is a prediposing factor for the development of atrial flutter. Patients with atrial enlargement were excluded from the series. The control group consisted of 11 age-matched patients with normal electrocardiograms and electrophysiology studies. The flutter group showed prolongation of the mean right intra-atrial conduction time at 50 msec (control of 37 msec, P less than 0.05), the mean interatrial conduction time at 92 msec (control of 44 msec, P less than 0.001) and the mean P wave duration at 132 msec (control of 112 msec, P less than 0.01). The flutter group also demonstrated a higher incidence of sinus node dysfunction and ventricular conduction disease compared to the control group. These data indicate that patients who develop atrial flutter have atrial conduction disease. Atrial conduction disease appears to be 1) a major prediposing factor for the development of atrial flutter and 2) a part of the fibro-degenerative conduction disease spectrum.

Arrhythmia, Sinus↗
PubMed1980

Effectiveness of amiodarone in resistant arrhythmias.

Amiodarone is used in the treatment of previously drug-resistant supraventricular and ventricular arrhythmias. We report our experience with amiodarone in 8 patients. Five patients had paroxysmal atrial flutter, one had paroxysmal atrial fibrillation, one had supraventricular tachycardia, and one ventricular tachycardia. Considerable improvement, both objectively and subjectively, was observed in all patients. Side effects were as follows: all patients had corneal microdeposits, one developed left bundle branch block which resolved on stopping amiodarone, and one reported constipation and abdominal pains. Six patients have been treated for 10-28 months; 3 developed tolerance at 4-14 months after the introduction of amiodarone therapy, but symptoms improved with increased dosage. It is important to watch for the development of tolerance to this drug.

Adult↗
PubMed1989

Prospective evaluation of transesophageal pacing for the interruption of atrial flutter.

PURPOSE: Although transesophageal pacing has been used successfully for the interruption of cardiac arrhythmias, the efficacy of this technique for the interruption of spontaneous atrial flutter remains poorly defined. The utility of transesophageal pacing to interrupt atrial flutter that was persistent despite standard antiarrhythmic drug therapy (mean duration: 70.3 days; range: one day to more than 365 days) was studied prospectively in 39 consecutive patients. PATIENTS AND METHODS: After written informed consent was obtained from each patient, transesophageal pacing was performed with a programmable stimulator, using the distal electrode as the cathode and the proximal electrode as the anode. All patients continued to receive a type 1 antiarrhythmic drug or amiodarone throughout the period of transesophageal pacing. The response to transesophageal pacing was classified as follows: (1) direct conversion; (2) indirect conversion; or (3) failure to interrupt atrial flutter. RESULTS: The mean stimulus amplitude and pulse duration required for atrial capture were 19.8 +/- 7.5 mA and 18.4 +/- 7.9 msec. Atrial flutter was successfully converted to sinus rhythm by transesophageal pacing in 82% of patients. In 38% of patients, atrial flutter was converted directly to sinus rhythm without another intervening arrhythmia (direct conversion). The mean pacing rate required for direct conversion was 341 +/- 27 beats/minute. In 44% of patients, the cycle length of atrial flutter was accelerated to less than 180 msec or was converted to atrial fibrillation with spontaneous conversion to sinus rhythm within 24 hours (mean 8.4 +/- 9.3 hours, indirect conversion). The mean pacing rate inducing accelerated atrial flutter or transient atrial fibrillation was 372 +/- 61 beats/minute (p = NS compared to direct conversion). Atrial flutter was not interrupted or atrial fibrillation was induced that did not spontaneously convert to sinus rhythm within 24 hours in an additional seven patients (18%). The underlying cardiac disease, age, previous drug therapy, atrial size, atrial flutter cycle length, history of prior atrial fibrillation, left ventricular function, and concomitant medical illnesses did not predict the efficacy of transesophageal pacing. CONCLUSION: The present study suggests that transesophageal pacing is highly effective for interrupting spontaneous atrial flutter that does not terminate with standard antiarrhythmic drug therapy.

Adult↗
PubMed2002

A mathematical model of human atrioventricular nodal function incorporating concealed conduction.

This work develops a mathematical model for the atrioventricular (AV) node in the human heart, based on recordings of electrical activity in the atria (the upper chambers of the heart) and the ventricles (the lower chambers of the heart). Intracardiac recordings of the atrial and ventricular activities were recorded from one patient with atrial flutter and one with atrial fibrillation. During these arrhythmias, not all beats in the atria are conducted to the ventricles. Some are blocked (concealed). However, the blocked beats can affect the properties of the AV node. The activation times of the atrial events were regarded as inputs to a mathematical model of conduction in the AV node, including a representation of AV nodal concealment. The model output was compared to the recorded ventricular response to search for and identify the best possible parameter combinations of the model. Good agreement between the distribution of interbeat intervals in the model and data for durations of 5 min was achieved. A model of AV nodal behavior during atrial flutter and atrial fibrillation could potentially help to understand the relative roles of atrial input activity and intrinsic AV nodal properties in determining the ventricular response.

Atrial Fibrillation↗
PubMed2004

Ibutilide-induced alterations in electrocardiographic and spatial vectorcardiographic descriptors of ventricular repolarization.

BACKGROUND: Ibutilide is used for the pharmacologic cardioversion of atrial fibrillation (AF) or flutter (AFl). Ibutilide-induced QT interval prolongation has been demonstrated previously. However, its effects on vectorcardiographic (VCG) descriptors of ventricular repolarization (VR) have not been studied so far. HYPOTHESIS: To evaluate the effects of ibutilide on electrocardiographic (ECG) and VCG descriptors of VR, one or two repeated 10-min infusions of 1 mg of ibutilide were given in 50 consecutively recruited patients (36 women, mean age 69.4 +/- 9.3 years) with AF or AFl of recent onset. METHODS: The maximum and the minimum QT intervals, QT dispersion, the rate-corrected QT maximum, and the spatial VCG descriptors, spatial T amplitude, and spatial QRS-T angle were calculated before (baseline ECG) and 30 min after the start of ibutilide infusion (postinfusion ECG). RESULTS: After ibutilide infusion, 40 (80%) patients were cardioverted to sinus rhythm (Group 1), while in the remaining 10 (Group 2) AF or AFl persisted. In both study groups, temporal measures of VR were significantly increased from baseline to the postinfusion ECG. In Group 1, spatial T amplitude and spatial QRS-T angle did not differ between those two ECGs, while in Group 2 spatial T amplitude was significantly increased (p = 0.005) and spatial QRS-T angle was significantly decreased (p = 0.002) post infusion compared with baseline ECG. CONCLUSIONS: While temporal measures of VR are significantly affected in all patients who receive ibutilide infusion for AF or AFl cardioversion, spatial VCG descriptors of VR are significantly altered only in those patients who fail to respond to the drug. A dose-related effect of ibutilide on the different aspects of VR should be suspected.

Aged↗
PubMed1994

Management outcome and follow-up of fetal tachycardia.

OBJECTIVES: The aim of this study was to evaluate fetal tachycardia and the efficacy of maternally administered antiarrhythmic agents and the effect of this therapy on delivery and postpartum management. BACKGROUND: Sustained fetal tachycardia is a potentially life-threatening condition in which pharmacologic therapy is reported to be effective. There is ongoing discussion about optimal management. METHODS: A group of 51 patients with M-mode echocardiographically documented fetal tachycardia was studied retrospectively. RESULTS: Thirty-three fetuses had supraventricular tachycardia; 15 had atrial flutter; 1 had two episodes of both; and 2 had ventricular tachycardia. Fetal hydrops was seen in 22 patients. Thirty-four fetuses received maternal therapy with either digoxin or flecainide as the first administered drug (additional drugs were given in 12). Drug treatment was successful in establishing acceptable rhythm control in 82% (84% without, 80% with hydrops). In the latter group the median number of drugs and number of days to conversion were higher. Three patients with fetal hydrops died. In 50% of cases, tachycardia reappeared at delivery: 9 neonates presented with atrial flutter, 14 with supraventricular tachycardia and 1 with ventricular tachycardia. Seventy-eight percent of the group had pharmacologic therapy by 1 month of age and 14% by 3 years. CONCLUSIONS: Fetal tachycardia can be treated adequately in the majority of patients, even in the presence of hydrops, and therefore emergency delivery might not be indicated. Digoxin and flecainide were drugs of first choice and produced no serious adverse effects in this series of patients. The majority of patients do not require prolonged therapy.

Atrial Flutter↗
PubMed1996

Unusual atrial pro-arrhythmic effect of flecainide: a contemporary review.

The authors report the case of a patient with drug-resistant atrial fibrillation, who developed, for more than 2 hours, a well-tolerated attack of palpitations, after taking 500 mg of flecainide acetate. The Holter monitoring demonstrated atrial flutter with 1:1 AV conduction and a ventricular rate at 220 bpm. This atrial pro-arrhythmic effect is rare and the mechanism is discussed.

Aged↗
PubMed1986

Incidence and clinical features of the quinidine-associated long QT syndrome: implications for patient care.

Quinidine therapy is one of the most common causes of the acquired long QT syndrome and torsade de pointes. In reviewing clinical data in 24 patients with the quinidine-associated long QT syndrome, 20 of whom had torsade de pointes, we have delineated several heretofore unreported or underemphasized features. (1) This adverse drug reaction occurred either in patients who were being treated for frequent nonsustained ventricular arrhythmias or for atrial fibrillation or flutter. (2) In patients being treated for atrial fibrillation, torsade de pointes occurred only after conversion to sinus rhythm. (3) Although most patients developed the syndrome within days of starting quinidine, four had torsade de pointes during long-term quinidine therapy, usually in association with hypokalemia. (4) Because of the large experience with this entity at our institution, we have been able to estimate the risk as at least 1.5% per year. (5) Twenty of the 24 patients had at least one major, easily identifiable, associated risk factor including serum potassium below 3.5 mEq/L (four); serum potassium between 3.5 and 3.9 mEq/L (nine); high-grade atrioventricular block (four); and marked underlying, (unrecognized) QT prolongation (two). Plasma quinidine concentrations were low, being at or below the lower limit of the therapeutic range in half of patients. The ECG features typically included absence of marked QRS widening, marked QT prolongation (by definition), and a stereotypic series of cycle length changes just prior to the onset of torsade de pointes. Torsade de pointes started after the T wave of a markedly prolonged QT interval that followed a cycle that had been markedly prolonged (usually by a post ectopic pause).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Signal-averaged electrocardiograms in patients with atrial fibrillation or flutter.

The signal-averaged QRS complex that is prolonged because of low amplitude late potentials predicts ventricular tachycardia. This study investigated if signal-averaged low amplitude atrial potentials predict atrial fibrillation or flutter (AFF). Low amplitude potentials were considered to be high-frequency, high amplitude P (HiFP) duration recorded between 50 and 250 Hz at 1.0 mm/microV amplitude minus unfiltered P (UnFP) duration at 0.1 mm/microV. In nine normals, HiFP averaged 115.6 msec +/- 9.8 SD. HiFP were wider in 26 control patients (133.5 msec +/- 15.7, p less than 0.005) but HiFP-UnFP (11.2 msec +/- 8.5) and signals less than 10 microV terminating HiFP inscription (21.7 msec +/- 23.4) were similar to normal values. Seventeen patients with paroxysmal or recently cardioverted AFF did not have significantly longer intervals than controls (HiFP averaged 138.8 msec +/- 23.0, HiFP-UnFP 13.2 msec +/- 9.3, and signals less than 10 microV 32.4 msec +/- 19.5). Therefore, signal-averaged P waves do not identify patients with AFF.

Adult↗
PubMed1990

Frequency and significance of cardiac rhythm disturbances in healthy elderly individuals.

The authors examined the prevalence and significance of cardiac rhythm disturbances in healthy elderly individuals. They selected 26 men with active lifestyles, aged 70-81 years, after clinical, routine blood tests, chest radiographs, echocardiography, resting and exercise electrocardiography, and Gated cardiac blood imaging evaluations. The men were submitted to continuous electrocardiographic monitoring during their daily routine. The recording time ranged from 838 to 1,432 min (average = 1,307 +/- 153 min). Clinical follow-up was done every six months. Sinus rhythm predominated in all subjects. The maximal, minimal, and average heart rate ranges (beats/min) were, respectively: during sleeping periods, 60-115 (85.8 +/- 13.2), 42-80 (56.6 +/- 8.7), 51-85 (64.0 +/- 8.8); and during awake periods, 85-150 (118.4 +/- 16.4), 50-85 (64.1 +/- 9.1), 61-90 (75.3 +/- 8.3). The longest sinus pauses were observed during sleep and ranged from 0.8 to 2.5 sec (1.25 +/- 0.34 sec). Atrial ectopic beats were observed in 20 individuals (76.9%). They were frequent in four (15.4%) and repetitive in nine (34.6%) of them. Short-lasting episodes of paroxysmal atrial tachycardia and paroxysmal atrial flutter were observed in one case each. Ventricular ectopic beats were recorded in 20 individuals (76.9%). They were frequent in 6 (23%) and multiform in 13 (50%) of them. Couplets were observed in 5 cases (19.2%) and episodes of nonsustained ventricular tachycardia were present in 3 individuals (11.5%). No symptoms were referred by any individual during recording. No clinical signs of heart disease or symptoms were noticed during the average 40 +/- 7.2 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

A controlled study on oral propafenone versus digoxin plus quinidine in converting recent onset atrial fibrillation to sinus rhythm.

UNLABELLED: Eighty-seven patients with recent onset atrial fibrillation (< or = 8 days) without clinical signs of heart failure were randomly allocated to one of the following treatments: (i) oral propafenone (600 mg as a loading dose followed after 8 h by 300 mg t.i.d.); (ii) intravenous digoxin as acute scheme (up to 1.125 mg/24 h) followed after 6 h by hydroquinidine chlorhydrate (total dose, 1350 mg); or (iii) placebo. The patients were submitted to Holter monitoring for 48 h. RESULTS: propafenone achieved higher successful conversion rates at 6, 12 and 24 h compared either with placebo (62% vs. 17%, 83% vs. 34%; 86% vs. 55%; P < 0.01, respectively) or with digoxin at 6 h (62% vs. 38%; P < 0.05) and digoxin plus quinidine at 12 h (83% vs. 48%; P < 0.05). At 48 h, a placebo conversion rate of 76% was observed with consequent lack of any significant difference with the active treatments. Mean conversion times within 48 h were 267 +/- 238 min for propafenone, 648 +/- 631 min for digoxin plus quinidine (P < 0.01 vs. propafenone) and 893 +/- 622 min for placebo (P < 0.001 vs. propafenone). Propafenone and digoxin plasma levels were within the therapeutic range. Asymptomatic phases of atrial flutter with > or = 2:1 atrio-ventricular conduction ratio were observed during Holter monitoring, before conversion to sinus rhythm, in four patients treated with propafenone, in one patient taking digoxin plus quinidine and in four patients with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Intravenous adenosine in the emergency department management of paroxysmal supraventricular tachycardia.

STUDY PURPOSE: To evaluate the efficacy of adenosine in the treatment of emergency department patients with spontaneous paroxysmal supraventricular tachycardia (PSVT). DESIGN: An eight-month prospective outcome study. POPULATION: Patients 16 or more years old with PSVT by surface ECG criteria. Patients were excluded if there was clinical or hemodynamic evidence of hypoperfusion. MEASUREMENTS: Patient age, sex, PSVT rate, pretreatment blood pressure, history of cardiac disease, chronic drug therapy, and response to IV adenosine. RESULTS: Twenty-three patients with 27 episodes of suspected PSVT met inclusion criteria. After IV adenosine, two patients were found to have atrial flutter, and one was found to have ventricular tachycardia. Twenty-four episodes of PSVT were diagnosed in the remaining 21 patients. There were eight male and 13 female patients with a mean age of 51 +/- 19 years (range, 16 to 80 years). Sixteen patients related a history of cardiovascular disease. The mean QRS rate during PSVT was 181 +/- 23. Twenty-three of 24 episodes (96%) were converted to sinus rhythm within 20 to 45 seconds of adenosine therapy. However, 13 of 23 of initial conversions (57%) were followed by recurrence of PSVT within five minutes. All 13 recurrences required therapy with other antiarrhythmic drugs for conversion to and maintenance of sinus rhythm. Complications of adenosine were noted in only four patients and were transient and clinically unimportant. CONCLUSION: IV adenosine effectively terminates PSVT in ED patients with spontaneous PSVT; recurrence of PSVT after adenosine is common in the ED population and should be treated with other antiarrhythmic agents, not repeated doses of adenosine; adenosine is useful in the differential diagnosis of tachyarrhythmias; and doubling the initial dose of adenosine to 12 mg would increase the likelihood of conversion with the first dose.

Adenosine↗
PubMed1994

Adenosine for the prehospital treatment of paroxysmal supraventricular tachycardia.

STUDY OBJECTIVE: To determine the efficacy and feasibility of adenosine for the treatment of paroxysmal supraventricular tachycardia (PSVT) in the prehospital setting. DESIGN: Prospective case series. SETTING: Large, urban, advanced life support emergency medical services system. PARTICIPANTS: One hundred twenty-nine adult patients with PSVT, as identified by paramedic personnel. Pregnant patients and those taking carbamazepine or dipyridamole were excluded. INTERVENTIONS: Dose of 12 mg adenosine by rapid i.v. push followed by a 5-mL saline flush and a repeat dose of 12 mg adenosine i.v. push if the patient's rhythm remained unchanged. MEASUREMENTS AND MAIN RESULTS: Six-second lead II rhythm strips and vital signs were documented before and 2 minutes after the administration of adenosine. Demographic information, past medical history, medications, number of adenosine doses given, and complications were recorded by the paramedic on a case-report form. One hundred six of 129 (82%) of the case-report forms included the rhythm strips from before and after adenosine administration. Actual initial rhythms were determined by a consensus panel. The initial rhythms were PSVT in 79% (84 of 106) of patients, atrial fibrillation in 12% (13 of 106), sinus tachycardia in 5% (five of 106), atrial flutter in 2% (two of 106), and ventricular tachycardia in 2% (two of 106). Eighty-five percent (71 of 84) of patients in PSVT were successfully converted to sinus rhythms; four (5.6%) of these patients required a second 12-mg dose. One patient in atrial fibrillation spontaneously converted to normal sinus rhythm and one patient in ventricular tachycardia converted after adenosine. All other patients not initially in PSVT remained in their initial rhythm. Complications occurred in 12 of 129 patients and included chest pain (five), flushing (three), shortness of breath (two), nausea (one), anxiety (one), dizziness (one), headache (one), and seizure (one). All complications were transient and required no treatment. Prior history of PSVT was the only variable associated with a higher rate of conversion (P = .029). CONCLUSION: Paramedics are able to accurately identify PSVT using a single lead. Adenosine is safe and effective treatment for PSVT in the prehospital setting. This series is the largest prehospital study of adenosine use to date.

Adenosine↗
PubMed2003

Utility of patient-activated cardiac event recorders in the detection of cardiac arrhythmias.

BACKGROUND: Patient-activated event recorders are useful for the diagnosis of arrhythmia in patients with palpitation and presyncope. However, the utility of event recorders in patients suspected of arrhythmia but presenting with other symptoms is not clear. Furthermore, the factors influencing their utility have not been evaluated. METHODS: Event recorder reports of six hundred and sixty consecutive patients referred due to clinical suspicion of cardiac arrhythmia were reviewed. We divided symptoms into four groups: palpitation, presyncope, chest tightness, and dyspnea. We calculated the diagnostic yield according to patients' symptoms reported on the record, and analyzed the factors affecting the utility of event recorders. RESULTS: The overall diagnostic yield was 64%, and those of palpitation, presyncope, chest tightness, and dyspnea were 66%, 57%, 51% and 60%, respectively. The most common five findings in our patients were sinus rhythm (36%), sinus tachycardia (30%), atrial premature complex (14%), ventricular premature complex (12%), and atrial fibrillation/atrial flutter (7%). The recording duration (8 +/- 4 days) was short in the present study, but the overall diagnostic yield was similar to those of previous ones. Women had lower diagnostic yields than men, especially in atrial flutter-fibrillation. The diagnostic yield was not influenced by age, ordered doctors, or history of cardiovascular disease. CONCLUSIONS; Patient-activated event recorders provided a good diagnostic yield in patients with different presentations of cardiac arrhythmia, and women had lower diagnostic yield in atrial flutter-fibrillation.

Arrhythmias, Cardiac↗
PubMed2000

Role of electrophysiological studies and arrhythmia intervention in repairing Ebstein's anomaly.

BACKGROUND: Repairing Ebstein's anomaly without correction of associated arrhythmia may result in sudden death. Catheter or surgical ablation is indicated for various symptomatic tachyarrhythmias in Ebstein's anomaly. METHODS: Between October 1973 and October 1997, 30 patients with Ebstein's anomaly underwent surgical repair in our hospital. Tricuspid valve replacement was performed in 13 patients, tricuspid annuloplasty and valvuloplasty in the remaining 17 patients. Preoperative electrophysiological studies were performed in 11 patients after 1980. Concomitant arrhythmia ablation was done in 10 patients: 4 for Wolff-Parkinson-White syndrome, 2 for atrioventricular (AV) nodal reentrant tachycardia, one for ventricular tachycardia and 3 for paroxysmal atrial flutter and fibrillation. RESULTS: No mortality or major morbidity occurred in those patients undergoing arrhythmia intervention. There were 7 deaths in total; 6 died suddenly, and the other died of purulent mediastinitis. None of the 6 sudden deaths underwent preoperative electrophysiological evaluation. The functional recovery was good in all survivals. CONCLUSIONS: We conclude that detailed preoperative electrophysiological evaluation in patients with Ebstein's anomaly is mandatory. Aggressive surgical intervention of the associated arrhythmias in addition to anatomic correction can reduce the sudden death in Ebstein's anomaly.

Adolescent↗