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 541 records · Page 30Linked to original sources
PubMed1984

Clinical pharmacology of calcium antagonists.

Verapamil, nifedipine, and diltiazem are effective in the treatment of stable effort angina and angiospastic (variant) angina. In addition, there is evidence that the agents are beneficial in patients diagnosed as having unstable angina. The efficacy of calcium antagonists for the treatment of effort angina appears to be augmented by combining them with beta-adrenergic blockers. Intravenous verapamil, but not nifedipine, is very effective in terminating paroxysmal supraventricular tachycardias caused by re-entrant mechanisms with or without involvement of accessory pathways (WPW syndrome). Verapamil is also effective in slowing the ventricular response to atrial fibrillation or flutter. The use of verapamil for the treatment of ectopic atrial or ventricular dysrhythmias is less well established and will require further evaluation.

Angina Pectoris↗
PubMed1983

Verapamil: an effective calcium blocking agent for pediatric patients.

Verapamil is a slow-channel calcium-blocking agent that has been released recently by the Food and Drug Administration for treatment of cardiac dysrhythmias in all age groups. Its primary action is to slow conduction in the atrioventricular node, thereby abolishing those types of supraventricular tachycardia using the atrioventricular node as a part of the reentry circuit or slowing the ventricular rate in someone with atrial flutter. Other investigations have shown that it is likely to relieve left ventricular outflow obstruction in patients with hypertrophic obstructive cardiomyopathy. Because of its potential widespread usefulness in the pediatric population, all pediatricians should be more aware of how it is used and the potential hazards. The methods of administration and treatment of overdoses as well as indications for usage, contraindications, and adverse reactions will be explained.

Administration, Oral↗
PubMed1978

[Discharge energy and the problems of anesthesia in the electrical cardioversion of paroxysmal arrhythmias].

The efficacy of electroimpulsive therapy with low energy discharges (up to 50 joules) in various paroxysmal arrhythmias was studied. A mild tranquilizer, seduxen (diazenam), was used as the anesthetic. Electroimpulsive therapy with low-energy discharges was found to produce a high effect in ventricular tachycardia and atrial flutter but a poor restorative effect in atrial fibrillation. The possibility of successful anesthesia with seduxen in electrical cardioversion of paroxysmal disorders of cardiac rhythm is concretized.

Adult↗
PubMed1979

Patient-initiated transtelephone transmission of electrocardiographic signals in the diagnosis of arrhythmias.

Thirty-one patients who had complained of recurrent palpitations were given transtelephone transmitters of electrocardiographic signals and instructed to use the transmitters while they were having symptoms. From the transcribed electrocardiograms sinus tachycardia was documented in 12 patients, paroxysmal atrial tachycardia in 7, atrial fibrillation in 4, atrial flutter in 3, frequent ventricular premature beats in 4 and ventricular tachycardia in 1. Patient-initiated transtelephone transmission of electrocardiographic signals was found to be an effective means of documenting the nature of symptomatic paroxysmal tachycardia.

Adolescent↗
PubMed1997

[Evaluation of hyperkinetic cardiac arrhythmia in chronic obstructive bronchopneumopathy].

Patients with chronic obstructive pulmonary disease (COPD), especially during acute exacerbations of their disease, show a greater incidence of cardiac arrhythmias than healthy subjects of the same age. The type of arrhythmias found may be supraventricular (premature atrial beats, paroxysmal supraventricular tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation) or ventricular (premature ventricular beats, sustained ventricular tachycardia, torsades de pointes, ventricular fibrillation) that may lead to sudden cardiac death. The pathogenesis of arrhythmias is complex and many factors may be involved such as hypoxemia, hypercapnia, respiratory acidosis, metabolic and respiratory alchalosis, hypokalemia, concomitant ischemic heart disease, chronic cor pulmonale, left ventricular diastolic dysfunction. Remarkable attention has been drawn to the possible arrhythmogenic effect of drugs such as theophylline, beta-adrenergic stimulants and digitalis which are commonly used in the therapy of COPD. Both of the main classes of bronchodilators (methylxanthynes and beta-adrenergic agonists), even when used together, apparently do not increase the incidence of dangerous cardiac arrhythmias. However, these drugs should be used with caution in the elderly, in patients with preexisting cardiac arrhythmias, with heart disease or with reduced hepatic function. In these cases Holter monitoring, repeated measurements of plasma drugs concentration and prompt hospitalization of high risk patients in Intensive Care Unit may be needed.

Adrenergic beta-Agonists↗
PubMed1998

A testing system for implantable cardioverter defibrillators.

Implantable cardioverter defibrillator (ICD) testing during the implantation process is important in order to avoid repeated induction of arrhythmias, which extends the implantation procedure and poses a risk to the patient. Hence, an in vitro testing system has been designed to assist optimal device programming and avoid repetitive inductions. The system includes a high-speed computer with A/D and D/A subsystems. Software has been designed to eliminate repeated arrhythmia induction by real-time capture and storage of the electrogram. Subsequently, the electrogram can be replayed into ICD software simulators at a variety of settings to determine candidate programming parameters. To validate the simulation system, signals were fed directly to an ICD via an attenuator. Output event markers were captured simultaneously with the signal into a digital file to assess the device performance. Four ventricular tachycardia (VT), three supraventricular tachycardia, (SVT), three atrial flutter (AFL), three atrial fibrillation (AF), and ten ventricular fibrillation (VF) passages were used to verify the system. Test settings were 110-160 beats/min for detection rate and 5 seconds for shock delay. The simulator and ICD detected the episodes for all passages at the 110 beats/min setting. For the setting of 160 beats/min, two VTs, two SVTs, three AFLs, and nine VFs were detected by the device, but no Afb triggered a shock. The simulator detection criteria were met by two VTs, two SVTs, three AFLs, ten VFs, and one AF. The mean detection time was 6,869-7,330 ms (110-160 beats/min) for the simulator and 7,840-8,170 ms for device. Comparison of results showed general agreement between simulator and device. Results demonstrated that device behavior at a variety of settings can be elucidated by the simulator for selection of optimal performance. The automated system can also function as a test bed for evaluation of new algorithms during device development and design.

Algorithms↗
PubMed1998

Fetal atrial flutter: diagnosis, clinical features, treatment, and outcome.

OBJECTIVES: To assess clinical features, treatment efficacy, and outcome of fetal atrial flutter. STUDY DESIGN: All atrial flutter cases seen in our unit between 1988 and 1995 were reviewed retrospectively and compared with the pooled data of 37 echocardiographically documented and published cases. RESULTS: Atrial flutter was found in 15 of 49 (30.6%) fetuses who had been referred because of clinically relevant tachyarrhythmia. Mean age at detection was 34+/-4 weeks' gestation. Atrial flutter was incessant in 11 and intermittent in 4, with a mean atrial rate of 442+/-65 beats/min and a mean ventricular rate of 216+/-28 beats/min. A predominance of 2:1 atrioventricular conduction was observed. In 5 of 15 cases another form of arrhythmia (supraventricular tachycardia, chaotic atrial rhythm, ventricular extrasystoles) coexisted with atrial flutter. Eleven fetuses were treated with maternal digoxin, and five subsequently converted to sinus rhythm. Four fetuses received no medication; of these four, two showed brief self-limited episodes of atrial flutter and two were delivered after detection of the arrhythmia. Only one fetus (6.7%), who did not respond to drug therapy, was delivered prematurely because of mild congestive heart failure. Seven neonates were in atrial flutter at birth; rhythm control could be easily achieved with sotalol or digoxin (n = 5), flecainide (n = 1), or electroconversion (n = 1) within the first 2 days of life without any relapse. CONCLUSION: Fetal atrial flutter accounts for approximately one third of all clinically relevant tachyarrhythmia. Although the suppression rate of incessant atrial flutter with digoxin is only 50%, this therapy may be useful for its positive inotropic and negative chronotropic properties. In our experience most fetuses with therapy-resistant atrial flutter and absence of 1:1 atrioventricular conduction do not experience congestive heart failure and do not need to be delivered prematurely. After birth, conversion to sinus rhythm was easily achieved in all neonates.

Anti-Arrhythmia Agents↗
PubMed1979

Verapamil in atrial fibrillation and atrial flutter.

A double-blind randomized study was performed to compare the efficacy of intravenous verapamil with saline in 28 patients with a rapid ventricular rate and atrial fibrillation or atrial flutter. Conversion of atrial fibrillation to sinus rhythm occurred in none of 14 patients after saline and in 3 of 20 patients (15%) 7 to 160 min after verapamil. The ventricular rate in atrial fibrillation was slowed greater than or equal to 15% in 2 of 14 patients (14%) by saline, in 17 of 20 patients (85%) by 1 dose of verapamil (p less than 0.001), and in 19 of 20 patients (95%) by 1 or 2 doses of verapamil (p less than 0.001). Conversion of atrial flutter to sinus rhythm occurred in none of 4 patients after saline and in 1 of 7 patients (14%) 105 min after verapamil. The ventricular rate in atrial flutter was slowed greater than or equal to 15% in none of 4 patients by saline, in 4 of 7 patients (57%) by 1 dose of verapamil, and in 7 of 7 patients (100%) by 1 or 2 doses of verapamil (p less than 0.001).

Adult↗
PubMed1982

Verapamil (Isoptin, Knoll; Calan, Searle).

Verapamil is a calcium antagonist that is pharmacologically different from other currently marketed antiarrhythmics. It is used for the acute treatment of PSVT and atrial fibrillation and flutter. It appears to be more effective than beta-adrenergic blocking agents in the treatment of PSVT. Approximately 80 percent of patients with PSVT will convert to normal sinus rhythm after verapamil 0.075-0.15 mg/kg. Atrial fibrillation and flutter seldom convert to sinus rhythm with verapamil, but it successfully reduces the ventricular rate in 90 percent of these patients. Verapamil is useful for the rapid conversion of PSVT to normal sinus rhythm and for the rapid control of ventricular rate in atrial fibrillation and flutter before other antiarrhythmics have taken effect. Because of its short plasma half-life, other agents or cardioversion can be used if verapamil is unsuccessful. The use of verapamil in the treatment of classical and variant angina, hypertrophic cardiomyopathy, and hypertension is being evaluated. Mild reduction in blood pressure and heart rate may occur with verapamil therapy. Caution must be exercised when verapamil is administered to patients with sinus node disease, advanced AV block, concomitant beta-adrenergic blocking agents, and digitalis intoxication.

Costs and Cost Analysis↗
PubMed1976

Spectrum of echocardiographic findings in bacterial endocarditis.

Forty-seven echocardiograms were obtained in 32 patients with bacterial endocarditis. Preexistent abnormalities were found in 14 patients. In five of them thought to have bacterial endocarditis on normal valves, echocardiography showed mitral stenosis (one), bicuspid aortic valve (two), and prolapse of mitral valve (two). Definite vegetations were seen in 22 patients--on the aortic valve in seven, the mitral valve in 12, and both valves in three. Ten patients had milder changes suggestive but not diagnostic of vegetations. In 12 patients, surgery confirmed the echocardiographic findings. Fourteen had systemic embolic episodes and all had echocardiographic evidence of vegetations. Abnormalities secondary to bacterial endocarditis, other than vegetations, were common. Twenty-one patients had left ventricular volume overload. Ten had a flail posterior leaflet of the mitral valve, three of which were confirmed surgically. Eight had abnormal coarsely fluttering echoes in the left ventricular outflow tract consistent with a prolapsing aortic valve or underlying aortic vegetations; four were confirmed by surgery. Five had signs of severe aortic regurgitation of recent onset (premature mitral valve closure) and all had confirmation by surgery. Echocardiographic abnormalities persisted after successful medical treatment. We conclude that echocardiography is helpful in patients with bacterial endocarditis. It permits recognition of unsuspected preexistent lesions and the characteristic vegetations, as well as the extent and nature of valvular damage secondary to bacterial endocarditis. However, echocardiography does not differentiate between active and healed lesions.

Adult↗
PubMed1984

Amiodarone treatment of critical arrhythmias in children and young adults.

The majority of sudden cardiac deaths in children occur in patients with prior arrhythmias and an abnormal heart. Amiodarone was given to 39 young patients (35 with an abnormal heart) with arrhythmias unresponsive to conventional treatment. Their age ranged from 6 weeks to 30 years with nine patients younger than 2 years of age. Atrial flutter was present in 16 patients, ventricular tachycardia in 14 patients and supraventricular tachycardia in 9 patients. The most common diagnosis (14 patients) was postoperative repair of congenital heart disease. The dose ranged from 2.5 to 21.6 mg/kg per day (mean 8.2). Elimination of arrhythmia (on 24 hour electrocardiography) occurred in 15 of 16 patients with atrial flutter, 11 of 14 with ventricular tachycardia and 5 of 9 with supraventricular tachycardia. Symptomatic side effects were: rash (three patients), headache (two patients), nausea (one patient) and peripheral neuropathy (one patient); seven patients had asymptomatic corneal microdeposits which normalized in all after the drug was discontinued. No side effects occurred in patients younger than 10 years of age. The following changed with treatment (p less than 0.05): heart rate decreased (three patients with atrial flutter and sick sinus syndrome required pacemaker implantation for bradycardia) and QTc increased; thyroxine (T4) and serum reverse triiodothyronine (T3) increased. During follow-up study (range 6 months to 3 years), 21 of the 39 patients continued to take amiodarone with complete control of arrhythmias, 9 were no longer taking the drug and 9 died (7 nonsudden and 2 sudden deaths). Amiodarone is an extremely effective treatment for infants and children with tachyarrhythmias resistant to conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Safety and efficacy of esmolol (ASL-8052: an ultrashort-acting beta-adrenergic blocking agent) for control of ventricular rate in supraventricular tachycardias.

Esmolol (ASL-8052) is a new intravenous beta-adrenergic blocking agent that has exhibited both cardiac selectivity and an extremely short half-life in animal studies. To assess its clinical efficacy, 16 patients were studied with a rapid ventricular rate associated with atrial flutter (n = 2), atrial fibrillation (n = 10), atrial tachycardia (n = 2) and multifocal atrial tachycardia (n = 2). During a 30 minute control period of observation, the ventricular rate ranged from 121 to 150 beats/min (mean 133.2 +/- 10.6). Using a double blind crossover method, esmolol was infused intravenously for a maximum of 60 minutes. Infusions of 50, 100, 150, 200, 250 and 300 micrograms/kg per min were given in consecutive 5 minute periods (during the first minute of each period, a loading dose of 500 micrograms/kg was given). Not all patients received the maximal dose. A response was defined as conversion to sinus rhythm or a 20% reduction in ventricular rate. One patient with atrial fibrillation associated with the Wolff-Parkinson-White syndrome did not respond. In the remaining 15 patients, their highest esmolol infusion rate was maintained for an additional 30 minutes. This resulted in a reduction in ventricular rate to a mean of 97.8 +/- 12.9 beats/min (range 72 to 119) (p less than 0.001). Conversion from flutter/fibrillation to sinus rhythm occurred in two patients. During the infusion, six had transient asymptomatic hypotension that was mild and manageable. After infusion, ventricular rate and blood pressure returned rapidly toward control values within 25 minutes in patients without conversion to sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1999

Surgical treatment of tricuspid regurgitation caused by Löffler's endocarditis.

A 25-year-old man with a history of bone-marrow-transplantation for the treatment of Löffler's endocarditis underwent surgery for massive tricuspid regurgitation with paroxysmal atrial flutter. Dense fibrosis in the right ventricular endocardium with complete obliteration of the apex was seen intraoperatively, and the right ventricular cavity was diminished. Annular dilatation of the tricuspid valve and entrapment of the posterior leaflet to the endocardial fibrosis were also seen. Annuloplication at the posterior leaflet was performed. In addition, the right atrial free wall was widely resected and the septal and inferior vena cava-tricuspid valve isthmi were cryoablated for the treatment of atrial flutter. Postoperative catheterization revealed rather high right ventricular end-diastolic pressure. However, tricuspid regurgitation disappeared with the increased cardiac output. Atrial flutter could not be induced by repetitive stimulation in the postoperative electrophysiological examination.

Adult↗
PubMed1996

Ionic mechanisms for prolongation of refractoriness and their proarrhythmic and antiarrhythmic correlates.

Drugs that prolong cardiac refractoriness exert antiarrhythmic effects, probably by reducing dispersion of refractoriness and thereby reducing the likelihood of reentrant excitation. This electrophysiologic effect can be achieved in fast-response tissues by sodium channel block or by action potential prolongation; drugs with either attribute can exert antiarrhythmic effects. However, both types of drugs can also cause proarrhythmic effects. For sodium channel blockers, proarrhythmic actions can be attributed to conduction slowing and include increased frequency of episodes of ventricular tachycardia as well as slowing of atrial flutter with 1:1 atrioventricular conduction and increases in ventricular rate. In addition, sodium channel block has been implicated as the mechanism underlying increased mortality with sodium channel blockers in the Cardiac Arrhythmia Suppression Trial (CAST); some data suggest that intercurrent ischemia increases this risk. For drugs that prolong action potentials, torsades de pointes is the most common proarrhythmic syndrome, occurring most often with underlying bradyarrhythmias and hypokalemia. The mechanism(s) underlying normal refractoriness and its modulation by antiarrhythmic drugs, as well as the mechanism(s) underlying these proarrhythmic syndromes, are discussed.

Action Potentials↗
PubMed1972

Immediate effects of intravenous verapamil in cardiac arrhythmias.

Verapamil was administered by intravenous injection to 181 patients with various cardiac arrhythmias. The automaticity of the cardiac pacemaker was slowed in sinus, idionodal, and idioventricular tachycardia. In atrial fibrillation the drug usually slowed the ventricular response and often made it regular. In some cases atrial flutter was converted to sinus rhythm, the ventricular response being reduced in the remainder. Conversion of paroxysmal supraventricular tachycardia to sinus rhythm was consistently achieved. A favourable response occurred in four patients in whom arrhythmias were associated with pre-excitation syndromes. There were no adverse clinical side effects.

Aged↗
PubMed1991

Electrical instability in patients undergoing surgery for atrioventricular septal defect.

Postoperative 24-hour Holter monitoring was performed in 106 patients with atrioventricular septal defect in order to identify the incidence of atrial and ventricular arrhythmias. Of the patients, 72 had separate atrioventricular orifices, including 13 with a small ventricular component to the defect, and 34 patients had a common atrioventricular orifice. Two groups of abnormal patients were found. First, patients with good electrical stability characterized by isolated atrial (9 patients) and ventricular (25 patients) extrasystoles falling in classes I and II of Lown. Second, patients with marked electrical instability characterized in one patient by repetitive atrial extrasystoles, in another by atrial flutter, in 2 by polymorphic ventricular extrasystole and in 8 by couplets or triplets. Electrical instability in individual patients was then compared, by means of logistic regression analysis, with operative, surgical and postoperative variables. There was no incidence of sudden death in our series. After surgical repair, ventricular arrhythmias were more frequent than atrial arrhythmias (33% vs. 10%) and were unrelated to the type of atrioventricular septal defect. Cardiac electrical instability after operation was significantly related to larger operative body size, higher postoperative end diastolic diameter of the right ventricle, larger size of the ventricular septal defect, coexistence of postoperative right bundle branch block and left anterior hemiblock. Conversely, the risk of arrhythmias was reduced by more recent operative data and by greater shortening fraction of the left ventricle.

Arrhythmias, Cardiac↗
PubMed1986

Conduction abnormalities detected by electrophysiologic testing following repair of ostium primum atrioventricular septal defect.

Since 1983 we have performed electrophysiologic studies in 6 patients who had previously undergone repair of an ostium primum atrioventricular septal defect. Information obtained during electrophysiologic studies was crucial in guiding appropriate pacemaker therapy in these patients. As judged from the resting electrocardiogram, sinus or junctional bradycardia was present in 3/6, atrial flutter / fibrillation in 2/6, and paced rhythm in 2 patients who had had ventricular pacemakers implanted for complete atrioventricular block. During maximal exercise testing 4 patients had reduced heart rates; 2 had sudden drops in heart rate at 1 min postexercise; 1 patient had exercise induced ventricular bigeminy; and 1 patient with atrial flutter and 2: 1-4: 1 block at rest developed 1: 1 conduction during Stage II with an effective ventricular rate of 220/min. During electrophysiologic studies, the maximum corrected sinus node recovery time was abnormal in five of the six, ranging from 410 to 5630 msec. There was no spontaneous atrial rhythm in the other patient. Complete atrioventricular block was present in 2 patients while the atrioventricular Wenckebach phenomenon occurred abnormally at atrial pacing cycle lengths greater than 450 msec in 2 others. Supraventricular tachycardia or atrial flutter/fibrillation, was either spontaneous or induced in 2/6 patients, while ventricular tachycardia was induced in 1/3 patients who underwent programmed ventricular stimulation. Electrophysiologic studies were important in unmasking severe sinus node disease in 3 patients and atrioventricular node disease in 2. We therefore recommend that electrophysiologic studies be strongly considered as part of the evaluation of conduction abnormalities following repair of ostium primum atrioventricular septal defect.

Adolescent↗
PubMed1975

The acute phase of myocardial infarction.

During the acute phase of myocardial infarction, two groups of patients are observed. Patients in the first group have no significant complications, and approximately 95 per cent of these patients recover fully without any specific therapy. Patients in the second group may have various complications, some of which are benign, whereas others may lead to a fatal outcome. The complications may be divided into four major types: 1. Cardiac arrhythmias and conduction defects. The tachyarrhythmias and bradyarrhythmias are the most frequently encountered complications in patients with acute myocardial infarction. Tachyarrhythmias include ventricular premature beats, ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial flutter, and atrial fibrillation. Bradyarrhythmias include sinus and junctional bradycardia and various degrees of heart block. Those patients who are unable to reach a hospital and die suddenly presumably succumb to ventricular fibrillation. 2. Left ventricular failure and cardiogenic shock. In more than 33 per cent of patients with acute myocardial infarction, a third heart sound and pulmonary rales may be heard. If they are present for only 24 hours, the physical findings may indicate an alteration of left ventricular failure. However, if they persist for a few days and disappear after medical therapy, mild left ventricular failure may be present. About 12 per cent of patients have acute pulmonary edema, and 10 per cent of patients develop cardiogenic shock. These two complications carry a high mortality rate (40 per cent and nearly 100 per cent respectively). 3. Rupture of the heart. Cardiac rupture may occur in the free wall, ventricular septum, and papillary muscles. These complications, although less frequently encountered, cause a number of deaths in patients with acute myocardial infarction. 4. Thromboembolism. Under this category are included pulmonary embolism, systemic arterial embolism, and systemic venous thrombosis.

Acute Disease↗