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 55 records · Page 3Linked to original sources
PubMed1981

[Prinzmetal's variant form of angina pectoris occurring with ventricular tachycardia, ventricular flutter and fibrillation].

After a brief literature survey, the author described a patient of 42, with its first stenocardia paroxysm, accompanied by tachycardia, clonic-tonic convulsion as MAS syndrome, loss of consciousness and spontaneous restoration. After 6 hours a second stenocardia paroxysm followed, when a gigantic ST segment elevation was recorded in precordial leads, appearance of paroxysmal ventricular tachycardia, ventricular fibrillation, loss of consciousness, restored via defibrillation. ST elevation faded by the 25 the minute. The changes are stressed to be most likely due to coronary spasm of r. descendens of the left coronary artery and to changes in the small myocardial vessels. The opinion that Prinzmetal stenocardia is a variant of angina pectoris is confirmed as well as that paroxysm could be with a lethal end due to ventricular fibrillation.

Adult↗
PubMed2003

[Cardiac arrhythmias during pregnancy--what to do?].

METHODS: Atrial premature beats are frequently diagnosed during pregnancy, supraventricular tachycardia (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable supraventricular tachycardia, initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the drug of first choice and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta(1) selectivity are first-line drugs; class Ic agents or the class III drug sotalol represent effective and therapeutic alternatives. Ventricular premature beats are also frequently present during pregnancy and benign in most of the unstable patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, ventricular fibrillation) are less frequently observed. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta(1) selectivity are regarded as drugs of first choice. If this therapy proves ineffective, class Ic agents or sotalol can be considered. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. CONCLUSIONS: The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.

Anti-Arrhythmia Agents↗
PubMed2005

Hospital discharge diagnoses of ventricular arrhythmias and cardiac arrest were useful for epidemiologic research.

OBJECTIVE: We investigated the validity of hospital discharge diagnosis regarding ventricular arrhythmias and cardiac arrest. METHODS: We identified patients whose record in the PHARMO record linkage system database showed a code for ventricular or unspecified cardiac arrhythmias according to codes of the International Classification of Diseases, 9th revision, clinical modification (ICD-9-CM). The validity of ICD codes for ventricular arrhythmias and cardiac arrest (427.1, 427.4, 427.41, 427.42, 427.5, 427.69) and ICD codes for unspecified cardiac arrhythmias (427.2, 427.60, 427.8, 427.89, 427.9) was ascertained through manual review of hospital clinical records. The positive predictive value (PPV) was calculated, and differences between characteristics of true and false positives were evaluated. RESULTS: The PPV of ICD codes for ventricular arrhythmias and cardiac arrest was 82% (95% confidence interval CI = 72-92). True positive results were associated with male gender (P = .09) and younger age (P = .05). Of the unspecified cardiac arrhythmias 10% (95% CI = 2-18) were identified as ventricular arrhythmias or cardiac arrest. CONCLUSION: Hospitalizations for ventricular cardiac arrhythmias and cardiac arrest (coded according to ICD-9-CM as paroxysmal ventricular tachycardia, ventricular fibrillation, ventricular flutter, ventricular premature beats, or cardiac arrest) have a high PPV and are useful for selecting events in epidemiological studies on drug-induced arrhythmias.

Data Collection↗
PubMed1995

Antiarrhythmic effect of the selective I1-imidazoline receptor modulator moxonidine on ouabain-induced cardiac arrhythmia in guinea pigs.

Moxonidine is a centrally acting antihypertensive agent with potent action on I1-imidazoline receptors. Moxonidine as an SIR modulator elicits a persistent reduction in circulating levels of epinephrine, demonstrating a reduction in sympathetic tone. In the first experiment the threshold dose of ouabain needed to induce ventricular arrhythmia and asystole was determined in guinea pigs, and the influence of moxonidine was tested. In a dose range of 0.1-0.4 mg/kg body weight i.v., moxonidine increased the threshold dose needed to induce ventricular tachycardia, premature ventricular beats, ventricular flutter, ventricular fibrillation, and asystole. The effect was dose-dependent and statistically significant. Clonidine, in a dose range of 0.2-0.8 mg/kg body weight i.v., also increased the threshold dose of ouabain necessary to induce different cardiac rhythm disturbances. Moxonidine was more effective than clonidine. Pretreatment with the alpha 2-receptor and I1-receptor-influencing substances efaroxan, idazoxan, and SKF 86466 attenuated the effect of moxonidine and clonidine. Efaroxan, idazoxan, or SKF 86466 alone reduced the threshold dose of ouabain necessary to induce cardiac arrhythmia as a sign for arrhythmogenic effects. The alpha 1-receptor antagonist prazosin had no influence on ouabain-induced arrhythmia. Pretreatment with prazosin reduced the moxonidine but not the clonidine effect. In the second experiment the influence of moxonidine on aconitine-induced extrasystoles (ES) in the spontaneously beating guinea pig auricle was investigated. Moxonidine in a dose of 10(-7)-10(-8) M reduced the number of ES. A 10-fold higher dose had no influence on ES number. The beta-blocking agent propranolol showed antiarrhythmic effects in both methods. The ouabain-induced cardiac arrhythmia is associated with increased sympathetic tone on central stimulation. The reduced sympathetic tone by centrally acting moxonidine via imidazoline receptors seems responsible for the antiarrhythmic effect of this drug. Clonidine also reduced the sympathetic tone via imidazoline receptor. The selectivity of clonidine to imidazoline receptors is less pronounced than is that of moxonidine. The interaction of moxonidine with imidazoline receptors is not clear. The possible interaction between imidazoline and alpha-adrenoceptors in relation to the antiarrhythmic effect of moxonidine or clonidine is also unknown. Modulation of imidazoline receptors by moxonidine could be an agonistic effect or an antagonism to an endogenous agonistic or antagonistic substance and vice versa.

Aconitine↗
PubMed1977

Electrocardiographic observation on goats with urea-ammonia poisoning and a consideration on the main cause of death.

Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.

Ammonia↗