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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most important symptoms in bradycardia are vertigo, dizziness and syncopy due to diminished cerebral blood sypply. Cardial symptoms are cardiac insufficiency and angina pectoris. By means of ECG, especially Holter-ECG, carotid sinus massage, atropin test and invasive methods (atrial stimulation, His-bundle ECG) sinu-nodal dysfunction, carotid sinus syndrome, bradyarrhythmia absoluta and AV-block can be diagnosed. Pharmacological treatment is only useful in acute situations. For symptomatic bradyarrhythmias the implantation of a Pacemaker is the therapy of choice. Individual treatment of the various types of bradyarrhythmia and the patients special needs is possible through the evolution of pacemaker technology.
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PMID:[Differential diagnosis and therapy of bradycardic arrhythmias]. 782 27

Syncope occurs in up to 20% of patients with supraventricular tachycardias and is suggestive of rapid and dangerous arrhythmias. Incidence, pathomechanism and consequences of syncope in supraventricular tachycardia are reviewed in this presentation. Frequent symptoms in supraventricular tachycardias are palpitations, dizziness or dyspnea. Syncope is more uncommon, however, if a sensation of rapid heart beat precedes a syncope, a causal relationship between arrhythmia and syncope has to be considered. When the surface ECG shows no abnormalities, Holter monitoring or exercise testing usually fail to record a suspected tachycardia, therefore, electrophysiologic study should be performed to verify the underlying arrhythmia. In patients with unexplained syncope supraventricular arrhythmias can be established in up to 15% of patients. However, interpretation of electrophysiologic results has to be performed carefully because functional abnormalities like dual AV nodal pathways can be found in up to 10% of asymptomatic patients. The prognostic value of syncope as a marker for rapid tachycardia or sudden cardiac death is still in discussion. Syncope in patients with Wolff-Parkinson-White syndrome may help to identify patients at risk for ventricular fibrillation due to rapid conduction over an atrioventricular accessory pathway during atrial fibrillation. Syncope in young patients (< 25 years) with Wolff-Parkinson-White syndrome was found to be associated with a short anterograde refractory period (< 220 ms) of the pathway. However, most of the studies were performed retrospectively in selected patients referred to the centers because of severe symptoms, therefore the predictive value of syncope in unselected patients with supraventricular tachycardia remains uncertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Syncope in supraventricular tachycardia. Incidence, pathomechanism and consequences]. 833 Aug 52

Transesophageal, electrophysiologic studies were conducted in 47 patients, with clinical and ECGgraphic diagnosis of paroxysmal reciprocating supraventricular tachycardia. After admission to hospital, the patients were enrolled in the study in accordance with the criterion concerning the exclusion of patients with signs and symptoms of severe heart pump failure (ie, NYHA III and IV class were excluded). The transesophageal study was performed during paroxysmal tachycardia in each patient to measure the V-A interval and to localize the site of reentry. Thereby, the patients could be grouped into 2 subsets, ie those with A-V nodal reentrant tachycardia (no. 30 patients) and those with accessory pathway reentrant tachycardia (no. 17 patients). Moreover, the prevalence in both subsets was evaluated in the following signs and symptoms: palpitations, dyspnoea, chest pain, pulsations in the neck, significant increase in urinary output, hypotension, dizziness, near-syncope, syncope, shock, focal brain injury. From the data analysis, significantly greater prevalence of palpitations in the neck resulted in the subset of patients with reentry confined to the A-V node (no. 20 cases) compared with those suffering from reentry via accessory pathway (no. 4 cases). Moreover the arterial pressure, in A-V nodal reentrant tachycardia, showed the lowest values and the best decreases, together with the finding of a more rapid trend to decline in comparison with the accessory pathway subset. On the other hand, no significant differences could be seen about the remaining symptoms. In an attempt to provide the reliable explanation for the differences found between the 2 subsets of study, concerning both the unpleasant pulsations in the neck and the pressure decrease, we postulated a remarkable role for the length of arrhythmic circle movement. The smaller dimensions of circuit limbs, in A-V nodal reentrant tachycardia, are likely to be the principle cause of the different clinical features of 2 types of reentry. We speculate actually that in susceptible patients the critical event is most likely to be A-V functional dissociation due to early and unphysiologic activation of atria by stimulus rapidly reentrant from the bottom portion of the AV node: the simultaneous occurrence, frequent in A-V node reentry, of both, atrial and ventricular mechanical activation, would result, however, in impairment of atrial haemodynamics due to development of cannon A waves, able either to activate a vasodepressor reflex from the atria or to stimulate instantaneous release of atrial natriuretic factor in the circulation. Further studies, however, are necessary to be performed on large cases-records, to confirm our hypothesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differences in the symptomatology of paroxysmal supraventricular tachycardias in relation to the different sites of localization of the arrhythmic reentry circuit. Clinical picture, semiologic and genetic aspects]. 845 Oct 24

In 102 patients with inducible supraventricular tachycardia (SVT), 56 women and 46 men aged 20-86 (mean, 52) years, underwent electrophysiologic study. SVTs observed at electrophysiologic study were atrial flutter or atrial fibrillation (32%), the "slow-fast" form of atrioventricular (AV) nodal reentrant tachycardia (45%), orthodromic AV reentrant tachycardia (25%), and atrial tachycardia (9%). More than 1 SVT occurred in some patients. Spontaneous symptomatic SVT frequency prior to oral flecainide varied from 3/day to 1/3 months (mean, 3/month). At electrophysiologic study and during SVT, intravenous flecainide, 2 mg/kg body weight, was given at an infusion rate of 10 mg/min up to a maximum dose of 150 mg. Patients were commenced on oral flecainide if SVT termination occurred during intravenous flecainide administration and if reinitiation was not possible after the total dose of flecainide had been given. In patients with AV nodal reentrant tachycardia and AV reentrant tachycardia further criteria for commencing oral flecainide were SVT termination by ventricular-atrial conduction block and persistent ventricular-atrial block after intravenous flecainide administration. Initial oral flecainide dosage was determined by assessing ability to reinitiate SVT after 50 mg, 100 mg, and the total dose of intravenous flecainide had been given. Eighty-nine patients (87%) remained free of symptomatic SVT over a mean follow-up period of 3.9 years (range, 3 months to 6.5 years). Two thirds were still taking the original dosage of flecainide and the rest were SVT-free on a higher dosage. Oral dosages ranged from 50 to 300 mg/day (median dosage, 100 mg twice daily) Nine patients experienced minor side effects, including, lethargy, dizziness, headache, and blurred vision. There were no deaths and no reports of major proarrhythmic events or other major adverse effects.
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PMID:Efficacy and safety of long-term oral flecainide acetate in patients with responsive supraventricular tachycardia. 860 96

Paroxysmal supraventricular tachycardia (PSVT) is a distinct clinical syndrome. Most patients present with the abrupt onset of palpitations, dizziness, dyspnea, or chest pain. The electrocardiogram (ECG) demonstrates a fast heart rate (150-250 beats per min), a regular rhythm, and most often, a narrow QRS complex. The P wave is usually hidden within the QRS complex. PSVT is caused by reentry, and the tachycardias are classified, electrophysiologically, according to the anatomic location of the reentry circuit. Atrioventricular nodal reentry is the most common form of PSVT. In A-V nodal reentry, there are two conducting pathways (alpha and beta) that have different conduction times and refractory periods; both pathways are confined to the A-V nodal and perinodal atrial tissue. The other common form of PSVT, termed atrioventricular reciprocating tachycardia, depends on an anatomically distinct, or "accessory," pathway that may conduct impulses between the atria and the ventricles, while bypassing the AV node. The two forms of PSVT may be distinguished in many cases by examining the 12-lead electrocardiogram. In the majority of cases of A-V nodal reentry, the atria and ventricles are depolarized simultaneously, and the P waves are hidden in the QRS complex. If the reentry circuit includes an accessory pathway, the P wave always follows the QRS, and usually the R-P interval exceeds 70 msec. Several principles should guide the management of PSVT: (a) Unstable patients require emergent electrical cardioversion; (b) A 12-lead ECG should be obtained immediately to confirm that the tachycardia has a narrow complex (ventricular tachycardia may masquerade as PSVT if only a single lead is examined); (c) Vagal maneuvers may be attempted (the Valsalva maneuver is safer and more efficacious, especially in the elderly); and (4) In most patients, adenosine is the first-line agent to treat PSVT. Contraindications to adenosine and drug interactions are noted in this article. In addition, the use of adenosine in wide complex tachycardias and the indications for admission and referral for electrophysiologic evaluation are discussed.
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PMID:Paroxysmal supraventricular tachycardias. 865 36

This study examined the incidence and significance of catheter-induced atrioventricular nodal block (AVNB) during a radiofrequency ablation procedure that uses stiff large-tip steerable ablation catheters. AVNB was noted in 10 (1.6%) of 613 consecutive patients undergoing radiofrequency ablation therapy for atrioventricular nodal (AVN) reentrant tachycardia (592 patients) or atrioventricular reentry tachycardia incorporating a midseptal accessory pathway (21 patients). Of these 10 patients, 9 underwent AVN modification for AVN reentrant tachycardia and 1 for ablation of a midseptal accessory pathway. One patient had two episodes of AVNB during two sessions undertaken because of recurrence of tachycardia. No patient had a preexisting conduction defect before the study. In all 10 patients, AVNB was transient, and it lasted for a mean of 9.1 +/- 19 minutes. It occurred during positioning of the ablation catheter in the junctional area before (8 patients) or after (2 patients) the start of radiofrequency current applications. Complete AVNB was noted on six occasions, second-degree AVNB on four occasions, and first-degree AVNB on one occasion. All blocks were associated with narrow QRS ventricular beats and with a site of block proximal to the His bundle. The mean ventricular heart rate during AVNB was 60 +/- 23 beats/min. Two patients had transient asystole, with one having loss of consciousness. No patient required special treatment for heart block. One-to-one conduction resumed after repositioning of the catheters, and the subsequent ablation procedure was successfully completed in 8 of the 10 patients. During a follow-up of 20 +/- 12 months, none of the patients had severe dizziness or syncope, and none required implantation of a permanent pacemaker. In conclusion, transient AVNB due to mechanical injury occurs during positioning of a stiff large-tip steerable ablation catheter in the junctional area. Delivery of radiofrequency current to the site that provokes catheter-induced AVNB should be avoided.
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PMID:Catheter-induced atrioventricular nodal block during radiofrequency ablation. 889 71

The purposes of this study were to describe: clinical symptoms in a sample of consecutive patients with supraventricular tachycardia (SVT); incidence of sudden death, syncope, and other disabling symptoms; whether these symptoms differ by tachycardia mechanism; and to identify predictor variables of syncope in patients with SVT. Data were collected from chart reviews of 167 consecutive patients with SVT admitted for radiofrequency ablation. Three patients (2%) had nonlethal cardiac arrest, and a total of 16% (26 of 183) received at least 1 external direct-current shock for arrhythmia management. Twenty percent of subjects (33 of 167) reported at least 1 episode of syncope which was preceded by palpitations. The most frequent symptoms were: palpitations (96%), dizziness (75%), and shortness of breath (47%). We found atrioventricular nodal reentrant tachycardia (AVNRT) in 64 patients, atrioventricular-reciprocating tachycardia (AVRT) in 59, atrial tachycardia in 22, and atrial flutter in 22. The symptom profiles of patients with AVNRT, AVRT, and atrial tachycardia were very similar, but differed significantly (p <0.05) from those reported in the atrial flutter group. Multivariate analysis showed that heart rate > or = 170 beats/min was the only independent risk factor for syncope. Chi-square analysis demonstrated that SVT patients with heart rate > or = 170 beats/min had significantly more dizziness and syncope. Thus, despite a low incidence of associated heart disease, and good left ventricular function, there was a high frequency of disabling, potentially life-threatening symptoms associated with episodes of SVT in this sample. SVT can have potentially lethal consequences, and is more disruptive than previously thought.
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PMID:Frequency of disabling symptoms in supraventricular tachycardia. 919 13

Symptomatic Improvement was evaluated in 64 patients with drug-refractory atrial fibrillation or atrial flutter who underwent atrioventricular (AV) nodal ablation and permanent pacemaker implantation. The arrhythmias were chronic in 40 patients and paroxysmal in 24 patients. All were refractory to multiple drugs (3.7 +/- 1.5) and had severe symptoms: palpitations (58 patients), dyspnea (n=58), dizziness (n=38), asthenia (n=37), and chest pain (n=20). All underwent AV nodal ablation and single- (n=39) or dual-chamber (n=25) pacemaker implantation. During follow-up of 20.4 +/- 17.8 months, palpitations improved in 100% of 58 patients who had palpitations before the ablation, dyspnea improved in 75% of 58 patients, chest pain in 95% of 20 patients, asthenia in 75% of 37 patients, and dizziness in 93% of 38 patients. Moderate to significant improvement in these symptoms was reported in 83% of patients and mild improvement in 5%. Before ablation, 77% of patients were in New York Heart Association functional class III or IV. After ablation, 19% of patients were in the same functional classes (P < 0.05). Thus, AV nodal ablation and pacemaker implantation in patients with drug-refractory atrial fibrillation or flutter was associated with significant improvement in presenting symptoms and functional capacity. A randomized, controlled study is needed to compare this form of therapy with other therapeutic modalities.
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PMID:Symptomatic improvement after AV nodal ablation and pacemaker implantation for refractory atrial fibrillation and atrial flutter. 937 44

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

We report a family in which the mother and her three sons suffered sick sinus syndrome and strabismus. Two members had a persistent left superior vena cava with drainage into coronary sinus. The illness in all members of this family was oligosymptomatic, and well tolerated with mild symptoms like dizziness, fatigue and exercise dyspnea associated with nodal rhythm. Three of them, had episodes of paroxysmal atrial fibrillation. All patients remain asymptomatic after pacemaker implantation.
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PMID:[Familial sick sinus syndrome associated to strabismus and persistent left superior vena cava]. 1097 40


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