Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten years ago a clinical method of recording the electrical activity of the His bundle in man with transvenously inserted electrodes was described. His bundle recording has permitted the breakdown of the P-R interval into three conduction intervals, i.e., intraatrial (P-A), A-V nodal (A-H), and His-Purkinje system (H-V). His bundle studies have demonstrated our inability to accurately predict from the surface electrocardiogram the exact location of most A-V blocks. First- and second-degree A-V block can occur in the atrium, A-V node or His-Purkinje system, and third-degree A-V block in the A-V node or His-Purkinje system. However, Mobitz type II block almost always occurs below the A-V node. Intraventricular conduction defects, especially of the so-called bifascicular block, have a high incidence of H-V time prolongation, indicating additional disease of the third fascicle or the main His bundle. The prognostic value of a prolonged H-V time in patients with and without chronic conduction defects remains controversial, with some agreement that patients with unexplained syncope or dizziness, normal sinus rhythm and 1:1 conduction, who show prolonged H-V times, should probably be paced permanently. No long-term studies exist regarding the value of the H-V time in predicting death or A-V block in patients with conduction defects secondary to acute myocardial infarction, congenital heart disease or after cardiac surgery. Electrophysiological studies have been extremely useful in the diagnosis and management of patients with accessory pathways and in the evaluation of ventricular and supraventricular arrhythmias. The most valuable test in diagnosing sinus node dysfunction is the sinus node recovery time. A clearly abnormal test in a patient with unexplained syncope or dizziness predicts an almost one hundred per cent relief of symptoms with permanent pacing.
 ...
PMID:Diagnostic and prognostic value of intracardiac electrophysiological studies. Ten years of experience. 38 29

In two patients with WPW syndrome Type A suffering from syncopes and dizziness intermittent high degree A-V block was observed. The analysis of the surface Ecg revealed in the first case a complete A-V block within the normal conduction system at the level of the A-V node. In the second case there was a constant left bundle branch block with intermittent block in the right fascicle (intermittent trifascicular block). In both cases the preexcitation syndromes could be best explained by accessory tracts bypassing the normal nodal system left side. One-to-one conduction through the bypass occurred only at a distinct range of cycle lengths, at lower frequencies the accessory tracts were refractory and a IInd or IIIrd degree A-V block occurred. However, outside this frequency zone some P waves were conducted through the accessory tracts without changes in cycle lengths. The findings support the thesis of at least two functionally different atrioventricular pathways in patients with preexcitation syndrome.
 ...
PMID:[Severe atrioventricular block in 2 cases with pre-excitation syndrome]. 96 Sep 77

Heart block was noted in 60 (35 complete and 25 second-degree) of 410 patients with acute inferior wall myocardial infarction. This group with heart block was compared to a control group of 30 patients with acute inferior wall infarction without heart block. The incidences of prior myocardial infarction and hypertension, in addition to the highest level of serum creatine phosphokinase and a maximum degree of ST-segment elevation in the inferior leads, were all greater in patients with heart block, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart block, while sinus nodal distrubances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart block was 28 percent compared to 13 percent for the control. It is concluded that patients with heart block complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker should be considered when specific indications are present and not routinely.
 ...
PMID:Heart block complicating acute inferior wall myocardial infarction. 126 67

A 69-year-old woman was referred for asthenia and dizziness when walking in the last two months. No clinical abnormalities were found, and sinus rhythm was present when lying down. On orthostatism and walking, advanced AV block developed. Atropine and isoproterenol ameliorated the AV conduction abnormality, suggesting a nodal block. The patient remained asymptomatic after pacemaker implantation.
 ...
PMID:Orthostatic and exercise-induced advanced nodal atrioventricular block. 151 40

Mexiletine is a Class IB antiarrhythmic which has basic and clinical electrophysiologic properties similar to lidocaine. Like other Class I antiarrhythmic agents, mexiletine blocks the rapid inward sodium current responsible for phase 0 of the action potential. It has been noted in the clinical electrophysiology laboratory to have minimal effect on sinus node function and AV nodal and His-Purkinje system conduction. Pharmacokinetic studies have shown that oral absorption is rapid with bioavailability of 80-90%. Mexiletine is predominantly metabolized by the liver with elimination half-life of 9 to 12 hours. The antiarrhythmic effects of the primary drug's metabolites remain to be defined. Hemodynamic studies have shown mexiletine to have a lesser negative inotropic effect than procainamide or disopyramide. Although mexiletine as a single agent successfully suppresses 60 to 80% of spontaneous ventricular arrhythmias, it has lower efficacy in suppression of induced ventricular arrhythmias. Multiple studies have shown that as monotherapy mexiletine is effective in preventing the induction of ventricular tachycardia in approximately 20% of patients. When used in combination with a Class IA antiarrhythmic drug for suppression of induced ventricular arrhythmias, multiple investigators have reported greater efficacy. Neurological side effects (tremor, dizziness, memory loss) occur in approximately 10% of patients while gastrointestinal side effects (nausea, anorexia, gastric irritation) occur in up to 40% of patients. Proarrhythmia or other serious toxicity from the drug is uncommon.
 ...
PMID:Mexiletine: pharmacology and therapeutic use. 218 14

Antidromic circus movement tachycardia was documented in 36 of 345 consecutive patients with Wolff-Parkinson-White syndrome undergoing detailed electrophysiologic evaluation. Twenty-six patients were men and 10 were women (mean age +/- standard deviation 26 +/- 12 years [range 12 to 45]). Multiple accessory pathways were identified in 12 of these 36 patients (33%). Ten of the patients (67%) with clinically documented antidromic tachycardia had multiple accessory pathways. Dizziness and syncope occurred in 61 and 50% of patients with antidromic circus movement tachycardia. Six patients had clinical documentation of atrial fibrillation, and 4 patients (11%) were resuscitated from ventricular fibrillation. In the 36 patients, 56 distinct antidromic tachycardias were recorded and several different pathways were observed. Orthodromic tachycardia was the most frequently associated arrhythmia (72%). Dual atrioventricular nodal pathways were present in 12 patients (33%); however, atrioventricular nodal tachycardia could be initiated in only 2 of them. Interruption of the accessory pathway was successfully performed in all 20 patients undergoing surgery.
 ...
PMID:Clinical and electrophysiologic characteristics of patients with antidromic circus movement tachycardia in the Wolff-Parkinson-White syndrome. 222 Jun 35

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of the Class I antiarrhythmic agent moricizine hydrochloride are reviewed. Moricizine is chemically similar to the phenothiazines but does not appear to block dopaminergic receptors. Its major electrophysiologic actions are a concentration-dependent decrease in maximum rate of phase 0 depolarization; increased rates of phase 2 and 3 repolarization, decreased action potential duration, and decreased effective refractory period. Moricizine causes a dose-related prolongation of the PR interval and of AV nodal, infranodal, and intraventricular conduction times but has little effect on ventricular repolarization. The antiarrhythmic and electrophysiologic effects are not correlated with plasma concentrations of the drug or its metabolites. Moricizine reduces the occurrence of ventricular premature contractions (VPCs), couplets, and nonsustained ventricular tachycardia. It appears to suppress symptomatic nonsustained ventricular tachycardia, sustained ventricular tachycardia, and ventricular fibrillation or flutter. Moricizine appears to be as effective as quinidine and more effective than disopyramide, propranolol, and imipramine but less effective than flecainide and encainide at reducing VPCs. Moricizine continues to be evaluated in the Cardiac Arrhythmia Suppression Trial, which was designed to assess the long-term benefit of arrhythmia suppression in patients with left ventricular dysfunction after myocardial infarction. Moricizine seems to be better tolerated than quinidine, disopyramide, and imipramine and to have less proarrhythmic potential than flecainide or encainide. Noncardiac adverse effects include dizziness, nausea, and headache. Cimetidine appears to decrease moricizine clearance, and decreased theophylline clearance has been reported in subjects given moricizine. The usual adult dosage of moricizine hydrochloride is 600-900 mg/day given in three divided doses; an every-12-hour regimen may be used in some patients. Because of the risk of proarrhythmic effects, indications are limited to treatment of documented life-threatening arrhythmias. Moricizine will compete with other agents as first-line therapy for life-threatening arrhythmias.
 ...
PMID:Moricizine: a new class I antiarrhythmic. 227 51

Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
 ...
PMID:Encainide. 251 80

Disabling presyncopal attacks were provoked in a patient with a sinus nodal disorder and cardiac pacemaker by treatment with antianginal vasodilators. At cardiac catheterization a severe fall in aortic pressure was documented during ventricular pacing, when desynchronized atrial contractions coincided with ventricular systoles. After withdrawal of the medication, no obvious changes in arterial pressure were associated with ventricular pacing, and the patient became free of dizziness. Vasodilating drugs may provoke episodic hypotension with characteristic features of the pacemaker syndrome.
 ...
PMID:Vasodilator therapy-induced pacemaker syndrome. 310 20

Atrial flutter is a supraventricular tachydysrhythmia believed to arise from electrophysiologic disturbances in the atria. It tends to be an unstable rhythm and is usually associated with intrinsic cardiac or pulmonary disease or adverse extrinsic influences on the heart. It is due to either a reentry mechanism or an increased atrial automaticity. Atrial depolarization is regular at a rate of 260 to 340 beats per minute. With a normal atrioventricular (AV) node there is usually a physiologic second-degree block with resultant 2:1 conduction. Higher degrees of AV block can occur in patients with AV nodal disease, increased vagal tone, or when certain drugs are in use. One-to-one conduction may occur in patients with accessory AV nodal pathways. In this situation, serious adverse effects are often seen, including palpitations, dizziness, syncope, angina, and dyspnea. Electrical cardioversion is the safest and most reliable way of terminating atrial flutter and its use should not be delayed in an unstable patient. In the nonemergent situation a variety of medications alone or in combination can be used to convert the rhythm or slow ventricular response.
 ...
PMID:Atrial flutter. 328 16


1 2 3 4 5 Next >>