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

Ninety symptomatic patients aged between 16 and 90 years were investigated by ambulatory continuous 24 hour electrocardiography. 75 of these patients underwent endocavitary exploration of atrioventricular conduction and sinus node function within 48 hour of ambulatory electrocardiography. Symptoms occurred during the recording in 30% patients, enabling the mechanism of the malaise to be determined. Every time that abnormalities in the zone surrounding the Tawara node were demonstrated by endocavitary recordings, the 24 hour electrocardiogramme showed the symptoms to be due to other causes than complete heart block. In 70% patients no symptoms were experienced but 58% of them had cardiac arrhythmias and particularly sinus node dysfunction (24 out of 37 patients) on the 24 hour electrocardiogramme. Comparing the results of these two methods of investigation, continuous electrocardiography appears to be a better technique for the diagnosis of sinus node dysfunction but endocavitary study of sinus node function would seem more suited to determine its severity. Endocavitary recordings seem more reliable in the investigation of paroxysmal atrioventricular blocks. These results demonstrate the complementary nature of these two methods in determining the causes of syncope and dizziness.
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PMID:[Comparison of 24 hours ambulatory electrocardiography and endocavitary recording in the diagnosis of heart rate disorders]. 10 88

Of the 353 patients followed in the pacemaker surveillance clinic between July 1976 and July 1977, 25 patients complained of episodes of dizziness and faintness. 20 of these had normal pacing function and pacemaker parameters at routine clinic testing. 18 patients had 'demand' units and 2 had fixed-rate pacemakers. The indication for permanent pacing was complete heart block in 16 patients and sinoatrial disease in 5 patients. At clinic follow-up, there was unequivocal evidence of vertebrobasilar insufficiency in 5 patients and postural hypotension in 4 patients. In 11 patients, the cause of presyncope was not evident at the clinic. All patients were monitored by 24-hour tape recording until an episode of pre-syncope occurred. In 8 patients, there was evidence of intermittent failure to pace associated with the episodes of presyncope. In 2 patients, an additional cause for presyncope was found at clinic examination. Ambulatory 24-hour tape monitoring of the electrocardiogram is an important adjunct to pacemaker follow-up especially when other methods such as transtelephone monitoring are not available in the United Kingdom. Routine electronic testing of pacemaker function does not always reveal intermittent abnormalities related to changes in threshold or unstable electrode positions.
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PMID:Ambulatory monitoring of the electrocardiogram: an important aspect of pacemaker surveillance. 61 42

This study analyzes the response to overdrive suppression of junctional pacemakers (JP) and correlates it with symptoms in 21 patients. Junctional rhythm (JR) was seen in 5 patients with intact A-V conduction, and in 16 with complete heart block, the JPs were located proximal to or within the His bundle (BH). Junctional recovery time (JRT) was measured following atrial or ventricular pacing during control and after atropine (2-2.5 mg). Control cycle length of the JR ranged from 835-2100 msec (mean 1402) and the corrected JRT (CJRT) ranged from 75 to greater than or equal to 7510 msec (mean 2966). Following atropine, the cycle length ranged from 660 to 2000 msec (mean 1115) and the CJRT ranged from 90 to greater than 6000 msec (mean 2050). All symptomatic patients were treated with permanent ventricular demand pacemakers and followed clinically from 6-72 months (mean = 35). Symptomatic patients could not be differentiated from asymptomatic patients on the basis of control heart rates, chronotropic response to atropine, and/or the site of origin of the JP as determined with BH recordings. However, presence or absence of symptoms of syncope and dizziness were well correlated with a CJRT greater than or less than 200 msec, respectively, either following atropine or during control. The determination of CJRT both before and after parasympathetic blockade provides a simpler and more reliable method for the therapeutic evaluation of patients.
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PMID:Junctional pacemakers in man. Response to overdrive suppression with and without parasympathetic blockade. 63 10

Fifty-one patients required the implantation of a Cordis Omnis-Stanicor permanent pacemaker. His bundle electrograms studies, which included right atrial pacing and sinoatrial (SA) node postsuppression recovery times, were performed prior to the implantations. Pacing and sensing thresholds were obtained in all patients. Syncope or episodes of dizziness were the presenting symptoms in virtually every patient. Twenty-eight of the 51 patients had the sick sinus syndrome. Only nine patients were in complete heart block, and an additional nine were in second-degree heart block. The His bundle electrogram technique was not particularly helpful in selecting the potential pacemaker candidate. The symptomatic patient with second- or third-degree heart block requires a pacemaker. In the sick sinus syndrome, the His bundle electrogram was a disappointing tool in detecting abnormalities. In chronic bundle branch block, the His bundle electrogram appears to play a major role. A prolonged H-V interval in a symptomatic patient, in whom a specific noncardiac cause cannot be identified, signifies that a pacemaker is required.
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PMID:His bundle electrograms in 51 patients requiring permanent transvenous pacemakers. 87 39

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.
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PMID:The clinical spectrum of chronic His bundle block. 100 Oct 51

The hemodynamic effects of a 10 mg bolus of edrophonium chloride followed by a continuous infusion of 0.25 to 1.0 mg per minute, were determined in unanesthetized patients with significant myocardial disease. The effect on heart rate of the drug was negated by studying a group of nine patients with complete heart block and permanently implanted ventricular pacemakers. After the 10 mg bolus, two of the nine patients experienced dizziness, nausea and abdominal cramps associated with a mild decrease in peripheral vascular resistance. There was no significant change in cardiac index, mean blood pressure, brachial artery upstroke time, corrected ejection time, or left ventricular systolic ejection time. This study demonstrated that the continuous infusion of 0.25 to 1.0 mg per minute of edrophonium chloride following a 10 mg loading dose, had no significant effect on myocardial function.
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PMID:Hemodynamic effects of edrophonium chloride (Tensilon) infusion. 111 89

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.
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PMID:Heart block complicating acute inferior wall myocardial infarction. 126 67

A 27-year old African woman with history of regular chloroquine ingestion presented with progressive deterioration of vision, easy fatiguability, dyspnoea, dizziness progressing to syncopal attacks. Ophthalmological assessment revealed features of chloroquine retinopathy, cardiac assessment revealed features of heart failure and a complete heart block with right bundle branch block pattern. The heart block was treated by pacemaker insertion and the heart failure resolved spontaneously following chloroquine discontinuation. She however remains blind.
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PMID:Chloroquine related complete heart block with blindness: case report. 162 52

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

Calcium channel blocking drugs are a chemically heterogenous group, so it might be expected that their effects on vascular smooth muscle, cardiac contractility, and conduction tissue may differ. However, the majority of adverse reactions are predictable from their pharmacological actions and may be conveniently grouped in the following categories: 1) vasodilatation, 2) negative inotropic effects, 3) conduction disturbances, 4) gastrointestinal effects, 5) metabolic effects, and 6) drug interactions. Vasodilatory symptoms, namely, dizziness, headaches, flushing sensation, and palpitation, are more likely with nifedipine. Peripheral edema is also common with nifedipine, but the mechanism is uncertain. For a given degree of vasodilation, the greatest negative inotropic effect is seen with verapamil first, diltiazem second, and nifedipine last. Calcium channel blocking drugs are contraindicated in hypertensive patients with second and third degree heart block, sick sinus syndrome, and severe heart failure. Verapamil and diltiazem have a significant effect on cardiac conduction, whereas nifedipine, in therapeutic doses, does not. Local gastrointestinal symptoms, such as nausea and constipation, are common with verapamil. None of the calcium channel blocking drugs have been reported to adversely affect lipid or protein metabolism. However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin. The significance of this finding needs to be explored further in hypertensive diabetics. Serum digoxin levels have been shown to increase after administration of verapamil and nifedipine, but there is no evidence that this change has any clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Side effects of calcium channel blockers. 328 Apr 92


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