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C R Kerr

Publications and source records attributed to C R Kerr.

90 records · Page 5Linked to original sources
PubMed1984

Stereospecific salivary excretion of tocainide enantiomers in man.

Saliva and plasma samples collected from four healthy volunteers who had received racemic tocainide by intravenous infusion for 20 minutes were analysed by a stereospecific and sensitive gas chromatographic method. The enantiomeric composition of mixed saliva obtained for a period of 48 hrs have been determined and compared with the corresponding plasma profiles. The concentration of each enantiomer in saliva tended to be greater than those in the corresponding plasma sample, such that the mean saliva to plasma ratio for S(+) tocainide was 2.07 +/- 0.50 (SEM) and for the R(-) isomer 3.683 +/- 0.76 (SEM). Marked intersubject variability was found in the saliva/plasma ratio of both isomers, however, the correlation of saliva/plasma concentrations in each volunteer was good and ranged from r = 0.910 to 0.987 for S(+) tocainide and r = 0.884 to 0.986 for R(-) tocainide. There was a 6-fold difference between saliva and plasma concentration of R(-) isomer in one subject whose saliva pH ranged from 6.9 to 7.1. The difference was only 3.5 fold in another subject whose saliva pH was consistently higher (7.4 to 7.5). Therefore, the saliva/plasma ratio appeared to depend on pH, increasing with decreasing pH. However, the correlation between the saliva/plasma ratio observed and the ratio predicted was poor. Mechanisms other than passive diffusion are likely to be involved in the transfer of tocainide enantiomers from plasma to saliva and are more pronounced with the levo isomer.

Adult↗
PubMed1983

Assessment of anaesthetic action of morphine and fentanyl in rats.

In 150 Sprague-Dawley rats, morphine and fentanyl dose-effect curves were determined for the following three end points--prevention of purposeful movement response to a noxious stimulus (PM), loss of righting reflex (RR), and prevention of heart rate increase to a noxious stimulus (HR). Accordingly, for each agent, three series of experiments were performed with intravenous administration of the following doses: morphine--3-10 mg X kg-1 for PM, 3-10 mg X kg-1 for HR, 35-55 mg X kg-1 for RR; fentanyl - 5-15 micrograms X kg-1 for PM, 18-30 micrograms X kg-1 for RR, 200-400 micrograms X kg-1 for HR. Dose-effect curves were calculated with the use of probit procedure and potency ratios were determined on the bases of ED50 values. It was found that potency ratios of morphine and fentanyl are different for the studied end points. The ratios of RR ED50 to PM ED50 were 7.8 for morphine vs 2.4 for fentanyl (p less than 0.001), the ratios of HR ED50 to PM ED50 were 1 and 33, respectively (p less than 0.001). These results suggest that blockade of movement response to noxious stimulation (which is usually regarded as an index for analgesic action of opioids) and blockade of heart rate increase to noxious stimulation (which is one of the goals of anaesthesia) is not necessarily induced by intravenous narcotic anaesthetics through the same mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1983

Role of specialized conducting fibers in the genesis of "AV nodal" re-entry tachycardia.

Recent reports have suggested that an accessory bypass tract connecting the His bundle to the atrium (His-atrial fiber) may form the retrograde limb of "AV nodal" re-entry tachycardia (AVNRT). We studied 12 patients with AVNRT in whom the presence of an accessory atrioventricular fiber (Kent fiber) was excluded. We investigated the possibility of a His-atrial (H-A) fiber by examining the nature of retrograde conduction and by assessing the necessity of the atrium as a part of the re-entry pathway. Retrograde conduction through the AV node had characteristics similar to retrograde conduction over a Kent bundle; that is, retrograde conduction times were short and did not vary. With echo beats (Ae) evoked during antegrade refractory period determination early premature beats resulted in prolongation of the AH interval with no change in HAe interval. During AVNRT the A'H':H'A' ratios ranged from 2.0-8.0 (mean 4.0 +/- 1.8) and with changes in tachycardia cycle length the H'A' interval remained constant. During retrograde refractory period determination, delay occurred below the AV node without change in the H-A interval. Estimations of retrograde conduction times by all 3 methods were not significantly different (p greater than 0.2). The pattern of retrograde conduction suggests anatomical or functional specialized fibers as the retrograde limb of the tachycardia. The necessity of the atria as a part of the re-entry circuit was assessed by the introduction of atrial premature beats (APBs) in the region of the atrial septum during AVNRT in 10 patients. APBs pre-excited the atria by 40-140 ms without changing the cycle length of the tachycardia, providing strong evidence against the participation of an extranodal His-atrial fiber in AVNRT. In conclusion, retrograde conduction during AVNRT appears to take place over a functional or anatomical specialized fiber within the AV node and not over an extranodal H-A fiber.

Adolescent↗
PubMed1983

Sustained "slow-fast" and "fast-slow" AV nodal re-entrant tachycardia in a patient with recurrent supraventricular tachycardia.

A case is presented of a 21-year-old woman with recurrent paroxysmal supraventricular tachycardia. Electrophysiologic study demonstrated the presence of both antegrade and retrograde dual AV nodal conduction pathways and both conventional slow-fast and atypical fast-slow forms of the AV nodal re-entrant tachycardia could be induced. Both tachycardias were successfully suppressed with a combination of digoxin and verapamil.

Adult↗
PubMed1983

Two mechanisms of arrhythmia induction by a DDD pacemaker: a case report.

A 68-year-old man with sick sinus syndrome and a history of intermittent atrial fibrillation was treated by implantation of a DDD pacemaker. He subsequently developed recurrent episodes of shortness of breath and tachycardia. Investigation revealed two different arrhythmias, both induced by the pacemaker: (1) a tachycardia in which the dual-chamber pacemaker system provided the antegrade limb and the AV node provided the retrograde limb and (2) a triggered, ventricularly paced tachycardia caused by the pacemaker sensing atrial fibrillation waves. Both rhythms were abolished by reprogramming to the DVI mode.

Aged↗
PubMed1983

The induction of atrial flutter and fibrillation and the termination of atrial flutter by esophageal pacing.

In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we prospectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 +/- 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40-340 ms (mean 166 +/- 72), pulse durations of 7.0-9.9 ms, and currents of 10-25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients. In one patient neither flutter nor fibrillation was induced by esophageal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160-220 ms (mean 176 +/- 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.

Adolescent↗
PubMed1983

The measurement of sinus node refractoriness in man.

We recently described a method for measuring sinus node refractoriness in the rabbit heart. Atrial premature beats either may result in reset return responses or may become interpolated because of encroachment on sinus node refractoriness. In previous studies with rabbits we defined the effective refractory period of the sinus node (SNERP) as the longest premature interval that is interpolated. This study presents results on the extension of this technique to the measurement of sinus node refractoriness in man. Out of 30 patients (12 with and 18 without sinus node dysfunction), SNERP could be measured in 26 at one or more basic cycle lengths. At a basic pacing cycle length of 600 msec, SNERP ranged from 250 to 380 msec (mean 325 +/- 39) in patients without sinus node dysfunction and from 500 to 550 msec (mean 522 +/- 20) in patients with sinus node dysfunction. This clear differentiation of patients with and without sinus node dysfunction by SNERP is in contrast to various results obtained by assessing sinus node function from sinus node recovery time and sinoatrial conduction time. Thus this study suggests the possible use of the measurement of SNERP in the assessment of sinus node function in man and its possible value in identifying patients with sinus node dysfunction.

Adolescent↗
PubMed1983

Sinus node dysfunction.

The syndrome of sinus node dysfunction has become increasingly recognized as a cause of symptoms and morbidity, particularly in the elderly population. This syndrome does not represent a homogeneous disease entity. Increased investigation has shown that many pathologic conditions and pathophysiologic mechanism may lead to one of the several clinical and electrocardiographic manifestations of the sick sinus syndrome. Attempts to improve diagnostic accuracy, identify underlying mechanisms and to predict the outcome of therapy have led to the development of various diagnostic tests. However, at present these have proven of limited clinical value and the mainstay of diagnosis remains ECG monitoring. Treatment is directed at the control of symptoms with pacemaker therapy for bradyarrhythmias and combined pacemaker and antiarrhythmic drug therapy for the bradycardiatachycardia syndrome.

Anti-Arrhythmia Agents↗
PubMed1983

Surgical treatment of Wolff--Parkinson--White syndrome.

The Wolff--Parkinson--White syndrome may be associated with life-threatening or disabling tachyarrhythmia, owing to the presence of an atrioventricular accessory pathway (Kent bundle). The first division of a Kent bundle was reported in 1969, but this surgery is still confined to a few centres. Between September 1981 and October 1982, 19 patients (13 men, 6 women) aged 16 to 46 years (mean 25 years) with the Wolff--Parkinson--White syndrome associated with refractory arrhythmia underwent surgery. Kent bundles were localized in the electrophysiology laboratory and by intraoperative cardiac mapping. The 19 patients had a total of 22 distinct Kent bundles. The bundles were divided using open-heart (13 patients) or closed-heart (6 patients) technique. All Kent bundles were confirmed as nonfunctioning before discharge. A delta wave recurred in two patients. The Kent bundle was not functional in one patient. The other is controlled by a drug that was previously ineffective. There were no complications or deaths. Kent bundles can be divided with minimal morbidity and a high success rate (more than 90%). Surgery is indicated in patients with refractory arrhythmias or in young patients who would be required to take medication for life.

Adolescent↗
PubMed1982

The electrophysiologic basis and management of symptomatic recurrent tachycardia in patients with Ebstein's anomaly of the tricuspid valve.

Twenty-two patients with Ebstein's anomaly were evaluated because of recurrent tachycardia. A total of 30 accessory pathways were present in 21 of the 22 patients. Twenty-six accessory pathways were of the atrioventricular (A-V) type while four were Mahaim fibers. Multiple accessory pathways were present in eight patients. Twenty-five of the 26 accessory A-V pathways were right-sided, either in the posterior septum (12 pathways) or the posterolateral free wall (13 pathways); one patient with corrected transposition of the great arteries had a left-sided accessory A-V pathway in a lateral free wall location. Patients with accessory A-V pathways had a long minimal ventriculoatrial (V-A) conduction time during reciprocating tachycardia (192 +/- 47 ms) and usually showed a persistent complete or incomplete right bundle branch block morphology. At surgery, preexcitation was invariably localized to the atrialized ventricle. The long V-A conduction time during reciprocating tachycardia appeared to consist of late activation of the local ventricle in the region of the accessory pathway with a further delay occurring before excitation of adjacent atrium presumably due to conduction over the accessory pathway. Accessory A-V pathways were successfully sectioned with no deaths in 13 of 15 patients. On the basis of these data, certain electrocardiographic findings encountered in the study of patients with recurrent tachycardia should point to the possibility of associated Ebstein's anomaly: morphology of the surface electrocardiogram suggesting preexcitation of the right posterior septum or right posterolateral free wall as well as the combination during reciprocating tachycardia of a long V-A interval and right bundle branch block.

Adolescent↗
PubMed1982

Cardiovascular effects of epinephrine and dipivalyl epinephrine applied topically to the eye in patients with glaucoma.

The cardiovascular effects of topical ophthalmological preparations of 2% epinephrine (EPI), 0.1% dipivalyl epinephrine (DPE), and placebo were studied in double-blind fashion in 20 patients with glaucoma. Both drugs and placebo produced a decrease in heart rate (2 +/- 3 beats/min) which, although small, was highly significant (p less than 0.001). Neither drug not placebo produced a significant effect on mean or systolic blood pressure (BP) over the group as a whole (p greater than 0.1). However, 5 of 20 patients responded to EPI with a significant rise in mean or systolic BP (defined as a change greater than mean change +/- 2 SD), whereas there were no such responses to DPE or placebo. One patient developed marked ventricular ectopy after EPI. We conclude that EPI may cause cardiovascular side effects in a high percentage of patients (25% in this study) through individual susceptibility rather than a predictable effect. DPE, a new epinephrine analogue, appears to be devoid of these effects.

Aged↗
PubMed1982

Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome.

We evaluated the electrophysiologic effects of disopyramide phosphate in 12 patients with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed during a control period and after administering i.v. disopyramide (four bolus doses of 9.5 mg/kg over 40 minutes superimposed on a continuous infusion at 1.0 mg/kg/hour). All patients were then restudied after 3 days on oral medication in doses of 800-1200 mg/day. In all patients we tried to induce reciprocating tachycardia and atrial fibrillation. The cycle length during reciprocating tachycardia was not changed by i.v. disopyramide, but increased after oral disopyramide, from 331 +/- 53 (+/- SD) to 370 +/- 68 msec (p less than 0.01). This increase occurred predominantly as a result of prolongation of retrograde conduction time in the accessory pathway. Despite prolonging cycle length during reciprocating tachycardia, disopyramide did not prevent its induction. The shortest and mean RR intervals during atrial fibrillation were used to assess antegrade refractoriness of the accessory pathway. Intravenous disopyramide prolonged the shortest RR from 169 +/- 18 to 226 +/- 24 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 329 +/- 62 msec (p less than 0.005). Oral disopyramide prolonged the shortest RR interval from 169 +/- 18 to 248 +/- 36 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 360 +/- 93 msec (p less than 0.001). After oral disopyramide, the episodes of atrial fibrillation were shorter and self-terminating. No acute hemodynamic side effects were observed, but five patients developed gastrointestinal or anticholinergic side effects on oral disopyramide. Seven patients elected to have surgical interruption of their accessory pathways and five have been successfully treated with oral disopyramide for 14-33 months. Disopyramide appears to have beneficial electrophysiologic effects in patients with Wolff-Parkinson-White syndrome. Prolongation of refractoriness in the accessory pathway markedly slows the ventricular response during atrial fibrillation and therefore prevents the development of life-threatening arrhythmias.

Administration, Oral↗
PubMed1982

Changes in ventriculoatrial intervals with bundle branch block aberration during reciprocating tachycardia in patients with accessory atrioventricular pathways.

During reciprocating tachycardia in patients with accessory atrioventricular pathways, the observation of changes in ventriculoatrial (VA) intervals with bundle branch block (BBB) aberration has been used to localize the site of the pathway and prove the participation of the pathway in the tachycardia. In this report we present the changes observed during BBB in 93 patients with single atrioventricular pathways in whom the site of their pathways was subsequently proved at the time of their surgical interruption. In patients with left or right free wall pathways, the minimum VA interval (VA min) increased by 61 +/- 19 msec with ipsilateral BBB, whereas no change occurred with contralateral BBB. The smallest increase in the VA interval was 35 msec. In 14 patients, shortening of the AH intervals resulted in changes in overall cycle length that were less than 35 msec. Patients with septal pathways all had changes in VA min of 25 msec or less with either right or left bundle branch block (RBBB or LBBB), which suggests that a clear differentiation between septal and free wall pathways can be made on the basis of changes in VA min. In patients with anteroseptal pathways, VA min intervals frequently prolonged with RBBB (16 +/- 9 msec) but not with LBBB. In patients with posteroseptal pathways, VA min frequently prolonged with LBBB (13 +/- 8 msec) but not with RBBB. Therefore, the observed changes in VA min with BBB may serve as an important indicator of the site of an accessory pathway and may provide guidance in the choice of surgical therapy.

Adolescent↗
PubMedDate not supplied

Effects of transient myocardial ischemia on the QT interval in man.

Prolongation of the QT interval may be associated with ventricular arrhythmias. Prolongation of the QT interval has been found during the evolution of acute myocardial infarction. To investigate the effect of transient myocardial ischemia on the QT interval, 80 patients admitted to the coronary care unit with unstable angina were studied, 60 retrospectively and 20 prospectively. The corrected QT intervals (QTc) in multiple leads were compared during ischemic pain to those recorded within 24 h in the absence of pain. During pain, the mean +/- SD QTc was 0.44 +/- 0.04 s which was identical to the mean QTc recorded without pain. The mean QTc during pain was not different between patients with and without ischemic electrocardiographic abnormalities, between patients with and without previous myocardial infarction or between patients with single and multiple vessel disease on angiography (P greater than 0.5). In conclusion, the QTc interval does not change during transient myocardial ischemia, regardless of previous infarction, extent of coronary artery disease or therapy with type 1 antiarrhythmic drugs.

Aged↗