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Biomedical subjects

C R Kerr

Publications and source records attributed to C R Kerr.

At least 73 records · Page 4Linked to original sources
PubMed1985

Incidence and clinical significance of accelerated junctional rhythm following open heart surgery.

Accelerated junctional rhythm following open heart surgery may lead to hemodynamic impairment due to loss of synchronized atrial contraction. Therefore, in this study we evaluated the frequency, duration, and hemodynamic effects of accelerated junctional rhythm in 30 patients undergoing coronary artery bypass (CAB) and in 30 undergoing valve replacement (VR). Accelerated junctional rhythm was defined as a rate greater than 55 bpm. Patients were continuously monitored postoperatively and rhythm strips obtained at least every 4 hours. Ten VR patients (33%) and four CAB patients (13%) exhibited accelerated junctional rhythm, the difference between these groups being significant (p less than 0.02). Nine of the 14 were hemodynamically compromised requiring inotropic support (9) and/or pacemaker insertion (2). The time of appearance of accelerated junctional rhythm ranged from immediate to 6 days (mean 26 +/- 52 hours, SD) and it lasted a mean of 16 +/- 22 hours. The rate ranged from 62 to 150 bpm. The sinus rate prior to the onset of accelerated junctional rhythm was significantly lower than the sinus rate in those not developing accelerated junctional rhythm. In conclusion, accelerated junctional rhythm is seen frequently following open heart surgery and may lead to hemodynamic deterioration. It is seen more frequently following VR, in approximately 33% of patients. Its manifestation appears to result from a combination of acceleration of junctional focus and slowing of sinus node discharge.

Coronary Artery Bypass↗
PubMed1985

Amplitude of atrial electrical activity during sinus rhythm and during atrial flutter-fibrillation.

The onset of atrial flutter or fibrillation in a patient with a DDD pacemaker may result in sensing of the atrial arrhythmia and an inappropriate ventricular pacing response. In order to assess the potential of this problem, we evaluated the amplitude of atrial electrograms recorded from the right atrial appendage during sinus rhythm and during atrial flutter or fibrillation during 19 episodes in 18 patients. In 11 episodes of fibrillation and eight episodes of flutter, there was no difference in amplitude of either unipolar or bipolar atrial electrograms compared to that recorded during sinus rhythm (p greater than 0.05). In 14 of 19 episodes, the direction of depolarization of the bipolar electrogram did not change appreciably between sinus rhythm and the atrial arrhythmia. In summary, there is insufficient difference between amplitude of atrial depolarizations recorded during sinus rhythm and atrial flutter or fibrillation to be differentiated reliably by DDD pacemakers.

Adult↗
PubMed1985

Transvenous atrial pacing following amputation of the atrial appendage at open heart surgery.

The right atrial appendage is frequently amputated at the time of open heart surgery. In this study we report implantation and chronic follow-up pacing data on 17 patients in whom either actively fixated screw-in leads or passively fixated tined "J" leads were implanted into the trabeculae at the base of the atrial appendage. Chronic follow-up demonstrated excellent chronic pacing thresholds and atrial sensitivity thresholds in those patients in whom these measurements could be made. It is therefore concluded that satisfactory atrial pacing can be achieved in patients who have previously undergone amputation of the atrial appendage during open heart surgery.

Adolescent↗
PubMed1985

Microvascular pressure, surface area, and permeability in isolated hindquarters of SHR.

The transvascular escape rate (TER) of labeled albumin is reported to increase in essential hypertension. However, the mechanism for this augmented rate of protein efflux is uncertain and may be related to increased microvascular permeability, surface area, and/or pressure. To determine the possible contributions of these mechanisms to increased TER of protein, the osmotic reflection coefficient for total plasma protein, capillary filtration coefficient, and effective capillary pressure were estimated in isolated hindquarters of age-matched (12-13 wk) spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar (WR) rats. Estimates of the reflection and filtration coefficients were not significantly different in SHR, WKY, and WR. However, capillary pressure was significantly greater in SHR than in normotensive controls. These results indicate that 1) skeletal muscle microvascular permeability and surface area are similar in SHR, WKY, and WR; 2) effective capillary pressure is greater in SHR than WKY or WR; and 3) if TER for protein is elevated in hypertensive skeletal muscle, the primary mechanism for this process may be increased convective transport of protein secondary to elevated microvascular hydrostatic pressure.

Animals↗
PubMed1985

Use of electrical pacemakers in the treatment of ventricular tachycardia and ventricular fibrillation.

Significant advances have been made in the therapy of ventricular arrhythmias. Many new antiarrhythmic drugs have expanded the medical armamentarium to treat ventricular tachycardia and ventricular fibrillation, and the use of intracardiac electrophysiologic studies has aided in predicting long-term drug efficacy. Major advances have also been made in the surgical treatment of arrhythmias. However, there remain a number of patients in whom ventricular arrhythmias remain a major therapeutic problem and, in some of these, electrical devices may aid in treatment. Overdrive pacing may prevent certain cases of ventricular arrhythmias, and antitachycardia devices may be useful in terminating paroxysmal ventricular tachycardia. In certain circumstances, internal cardioversion or defibrillation may be an alternative. At present, antitachycardia pacing and internal countershock must be considered as forms of therapy to be used when medical and surgical therapy are impractical or have failed. Careful selection is necessary to delineate patients in whom these forms of therapy may be indicated.

Cardiac Catheterization↗
PubMed1985

Applicability of capillary gas liquid chromatography to the measurement of free fraction of disopyramide in human plasma.

A sensitive and specific capillary gas liquid chromatographic nitrogen/phosphorus selective detection technique was used to measure unbound disopyramide in human plasma. The concentration dependent protein binding of disopyramide was examined. Various concentrations of disopyramide alone ranging from 0.5 to 10.0 micrograms/ml in 0.4 ml of isotonic phosphate buffer (pH 7.4) were dialyzed for 6 hours at 37 degrees C, against 0.4 ml blank plasma from five healthy volunteers. The concentration-dependent binding of disopyramide was confirmed. The average free fraction for disopyramide at concentrations of 0.5, 1.0, 2.0, 3.0, 4.0, 5.0 and 10.0 micrograms/ml were 0.14, 0.15, 0.20, 0.27, 0.30, 0.34 and 0.53, respectively.

Chromatography, Gas↗
PubMed1984

Simultaneous quantitation of disopyramide and its mono-dealkylated metabolite in human plasma by fused-silica capillary gas chromatography using nitrogen-phosphorus specific detection.

A nitrogen-specific detector gas-liquid chromatographic assay method is reported which provides improved selectivity and sensitivity for disopyramide and its mono-N-dealkylated metabolite using a crosslinked fused-silica capillary column. The quantitation of disopyramide and mono-N-dealkylated disopyramide was accomplished by injecting trifluoroacetic anhydride-treated samples containing derivatized internal standard p- chlorodisopyramide , into a gas chromatograph equipped with a nitrogen--phosphorus detector and an automatic liquid sampler. A 25 m X 0.31 mm crosslinked, 5% phenylmethyl silicone-coated fused-silica column was utilized and samples were injected using the splitless injection mode. Linearity was observed in the range 0.05-5.00 micrograms/ml for disopyramide and 0.02-3.00 micrograms/ml for the mono-N-dealkylated metabolite. The coefficient of variation was found to be within 10% for both compounds in the concentration range studied.

Chromatography, Gas↗
PubMed1984

Morphine-halothane interaction in rats.

The effects of morphine, halothane, and their various combinations on the purposeful movement (PM) response and the heart rate (HR) increase caused by noxious stimulation were studied in 250 rat experiments. Doses that block the PM and HR responses for the single agent and for combinations were determined with a probit procedure and compared with an isobolographic analysis. As was evidenced by the PM response, the combined anesthetic effect of morphine and halothane, with some deviations, may be defined as additive. It also was found that the combined administration of morphine and halothane results in an antagonism for suppression of the HR increase to noxious stimulation. Halothane antagonized morphine to a much greater extent than morphine to halothane.

Animals↗
PubMed1984

Failure to pace following high dose antiarrhythmic therapy--reversal with isoproterenol.

A patient with resistant ventricular tachycardia treated with a combination of antiarrhythmic agents is described. Sudden onset of a wide complex ventricular rhythm with periods of asystole and failure to achieve transvenous pacing were observed, presumably due to antiarrhythmic drug toxicity. Inability to pace was reversed by the infusion of isoproterenol.

Amiodarone↗
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↗