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Biomedical subjects

S Furman

Publications and source records attributed to S Furman.

At least 181 records · Page 10Linked to original sources
PubMed1985

Dual chamber pacemakers: upper rate behavior.

Upper rate management of a dual chamber pacemaker requires sensing of the atrium and limitation of ventricular response to desired levels. Limitation of ventricular rate response is accomplished by setting atrial channel refractoriness which consists of two separate and continuous intervals, the atrioventricular interval (AV interval) and the atrial refractory interval, after the ventricular pace or sense event (AR interval). A P-wave that falls within the total atrial refractory interval (TARI) remains unsensed and one that falls beyond the TARI is sensed. If the upper rate limit interval (URI) is programmed to equal the TARI, the upper rate limit will occur by development of sudden AV block. If the URI is of greater duration (lower allowed rate) than the TARI, the difference in interval between the two is the Wenckebach interval (WI) and is the duration of a response plateau, when the atrial coupling interval is less than the upper rate interval. All dual chamber timing cycles can be interpreted in terms of atrial refractoriness and upper rate limitation with consideration of the lower rate interval, and the ventricular refractory and blanking intervals.

Bradycardia↗
PubMed1985

Maintenance of exercise stroke volume during ventricular versus atrial synchronous pacing: role of contractility.

Although atrial synchronous and rate-responsive ventricular pacing have been compared, the importance of maintaining synchronized atrial systole in addition to rate responsiveness has been incompletely defined. That is, the effects of these two pacing modes on cardiac volumes and contractility have not been studied. Accordingly, 16 patients with normal ventricular function were studied while in the upright position and at rest with gated radionuclide ventriculography during both atrial synchronous and ventricular pacing. Twelve of these patients were also studied during low-level upright exercise (300 kilopond-meters). Rest and exercise ventricular pacing heart rates were matched to those recorded with synchronous pacing. Ventricular volumes were determined with a counts-based method. The ejection fraction and peak systolic pressure/end-systolic volumes or contractility between the two pacing modes. However, during exercise to identical heart rates, blood pressures, and workloads, although stroke volume was the same during exercise with atrial synchronous and ventricular pacing (78 +/- 13 vs 75 +/- 12 ml), end-diastolic and end-systolic volumes were lower with ventricular pacing than with atrial synchronous pacing (end-diastolic volume 101 +/- 13 vs 113 +/- 16 ml, p less than .001; end-systolic volume 26 +/- 4 vs 35 +/- 7 ml, p less than .001). Stroke volume during ventricular paced exercise was maintained at atrial synchronous pacing levels by means of increased contractility (ejection fraction of 74 +/- 4% during ventricular pacing vs 69 +/- 5% during atrial synchronous pacing, p = .002; peak systolic pressure/end-systolic volume ratio of 6.51 +/- 1 during ventricular pacing vs 4.85 +/- 1 during atrial synchronous pacing, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Affinity of antibody at a secretory site in the rat.

Sprague-Dawley rats were administered DNP-BGG on day one of pregnancy by either local mammary gland vicinity injection or by gastric intubation. All rats later received local mammary gland vicinity injection of DNP-BGG on day 11 of pregnancy. Milk and serum were collected post-parturition. IgA and IgG antibody was separated in the milk and IgG antibody in the serum. The relative average affinity constant (KO) was determined by a modification of the Farr assay. Milk IgG affinity was found to be considerably higher than the affinity of IgG in the serum. IgA affinity in the milk of rats which received the antigen by gastric intubation demonstrated antibody affinity much greater than the affinity of milk antibody in rats which simply received mammary gland vicinity injection (1.8 x 10(8) vs. 1.4 x 10(6) l/M). The results indicate that much of the IgG antibody in milk may be locally synthesized. Gut-associated lymphoid tissue may act as a source of antigen specific memory cells for peripheral secretory tissues.

Animals↗
PubMed1985

The pacemaker syndrome.

The pacemaker syndrome is a complex of clinical signs and symptoms related to the adverse hemodynamic and electrophysiologic consequences of ventricular pacing in the absence of other causes. Neurologic symptoms or those suggesting low cardiac output or congestive heart failure, temporally related to the onset of ventricular pacing, are indicative of the pacemaker syndrome. The evolution of a clinically recognized syndrome, an analysis of possible mechanisms and clinical manifestations, and diagnostic approaches and their implications for management are discussed.

Adaptation, Physiological↗
PubMed1985

Pacemaker syndrome: definition and evaluation.

The pacemaker syndrome is an iatrogenic disorder that can result from hemodynamic sequelae of ventricular pacing. Symptoms range from fatigability to syncope and occur during the time the ventricles are being stimulated by the pulse generator. Postulated mechanisms include loss of atrioventricular synchrony, vasodepressor reflexes, and retrograde atrial activation. Prevention is attempted by selection of the appropriate pacing mode for the individual patient. Remission results from restoration of atrioventricular synchrony.

Adaptation, Physiological↗
PubMed1985

The role of implantable pacemakers in the therapy of tachycardias.

Antitachycardia electrical stimulation involves significant problems of sensing the cardiac rhythm and determining whether a tachycardia exists. The simple algorithms developed for bradycardia pacing are inadequate for tachycardia pacing. Electrogram signal analysis and cardiac activation analysis with at least two leads will be required to make a device diagnosis of a tachycardia. Termination of a tachycardia reliably and consistently is difficult and has only been accomplished uniformly by defibrillation. Further development of devices which are multimodal in termination capability is necessary. A registry for tachycardias and for tachycardia management is required to provide concentrated and analyzable data from a modality as yet infrequently used.

Anti-Arrhythmia Agents↗
PubMed1984

Stability of AV conduction in sick sinus node syndrome patients with implanted atrial pacemakers.

Single-chamber atrial pacing is effective in the management of sinus node dysfunction, subject to the uncertainty of long-term atrioventricular conduction. Despite the accepted observation that many patients with sinus node dysfunction also have atrioventricular conduction disease, data do not exist on the development of atrioventricular block in those patients with permanent single-chamber atrial pacing. Of 70 patients who received single-chamber atrial pacing from 1967 to 1982 (mean duration of pacing was 33 months), only two patients of 58 (3.4%) of those with sinus node dysfunction developed atrioventricular (AV) block--after 14 months in one patient and after 23 months of successful atrial pacing in the other. None of the 12 patients paced for tachyarrhythmia management developed AV block. Of the 70 patients, 37 had assessment of AV conduction by incremental atrial pacing at the time of implant and 20 patients underwent atrial pacing on the basis of surface ECG and clinical judgment. Electrophysiologic studies were conducted only in those patients being paced for control of supraventricular arrhythmias. Only 5 of the 70 patients required conversion to ventricular pacing for technical difficulties; three of these conversions occurred in the early 1970's before the advent of atrial tined or J leads; one was for irreparable lead fracture and only one occurred in a patient with a newer design atrial lead. In conclusion, progression to AV block in patients with permanent atrial pacing is uncommon; formal electrophysiologic studies are necessary mainly in patients with supraventricular arrhythmias; and in the majority of patients, AV conduction can be assessed at the time of implant. Continued improvement in atrial leads should make atrial pacing even more successful.

Adult↗
PubMed1984

"Pseudo-endless loop" tachycardia in an AV universal (DDD) pacemaker.

A 3-beat episode of ventricular arrhythmia was recorded in a patient with an AV universal (DDD) pacemaker. This arrhythmia mimicked "endless loop" tachycardia (ELT) because it appeared following a ventricular premature contraction (VPC), its rate approached the preset upper-rate limit and the regular P waves disappeared during the episode. However, as retrograde conduction was absent ELT could not exist. The mechanism of this arrhythmia was based on a combination of interference by VPC of the regular sequence of QRS complexes produced by P wave and the pacemaker commitment to maintain an upper rate limit by prolongation of the programmed pacemaker AV delay.

Electrocardiography↗
PubMed1984

DDD/DDT pacemakers in the treatment of ventricular tachycardia.

The possibility of adapting multimode dual-chamber pacemakers for programmed and burst stimulation was explored in a group of patients with ventricular tachycardia. The potential usefulness and pitfalls of these pacemakers were exemplified in one patient, presented in detail. The implanted DDD pacemaker was programmed to an all-synchronous mode (DDT), permitting programmed ventricular stimulation through synchronization with chest wall stimulation provided by a standard external programmable stimulator. With the ventricular sensing refractory period shortened to 200 ms, both programmed electrical stimulation and burst pacing for termination of induced tachycardias were possible. When medications failed to offer protection against the patient's tachycardias, the ventricular sensing refractory period (and minimum stimulation interval) was increased to 300 ms, thereby permitting burst pacing at up to 200 beats/minute for termination of spontaneous episodes. After many trials to confirm the efficacy of such stimulation, and the lack of muscle potential triggering, the patient was discharged home with the pacemaker in the DDT mode. He was instructed to go to his local emergency room, and was equipped with a portable device to trigger his implanted unit. Subsequently, the patient had successful termination of several spontaneous episodes of ventricular tachycardia in an emergency room. Later, he began to experience palpitations during certain exercises, and it was found that the implanted unit was being triggered by pectoral myopotentials. The unit was therefore reprogrammed to decrease the sensitivity, and the patient was again discharged. The need for careful evaluation and close follow-up is emphasized to maximize the benefits and to minimize the very serious potential risks of this pacing mode.

Action Potentials↗
PubMed1984

Implantation techniques of antitachycardia devices.

Implantation of a defibrillator may be by a mixed technique of transvenous leads and subcostal thoracotomy. An alternative approach is placement of all defibrillator leads and possible pacemaker leads via median sternotomy. All sensing leads, either for a defibrillator or a pacemaker, should be bipolar to provide maximal rejection of interference signals. Interpretation of the electrogram requires analysis of the pathologic electrogram to distinguish it from the "normal" electrogram for that patient and may require several leads to determine the activation sequence which will allow diagnosis of a tachycardia in a fashion similar to that performed by a human observer.

Electric Countershock↗