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Biomedical subjects

R R Hope

Publications and source records attributed to R R Hope.

29 records · Page 2Linked to original sources
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed.

Animals↗
PubMed1977

The induction of ventricular arrhythmias in acute myocardial ischemia by atrial pacing with long-short cycle sequences.

Recent studies emphasize the importance of heart rate in the genesis of ventricular arrhythmias during myocardial ischemia. The role of alterations in rhythm has not previously been systematically investigated. In 20 dogs subjected to acute myocardial ischemia and crushing of the sinus node, standard electrocardiographic leads were recorded, as well as His bundle and epicardial electrograms from the normal and ischemic areas. Abrupt pauses in regular atrial pacing did not cause arrhythmias prior to the onset of ischemia; however, during ischemia, atrial pacing with intermittent abrupt pauses resulted in the induction of ventricular arrhythmias beginning after the second conducted beat following each pause (ventricular premature beats, 20/20; ventricular tachycardia, 19/20; and ventricular fibrillation, 8/20). Onset of the arrhythmia was associated with increased delay in activation of ischemic epicardium and fractionation of the electrogram potential of the second conducted impulse. Typical Gouaux-Ashman phenomenon was an incidental observation. Unlike the Gouaux-Ashman phenomenon, which is restricted to the His-Purkinje system, the phenomenon we observed orginated within ischemic myocardium. In vitro studies indicate that the underlying mechanism may be related to postrepolarization refractoriness induced by ischemia.

Animals↗
PubMed1976

Selective versus non-selective His bundle pacing.

His bundle pacing was achieved in 10 anaesthetized open chest dogs by stimulation from bipolar electrode catheters positioned in the aortic root and right heart. Recordings were taken directly through plunge wires from the right atrium, high ventricular septum, and epicardial sites on the right and left ventricles. Six types of response were seen during A-V junctional stimulation: (1) low atrial pacing; (2) combined atrial and His bundle pacing; (3) His bundle pacing; (4) combined atrial, ventricular septal, and His bundle pacing; (5) combined septal and His bundle pacing; and (6) ventricular pacing. Pacing of the His bundle in combination with the atrium and/or ventricular septum is designated as non-selective, whereas stimulation of the His bundle alone is considered selective pacing. Non-selective His bundle pacing can be recognized from the surface leads by changes in onset and amplitude of the QRS with appreciable T-wave alterations. Although electrode position was an important determinant of the type of pacing achieved, a variety of patterns of stimulation resulted from variation in the modalities of the pacing stimulus, ie, polarity, intensity, and duration. Unless these factors are considered, selective His bundle pacing may not be achieved.

Animals↗
PubMed1976

Hierarchy of ventricular pacemakers.

To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence.

Animals↗
PubMed1975

Cyanosis and unrecognised atrial septal defect in children.

Two unusual cases of cyanosis and atrial septal defects are presented. Relative hypoplasia of the right ventricle was an associated feature. In both cases cyanosis was the presenting symptom and the usual clinical signs of atrial septal defect were absent. Chest x-rays and electrocardiograms were normal and the correct diagnosis was not made until after cardiac catherisation.

Adolescent↗