Jackson H. Stuckey

Effect of pacemaker site on cardiac output and ventricular activation in dogs with complete heart block

Abstract The sequence of ventricular activation was recorded in dogs with complete heart block while the heart was paced from each of 11 ventricular sites; cardiac output was determined while the heart was paced from each of 8 ventricular sites at rates of 90, 120 and 150 per minute. The following conclusions were reached: 1. 1. Each ventricular pacemaker site results in a specific pattern of ventricular activation. 2. 2. Differences of over 100 per cent in cardiac output were recorded when the heart was paced from different ventricular sites at the same pacemaker rate. 3. 3. The optimal pacemaker rate is dependent upon the ventricular site selected for the implantation of the pacemaker electrode and the condition of the cardiovascular system. 4. 4. The hemodynamic effectiveness of the left ventricular pacemaker sites is inversely related to the muscle mass activated by muscle conduction. 5. 5. The hemodynamic effectiveness of right ventricular pacemakers is dependent upon the pattern of left ventricular depolarization. 6. 6. The hemodynamically more effective left ventricular pacemaker sites resulted in higher cardiac outputs than any of the right ventricular sites tested. 7. 7. The changes in cardiac performance when the heart is paced from various pacemaker sites is best explained by varying degrees of asynchrony during ventricular contraction and/or the position of the atrioventricular valves early in ventricular systole. 8. 8. The clinical implications of this study have been considered.

Functional Properties of the Atrioventricular Conduction System

Experiments were designed to study A-V transmission of premature atrial responses by recording electrical activity directly from selected parts of the conducting system. This experimental design permits a more exact interpretation of results than is the case when records are obtained only from the atria and ventricles. Two types of experiments have been conducted in studies of the response of the specialized conducting system of the mammalian heart to premature activation. Records of transmembrane potentials from single fibers of the A-V node and Purkinje system show that premature responses may show a reduced rate of rise and amplitude and thus may be conducted slowly or may decrement completely. Under other conditions, premature responses may show local delay or block because they arise from a local response of considerable duration. Records obtained directly from different parts of the in situ specialized conducting system show that the same phenomena probably occur in the intact, normal heart. These properties of the various fibers of the conducting system, in conjunction with the normal local differences in action potential duration, conduction velocity, and excitability, seem to account quite adequately for the variations which have been noted during A-V propagation of premature responses. On the basis of these results, it seems unnecessary to postulate a dual A-V conducting system in the mammalian heart.

Effects of ischemia and hypoxia on the specialized conducting system of the canine heart

Abstract Close bipolar electrodes have been attached at selected locations on the epicardium and endocardium of in situ canine hearts during total cardiopulmonary bypass. Records from various parts of the atrium, specialized conducting system, and ventricle have been obtained during ischemia and severe hypoxia. Atrial and A-V nodal conduction were the most sensitive to ischemia and hypoxia. The specialized conducting system was least affected by ischemia, and the peripheral Purkinje system was the most resistant. Ventricular fibrillation occurred in all experiments during ischemia but was not produced by hypoxia. Recordable electrical activity was abolished after 40 minutes of ischemia. During 120 minutes of severe hypoxia, electrical activity in the atrium was depressed, whereas that in the specialized conducting system distal to the A-V node was not markedly affected. In view of the striking differences between the effects of ischemia and hypoxia on the specialized conducting system distal to the A-V node, it is concluded that a lack of oxygen may not be so important as other factors, such as the retention of metabolites and changes in blood pH and electrolyte concentrations which occur during ischemia.

Electrical Activity During the P-R Interval

Electrical activity of the specialized conducting system (His bundle, bundle branches, false tendons and peripheral Purkinje fibers) of canine hearts has been recorded in situ through electrodes attached to the endocardium during total cardiopulmonary bypass. Simultaneous records from multiple sites have been correlated with electrocardiograms to indicate the sequence of activation of the specialized conducting system during normal and retrograde activation and during vagal stimulation. The results obtained indicate that the method employed has several advantages among which are an absence of injury at the recording site and an applicability to chronic studies.

On the Cause of Ventricular Asystole during Vagal Stimulation

In anesthetized dogs the vagus nerve was stimulated for 2 min; during the first minute the ventricles were driven at a rate higher than the control sinus rate; after discontinuation of the drive, the duration of asystole was prolonged. When the ventricles were driven at a rate lower than the sinus rate during vagal stimulation the subsequent asystole was shortened. Slowing sinus activity by graded vagal stimulation before maximal vagal stimulation led to a shorter asystole. Driving the ventricles at a rate higher than the sinus node rate before vagal stimulation resulted in longer asystole. In animals with chronic atrioventricular block, “overdriving” the ventricles resulted in subsequent temporary inhibition of ventricular pacemakers. In dogs with atrioventricular block, coronary sinus plasma potassium increased during the period of ventricular overdriving, and the magnitude of the rise was a function of the driving rate. These results support the concept that ventricular asystole results from the suppressive action of the fast rate imposed by the sinus node upon the slowly discharging ventricular pacemakers. Suppression of sinus node activity by the vagus reveals the rate-dependent inhibition of ventricular pacemakers. The mechanism of inhibition may be related to changes in ionic concentration gradients.

Activation of the interventricular septal myocardium studied during cardiopulmonary bypass

Abstract The sequence of activation of the right and left surfaces of the interventricular septum of the canine heart has been studied by means of bipolar electrograms recorded under direct vision from multiple selected points in the in situ heart during total cardiopulmonary bypass. Earliest activity is almost simultaneous on both sides of the septum; depolarization of septal musculature is first recorded, on the right, from the septum above and anterior to the anterior papillary muscle and, on the left, from the central septum either above or below the midline. Records of septal activation after bundle branch block show that all of the anterior and middle parts of the right surface, including the anterior papillary muscle, are dependent on the right bundle branch for normal activation, and all of the left surface is dependent on the left bundle branch. In some animals the posterior and basal parts of the right surface are normally activated from some part of the left bundle branch.

On the Sympathetic Control of Ventricular Automaticity THE EFFECTS OF STELLATE GANGLION STIMULATION

The effects of stellate ganglion stimulation on idioventricular automaticity were studied in anesthetized dogs. An idioventricular rhythm was obtained in one series of animals by ligating the His bundle and in the other by stimulating the vagus. On isolation of the left stellate ganglion, the idioventricular rate fell by 5 beats/min which is compatible with a rate of “tonic” discharge of about 3 impulses/sec. On stimulation of the stellate ganglia at increasingly higher frequencies, the idioventricular rate accelerated progressively and the frequency-response curve was sigmoid. When the stimulation frequency was increased above 10 to 15 pulses/sec, there was no further enhancement of ventricular automaticity. The ventricular rates attained during sympathetic stimulation rarely exceeded 70/min. The interval between the initiation of sympathetic stimulation and the maximal ventricular acceleration was shorter at higher stimulation frequencies. The effects of right and left stellate stimulation on the rate of idioventricular pacemakers were comparable. Reflex vagal inhibition had little influence on the acceleratory action of the sympathetic nerves on the idioventricular pacemakers since in dogs with atrioventricular block the results before and after vagotomy were similar. Furthermore, the idioventricular rhythm during vagally induced block increased on sympathetic stimulation to values comparable to those obtained in dogs with surgically induced block.

Direct Measurement of Conduction Velocity in In situ Specialized Conducting System of Mammalian Heart.

Summary By use of a pump-oxygenator and cardiopulmonary bypass, bipolar electro-grams have been recorded under direct vision from the bundle of His, the right and left bundle branches and peripheral Purkinje system of dog hearts. Conduction velocity from the bundle of His to bundle branches is 1.0-1.5 m/sec, while in the false tendons this value is 3-4 m/sec at 36°C.

Activation of subendocardial Purkinje fibers and muscle fibers of the left septal surface before and after left bundle branch block

Abstract Through utilization of a technique developed in this laboratory it has been possible to study the sequence of activation of the Purkinje fibers and muscle fibers beneath the endocardium of the left interventricular septal surface at the same 21 specific points before and after left bundle branch block (LBBB). It has been demonstrated that activation of the Purkinje system (P) at a specific point on the septum precedes that of the adjacent muscle fibers both before and after LBBB. It is concluded, therefore, that activation of the muscle fibers of the left septal surface is a direct result of excitation spreading to these fibers from the subendocardial Purkinje network both before and after LBBB. After LBBB the time required for complete activation of the left septal surface is considerably less than the control value; this finding is consistent with the concept that, after LBBB, activity spreads within the homolateral subendocardial Purkinje system, which has been activated simultaneously at multiple points, and then spreads to the adjacent muscle fibers of the left septal surface. Representative recordings from all points on the specialized conducting system (SCS) have been presented, including bipolar electrograms from the bundle of His (BH), right bundle branch (RBB), right Purkinje-papillary junction (RPPJ), free-running Purkinje fibers which extend from the base of the right anterior papillary muscle to the endocardium of the wall of the right ventricle (FRP), left bundle branch (LBB), anterior false tendon of the left ventricle (AFT), left anterior Purkinje-papillary junction (LAPPJ), and peripheral Purkinje fibers of the left septal surface at multiple sites (P). In order to facilitate the orderly presentation of data, a system of nomenclature based on the abbreviation for each of the anatomic points from which electrical potentials are recorded has been suggested for use in studying the specialized conducting system (SCS) of the heart.

Role of the Sympathetic Nervous System in the Sinus Node Resistance to High Potassium

The resistance of sinus node automaticity to high potassium (K) levels was studied in anesthetized dogs by perfusing the sinus node artery with oxygenated Tyrodes solution containing different K concentrations. The following results were obtained. (1) Sinus node automaticity persisted at a K concentration of 21.6 mM, although the pacemaker site tended to shift in and out of the node at this concentration. (2) Sinus node dominance at high K concentrations was progressively lost as sympathetic influences were progressively eliminated. (3) Sinus node pacemaker activity was suppressed at a K concentration lower than 21.6 mM when calcium was omitted from the perfusion fluid. (4) The pacemaker site shifted consistently from the sinus node towards the atrioventricular node at high K concentrations after the elimination of sympathetic activity (5) The transient sinus tachycardia caused by high K concentrations persisted after bilateral vagotomy. It is concluded that catecholamines participate in the resistance of the sinus node to K, suggesting that the difference in resistance to high K concentrations between the sinus node and Purkinje fibers may, in part, result from the more abundant innervation of the sinus node.