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Biomedical subjects

C W Balke

Publications and source records attributed to C W Balke.

49 records · Page 3Linked to original sources
PubMed1988

Differential effects of procainamide, lidocaine and acetylstrophanthidin on body surface potentials and epicardial conduction in dogs with chronic myocardial infarction.

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecting the more subtle effects on conduction caused by lidocaine and acetylstrophanthidin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Interaction of metoprolol and lidocaine on the ventricular fibrillation threshold in the anesthetized dog.

In the present study, we evaluated the antiarrhythmic interaction (s) of metoprolol and lidocaine in 16 dogs using the ventricular fibrillation threshold (VFT) method. The right ventricle was stimulated with a 100 Hz train of 12.4 ms pulses delivered after every eighth atrial paced beat at a basic cycle length of 300 ms. Lidocaine dosage was 2 mg/kg followed by a 70 micrograms/kg/min infusion and metoprolol dosage was a 75 micrograms/kg bolus. In Group 1, lidocaine was followed by metoprolol; in Group 2, first lidocaine then metoprolol and again lidocaine were given; and in Group 3, dogs received first metoprolol, then lidocaine, and subsequently metoprolol. Drug dose intervals were 45 min. In Group 1, lidocaine elevated the VFT to 149% +/- 20% and metoprolol to 204% +/- 30% of control, (p less than 0.01). In group 2, the VFT remained elevated after the second lidocaine administration (p less than 0.05 vs. Group 1). In Group 3, the VFT was increased by metoprolol to 227% +/- 30% of control (p less than 0.01). Interestingly, defibrillation induced by the combination of metoprolol and lidocaine occurred after 3.2 +/- 0.5 s in four out of 16 animals (p less than 0.05). This "chemical" defibrillation never occurred when only metoprolol or lidocaine alone was administered. Fibrillation was often more organized in the presence of the combination of metoprolol plus lidocaine, which might relate to the observed defibrillation associated with metoprolol plus lidocaine. In conclusion, the combination of metoprolol and lidocaine has no proarrhythmic effects and may enhance the electrical stability of the ventricles as measured by the VFT method.

Anesthesia↗
PubMed1988

Mechanisms of depressed conduction from long-term amiodarone therapy in canine myocardium.

Amiodarone therapy leads to a significant impairment in myocardial conduction, yet it causes only a modest decrease in the maximum rate of depolarization of the action potential (dV/dT). To determine whether the decrease in dV/dT solely accounts for the impaired myocardial conduction or whether passive membrane properties may also be involved, we studied 21 ventricular epicardial tissues from 14 beagles; six dogs received long-term treatment (3-6 weeks) of amiodarone orally, and the remaining dogs served as controls. Amiodarone therapy was associated with a decrease in conduction velocity (0.41 +/- 0.15 vs. 0.56 +/- 0.05 m/sec; p less than 0.01). There was a trend toward a decrease in dV/dT and a significant decrease in the space constant (0.69 +/- 0.27 vs. 1.05 +/- 0.25 mm; p = 0.01), of which the latter correlated closely with the decrease in conduction velocity measured in the amiodarone-treated tissues (r = 0.85, p less than 0.05). These data indicate that the decrease in myocardial conduction velocity caused by amiodarone is primarily due to effects on overall resistance to passive current flow rather than effects on the inward sodium current.

Action Potentials↗
PubMed1988

Interaction of fiber orientation and direction of impulse propagation with anatomic barriers in anisotropic canine myocardium.

We developed a computer model of the interaction of impulse propagation with anatomic barriers in uniformly anisotropic tissue. Its predictions were confirmed experimentally by using an in vitro cut to create a 6 X 1-mm anatomic barrier in 12 canine epicardial strips. The model predicted that long, thin barriers located parallel to the direction of impulse propagation would have little effect in delaying conduction regardless of the arrangement of cardiac fibers. In this situation, the mean experimental ratio of postcut to control conduction times across the barrier was 1.05:1.00 in 10 tissues. When impulses were proceeding perpendicular to an anatomic barrier, significant distal conduction delay was predicted and found to occur only when the conduction from pacing to recording sites was initially longitudinal to fiber orientation (mean experimental ratio, 2.34:1.00 in five tissues) but not transverse to fiber orientation (ratio, 1.08:1.00 in five tissues). We conclude that the direction of initial impulse propagation and the orientation of myocardial fibers have large effects on the degree to which anatomic barriers delay activation in cardiac tissue. These findings may have implications for the participation of anatomic barriers in reentrant circuits.

Animals↗
PubMed1988

Effects of cellular uncoupling on conduction in anisotropic canine ventricular myocardium.

Experiments were performed on canine superfused ventricular epicardial tissue slices to determine the effects of 1.0-2.0 mM heptanol, an uncoupling agent, on conduction longitudinal and transverse to myocardial fiber orientation. Conduction velocities were measured between proximal and distal pairs of epicardial electrodes oriented transverse and longitudinal to the direction of a conducted wavefront evoked by pacing at a basic cycle length of 2,000 msec from one margin of the tissue before and after the addition of heptanol. In a separate group of tissues, the dual bipolar orthogonal electrode was used to sequentially map epicardial activation at 40 to 45 sites in a 1 cm x 2 cm area before and 30 minutes after the introduction of heptanol. In a third group of tissues, transmembrane potentials were recorded with standard microelectrode techniques to determine the effects of heptanol on action potential characteristics. Heptanol did not significantly effect action potential amplitude or maximum rate of depolarization. After 1.0 mM heptanol, conduction velocity began to decrease in 1-2 minutes and reached a steady state in 15-20 minutes. Conduction velocity in the longitudinal direction decreased from a control value of 0.56 +/- 0.13 to 0.46 +/- 0.10 M/sec (+/- SD) at 30 minutes after heptanol (p = 0.005). In the transverse direction, it decreased from 0.24 +/- 0.09 to 0.17 +/- 0.05 M/sec (p = 0.002). The ratio of longitudinal to transverse conduction velocities increased from 2.54 +/- 1.00 to 2.94 +/- 0.82 (p = 0.042). Thus, heptanol preferentially slowed conduction in the transverse direction. Because heptanol did not greatly influence active membrane properties, we used cable equations to calculate the time course of the change in effective junctional resistivity, which rose from 133.2 omega.cm before heptanol to 312.2 omega.cm 30 minutes after heptanol administration. We conclude that heptanol slows conduction velocity by selectively increasing junctional resistivity. The preferential slowing of conduction in the transverse direction is most likely due to the fact that more junctional resistances are encountered per unit distance in the transverse than in the longitudinal direction.

Action Potentials↗
PubMed1987

Comparison of amplitude-modulated (direct) and frequency-modulated ambulatory techniques for recording ischemic electrocardiographic changes.

Continuous ambulatory electrocardiographic monitoring of ST-segment configuration has become a useful technique for evaluation of myocardial ischemia. Concern that direct or amplitude-modulated (AM) recording and playback systems have inherent limitations that cause inaccurate ST-segment recordings has led to preference for frequency-modulated (FM) devices. To determine the accuracy of AM and FM ambulatory electrocardiographic systems, the signal was compared from the same set of 2 bipolar leads simultaneously recorded by standard electrocardiography and AM and FM recorders in 14 patients during treadmill exercise. Also, simultaneous AM and FM recorders were compared in 9 ambulatory patients in 16 monitoring sessions. The AM recording system accurately reproduced ST segments recorded during treadmill exercise (range 4.0 mm of ST-segment depression to 2.0 mm of ST elevation) when measured at the J point (r = 0.91, p less than 0.0001), and 0.08 second after the J point (r = 0.95, p less than 0.0001). FM recording was equally accurate (r = 0.89 and 0.95, respectively, p less than 0.0001). Similarly, during ambulatory recording, the AM technique accurately recorded maximal ST depression in each episode as recorded by the FM device (28 episodes, range 0 to 3 mm of ST depression, r = 0.85, p less than 0.0001). Both AM and FM ambulatory electrocardiographic systems can accurately reproduce ST-segment deviation associated with ischemia and can be used to monitor transient ST-segment changes in patients with coronary artery disease.

Ambulatory Care↗
PubMed1987

Malnutrition among hospitalized patients. A problem of physician awareness.

Between 25% and 50% of patients admitted to an acute medical service are malnourished. Physicians are often unaware which patients are admitted at nutritional risk and make no attempt to arrest further nutritional decline until a dramatic deterioration has occurred. We studied all patients admitted to an acute medical ward service before and after their physicians were taught to recognize nutritional deficiency early and to intervene appropriately. During the initial period, the house staff correctly identified two (12.5%) of 16 patients as being malnourished. During the posteducation period, physicians correctly identified all 14 patients admitted at nutritional risk (100%), using a simple screening device that required only routine admission data. In all cases, the appropriate nutritional intervention was subsequently made. Results were further validated using a pretest and posttest, showing a significant improvement in nutritional knowledge. We conclude that physicians are not presently being taught to recognize malnutrition, that such malnutrition is latrogenically worsened in the hospital, and that physician education can effectively correct this problem.

Clinical Competence↗
PubMed1981

Reperfusion ventricular tachyarrhythmias: correlation with antecedent coronary artery occlusion tachyarrhythmias and duration of myocardial ischemia.

The incidence and severity of reperfusion ventricular tachyarrhythmias were correlated with : (1) the duration of antecedent acute coronary artery occlusion and (2) the incidence, severity, and time course of ventricular tachyarrhythmias occurring during the antecedent period of coronary occlusion in 98 dogs studied postligation for 5 to 60 minutes. The incidence of reperfusion ventricular fibrillation (VF) increased significantly as coronary artery ligation periods were lengthened from 5 minutes to either 20 minutes (2 of 19 dogs vs 12 of 18 dogs, p less than 0.001) or 30 minutes (16 of 24, p less than 0.001), but notably decreased when reperfusion was delayed further from 30 minutes to 60 minutes after coronary artery ligation (4 of 18 dogs, p less than 0.001). Seven dogs were resuscitated from VF during coronary ligation and all seven suffered VF on reperfusion, whereas 37 dogs were arrhythmia-free during ligation and only one (3%, p less than 0.001) had VF on reperfusion. In addition, reperfusion ventricular tachyarrhythmias correlated with the occurrence of both immediate ventricular tachyarrhythmias (those peaking at 5 to 6 minutes postligation) and delayed ventricular tachyarrhythmias (those peaking at 18 minutes' postligation) of the antecedent acute ligation period. These observations provide a further basis for improved clinical understanding and management of potentially malignant tachyarrhythmias consequent to early myocardial reperfusion following acute myocardial ischemia and infarction.

Animals↗
PubMed1980

Intramyocardial activation in early ventricular arrhythmias following coronary artery ligation.

Subendocardial, subepicardial and intramyocardial activation in the ischemic zone was investigated in 20 anesthetized open chest dogs 0-30 minutes after the ligation of the left anterior descending coronary artery. Single and composite electrograms and lead 2 of the ECG were recorded. Coronary artery ligation produced marked delay, fragmentation, and reduction in amplitude in the electrical activity of the subepicardial and intramyocardial muscle layers. The activation remained synchronous in the subendocardial muscle layers. Extension of electrical activity in the ischemic subepicardium and intramyocardium beyond the T wave of the surface ECG preceded the onset of immediate ventricular arrhythmias (IVA) during the initial ten minute period after coronary artery ligation. However, a second surge of delayed ventricular arrhythmias (DVA), 10-30 minutes after ligation, was not associated with the appearance of diastolic electrical activity in any of the subepicardial or myocardial layers. It appears that subepicardial as well as intramyocardial reentry could play an important role in the genesis of the immediate ventricular arrhythmias (1-10 minutes after ligation). In contrast, no obvious reentrant activity as evidenced by delayed and fragmented electrical activity could be observed in the electrogram from any of the myocardial electrical activity could be observed in the electrogram from any of the myocardial layers with the appearance of delayed ventricular ectopic activity 10-30 minutes after ligation.

Animals↗
PubMed1979

Two periods of early ventricular arrhythmia in the canine acute myocardial infarction model.

The time course of ventricular arrhythmias in the early period (0--30 minutes) after ligation of the left anterior descending coronary artery was studied in 41 open-chest mongrel dogs anesthetized with pentobarbital sodium (Nembutal). ECGs and seven single and composite electrograms from various regions in and around the ischemic zone were recorded throughout the experiments. Two periods of ventricular arrhythmias were clearly seen. The first occurred 2--10 minutes after coronary ligation, peaking at 5--6 minutes, and was designated as immediate ventricular arrhythmias (IVAs). There was a distinct correlation between incidence, severity, onset and termination of IVA and the degree of local delay and fragmentation of the normal sinus activation spread in the ischemic subepicardial zone. The second wave of ventricular arrhythmias occurred 12--30 minutes after ligation independently of the previous increased delay and fragmentation of activation in the ischemic subepicardium. Delayed ventricular arrhythmias (DVAs) were as severe as IVAs--there were nine instances of ventricular fibrillation during DVA and seven during IVA. While the mechanism of IVA is most probably related to reentry accompanied by delay and fragmentation of ischemic subepicardial activation, the mechanism of DVA remains unclear. Our evidence suggests that DVAs are also reentrant, with the reentry pathways located in deep myocardial structures or involving microscopic pathways at the Purkinje muscle junction.

Acute Disease↗