Bipolar Electrogram Amplitude Research Articles

Are the Cardiovascular Effects of Gentamicin Similar to Those of Calcium Antagonists?

Cardiac and coronary vasodilator effects of gentamicin (GM) were investigated in isolated, blood-perfused papillary muscle, sino-atrial (SA) node and atrioventricular (AV) node preparations of dogs. GM (0.3-100 μmol) was injected intraarterially. GM produced an increase in coronary blood flow in all preparations. In paced papillary muscle preparations, GM reduced the force of contraction. In spontaneously beating papillary muscle preparations, GM decreased the rate of . automaticity and the force of contraction. In SA node preparations, GM decreased the sinus rate. In AV node preparations, GM injected into the posterior septal artery (which supplies the AV node) increased AV conduction time and in large doses, produced third-degree AV block. In the same preparations, GM in large doses injected into the anterior septal artery (which supplies the His-Purkinje-ventricular system) prolonged AV conduction time (i.e., intraventricular conduction time) and reduced the amplitude of ventricular bipolar electrograms. The order of potencies of GM on the above cardiovascular variables is as follows: Coronary blood flow≥ventricular muscle contraction>ventricular automaticity>SA nodal automaticity>AV nodal conduction>intraventricular conduction. This cardiovascular profile is different from those of organic calcium-antagonists, but rather similar to that of manganese ions, reflecting its own mechanism of action.

Are the cardiovascular effects of gentamicin similar to those of calcium antagonists?

Cardiac and coronary vasodilator effects of gentamicin (GM) were investigated in isolated, blood-perfused papillary muscle, sino-atrial (SA) node and atrioventricular (AV) node preparations of dogs. GM (0.3-100 mumol) was injected intraarterially. GM produced an increase in coronary blood flow in all preparations. In paced papillary muscle preparations, GM reduced the force of contraction. In spontaneously beating papillary muscle preparations, GM decreased the rate of automaticity and the force of contraction. In SA node preparations, GM decreased the sinus rate. In AV node preparations, GM injected into the posterior septal artery (which supplies the AV node) increased AV conduction time and in large doses, produced third-degree AV block. In the same preparations, GM in large doses injected into the anterior septal artery (which supplies the His-Purkinje-ventricular system) prolonged AV conduction time (i.e., intraventricular conduction time) and reduced the amplitude of ventricular bipolar electrograms. The order of potencies of GM on the above cardiovascular variables is as follows: Coronary blood flow greater than or equal to ventricular muscle contraction greater than ventricular automaticity greater than SA nodal automaticity greater than AV nodal conduction greater than intraventricular conduction. This cardiovascular profile is different from those of organic calcium-antagonists, but rather similar to that of manganese ions, reflecting its own mechanism of action.

Cardiovascular profile of AN-132, a new diamine derivative antiarrhythmic agent, revealed in the isolated, blood-perfused dog heart.

The cardiac and coronary effects of AN-132, a new antiarrhythmic agent, were investigated in isolated, blood-perfused atrioventricular (AV) node, sinoatrial (SA) node and papillary muscle preparations of dogs. AN-132 was administered intraarterially. In AV node preparations, whether injected into the anterior septal artery (ASA; supplying the His-Purkinje-ventricular system) or the posterior septal artery (PSA; supplying the AV node), AN-132 prolonged AV conduction time and produced second- or third-degree AV block at large doses in some preparations. Moreover, only when injected into the ASA AN-132 produced a broadening and diminution of amplitude of bipolar electrograms obtained from the right bundle branch and the ventricular septum. In SA node preparations, AN-132 decreased sinus rate and produced atrial standstill at large doses in some preparations. In paced papillary muscle preparations, AN-132 reduced the force of contraction. In spontaneously beating papillary muscle preparations, AN-132 decreased the rate of automaticity and the force of contraction. In all preparations, AN-132 produced a transient increase in blood flow only at large doses. The order of potencies of AN-132 based on the doses that produced 15% suppressions of the above cardiovascular variables was as follows: cardiac muscle contraction greater than ventricular automaticity greater than or equal to intraventricular conduction greater than AV nodal conduction greater than or equal to coronary blood flow greater than SA nodal automaticity.

Failure of the automatic implantable defibrillator to detect ventricular fibrillation

Some of the reported problems with the use of the automatic implantable defibrillator (AID) include inappropriate discharge, 1–3 failure to defibrillate because of excessively high defibrillation thresholds 3–5 and failure to sense ventricular fibrillation (VF) in patients who also have pacemakers. 1,2 In this report, we describe another potential problem: the failure of an AID to sense VF because of variable bipolar epicardial electrogram amplitudes during VF.

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.

Transesophageal atrial pacing threshold: Role of interelectrode spacing, pulse width and catheter insertion depth

This study evaluated the role of interelectrode spacing, pulse widths > 10 ms, and depth of esophageal insertion on minimizing transesophageal atrial pacing threshold in 30 patients aged 1 day to 77 years. Interelectrode spacings of 15, 22 and 28 mm were evaluated by establishing strength-duration curves in 2 or more serial studies in 12 patients; electrode spacing had no effect on pacing threshold. In 23 patients studied with 22-mm electrode spacing, pulse widths of 15 and 20 ms had no significant effect on current threshold requirements compared with 10-ms pulse widths. In 20 patients, pacing threshold and esophageal electrograms were obtained at 1.0- to 2.5-cm intervals with a 22-mm lead using a pulse width of 10 ms. Average minimal pacing threshold was 10.2 mA (range 4.5 to 20). The site of minimal pacing threshold was highly correlated with patient height (r = 0.987), and occurred within 1.1 cm (0 to 2.5 cm) of the site of the maximal bipolar atrial electrogram amplitude and 0.95 cm (0 to 3 cm) of the site of the maximal unipolar atrial electrogram. Bipolar electrode spacing of 15, 22 or 28 mm has little effect on transesophageal pacing threshold. In most patients, pulse widths > 10 ms do not significantly decrease pacing threshold. Correct catheter insertion depth is critical to minimize pacing threshold and may be predicted by either the site of the maximal atrial electrogram amplitude or patient height.

Effect of ethanol on electrogram changes and regional myocardial blood flow during acute myocardial ischaemia.

Acute occlusion of the left anterior descending coronary artery in dogs produced delayed conduction and diminished amplitude of bipolar electrograms recorded from ischaemic zones. Intravenous infusion of ethanol (1.2 g . kg-1), before coronary artery occlusion, delayed conduction and reduced the amplitude of electrograms recorded in normal myocardium, but attenuated ischaemia-induced electrogram changes produced by the subsequent occlusion. Ethanol (0.6 g . kg-1 iv) did not significantly alter activation of electrograms recorded from normal myocardium, but reduced ischaemia-induced electrogram changes and decreased the incidence of ventricular fibrillation elicited by rapid ventricular pacing from five of eight to one of eight dogs. Infusion of 10 or 30% (V/V) ethanol directly into a non-occluded coronary artery significantly increased conduction time and reduced electrogram amplitude recorded in the epicardium perfused by that coronary artery. These effects were more pronounced when ethanol was infused into an occluded coronary artery distal to the site of occlusion. Ethanol did not alter regional myocardial blood flow determined by labelled microspheres during ischaemia. Thus, despite a direct depressant effect on extracellular electrical activity recorded from normal and ischaemic myocardium, ethanol reduced the severity of ischaemia-induced electrogram alterations and decreased the incidence of ventricular fibrillation when given intravenously prior to coronary artery occlusion.

Inhibition of excitation-contraction coupling in the ventricular myocardium of the dog by SKF 24260.

1. The effects of SKF 24260 on the coronary vasculature and on the electrical and mechanical activities of the ventricular myocardium were studied by the use of papillary muscle preparations of the dog. The preparation was cross-circulated from a donor dog through the anterior septal artery, and driven at a rate of 120 beats/min. Drugs were injected into the anterior septal artery. 2. SKF 24260, in doses of 0-01-100 mug, caused a dose-dependent increase in the rate of blood flow through the anterior septal artery; the mean dose producing a 100% increase in blood flow rate was about 0-7 mug. 3. SKF 24260 in doses of 0-01-0-03 mug produced a slight increase in developed tension of papillary muscles. With 0-1-0-3 mug of SKF 24260 the increase was preceded by a transient decrease, and with doses larger than 1 mug the drug caused a dose-dependent decrease. The mean dose producing a 50% decrease in developed tension was about 2-8 mug. 4. SKF 24260 failed to affect the amplitude and shape of bipolar electrograms even in doses of 39-100 mug which completely abolished the developed tension. 5. The decrease in the developed tension caused by SKF 24260 was overcome by exogenous calcium; the increase in the developed tension in response to exogenous calcium was antagonized by SKF 24260. 6. These results indicate that the dilator action of SKF 24260 on the coronary vasculature is more prominent than the negative inotropic action on the ventricular myocardium, and suggest that the negative inotropic action is probably due to antagonism of the role of calcium in excitation-contraction coupling.