Simultaneous right atrial appendage sensing with a target tip, a solid tip and J orthogonal electrodes.

To compare the sensing characteristics of a solid tip, target tip (Medtronic) and orthogonal electrodes within the right atrial appendage, atrial electrograms were simultaneously recorded from 2 pacing leads in 11 patients. No significant differences were noted between atrial electrograms derived from target tip or a solid tip electrode in contact with atrial myocardium. Mean values for P-wave amplitudes of 3.0 vs 3.1 mV and slew rates 0.4 V/s vs 0.6 V/s, and QRS amplitudes of 1.0 vs 1.2 mV and slew rates 0.4 vs 0.2 V/s were obtained. The frequency content was also similar, with spectral maxima at 8 vs 9 Hz (P wave) and 7 vs 6 Hz (QRS). In contrast, atrial electrocardiograms derived from the orthogonal electrodes were significantly different: P-wave amplitude of 6.1 mV (p less than 0.025) and slew rate of 1 V/s and QRS of 0.13 mV and slew rate of 0.04 V/s. Spectral analysis was also dissimilar with maxima at 34 Hz (P wave) and 3 Hz (QRS). Orthogonal noncontacting sensing electrodes positioned within the atrial appendage offer substantially better electrographic P-wave amplitude detection and QRS rejection than contacting tip electrodes. These leads yield a significant improvement when discriminate atrial sensing is required.

Sensing and pacing with floating electrodes in the right atrium and right atrial appendage.

Unipolar and bipolar floating atrial electrograms from 58 pacemaker patients were recorded and compared. Twenty-four floating unipolar electrodes and 29 floating bipolar electrodes were used at mid-right atrial level and five orthogonal atrial J leads within the right atrial appendage. Each signal was analyzed in the time domain: peak to peak deflection of P wave and QRS complex, duration of P wave and QRS complex and slew rate; and in the frequency domain: maximum of the energy spectrum and frequency at which a decrease of 3 dB from the maximal amplitude occurred. Atrial P (1.31 +/- 0.94 mV, mean +/- SD) and QRS (1.0 +/- 0.56 mV) waves from unipolar floating electrodes were comparable, whereas they were significantly different from bipolar floating electrodes (1.15 +/- 0.77 mV and 0.25 +/- 0.39 mV). Amplitudes of P waves from orthogonal J leads were largest (3.1 +/- 2.6 mV) and QRS complexes (0.21 +/- 0.13 mV) smallest. The P waves had the highest frequency content (17.1 +/- 19.4 Hz). It is concluded that atrial electrograms from orthogonal electrodes (bipolar or orthogonal J) offer superior sensing characteristics because of the large amplitude P wave and discriminating power between P and QRS waves (P/QRS voltage 15:1). An orthogonal J lead can thus be used for P synchronous pacing at the atrial level, whereas an orthogonal ventricular lead can be used for rate-response pacing systems.

Orthogonal atrial appendage sensing.

The characteristics of electrograms derived from a solid platinum-iridium pacing catheter tip in contact with the right atrial appendage are compared to those derived from a Target-tip electrode. Both are then compared to electrograms from two noncontacting orthogonal electrodes positioned more proximally within the atrial appendage. Wave form morphology and spectral energy distribution were determined for the three sets of electrograms. It is concluded that orthogonal electrodes placed within the atrial appendage may offer enhanced atrial sensing required by more sophisticated pacemakers.

Clinical and induced ventricular tachycardia in a patient with myotonic dystrophy.

A 20 year old patient with myotonic dystrophy presented with hemodynamically significant ventricular tachycardia at a rate of 230 beats/min requiring cardioversion. Two days later, the identical tachycardia was reproducibly initiated and terminated in the electrophysiology laboratory using two extrastimuli in the right ventricle. Trials of procainamide and quinidine were not successful in controlling the induced rhythm and amiodarone was administered. On restudy with amiodarone, ventricular fibrillation was induced using a single extrastimulus. This case suggests that ventricular tachyarrhythmias may contribute to the known cardiac morbidity and mortality in myotonic dystrophy.

Orthogonal ventricular electrogram sensing.

Inappropriate demand pacing is most commonly due to improper ventricular electrogram sensing. Filters and programmable sensitivities improve electrogram sensing of conducted beats, but paced electrograms cannot be sensed by conventional unipolar or bipolar systems. A permanent pacing lead with a standard tip electrode and three orthogonal 0.8 mm2 sensing electrodes located circumferentially 2 cm proximal to the pacing tip was tested in 22 patients. The tip electrode was placed in the right ventricular apex in standard pacing position. Orthogonal electrodes were not in contact with ventricular myocardium. Orthogonal ventricular electrograms from 54 electrode pairs were compared with unipolar tip electrograms during conducted rhythms and paced beats. Tip ventricular electrograms averaged 12.8 mV with 3.04 mVT waves. Orthogonally recorded ventricular electrograms during conducted beats averaged 8.86 mV with T waves of 1.57 mV. During pacing, tip ventricular electrograms were obscured by the stimulus artifact and repolarization events. Orthogonal ventricular electrograms, however, demonstrated small discrete stimuli of 1.99 mV followed by discrete ventricular electrograms of 9.19 mV and T waves of 1.9 mV. Orthogonal ventricular electrograms compared favorably with contacting tip electrograms during conducted beats and provided a redundant sensing capability. During pacing, orthogonal ventricular electrograms allowed the capability for capture verification. A new pacing catheter allows for improved ventricular electrogram sensing and capture verification.

Orthogonal electrogram sensing.

Intracardiac electrogram sensing is the afferent limb of demand pacing systems. Under- and over-sensing at the ventricular level has been demonstrated in almost 50% of implanted unipolar pulse generators, and atrial electrogram sensing problems are more common. A unique dedicated sensor employing noncontacting and circumferentially placed orthogonal electrodes was tested at both the atrial and ventricular levels. Electrograms demonstrated voltages similar to those recorded from contacting electrodes, but with complete far-field rejection of signals from the opposite chamber. Orthogonal electrograms allowed for activation sequencing and capture verification as well.

Lidocaine clinical pharmacokinetics.

A review of the clinical pharmacokinetics of lidocaine is presented. Available evidence suggests that antiarrhythmic effects are reasonably well correlated wih plasma concentration. Adverse effects also covary with plasma concentration, but available evidence suggests that the correlation is not strong. A simple, multiple-bolus loading schedule appears to be superior to techniques using loading infusions; most of the multiple-bolus protocols mandate that only enough drug be given to attain the desired pharmacologic effect. In contrast, the loading infusion protocols almost invariably require the administration of a fixed dose, regardless of what fraction of the dose has been given when arrhythmia suppression is achieved. Since multiple-bolus and constant-rate infusion techniques have been shown to reduce substantially the incidence of primary ventricular fibrillation, they should be considered appropriate prophylactic and treatment regimens for acute myocardial infarction patients.

A new orthogonal lead for P synchronous pacing.

P synchronous pacing has long been identified as advantageous for patients with atrioventricular conduction defects and intact sinus node function. Prior endocavitary systems have been infrequently employed, because of unreliable P wave sensing from standard ring electrodes in the atrium or the requirement for a second atrial sensing lead. A single endocardial lead employing a unipolar ventricular stimulating electrode and an orthogonal P wave sensing design was developed and tested in 22 patients undergoing electrophysiologic study or pacemaker implantation. Thirteen centimeters from the stimulating tip of a standard permanent pacing lead, three or four electrodes with a surface area of one millimeter squared, equidistant from the tip, were placed circumferentially about the catheter. With the catheter tip normally placed in the right ventricular apex, atrial sensing electrodes were positioned in the mid-high lateral right atrium, adjacent to, but not affixed to, the right atrial wall. Bipolar orthogonal leads X and Y were obtained. In 22 patients, during sinus rhythm, atrial electrogram voltages in the X axis of 2.47 plus or minus 1.6 millivolts and 2.32 plus or minus 1.6 millivolts in the Y axis were recorded. QRS voltages of 0.078 millivolts and 0.073 millivolts, respectively, allowed dramatic ability to discriminate P from QRS complexes (P/QRS equals 32/1). There was no change in QRS or unipolar ventricular pacing. A single catheter designed for P synchronous pacing employing circumferentially placed atrial sensing electrodes has demonstrated unique atrial sensing voltages with excellent QRS signal rejection.

Factors influencing serum protein binding of lidocaine in humans.

Several factors that may affect protein binding of lidocaine in human serum were studied in normal volunteers. Evidence was obtained for the presence of two classes of lidocaine binding sites with strikingly different affinity constants (k) and capacities (nP); k1 equals 1.3 x 10(5)M(-1), n1P1 equals 1.7 x 10(-5)M, and k2 equals 6.4 x 10(1)M(-1), n2P2 equals 6.9 x 10(-3)M. The low affinity binding sites are probably on serum albumin, whereas the high affinity site may be located on alpha 1 acid glycoprotein. At a lidocaine serum concentration of approximately 1.4 microgram/ml, it was observed that acidosis (pH 7.4 leads to 7.2) caused lidocaine-free fraction to increase from 0.29 to 0.36 (p less than 0.01) and that the addition of the lidocaine metabolites 3-hydroxylidocaine, 4-hydroxylidocaine, monoethylglycinexylidide, and glycinexylidide had no effect on the binding of lidocaine. Bupivacaine, disopyramide, and quinidine (in concentrations that are observed clinically) caused a significant increase (p less than 0.01) in the free fraction of lidocaine in serum (23%, 21%, and 34%, respectively. Interestingly, N-depropyl disopyramide, dihydroquinidine, procainamide, N-acetyl procainamide, and propranolol had no effect on lidocaine binding.

Factors influencing procainamide total body clearance in the immediate postmyocardial infarction period.

Fifteen acute myocardial infarction patients (only one of whom had evidence of significant renal dysfunction) received a constant-rate intravenous infusion of procainamide at one rate for a least 24 hours. Steady-state plasma levels achieved during these infusions were used to calculate total body clearance (C/B). Linear regression analysis of C/B versus a variety of clinical and laboratory patient characteristics yielded only body weight (or parameters derived from it) as a significant covariant (r = 0.713, P less than or equal to 0.005). Interestingly, the data from these 15 patients suggest that the presence of a significant degree of heart failure at the start of therapy did not result in a significant decrease in C/B (C/B = 5.9 ml/min/kg when class 0-I failure was present at the start of therapy and C/B = 5.5 ml/min/kg when class III-IV failure was present). If the data from five other patients who were studied previously are added to the group reported here, the conclusions reached would be the same. These data suggest that in patients with good renal and hepatic function, initial procainamide infusion rate could be selected on the basis of body weight and need not consider the initial presence of moderate heart failure. However, intense clinical monitoring for signs of impeding serious toxicity is strongly recommended since the observed regression line did not predict total body clearance accurately in 10-15 per cent of the patients studied.

Initial ventricular activation in left-sided intraventricular conduction defects.

Nine patients with ECG evidence of rate-related left bundle branch block (LBBB) were studied using His bundle electrograms, electrograms from the right ventricular (RV) apex and vectorcardiograms recorded as heart rate was increased to produce LBBB. In five patients, when LBBB occurred, initially normal septal activation reversed and the HV intervals increased 10-30 msec, while the H-RVA interval did not change (group 1). Four patients had initially normal QRS duration (90-100 msec) but reversed septal activation (group 2). When LBBB developed there was no shift in either the HV interval or H-RVA interval. Only the QRS complex itself widened to distinguish these patients from group 1. These studies defined ventricular septal activation in normal conduction and in complete LBBB (group 1) and incomplete LBBB (group 2). The conduction patterns of group 1 and 2 patients are similar but are both markedly different from normal.

Procainamide accumulation kinetics in the immediate postmyocardial infarction period.

The rate of change of plasma procainamide concentration during 36 hours of constant-rate intravenous infusion was examined in five acute myocardial infarction patients. It was observed that a steady-state plasma concentration was established in about 16 hours, which is consistent with simulations of plasma concentrations based on pharmacokinetic constants obtained from studies in young healthy volunteers. However, the steady-state level that was attained in these patients was markedly higher than that which the simulations predicted. Thus, on the average, acute myocardial infarction patients have lower total body clearances of procainamide than normal volunteers.

Microdetermination of procainamide in human serum.

An electron-capture GLC method to measure procainamide (0.1-1 microgram/sample) in human serum was developed. An internal standard, p-amino-N-[2-(dipropylamino)ethyl]benzamide, is added to the serum before the sample is alkalinized with pH 10.5 phosphate buffer and extracted with ethyl acetate. The ethyl acetate phase is evaporated to dryness, and the residue is reacted with pentafluoropropionic anhydride. N-Pentafluoropropionyl derivatives of the drug and the internal standard had retention times of 5 and 8 min, respectively, when chromatographed at 235 degrees on a 1-m (4-mm i.d.) glass column packed with 5% OV-17 (carrier gas flow of 40 ml/min). The coefficient of variation was less than 5% for spiked standards. Furthermore, N-acetylprocainamide added to samples did not interfere. One hundred and eighty-six samples from 16 patients receiving procainamide intravenously were assayed by this GLC procedure and by a standard colorimetric method. Linear regression analysis yielded a correlation coefficient of 0.985 (slope, 1.040; intercept, 0.015).