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D L Rollins

Publications and source records attributed to D L Rollins.

At least 19 recordsLinked to original sources
PubMed1998

Locally propagated activation immediately after internal defibrillation.

BACKGROUND: Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS: In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS: LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.

Animals↗
PubMed1997

Effects of transvenous electrode polarity and waveform duration on the relationship between defibrillation threshold and upper limit of vulnerability.

BACKGROUND: The upper limit of vulnerability (ULV) hypothesis for defibrillation predicts that maneuvers that alter the ULV will cause a similar alteration in the defibrillation threshold (DFT). The purpose of this study was to test this prediction by evaluating the effects of electrode polarity and waveform duration on the relationship between the DFT and the ULV. METHODS AND RESULTS: Platinum spring electrodes were placed in the right ventricular (RV) apex and the superior vena cava in 12 pigs. Strength-duration curves were constructed for the DFT and ULV for each electrode polarity with monophasic waveforms (6 pigs) of different durations (2 to 14 ms) and biphasic truncated exponential waveforms (6 pigs) having phase 1 equal to 4 ms and phase 2 of different durations (0 to 10 ms). ULV data were gathered by scanning of the T wave. The ventricular pacing threshold (VPT) and ventricular fibrillation threshold (VFT) were also determined with these same waveforms. For the RV electrode as a cathode for monophasic and the first phase of biphasic stimuli, VPTs for the same waveform duration were significantly lower than for the configuration with the RV electrode as an anode. VFTs were not significantly different for the two electrode polarities with either monophasic or biphasic waveforms. The DFT changed in a fashion similar to the ULV with changes in electrode polarity and phase duration for both monophasic and biphasic waveforms. The ULV and DFT for each waveform duration for each polarity were strongly correlated (r=.83 to .99). CONCLUSIONS: The almost identical changes in ULV and DFT with changes in electrode polarity and waveform duration provide new evidence to support the ULV hypothesis of defibrillation.

Animals↗
PubMed1996

Effect of changing capacitors between phases of a biphasic defibrillation shock.

BACKGROUND: In this study, we examined the effect of changing capacitor values between phases of a biphasic waveform with the goal of lowering leading edge voltage (LEV), total delivered energy (TDE), and total stored energy (TSE). METHODS: Defibrillation thresholds were determined in 18 open-chest swine using epicardial patch electrodes. In part I, three combinations of capacitors were tested: 150:150 microF; 150:300 microF; and 300:150 microF. Waveform durations were 6/0, 6/2, 6/4, 6/6, and 6/8 ms. In part II, phase 1 capacitance was 150 microF. Three phase 2 capacitance values were used: 150 microF; 75 microF; and 37.5 microF. Phase 2 LEV was a multiple of phase 1 trailing edge voltage: x 0.5; x 0.75; x 1; x 2; x 3; and x 4. A 3.5/2.0 ms biphasic waveform was used. In part III, thresholds were determined for two sets of capacitor values, which can be created by switching a pair of capacitors from in parallel to in series, 150:37.5 microF and 300:75 microF, and nine waveform durations, 4/0, 4/2, 4/4, 6/0, 6/3, 6/6, 8/0, 8/4 and 8/8 ms. RESULTS: In part I, the 300:150 microF system defibrillated with the lowest LEV, TDE and TSE were not different for any of the biphasic waveforms tested except for the 6/8 ms, which was higher. In part II, there was no difference in LEV among any of the three phase 2 capacitor values. LEV was lowest for the x 2, x 3, x 4 multipliers. Peak voltage was lowest for the x 1 and x 2 multipliers. TDE was lowest for the x 0.5, x 0.75, x 1, and x 2 multipliers. In part III, the 300:75 microF system defibrillated at a lower LEV than did the 150:37.5 microF system. The 150:37.5 microF system defibrillated at a lower total delivered energy than did the 300:75 microF. CONCLUSION: These results suggest that defibrillation can be accomplished with lower LEV, TDE, and TSE if two capacitors are switched from a parallel configuration to a series configuration between phases of the biphasic waveform.

Animals↗
PubMed1996

Effects of polarity for monophasic and biphasic shocks on defibrillation efficacy with an endocardial system.

Electrode polarity has been reported to be one of the factors that affect defibrillation efficacy. We studied the influence of polarity on defibrillation efficacy when monophasic and biphasic waveforms were used with an endocardial lead system. In six anesthetized pigs, defibrillation catheters were placed in the right ventricular (RV) apex and at the junction of the superior vena cava (SVC) and right atrium. Monophasic shocks were 6 ms in duration, while for biphasic shocks the first phase was 6 ms and the second was 4 ms in duration. Four electrode configurations were tested: R:S, M (the RV electrode, cathode; the SVC electrode, anode, with a monophasic shock); S:R: S, B(the RV electrode, first phase cathode; the SVC electrode, first phase anode, with a biphasic shock); S:R, B. Defibrillation probability of success curves were determined using an up/down protocol requiring 15 shocks for each configuration. For monophasic shocks, total delivered energy at the 50% probability of success point was significantly lower when the RV electrode was an anode than when it was a cathode (R: S, M: 24.4 +/- 7.4 J [mean +/- SD] vs S:R, M: 16.4 +/- 5.5 J; P < 0.05). For biphasic shocks, total energy was not affected by polarity reversal of the electrodes (R:S, B: 8.7 +/- 1.4 J vs S:R, B: 8.4 +/- 2.5 J; P = NS). The endocardial electrode configuration with the RV electrode as an anode requires less energy for defibrillation with a monophasic but not a biphasic waveform.

Animals↗
PubMed1996

Epicardial sock mapping following monophasic and biphasic shocks of equal voltage with an endocardial lead system.

INTRODUCTION: The reason for the increased defibrillation efficacy of biphasic shocks over monophasic shock is not definitely known. METHODS AND RESULTS: In six anesthetized pigs, we mapped the epicardium after transvenous defibrillation shocks to compare the activation patterns following successful biphasic shocks with unsuccessful monophasic shocks of the same voltage. The heart was exposed and a 510-electrode sock with approximately 4-mm interelectrode spacing was pulled over the entire ventricular epicardium and sutured to the pericardium. Defibrillation catheters were placed in the right ventricular apex and in the superior vena cava. Paired monophasic 12 msec and biphasic 6/6 msec defibrillation shocks were given using an up-down protocol to keep shock strength between the defibrillation thresholds for the two waveforms so that the biphasic shock was successful while the monophasic shock was not. Activation fronts immediately following 60 paired shocks were recorded and analyzed by animated maps of the first derivative of the electrograms. The ventricles were divided into apical (I), middle (II), and basal (III) thirds, and early sites, i.e., the sites from which activation fronts first appeared on the epicardium following the shock, were grouped according to their location. Postshock intervals, i.e., the time from the shock until earliest epicardial activation occurred, were also determined. No ectopic activation fronts followed the shock in 20 biphasic episodes. In the other 40 paired episodes, the number of early sites was smaller after biphasic shocks than after monophasic shocks [monophasic: 198 (total), 3.3 +/- 0.9 (mean +/- SD) per shock episode; biphasic: 67, 1.1 +/- 1.0, P < 0.05]. For biphasic but not monophasic shocks, early sites were less likely to arise from the middle (II) and basal (III) thirds than from the apical third (I) [monophasic: I: 84 (42%), II: 68 (34%), III: 46 (23%); biphasic: I: 49 (73%), II: 10 (15%), III: 8 (12%), P < 0.05]. Postshock intervals were significantly shorter for monophasic shocks (54 +/- 14 msec) than for biphasic shocks (75 +/- 23 msec, P < 0.05). CONCLUSION: The decreased number of activation fronts and the longer delay following the shock for the earliest epicardial appearance of those activation fronts that do occur may be responsible for the increased defibrillation efficacy for biphasic shocks.

Animals↗
PubMed1996

Transmembrane potential changes caused by shocks in guinea pig papillary muscle.

To study transmembrane potential (Vm) changes (delta Vm) caused by extracellular field stimulation, Vm was recorded in 10 guinea pig papillary muscles by a double-barrel microelectrode. A 10-ms shock was delivered during the action potential plateau or during diastole. Six shock strengths (1.8 +/- 0.4, 3.8 +/- 0.7, 5.6 +/- 0.9, 7.2 +/- 1.1, 11.1 +/- 1.9, and 17.8 +/- 1.5 V/cm) were given with both polarities. The tissue was then treated with either 30 microM tetrodotoxin (TTX; n = 5) or 30 microM TTX plus Ca(2+)-free (n = 5) perfusion. For shocks during the action potential plateau, delta Vm caused by the six potential gradients was 22.4 +/- 9.6, 43.6 +/- 17.4, 54.7 +/- 17.9, 60.4 +/- 18.1, 65.4 +/- 13.7, and 66.4 +/- 12.2 mV for shocks causing depolarization and 41.1 +/- 16.5, 68.3 +/- 22, 80.5 +/- 20.4, 84.0 +/- 19.5, 93.6 +/- 16.3, and 98.9 +/- 15.4 mV for shocks causing hyperpolarization. The relationship between delta Vm and shock potential gradient was not linear. During diastole, hyperpolarizing shocks induced initial hyperpolarization, then depolarization followed again by hyperpolarization. A new depolarization upstroke occurred immediately after the shock. After TTX or TTX plus Ca(2+)-free perfusion, point stimuli 10 times diastolic threshold could not induce an action potential, but a shock field of 1.8 +/- 0.2 V/cm still induced action potentials. The peak value of depolarization measured with respect to resting potential (-87 +/- 5 mV) during the hyperpolarizing shock decreased from +14 +/- 22 before to -66 +/- 30 mV with TTX perfusion (P < 0.01). The fast upstroke rate of depolarization both during and immediately after the end of hyperpolarizing shocks was inhibited by TTX perfusion. Thus 1) the relationship between delta Vm and shock potential gradient is not linear; 2) field but not point stimulation can induce an action potential when Na+ channels are inactivated; and 3) during diastole Na+ channels are activated twice by a 10-ms hyperpolarizing shock, once during shock-induced hyperpolarization and again immediately after the end of the shock.

Action Potentials↗
PubMed1995

Improved defibrillation threshold with a new epicardial carbon electrode compared with a standard epicardial titanium patch.

BACKGROUND: Recent studies show that depending on the type of shock morphology used, 5% to 15% of patients requiring implantable defibrillators cannot be treated with a nonthoracotomy system. In these cases, an epicardial patch-based system becomes necessary. In this study, we investigated a newly developed epicardial carbon electrode as an alternative to a standard epicardial titanium patch. METHODS AND RESULTS: A tubular epicardial braided carbon electrode of 7F diameter and 14-cm length applied in a U-shape to the epicardium was compared with a standard left ventricular epicardial 15-cm2 titanium mesh patch (CPI Inc). As cathode, a CPI endocardial lead, a Medtronic lead, or a carbon-platinum-iridium prototype electrode was used. Ventricular fibrillation was induced with a 60-Hz generator and allowed to continue for 10 seconds before a shock was given. Two different biphasic shock waveforms (3.2/2- and 6/6-millisecond) were delivered by the six electrode configurations. Eight dogs (weight, 24.5 +/- 1.3 kg) underwent an up-down defibrillation protocol. The order of testing the epicardial electrodes, the endocardial cathodes, and the waveform was randomized. With the epicardial carbon electrode, the mean defibrillation threshold (DFT) energy decreased 39% to 56% and the voltage decreased 24% to 35% compared with the titanium patch: from 8.3 +/- 2.5 to 4.9 +/- 3.6 J with the CPI lead and the 3.2/2-millisecond waveform, from 6.2 +/- 2.5 to 2.9 +/- 2.1 J with the carbon-platinum-iridium prototype, and from 6.4 +/- 3.4 J to 3.5 +/- 2.6 J with the Medtronic lead (P < or = .05). The DFT determinations with the 6/6-millisecond biphasic waveform showed a similar trend with slightly higher values. CONCLUSIONS: Compared with a titanium patch, the new braided epicardial electrode significantly decreases the defibrillation energy requirements. This effect can be maximized by using an endocardial carbon-platinum-iridium prototype as cathode and a short duration biphasic waveform.

Animals↗
PubMed1995

Influence of malpositioned transvenous leads on defibrillation efficacy with and without a subcutaneous array electrode.

Some patients cannot receive a transvenous lead system because of high defibrillation thresholds (DFTs). We hypothesized that a right ventricular (RV) catheter electrode not extending as far as possible into the RV apex could cause high DFTs. Recently, a subcutaneous array (SQA) electrode has been shown to lower DFTs substantially. We compared the influence of a malpositioned RV catheter electrode on defibrillation efficacy for endocardial lead systems with and without a SQA. In eight anesthetized pigs, defibrillation catheters were placed in the RV apex and near the junction of the superior vena cava (SVC) and right atrium. SQA, formed by three elements, each 20 cm in length, was placed in the left thorax. DFTs were determined for a biphasic waveform using an up/down protocol with the RV catheter at the apex and with it repositioned 1-cm and 2-cm proximal to the apex. The mean DFT energies for the configurations with a SQA were less than those without a SQA for every catheter position. The placement of the RV catheter away from the apex caused an increase in defibrillation energy for the configurations without a SQA (apex: 17.1 +/- 3.8 J [mean +/- SD]; 1 cm: 20.1 +/- 4.6 J; 2 cm: 27.6 +/- 9.5 J; P < 0.05), but not for the configurations with a SQA (apex: 12.2 +/- 2.2 J; 1 cm: 12.3 +/- 2.9 J; 2 cm: 12.1 +/- 0.9 J: P = NS). These results suggest that a malpositioned RV catheter electrode, at the time of implantation or by late dislodgment, significantly elevates DFTs for a total endocardial system but not for a system that includes a SQA.

Animals↗
PubMed1995

Responses of the transmembrane potential of myocardial cells during a shock.

INTRODUCTION: The purpose of this investigation was to study the transmembrane potential changes (delta Vm) during extracellular electrical field stimulation. METHODS AND RESULTS: Vm was recorded in seven guinea pig papillary muscles in a tissue bath by a double-barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 microns) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten S1 stimuli, an S2 shock field created by a 10-msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 +/- 0.1, 2.9 +/- 0.2, 6.1 +/- 0.6, and 8.8 +/- 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak delta Vm caused by the above four potential gradients were 21.1 +/- 8.2, 33.6 +/- 13.6, 49.9 +/- 24.2, and 52.3 +/- 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 +/- 14.2, 56.6 +/- 16.4, 83.1 +/- 19.4, and 92.9 +/- 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though delta Vm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 +/- 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 +/- 0.1 to 8.8 +/- 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 +/- 1.8 to 1.6 +/- 0.7 msec for depolarizing shocks and from 6.0 +/- 3.1 to 3.4 +/- 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, than depolarization, followed again by hyperpolarization. CONCLUSION: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between approximately 2 and 9 V/cm.

Animals↗
PubMed1995

Alteration of ventricular fibrillation by propranolol and isoproterenol detected by epicardial mapping with 506 electrodes.

INTRODUCTION: We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation. METHODS AND RESULTS: We used a 528-channel mapping system to quantify the effects of the beta-antagonist, propranolol, and the beta-agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 x 23) electrodes spaced 1.12 mm apart and covering about 5% of the ventricular epicardium was sewn to the anterior right ventricle in 18 pigs (30 kg). Propranolol (0.25 to 0.4 mg/kg) increased the refractory period at a right ventricular epicardial site while isoproterenol (3 to 5 micrograms/min) shortened it. Ventricular fibrillation was induced by programmed stimulation, and unipolar electrograms were recorded from the 506 plaque electrodes for 2 seconds beginning 1, 15, and 30 seconds after the onset of fibrillation. Active epicardial recording sites were identified from the first derivative of the unipolar potentials (dV/dt) detected at each electrode. Then, neighboring active sites were grouped into activation fronts by computer analysis. In six pigs the effect of repeated inductions of ventricular fibrillation was assessed by comparing ventricular fibrillation after saline with a preceding control episode of fibrillation. Each activation front excited 40% +/- 46% of the mapped region before blocking. No changes were observed with saline and multiple inductions of fibrillation. In another six pigs, ventricular fibrillation after propranolol was compared with a preceding control episode of fibrillation. Ventricular fibrillation after propranolol exhibited a decreased activation rate per epicardial recording site and fewer activation fronts per second. There was no change in the amount of tissue excited by each activation front or the number of reentry cycles per activation front compared with control. In addition, there was no change in the maximum negative dV/dt detected per activation at an epicardial site. In six pigs ventricular fibrillation during isoproterenol was compared with control episodes of ventricular fibrillation before and 45 minutes after washout of the drug. The control episodes of fibrillation were not different from each other. Compared with control, ventricular fibrillation during isoproterenol exhibited an increased activation rate per epicardial site, an increased amount of tissue excited by each activation front, and an increased maximum negative dV/dt for each activation. There was no change in the number of activation fronts per second or the number of reentry cycles per activation front compared with control. CONCLUSION: Quantitative analysis revealed that propranolol and isoproterenol do not have symmetrically opposite effects on ventricular fibrillation. Propranolol decreased the number of activation fronts while isoproterenol increased the amount of tissue excited by each activation front. Thus, drugs that alter ventricular refractoriness or excitability alter ventricular fibrillation.

Animals↗
PubMed1995

Regional capture of fibrillating ventricular myocardium. Evidence of an excitable gap.

Previous investigations have suggested that during ventricular fibrillation (VF) pacing stimuli are incapable of evoking propagated ventricular activations. To determine whether regional myocardial capture could be achieved during rapid pacing in VF, extracellular unipolar potentials were sampled (2 kHz) and recorded from 506 Ag-AgCl electrodes arranged in a rectangular grid (22 x 23, 1.12-mm spacing) embedded in a plaque overlying two pacing electrodes in the epicardium of the anterobasal right ventricle in pentobarbital-anesthetized pigs (25 to 30 kg, n = 6). During separate episodes of electrically induced VF, two bursts of 40 monophasic stimuli (10 mA, 2-millisecond duration) were asynchronously applied to the stimulating electrodes in either a bipolar, unipolar anodal, or unipolar cathodal mode. Evidence of regional capture was provided by (1) animating the first temporal derivative of the extracellular potentials, (2) analyzing inter-beat interval patterns, and (3) employing the Karhunen-Loeve decomposition method to quantify the repetitiveness of spatio-temporal patterns of activation. Regional capture of ventricular myocardium during VF was observed when pacing stimuli fell late in the local myocardial activation interval and when the pacing cycle length was 80% to 115% of the mean subplaque activation cycle length. When myocardial activations became phase locked to the pacing stimuli, repeatable spatiotemporal patterns of activation followed each stimulus. Poincaré sections at the plaque border revealed that during VF prior to pacing, interbeat intervals were irregular but were driven by pacing to stable fixed values at times corresponding to our qualitative declaration of regional capture. A similar correspondence was demonstrated between the time of capture, defined by direct observation of the activation patterns, and a rise in the power contained in the first two spatial modes of a Karhunen-Loeve decomposition. These data demonstrate that appropriately timed stimuli produce regional capture of fibrillating right ventricular myocardium in the pig and support the existence of an excitable gap during VF in this model.

Animals↗
PubMed1993

Effective defibrillation in pigs using interleaved and common phase sequential biphasic shocks.

Previous studies have shown that low internal defibrillation thresholds (DFTs) can be attained by using two pairs of electrodes and combining biphasic shocks with sequential timing. The purpose of this two-part study was to test the defibrillation efficacy of two new shock sequences, an interleaved biphasic, and a common phase sequential biphasic, that utilized two pairs of electrodes and were developed from the concept of sequential biphasic shocks. In the first part, defibrillation catheters were placed in the right ventricle and the superior vena cava of six anesthetized pigs. A small patch electrode was placed on the LV apex through a subxiphoid incision and a cutaneous patch was placed on the left thorax. The mean DFT energies for the interleaved biphasic (5.2 +/- 0.4 J) and the common phase sequential biphasic waveforms (5.4 +/- 0.4 J) were substantially less (P < 0.0001) than those for either the sequential monophasic (10.6 +/- 1.0 J) or single biphasic waveforms (9.0 +/- 1.0 J). In the second study, which used nine anesthetized pigs, the importance of phase reversal was demonstrated by the finding that the DFT energy of a common phase sequential biphasic shock (6.2 +/- 0.4 J) was much less than a common phase sequential monophasic shock (17.9 +/- 1.3 J, P < 0.0001); furthermore, the average DFT for four common phase sequential biphasic configurations (5.7 +/- 0.2 J) was much less than for a configuration that was similar except that current flow was not reversed in one phase so that no biphasic effect was present (19.7 +/- 1.2 J). The efficacy of common phase sequential biphasics was comparable to that of sequential biphasics. The effectiveness of sequential biphasics, interleaved biphasics, and common phase sequential biphasics is possibly due to two mechanisms: (A) an increase in the potential gradient during a later phase in regions that were low during the first phase, and (B) the exposure of most of the myocardium to a biphasic shock that reduces the minimum extracellular potential gradient needed to defibrillate.

Animals↗
PubMed1993

Is the second phase of a biphasic defibrillation waveform the defibrillating phase?

Why some biphasic waveforms defibrillate with lower energies than monophasic waveforms of similar duration is unknown. One hypothesis is that the first phase of a biphasic waveform acts as a conditioning, hyperpolarizing prepulse to prepare for defibrillation by a second depolarizing phase. To test whether the second phase of a biphasic waveform is the defibrillating phase, three monophasic waveforms, an ascending ramp (A), a square wave (S), and a descending ramp (D), were compared to three biphasic waveforms with A, S, or D in the first phase (biphasic first phase) and three biphasic waveforms with A, S, or D in the second phase (biphasic second phase). Two defibrillation thresholds for each waveform were performed in 18 open chest pigs and mean defibrillation thresholds were compared. In nine pigs 16-msec monophasic and 16/16-msec biphasic waveforms were ranked by mean current and energy at defibrillation threshold. The ranks were the same for monophasic and biphasic second phase waveforms: for mean current A < S = D and for energy A < S < D. The ranks were different for the biphasic first phase waveforms: for mean current S < A = D and for energy S < A = D. Although ranks for the 16-msec monophasic waveforms matched those for the 16/16-msec biphasic second phase waveforms, the biphasic waveforms had higher mean currents and energies at defibrillation threshold. In nine pigs defibrillation thresholds for 6-msec monophasic and 6/6-msec biphasic waveforms were ranked. For mean current the ranks were monophasic: A < S = D; biphasic first phase: A = S = D; and biphasic second phase: S = D < A. For energy the ranks were monophasic: A = S < D; biphasic first phase: A = S = D; and biphasic second phase: S = D < A. Thus, ranks for the 6-msec monophasic waveforms differed from those for the 6/6-msec biphasic second phase waveforms. For 16/16-msec biphasic waveforms, less effective for defibrillation than corresponding 16-msec monophasic waveforms, these results support the hypothesis that the second phase of a biphasic waveform defibrillates since the defibrillation efficacy of a 16/16-msec biphasic waveform is related to the defibrillation efficacy of its second phase waveshape. However, for clinically useful 6/6-msec biphasic waveforms, more effective for defibrillation than 6-msec monophasic waveforms, the hypothesis is not supported because the ability of a 6/6-msec biphasic waveform to defibrillate is unrelated to the defibrillation efficacy of its second phase waveshape.

Animals↗
PubMed1993

Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs.

This study determined the response of action potentials during ventricular fibrillation (VF) to timed monophasic and biphasic shocks. A floating glass microelectrode was used to record intracellularly from the anterior right ventricle in 10 open-chest dogs. After 10 seconds of electrically induced VF, 5-millisecond monophasic and 2.5/2.5-millisecond biphasic shocks or 16-millisecond monophasic and 8/8-millisecond biphasic shocks were given via mesh electrodes on either side of the microelectrode. Monophasic and biphasic truncated exponential shocks of 5 V/cm were given with coupling intervals timed from the beginning of a VF action potential to the shock ranging from 50 to 70 milliseconds in 5-millisecond increments. Each coupling interval for each waveform was tested during a different VF episode. The interval between successive activations during VF was 86 +/- 15 milliseconds (mean +/- SD). The refractory period during VF was 61 +/- 5 milliseconds for 5-millisecond monophasic shocks and 66 +/- 6 milliseconds for 2.5/2.5-millisecond biphasic shocks (P < .05). At each coupling interval, action potential duration at 50% repolarization (APD50) was significantly prolonged by the shocks compared with the mean preshock APD50 (P < .05). ADP50 duration increased significantly with increases in the coupling interval (P < .05) for both monophasic and biphasic waveforms. For all coupling intervals together, APD50 prolongation as a percent of the mean preshock APD50 was 170 +/- 55%, 192 +/- 45%, 151 +/- 44%, and 175 +/- 45% for 5- and 16-millisecond monophasic and 2.5/2.5- and 8/8-millisecond biphasic waveforms, respectively. This APD50 prolongation was greater for monophasic than biphasic shocks and was greater for longer than shorter waveforms (P < .05). Thus, during VF, (1) the refractory period for 5-V/cm truncated exponential waveforms lasting 5 milliseconds is approximately 75% of the VF activation interval; (2) the refractory period is shorter for monophasic than for comparable biphasic waveforms; (3) both monophasic and biphasic 5-V/cm shock fields cause prolongation of action potential duration; (4) prolongation of action potential duration increases as the coupling interval increases; and (5) prolongation of action potential duration is greater for monophasic shocks and for longer shock waveforms.

Action Potentials↗
PubMed1992

High ligation of the greater saphenous vein for treatment of lower extremity varicosities: the fate of the vein and therapeutic results.

This study was carried out to determine the subsequent fate of the greater saphenous vein and the efficacy of its high ligation along with surgical excision or sclerotherapy of varicosities. From 1988 to 1990, 22 patients underwent high ligation and sclerotherapy, 22 underwent high ligation and varicose vein excision, and four underwent high ligation alone. There were 36 women and 12 men patients. The average patient age was 48. Sixty limbs were scanned by duplex ultrasound pre- and postoperatively to determine the status of the greater saphenous vein. Average follow-up time was 10 months. Patients and surgeons rated the results of therapy for ablation of varicosities and alleviation of symptoms. Surgical complications were evaluated. At postoperative scan, 47 greater saphenous veins (78%) were found to be completely patent, nine (15%) were thrombosed for a short segment (less than 10 cm) and four (7%) were more significantly thrombosed. Those limbs in which high ligation and sclerotherapy were performed had the highest complete patency rate (96%). Patient and surgeon satisfaction was good to excellent in every case. The only complications were three symptomatic greater saphenous vein thromboses. Although follow-up is relatively brief, complete patency of the ligated greater saphenous vein was found in most cases. High ligation allows preservation of a patent greater saphenous vein, which can be used as an arterial conduit at a later date and gives therapeutic results comparable to stripping without the additional morbidity.

Combined Modality Therapy↗
PubMed1992

Defibrillation electrode configurations developed from cardiac mapping that combine biphasic shocks with sequential timing.

Previous canine mapping studies of the transvenous defibrillation lead configuration of right ventricle (RV) to left R2 patch (P) revealed regions of low potential gradient in the left ventricular apex (A) and the right ventricular outflow tract (O). Thus 16 new lead configurations were tested in eight dogs, which incorporated electrodes in A and O to raise the gradient. When used in conjunction with two sequential biphasic shocks, the average defibrillation threshold energy from these configurations was 57% lower than that produced by a single biphasic shock delivered through RV-->P (phase 1 cathode-->anode, p < 0.001). Of the 16 configurations tested, the most effective was RV-->P followed by A-->O. When the shocking order of this configuration was reversed in another eight dogs, no difference in defibrillation efficacy was noted. In individual configurations of RV-->P and A-->O that used a single biphasic shock, defibrillation was not effective. Finally, when two sequential biphasic shocks were delivered to the same two electrodes in seven other dogs, the defibrillation efficacy was low. Thus configurations that use two sequential biphasic shocks can produce low defibrillation thresholds when the shocks are delivered to two different sets of electrodes. The high efficacy may be caused by one shock increasing the potential gradient in regions of low potential gradient that are produced by the other shock.

Animals↗
PubMed1992

High-current stimuli to the spared epicardium of a large infarct induce ventricular tachycardia.

BACKGROUND: Previous studies have demonstrated that both ventricular tachycardia (VT) and ventricular fibrillation (VF) may begin as figure-eight reentry: VT with a longer cycle length from spared tissue adjacent to an infarct by programmed stimulation and VF with a shorter cycle length from noninfarcted tissue by a large premature S2 stimulus. These results suggest that the type of tissue or cycle length of the arrhythmia rather than the mode of induction determines whether the figure eight becomes sustained VT or degenerates into VF. Thus, a protocol similar to that by which a VF threshold is determined may induce VT rather than VF when performed in the spared tissue over an infarct. METHODS AND RESULTS: In 10 dogs, 4 days after occlusion-reperfusion of the left anterior descending coronary artery, 10 S1 stimuli were delivered from a total of 34 right and left ventricular sites outside the infarct. An epicardial S2 stimulus over the infarct was increased in 10-mA steps and introduced in diastole at decreasing cycle lengths of 5 msec until VT or VF was induced. Sustained monomorphic figure-eight VT was induced from 24 S1 sites and VF from nine (p = 0.03). The mean cycle lengths for the initial six arrhythmic cycles was 152 +/- 33 msec for VT and 115 +/- 13 msec for VF (p less than 0.001). Mean transmural infarct extent was 80% in five dogs with only VT, 63% in three dogs with both VT and VF, and 15% in two dogs with only VF. Different morphologies of VT were induced by changing the S1 site, the S2 strength, or the S1S2 coupling interval. In 25 of the 34 arrhythmias, the central part of the initial figure-eight pathway was oriented opposite the S1 activation sequence in that region. CONCLUSIONS: A large S2 stimulus over a nontransmural infarct induces VT if the spared myocardium is thin. This study introduces a useful technique for inducing sustained monomorphic VT in which the location and direction of the figure-eight pathway are known a priori and in which different morphologies of sustained VT can be produced by changing the S1 site.

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