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Biomedical subjects

W M Smith

Publications and source records attributed to W M Smith.

At least 109 records · Page 6Linked to original sources
PubMed1993

The effect of phase separation on biphasic waveform defibrillation.

It has been hypothesized that the defibrillation efficacy of a biphasic shock is caused by the large change in voltage between the two phases. This study examined the effects of separating the two phases in time thus splitting in half the rapid voltage change at phase reversal. The study was performed in three parts each using six dogs. Part I determined defibrillation thresholds (DFTs) for two exponentially truncated biphasic waveforms (3.5/2 msec and 6/6 msec) with interphase time delays of 0, 1, 2, 3, 4, 6, 8, and 10 msec. In Part II, probability of success curves were generated using an up down method with 15 shocks for each delay for the 3.5/2 msec biphasic waveform with interphase delays of 0, 2, 3, 4, and 5 msec. In Part III, DFTs were determined using a 3.5/2 msec and 6/6 msec biphasic as well as a third waveform that consisted of two sequential 6-msec pulses of the same polarity with interphase delays of 0, 5, 10, 15, 20, 25, 50, and 100 msec. In all three parts the defibrillating cathode was a 6.17 cm2 transvenous spring electrode positioned in the RV apex and the anode was a 113 cm2 cutaneous left chest wall electrode patch. With all waveforms, the trailing edge voltage of the first phase was equal to the negative of the leading edge voltage of the second phase. There was no statistical difference in DFTs or in 50% successful defibrillation points for phase separations from 0 to 6 msec and 0 to 5 msec for Parts I and II, respectively. In Part I there was a significant increase in DFTs for phase separations of 8 and 10 msec compared to a phase separation of 0 msec. In Part III there was no significant difference for separations of 0 and 5 msec; however, there was a significant increase in DFT requirements for separations from 5 to 50 msec, which then decreased with a separation of 100 msec for all three waveforms tested. In conclusion, defibrillation efficacy was unchanged with phase separations up to 6 msec. With phase separation, the rapid voltage change during phase reversal is split in half and, thus, cannot explain the improved efficacy of biphasic waveforms.

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

A quantitative measurement of spatial order in ventricular fibrillation.

INTRODUCTION: The degree of organization in ventricular fibrillation (VF) is not known. As an objective measurement of spatial order, spatial correlation functions and their characteristic lengths were estimated from epicardial electrograms of pigs in VF. METHODS AND RESULTS: VF was induced by premature stimulation in five pigs. Electrograms were simultaneously recorded with a 22 x 23 array of unipolar electrodes spaced 1.12 mm apart. Data were obtained by sampling the signals at 2000 Hz for 20 minutes immediately after the initiation of FV. Correlations between all pairs of signals were computed at various times. Correlation lengths were estimated from the decay of average correlation as a function of electrode separation. The correlation length of the VF in pigs was found to be approximately 4 to 10 mm, varying as fibrillation progressed. The degree of correlation decreased in the first 4 seconds after fibrillation then increased over the next minute. CONCLUSION: The correlation length is much smaller than the scale of the heart, suggesting that many independent regions of activity exist on the epicardium at any one time. On the other hand, the correlation length is 4 to 10 times the interelectrode spacing, indicating that some coherence is present. These results imply that the heart behaves during VF as a high dimensional, but not random, system involving many spatial degrees of freedom, which may explain the lack of convergence of fractal dimension estimates reported in the literature. Changes in the correlation length also suggest that VF reorganizes slightly in the first minute after an initial breakdown in structure.

Animals↗
PubMed1993

Internal cardioversion of atrial fibrillation in sheep.

BACKGROUND: The cardioversion efficacy of multiple defibrillation waveforms and electrode systems was compared in a sheep model of atrial fibrillation. METHODS AND RESULTS: Sustained atrial fibrillation could be induced with rapid atrial pacing in 23 (55%) of the animals. This study was performed in four parts. Six sheep with sustained atrial fibrillation were used for data analysis for each part, except in part 4 where five sheep without sustained atrial fibrillation were used. In part 1, four lead systems and four single capacitor truncated exponential defibrillation waveforms (two monophasic and two biphasic) were tested. In part 2, two transvenous lead systems were compared; one was a right-to-left system with one electrode located in the right side of the heart and the other electrode located in the left side of the heart, and the other was a totally right-sided system with both electrodes located in the right side of the heart. Eight (four monophasic and four biphasic) waveforms were tested with each lead system. In part 3, eight transvenous lead systems were compared, and two waveforms (one monophasic and one biphasic) were tested with each lead system. For parts 1-3, probability of success curves were determined for each waveform/lead system configuration using an up-down technique with 15 shocks per configuration. In part 4, shocks were synchronized to the QRS and given through two lead configurations during sinus rhythm in 20-V steps starting with 40 and ending with 500 V, and two waveforms were tested with each lead system (one monophasic and one biphasic). Ventricular fibrillation thresholds were determined by giving shocks during the T wave of sinus rhythm. For part 1, the three lead systems that used only intravenous catheter electrodes had significantly lower defibrillation requirements than the catheter-to-chest wall patch system. A 3/3-msec biphasic waveform had significantly lower defibrillation requirements than any of the other three waveforms in part 1. In part 2, the 3/3-msec biphasic waveform with a right-to-left lead system configuration had significantly lower defibrillation requirements than any other waveform lead system combination tested, and for each waveform tested, the right-to-left configuration had significantly lower requirements than the totally right-sided configuration. In part 3, for each waveform the right-to-left configuration had significantly lower voltage and energy requirements than the corresponding totally right-sided configuration. Furthermore, in part 3, waveform/lead configurations that probably generated high potential gradients near the sinoatrial node and near the atrioventricular node resulted in more postshock conduction disturbances. In part 4, there were no episodes of ventricular arrhythmias with shocks synchronized to the QRS. However, with synchronization to the T wave, ventricular fibrillation was induced in all five animals with the minimum tested voltage, which was 40 V. CONCLUSIONS: This acute model yielded sustained atrial fibrillation in approximately 55% of the animals. Cardioversion of atrial fibrillation in sheep is possible with very low energy requirements using transvenous electrode systems (50% successful energy of 1.3 +/- 0.4 J for the 3/3-msec biphasic waveform with a right-to-left lead system). The biphasic waveform had the lowest defibrillation requirements of any waveforms tested, and right-to-left lead systems resulted in lower defibrillation requirements than totally right-sided lead systems. Also, lead systems that probably generated high potential gradients near the sinoatrial and atrioventricular node areas resulted in more frequent episodes of postshock conduction disturbances. Furthermore, synchronization of the shock to the QRS was vital to avoid potentially lethal postshock ventricular arrhythmias...

Animals↗
PubMed1993

Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs.

To study the mechanism of defibrillation and the reason for the increased defibrillation efficacy of biphasic waveforms, the potential gradient in a 32 x 30-mm region of the right ventricle in 15 dogs was progressively lowered in four steps while a strong potential gradient field was maintained throughout the rest of the ventricular myocardium. The volume of right ventricle beneath the plaque was 10 +/- 2% of the total ventricular mass. A 10-msec monophasic (eight dogs) or 5/5-msec biphasic (seven dogs) truncated exponential shock 30% above the defibrillation threshold voltage was given via electrodes on the left ventricular apex and right atrium to create the strong potential gradient field. Simultaneously, a weaker shock with the same waveform but opposite polarity was given via mesh electrodes on either side of the small right ventricular region to cancel part of the potential difference in the region and to create one of the four levels of potential gradient fields. Shock potentials and activations were recorded from 117 epicardial electrodes in the small region, and in one dog global epicardial activations and potentials were recorded from a sock containing 72 electrodes. Each gradient field was tested 10 times for successful defibrillation after 10 seconds of electrically induced fibrillation. For both monophasic and biphasic shocks, the percentage of successful defibrillation attempts decreased (p < 0.05) as the potential gradient decreased in the small region. Defibrillation was successful approximately 80% of the time for a mean +/- SD potential gradient of 5.4 +/- 0.8 V/cm for monophasic shocks and 2.7 +/- 0.3 V/cm for biphasic shocks (p < 0.05). No postshock activation fronts arose from the small region for eight waveform when the gradient was more than 5 V/cm. For both waveforms, the postshock activation fronts after the shocks were markedly different from those just before the shock and exhibited either a focal origin or unidirectional conduction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Optical measurements of transmembrane potential changes during electric field stimulation of ventricular cells.

We evaluated transmembrane potential changes at the ends of isolated rabbit ventricular myocytes during defibrillation-strength shocks given in the cellular refractory period. The myocytes were stimulated (S1 pulse) to produce an action potential. Then a constant-field shock (S2 pulse) with an electric field of 20 or 40 V/cm was given at an S1-S2 interval of 50 msec. The cells were stained with potentiometric dye (di-4-ANEPPS), and the cell end facing the S2 anode or cathode was illuminated with a laser while the fluorescence was recorded. During S2, the cell end facing the S2 cathode became more positive intracellularly, whereas the cell end facing the S2 anode became more negative intracellularly. The S2-induced transmembrane potential change at the cell end (delta Vm) was determined relative to the amplitude of the S1-induced action potential (APA) in each recording (i.e., delta Vm/APA). In Tyrode's solution containing 4.5 mM potassium, delta Vm/APA for 40-V/cm S2 was 1.36 +/- 0.34 at the cell end facing the S2 cathode and -1.65 +/- 0.61 at the cell end facing the S2 anode (n = 9). For the 20-V/cm S2, delta Vm/APA was 0.61 +/- 0.33 at the cell end facing the S2 cathode and -0.71 +/- 0.33 at the cell end facing the S2 anode (n = 6). The delta Vm/APA was not significantly influenced by 20 mM diacetyl monoxime. These results indicate that large delta Vm values occurred at the ends of the cells during S2. The calculated values of delta Vm, assuming a nominal APA of 130 mV, were 177 and -214 mV for the 40-V/cm S2 and 79 and -93 mV for the 20-V/cm S2. The delta Vm was correlated with cell size (r > or = 0.95) and agreed with values predicted by the S2 electric field strength multiplied by half of the cell length to within 27%. When the potassium concentration was increased to 20 mM, delta Vm/APA for 40 V/cm S2 increased 85% and 67% at the cell ends facing the S2 cathode and anode, respectively (n = 9, p < 0.005 versus 4.5 mM potassium), consistent with reduced APA. Thus, with normal or elevated extracellular potassium, transmembrane potential changes at the ends of cells during defibrillation-type stimulation are large enough to produce activation or recovery of voltage-dependent ion channels and may produce the effects responsible for defibrillation.

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↗
PubMed1993

Long-range safety and protective benefits of angiotensin-converting enzyme inhibitors for hypertension. Do we need more clinical trials?

Inhibition of the renin-angiotensin system is being applied with considerable success to the treatment of hypertension and heart failure. Angiotensin-converting enzyme (ACE) inhibitors are the only currently available agents that can achieve this objective. In general, the major therapeutic effects of these agents in the treatment of mild to moderate hypertension or of heart failure are exerted on the vascular tissue through inhibition of the renin-angiotensin system and, secondarily, of the sympathetic nervous system. When cardiovascular functional reserve is diminished and autoregulation of regional and systemic blood flow is strained, however, ACE inhibitors may affect other organ functions (heart, kidneys, and possibly brain), hormones other than the renin system, and local tissue humoral systems. The interrelations between the renin-angiotensin system and several other vasoactive systems--including circulating and locally generated tissue hormones and centrally acting neurohormonal factors--are complex and unclear. A better understanding of these mechanisms and interrelations would allow for a more rational therapeutic use of these agents. Unknown also are the clinical effects of prolonged ACE inhibition. Whether the use of ACE inhibitors can provide primary cardiorenal protection requires proof through definitive clinical trials.

Angiotensin-Converting Enzyme Inhibitors↗
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

Adenosine versus verapamil in the treatment of supraventricular tachycardia: a randomized double-crossover trial.

The safety and efficacy of verapamil and adenosine in the acute termination of supraventricular tachycardia were compared in a randomized double-crossover trial. Of 32 eligible patients with either spontaneous or induced narrow complex tachycardia, seven (22%) patients experienced conversion to sinus rhythm with carotid sinus massage. The other 25 patients were randomly assigned to receive either adenosine (n = 14) or verapamil (n = 11). Relative drug efficacies were 100% for adenosine versus 73% for verapamil, p = NS. Adenosine given at less than or equal to 120 micrograms/kg caused conversion in 12 (86%) of 14 patients. The other two patients required 20 mg adenosine for conversion. After conversion the systolic blood pressure increased significantly in the adenosine group but not in the verapamil group. Reinitiation of tachycardia occurred in two (14%) of 14 patients randomized to the adenosine group. Serious adverse hemodynamic effects were observed in one (9%) of 11 patients randomized to verapamil. The incidence of conversion arrhythmias was similar in both treatment groups (adenosine 57%, verapamil 50%, p = NS).

Adenosine↗
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.

Animals↗
PubMed1992

Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation.

BACKGROUND: Potential gradient field determination may be a helpful means of describing the effects of defibrillation shocks; however, potential gradient field requirements for defibrillation with different electrode configurations have not been established. METHODS AND RESULTS: To evaluate the field requirements for defibrillation, potential fields during defibrillation shocks and the following ventricular activations were recorded with 74 epicardial electrodes in 12 open-chest dogs with the use of a computerized mapping system. Shock electrodes (2.64 cm2) were attached to the lateral right atrium (R), lateral left ventricular base (L), and left ventricular apex (V). Four electrode configurations were tested: single shocks of 14-msec duration given to two single anode-single cathode configurations, R:V and L:V, and to one dual anode-single cathode configuration, (R+L):V; and sequential 7-msec shocks separated by 1 msec given to R:V and L:V (R:V----L:V). Defibrillation threshold (DFT) current was significantly lower for R:V----L:V than for the other configurations and markedly higher for L:V. Despite these differences, the minimum potential gradients measured at DFT were not significantly different (approximately 6-7 V/cm for each electrode configuration). Potential gradient fields generated by the electrode configurations were markedly uneven, with a 15-27-fold change from lowest to highest gradient, with the greatest decrease in gradient occurring near the shock electrodes. Although gradient fields varied with the electrode configuration, all configurations produced weak fields along the right ventricular base. Early sites of epicardial activation after all unsuccessful shocks occurred in areas in which the field was weak; 87% occurred at sites with gradients less than 15 V/cm. Ventricular tachycardia originating in high gradient areas near shock electrodes followed 11 of 67 successful shocks. CONCLUSIONS: These data suggest that 1) defibrillation fields created by small epicardial electrodes are very uneven; 2) achievement of a certain minimum potential gradient over both ventricles is necessary for ventricular defibrillation; 3) the difference in shock strengths required to achieve this minimum gradient over both ventricles may explain the differences in DFTs for various electrode configurations; and 4) high gradient areas in the uneven fields can induce ectopic activation after successful shocks.

Animals↗
PubMed1992

Three-dimensional potential gradient fields generated by intracardiac catheter and cutaneous patch electrodes.

BACKGROUND: Defibrillation may be improved if electrode configurations can be found that create a larger and more even voltage gradient field across the heart. This study determined the magnitude of the shock gradient fields generated by four nonthoracotomy electrode configurations for defibrillation. METHODS AND RESULTS: In six dogs, a catheter was inserted containing a right ventricular apical electrode (V) and a right atrial electrode (A). A cutaneous patch electrode (P) was placed on the left lateral thorax. Shock potentials were recorded simultaneously from 128 electrodes in the left ventricular and right ventricular subepicardium and subendocardium, ventricular septum, and atria. With the chest closed, 50-mA shocks were given during diastole via the following lead configurations: V----A (V, cathode; A, anode); V----P; V----A+P; and V+A----P. Potential gradients were calculated at the subepicardium and subendocardium in millivolts per centimeter per volt of shock. In most dogs, the V----A+P configuration produced higher gradients throughout the ventricles than did V----A, V----P, or V+A----P. The maximum potential gradient was smaller for the V+A----P configuration than for V----A, V----P, or V----A+P. The gradient fields for the configurations with the catheter alone or combined with P were uneven. CONCLUSIONS: It is possible to estimate shock gradient fields in three dimensions. Of the four configurations tested, V----A+P produced the highest gradients and V+A----P produced the lowest high gradient. The gradient fields were uneven throughout the ventricles.

Animals↗
PubMed1992

Effect of pulse separation between two sequential biphasic shocks given over different lead configurations on ventricular defibrillation efficacy.

BACKGROUND: Two sequential biphasic shocks delivered over separate lead configurations markedly improve defibrillation efficacy compared with a single shock alone. We investigated the effect of varying the intershock interval between sequential biphasic shocks on defibrillation. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were obtained in six dogs for shock separations ranging from 0.2 to 125 msec. The first shock was given from a catheter electrode in the right ventricular apex to a patch on the left lateral thorax; the second was from a small patch on the left ventricular apex to a catheter electrode in the right ventricular outflow tract. When the interval between shocks was less than or equal to 10 msec or greater than or equal to 75 and less than or equal to 125 msec, the mean DFTs were less than that previously found for the first shock by itself (4.2 versus 7.4 J, p = 0.002). At a separation of 50 msec, however, there was a marked rise in the DFT to 27 J. The mean DFT for the second shock at a delay of 50 msec was not different from the mean DFT previously found for the second shock by itself (7.2 versus 7.0 J). These results were confirmed in another six dogs using defibrillation probability-of-success curves. In 12 other dogs, probability-of-success curves were generated for delays between shocks as a percentage of the activation interval during ventricular fibrillation. Minimum defibrillation energy requirements were at two separations, 0.2 msec and 90% of the activation interval. CONCLUSIONS: The optimal intershock interval between two sequential biphasic shocks is either less than or equal to 10 msec or greater than or equal to 75 and less than or equal to 125 msec. The marked rise in the DFT at a shock separation of 50 msec, requiring more energy than that for the first shock alone, suggests that the second shock at this time delay is likely to reinduce fibrillation after it is halted by the first shock until the second shock is strong enough to defibrillate independently of the first shock.

Animals↗
PubMed1992

Effect of field stimulation on cellular repolarization in rabbit myocardium. Implications for reentry induction.

We have investigated the effects of electric field stimulation on membrane repolarization in rabbit papillary muscles and assessed the consequences of these effects for the dispersion of intracellular potentials and the production of a propagation wave front or unidirectional block in relatively refractory tissue. The stimuli studied had electric field strength of 0.25-14 V/cm, duration of 2 msec, and field orientation along or across the myocardial fibers. The field strengths to excite the muscles in diastole were 0.68 or 1.23 V/cm for stimuli oriented along or across the fibers, respectively (p less than 0.01, along versus across). A 2.5-V/cm stimulus given near the end of the action potential (AP) produced either no response or, after increasing the stimulus delay only 2-3 msec, a full response with almost no AP durations that were intermediate. For stimulation along and across the fibers, respectively, given at 70% of the AP duration, a 4-V/cm stimulus produced AP prolongation (measured at 90% repolarization) of 20% and 4% (p less than 0.05), an 8-V/cm stimulus produced AP prolongation of 36% and 20% (p less than 0.05), and a 14-V/cm stimulus produced AP prolongation of 36% and 30% (p = NS). For either orientation, AP prolongation by stimuli of 8 V/cm or 14 V/cm increased gradually as the stimulus delay was increased. The different effects in relatively refractory tissue of stimuli of 2.5 V/cm compared with 8 V/cm can explain the propagation wave front and block that occur with electrically induced functional reentry in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

Existence of both fast and slow channel activity during the early stages of ventricular fibrillation.

Although sodium channels have been reported to be inactive after 5-10 minutes of ventricular fibrillation (VF), their state during early VF is unknown. In 12 open-chest dogs, a floating glass microelectrode was used to record intracellular action potentials from the right ventricle during pacing and during electrically induced VF. Before any drug was administered, an initial episode of VF was continuously recorded for at least 20 seconds followed by defibrillation. Recordings were made during VF episodes after superfusion for 15 minutes around the microelectrode site by low (2.8 x 10(-5) M) and high (10(-4) M) concentrations of tetrodotoxin (TTX) in five dogs, or by low (4 microM) and high (100 microM) concentrations of verapamil in another four dogs. In three dogs, VF was induced without drugs three times to determine if the effects observed in the previous dogs were caused by the drugs or by successive episodes of VF. Ten consecutive action potentials were analyzed at the onset and after 5, 10, 15, and 20 seconds of VF. Action potential amplitude and duration during paced rhythm or VF were not changed by the local perfusion of either TTX or verapamil. In the TTX group, the maximum upstroke rate of depolarization of an action potential (Vmax) during paced rhythm was 104 +/- 14 V/sec for control cycles before any drug was given, 86 +/- 15 V/sec for the low TTX concentration, and 55 +/- 14 V/sec for the high TTX concentration (p less than 0.05 versus other two). Vmax decreased from 55 +/- 32 V/sec at the beginning of VF to 37 +/- 27 V/sec after 20 seconds of VF for predrug VF, from 39 +/- 20 V/sec to 18 +/- 11 V/sec for low-dose TTX VF, and from 18 +/- 13 V/sec to 12 +/- 7 V/sec for high-dose TTX VF (p less than 0.05 among the three groups). In the dogs receiving verapamil, VF was still inducible with Vmax not significantly different from predrug VF at the onset and after 5 or 20 seconds of VF but with Vmax smaller (p less than 0.05) for verapamil than for predrug VF after 10 or 15 seconds of VF. In three dogs, Vmax was not significantly different during three successive episodes of VF when no drug was given between the episodes.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗