Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Defibrillators”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources
PubMed1982

Determination of safety factor for defibrillator waveforms in cultured heart cells.

We studied excitation thresholds and arrhythmias produced in cultured chick embryo myocardial cells subjected to electric shocks using rectangular, untruncated resistor-capacitor (RC), and critically damped resistor-inductor-capacitor (RLC) waveforms with variable intensities while photocell mechanograms were recorded. Strength-duration curves for excitation and production of a specific postshock arrhythmia (4-s arrest) were constructed. Excitation curves closely resembled those for in situ defibrillation threshold (or specific % success). The ratio between the shock intensity producing a 4-s arrest and that producing excitation at each duration (termed the "safety factor") was determined. Waveforms with a large safety factor in vitro defibrillated most effectively in situ with little postshock dysfunction. Waveforms with low safety factors had a low rate of success in situ and produced much postshock dysfunction. Safety factor of monophasic clinical waveforms were lower than that of the 5-ms rectangular wave. The close correspondence between in vitro safety factor and in situ defibrillating effectiveness, as reported in the literature, suggests that the cell culture system is an effective screening system for determining waveforms that will improve the efficacy and safety of defibrillation procedures.

Animals↗
PubMed1987

Improved cardiac cell excitation with symmetrical biphasic defibrillator waveforms.

According to the most commonly accepted hypothesis, ventricular defibrillation is produced by exciting cells in a critical mass of the ventricle. For monophasic defibrillator waveforms, this hypothesis correctly predicts a direct correlation between defibrillation threshold in the transthoracic calf model and excitation threshold for extracellular field stimulation in the cultured cell model. To further test the hypothesis, we determined whether symmetrical biphasic waveforms, which reduce defibrillation threshold in the calf to approximately 65% of that of the corresponding monophasic waveform (14), decrease excitation threshold in the cultured cell model. Experiments were performed on 100- to 250-microns aggregates from 10- to 12-day-old chick embryos. Excitation threshold strength-duration curves obtained at extracellular potassium (Ko) = 6.5 mM and pacing interval of 1,000 ms showed a significant reduction for symmetrical biphasic rectangular waveforms, when compared with the corresponding monophasic waveforms for durations greater than 3 ms. At the rheobase, the threshold ratio between the biphasic and monophasic waveforms was 0.63 (SE = 0.02). Transmembrane potentials during stimulation showed that excitation takes place during the second portion of the biphasic waveform for intensities that are subthreshold for the monophasic waveform. The relative effectiveness of the biphasic waveform (5-ms duration) increases under "fibrillation conditions" of short pacing interval (300 ms) and high extracellular potassium (10.5 mM). These results show that symmetrical biphasic waveforms decrease excitation threshold in the cultured cell model and that the degree of threshold reduction is dependent on Ko and beat rate.

Animals↗
PubMed1990

Nature of defibrillation: determinism versus probabilism.

The gradual transitions that are found between unsuccessful and successful shock strengths in percent success or dose-response curves suggest that defibrillation is a probabilistic phenomenon. This concept appears to be reinforced by the fact that a frequency distribution is observed in defibrillation threshold data and that a dose-response relationship is also obtained by integration of the frequency distribution. The purpose of this study was to investigate whether a deterministic threshold model (based on experimental results) could produce 1) gradual transitions in dose-response curves, and 2) a threshold frequency distribution for individual subjects. In the experimental phase of the study, a linear deterministic relationship was found between transthoracic threshold current and defibrillation episode number (other variables held constant) in pentobarbital-anesthetized dogs. The correlation coefficient for each dog was between 0.77 and 0.98 (P less than 0.01), and both positive and negative slopes were found. Based on these results, threshold current was modeled for computer simulation as a linear function of episode number. The model was thus purely deterministic with no random variability. For each simulated experiment, several parameters were varied: order of shocks (increment, decrement, random order), slope of threshold function, and percent error of the initial threshold. Several hundred computer simulations were performed to determine the effect of varying these parameters. In all cases, threshold-frequency distributions and sigmoidal dose-response curves with gradual transitions were produced. The results of this investigation demonstrate that the apparent probabilistic behavior of defibrillation can be produced by a deterministic relationship.

Animals↗
PubMed1991

Defibrillation shocks increase myocardial pacing threshold: an intracellular microelectrode study.

Defibrillation is known to cause inability to pace the heart acutely, but the mechanism is unknown. This study used microelectrode techniques to directly evaluate the effect of defibrillation shocks on the pacing threshold and membrane potentials from superfused guinea pig papillary muscles. Failure of pacing stimuli to induce action potentials (pacing failure) followed shocks of 50-200 V/cm, with pacing failure duration correlated with shock intensity. Increasing pacing strength from one to three times diastolic threshold decreased the incidence and duration of pacing failure. Decreased extracellular calcium concentration and verapamil added to the superfusate increased the duration of pacing failure. Membrane potential depolarization occurred after shock, but pacing failure did not correlate with depolarization magnitude. We conclude that defibrillation shocks directly cause shock intensity-dependent increase of myocardial pacing threshold. The pacing threshold of the myocardium can be increased after defibrillation shock independent of hypoxia or shock-induced depolarization and may involve membrane changes in calcium handling.

Action Potentials↗
PubMed1994

Dysfunction and safety factor strength-duration curves for biphasic defibrillator waveforms.

Newly developed biphasic waveforms significantly lower defibrillation threshold in animal and clinical models. However, underlying mechanisms and optimum waveform shape are unknown. Defibrillation shocks produce dysfunction; safety factor, the ratio of shock intensity inducing dysfunction to that producing stimulation of partially refractory cells, is an important parameter for defibrillator waveforms. We determined dysfunction and safety factor strength-duration curves for symmetric and asymmetric (50% undershoot) monophasic and biphasic rectangular (0%-tilt) waveforms. Dysfunction threshold, defined as the voltage producing a 4-s postshock contractile arrest, was determined for waveforms with total durations from 1 to 40 ms. For all waveforms, dysfunction threshold decreased with waveform duration. At all durations, dysfunction threshold was similar for symmetric monophasic and biphasic waveforms with the same total duration. In contrast, asymmetric biphasic waveforms increased dysfunction threshold 14 +/- 3% (P < 0.005) compared with monophasic control waveforms. Because long-duration, low-tilt, biphasic waveforms improve excitation threshold for refractory cells, they should improve defibrillation threshold. Asymmetric waveforms have the additional advantage of improving safety factor by reducing postshock dysfunction.

Animals↗
PubMed1998

Defibrillation depresses heart sarcoplasmic reticulum calcium pump: a mechanism of postshock dysfunction.

Presently, the only therapy for ventricular fibrillation is delivery of high-voltage shocks. Despite "successful defibrillation," patients may have poor cardiac contractility, the mechanisms of which are unknown. Intracellular Ca2+ handling by the sarcoplasmic reticulum (SR) plays a major role in contractility. We tested the hypothesis that defibrillation shocks interfere with Ca2+ transport function of cardiac SR. Rats anesthetized with pentobarbital sodium had bilateral electrodes implanted subcutaneously for transthoracic shocks. A series of 10 shocks, 10 s apart, at 0-250 V was delivered from a trapezoidal defibrilator. The hearts were rapidly removed, SR-enriched membrane vesicles were isolated, and ATP-dependent Ca2+ uptake and Ca(2+)-stimulated ATP hydrolysis were determined. There was a marked, shock-related decline in Ca2+ uptake, whereas adenosinetriphosphatase activity remained unaltered. The polypeptide compositions were similar in control and shocked SR. In Langendorff hearts, shocks also decreased contractility and slowed relaxation. These data indicate that shocks with current densities similar to defibrillation depress Ca(2+)-pumping function of cardiac SR because of uncoupling of ATP hydrolysis and Ca2+ transport. Shock-induced impairment of Ca2+ pump function may underlie postshock myocardial dysfunction.

Animals↗
PubMed2002

Impact of myocardial ischemia and reperfusion on ventricular defibrillation patterns, energy requirements, and detection of recovery.

BACKGROUND: Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF. METHODS AND RESULTS: The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5xE-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for > or = 30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5xE-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6+/-5.3 seconds. CONCLUSIONS: Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.

Animals↗
PubMed1999

Comparison of naive sixth-grade children with trained professionals in the use of an automated external defibrillator.

BACKGROUND: Survival after out-of-hospital cardiac arrest (OHCA) is strongly influenced by time to defibrillation. Wider availability of automated external defibrillators (AEDs) may decrease response times but only with increased lay use. Consequently, this study endeavored to improve our understanding of AED use in naive users by measuring times to shock and appropriateness of pad location. We chose sixth-grade students to simulate an extreme circumstance of unfamiliarity with the problem of OHCA and defibrillation. The children's AED use was then compared with that of professionals. METHODS AND RESULTS: With the use of a mock cardiac arrest scenario, AED use by 15 children was compared with that of 22 emergency medical technicians (EMTs) or paramedics. The primary end point was time from entry onto the cardiac arrest scene to delivery of the shock into simulated ventricular fibrillation. The secondary end point was appropriateness of pad placement. All subject performances were videotaped to assess safety of use and compliance with AED prompts to remain clear of the mannequin during shock delivery. Mean time to defibrillation was 90+/-14 seconds (range, 69 to 111 seconds) for the children and 67+/-10 seconds (range, 50 to 87 seconds) for the EMTs/paramedics (P<0.0001). Electrode pad placement was appropriate for all subjects. All remained clear of the "patient" during shock delivery. CONCLUSIONS: During mock cardiac arrest, the speed of AED use by untrained children is only modestly slower than that of professionals. The difference between the groups is surprisingly small, considering the naïveté of the children as untutored first-time users. These findings suggest that widespread use of AEDs will require only modest training.

Adult↗
PubMed2001

Successful ventricular defibrillation by the selective sodium-hydrogen exchanger isoform-1 inhibitor cariporide.

BACKGROUND: Sodium-hydrogen exchanger isoform-1 (NHE-1) activation worsens functional myocardial abnormalities associated with ischemia and reperfusion. We hypothesize that these abnormalities may limit cardiac resuscitation from ventricular fibrillation (VF) and investigated whether NHE-1 inhibition with the benzoylguanidine derivative cariporide could improve resuscitability, postresuscitation myocardial function, and short-term survival in isolated heart and intact rat models of VF. Methods and Results-- In the isolated rat heart, VF was induced for 25 minutes. Perfusion was interrupted for the initial 10 minutes and restarted at 10% of baseline flow for the remaining 15 minutes (simulating chest compression). Cariporide ameliorated ischemic contracture, prevented postresuscitation diastolic dysfunction, and favored earlier return of contractile function. In the intact rat, cariporide, injected into the right atrium before chest compression was started (after 6 minutes of untreated VF), prompted spontaneous defibrillation between minutes 7 and 9 of chest compression in 6 of 8 rats. In contrast, electrical defibrillation was required in each of 8 control rats after completion of a predetermined 16-minute interval of VF. After resuscitation, cariporide-treated rats had less ventricular ectopic activity and normalized their hemodynamic function faster. Electrical defibrillation was then timed in control rats to match the time when spontaneous defibrillation occurred in cariporide-treated rats. With comparable VF duration, postresuscitation hemodynamic dysfunction was ameliorated by cariporide, but only when more severe ischemia was modeled by prolongation of the interval of untreated VF from 6 to 10 minutes. CONCLUSION: NHE-1 inhibition may represent a novel and remarkably effective intervention for resuscitation from VF.

Animals↗
PubMed1977

Transthoracic ventricular defibrillation in the 100 kg calf with unidirectional rectangular pulses.

The effectiveness in reversing ventricular fibrillation of 30 seconds duration of unidirectional rectangular-wave shocks having pulse widths of 0.5 through 64 msec, pulse amplitudes of 35, 50, 70, 100, and 140 amp, and pulse energies of 109 through 1,660 J was studied in 3,303 transthoracic fibrillation-defibrillation episodes in 100 kg calves. A total of 38 animals were used in the study. Postdefibrillation electrocardiograms were recorded. Families of curves of percent successful defibrillation vs pulse duration, percent successful defibrillation vs pulse energy, duration of postdefibrillation complete block or standstill vs energy, and time required for a return to normal sinus rhythm vs energy were derived. The most effective waveform studied (70 amp--8 msec--862 J) yielded defibrillation on the initial attempt in 93% of 120 episodes. In general, the duration of complete block or standstill and the time required for a return to normal sinus rhythm increased with increasing pulse current and pulse energy.

Animals↗
PubMed1979

Scaling current and energy with body weight: requirements for the transthoracic ventricular defibrillation of calves as they grow from 50 to 150 kg.

To test the hypothesis that the effectiveness of a shock in achieving ventricular defibrillation is relatively independent of body weight if electrode diameter is proportional to the one-third power and current is proportional to the two-thirds power of weight, we studied defibrillation rates in 10 calves as they increased weight. At 50 kg, each calf was subjected to 20 fibrillation-defibrillation episodes using 10.3-cm diameter electrodes and 32-amp, 4-msec rectangular pulses for defibrillation. Two days after the original study, each calf underwent 20 additional episodes involving 44-amp pulses. With the specified scaling of electrode diameter and pulse amplitude, the two studies were repeated at weight intervals of 25 kg as the animals grew. Six calves survived. In the study that started with 32-amp pulses, first-shock success values of 28%, 49%, 66%, 51% and 23% were found in the six surviving calves at 50, 75, 100, 125 and 150 kg, respectively. The corresponding values were 93%, 96%, 93%, 94% and 91% in the study that started with 44-amp pulses. While the results of the 32-amp study fail to support our initial hypothesis, those obtained in the 44-amp current study appear compatible with the hypothesis.

Animals↗
PubMed1981

Transthoracic resistance in human defibrillation. Influence of body weight, chest size, serial shocks, paddle size and paddle contact pressure.

Successful defibrillation depends on delivery of adequate electrical current to the heart; one of the major determinants of current flow is transthoracic resistance (TTR). To study the factors influencing TTR, we prospectively collected data from 44 patients undergoing emergency defibrillation. Shocks of 94-450 J delivered energy were administered from specially calibrated Datascope defibrillators that displayed peak current flow, thereby permitting determination of TTR. Shocks were applied from standard (8.5-cm diameter) or large (13 cm) paddles placed anteriorly and laterally. First-shock TTR ranged from 15-143 omega. There was a weak correlation between TTR and body weight (r = 0.45, p less than 0.05) and a stronger correlation between TTR and chest width (r = 0.80, p less than 0.01). Twenty-three patients who were defibrillated using standard 8.5-cm paddles had a mean TTR of 67 +/- 36 omega (+/- SD), whereas 21 patients who received shocks using paddle pairs with at least one large (13 cm) paddle had a 21% lower TTR of 53 +/- 24 omega (p = 0.05, unpaired t test). Ten patients received first and second shocks at the same energy level; TTR declined only 8%, from 52 +/- 19 to 48 +/- 16 omega (p less than 0.01, paired t test). In closed chest dogs, shocks were administered using a spring apparatus that regulated paddle contact pressure against the thorax. Firmer contact pressure caused TTR to decrease 25%, from 48 +/- 22 to 36 +/- 17 omega (p less than 0.01, paired t test). Thus, human TTR varies widely and is related most closely to chest size. TTR declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and increases in current flow can be achieved by using large paddles and applying firm paddle contact pressure.

Animals↗
PubMed1985

Automated impedance-based energy adjustment for defibrillation: experimental studies.

In defibrillation, current flow depends on the energy selected and the transthoracic impedance. If transthoracic impedance is high, current flow may be inadequate to defibrillate. We developed a method by which high transthoracic impedance is automatically compensated for by an increase in operator-selected energy when impedance is high. Transthoracic impedance was predicted in advance of the first shock by passing a low-level current between the defibrillator electrodes during the defibrillator charge cycle; a microprocessor monitored current flow and determined impedance. In 28 mongrel dogs we manipulated transthoracic impedance by placing glycerin-soaked gauze pads between the paddle electrodes and the chest. If the predicted impedance exceeded a preset value, the delivered energy was automatically increased by 40% or 100%. Using this impedance-based energy adjustment technique, we found significant improvements in current flow and success rate of shocks when energy was automatically increased to compensate for high transthoracic impedance. The use of transthoracic impedance as a basis for energy adjustment appears a promising technique to minimize the hazards of high electrical energy; it allows low-energy shocks in most patients while avoiding inappropriate low energies in patients with high impedance. Clinical trials are justified.

Animals↗
PubMed1986

Some factors affecting bubble formation with catheter-mediated defibrillator pulses.

Factors affecting bubble formation during delivery of defibrillator pulses to arrhythmogenic cardiac tissue via a catheter are unknown. We investigated the role of energy, electrode surface area, interelectrode distance, and electrode polarity on bubble formation and on current and voltage waveforms during delivery of damped sinusoidal discharges from a standard defibrillator to anticoagulated bovine blood. Gas composition was studied with mass spectrometry. Defibrillator energy settings were varied between 5 and 360 J. The principal catheter used for study was a Medtronic 6992A lead. Additional electrodes tested included 2, 5, and 10 mm long No. 6F, 7F, and 8F copper electrodes. Interelectrode distances used to assess the effect of anode-cathode spacing were 1, 5, 10, and 20 cm. Bubble volume increased linearly from 0.043 to 0.134 ml per cathodal pulse and from 0.030 to 3.50 ml per anodal pulse as energy settings were increased from 5 to 360 J (r = .99). Typical smooth waveforms for both current and voltage were seen only in the absence of bubbles. The voltage waveform was distorted for each cathodal pulse of 100 J or more and for each anodal pulse of 10 J or more only if bubbles were present. The effect of electrode surface area on bubble formation was tested at a 200 J energy setting and at a 10 cm interelectrode distance with the use of cathodal pulses. Bubble formation varied inversely with electrode surface area (r = .876). Bubble formation, however, varied minimally as interelectrode spacing was changed from 1 to 20 cm. The effect of polarity on bubble formation when the Medtronic 6992A distal electrode and an 8.5 cm disk electrode separated by 10 cm were used was highly significant. For a 200 J pulse, bubble formation with the catheter as anode was 3.30 +/- 0.10 ml and with the catheter as cathode it was 0.070 +/- 0.002 ml (p less than .001). Mass spectrometry of both anodal and cathodal gas samples demonstrated the constituents of the gas bubble to include a variety of gases, which is inconsistent with simple electrolytic production of the bubbles observed. The predominance of nitrogen in either polarity sample suggested that the principal source of the bubble was dissolved air. In summary, bubble formation at an electrode receiving damped sinusoidal outputs from a standard defibrillator does not vary significantly with varying interelectrode distance. However, it is directly proportional to energy and inversely proportional to electrode surface area. Anodal catheter discharges produce considerably more bubbles than do cathodal discharges.(ABSTRACT TRUNCATED AT 400 WORDS)

Catheterization↗
PubMed1986

Effects of varying electrode configuration with catheter-mediated defibrillator pulses at the coronary sinus orifice in dogs.

We compared two methods of delivering single damped sine-wave defibrillator pulses to the coronary sinus orifice in 20 dogs. Ten dogs had "unipolar" (coronary sinus to precordial disc) and 10 had "bipolar" (coronary sinus proximal to coronary sinus distal electrode) discharges. Delivered voltage, current, and energy were recorded during each pulse. Electrophysiologic testing was done before and 4 weeks after the procedure. Histologic examination of the atrioventricular groove was done at 1 mm serial sections. For the unipolar configuration a 200 J defibrillator pulse resulted in a peak voltage of 3370 +/- 125 V, a peak current of 21 +/- 4 A, and a delivered energy of 253 +/- 29 J as compared with 3010 +/- 99 V, 70 +/- 4 A, and 144 +/- 18 J, respectively, for the bipolar configuration (p less than .001). Three dogs (two with bipolar, one with unipolar pulses) had gross coronary sinus rupture and died from acute pericardial tamponade. In addition, irrespective of electrode configuration, all dogs showed microscopic rupture of the coronary sinus internal elastic membrane. Transmural atrial scarring occurred in all 10 dogs that received a unipolar pulse but in only two dogs that received a bipolar pulse (p = .0004). Unlike the atrium, injury to the left ventricle was limited in both groups. Similarly, injury to the periannular myocardium was inconsistent and not transmural in either group. No significant electrophysiologic changes were observed. With the present technique, unipolar rather than bipolar catheter-mediated defibrillator pulses result in transmural atrial injury that might prevent accessory pathway conduction. Regardless of electrode configuration, high-energy defibrillator pulses consistently cause some degree of coronary sinus rupture, most likely related to a barotraumatic mechanism.

Animals↗
PubMed1990

An analysis of the cost effectiveness of the implantable defibrillator.

The automatic implantable defibrillator has been shown to decrease the mortality of patients who have survived cardiac arrest due to ventricular tachycardia or fibrillation and are at high risk for recurrence. We performed a cost-effectiveness analysis of this seemingly expensive new technology with data obtained from the 1984 Medicare data base, the medical literature, Medicare carriers, individual pharmacies and hospitals, and expert opinion. Analyzing combinations of principal and secondary discharge diagnoses across 18 diagnosis-related groups, we estimated the cost of hospitalization for a comparison group of patients. Hospitalization costs for the defibrillator group were obtained from reported empirical data. Rehospitalization rates and other health-care use estimates were solicited from an expert panel of physicians, and mortality rates for both groups were obtained from the literature. Using a decision-analytic model, we estimated that the net cost effectiveness of the defibrillator, when used in the high-risk patient, is approximately $17,100 per life-year saved, with sensitivity analyses suggesting that the true value lies between $15,000 and $25,000. This estimate is well within the range that is currently accepted by the US medical care system for other life-saving interventions. We also estimated the cost effectiveness of the defibrillator in a 1991 scenario to be $7,400 per life-year saved, when the device would have greater longevity, would be programmable, and would not require a thoracotomy. Sensitivity analyses suggest that the true value lies between a value that is cost saving (less expensive than pharmacologic therapy) and $19,600 per life-year saved.

Arrhythmias, Cardiac↗
PubMed1992

Effects of lidocaine on relation between defibrillation threshold and upper limit of vulnerability in open-chest dogs.

BACKGROUND: The purpose of the present study was to test the effects of lidocaine on the relation between the defibrillation threshold and the upper limit of vulnerability. METHODS AND RESULTS: The shock strength associated with a 50% probability of successful defibrillation (DFT50) and the shock strength associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) were determined in 11 open-chest dogs by using the delayed up-down method before and during lidocaine (seven dogs) or normal saline (four dogs) infusion. The ventricles were paced at a cycle length of 300 msec. Shocks of various strengths were then given via a patch-patch electrode configuration on the anterior and posterior surfaces of the ventricle to determine the ULV50. Once ventricular fibrillation was induced, shocks were given 15-20 seconds later via the same electrode configuration to determine the DFT50. Lidocaine infusion resulted in a serum level of 15 +/- 4 micrograms/ml. This was associated with a lengthening of the QT interval but not with the widening of the QRS complex. In all dogs, both the ULV50 and the DFT50 increased significantly when tested during lidocaine infusion. Mean ULV50 during lidocaine infusion was 496 +/- 70 V or 13.1 +/- 4.3 J, which were significantly higher than the baseline values of 333 +/- 67 V or 5.3 +/- 2.2 J (p less than 0.001 for both voltage and energy). Mean DFT50 during lidocaine infusion was 407 +/- 41 V or 8.7 +/- 1.7 J, which were significantly higher than the baseline values of 300 +/- 38 V and 4.4 +/- 1.1 J (p = 0.004 for voltage and p = 0.013 for energy). The r values between the ULV50 and the DFT50 were 0.79 (p = 0.037) for voltage and 0.80 (p = 0.030) for energy at baseline and 0.85 (p = 0.016) for voltage and 0.88 (p = 0.009) for energy during the lidocaine infusion. However, the increments of the ULV50 (163 +/- 88 V or 7.8 +/- 4.6 J) were significantly greater than the increments of the DFT50 (107 +/- 51 V or 4.4 +/- 1.9 J, p = 0.035 for voltage and p = 0.023 for energy). Normal saline infusion did not alter DFT50 or ULV50. CONCLUSIONS: Lidocaine infusion significantly increases both ULV50 and DFT50. These results are compatible with the upper limit of vulnerability hypothesis of defibrillation. However, the greater increase of the upper limit of vulnerability than the defibrillation threshold with lidocaine infusion indicates that other factors may also need to be considered to explain the results.

Algorithms↗
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↗