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Biomedical subjects

R A Malkin

Publications and source records attributed to R A Malkin.

At least 19 recordsLinked to original sources
PubMed2003

Frequency dependence of the cardiac threshold to alternating current between 10 Hz and 160 Hz.

It is still unclear what fundamental criteria influence the ability of alternating current (AC) to induce ventricular fibrillation (VF) in vivo. As the VF threshold has a bowl-shaped relationship with frequency (showing a minimum threshold at some frequency), similar to the nervous system, one proposed model has assumed that the mechanisms underlying AC stimulation of nerves are at work for VF induction. More recent work has suggested a second approach, whereby a simple RC-like model is sufficient to understand the cardiac AC stimulation threshold's frequency dependence, suggesting that some unarticulated mechanism is at work for VF. The paper directly tests these two models. In 12 intact dogs and 20 intact guinea pigs, DC pulses were used to stimulate AC square and AC sine waves at 10, 20, 40, 80 and 160 Hz. All electrodes were endocardial, with the return electrode being on a paw or thorax. It was found that, for square and sine wave stimulation in both dogs and guinea pigs, the stimulation threshold increased monotonically with frequency from 10 Hz up to 160 Hz (p < 0.01 for dogs and guinea pigs). Between 80 and 160 Hz, the AC stimulation threshold doubled, exactly as predicted by an RC model. It was concluded that the AC stimulation threshold is not bowl-shaped and is best understood with an RC model. As the VF threshold does exhibit a bowl-shape with frequency, as opposed to the stimulation threshold which does not, the VF induction frequency dependence must have different origins.

Animals↗
PubMed2001

Excitation of a cardiac muscle fiber by extracellularly applied sinusoidal current.

INTRODUCTION: The goal of this study was to examine the effect of AC currents on a cardiac fiber. The study is the second in a series of two articles devoted to the subject. The initial study demonstrated that low-strength sinusoidal currents can cause hemodynamic collapse without inducing ventricular fibrillation. The present modeling study examines possible electrophysiologic mechanisms leading to such hemodynamic collapse. METHODS AND RESULTS: A strand of cardiac myocytes was subjected to an extracellular sinusoidal current stimulus. The stimulus was located 100 microm over one end. Membrane dynamics were described by the Luo-Rudy dynamic model. Examination of the interspike intervals (ISI) revealed that they were dependent on the phase of the stimulus and, as a result, tended to take on discrete values. The frequency dependency of the current threshold to induce an action potential in the cable had a minimum, as has been found experimentally. When a sinus beat was added to the cable, the sinus beat dominated at low-stimulus currents, whereas at high currents the time between action potentials corresponded to the rate observed in a cable without the sinus beat. In between there was a transition region with a wide dispersion of ISIs. CONCLUSION: The following phenomena observed in the initial study were reproduced and explained by the present simulation study: insignificant effect of temporal summation of subthreshold stimuli, frequency dependency of the extrasystole threshold, discrete nature of the ISI, and increase in regularity of the ISI with increasing stimulus strength.

Action Potentials↗
PubMed2001

Mechanisms by which AC leakage currents cause complete hemodynamic collapse without inducing fibrillation.

INTRODUCTION: The first study of weak alternating current (AC) stimulation in closed chest humans showed that complete hemodynamic collapse can occur below the threshold for inducing ventricular fibrillation (VF), a heretofore unknown danger to patients. This article, and the accompanying simulation article, explore the mechanisms responsible for the collapse. METHODS AND RESULTS: A quadripolar pacing catheter was placed in the right ventricle (RV) of six dogs. The tip of the catheter (17 mm2) carried 5 seconds of AC stimulation ranging from 10 to 160 Hz and 10 to 1,000 microA. The lead II body surface ECG, femoral artery pressure, and a bipole from the proximal pair of electrodes on the RV catheter were recorded 2 seconds before, during, and 2 seconds after stimulation. Based on the blood pressure, every episode was categorized as VF, COLLAPSE without VF, extrasystolic without COLLAPSE (EFFECT), or having caused no effect (NSR). The electrical activation interval (interspike interval [ISI]) from the RV bipole was compared with the mechanical activation interval, determined from M-mode ultrasound. COLLAPSE is associated with a short ISI (NSR = 408+/-110 msec; EFFECT = 305+/-113 msec; COLLAPSE = 179+/-25 msec; P < 0.001) with a high degree of regularity (P < 0.001): coefficient of variation of ISI for COLLAPSE (0.038+/-0.069) versus VF (0.389+/-0.222), EFFECT (0.420+/-0.241), and NSR (0.016+/-0.048). Electrical activation and mechanical activation rates occurred at integer multiples of the AC stimulation period. CONCLUSION: COLLAPSE (86+/-37 microA; minimum 50 microA in two animals) occurs below the VF threshold (108+/-28 microA) by causing rapid, regular excitation.

Action Potentials↗
PubMed2001

Defibrillation and the geometry of the heart: a novel measurement with implications for defibrillation mechanisms.

We present a novel measurement for studying defibrillation mechanisms: the time course of changes in the size of the left ventricular (LV) cavity within 500 ms following defibrillation. Mechanical changes can be linked to electrical mechanisms via an understanding of excitation-contraction coupling. Eight mongrel dogs were internally defibrillated 5-50 seconds (including backup shocks) after the onset of 20 ventricular fibrillation (VF) episodes per animal. Two dimensional, short axis, LV cavity, ultrasound images were recorded at 30 frames per second just prior to inducing VF, during defibrillation and following the shock. Each frame was individually analysed to yield the LV cavity area as a function of time. Defibrillation shocks were followed by a highly reproducible phenomenon: (1) a dramatic and rapid increase in LV area, (2) a more or less prominent LV area plateau and (3) a decrease in the LV area. The peak fractional area increase ranged from 1.65 to 4.64 times larger than the baseline (LV area just prior to defibrillation), averaging 2.18 +/- 0.686. Successful shocks took significantly longer (p < 0.01) to return to 1.3 times the baseline (407 +/- 209 ms) than unsuccessful shocks (296 +/- 130 ms). Extrapolating to electrical mechanisms, our novel measurement demonstrates that defibrillation causes immediate relaxation and therefore suggests a significant role for deexcitation in defibrillation.

Animals↗
PubMed2000

Hemodynamic collapse, geometry, and the rapidly paced upper limit of ventricular vulnerability to fibrillation by T-wave stimulation.

There is an upper limit to the vulnerability (ULV) of the ventricles to fibrillation (VF) induced by T-wave stimuli. Across species, disease states, and pharmacological treatments, the ULV is correlated to the defibrillation threshold (DF50). However, one factor known to increase the ULV far above the DF50 is rapid pacing. In this article we test the hypothesis that this increase is owing to an accompanying hemodynamic collapse or geometric change. In 18 dogs, T-wave stimuli were delivered from transvenous defibrillating electrodes. The T-wave shock strength that induced VF 50% of the time (the ULV50) was measured using a 10-step Bayesian up-down protocol. T-wave stimuli were delivered after 15 paced beats at one of several rates: normal (80% of the R-R interval), rapid (the interval just fast enough to cause hemodynamic collapse), or 10 milliseconds greater than rapid (which did not cause hypotension). We measured the geometry of the left ventricle at the moment of T-wave stimulation using linear ultrasound. Rapid pacing significantly increased the ULV50 above the normal rate ULV (507 +/- 62.9 vs 379 +/- 70.6 V, P < .005, n = 18), even in the subset without hemodynamic collapse (505 +/- 84.4 vs 394 +/- 66.5 V, P < .005, n = 6). No significant geometric changes were noted between rapid (19.8 mm) and normal (20.6 mm, n = 6, P < NS) pacing, but QT interval reduction appears to correlate with the ULV50 (QT vs ULV50, r > 0, P < .01). Rapid pacing can dramatically increase the measured ULV50. The most likely cause is a concurrent change in the electrophysiology, eg, QT or APD, of the myocardium. As the only known factor to consistently alter the relationship between ULV and the DF50, rapid pacing offers a unique opportunity for the study of the link between defibrillation and ULV testing.

Animals↗
PubMed2000

A simulation study evaluating the performance of high-density electrode arrays on myocardial tissue.

Multielectrode arrays used to detect cellular activation have become so dense (electrodes per square millimeter) as to jeopardize the basic assumptions of activation mapping; namely, that electrodes are points adequately separated as to not interfere with the tissue or each other. This paper directly tests these assumptions for high-density electrode arrays. Using a finite element model with modified Fitzhugh-Nagumo kinetics, we represent electrodes as isopotential surfaces of varying widths and spacing ratio (SR) (center-to-center spacing divided by electrode width). We examine the signal strength and ability of a single electrode to detect activation due to a passing wavefront. We find that high-density arrays do not cause significant wavefront curvature or alter activation timing in the underlying tissue. Relationships between signal strength, cross talk, and array design are explained by the interaction of the propagating wavefront and induced sources on the isopotential electrodes. Sensitivity analysis shows that these results may be generalized to a wide range of physiologically relevant designs and applications. We conclude that electrode array designs in which electrode spacing greatly exceeds electrode diameter are overly conservative and that arrays with a SR of less than 2.0 may perform successfully in electrophysiological studies.

Animals↗
PubMed2000

Construction of a very high-density extracellular electrode array.

Cellular activation mapping (specifying in time and space the electrical activation sequence of cells) is a well-established basic research tool in cardiac, neural, and gastric physiology. Much recent research in cardiac mapping has focused on large arrays (>200 electrodes) with small electrodes (<500 microm). Construction of such arrays using standard techniques is tedious and yields irregular electrode spacing. We present a novel construction technique that rapidly produces large arrays with regularly spaced small electrodes. For methods, fine-pitch copper ribbon cables, insulated with either polyvinylchloride (PVC) or polyimide (flexible printed circuit; FPC), were assembled together such that the active surface was the cut end of the cable. The cut end was sanded and polished, then coated with silver and sometimes silver chloride. Once completed, the alternating current (AC) root-mean-square (rms) potential was measured between two adjacent, individual electrodes. Polarization testing was conducted according to a previously reported protocol (Witkowski FX and Penkoske PA. J Electrocardiol 21: 273-282, 1988). Activation mapping was conducted in the open-chest guinea pig with both pacing- and defibrillation- strength stimuli. In terms of results, four PVC and three FPC arrays were constructed, ranging from 4 to 400 electrodes. Two hours of labor were needed to create a complete electrode array, independent of the number of electrodes, including connectors and silver/silver chloride coating. As expected, the addition of a silver/silver chloride coating significantly reduced (0.76-0.42 mV, P < 0.001) the AC rms potential difference between two electrodes. A nearly immediate recovery of the potential difference between adjacent pairs of silver/silver chloride electrodes was observed after defibrillation stimuli.

Animals↗
PubMed1999

Cardiovascular collapse caused by electrocardiographically silent 60-Hz intracardiac leakage current. Implications for electrical safety.

BACKGROUND: The national standard for safe 60-Hz intracardiac leakage current under a single-fault condition is 50 microA. This standard is intended to protect patients from alternating current (AC) at levels below the threshold for sensation, but the minimum unsafe level for AC in closed-chest humans is not known. To determine this value, we studied 40 patients at testing of implantable cardioverter-defibrillators using a programmable source of 60-Hz AC. METHODS AND RESULTS: We applied AC for 5-second test periods in increasing strengths until ventricular fibrillation (VF) was induced or 1 mA was reached. Two current paths were tested: bipolar, between tip and ring electrodes of a right ventricular pacing catheter, and unipolar, from tip to a remote electrode. We observed a characteristic sequence of 3 responses as AC was increased: (1) intermittent ventricular capture with QRS morphology identical to pacing through the electrodes (minimum value, 20 microA); (2) continuous capture at cycle length 282+/-88 ms (minimum value, 32 microA); and (3) VF persisting after AC termination (minimum value, 49 microA). Continuous capture caused loss of pulsatile arterial pressure and cardiovascular collapse (mean arterial pressure, 32+/-8 mm Hg) for the duration of AC with no ECG evidence of AC stimulation. Thus, the clinical picture was that of hypotensive ventricular tachycardia (VT). The continuous-capture threshold was </=50 microA in 9 patients (22%) for bipolar AC and in 5 (12%) for unipolar AC. All patients showed continuous capture over a wide range for both bipolar AC (68+/-18 to 216+/-238 microA) and unipolar AC (84+/-27 to 278+/-226 microA). CONCLUSIONS: Leakage current causes cardiovascular collapse at levels below the VF threshold. Stimulation by silent AC that is neither felt nor visible on the ECG presents as hypotensive VT. In patients with intracardiac electrodes, leakage current less than or equal to the present standard of 50 microA may cause VT or VF. The safety standard for leakage current lasting >/=5 seconds should be </=20 microA. This standard should be based on the continuous-capture threshold.

Electric Stimulation↗
PubMed1999

Experimental cardiac tachyarrhythmias in guinea pigs.

Despite years of intense research into the mechanisms of defibrillation, there remain many unanswered questions. In many fields, hypotheses are first tested in rodent models before confirming the results in larger animals. This work suggests the guinea pig as a rodent model for defibrillation. Twenty-eight guinea pigs were studied, all male retired breeders weighing over 900 g. T-wave stimuli (upper limit of vulnerability [ULV]) were given after 15 rapid pacing beats, since the rapid pacing has been suggested to extend the tachyarrhythmia. Defibrillation (DF) was attempted after 5 seconds. The correlation between the ULV50 and DF50 in guinea pigs (0.82, n = 8) is very close to that seen in dogs (0.85). Also, the sensitivity of the DF50 to waveform is similar (476 +/- 176 for monophasic vs 364 +/- 94 V for biphasic P < 0.005, n = 10). The dose-response curve widths (2.3 +/- 1.7 for ULV vs 1.9 +/- 1.8 for defibrillation, n = 10) show the same trend of increasing curve widths for ULV, and similar magnitude to dogs (mean 1.8). We rarely (<1.5%) observed spontaneous conversion in less than 10 seconds. The guinea pig can be used as a model for defibrillation as it shows many of the same characteristics as dogs.

Animals↗
PubMed1999

A four-shock Bayesian up-down estimator of the 80% effective defibrillation dose.

INTRODUCTION: New defibrillation techniques are often compared to standard approaches using the defibrillation threshold. However, inference from thresholding data necessitates extrapolation from reactions to relatively ineffective shocks, an error prone procedure requiring large sample sizes for hypothesis testing and large safety margins for defibrillator implantation. In contrast, this article presents a clinically validated statistical model of a minimum error, four-shock defibrillation testing protocol for estimating the 80% effective defibrillation strength for a given patient (ED80). METHODS AND RESULTS: A Bayesian statistical model was constructed assuming that the defibrillation dose-response curve is sigmoidal, and the ED80 is between 150 and 750 V. The model was used to design a minimum predicted error testing protocol and estimates. To prospectively validate the testing protocol and estimates, 170 patients received voltage-programmed biphasic testing. Four fibrillation episodes were induced and terminated in each patient according to the Bayesian up-down protocol. In addition, a validation attempt was made at the estimated ED80 rounded up to the nearest 50 V. In order to estimate the safety margin, in 136 patients, a defibrillation attempt was made at the rounded ED80 + 100 V. Of the 170 attempts at the rounded ED80, 143 (84%) attempts terminated fibrillation. Of the 136 attempts at the rounded ED80 + 100 V, 133 (98%) were effective. CONCLUSIONS: The four-shock Bayesian up-down protocol is the first clinical protocol to accurately predict an ED80 voltage. A 100 V increment above the ED80 provides an adequate safety margin. This simple and accurate method for estimating a highly effective defibrillation dose may be a valuable tool for population-based clinical hypothesis testing, as well as defibrillator implantation.

Adult↗
PubMed1999

Defibrillation and the upper limit of vulnerability to fibrillation in a transthoracic guinea pig model.

Recent studies have shown sustained tachyarrhythmias in guinea pigs. We hypothesized that guinea pigs could be used as a model of ventricular fibrillation, focusing on defibrillation waveform efficacy and the upper limit of vulnerability to fibrillation. In 10 male guinea pigs, an esophageal/apical pacing electrode configuration was used. The electrocardiogram (ECG) and arterial blood pressure were continuously monitored. T-wave and defibrillation shocks were applied transthoracically. A modified up-down protocol was used. After up-down testing was completed, a tachyarrhythmia was induced without electrical termination. All animals died of a sustained tachyarrhythmia. The monophasic DFT50 (the 50% successful defibrillation voltage, 496 +/-176 V) was larger than the biphasic DFT50 (364+/-94 V, P < .005). The upper limit of vulnerability to fibrillation (ULV50) (the 50% successful induction voltage) was correlated with the DFT50 for both monophasic (r = .82, P < .005) and biphasic shocks (r = .88, P < .005). Its low cost and ease of handling may make the guinea pig a preferred model for some fibrillation and defibrillation studies.

Animals↗
PubMed1999

Open-thorax guinea pig model for defibrillation.

BACKGROUND AND PURPOSE: Guinea pigs are used as models for study of ventricular tachyarrhythmias (VT); however, the tachyarrhythmia often is transient and does not persist. We developed an open-thorax guinea pig model of sustained ventricular fibrillation (VF). METHODS: Bilateral thoracotomy was performed on eight guinea pigs weighing 865 to 1,464 g, and two sutures were positioned in the right ventricular apex for the purpose of pacing. Two methods were used to induce VF: a 50-Hz burst (normal pacing), and an initial 15 beats at 70% of the R-R interval followed by a 100-Hz burst for 84 beats (rapid pacing). Fifteen attempts at inducing VF were performed by use of each method. Blood pressure was recorded before and after development of VF, which was defined as VT with mean blood pressure consistently <10 mm Hg. A final observation was obtained using the normal pacing method without defibrillation. RESULTS: Use of both methods successfully induced VF. A significant relationship between body weight >1,021 g and ability to sustain and survive VF was detected. CONCLUSION: The guinea pig is a useful rodent model for the study of VF and defibrillation.

Animals↗
PubMed1998

The effect of inducing ventricular fibrillation with 50-Hz pacing versus T wave stimulation on the ability to defibrillate.

When testing an ICD, there are at least two techniques for inducing ventricular fibrillation: (1) high frequency (approximately equal to 50 Hz) pacing; and (2) a single T wave stimulus. It is generally assumed that these two methods yield similar results. This study directly tested this assumption. In six dogs, one defibrillation electrode was placed in the right ventricular (RV) apex and the second was placed cutaneously on the left thorax. All defibrillation and T wave stimuli were biphasic between these two electrodes. Pacing was monophasic from the tip of the RV catheter to the cutaneous patch. The voltage which defibrillates 50% of the time (DF50) was measured using a 10-step Bayesian up-down method. Observations for two DF50 measurements were randomly interleaved. For one DF50 measurement, fibrillation was induced with 99 pacing stimuli at a 20-ms pacing interval (50-Hz pacing). For the second DF50 measurement, fibrillation was induced with a single defibrillation shock of approximately 1/2 J delivered at a time corresponding to the peak of the T wave in the lead II electrogram (T wave stimuli). The average DF50 when measured after fibrillation induced with 50-Hz pacing was 379 +/- 54.6 V, as compared to 382 +/- 50.3 V when fibrillation was induced with T wave stimuli. The difference of 3 V was not statistically significant. If these results are confirmed in humans, it is reasonable to assume that the efficacy of a defibrillation shock is the same whether T wave stimuli or 50-Hz pacing are used to induce fibrillation.

Animals↗
PubMed1998

Improved guinea pig model of cardiac tachyarrhythmias.

Guinea pigs are frequently used as models for ventricular tachyarrhythmias, including polymorphic ventricular tachycardia (VT) and ventricular fibrillation. However, applications of the model for short-term therapies are limited because the arrhythmias are transient, typically lasting <5 sec. Thus, spontaneous termination cannot be easily distinguished from effective short-term therapy in standard models. Results of this study confirmed an improved induction method that consistently extends the arrhythmias to 30 sec or longer. In 10 (400- to 1200-g) male guinea pigs, a pacing electrode was advanced in the esophagus. The anode for pacing was a wire advanced through a 20-gauge needle across the diaphragm toward the ventricular apex. Two 12-mm-diameter electrodes were placed on the skin on opposing aspects of the thorax for T-wave stimulation. The blood pressure in the carotid artery was continuously monitored. Two traditional methods were used to induce VT: 2 sec of a 50-Hz square wave, and a single 200 V/5 ms transthoracic stimulus at the peak of the T-wave after pacing at 80% of the intrinsic R-R interval. A third novel method also was used: a single 200 V/5 ms transthoracic stimulus at the peak of the T-wave after a rapid pacing sequence. The rapid pacing sequence was a 25-stimulus sequence, which accelerated to end with 15 beats at the shortest pacing interval for which all pacing stimuli captured. A tachyarrhythmia was defined as any abnormally rapid surface electrocardiographic waveform lasting at least 2 sec after termination of the initiating stimulus. Between 5 and 23 attempts were made to induce tachyarrhythmias in each animal. In four additional animals (>800 g), the efficacy of an established short-term therapy for tachyarrhythmias was measured, using the proposed rapid pacing model. All arrhythmias induced by use of the three induction methods were polymorphic VT accompanied by complete hemodynamic collapse. In hearts weighing >2.5 g (body mass >800 g), 100% of arrhythmia episodes were sustained for 30 sec or longer when initiated after rapid pacing, as opposed to only 55% sustained by use of other induction methods (P < 0.01). The efficacy results for the established short-term therapy matched those previously reported for 100-kg calves. A brief period of rapid pacing facilitates initiation of consistent, sustained ventricular tachyarrhythmias in large guinea pigs, eliminating spontaneous termination as a confounding factor in the study of short-term therapies.

Animals↗
PubMed1997

Statistical analysis of signals from an intracavitary probe in a diseased heart.

A model study introduces the use of statistical signal processing to analyse the signals from an intracavitary probe. A complete derivation is given for the detection of one type of arrhythmogenic substrate, myocardial infarctions (MIs). Both the use of statistical signal processing and the detection of VT substrates, as opposed to activation maps, are unique. A quasi-stationary electromagnetic model with simplified geometry is presented. The model is used to simulate ventricular pacing in the presence of MI. The likelihood ratio is used for detection. A tabulation of the results from this model shows that an intracavitary probe can be used to detect MIs as small as 400 mm2 in 1 mV of noise with a detectability index of 0.495, where 0.5 indicates perfect detection. Sensitivity to noise can be reduced by analysing multiple heart beats. The results are only slightly affected by changing the probe from a cage frame design, which mechanically supports the electrodes on thin spokes, to a balloon design, which supports the electrodes on the surface of an insulating balloon.

Computer Simulation↗
PubMed1997

An up-down Bayesian, defibrillation efficacy estimator.

In both the clinic and the laboratory, efficacy estimators are used to estimate the shock strength required to achieve a given defibrillation success rate. In the clinic, efficacy estimators are used to estimate highly effective doses (i.e., the shock strength that defibrillates 95% of the time), in order to choose the setting for an ICD. Efficacy estimators are used in the laboratory to compare defibrillation techniques and configurations. Current efficacy estimators are inadequate because they are either difficult to use, can only estimate the shock strength that defibrillates 50% of the time, or do not yield desirable accuracy (low RMS error). This article presents a Bayesian estimation technique that forces the difference between successive test shock strengths (step-size) to be a fixed value after each measurement. Constraining the difference dramatically reduces the computational complexity of the up-down Bayesian method. This new, up-down Bayesian protocol can be used with up to 15 measurements to estimate the shock strength for any given success rate. Simulations show that the added constraint (fixed step-size) only slightly increases the rms error, as compared to the optimum Bayesian protocol. Our simulations also show that protocols can be generated for shock strengths rounded to the nearest 1, 10, or 50 V. without a great increase in RMS error. Experimental results from a subset of all the simulations are reported from six animals, showing a < -2.4% difference between the simulated and measured errors.

Animals↗
PubMed1997

The ventricular defibrillation and upper limit of vulnerability dose-response curves.

INTRODUCTION: A stimulus delivered in the T wave of a paced cardiac cycle can induce ventricular fibrillation (VF). If the stimulus strength is increased, the probability of inducing VF decreases. This study determines an ideal mathematical model (a dose-response curve) for the relationship between the shock strength and the probability of inducing VF or defibrillating. METHODS AND RESULTS: Defibrillating electrodes were implanted in the right ventricle and superior vena cava in 16 pigs. The electrode in the vena cava was electrically connected to a cutaneous patch. The same electrodes were used for both VF induction and defibrillation. T wave stimuli were given at the peak of the T wave according to a modified up-down protocol (40 V up, 20 V down). When a T wave stimulus induced VF, a defibrillation stimulus was delivered 10 seconds later, also according to the modified up-down protocol. Exponential, logistic, log-dose logistic, piecewise linear and Box-Tiao dose-response curves were fit to the resulting data using the maximum likelihood method. For the defibrillation data, it was found that only the logistic and Box-Tiao curves fit all of the animals (P < 0.05). For VF induction, only the Box-Tiao curve fit all of the animals (P < 0.05). Extrapolating along a dose-response curve that did not fit to a shock strength with a very low probability of inducing VF or a very high probability of defibrillating yielded errors as great as 610 V. CONCLUSION: The Box-Tiao dose-response curve is the best single choice for fitting VF induction or defibrillation datasets.

Animals↗