Radio-frequency ablation: effect of voltage and pulse duration on canine myocardium.

The purpose of this investigation was to examine in vivo the relationship of radio-frequency (RF) pulse voltage and duration on the volume of tissue injury. RF 500-kHz pulses of 20-, 40-, and 60-V amplitude (RMS) were applied to the epicardium of 18 dogs for pulsing periods of 5-20 s. Systematic and quantitative tissue analysis was then performed after 30 days. No chronic lesions were evident on microscopic examination for 20-V RF pulse applications up to 15 s. Application of 20-V pulses for 20 s produced small lesions having a volume of 2.4 +/- 0.7 mm3. At 40 V, the volume of tissue injury ranged from 39.1 +/- 10.3 mm3 for 5 s of pulse application to 128.8 +/- 24.8 mm3 for 20 s of pulse application. Over the first 15 s of 40-V pulse application, the volume of tissue injury increased as pulse application time increased. There was no further increase in tissue injury for 40-V pulsing durations greater than 15 s. At 60 V, volumes of tissue injury ranged from 122.7 +/- 33.5 mm3 at 5 s to 313.6 +/- 73.7 mm3 at 20 s. Lesion size increased significantly for pulse durations of up to 10 s. Thereafter, 60-V pulses yielded little increase in tissue injury. In addition, persistent 60-V pulsing for periods greater than 9 s duration resulted in arcing and tissue vaporization in 28% of the applications. Thus RF energy is limited in its ability to create safe and effective tissue injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Biophysical and anatomical considerations for safe and efficacious catheter ablation of arrhythmias.

The development of catheter ablation techniques for therapy of cardiac arrhythmias continues to evolve. Although many patients have benefited from catheter ablation procedures, failure to ablate the arrhythmogenic substrate and complications from the pulse used in these procedures remain too frequent occurrences. The purpose of this review is to focus on these problems of inefficacy and safety with attention directed to the role various direct current and radiofrequency pulses have had in the genesis of these difficulties.

Effect of voltage and charge of electrical ablation pulses on canine myocardium.

Multiple paired lesions produced by a train of high-voltage low-charge rectangular pulses (20 A, 30 microsecond) and a train of low-voltage high-charge rectangular pulses (2 A, 300 microsecond) were made to the left ventricular epicardium of 23 dogs to determine the relative influence of voltage and charge delivery on injury of canine myocardium. Both pulsing methods contained equal amounts of energy (15 J) delivered over equal periods of time (100 ms), and both pulsing methods were nonarcing and therefore nonbarotraumatic. The volume of cardiac tissue injury resulting from both types of pulses was then evaluated from planimetered serial histological sections after 1, 10, and 30 days. Over the 30-day period, lesion size progressively decreased to 56% of its original value for the high-voltage low-charge pulse. In contrast, lesion size from the low-voltage high-charge pulse remained relatively constant, decreasing only 12% of its original value. These results indicate that when energy delivery is held constant, voltage, not charge, is the dominant mediator of cell injury. Also, cells subjected to high voltages appear to recover partially over time with significantly less constancy of tissue injury than that seen with low-voltage high-charge pulses.

Cardiac, ventilatory and metabolic responses of two ecologically dissimilar species of fish to waterborne cyanide.

Changes in heart rate, ventilatory activity and oxygen consumption were determined in trout (Salmo gairdneri) and brown bullhead catfish (Ictalurus nebulosus) during exposure to a steadily increasing concentration of waterborne cyanide selected to produce death in 8-9 hours for each species. The lethal cyanide concentration for the bullheads was an order of magnitude higher than for trout. Trout developed an immediate and gradually increasing bradycardia throughout the exposure period. Cyanide produced tachycardia in the bullhead followed by a gradual onset of bradycardia as the concentration of cyanide was raised. Pericardial injection of atropine (a muscarinic cholinergic antagonist) indicated that bradycardia in the trout was due initially to increased vagal tone but later due to the direct effect of cyanide on the heart. Hyperventilation in the trout persisted throughout the exposure period, although the rate and amplitude fluctuated and was variable between individual fish. During the last hour of exposure (highest cyanide concentration), ventilation was characterized by rapid, shallow breaths followed by a sudden respiratory arrest. The bullheads exhibited hyperventilation during the first 3 hours of exposure followed by a gradual, linear drop in ventilation rate and amplitude until death occurred. Cardiac and ventilatory responses in both species were attributed to stimulation of central and peripheral chemoreceptors by cyanide. Evidence is presented which suggests the initial response in the bullheads was due, at least in part, to gustatory stimulation by the cyanide. Oxygen consumption of the trout remained above pre-exposure levels for the majority of the test period. Oxygen consumption in the bullhead paralleled the changes in heart and ventilatory rates. Whole-body lactate levels of fingerlings of both species during cyanide exposure were measured to estimate the extent of anaerobiosis. Whole-body lactate levels were much greater in the bullheads than the trout, indicating a higher capacity for anaerobiosis, possibly due to a greater fuel supply. Overall, the trout responded to cyanide in a manner similar to that produced by environmental hypoxia whereas the bullheads experienced a gustatory stimulus which masked the hypoxia-like response.