The efficacy of self-adhesive electrode pads for defibrillation and cardioversion was assessed in 80 patients who received 267 shocks from self-adhesive pads. In all but two patients, defibrillation or cardioversion was achieved at least once. The pads were equally effective when used in the apex-anterior or apex-posterior position. The transthoracic impedance using self-adhesive pads was 75 +/- 21 ohms (mean +/- standard deviation), which is similar to previously reported transthoracic impedance in defibrillation, using standard hand-held electrode paddles of 67 +/- 36 ohms. It is concluded that self-adhesive electrode pads are effective for defibrillation and cardioversion.
The purpose of this study was to determine the effect of the antiarrhythmic drugs lidocaine and bretylium on the minimal energy requirement for transthoracic defibrillation--the defibrillation threshold. Closed chest dogs were anesthetized with chloralose or pentobarbital; lidocaine was administered at varying rates for 2 hours and defibrillation threshold periodically redetermined. Similar protocols were followed for bretylium. Serum lidocaine levels from therapeutic to toxic ranges were obtained, and up to a 60% (p less than 0.05) increase in defibrillation threshold in the pentobarbital-anesthetized dogs was demonstrated. In chloralose-anesthetized dogs the lidocaine effect was modest, with only a 10 to 20% rise in defibrillation threshold (p = NS) despite similar increases in serum lidocaine levels. Thus, lidocaine increases the minimal energy requirements for transthoracic defibrillation, but this effect is in part anesthesia-related, indicating a lidocaine-pentobarbital interaction. When phentolamine was administered to chloralose-anesthetized dogs receiving lidocaine, defibrillation threshold rose 13% (p less than 0.05); this suggests that alpha-adrenergic receptor blockade is at least in part the mechanism of the pentobarbital-lidocaine interaction on defibrillation threshold. Bretylium with either anesthetic had no significant effect on defibrillation threshold.
After permanent coronary artery occlusion, the extent of two-dimensional echocardiographically detected dyskinesis correlates well with infarct size. Reperfusion after coronary artery occlusion decreases infarct size; however, contractile function of myocardium salvaged in this way may remain depressed for several weeks. The purpose of this study was to explore the relationship between echocardiographically detected dyskinesis and infarct size in reperfused myocardium. We hypothesized that after transient coronary artery occlusion, the relationship between dyskinesis and infarct size would be altered because of the prolonged depression of contractile function after reperfusion so that dyskinesis would not predict infarct size. We also wanted to explore two related questions: (1) Does inotropic stimulation of reperfused myocardium result in improved systolic function in segments that are dysfunctional but not necrotic? (2) Does the relationship between infarct size and coronary risk region, which is linear in myocardium subjected to permanent coronary occlusion, remain linear in myocardium subjected to a sequence of occlusion and reperfusion? Thirty-seven sedated dogs with preplaced circumflex occluders underwent 1 or 2 hr of coronary artery occlusion, then 2 or 10 days of reperfusion. The percentage of the left ventricle that was dyskinetic was estimated from short-axis two-dimensional echocardiograms at the chordal and papillary muscle level obtained at control, after 1 or 2 hr of occlusion, after 20 min of reperfusion, and after 2 or 10 days of reperfusion. At 2 or 10 days of reperfusion, echocardiograms were also obtained during infusion of dobutamine. Area at risk was determined from postmortem barium-gelatin angiography and infarct size was determined at pathologic examination. We found a significant linear correlation between infarct size and risk region size in reperfused myocardium. Significant dyskinesis was present at 60 or 120 min of occlusion and decreased by 5% to 60% of the occlusion value after 2 days of reperfusion. There was no further change in extent of dyskinesis between 2 days and 10 days of reperfusion. There was no significant correlation between infarct size and percent dyskinesis at either 2 days (r = .09) or 10 days (r = .29) of reperfusion, in contrast to the good correlation we have previously demonstrated between dyskinesis and infarct size 2 days after permanent coronary artery occlusion. Infusion of dobutamine at 2 and 10 days did not result in significantly decreased dyskinesis. Thus, in this canine preparation the extent of dyskinesis resulting from 1 or 2 hr of circumflex occlusion is reduced by reperfusion but fails to correlate with infarct size. These findings suggest that the extent of regional dyskinesis early after acute thrombolysis may not predict the final extent of myocardial injury or salvage. Circulation 71, No. 6, 129271, No. 6, -130071, No. 6, , 1985 ISCHEMIC REGIONAL DYSKINESIS -systolic expansion of the left ventricle with consequent wall thinning -was...
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