Application and evaluation of automated arrhythmia monitoring in the coronary care unit.
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Biomedical subjects
Publications and source records attributed to J Hulting.
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Ten patients with various heart diseases and ventricular arrhythmia received a single oral dose of disopyramide (DE) 200 mg. The ECG was recorded continuously for about 50 h from 2-4 h before drug administration. A statistically significant reduction in the number of ventricular ectopic beats (VEBs) was seen 1.0-3.5 h after drug intake; the average number of VEBs per 30 min decreased from 317 during the control period to 92 by 1.0-3.5 h after treatment and if one patient who did not respond is excluded, the corresponding figures were 272 and 14, respectively. Consecutive VEBs were seen in seven patients before DE was given and decreased significantly (p less than 0.05) 1.5-5.5 h after drug administration. There was no change in the PQ interval, the QRS interval showed a slight increase, whereas the QT interval was prolonged 0.5-4 h after administration of DE. A specific gas chromatographic method was used for DE assay in plasma and urine. Absorption was rapid in all patients. Urinary excretion during the first 48 h after drug intake varied between 35 and 75%. The lowest effective antiarrhythmic concentration estimated in six patients ranged from 1.4 to 7.0 mug/ml. beta-Phase half-life in five patients was between 10.3 and 22.1 h.
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Antiarrhythmic and hemodynamic effects of i.v. disopyramide phosphate (1.7 mg/kg b.wt. over 2 min) have been studied in nine patients, several in various degrees of cardiac decompensation, with sinus rhythm and persistent ventricular ectopic beats (VEBs). In one case with primary cardiomyopathy, with greater than 30 VEBs/min, disopyramide (DE) abolished the arrhythmia for 30 min, but precipitated brief dysponea. Other side-effects were tolerable and mainly attributable to anticholinergic effects of the drug. DE either abolished or significantly reduced the arrhythmia in all cases. For 30 min, only one patient showed VEBs, and in three patients no VEBs were seen for three hours. Changes in cardiac output and pulmonary artery (PAP) and central aortic pressures were measured in eight patients. Negative inotropic effects were indicated in seven by an increased diastolic PAP/stroke volume ratio and in seven by a decreased central aortic (dp/dt)max. Patients with high control values for diastolic PAP showed marked reductions in cardiac output, stroke volume and stroke work. In predicting myocardial depressant effects of DE, the control values for diastolic PAP seemed to be superior to central venous pressure, cardiac index and systolic time intervals. Mean arterial pressure measured 5 and 10 min after drug administration showed no significant change, indicating that vasoconstrictor reflexes were well preserved, and a pressure level significantly above the control value was reached from the 20th min. It is concluded that DE is potent in suppressing VEBs but exerts negative inotropic effects that may be of clinical importance. The optimal antiarrhythmic dose is probably lower than that used in the present study.
A digital system for real-time arrhythmia monitoring in the coronary care unit has been designed. The system is based on an algorithm for discrimination between normal complexes and ventricular ectopic beats (VBs). A beat is classified as normal if the absolute difference from a running average of the patient's normal QRS is below an adaptive threshold. To prevent artifacts and beats of non-ventricular origin from being falsely interpreted as VBs, each abnormal beat is correlated with a typical VB waveform, incorporated into the program. A VB is recognized only when the correlation coefficient exceeds 0.8. In a performance study, ECGs from 15 patients were recorded on magnetic tape and replayed to the computer. Independent evaluation by two physicians showed a total of 1 306 VBs, 94% correctly classified by the computer. In the group labelled "suspected VBs" the detection rate was lower (average 69%). Out of the whole number of complexes (53 260), 0.45% were falsely interpreted as VBs by the computer. Artifacts giving rise to false VBs are included in this figure. The causes of false positive and false negative VBs were thoroughly investigated and on the basis of these results, possible improvements in the system are discussed.
Administration of disopyramide phosphate (DE) i.v. in two doses, 30 min apart, to a patient with ventricular tachycardia was accompanied by no, or only slight, changes in systemic arterial pressure (SAP), cardiac output (Q), stroke work (SW), and pulmonary artery diastolic pressure (PADP). Heart rate fell from 123 to 103/min. Following reversion to sinus rhythm, which occurred 60 min after the second dose of DE at a serum concentration greater than 4.3 mug/ml, Q ans SW showed significant increases above their control values. PADP fell from 20 to 6 mmHg whereas the mean SAP remained largely unchanged. There seemed to be no adverse effects of drug administration. In this patient, recurrent attacks of ventricular tachycardia not responding to conventional antiarrhythmic treatment could be prevented by oral DE in a dose of 800 mg/day.
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