Transesophageal electroventilation. Optimization and improvement.

For electroventilation, short duration pulse trains (0.1 ms) were applied between two axillary pads (transchest) and compared with transesophageal electroventilation where pulses passed between the same pads to an esophageal electrode in apneic, pentobarbitone-anesthetized pigs. Significantly greater tidal volumes were produced by transesophageal electroventilation in comparison with transchest. As measured by maintained tidal volumes, duration of inspiratory air flow, peak flow, percentage hemoglobin oxygen saturation (%SaO2), and end tidal carbon dioxide concentration (ETCO2), the optimal requirements for transesophageal electroventilation were pulse frequency 40 Hz, 0.7 s duration pulses, at 60 to 100 V, pulse width 0.1 ms, with the esophageal electrode proximal to the gastroesophageal junction without producing brachial plexus stimulation. The efficiency of transesophageal electroventilation falls off rapidly following ventricular fibrillation. Thus, the application of this technique would be in respiratory arrest with maintained circulation, eg, in drug-induced respiratory depression, severe smoke inhalation, severe emphysema, high cervical cord lesion, and weaning from prolonged mechanical ventilation.

Effect of nifedipine on arrhythmias in the acute phase of myocardial infarction.

In a double-blind placebo-controlled trial to study the effect of nifedipine on ventricular arrhythmias among patients with acute myocardial infarction, 434 patients with suspected myocardial infarction were randomized within 6 h from the onset of chest pain to treatment with nifedipine (p = 217) or placebo (p = 217). During the 48-h treatment period, a 10-mg capsule containing active drug or placebo was administered sublingually every 4 h for 24 h, then orally every 4 h for the next 24 h. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). Twenty-four hour ECG tape analysis during 1-5 h from onset of chest pain showed that there was no significant difference in the number of patients with ventricular ectopics, ventricular couplets, ventricular tachycardia (3-9 beats), self terminating or sustained ventricular tachycardia between the two treatment groups. Also during the greater than 5-24 h from onset of chest pain, the numbers of patients with ventricular ectopics, multifocal, bigeminal or couplets, self-terminating ventricular tachycardia or sustained ventricular tachycardia did not differ significantly. However, there was a significant reduction in the number of patients with short runs of ventricular tachycardia (3-9 beats) in the nifedipine-treated group. There was no significant difference among patients with ventricular fibrillation between the two treatment groups.

Effect of nifedipine on enzymatically estimated infarct size in the early phase of acute myocardial infarction.

In a double blind placebo controlled trial, 434 patients with suspected myocardial infarction were randomised to treatment with nifedipine (n = 217) or placebo (n = 217) within six hours from the onset of chest pain. During the treatment period of 48 hours, a 10 mg capsule containing nifedipine or placebo was given sublingually every four hours for 24 hours, then orally every four hours for the next 24 hours. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). The median delay time to intervention with nifedipine in patients with acute myocardial infarction was 111 minutes. Infarct size was assessed by the estimation of release of creatine kinase isoenzyme MB and creatine kinase from blood samples taken every four hours for 48 hours. The total mean (SEM) creatine kinase MB released was 406.4 (27.2) IU/l in the nifedipine group and 345.7 (20.5) IU/l in the placebo group. Total mean (SEM) creatine kinase released was 2749.6 (165.1) IU/l in the nifedipine group and 2698.4 (145.9) IU/l in the placebo group. In hospital mortality was similar for both the nifedipine and placebo groups (6.6% and 5.8% respectively). Treatment with nifedipine in the early phase of acute myocardial infarction seems to have no effect on enzymatically measured infarct size.