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A ventricular inhibited demand cardiac pacemaker was inhibited in the presence of intimate contact between the active temporary bipolar electrode ring and a rejoined inactive permanent bipolar electrode tip. Electromagnetic interference effects, lack of insulation, lead breaks, and loose connections were all ruled out as the cause of pacemaker suppression. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor about cardiac pacing.

Recent experience with implanted cardiac pacemakers in nine young patients is reported. Advance in technology include improved pacemaker generator design and placement, and improved lead design and placement. No patients died; our only complication, failure to capture, required repositioning of the lead. All pacemaker replacements were elective. This series helps to define the more favorable current prognosis for the young patient needing pacemaker therapy.

A case of recurrent massive pulmonary embolization through a modified Miles' clip two weeks after successful emergency pulmonary embolectomy is reported. Vena caval ligation is probably a safer alternative in these critically ill patients.

Recommendations regarding the safe waiting period between discontinuing chronic oral propranolol therapy and beginning cardiopulmonary bypass have varied from a few hours to 2 weeks. In the present study, utilizing adult dogs, propranolol was discontinued 8 or 48 hours prior to surgery. A reduction in cardiac output and elevations of left ventricular end-diastolic pressure, peak systolic pressure, and systemic resistance were noted when cardiac function was evaluated following the induction of anesthesia and prior to undertaking cardiopulmonary bypass. The magnitude of these differences was directly related to the degree of volume loading and inversely related to the interval between the last dose of propranol and the determination of cardiac function. Reduction of heart rate was the most evanescent of propranolol's hemodynamic effects as the marked bradycardia which persisted throughout the course of propranolol therapy was no longer evident 8 hours after the last oral dose of the drug. Following total cardiopulmonary bypass of 1 hour's duration, undertaken 8 hours after the last oral dose of propranolol, cardiac output and left ventricular end-diastolic pressure had returned to normal but peak systolic pressure and systemic resistance remained significantly elevated, When 48 hours had elapsed between discontinuing propranolol and beginning cardiopulmonary bypass, postbypass cardiac function was essentially normal with only slight persistent elevations of peak systolic pressure and systemic resistance detected. When the combined effects of ischemic heart disease and propranolol therapy, the altered metabolic and hemodynamic effects of different routes of drug administration, and the varying durations of cardiopulmonary bypass are taken into consideration, some of the discrepancies between previously reported clinical and experimental findings regarding the duration of persistent propranolol effects can be understood. The clinical course is usually benign in patients who have received propranolol to within a few hours of surgery without specific indication. However, it is often complicated when the drug is continued until just prior to surgery in patients dependant on propranolol for pain or arrhythmia control. In patients demonstrating propranolol dependence, control of symptoms with intra-aortic balloon counterpulsation is recommended followed by the gradual withdrawal of propranolol and elective aortocoronary bypass surgery.