Copyright © 1989 by the European Society of Cardiology.
© 1989 The European Society of Cardiology
Thoracic epidural anaesthesia in patients with unstable angina pectoris
*Department of Internal Medicine I, Section of Cardiology, University of Gothenburg, Sahlgren's Hospital Gothenburg Sweden
**Department of Anaesthesia and Intensive Care Gothenburg Sweden
Received 24 May 1988; revised 7 October 1988; .
Correspondence and reprints requests to: Sven-Erik Richsten, M.D.Ph.D., Department of Anaesthesia and Intensive Care, Sahlgren's Hospital, S-413 45 Gothenburg, Sweden.
Abstract
The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated wth nitroglycerin infusion for gt;24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest < 2 days after infarction. 4.4 ± 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments ( Th1-7) for 98 ± 9min. Heart rate decreased significantly from 70 ± 3 to 64 ± 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 ± 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 ±0.3 the first day to 0.9 ± 0.3 the fourth day (P>0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.
Exercise stress testing was performed on eight patients three to five days after the start of thoracic epidural anaesthesia. At a comparable workload, ST-segment depression was significantly (P>0.05) less pronounced during anaesthesia ( – 0.6 ± 0.1 mm) compared with control ( – 1.3 ± 0.2mm). The respective heart rate values were 95 ± 7 and 107 ± 7 beats min -1 (P > 0.05), while systolic or diastolic blood pressure did not differ between the two conditions.
We conclude that blockade of cardiac sympathetic afferents and efferents by means of thoracic epidural anaesthesia can effectively treat pain and stabilize patients with unstable angina pectoris refractory to medical treatment. Furthermore, thoracic epidural anaesthesia attenuates stress-induced myocardial ischaemia; thus, it may be an efficient supplementary treatment for the control of pain and for stabilizing patients with unstable angina pectoris during diagnostic procedures and prior to coronary surgery or angioplasty.
Key Words: Unstable angina pectoris • thoracic epidural anaesthesia • local anaesthetics
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