Why the study?
Does high thoracic epidural anaesthesia with bupivacaine prevent the mobilization of circulatory reserves during hypercapnia-induced sympathetic stimulation in elderly patients?
Does high thoracic epidural anaesthesia with bupivacaine prevent the mobilization of circulatory reserves during hypercapnia-induced sympathetic stimulation in elderly patients?
High thoracic epidural anesthesia with 0.5% bupivacaine is insufficient to completely block sympathetic innervation to the heart during hypercapnia-induced sympathetic stimulation in elderly patients.
Answers are grounded in this paper and cite their sources.
High thoracic epidural anaesthesia may not fully blunt hypercapnic sympathetic responses in elderly patients; leaves open optimal block strategies for circulatory control.
Circulatory changes and the degree of sympathetic block were evaluated in 15 elderly patients with high thoracic epidural anaesthesia (T1-T5). Bupivacaine 5-6 ml 0.5% was injected via an epidural catheter at the T3-level. The quality of the sympathetic block was determined with the Valsalva manoeuvre. Induced hypercapnia was used to quantify the degree of sympathetic block. Following thoracic epidural anaesthesia (TEA), cardiac output, stroke volume and arterial blood pressure decreased. During hypercapnia, heart rate and arterial blood pressure increased both before and after established TEA. Thus the block of the sympathetic innervation to the heart with a high TEA using 0.5% bupivacaine was not sufficient to prevent mobilization of circulatory reserves during sympathetic stimulation. The most likely explanation is considered to be the lack of neural block of the efferent nerves leading to the adrenal medulla and the peripheral vascular bed.
No takes yet. Share an insight, caveat, or question.
Sundberg et al. (1987) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: