Groeben H, Schwalen A, Irsfeld S, Lipfert P, Hopf H B
Institut für Klinische Anaesthesiologie, Heinrich-Heine-Universität Düsseldorf.
Acta Anaesthesiol Scand. 1995 May;39(4):523-6. doi: 10.1111/j.1399-6576.1995.tb04112.x.
Whether or not neural blockade of pulmonary sympathetic innervation is of relevance for airway resistance in patients with chronic obstructive pulmonary disease (COPD) is unknown. Accordingly we evaluated airway resistance during sympathetic blockade by high thoracic epidural anaesthesia in patients with COPD. Before and 45 min after thoracic epidural injection of bupivacaine 0.75% (6-8 ml; n = 10) total respiratory resistance (oscillometry, ROS), vital capacity (VC), forced expiratory vital capacity in 1 s (FEV1, [%VC]), functional residual capacity (FRC; helium dilution method), and arterial blood gases were measured. Three additional patients received bupivacaine intravenously (1.2 mg.min-1 for 45 min), another three received saline epidurally. Sensory blockade covered segment C5 through T8. As an indicator of widespread sympathetic blockade including the lungs, skin temperature increased significantly on thumb and little toe. Despite pulmonary sympathetic denervation ROS, FEV1, and FRC remained unchanged, while VC decreased slightly, probably due to intercostal muscle blockade. Blood gases remained constant. Neither intravenous bupivacaine nor epidural saline evoked directional changes. Since, in contrast to beta-adrenoceptor blockade, pulmonary sympathetic denervation did not increase airway resistance in patients with COPD, neural sympathetic blockade seems to be of no relevance for airway resistance in these patients.
