Physiology and pathophysiology of thoracic sympathetic blockade

Sympathetic innervation of the heart and lung is mediated by fibres originating from the thoracic segments T1–4. Sympathetic stimulation in healthy subjects causes coronary vasodilation, whereas stenotic coronary arteries show vasoconstriction in response to sympathetic stimulation. Thus, in patients at risk of ischaemia, high thoracic epidural anaesthesia (TEA) should dilate constricted coronary vessels, decrease heart rate and myocardial metabolism, and improve cardiac function by reducing pre- and afterload and optimizing oxygen availability. The pulmonary effects include an improved postoperative diaphragmatic function in lambs and humans and enhanced respiratory function parameters. Hypoxic pulmonary vasoconstriction, an important mechanism for the maintenance of adequate oxygenation after induction of general anaesthesia, is not affected by TEA in dogs. Beneficial effects of epidural sympathetic blockade on myocardial perfusion and function, and on pulmonary parameters, can only be achieved by a thoracic blockade, whereas lumbar epidural anaesthesia may exert adverse effects due to a compensatory increase of thoracic sympathetic activity.