How are haemodynamic and metabolic responses to haemorrhage influenced by segmental thoracic and thoracolumbar epidural analgesia? An experimental study in dogs

To determine the effects of the spread of sympathetic blockade administered prior to haemorrhage on haemodynamic and metabolic responses 10 haemorrhage, we compared these responses among dogs treated by segmental thoracic epidural analgesia, thoracolumbar epidural analgesia and general anaesthesia. Group 1 of six dogs received 0.2% halothane plus epidural analgesia ranging from C 4 to T 5 , group 2 of seven 0.2% halothane plus epidural analgesia ranging from C 5 to L 7 , and group 3 of eight 0.9% (1 MAC) halothane anaesthesia. A volume of 35 ml · kg ‐1 was bled over 30 min. The haemodynamic, metabolic and catecholamine variables were measured repeatedly at 30‐min intervals for 2.5 h. The mean arterial pressure decreased significantly in all groups immediately after haemorrhage. It recovered to 80–90 mmHg at 2–2.5 h in groups 1 and 3 but remained at 20–30 mmHg in group 2. The cardiac output decreased significantly in all groups. The systemic vascular resistance increased significantly in group 1 but decreased significantly in group 2. In group 3 it decreased significantly but soon recovered. Arterial pH and base excess decreased significantly in all groups immediately after haemorrhage. After that, base excess recovered slowly in groups 1 and 3 but decreased further in group 2. The plasma epinephrine concentration increased immediately after haemorrhage and then decreased slowly in groups 1 and 3. In group 2 it remained unchanged at the lower level. The decreases in mean arterial pressure, systemic vascular resistance and base excess were significantly larger in group 2 than in groups 1 and 3. These results demonstrate that the haemodynamic and metabolic changes after haemorrhage are milder under segmental thoracic epidural analgesia or 1 MAC halothane anaesthesia than under thoracolumbar epidural analgesia. Widespread epidural analgesia would weaken haemodynamic and metabolic compensatory responses to haemorrhage.