Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia

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Abstract
Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3‐L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8‐T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats · min‐1 while thoracic impedance increased from 25.5 to 26.5 ohm. End‐systolic diameter (ESD) and end‐diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats · min‐1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head‐down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol·1‐1, vasopressin from 3 and 2 to 152 and 46 pmol·1‐1, and aldosterone from 282 and 229 to 383 and 485 pmol·‐1, respectively. The established level of analgesia suggests that the changes in circulatory and hormonal variables as well as successful resuscitation of the subjects with saline in the head‐down position conform to central blood volume depletion leading to increased vagal tone. During epidural anaesthesia presyncopal symptoms were preceded by an approximately 13% reduction in left ventricular diameters.