Intraoperative change in baroreceptor function during carotid endarterectomy

Abstract Background Labile blood pressure following carotid endarterectomy (CEA) is common and is associated with perioperative myocardial infarction and intracranial haemorrhage. Previous studies have identified that alteration in carotid baroreceptor function is responsible for the blood pressure changes although the mechanism remains unclear. This study aimed to identify the mechanism by which CEA affects baroreceptor function. Methods Fifty patients were recruited prospectively and underwent estimation of baroreceptor sensitivity (BRS) during a 10-min period of supine bed rest using electrocardiography and Finapres, 2 days before and 2 days to 6 weeks after surgery. During surgery continuous measurements of blood pressure (intra-arterial) and heart rate were recorded on to digital audio tape for postoperative analysis. During analysis the operation was divided into different stages to identify at which stage baroreceptor function altered. Particular attention was paid to initial clamping of the carotid artery, performance of the endarterectomy and final restoration of blood flow. In addition the carotid sinus area was stimulated by stroking the inside of the artery before and after removal of the plaque. Autonomic activity was calculated using power spectral analysis of beat-to-beat blood pressure and the R–R interval from the electrocardiograph. BRS was estimated by calculation of the square root of the ratio of the powers of R–R interval and systolic blood pressure to give the alpha index which has been shown to correlate well with BRS calculated by means of standard pharmacological techniques. Results For this cohort of patients BRS was significantly reduced 2 days after surgery compared with the preoperative recordings (2·8(0·4) to 5·6(0·8)). Six weeks after operation BRS had improved but had not achieved preoperative levels (3·8(0·6) to 5·6(0·8)). During surgery, patients with good baroreceptor function identified before operation experienced a rise in blood pressure on initial carotid clamping indicating that dissection had not affected the baroreceptor mechanism. Similarly, intraluminal stimulation of the carotid sinus area with the plaque in situ produced a decrease in blood pressure indicating good baroreceptor function. After removal of the plaque, repeating the intraluminal stimulation did not produce a decrease in blood pressure indicating disruption of the baroreceptor mechanism. Conclusion Removal of the atheromatous plaque during CEA adversely affects carotid baroreceptor function. The baroreceptor mechanism is disrupted but not completely destroyed and gradually improves in the weeks following surgery.