Carotid endarterectomy (CEA) is the recommended treatment to prevent future cardiovascular events in patients with a symptomatic high degree stenosis of the internal carotid artery (ICA). Besides these symptoms, stenosis of the ICA jeopardizes the cerebral perfusion and may affect cerebral auto-regulation (CA), indicating that cerebral perfusion becomes dependent on changes in blood pressure . Therefore, to preserve cerebral perfusion during surgery and to prevent ‘watershed’ stroke, intraoperative hypotension needs to be avoided and the suggested blood pressure that should be maintained intraoperatively is an arterial pressure between baseline blood pressure measured on the nursing ward the day before surgery and 20% above this blood pressure .
To do so, different short-acting vasopressor agents can be used, such as phenylephrine or ephedrine . If existing at all, preference for either of these agents is solely based on the discretion of the attending anesthesiologist. Furthermore, ephedrine and phenylephrine are widely accepted and, when heart rate is in the normal range, applied in cardiovascular surgery on the basis of individual preference. Both agents have a different mechanism of action. Phenylephrine (an α-agonist) increases blood pressure purely by vasoconstriction, whereas ephedrine (a combined α- and β-agonist) increases blood pressure by a combination of vasoconstriction and an increase in heart rate and a subsequent rise in cardiac output .
Besides the difference in systemic hemodynamics, the perfusion of the brain reacts differently. In healthy subjects, with intact CA, the frontal lobe cerebral tissue oxygenation (rSO2) decreases during phenylephrine administration while it is preserved with ephedrine use [4, 5]. It is suggested that the increase in cardiac output observed during ephedrine use can explain this difference in rSO2. It is unknown how in the situation of impaired CA, as often observed in patients undergoing a CEA, the rSO2 and vasomotor tone react after administration of phenylephrine or ephedrine. Thus, the optimal drug to maintain cerebral perfusion in CEA patients, with an impaired CA is unknown. If during the use of one of the two agents cerebral perfusion would be better maintained or even increased this would clearly influence the choice for the desired agent.
In our institution, we routinely monitor rSO2 using near infrared spectroscopy (NIRS) and middle cerebral artery blood velocity (V
MCA) measured by transcranial Doppler (TCD) during CEA. To study the effect of both vasopressors on these parameters, we retrospectively analyzed the effect of phenylephrine and ephedrine induced changes in mean arterial pressure (MAP) on rSO2 and V
MCA in 11 CEA patients. We noticed that phenylephrine and ephedrine both increased MAP and V
MCA in patients undergoing carotid endarterectomy. However, an increase in MAP induced by phenylephrine has a lowering effect on the rSO2, while ephedrine had an increasing effect on the rSO2.
This pilot study indicated that the use of ephedrine should be preferred above the use of phenylephrine for correction of hypotension during CEA. However, the numbers of patients were small and the dose of agent applied not standardized. Therefore, a prospective study to analyze the effect of both ephedrine and phenylephrine on cerebral perfusion during CEA is needed to make a recommendation.