Should we increase mean arterial pressure, no matter what the means, to secure brain oxygenation during anesthesia?

Following the publication of our studies on the influence of vasopressors on cerebral blood flow/oxygenation, Meng et al. published their study supporting our data.

The aims of this study were to evaluate the impact of administrating bolus injection of phenylephrine and ephedrine on frontal lobe oxygenation in anesthetized patients undergoing elective surgery and to identify the variables that are responsible for the changes in frontal oxygenation induced by phenylephrine and ephedrine.

Initially, thirty-three patients were enrolled in this study. Of these 33 patients, they authors were able to administer the drugs and complete all measurements in 29 patients. Phenylephrine or ephedrine was administered as soon as patients were experiencing anesthesia-related hypotension, defined as at least a 20% reduction in mean arterial pressure or mean arterial pressure below 60 mmHg).  Of note, bolus injections were administered and measurements were performed before the beginning of surgery.

Frontal lobe oxygenation (near-infrared spectroscopy), cardiac output (oesophageal Doppler). mean arterial pressure (intra-arterial catheter system), end-tidal carbon dioxide (gas analyzer built in the anesthesia machine) and depth of anesthesia (BIS monitor) were recorded before each bolus injection, at the maximal impact of the drugs and at the lowest frontal lobe oxygenation monitored following the maximal impact of the drugs.

The 2 figures below present mean and individual changes in mean arterial pressure, cardiac output and frontal lobe oxygenation with both agents. The administration of phenylephrine (A, B, C in both figures) was efficient at increasing mean arterial pressure, but was associated with a reduction cardiac output and frontal lobe oxygenation. The administration of ephedrine (D, E, F in both figures) was also efficient at increasing mean arterial pressure. However, cardiac output and frontal lobe oxygenation remained unchanged. Interestingly, cardiac output was identified as the variable associated most significantly with frontal lobe oxygenation.

This study supports the existing link between changes in cardiac output and cerebral oxygenation reported in different circumstances and study designs. The potential mechanisms underlying the modulation of cerebral oxygenation by cardiac output could be sympathetically mediated vasoconstriction induced by a lowering in cardiac output or it could also depend on the distribution of circulating blood volume.

Should we increase mean arterial pressure, no matter what the means, to secure brain oxygenation during anesthesia?

If treating hypotension is an attempt to avoid organ ischaemia and hypoxia, we are actually achieving the opposite result (decreased cerebral oxygenation) by administering phenylephrine, as demonstrated in this study a quantitative NIRS device and in pressure studies using a trend NIRS device.

Thus, the routine and indiscriminate use of vasopressors might be less beneficial than previously thought.

Phenylephrine represents a first-line agent used to maintain mean arterial pressure in hypotensive states because of minimal impact on heart rate. Conversely, ephedrine is not considered a first-line agent, especially when the elevation in heart rate is undesirable. Further research is needed to better understand if these acute changes in frontal lobe oxygenation following administration of phenylephrine are associated with adverse post-surgical outcomes and if administration of ephedrine (rather than phenylephrine) is related to better post-surgical outcomes.

References

Meng L, Cannesson M, Alexander BS, Yu Z, Kain ZN, Cerussi AE, Tromberg BJ, Mantulin WW. Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients. Br J Anaesth. 2011;107:209-217

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