In Reply

We would like to thank Dr. Williams for responding to our editorial,1which appeared in the February 2012 issue of ANESTHESIOLOGY.Dr. Williams makes the point that patients sedated for endovascular treatment of acute ischemia may have higher arterial carbon dioxide partial pressure levels than patients treated for the same problem but receiving a general anesthetic. There are two points to this argument. The first is that patients receiving general anesthesia have a lower arterial carbon dioxide partial pressure than patients sedated without a general anesthetic. The second is that vasodilation from retention of carbon dioxide in the sedated patients will dilate the cerebral vasculature and protect penumbral areas by that mechanism.First, with a general anesthetic the partial pressure of carbon dioxide can be regulated to whatever level is required. It is incorrect to assume that the patient will be hyperventilated and thereby have a lower carbon dioxide partial pressure than will be achieved without intubation, although that may be the case if the anesthesiologist hyperventilates the patient. Dr. Williams is also correct that sedation may cause the patient to hypoventilate and retain carbon dioxide.Second, it is assumed that ischemic cerebral regions dilate anyway. Cerebral blood flow is probably pressure dependent in the penumbra. The issue of where to keep the partial pressure of carbon dioxide has been discussed extensively in management of patients receiving carotid endarterectomy under general anesthesia.2–4What was found was that it was difficult to predict the effect of dilating or constricting the surrounding healthy tissue on the ischemic cerebral areas. If you increase the partial pressure of carbon dioxide, dilate the noninvolved cerebral areas, you may shunt blood to normal brain tissues away from ischemic areas, referred to as “countersteal.”2–4On the other hand, if you decrease the partial pressure of carbon dioxide, constricting the noninvolved cerebral areas, you may not increase blood flow to the ischemic areas because they are limited already by the thrombus, which occludes the lumen, and you may cause the noninvolved areas to become relatively ischemic.3,5We still think that the overwhelming evidence from stroke management and from this paper is for maintenance of systolic blood pressures more than 140 mmHg and less than 200 mmHg as the best strategy to provide cerebral perfusion to ischemic brain through whatever collaterals may be available. Davis et al. did not provide any data related to end-tidal partial pressure of carbon dioxide.6

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