Letter to the Editor

To the Editor: In the January issue of this journal, Bassan and colleagues reported disturbed cerebral autoregulation in 5/ 43 (13%) critically ill infants with congenital heart disease who underwent cardiopulmonary bypass surgery (1). Spontaneous changes in MAP, NIRS, and CBFV were correlated to quantify the pressure passive index (PPI 0 = intact autoregulation). In this patient population, the task is technically challenging, and the investigators should be commended for studying cerebral autoregulation in this group of patients at risk of long-term neurologic sequelae. While the authors have correctly stated that doing tilt or static testing in these children is problematic, they should have discussed the limitations of the methodology used in this study to determine autoregulatory capacity. The difficulty in quantifying the incidence of impaired autoregulation using spontaneous correlation analysis of physiologic variables is that one cannot be sure that the autoregulatory system was indeed stimulated and that the changes in CBFV or NIRS were due to changes in MAP. Cerebral autoregulation is a homeostatic system controlled by a feedback loop with as yet undefined metabolic/neural mechanism. To trigger this homeostatic mechanism, a sufficient stimulus must be furnished. At the same time, the stimulus must not be coupled with other factors that may alter blood flow independently. For example, if cerebral metabolic rate is increased for whatever reason during the study, MAP and CBFV will all increase, and cerebral oxygen saturations may or may not increase due to flow metabolism coupling. Since cerebral metabolic rate was neither measured nor specifically controlled during the study period, one cannot be sure that the observed phenomenon represents impairment of the autoregulatory process rather than preservation of flow metabolism coupling. This criticism is not to detract the potential value of these autoregulation studies, but we must be cognizant of the limitations of the method, which in our opinion, at best provide a qualitative rather then quantitative assessment of cerebral autoregulation. The authors also report increased odds of impaired autoregulation with hypercapnea (ET-CO₂ ≥ 40 mm Hg). However, in critically ill patients, ET-CO₂ may underestimate PaCO₂. An analysis of the relationship between PaCO₂ and autoregulatory capacity would provide more useful information.