Effect of Hyper- and Hypocapnia on Cerebral Arterial Compliance in Normal Subjects
Emmanuel Carrera, Dong‐Joo Kim, Gianluca Castellani, Christian Zweifel, Peter S. Smielewski, John Douglas Pickard, Marek Czosnyka
Abstract
Emmanuel Carrera, Dong‐Joo Kim, Gianluca Castellani, Christian Zweifel, Peter S. Smielewski, John Douglas Pickard, Marek Czosnyka
Abstract
BACKGROUND: Changes in partial pressure of carbon dioxide (PaCO2) are associated with a decrease in cerebral blood flow (CBF) during hypocapnia and an increase in CBF during hypercapnia. However, the effects of changes in PaCO2 on cerebral arterial compliance (Ca) are unknown. METHODS: We assessed the changes in Ca in 20 normal subjects using monitoring of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV). Cerebral arterial blood volume (CaBV) was extracted from CBFV. Ca was defined as the ratio between the pulse amplitudes of CaBV (AMPCaBV ) and ABP (AMPABP). All parameters were recorded during normo-, hyper-, and hypocapnia. RESULTS: During hypocapnia, Ca was significantly lower than during normocapnia (.10±.04 vs. .17±.06; P<.001) secondary to a decrease in AMPCaBV (1.3±.4 vs. 1.9±.5; P<.001) and a concomitant increase in AMPABP (13.8±3.4 vs. 11.6±1.7 mmHg; P<.001). During hypercapnia, there was no change in Ca compared with normocapnia. Ca was inversely correlated with the cerebrovascular resistance during hypo- (R2=0.86; P<.001), and hypercapnia (R2=0.61; P<.001). CONCLUSION: Using a new mathematical model, we have described a reduction of Ca during hypocapnia. Further studies are needed to determine whether Ca may be an independent predictor of outcome in pathological conditions.
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BACKGROUND: Changes in partial pressure of carbon dioxide (PaCO2) are associated with a decrease in cerebral blood flow (CBF) during hypocapnia and an increase in CBF during hypercapnia. However, the effects of changes in PaCO2 on cerebral arterial compliance (Ca) are unknown. METHODS: We assessed the changes in Ca in 20 normal subjects using monitoring of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV). Cerebral arterial blood volume (CaBV) was extracted from CBFV. Ca was defined as the ratio between the pulse amplitudes of CaBV (AMPCaBV ) and ABP (AMPABP). All parameters were recorded during normo-, hyper-, and hypocapnia. RESULTS: During hypocapnia, Ca was significantly lower than during normocapnia (.10±.04 vs. .17±.06; P<.001) secondary to a decrease in AMPCaBV (1.3±.4 vs. 1.9±.5; P<.001) and a concomitant increase in AMPABP (13.8±3.4 vs. 11.6±1.7 mmHg; P<.001). During hypercapnia, there was no change in Ca compared with normocapnia. Ca was inversely correlated with the cerebrovascular resistance during hypo- (R2=0.86; P<.001), and hypercapnia (R2=0.61; P<.001). CONCLUSION: Using a new mathematical model, we have described a reduction of Ca during hypocapnia. Further studies are needed to determine whether Ca may be an independent predictor of outcome in pathological conditions.
Key concepts: Normocapnia, Hypocapnia, Hypercapnia, Medicine, Cerebral blood flow, Anesthesia, Blood pressure, Cardiology