Cerebral vasomotor reactivity: steady-state versus transient changes in carbon dioxide tension

Abstract

Cerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension (P aCO 2) is assessed during steady-state or transient changes in P aCO 2. This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in P aCO 2; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal carbon dioxide tension (P ET , CO 2) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus P ET , CO 2) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in P ET , CO 2 of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in P ET , CO 2. The linear regression for CBFV versus P ET , CO 2 (P = 0.65) and CVCI versus P ET , CO 2 (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus P ET , CO 2 (P < 0.01) and CVCI versus P ET , CO 2 (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2 is similar regardless of the employed methodology to induce changes in P aCO 2 and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

Figure 1. Representative illustration of middle cerebral artery blood velocity (CBFV), mean arterial blood pressure (MAP) and end-tidal carbon dioxide () during steady-state and simplified rebreathing-induced hypercapnia from one subject

A and B depict CBFV, MAP and responses during steady-state elevations in of 5 and 10 Torr, respectively, while C depicts the responses during the modified rebreathing protocol. The continuous vertical lines in A and B show the period (45 s) when the steady-state measures were obtained, while the dashed vertical lines in A–C show the start and end of the hypercapnic periods.

Figure 2. Cerebral vasomotor reactivity during steady-state and simplified rebreathing-induced hypercapnia

A illustrates a representative relationship between CBFV and , while B illustrates a representative relationship between cerebrovascular conductance index (CVCI) and from one subject. C depicts the individual (lines) and the group-averaged relationship (vertical bars) between CBFV and (i.e. cerebral vasomotor reactivity) during steady-state and rebreathing-induced increases in . D depicts the individual (lines) and the group-averaged relationship (vertical bars) between CVCI and changes in (i.e. cerebral vasomotor reactivity) during steady-state and rebreathing-induced increases in . The cerebrovascular response to hypercapnia was similar regardless of the method (i.e. steady state and modified rebreathing) of inducing hypercapnia or the analysis approach (i.e. CBFV and CVCI).

Figure 3. Cerebral vasomotor reactivity during simplified rebreathing-induced hypercapnia with (hyperventilation + rebreathe) and without a prior period of hyperventilation (rebreathe)

A illustrates a representative relationship between CBFV and , while B illustrates a representative relationship between CVCI and from one subject. C depicts the individual (lines) and the group-averaged relationship (vertical bars) between CBFV and (i.e. cerebral vasomotor reactivity) during hyperventilation + rebreathe and rebreathe only. D depicts the individual (lines) and the group-averaged relationship (vertical bars) between CVCI and changes in (i.e. cerebral vasomotor reactivity) during hyperventilation + rebreathe and rebreathe only. The cerebrovascular response to hypercapnia was significantly blunted when the rebreathing was preceded by a brief period of hyperventilation-induced hypocapnia (hyperventilation + rebreathe).