Cerebral autoregulation can be studied in static or in dynamic conditions. Static autoregulation refers to changes in steady-state CBF recorded after an increase in blood pressure induced by the infusion of a vasopressor drug .
Dynamic autoregulation refers to continuous changes in CBF either in natural conditions, by the calculation of a transfer function from the spectral analysis of blood pressure and flow signals , or by the calculation of a rate of correction of flow per unit of change in blood pressure . While static and dynamic cerebral autoregulation measurements have shown to be correlated , the agreement of both approaches in hypoxia is not known and it remains uncertain whether pharmacological manipulations of blood pressure might be without intrinsic influence on the autoregulation process. Therefore, it seems preferable to evaluate cerebral autoregulation in dynamic rather than in static conditions.
Van Osta et al. investigated the effects of hypoxic breathing on dynamic cerebral autoregulation and CCP in 15 normal volunteers and correlated the results to an AMS score obtained after 6 hours of hypoxic exposure in a hypobaric chamber . Cerebral blood flow velocity was measured by transcranial Doppler and blood pressure by finger plethysmography in normoxia (fraction of inspired O2, FIO2 0.21) and after a short period of hypoxic breathing (FIO2 0.12). A dynamic CBF autoregulation index (ARI) and a CCP were calculated from continuous recordings of CBF velocity and blood pressure during transient hypotension induced by the sudden release of inflated bilateral thigh cuffs.
In such experiments, blood pressure falls 15 to 25% for 20 to 30 s, while the CBF initially follows in parallel but returns to baseline in 5 to 7 s. The normal response of CBF to a fall in blood pressure is a 20% correction per second, yielding an ARI of around 5 . An ARI of 10 corresponds to a perfect autoregulation and an ARI of 0 to no autoregulation at all . The same measurements allow the plotting of blood pressure as a function of CBF, as both are initially rapidly decreased after cuff release. The first seconds of these pressure and flow changes are passive and are best described by a linear approximation. The extrapolation of linear pressure-flow relationships to the pressure axis defines a critical closing pressure. The experimental setting with pressure and flow recordings for the calculations of both ARI and CCP, in normoxia and in hypoxia, is illustrated in figures 1 to 3.
Van Osta et al. correlated these measurements to an AMS score sampled after 6 hours in a hypobaric chamber at a simulated altitude of 4260 m. Hypoxia decreased CCP from by 18% (p < 0.05) and ARI by 17% (p < 0.05). There was a negative correlation between baseline normoxic ARI and AMS score (r = - 0.54, p < 0.05) and a positive correlation between ARI and CCP in hypoxia (r = 0.61, p < 0.05). These results suggested that hypoxia-induced impairment of cerebral hemodynamics might play a role in the pathogenesis of AMS .
Van Osta et al. then measured CBF, blood pressure, ARI and CCP at 490 m and 20 hours after arrival at 4559 m, in 35 healthy volunteers . These
subjects had been randomized to tadalafil, dexamethasone or placebo as part of a study on the pharmacological prevention of high-altitude pulmonary edema . Altitude was associated with an increase in a cerebral sensible AMS (AMS-C) score (p<0.001), without change in average CBF, ARI, or CCP. However, the AMS-C score was negatively correlated to ARI (r = - 0.47, p<0.01). The ARI and CCP were positively correlated to arterial oxygenation. The AMS-C score was lower in dexamethasone-treated subjects compared to high-altitude pulmonary edema-sensible controls. A stepwise multiple linear regression analysis on arterial PCO2, SaO2, and baseline or altitude ARI, identified altitude ARI as the only significant predictor of the AMS-C score (p=0.01). These results supported the notion that impaired dynamic autoregulation of CBF could play a role in AMS symptomatology .
Thus cerebral hemodynamic studies so far fit with the notion that AMS and high altitude cerebral edema are at the extremes of a spectrum of progressively severe hypoxia-induced vasogenic cerebral edema. This would explain the striking clinical similarities between of AMS and cerebral edemas of other causes, such as cerebral vein thrombosis. This would certainly account for the efficacy of therapies aimed at the decrease of vasogenic cerebral edemas, such as high doses of corticosteroids .
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