Autoregulation

Abstract: Cerebral blood flow was studied by the arteriovenous oxygen difference method in patients with severe hypertension and in normotensive controls. The blood pressure was lowered to study the lower limit of autoregulation (the pressure below which cerebral blood flow decreases) and the pressure limit of brain hypoxia. Both limits were shifted upwards in the hypertensive patients, probably as a consequence of hypertrophy of the arteriolar walls. These findings have practical implications for antihypertensive therapy.When the blood pressure was raised some patients showed an upper limit of autoregulation beyond which an increase of cerebral blood flow above the resting value was seen without clinical symptoms. No evidence of vasospasm was found in any patient at high blood pressure. These observations may be of importance for the understanding of the pathogenesis of hypertensive encephalopathy.

Abstract: Objectives. Premature infants experience brain injury, ie, germinal matrix–intraventricular hemorrhage (GMH-IVH) and periventricular leukomalacia (PVL), in considerable part because of disturbances in cerebral blood flow (CBF). Because such infants are susceptible to major fluctuations in mean arterial blood pressure (MAP), impaired cerebrovascular autoregulation would increase the likelihood for the changes in CBF that could result in GMH-IVH and PVL. The objectives of this study were to determine whether a state of impaired cerebrovascular autoregulation could be identified reliably and conveniently at the bedside, the frequency of any such impairment, and the relation of the impairment to the subsequent occurrence of severe GMH-IVH and PVL. Patients and Methods. To monitor the cerebral circulation continuously and noninvasively, we used near-infrared spectroscopy (NIRS) to determine quantitative changes in cerebral concentrations of oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (Hb) from the first hours of life. Our previous experimental study showed a strong correlation between a measure of cerebral intravascular oxygenation (HbD), ie, HbD = HbO2 − Hb, determined by NIRS, and volemic CBF, determined by radioactive microspheres. We studied 32 very low birth weight premature infants (gestational age: 23–31 weeks; birth weight: 605-1870 g) requiring mechanical ventilation, supplemental oxygen, and invasive blood pressure monitoring by NIRS from 1 to 3 days of age. MAP measured by arterial catheter pressure transducer and arterial oxygen saturation measured by pulse oximetry were recorded simultaneously. The relationship of MAP to HbD was quantitated by coherence analysis. Results. Concordant changes (coherence scores >.5) in HbD and MAP, consistent with impaired cerebrovascular autoregulation, were observed in 17 of the 32 infants (53%). Eight of the 17 infants (47%) developed severe GMH-IVH or PVL or both. Of the 15 infants with apparently intact autoregulation, ie, coherence scores .5. Conclusions. We conclude that NIRS can be used in a noninvasive manner at the bedside to identify premature infants with impaired cerebrovascular autoregulation, that this impairment is relatively common in such infants, and that the presence of this impairment is associated with a high likelihood of occurrence of severe GMH-IVH/PVL.

Abstract: Assessment of cerebral autoregulation is an important adjunct to measurement of cerebral blood flow for diagnosis, monitoring or prognosis of cerebrovascular disease. The most common approach tests the effects of changes in mean arterial blood pressure on cerebral blood flow, known as pressure autoregulation. A 'gold standard' for this purpose is not available and the literature shows considerable disparity of methods and criteria. This is understandable because cerebral autoregulation is more a concept rather than a physically measurable entity. Static methods utilize steady-state values to test for changes in cerebral blood flow (or velocity) when mean arterial pressure is changed significantly. This is usually achieved with the use of drugs, shifts in blood volume or by observing spontaneous changes. The long time interval between measurements is a particular concern in many of the studies reviewed. Parallel changes in other critical variables, such as pCO2, haematocrit, brain activation and sympathetic tone, are rarely controlled for. Proposed indices of static autoregulation are based on changes in cerebrovascular resistance, on parameters of the linear regression of flow/velocity versus pressure changes, or only on the absolute changes in flow. The limitations of studies which assess patient groups rather than individual cases are highlighted. Newer methods of dynamic assessment are based on transient changes in cerebral blood flow (or velocity) induced by the deflation of thigh cuffs, Valsalva manoeuvres, tilting and induced or spontaneous oscillations in mean arterial blood pressure. Dynamic testing overcomes several limitations of static methods but it is not clear whether the two approaches are interchangeable. Classification of autoregulation performance using dynamic methods has been based on mathematical modelling, coherent averaging, transfer function analysis, crosscorrelation function or impulse response analysis. More research on reproducibility and inter-method comparisons is urgently needed, particularly involving the assessment of pressure autoregulation in individuals rather than patient groups.