1 Cambridge, UK 2 Nottingham, UK
EditorWe read with interest the article by Sherman and colleagues.1 We would like to comment on the methods used to estimate critical closing pressure and cerebral perfusion pressure.
The formula used to calculate critical closing pressure in this article omits the influence of cerebrovascular wall tension. It actually equates critical closing pressure with intracranial pressure. As shown earlier, critical closing pressure consists not only of intracranial pressure but also of a factor representing arterial vascular wall tension.2 Moreover, the method used to calculate critical closing pressure can be questioned. Basing the linear function (of which the x-axis intercept is considered to be critical closing pressure) on diastolic and mean values only, thus omitting the systolic values, would only be appropriate if the upstroke of the pulse wave were linear, which is not always the case.
The formula that was used to estimate cerebral perfusion pressure was originally a simplification of Aaslids approach.3 However, there is a relevant difference between what Aaslid validated and what Sherman and colleagues, based on Belfort and co-workers,4 used. The original Aaslid formula is:
eCPP = FVm x (F1 (MAP))/(F1 (FVm))
(F1=amplitude of the fundamental frequency components, eCPP=estimated cerebral perfusion pressure, FVm=mean flow velocity, MAP=mean arterial pressure). The substitution of the amplitude of the fundamental frequency components with the differences between mean and diastolic values introduces an error that is especially relevant under conditions where intracranial pressure is assumed to be normal. The behaviour of diastolic velocity becomes important when intracranial pressure is high. However, in patients who are assumed to have normal intracranial pressure, mean arterial pressure is the best estimator of cerebral perfusion pressure. Methods that estimate cerebral perfusion pressure as a fraction of mean arterial pressure, the fraction being derived from the transcranial Doppler waveform, are generally more accurate.5 Using our own material collected in head injured patients,6 we can confirm the prediction that using the distance between mean and diastolic values for flow velocity or blood pressure weakens the estimation of cerebral perfusion pressure.
We would like to emphasize that these comments are of a methodological nature, and we do not imply that using different formulae to estimate critical closing pressure or cerebral perfusion pressure would have changed the results.
L. A. Steiner
M. Czosnyka
Cambridge, UK
EditorWe thank Steiner and Czosnyka for their interest in our study. They raise interesting points regarding non-invasive methods of estimating cerebral perfusion pressure and critical closing pressure using transcranial Doppler ultrasonography.
Steiner and Czosnyka state that Belforts formula, that we have used in our study1 to calculate critical closing pressure, omits the influence of cerebral vascular wall tension. However, they have not referred to any published data to support their rather generalized statement. Their referenced studies in head-injured patients,5 6 do not directly assess the performance of Belforts formula during changes in vascular wall tension and, in our opinion, do not address the issue. As they have acknowledged, since Aaslids study,3 a number of formulae have been described to estimate critical closing pressure and cerebral perfusion pressure. All these are based on systolic, diastolic or mean flow velocities as related to systolic, diastolic or mean arterial pressures. The basic principle remains the same [i.e. P=FxR (P=perfusion pressure, F=flow, R=resistance)]. In most of these formulae, the flow is represented by mean flow velocity, and the resistance is represented by the ratio between instantaneous pressure and flow,3 or the ratio between changes in pressure and flow during cardiac cycle.4 In theory, any relationship between pressure and flow in an elastic vessel during pulsatile flow, whether based on systolic, diastolic or mean values during the cardiac cycle, when extended to the point of critical closing pressure (which is never measured directly), assumes that the vessels elastic behaviour remains constant throughout its diameter. Therefore, in the strict sense, Belforts assumption is no different from the assumptions made by any other methods.
In practical terms, as far as we are aware, none of the recently described methods are fully validated; in particular, it is not clear from existing literature as to which formula is most appropriate under given pathophysiological conditions. We have recently conducted bench model studies to validate different formulae.7 8 Our data suggests that Belforts formula can reliably estimate changes in critical closing pressure related to either changes in intracranial pressure,7 or changes in systemic vascular compliance.8 In another recent study, we have shown that in human volunteers, where intracranial pressure can be assumed to be normal, changes in critical closing pressure, subsequent to changes in end-tidal carbon dioxide, can be reliably predicted and estimated by Belforts formula.9 10 The results of this study are similar to those published by Weyland and colleagues,11 who assessed critical closing pressure using regression lines between instantaneous pressure and flow velocity points in a given cardiac cycle. These studies conclude that arterial tone is the main determinant of downstream pressure of cerebral perfusion in patients or subjects without intracranial hypertension, and provide direct evidence that Belforts method is capable of detecting changes in this phenomenon. The results of these studies also give us sufficient ground to suggest that the concern raised by Steiner and Czosnyka, that Belforts method omits the influence of cerebrovascular wall tension, is unfounded.
R. Sherman
R. P. Mahajan
Nottingham, UK
References
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