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Euro-Neuro'98: First International Update on Neuro-Anaesthesia and Neuro-Intensive Care; Genk, Belgium, 5-7 February 1998

Cerebral blood flow measurement

van Aken, J.

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European Journal of Anaesthesiology: January 1998 - Volume 15 - Issue - p 59-60

Abstract F2

Although measurement of cerebral blood flow (CBF) using a variety of techniques has been employed for more than four decades for clinical research purposes, CBF determinations have not been generally applied in clinical practice. The current status of CBF measurements in clinical neurosurgery is very much like that of intracranial pressure measurement 30 years ago [1].

While continuous monitoring of the systemic circulation using pulmonary artery catheters and invasive blood pressure monitoring has become widely available clinically, monitoring of blood flow in specific organs is still unsolved. This is especially true for bedside moinitoring of the CBF. There are two reasons for this:

  1. the anatomical location of the brain within the skull makes access difficult and complicated and requires very expensive technology;
  2. there is a demand for minimal invasive techniques and a limit to examination due to the patient's specific situation (namely, minimal handling in craniocerebral trauma or surgery).

Therefore, for the moment, most clinicians must rely on their clinical judgement in monitoring the electro-physiological or metabolic consequences of changes in CBF; in other words, they must rely on indirect methods to evaluate CBF [2].

Below the reasons why CBF should be monitored (indirectly or directly) are discussed and a few techniques that are currently available for the bedside determination of CBF are briefly described.

The measurement of CBF is intended to answer several questions including the following:

  1. is the level of CBF near the ischaemic treshold?
  2. is CBF in the hyperaemic range?
  3. is CBF raising or falling?
  4. is autoregulation or PaCO2 response abnormal?
  5. does therapy have the desired effect on CBF?

Most indirect CBF monitoring techniques, namely jugular venous oxygen saturation (SjvO2), EEG and monitoring of the cerebral perfusion pressure(CPP), will provide information by means of the description of the consequences of a CBF decrease as a result of a decreasing CPP [3].

As CPP decreases toward the lower limit of autoregulation (approximately 50 mmHg), arterial vessels dilate and cerebral blood volume (CBV) increases.

At the lower limit of autoregulation, however, the ability to dilate further is exhausted and the circulation cannot decrease resistance any further to maintain flow, and CBF begins to decline passively as CPP decreases further.

At first, an increase in oxygen extraction compensates for the passive decline in CBF. When oxygen extraction is maximal, cerebral oxygen consumption (CMRO2) begins to decrease. Accordingly, synaptic transmission becomes impaired and eventually fails completely, as manifested by an isoelectric EEG. At this point, there is sufficient energy available to keep the neurons alive, but neuronal work is abolished.

Proceeding to even lower levels results in membrane failure (Na+, Ca2+ and water enter, and K+ exits the cell; this is cytotoxic oedema). Such reductions in CBF are in the lethal range and result in infarction immediately, if not corrected. These metabolic consequenses of reduced CBF are the same for any mode of flow reduction.

However, the indirect monitoring methods do not provide an evaluation of the CBF that is sufficiently sensitive or specific. Only three techniques are more or less suited as bedside CBF monitors. These include two indirect methods, the transcranial Doppler (TCD) and the measurement of the arteriovenous oxygen difference (AVDO2) via the jugular bulb catheter and one direct method, the inhalation or intravenous Xe133 method.

The TCD and the AVDO2 will be discussed extensively in the next lextures in this session. The Xe133 clearance technique for measuring CBF has been used longer and more extensively for the study of patients with craniocerebral trauma and subarachnoid haemorrhage than any other CBF monitoring technique. This technique has many advantages and is the mainstay of CBF measurement in many ICU departments.

Several other promising techniques are not discussed here because they are not clinically relevant or are still in an experimental stage (e.g. laser Doppler, oxygen tissue tension, spectroscopy).

The vision of optimal neurological monitoring determining regional blood flow and various metabolic parameters, online positron emission tomography(PET), is still far in the future.

In the meantime, the hydrogen clearance technique has proved to be highly beneficial in the ICU [4] and the operating room [5].

The focus on these techniques does not imply that other CBF methods have no role in the management of neurosurgical patients. The choice of a CBF measurement technique depends on many considerations: local availability of equipment and expertise, cost, subject (human vs. animal), desired anatomical resolution, and so on.

For a comprehensive overview of the CBF techniques available for the moment most neuro-anaesthesia textbooks can be recommended. Often one chapter is dedicated to the enumeration of the advantages and disadvantages of each technique.

References:

1Martin NA, Doberstein C. Cerebral blood flow measurement in neurosurgical intensive care. Neurosurg Clin N Am, 1994; 5: 607-618.
2 Germann P, Urak G, Donner A, et al. Regional cerebral blood flow measurement. Acta Anaesth Scand, 1997; 41 (Suppl. 111): 37-40.
3 Young WL, Omstein E. Cerebral and spinal cord blood flow. In: Cottrell JE, Smith DS, eds: Anesthesia and Neurosurgery, Mosby St Louis, 1994: 17-57.
4 Shiozaki T, Sugimoto H, Taneda M, et al. Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury. J Neurosurg, 1993; 79: 363-368.
5 Van Aken J, Van Poucke S, Ongenae M, Mortier E, Rolly G, De Ley G. A propofol based anesthesia impairs the responsiveness of cerebral blood flow to hypocapnia in patients with a brain tumor. Anesth Analg, 1997; 84: S374.

Section Description

The publication of this supplement has been supported by an eductional grant from Abbott Pharmaceuticals

Session F: Update on neuro-monitoring

© 1998 European Society of Anaesthesiology