1 Klinik für Anästhesiologie, Universitätsklinikum der RWTH Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany. 2 Institut für Pathophysiologie, Universitätsklinikum Essen, Germany. 3 Zentrum Anaesthesiologie, Rettungs- und Intensivmedizin, Georg-August-Universität, Göttingen, Germany. 4 Klinik für Anästhesiologie und Operative Intensivmedizin Städtische Kliniken, Oldenburg, Germany
Corresponding author. E-mail: wbuhre@ukaachen.de
Accepted for publication: November 4, 2002
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Abstract |
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Methods. We studied 20 mechanically ventilated patients with severe head injury, in whom ICP was monitored by epidural pressure transducers. AP was measured with a radial artery cannula. Blood flow velocity in the middle cerebral artery (VMCA) ipsilateral to the site of ICP measurement was measured with a 2 MHz transcranial Doppler probe. All data were recorded by a microcomputer from analoguedigital converters. ZFP was extrapolated by regression analysis of APVMCA plots and compared with simultaneous measurements of ICP.
Results. ZFP estimated from APVMCA plots was linearly related to ICP over a wide range of values (r=0.93). There was no systematic difference between ZFP and ICP. Limit of agreement (2 SD) was 15.2 mm Hg. Short-term variations in ICP were closely followed by changes in ZFP.
Conclusion. Extrapolation of cerebral ZFP from instantaneous APVMCA relationships enables detection of severely elevated ICP and may be a useful and less invasive method for CPP monitoring than other methods.
Br J Anaesth 2003; 90: 2915
Keywords: brain, blood flow; brain, intracranial pressure; head, injury
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Introduction |
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Patients and methods |
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Arterial oxygen saturation and carbon dioxide tension were measured at the beginning and end of each set of measurements. Blood flow velocity was measured in the middle cerebral artery (VMCA) on the same side as the site of ICP measurement, with a 2 MHz Doppler device (TC 2000; EME, Ueberlingen, Germany). After finding the blood flow velocity curve in the middle cerebral artery, the depth of insonation was adjusted to obtain signals from the proximal segment (M1) of the middle cerebral artery.79 Then, the Doppler probe was fixed with a probe holder device (IMP monitoring probe holder; EME), and the position of the probe was left unchanged until the end of the study period. Arterial blood pressure and VMCA curves were sampled with an analogue digital converter at a frequency of 50 Hz and the data were stored on a microcomputer for further calculation.
EDP was calculated by extrapolation of Doppler-derived pressureflow velocity plots as described recently.4 Since cerebral blood flow stops if MAP equals EDP, EDP would be the same as arterial pressure when cerebral blood flow was zero. In patients with spontaneous circulation, ZFP cannot be measured directly; therefore ZFP was determined in the present study using instantaneous arterial pressure flow velocity plots (APVMCA).4 Arterial pressure and VMCA data of single heart-beats were plotted against each other and extrapolated to zero flow using linear regression analysis.4 As pressure and flow were measured at different locations, compensation for time delay was done by iterative regression analysis until hysteresis of APVMCA plots was minimized.4 The pressure axis intercept of these plots represents ZFP data of the cerebral circulation.4 For each measurement, two respiratory cycles were selected randomly and extrapolated ZFP data of these heart-beats were averaged for further analysis.
Statistics
Haemodynamic data in Table 1 are given as mean (SD). Directly measured ICP and calculated ZFP data were compared according to the method of Bland and Altman.10 Bias between methods was determined as the mean difference between ZFP and ICP. The precision of both methods was given by the limits of agreement (2 SD of the difference between methods). In addition, correlation analysis was performed to assess the relationship between ICP and ZFP.
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Results |
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Discussion |
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Basic physiology predicts that blood flow through an organ will stop if the difference between the upstream and the downstream pressure is abolished; thus, the arterial pressure at zero flow will be the same as the EDP of the vascular bed. Because of the peculiar anatomy of cerebral veins and the rigidity of the cranium, the EDP of the cerebral circulation is determined by ICP if intracranial hypertension is present and indicates ZFP under these conditions.
To assess ZFP, several experimental studies have used stop-flow methods. Other studies extrapolated to ZFP by curve-fitting of pressureflow plots. In most of these studies, paired pressureflow data were derived from variation in blood flow by different interventions using repeated flow measurements. In our study, ZFP was measured by extrapolation from instantaneous pressureflow velocity relationships, using the physiological variations in blood pressure and blood flow during the cardiac cycle. This method has been used previously to calculate the EDP in the coronary circulation11 12 and has been used recently to assess the EDP of the cerebral circulation in a clinical setting.1315
We found close agreement between mean ICP and mean ZFP. The lack of a systematic difference confirms the hypothesis that ZFP, as extrapolated from instantaneous pressureflow velocity plots, represents the EDP of the cerebral circulation in patients with intracranial hypertension. The relationship between individual ICP and ZFP data additionally shows satisfactory agreement between the two methods of measurement. There may be individual differences between ZFP and ICP for different reasons.
First, extrapolation of ZFP from pressureflow velocity plots requires high-quality recordings of both arterial pressure and middle cerebral artery blood flow velocity. In some patients poor resolution of Doppler flow measurements may cause errors in extrapolating ZFP. Damping of arterial pressure measurements may cause similar problems. As the arterial pressure curve was from the radial artery, there was a time delay between pressure and flow, and such a delay requires correction. If this correction is inaccurate there may be residual hysteresis of the pressureflow velocity plots.4
Secondly, direct measurements of ICP may also be subject to methodological inaccuracy, which could cause differences between ZFP and ICP. In particular, epidural measurements are not accepted as a gold standard in determining ICP. A parallel study compared the EDP from pressureflow velocity plots with ICP measured by intraventricular pressure recordings in patients with and without intracranial hypertension.16 The limits of agreement were comparable (16.2 vs 15.2 mm Hg in our patients), suggesting that individual differences between EDP and ICP are a physiological rather than a methodological problem.16 From the physiological point of view, ZFP is a measure of cerebral EDP, whereas ICP represents an indirect estimate of tissue pressure. This is true whether a pre- or a postcapillary Starling resistor determines the EDP. Particularly in patients with high cerebral vasomotor tone, EDP may be greater than ICP if critical closing pressure is located at the precapillary (arteriolar) level, as we found in patients with intracranial normotension during deliberate changes in arterial carbon dioxide tension.4 13
Czosnyka and colleagues,17 in a similar clinical study, investigated the relationship between cerebral ZFP (as a measure of critical closing pressure) and ICP. In contrast to our results, the correlation between critical closing pressure and ICP was weak (r=0.41) and the authors concluded that critical closing pressure cannot be used to estimate ICP. This difference in results may be explained by the method of ZFP determination. Czosnyka and colleagues17 calculated the zero flow intercept point by extrapolation of systolic and diastolic pressureflow velocity data pairs only. Recording of systolic data at a sampling rate of 50 Hz may give rise to considerable errors in the extrapolation of ZFP if the remaining data from pressureflow velocity changes during the cardiac cycle are neglected. Hysteresis of pressureflow velocity plots because of a time delay in one of signals cannot be detected.
However, in the study of Czosnyka and colleagues17 the highest deviation between critical closing pressure and ICP was found in patients with intact autoregulation, i.e. in the presence of significant vasomotor tone; no significant difference was observed in patients with disturbed autoregulation. Correspondingly, the relative differences between ZFP and ICP in our study were greatest at low and moderate ICP values, when vasomotor tone was more likely to have a greater effect than the influence of ICP on EDP.
Extrapolation from instantaneous pressureflow velocity relationships enables determination of EDP on a beat- to-beat basis. This gives high temporal resolution, shown by on-line recordings of short-term variations in EDP. The example in Figure 3 shows variations in ICP caused by intermittent positive pressure ventilation closely paralleled by changes in ZFP. The temporal resolution of ZFP from instantaneous pressureflow relationships is sufficient to detect cyclic changes in EDP, e.g. abrupt increases in ICP (A-waves), which are of pathophysiological relevance.
In a number of patients with refractory intracranial hypertension, zero flow in the cerebral circulation occurred during diastole. The recording of pressureflow velocity plots in these patients enabled validation of our technique of curve-fitting and extrapolation as the true ZFP data, i.e. the arterial pressure that co-indicates complete cessation of blood flow in the middle cerebral artery. The analysis of these plots shows that the linearity of the arterial pressureVMCA relationship is maintained even at very low flow velocities. The close agreement between the true ZFP and ICP adds further evidence that ICP at extreme levels of intracranial hypertension indeed represents the EDP of the cerebral circulation.
The clinical values of ZFP extrapolation are several. First, transcranial Doppler sonography and arterial pressure monitoring are only moderately invasive, so that ICP can be estimated without breaching the cranium. This may be particularly useful if ICP measurement is not readily available or contraindicated because of coagulation disorders. Furthermore, more than one-third of patients with severe head injury develop intracranial hypertension within the first 24 h without signs of increased ICP in the initial CT scan.2 18 Patients with cerebral injury could be screened by quantitative assessment of EDP to examine the indication for direct ICP measurement.
In summary, we conclude that ZFP and ICP do not differ systematically and are closely related to each other in patients with severe head injury associated with moderate to severe intracranial hypertension. However, in the subgroup of patients with moderately elevated ICP, ZFP and ICP may be different entities. Estimation of ZFP from instantaneous pressureflow velocity plots allows clinical detection of severe intracranial hypertension if other methods fail or are not available. From a physiological point of view, ZFP may, in principle, be the more rational measure to assess cerebral downstream pressure and estimate cerebral perfusion pressure.
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References |
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