OBJECTIVE: To propose a new coefficient, which contains information about both the absolute ICP and the position of the 'working point' on the pressure-volume curve. METHOD: ICP was monitored continuously in 187 sedated and ventilated patients. The RAP coefficient was calculated as the running (3 minutes) correlation coefficient between slow changes in pulse amplitude and mean ICP. RAP has value 0 on the flat part of the Pressure-Volume Curve and +1 on the ascending exponential part. Then RAP decreases to zero or becomes negative when ICP increases further and affects cerebrovascular pressure-reactivity (which flattens the pressure-volume curve). Variable tICP = ICP* (1 - RAP) has been called 'trueICP'. It magnifies the critical values of ICP when cerebrovascular reactivity is exhausted and dampens those states where absolute ICP is elevated but vascular reactivity is not affected. RESULTS: Both Mean ICP and RAP were independently correlated with outcome (ANOVA:ICP-GOS: F = 22; p < 0.00001, RAP-GOS: F = 9; p < 0.001). 'TrueICP' had stronger association with outcome: F = 28; p < 0.000001. Mortality in those patients having 'trueICP' above the threshold of 19 mm Hg was above 80%, while the mortality in those having cICP below 19 mm Hg was only 20% (F = 80; p < 10(-8)). 'TrueICP' was also suitable for continuous monitoring: sustained rise in tICP above 19 mm Hg was strongly associated with fatal complications. CONCLUSION: The proposed variable is a powerful predictor of fatal outcome following head injury. It is sensitive to both the rising absolute ICP and the critical loss of cerebrovascular regulation.
OBJECTIVE: To propose a new coefficient, which contains information about both the absolute ICP and the position of the 'working point' on the pressure-volume curve. METHOD: ICP was monitored continuously in 187 sedated and ventilated patients. The RAP coefficient was calculated as the running (3 minutes) correlation coefficient between slow changes in pulse amplitude and mean ICP. RAP has value 0 on the flat part of the Pressure-Volume Curve and +1 on the ascending exponential part. Then RAP decreases to zero or becomes negative when ICP increases further and affects cerebrovascular pressure-reactivity (which flattens the pressure-volume curve). Variable tICP = ICP* (1 - RAP) has been called 'trueICP'. It magnifies the critical values of ICP when cerebrovascular reactivity is exhausted and dampens those states where absolute ICP is elevated but vascular reactivity is not affected. RESULTS: Both Mean ICP and RAP were independently correlated with outcome (ANOVA:ICP-GOS: F = 22; p < 0.00001, RAP-GOS: F = 9; p < 0.001). 'TrueICP' had stronger association with outcome: F = 28; p < 0.000001. Mortality in those patients having 'trueICP' above the threshold of 19 mm Hg was above 80%, while the mortality in those having cICP below 19 mm Hg was only 20% (F = 80; p < 10(-8)). 'TrueICP' was also suitable for continuous monitoring: sustained rise in tICP above 19 mm Hg was strongly associated with fatal complications. CONCLUSION: The proposed variable is a powerful predictor of fatal outcome following head injury. It is sensitive to both the rising absolute ICP and the critical loss of cerebrovascular regulation.
Authors: Frederick A Zeiler; Ari Ercole; Manuel Cabeleira; Erta Beqiri; Tommaso Zoerle; Marco Carbonara; Nino Stocchetti; David K Menon; Peter Smielewski; Marek Czosnyka Journal: Acta Neurochir (Wien) Date: 2019-05-03 Impact factor: 2.216