Influence of an increased intracranial pressure on cerebral and systemic haemodynamics during endoscopic neurosurgery: an animal model A.F. Kalmar, G.

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Influence of an increased intracranial pressure on cerebral and systemic haemodynamics during endoscopic neurosurgery: an animal model A.F. Kalmar, G. De Ley, C. Van Den Broecke, J. Van Aken, M.M.R.F. Struys, M.M. Praet, E.P. Mortier British Journal of Anaesthesia Volume 102, Issue 3, Pages 361-368 (March 2009) DOI: 10.1093/bja/aen381 Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 1 Example of pressure waveform during placement of the occipital needle. A linear pressure increase during tissue penetration is followed by a sudden decrease upon entering into the cisterna magna. At that moment, a pulsatile waveform matching a normal ICP of around 6 mm Hg is observed. Low-frequency ventilatory pulsations are superimposed to high-frequency cardiac pulsations. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 2 The evolution of the MAP and HR during the first 200 s upon induction of intracranial hypertension. At time 0, the ICP is increased. A two-fold increase of the initial arterial pressure is seen in Groups N and L compared with a three-fold increase in Group S. In all three groups, the MAP increases significantly after induction of intracranial hypertension (P<0.01). In the N group, tachycardia and bradycardia are observed after induction of intracranial hypertension. In the L group, there is a tendency towards bradycardia. In the N and L groups, no significant change in HR is observed after induction of intracranial hypertension. In the S group, there is a significant induction of tachycardia within seconds after induction of intracranial hypertension (P<0.01). Compared with the N group, there was no significant decrease of the initial MAP (P=0.06) or HR (P=0.53) in the L group, but there was a significant decrease of initial MAP (P<0.01) and HR (P<0.01) in the S group. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 3 Typical recording of the sudden change in arterial blood pressure (ABP) in response to an increased ICP during an S group experiment. Inspiratory sevoflurane concentration of 8% results in a low initial ABP and causes bradyarrhythmia. Five seconds after increasing the ICP, the arrhythmia resolves and a Cushing reflex initiates. Notice a low pulse pressure of the ICP (PPICP) at 0–7 s, an absent PPICP when ICP>ABP, and relatively high PPICP when ICP=MAP. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 4 Hct levels before and after CPP suppression indicate the infused fluid was resorbed into the vascular compartment. All samples are from the sevoflurane group. Since in some of the animals, the second blood sampling via the tail artery was not possible, only 10 coupled data points were obtained. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 5 The pulse pressure of the ICP (PPICP) shows a very reproducible pattern in relation to the CPP. When the ICP is low, a low PPICP is seen; when the ICP increases towards the ABP, the PPICP increases to its maximum, and when the ICP increases to above the systolic arterial pressure, the PPICP decreases to almost zero. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions

Fig 6 After cessation of the infusion, the ICP decreases exponentially from 100.3 mm Hg to its baseline value. Within 2.4 s, the ICP has decreased to 1/e (=37%) of its baseline value, thus τ=2.4 s. British Journal of Anaesthesia 2009 102, 361-368DOI: (10.1093/bja/aen381) Copyright © 2009 British Journal of Anaesthesia Terms and Conditions