Commentary 6.1.2.



Karel Zítko

If artificial ventilation is indicated with a patient with the brain injury, we will ventilate to take physiological parameters (see Commentary 4.1.2.). We will use hyperventilation for the treatment of the intracranial hypertension which is done by neurological status or by assessment of intracranial pressure (ICP). We will not hyperventilate untill 24 mmHg (3 kPa).

The use of hyperventilation in the brain injury is a controversial issue1. As hyperventilation is used PaCO2 is decreased and the vasoconstriction of brain blood vessels occur. In this way the whole cerebral blood volume (CBV) and also cerebral blood flow (CBF) will decrease and that will manifest itself by the decrease of intracranial pressure (ICP). Worse final outcome was demonstrated with the patients who were hyperventilated long2.

The lowering of ICP is nevertheless transiet. Hyperventilation can moreover generate an exacerbation of the brain ischemia just for its influence on vasoconstriction of the brain blood vessels3. An extreme hypocapnia has further side-effects: the rise of respiratory alcalosis with the inducement of cardiovascular parameters (mainly lowering of cardiac output with the decrease of arterial tension) and metabolic effects which bring to bear on the whole organism.

1. Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: The eclusive role of ischemia. J Neurosurg 1991;75:685-693.
2. Muizelaar JP, Marmarou A, Ward JD et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg 1991; 75:731-739.
3. Marion DW, Carlier PM, Obrist WD, Darby JM: Treatment of cerebral ischemia improves outcome following severe traumatic brain injury. Abstract. 2nd International Neurotrauma Symposium, Glasgow 1993:072.

Last updated: 1999-09-06