Background: Intracranial pressure (ICP) may increase in tracheally intubated subjects during periods of movement (e.g., 'bucking' and coughing). Recent research has suggested that factors other than passive congestion of the cerebral vessels, resulting from increases in central venous pressure, may contribute to the ICP response. The current study evaluated this issue in a canine model of intracranial hypertension and additionally evaluated the relationship between ICP and static increases in superior vena caval pressure. Methods: Six dogs were lightly anesthetized with 0.65% end-expired halothane in oxygen and nitrogen, and ventilation was mechanically controlled. Intracranial pressure was increased to a stable baseline of 15- 20 mmHg using a subarachnoid infusion of warm 0.9% saline solution. The following variables were quantified before, and for 6 min after, initiating a 1-min noxious stimulus to the trachea and skin: ICP, central venous pressure, electromyograms (masseter, deltoid, and intercostal muscles), intrathoracic pressure, and cerebral perfusion pressure (defined as mean arterial pressure -ICP). Later, the protocol was repeated in the presence of neuromuscular block with pancuronium. Finally, in the same dogs, occlusion of the superior vena cava at its junction with the right atrium was used to increase superior vena caval pressure in 5-mmHg increments, from 5 to 30 mmHg, so that the resulting increases in ICP could be quantified. Results: In unparalyzed dogs whose heads were maintained at the level of the right atrium, there was a 22- mmHg increase in ICP at 1 min after initiating the noxious stimulus (P < 0.05). The ICP increase was related to electromyogram activation and a 6- mmHg increase in central venous pressure; however, it was not associated with significant increases in intrathoracic pressure or cerebral perfusion pressure. Treatment with pancuronium abolished the electromyographic, ICP, and central venous pressure responses to noxious stimulus. When superior vena caval pressure was statically manipulated, the resulting ICP increase was only one half the magnitude of the superior vena caval pressure increase. After elevating the head 14 cm, the ratio of ICP to superior vena caval pressure increases was reduced to one third. Conclusions: If these results apply to humans, it was concluded that increases in ICP that accompany movement in tracheally intubated patients may arise from two complementary factors: (1) cerebrovascular dilation that correlates with electromyographic activity and is mediated by ascending neural pathways that transmit proprioreceptive information, and (2) passive venous congestion that results from any increase in central venous pressure. The influence of the latter factor can be reduced by elevating the head.
- Blood pressure, brain: blood volume; intracranial pressure
- Circulation: central venous pressure; mean arterial pressure
- Muscle: afferent activity; electromyograms; skeletal
- Neuromuscular relaxants: pancuronium