Effect on cerebral hemodynamics and brain function

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Elevated intrathoracic pressure caused by mechanical ventilation with PEEP may influence cerebral hemodynamics by several mechanisms, particularly if cerebral blood flow regulation is impaired and pressure dependent. PEEP-related changes in the systemic circulation (decreased venous return, decreased mean arterial pressure (MAP)) will decrease cerebral arterial inflow. Moreover, application of PEEP may increase cerebral venous pressure and intracranial pressure (ICP), and thus further decrease cerebral perfusion pressure (CPP = MAP - ICP) and cerebral venous outflow.

PEEP increases intracranial pressure by direct transmission of elevated pleural pressure through the intervertebral foramina to the spinal and cerebral subarachnoid spaces, and, in some cases, by Paco2 elevation as the ratio of physiological dead-space to tidal volume may be increased with the application of PEEP. However, the main transmission of elevated intrathoracic pressure occurs via the systemic and cerebral venous system.

PEEP increases right atrial, internal jugular, and vertebral venous plexus pressures. This is transmitted to the dural sinuses and, at least partially, to cerebral veins with a subsequent rise in intracranial pressure. The magnitude of these changes depends on the amount of PEEP applied and on pulmonary compliance (the stiffer the lung, the less pressure is transmitted to the brain). The transmission of raised atrial pressure to the intracranial contents could be particularly dangerous in patients with pre-existing intracranial hypertension. Abrupt increases of intracranial pressure and decreases in cerebral compliance were observed during application of PEEP in dogs and rabbits with mass lesions artificially produced by inflation of an intracranial balloon.

Conversely, while studying the effect of PEEP in a similar dog model, Huseby.efa/ (1981) found that intracranial hypertension diminished the increase in intracranial pressure for a given level of PEEP. They postulated that there is a compensatory waterfall mechanism with a significant pressure gradient between the cortical veins, which are compressible by the intracranial pressure, and the sagittal venous sinus which is not influenced by intracranial pressure changes. When the intracranial pressure is low, the cortical veins are largely open so that increases in the sagittal sinus pressure are easily transmitted to the intracranial contents, limiting cerebral venous outflow and increasing cerebral blood volume. In contrast, when intracranial pressure is elevated, cortical veins become compressed and the increased pressure gradient between the cortical veins and the sagittal sinus prevents the pressure rise in the sagittal sinus from affecting intracranial pressure ( Fig 2). Another possible compensatory mechanism for elevated cerebral venous pressure is the opening of additional anastomotic channels with a redistribution of cerebral venous outflow.


Fig. 2 Schematic illustration of the intracranial space during raised intracranial pressure (ICP). The arrows indicate the position of the hypothesized Starling resistor. Here, the mean arterial pressure (MAP) is greater than intracranial pressure, which is greater than the sagittal sinus pressure (SSP). The cortical vein pressure ( Pcv) cannot fall below the intracranial pressure, and thus flow is dependent on MAP - ICP and independent of small changes in the sagittal sinus pressure. (Reproduced with permission from Huseby.elal,., (.1.98.1.))

The waterfall concept was recently contested by Asgeirss^ who postulated that cerebral venous outflow is regulated by a venous resistance situated at the outflow orifice and directly related to the variations of interstitial tissue pressure; furthermore, they claimed that cortical veins were neither compressed nor collapsed, but remained dilated during increases in intracranial pressure.

The evidence regarding the potential effects of PEEP in patients with brain lesions is conflicting. Some authors have found no clinically significant rise in intracranial pressure on use of PEEP, although others have reported increases in intracranial pressure and neurological deterioration following application of PEEP in patients with decreased cerebral compliance.

The overall effects of elevated intrathoracic pressure on cerebral hemodynamics depend on the interactions of pulmonary and cerebral compliance, the status of cerebral and systemic circulation, and any improvement in respiratory function obtained by ventilation with PEEP. In patients with impaired autoregulation, high intracranial pressure, and reduced cerebral perfusion pressure, the lowest possible intrathoracic pressure should be employed. Moderate head elevation (15-30 per cent), which may decrease the jugular venous pressure, was proposed for the management of these patients. However, conflicting results regarding the beneficial effect of this maneuver and its influence on cerebral perfusion pressure have recently been presented ( Asg.eirs.son.and G.ra,n.d.e...,1...,9..9.4).

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