Central venous pressure elevations are associated with intracranial pressure spikes in a model of acute obstructive sleep apnea.

Obstructive sleep apnea (OSA) is associated with increased cerebrovascular disease, but acute intracranial dynamics during obstructive events remain uncertain. We hypothesized that negative intrathoracic pressure elevates intracranial pressure (ICP) by increasing central venous pressure (CVP) and impairing cerebral venous outflow. In an anesthetized porcine model, we measured ICP during simulated OSA with intermittent negative airway pressure (INAP) or positive end-expiratory pressure (PEEP) under controlled blood gas conditions. INAP consistently produced post-apneic ICP surges (+10 mmHg) that were time-locked to CVP spikes with strong ICP-CVP coupling during INAP (r = 0.74) and moderate pooled correlation across all epochs (r = 0.48). Pooled associations with arterial blood pressure (r = -0.02) and cerebral blood flow (r = 0.24) were negligible. The magnitude of responses was modulated by blood gases: hyperoxia attenuated ICP/CVP changes, whereas hypercapnia augmented pressure surges and was associated with modest changes in global cerebral blood flow without proportionally increasing peak ICP. PEEP was accompanied by immediate increase in ICP and CVP, consistent with direct pressure transmission to the venous system. Collectively, these findings support a venous-mechanical contribution as a key driver of acute ICP elevation during obstructive events, with chemoregulatory effects modulating the response, and provide a hemodynamic context for OSA's established cerebrovascular risk associations.