Key result
Elevated intracranial pressure was associated with a mean increase in model-derived intracranial elastance of 1.0 mm Hg/mL and venous outflow resistance of 0.9 mm Hg × s/mL.
Why the study?
Intracranial pressure waveforms convey key physiological information but are typically analyzed qualitatively, prompting the development of a minimized model to estimate intracranial elastance and venous outflow resistance from arterial and intracranial pressure waveforms.
Does a minimized model of intracranial physiology allow for estimation of intracranial elastance and venous outflow resistance from arterial pressure and ICP waveforms in patients with severe brain injury?
Observational (n=15)
Does a minimized model of intracranial physiology allow for estimation of intracranial elastance and venous outflow resistance from arterial pressure and ICP waveforms in patients with severe brain injury?
Effect estimate: mean increase of 1.0 mm Hg/mL and 0.9 mm Hg × s/mL
A minimized mathematical model can closely replicate measured ICP waveforms and estimate intracranial elastance and venous outflow resistance using readily available clinical parameters in brain injury patients.
Model may aid single-cycle ICP analysis in brain injury; leaves open clinical adoption pending validation.
Introduction The intracranial pressure (ICP) waveform conveys important information regarding the state of intracranial physiology, but in clinical practice it is typically analyzed in a qualitative fashion. We sought to develop a minimized model of intracranial physiology that describes intracranial dynamics occurring in a single cardiac cycle. By using an abridged model to which inputs of measured arterial and ICP waveforms from patients with brain injury can be applied, we aimed to derive estimates of intracranial elastance and venous outflow resistance. Methods The minimized model has two capacitor elements, representing arterial wall and intracranial compliance, and two resistance elements, representing intracranial viscoelasticity and venous outflow resistance. We use a parameter optimization method to achieve estimates of intracranial elastance and venous outflow resistance. We studied patients with brain injury in the neurointensive care unit who underwent ICP monitoring and analyzed data from periods of normal and elevated ICP. Results We studied 375 ICP waveforms in 15 patients. Model-derived waveforms corresponded closely to measured ICP waveforms at both normal and elevated ICP. Model-derived estimates of intracranial elastance and venous outflow resistance both increased significantly when ICP was elevated (mean increase of 1.0 mm Hg/mL and 0.9 mm Hg × s/mL, respectively). Conclusions The minimized model closely replicates measured ICP waveforms and allows for estimation of intracranial elastance and venous outflow resistance in patients with brain injury from readily available clinical parameters.
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Nassir et al. (2026) conducted an observational in Severe brain injury (n=15). Elevated intracranial pressure (ICP) vs. Normal ICP was evaluated on Intracranial elastance and venous outflow resistance (mean increase of 1.0 mm Hg/mL and 0.9 mm Hg × s/mL). Elevated intracranial pressure was associated with a mean increase in model-derived intracranial elastance of 1.0 mm Hg/mL and venous outflow resistance of 0.9 mm Hg × s/mL.
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