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Experiments were performed in a group of 19 healthy, non-smoking volunteers. The experiment consisted of three apnoeas, sequentially: 30 s apnoea, 60 s apnoea and maximal, that could be done, apnoea. The breath-hold was separated for 5 minutes rest. The following parameters were measured and obtained for further analysis: blood parameters, artery diameter of the internal carotid artery, end-tidal CO2 in expired air, the cardiac (from 0.5 to 5.0 Hz) and slow (< 0.5 Hz) components of subarachnoid space width signal. As a result of the experiment, we observed two different reactions, using the same experimental procedure. It seemed to indicate two different operating modes and two separate models. As a consequence, there are two subsets of slow subarachnoid space width responses to breath-hold in humans. A positive subarachnoid space width changes (slow) component depends on changes in heart rate, pulsatility index and cerebral blood flow velocity. A negative subarachnoid space width changes component is driven by heart rate changes and pulsatility index changes. The different heart-generated arterial pulsation response to experimental breath-hold provides new insights into our understanding of the complex mechanisms governing the adaptation to apnoea in humans. We propose a mathematical methodology that can be used in further clinical research.

Modeling of Cardiac Component of Subarachnoid Space Changes in Apnoea Resulting as a Function of Blood Pressure and Blood Flow Parameters - Two Mechanizm of Regulation