Investigators have recently shown that the Systolic 1 based pulsatile apparent resistance (S1-PaR) is more sensitive to an increase in intracranial pressure than a simple pulsatility index (PI) based upon middle cerebral artery flow velocity (MCAFV) alone. S1-PaR is a so-called blood pressure (BP) corrected PI. It is designed to detect a difference between middle cerebral artery PI and arterial blood pressure PI.
The apparent resistance is defined by aR = BP / MCAFV similar to Ohm's law: R = I / V: resistance is current divided by voltage (difference).
Central to the work of Neuromon B.V. is the theory of arterial acceleration. This theory proposes that the pressure wave of the heart is amplified by a shortlasting contraction in the conducting vessels of the arterial tree: Sys1. The second phase of systole (Sys2) is the result of the stroke volume being ejected into the aorta. The propagation of the Sys1 is presumably faster than of Sys2, since the first is based upon a rapidly spreading depolarization within the smooth muscle cells of the arterial wall via the abundant presence of gap junctions. The propagation of the Sys2 wave is slower since it is dampened by the visco-elastic properties of the arterial tree.
Arterial acceleration increases the penetration force of the Sys1 component, whereas Sys2 and diastolic flow velocity will be more sensitive to intracranial pressure elevation. This is typically the case when systolic spikes are seen in the MCAFV signal: only allowing flow during Sys1 and none during Sys2 and the diastolic phase.
Therefore, the relation between arterial blood pressure and MCAFV will be different during Sys1 compared to diastole. This leads to the definition of the PaR:
S1-PaR = (ED_aR - Sys1_aR) / TAVM_aR (with TAVM as abbreviation for time averaged mean).
The working of this parameter can be demonstrated in Neuromon's cardiovascular simulation. Let's start with simple settings of the model: no reflex activity but with arterial acceleration active.
In the simulation (red curve is arterial blood pressure (ABP) and blue curve is right middle cerebral artery flow velocity (MCAFV)):
This gives us the following results:
And the following waveforms (red curve is arterial blood pressure (ABP) and blue curve is right middle cerebral artery flow velocity (MCAFV)):
After normalization (dividing both signals by their time averaged means) and swapping the x- and y-axis:
Under these circumstances the relation between ABP and MCAFV (aR: symbolized by the angle of the lines with the x-axis) is similar during systole and diastole. Deviations from the ideal curve are partly due to a time lag between MCAFV-Sys2 in relation to ABP-Sys2. (Note that the pulsatility index (PI) is the width of the graph projected along the x-axis.)
What happens during elevated ICP? In the model ICP is assumed constant and adds up to normal venous pressure lowering the arterio-venous pressure difference that drives the blood flow.. During diastole, the relative effect of elevated ICP is larger than during systole and it may even lead to the cessation of flow at the so called critical closing pressure (CCP). Settings of the model (note: intracranial pressure):
The simulation (red curve is arterial blood pressure (ABP) and blue curve is right middle cerebral artery flow velocity (MCAFV)):
Leading to the following results:
And the following waveforms (red curve is arterial blood pressure (ABP) and blue curve is right middle cerebral artery flow velocity (MCAFV)):
After normalization (dividing both signals by their time averaged means) and swapping the x- and y-axis:
The increase in ICP brings the MCAFV closer to zero and under these circumstances the relation between ABP and MCAFV (aR: symbolized by the angle of the lines with the x-axis) is quite different during systole and diastole resulting in an increased value of S1-PaR. (Note that the PI is the width of the graph projected to the x-axis.)
S1-PaR = (ED_ABP/TAVM_ABP) / (ED_MCAFV/TAVM_MCAFV) - (S1_ABP/TAVM_ABP) / (S1_MCAFV/TAVM_MCAFV)
Comparing different parameters for a range of ICP values:
S1-PaR and PI rapidly increase when the end diastolic flow velocity becomes zero (at ICP > 30 mmHg). The CrCP increases more steadily since it is calculated over the full beat to beat average and the effect of the diastolic flow velocity becoming zero is more gradual.
