The objective is to identify the cause of the hemodynamic aberrance in the usual care group with 5 patients leading to 100% ihm; vs the sepsis protocol cohort with 11 patients @ 90.05% ihm with a median hospital stay of 5 days (pre‐ad to ER as, 0 hr. till 120 hrs. (5 days) ± 48 hrs. with a max.7 days). GCS 3‐8 (Ref: Fig 3. NCT01663701(PMID: 28973227). Neurology (Monitoring parameters): EI: (None): VI: Intubated‐IT; MI: M:1 (None). Geometry: PMN 8‐15μm, eosinophils ~15 μm, basophils ~12‐15 μm, monocytes ~14‐25 μm, lymphocytes~8‐15 μm, platelets ~2‐3 μm, RBC ~ 7.7 ± 0.7 μm; capillaries (med. size) internal diameter 6 μm, wall thickness, 1 μm, length ~0.1cm, ~blood viscosity 0.03 cm/s (human) (p48, 63: ISBN 9780128024089). Flow Regimes: Re < 2100 ÜLaminar; 2100 < Re < 4200 ÜTransition; 4200 < ReÜTurbulent (Table 1.3 p22). Approximation of Flow Regimes: 0 < Re < 1 Ü highly viscous laminar creeping motion; 1 < Re < 100 Ü Laminar strong Re dependence; 100 < Re < 103Ü Laminar, (boundary layer theory‐separation‐APG!); 103< Re < 104 Ü Transition to turbulence; 104 < Re < 106Ü Turbulent, moderate Re dependence; 106 < Re < ∞ Ü Turbulent, slight Re dependence (Table 1.2, p21). Blood Vessels(Canine): Systemic arterioles, mean diameter (mm): 0.050, number of vessels 2.8X106, mean length(mm) 1.2, total cross section cm2): 55, total volume of blood (ml) 7; capillaries: mean diameter (mm) 0.008, number of vessels, 2.7X109, mean length (mm) 0.65, total cross section (cm2) 1357.0, total volume of blood (ml) 88, total percentage of total blood vol: 5 ml; Pulmonary arterioles, mean diameter (mm): 0.100, number of vessels 1.5X108, mean length(mm) 0.7, total cross section cm2: 120, total volume of blood (ml) 8; capillaries: mean diameter (mm) 0.008, number of vessels, 2.7X109, mean length (mm) 0.5, total cross section (cm2) 1357.0, total vol of blood (ml) 68, total % of total blood vol: 4 ml; (Table 3.1p85, ISBN: 9781439845165; Ref Table 2.1 p 63 ISBN 9780128024089). Gov.Eq: Eq 2.1 to Eq 2.6 (p73). Derivation: ERP induced in the flow against an APG, the fluid particles near and within the boundary layer due to their low kinetic energy flow in the opposite direction, cannot surmount the APG, thus eddies are formed. Because of local flow reversal zone, which curtails the pressure in the fluid, and pressure in the flow separation the region is low, causing low pressure, flow deceleration(upstream) with drag force (form drag) fluid profile entering branching of mother blood vessels to daughter vessels thrusting toward the inner wall (δP/δx >0; Fig 2.10, p73) resulting flow separation at BL and yield APG (Fig 2.10, refer flow separation regions); While Fig 2.11 presents the effect of APG on velocity profile for parabolic shape: δP/δx< 0; transition: δP/δx ̴ 0; flow separation (region) at δP/δx >0, forming recirculation zone where vortex shedding and eddie formation occur (Fig 2.11, panel c. p73 ISBN 9780128024089). Prospect: Taken together, plausibly aforesaid fluid flow pattern in metarteriole of limbic system (& arborvitae – cerebellar), provided a microsphere of incubator (anaerobic‐aerobic) for ClPr, consequent toxemia/toxic shock ÜCCP ÜCEP.
Read full abstract