Genesis of Antibiotic Resistance (AR) LXXV: Turbulence Modeling of Simplified Severe Sepsis Protocol‐2 (SSSP‐2), NCT01663701: Simulation of Contributing factors that Protract & Métier Torque Thrusted LPE Aggregates’ in Coandă effect Cause Critical Closing Pressure (CCP)

Abstract

Hypothesis: EGDT-ERP is directly inducing blood volume expansion, altering the BP, alter the velocity, shear stress, hematocrit forming an LPE aggregate’ and an adverse pressure gradient in vivo smite NFP lead to CCP subsequent CVA/comatose. An effort is made to test a unifying (holistic) hypothesis that has the potential to lull LPE aggregates, alongside AR clinical persisters in the cerebrovascular capillary bed with intrinsic torque of LPE (bluff body) in tandem dragging on the capillary lumen, alongside LE (large eddies), vortices would rupture true capillaries eliciting CCP in an asymmetric velocity profile through anisotropic mode with the collapse of NFP is tested with fluid flow. Geometry: We take inspiration from the impact of torque-drag of a moving object in time sequence: a: torque- and drag sustain damage to the runway – correlate LPR torque – drag on the capillary bed: https://www.youtube.com/watch?v=DFOynlRYT54YouTube©– (time scale: seconds)– b: https://www.youtube.com/watch?v=u5axFVRdNRU; c:splash on the landing: https://www.youtube.com/watch?v=9poWj5eu5rE- (time scale: seconds) – d:https://www.youtube.com/watch?v=2u7jY3V-GJ0– rejected take-off – LPE aggregates lead abrupt occlusion; Governing equations: Darcy's law: Q=kA∆P/μl, -Eq3.27, where Q=discharge flow rate, k=permeability, A= cross-section of the media (blood), ∆P=pressure drop, μ=viscosity, L=length, derived eq. 3.28 – 3.34; (p104-105, ISBN 9780128024089); Torque: τ = r x F, where force F, that act on a particle at position, r(p250 eq;7.6 (ISBN 9780521198110). Experimental Observation: The following experimental observations is an archetype for our hypothesis ad hoc momento. PMID:27319318: Fig2 b, d, f, h compares to the Fig 1, III and V, E, would be lysed passing through the occlusion, releasing lysate, in turn, activating L, P, and E forming LPE; Fig 3d-F represent an LPE aggregate in vivo of sepsis cohort in NCT01663701; Fig 4c the stenosed vessels energy level declined; Fig 5c location II, high energy location VI favor LPE aggregate upstream causing CCP; penultimate to losing NFP, CVA cloture comatose. PMID: 31297646: indicate that RBC(E) aggregate occurs upstream of stenosis forming thin cell free layer (CFL) and decreased flow velocity are in favor of our hypothesis. PMID 31010931 Fig 5 C in the CLP group continuous accumulation of heparin sulfate in the hippocampus of sepsis model (PMID 31297646, PMID 29195076), Fig 7E, implicit of LPE aggregate at the arterial end of the capillary bed;p9213 reinternalize cecum–a trauma-lack≡DDx!; ( PMID: 30720464 PMID: 31337421; PMID: 31201739), patient-specific, TM-CFD; Simulation: Our effort to simulate for water/sewage flow system indicate that a. monitors the aggregate formation, b. utilizes the degreaser/blood-thinning agent, c. coating the pipe agents to repair glycocalyx-endothelium to restore the structure and laminar flow. At present, attempting the simulation of role of CFL in eliciting the adverse pressure gradient / vasomotion in the terminal arteriole - exchange vessels - postcapillary venule in vivo.