Genesis of Antibiotic Resistance (AR) LXXXIV: Turbulence Modeling(TM) of Hemodynamics in Simplified Severe Sepsis Protocol‐2 (SSSP‐2)‐NCT01663701: ISP Afloat Transient APG Thrust VKVS to Hypoxia Rouse Erythropoiesis penultimate to GCS 3, and IHM

Abstract

Based on the theoretical inferences from the CFD pertaining to VKVS/vortices/shedding frequency/vortex‐induced vibration/ hysteresis effect, Shed Vortex, and Karman/symmetric vortex shedding, Courtesy: Flow‐3D HydroÒ, COMSOL Multiphysics®, © 2021, NASA‐U.S: https://earthobservatory.nasa.gov/images/85989/canary‐islands‐kick‐up‐von‐karman‐vortices, Harvard Natural Sciences Lecture Demonstrations http://sciencedemonstrations.fas.harv… https://www.youtube.com/watch?v=_Hbbkd2d3H8, Vortex shedding; https://www.youtube.com/watch?v=ahohd8ceGR4, and hemodynamic data from NCT01663701, here we present a plausible physiological basis for the effect of fluid bolus augmented VKVS, eliciting ISP, thrust skewed viscosity/velocity profile in congruence hitherto ISP, which may have been the cause that leads to precipitous ihm in the usual care cohort of SSSP‐2 (PMID: 28973227). Hypothesis:ISP dependent APG elicit spasmodic hypoxia to hyperbolic erythropoiesis penultimate to Comatose (GCS 3) to CCP and ihm in 24 hrs. Geometry: Part I: RBC, Platelets, WBC: detailed geometry of RBC, Platelets, WBC, p47‐56; Part II: Approximate geometry, blood velocity, and function of human blood vessels, Table 2.1; 2,2; 2.3; p63; ISBN 9780128024089; Governing Equation: Segmental Cerebral Perfusion Pressure Equation for The Intracranial Compartment: SPP = Pd − ICP = FFR · CPP − Ge · (1 − FFR) · (ICP − Pe), where, SPP is segmental perfusion pressure for the intracranial compartment, Pd—intracranial inflow pressure, ICP—intracranial pressure, Pa—systemic arterial pressure, FFR—Pd/Pa is the fractional flow reserve of the common inflow, CPP=Pa–ICP is cerebral perfusion pressure, Ge is the ratio of extracranial vascular conductance to total (intra‐extracranial) vascular conductance, and Pe is extracranial outflow pressure. (PMCID: PMC8032738; PMID: 33833266). Derivation and Prospects (Physiological Connotation): Earlier we have illustrated the resuscitation (of fluid bolus) induced fluid volume expansion evoked APG exert low shear force on cerebral arterial, endothelium engendering a pro‐thrombotic milieu (vasoconstrictive) (PMID: 17699225), enhancing the ZoO. Such conditions may impart a mechanical trauma to the RBC/WBC/platelets as a function of time in a flow ‐dependent shear forces (PMID: 19033138) evoking turbulence (Recrit= 2000) and increased stress on RBC (PMID: 27048168). Steal mechanism (hypoperfusion) (PMID: 23396797) can induce oscillating acute or chronic ischemia eliciting HIF‐1 in turn erythropoietin production and erythropoiesis (PMPMID: 26927670). As a function of time, such altering blood viscosity dependent velocity pattern in the upstream of the ZoO – blunt‐body/streamline bodies, possibly rupture and cause cerebral hemorrhage (CVA!). Taken together, it is suggested that aforesaid in vivo milieu would likely to be the cause for ihm in less than 24 hrs. in the usual care cohort of NCT01663701. Efforts are in progress to understand the rupturing mechanism(s).