Genesis of Antibiotic Resistance (AR) LXXXV: Turbulence Modeling(TM) of Hemodynamics in Simplified Severe Sepsis Protocol‐2 (SSSP‐2)‐NCT01663701: Clinical Connotation of Monitoring ISP [BP(PP), MAP, CBF, ICP, CPPopt, Comatose GCS 3, and CCP] for Attenuation of IHM
Authors: Montoya Hector , Flores Jorge , Kannan Subburaj 
Published: May 2022

Based on the theoretical inferences derived from industrial CFD modules: Flow‐3DÒ Hydro FD simulation Model 04; 05_sediment_transport FLOW‐3D HydroÒ, (Courtesy: Flow‐3D HydroÒ), The Beauty of Vortex Streets, May 5, 2021; Curve Fitting of Solution Data in COMSOL Multiphysics®, July 27, 2021 © 2021 BY COMSOL INC., https://earthobservatory.nasa.gov/images/90734/two‐views‐of‐von‐karman‐vortices (NASA). and hemodynamic data (SSSP‐2), here we present a plausible physiological basis for the benefit of monitoring ISP for attenuation 100% ihm in the usual care cohort of SSSP‐2 (PMID: 28973227). Hypothesis & Rationale:Monitoring the ISP‐induced transient APG, eases the point of care clinical intervention for the recovery from GCS3 to homeostasis. Geometry: RBC, WBC, platelets, p47; Whole blood viscosity ~ 3 centipoise (cP) or ~0.003 Pascal second (Pa. s) p53; Blood velocity in the Human Blood Vessels: table 2.1 p63, Blood Vol. Distribution: Table 2.2, p64; Stress–Strain Curve, Fig 2.15 p 78; ISBN:9780128024089. Gov Eq: Segmental Cerebral Perfusion Pressure Equation for The Intracranial Compartment: SPP = Pd − ICP = FFR · CPP − Ge · (1 − FFR) · (ICP − Pe) (PMCID: PMC8032738; PMID: 33833266). Derivation & Prospects:ISP has been shown to induce cerebral hypoperfusion in turn vasogenic edema altering contralateral/ipsilateral CBF due to increased blood flow through the anterior communicating artery (Acom). Case Report (PMCID: PMC7332508; PMID: 32637214): A 72‐year‐old male presented with the right‐sided hemiparesis and underwent MRI. MR imaging show an acute infarction of the left frontal lobe [Figure 1] and bilateral internal carotid artery (ICA) stenosis (NASCET: Rt: 90%, peak systolic velocity 425 cm/s and Lt: NASCET 70%, peak systolic velocity 212 cm/s). After 2 months, SPECT showed an decrease in CBF in the right cerebral hemisphere [Figure 2a]. INVOS‐4100 cerebral oximeter based determination of the effect of carotid clamping and shunting on oxygen saturation (rSO2) showed rSO2 readings were lower than ipsilateral rSO2 readings. SPECT showed a decrease in CBF around the infarction [Figure 2b]. SPECT indicated a contralateral increase in CBF [Figure 2b]. Tx, with free‐radical scavenger(Rx), showed an improvement in CBF, and laterality disappeared 2 weeks after CEA [Figure 2c and d]. The CBF of both sides equaled 2 weeks later [Figure 3]. Subsequent MR imaging with fluid‐attenuated inversion recovery (FLAIR) images showed a local high‐intensity lesion around a previous infarction in comparison with before CEA [Figure 4a and b]. FLAIR MR imaging 2 weeks after initial surgery confirmed the complete disappearance of the high‐intensity lesion [Figure 4c]. Taken together, the focal vasogenic edema induced neurologic impairment is shown to be alleviated by treating edema and cerebral ischemia while monitoring hemodynamic parameters. This model could be applied for the attenuation of fluid bolus augmented VKVS, collapsing of cerebral vessels leading to 100% ihm, in the usual care group in SSSP‐2 (PMID: 28973227).