Genesis of Antibiotic Resistance (AR) LXXX: Turbulence Modeling(TM) of Hemodynamics in Simplified Severe Sepsis Protocol‐2 (SSSP‐2)‐NCT01663701: Temporal Correlation of Fluid Bolus, CPPopt(PRx), “Zone of Obstruction”, Comatose (GCS 3), and In‐Hospital Mortality (ihm)

Abstract

Based on Flow‐3DÒ Hydro FD simulation Model 04 (Courtesy: Flow‐3DÒ) and fluid flow patterns, here we present a plausible scheme of hemodyn. sequel in ERP induced fluid volume expansion, that lead to 100% ihm usual care cohort of SSSP‐2 (PMID: 28973227). Rationale: From the pressure‐volume curve of D ICP vs DCBV (ΔV cm3) of the intracerebral space Figure1. https://cppopt.org/prx/ (PMID: 632857) it is proposed that subsequent to fluid bolus, the patients in usual care and sepsis protocol cohort of SSSP‐2 may have had a good compensatory reserve (part I) within< 24hrs. The exponential part of the curve (part II) would likely represent the patients who have had a poor compensatory reserve with a slow ΔV of the intracerebral space (CBV) that caused a significant change in the ICP in less than ~48 hrs. The cause of 100% ihm in usual care cohort, could be derived as the patients with high CBV and consequently high ICP levels (part III)that lead to cerebral vessels collapse and impairing pressure‐volume relationship implied in impaired positive brain vessel function index possibly by capillary pruning‐string events within ~ 48hrs to ~72 hrs. An increase in CVP, lead to an anaerobic milieu to spur the growth of anaerobic AR‐ClPr (G+/G‐) bacilli merging with “Zone of Obstruction” (ZoO), hitherto DDx, CC/MCC/CCI/DRG, Comorbidity–polypharmacy score (CPS) and ultimately Comatose (GCS 3‐8) (PMID: 31474933). Hemodynamically, when there is an ÝABP/ CPP/CBV the arterioles dilate and hence the CBF, CBV and consequently the ÝICP. Geometry: (Table 2.1 p63, ISBN: 9780128024089). Hemodyn/neurol monitoring parameters:CPPopt, CVP ≥ 8 cm H20, ScVO2 ≤ 70%, GCS 3‐8, and time to event 120 hrs ± 48 hrs. Governing. Equation(s): Dimensional form of Momentum equation (9.10) at the wall u= v=0, considering the pressure gradient dp/dx<0, then [d2u/dy2]y=0=1/μ *dp/dx Eq 9.42; Fig 9.5 Flow separation and formation of wake behind ZoO (LPE Aggregates ‐Toxins of AR‐ClPr origin) form blunt bodies/streamline bodies referred as “ZoO” of unknown dimension; Fig 9.6 velocity distribution within a boundary layer; considered panel a: favorable pressure gradient = dp/dx<0; panel b: APG = dp/dx>0 (p468 – 471; ISBN:13:978‐0071329194). Derivation & Prospect: Subsequent to fluid bolus, within 120 hrs., BLS occurs expediting the ZoO, in metarteriole, capillary bed, and arteriovenous anastomosis doffing off vaso vasorum in turn vasomotion of the limbic region in particular cingulate nuclei, Amygdala, amygdaloid body, thalamic nuclei, parahippocampal gyrus, hypothalamus. Such an increase in CPPopt, and CBV engendered APG, eddies, ZoO, in cerebral pre‐capillary bed followed by a vasoconstriction of capillary sphincters, the collapse of arteriovenous anastomosis, possible occlusion of thoroughfare channel in true capillaries form a cyclical aerobic‐anaerobic milieu in vivo (en vivo) for the growth G+/G‐ AR‐ClPr, in turn spur toxic shock syndrome, CCP to GCS 3 consequential 100% ihm, within 120 hrs. in SSSP‐2.