Genesis of Antibiotic Resistance (AR) LXXVI: Turbulence Modeling of Hemodynamics in Simplified Severe Sepsis Protocol‐2 (SSSP‐2)‐NCT01663701(ERP‐EGDT): Mechanism(s) Time‐dependent Fluid Volume Overload Elicit Adverse Pressure Gradient (APG) in metarteriole
Authors: Puente Raul , Padilla Natalie , Kannan Subburaj 
Published: May 2022

NCT01663701(PMID: 28973227) observed that usual care group, 5 patients @ 100% in‐hospital mortality (ihm); and the sepsis protocol cohort with 11 patients @ 90.05% ihm with a median hospital stay of 5 days (Usual Care: BP: 96/61mmHg, PP: 35mmHg; MAP: 72mmHg; Sepsis Protocol: BP: 95/61 mmHg; PP: 34 mmHg; MAP: 73mmHg; SAPS3≥56, JVP, > ‐2 cm H2O @ implicit hypovolemia (JVP: 6 to 8 cm above the right atrium; elevated: JVP > 9 cm, (Ref: Fig 3. p1239). Objective: to determine the effect(s) of fluid resuscitation on hemodynamic parameters in usual care cohort vs sepsis protocol cohort. Hemodynamic Parameters(Normal): i. BP: SBP/ DBP: 120/80mmHg; ii. PP: 40 mmHg; iii. MAP: 70 – 105 mmHg; iv. SPV: <5 mmHg ‐ >5mmHg; v.PPV: <10% >13‐15%; vi. SVV: <10% ‐13‐15%>; vii. RAP: 2 – 6 mmHg; viii. RVP: RVSP 15 – 25 mmHg; ix. RVDP: 0–8 mmHg; x: PAP: PASP: 15 – 25 mmHg / PADP: 8–15 mmHg; xi. MPAP: 10 – 20 mmHg; xii. PAWP: 10 – 20 mmHg; xiii. LAP: 6 – 12 mmHg; xiv.CO: 4.0 – 8.0 l/min; xv.CI: 2.5 – 4.0 l/min/m2; xvi.SV: 60 – 100 ml/beat; xvii. SVI: 33 – 47 ml/m2/beat; xviii. SVR: 800 – 1200 dynes · sec/cm5; xviii. SVRI: 1970 – 2390 dynes · sec/cm5/m2; xix. PVR: <250 dynes · sec/cm5; xx. PVRI: 255 – 285 dynes·sec/cm5/m2; xxi. LVSW: 58 – 104 gm‐m/beat; xxii. LVSWI: 50 – 62 gm‐m/m2/beat; xxiii. RVSW: 8 – 16 gm‐m/beat; xxiv. RVSWI: 5 – 10 gm‐m/m2/beat; xxv.CPP: 60 – 80 mmHg; xxvi. RVEDV: 100 – 160 ml; xxvii. RVESV: 50 – 100 ml; xxviii. RVEF: 40 – 60%; Oxygenation Parameters(Normal): i. PaO2 = 80–100 mmHg; ii. PaCO2 = 35 – 45 mmHg; iii. SpO2 / SaO2 = 95 – 100%; iv. Mixed SvO2 = 60 – 80%; v. CaO2 = 17 – 20 ml/dl; vi. CvO2 = 12 – 15 ml/dl; vii. A‐V O2 Content Difference (C(a‐v) O2) = 4–6 ml/dl; viii. DO2 =950‐1150 ml/min; ix. Oxygen DO2I = 500 – 600 ml/min/m2; x. VO2 = 200 ‐250 ml/min; xi. VO2I = 120 – 160 ml/min/m2; xii. O2ER = 22 – 30%; xiii. O2EI = 20 – 25%; Rationale: Based on the eTable 1. and eTable 2. it is inferred that patients in this study are pre‐disposed to unknown level of infectious diseases burden with AR clinical persister(s)(ARClPr) (DRI, RM, ARF, AR Stewardship data!) with concurrent loss of glycocalyx (patient specific), in the pre‐capillary vessels. ERP induced APG: As per eTable 3, subsequent to fluid bolus for usual care/sepsis protocol cohort, a low‐pressure upstream (arteriole‐metarterioles) transition to a high‐pressure downstream (venules‐venous) induced transition from hypoxia to normoxia/hyperoxia alter the hematocrit, viscosity, blood vessel resistance, velocity profile causing an alteration as shown: ArterioleÜterminal arterioleÜpre‐capillary sphinctersÜmetarterioleÜ pre‐capillary sphincters
ÜTrue CapillariesÜThoroughfare channel/preferential channelsÜ post capillary venulesÜvenulesÜveins (with valves) where a slow free stream dp/dx=0; at the BLS, slow down going into negative velocities in metarterioles with reperfusion‐induced injuries w/o by rolling LPE aggregates, elicit reverse flow forming APG (an anaerobic milieu). Prospects: Efforts are in progress to identify/locate the source, cause(s) and effect(s) of ERP‐EGDTÜ APGCBBLSÜReg. Expr. of ARGRÜARClPrÜClinical End Point.