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, gt; -2 cm H2O @ implicit hypovolemia (JVP: 6 to 8 cm above the right atrium; elevated: JVP gt; 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: lt;5 mmHg - gt;5mmHg; v.PPV: lt;10% gt;13-15%; vi. SVV: lt;10% -13-15%gt;; 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: lt;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 sphinctersÜTrue 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.
