Genesis of Antibiotic Resistance (AR) LXXIX: Turbulence Modeling of Hemodynamics in Simplified Severe Sepsis Protocol‐2 (SSSP‐2)‐NCT01663701: Linear Correlation of CPPopt, GCS 3‐8 and in hospital mortality (ihm)
Authors: Quiroz Aida , Camacho Cheyenne , Kannan Subburaj 
Published: May 2022

The objective is to determine the cause and effect relationship between ERP induced fluid volume expansion, neurological monitoring parameters that determine the CPPopt, Comatose GCS 3‐8, and ihm of the usual care cohort vs sepsis protocol cohort in the time scale of pre‐ad to ER as, 0 hr. till 120 hrs. (5 days) ± 48 hrs. (7 days maximum hospital stay). Coma Scale used (vs Four Score (Ann. Neurol 2005; 58:585)): (NC 5‐37: ISBN‐10:1‐4963‐0553‐1). Eye Opening(E): E1: None; Best Motor Response(M): M1= no response; Best Verbal Response(V): V1= No response; (E1+M1+V1=GCS3). DDx: Dysfxn of brainstem RAS, thalamic relay nuclei, and/or b/l diffuse dysfxn of cerebral hemispheres (verbatim ‐ NC‐5‐38). GCS < 8 =Unconscious; GCS 4‐3=Coma Grade III –IV deep coma (p167; ISBN: 978‐1‐59103‐261‐8). Geometry: Table 2.1, p 63, ISBN 9780128024089. Hemodynamic & Neurologic Monitoring Parameters (Normal): i. Mean Arterial Pressure (MAP): 70 mmHg to 100 mmHg @ BP 120mmHg/80mmHg; PP 40 mmHg; PI: 0.02% weak pulse to 20% strong pulse; PaO2 by arterial blood gas (ABG) test: 75‐100 mmHg; SpO2: 95%‐100%; ii. Cerebral Perfusion Pressure(CPP): 60‐80mmHg; iii. Intra Cranial Pressure (ICP): 5‐10mmHg; iv. Pulsatility Index (PI) or Gosling index: 1.36 – 1.56; v. Resistive Index (RI): 0.6–0.8; vi. Central Venous Pressure (CVP):0‐5mmHg; vii. pO2 > 12kPa; viii. CPPopt <10 mmHg = hypo perfusion; CPPopt >10 mmHg = hyper perfusion (D CPPopt= CPP‐ CPPopt ±10 mmHg) (PMID: 33420669); ix. Pressure Reactivity Index (PRx)(PMID: 21852615); x.Brain tissue oxygenation (Oxygen reactivity index – ORx) 0.6 to +0.7 (PMID: 21852615); xi: Total oxygenation reactivity index – (TOx): (PMC4957667). Governing Equation(s): D CPPopt= CPP‐CPPopt ±10 mmHg. Derivation: The following presentation is derived for neurogenic shock:ÞBP, ÞPP, ÞCO, ÞCVP, ÞPASP, ÞPADP, ÞPAWP, ÞSVR, ÞSvO2, Ý/N. PVR @ hypovolemia, ÜPerfusionÞ dysfunction of sym. Sti., Ý vasodilation. and systemic hypoperfusion (p10‐44): Septic shock: As per baseline characteristics of NCT01663701, it is predicted that G‐ bacilli of HAI, and G+ ClPr: S. aureus, Streptococcal species induced iv line sepsis: Infectious toxins of ClPr originÜLPE aggregate(s) damaged capillary bed Üpermeability Ý/vasodilation Üloss of NFPÜabsolute 3rd spacing Ü hypovolemia Ü BPÞ, Ü hypoperfusion Ü GCS3‐8 ÜCCP Ü CEPÜ ihm. p10‐45: ISBN 9780932887566. Prospects: Here we present a correlation ERP and time‐dependent progression of comatose to ihm in usual cohort. Part I: Patients on the flat part of the curve have a good compensatory reserve. Part II: Patients on the exponential part of the curve (part II) have a Þ compensatory reserve meaning that a slow change in the volume (ΔV) of the intracerebral space (CBV, ICP depending on the medical history of individual patient). Part III: This part of the curve likely corresponds to patients in the usual cohort (NCT01663701) imply the onset of GCS 3‐8 due to initial ÝCBV, ÝICP, and subsequent irreversible collapse of cerebral vessels. Source: https://cppopt.org/prx/. Such scenario may have been the clinical incidence for 100% ihm in the NCT01663701, usual care cohort.