(812.13) 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)
Tuesday, April 5, 2022
12:30 PM – 1:45 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
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 lt; 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 amp; 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 gt; 12kPa; viii. CPPopt lt;10 mmHg = hypo perfusion ; CPPopt gt;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.
