Role of pCO2 (AV gap) of Multi Organ Dysfunction Syndrome

Abstract

Recruitment of Microcirculatory-Mitochondrial (RMM) reduces Microcirculatory-Mitochondrial Distress Syndrome (MMDs), and Syndrome of Multi-Organ Dysfunction (MODs), by accelerated speed of delivery and return of blood flow which directly leads to a decrease in tissue hypoxia marker pCO2 (AV gap) and respectively with ↓ many other Endogenous Toxic Substances (ETS). In cases of pulmonary damage with ↑ pCO2 & ↓ Oxygenation Index PaO2/FiO2 ↓ 300 the development of Acute Respiratory Distress Syndrome (ARDs), MMDs are also aggravated at ↑ with pCO2 AV gap. RMM also needs additional support of Multiple Organ Therapies-Multi-Organ Supportive Therapy (MOST), Alveolar Recruitment, Extracorporeal Life Support Organization (ELSO), Modeling of the Index of Extravascular Lung Fluid, EVLWI, Th4- Th5 Thoracic Epidural Block, Active detoxification methods. The absence of decreasing of the pCO2 tissue hypoxia marker at the pCO2 AV gap ↓ 5.0 mmHg, after RMM proves the mitochondrial eu-energetic metabolic remodeling with the elimination of the hypo(an)ergic mitochondria performed by lysosomal clearance (mitophagy) makes the predominance eu-ergic mitochondria with the normalization of mitochondrial Ca++-uniporter-channel and mitochondrial permeability pore transition which productively inactivate the toxic forms of oxygen and nitrogen.