Pneumolysis in COVID-۱۹: pathophysiology and high altitude implications

سال انتشار: 1399
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 131

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شناسه ملی سند علمی:

BIOCONF21_0512

تاریخ نمایه سازی: 7 شهریور 1400

چکیده مقاله:

Severe lung compromise in COVID-۱۹ patients often evolves to life-threatening hypoxemia. The mechanisms involved are not fully understood. Their understanding is crucial to improve the outcomes. Initially, pastexperience lead to the implementation of standardized protocols assuming this disease would be the same as SARS-CoV. Impulsive use of ventilators in extreme cases ended up in over ۸۸% fatality. Medical and physiological high altitude acute and chronic hypoxia experience with COVID-۱۹ hypoxemia grants a new insight. A pathophysiological analysis is performed based on literature review and histopathological findings. Application of the Tolerance to Hypoxia formula = Hemoglobin/PaCO۲ +۳.۰۱ to COVID-۱۹, enlightens the critical hypoxemia. Pneumolysis is an acute infectious disease marked by inoculation of the Coronavirus-۲RNA or other viruses within the pneumocytes, viral intra-cellular replication and pneumocyte destruction (generally not compromising the bronchioles), accompanied by inflammation, edema, capillary vasodilatation, the formation of hyaline membranes, and micro-abscesses, nuclear atypia, characterized by non-productive cough, initial silent hypoxemia, and sudden onset of difficulty in breathing, fatigue, tachycardia and rapid progression to a reduced lung gas exchange area and subsequent fibrosis. First known use: Jun ۱۳, ۲۰۲۰. The adequate interpretation of the histopathological lung biopsy photomicrographs reveals these alterations. The three theoretical pathophysiological stages of progressive hypoxemia (silent hypoxemia, gasping, and death zone) are described. At high altitude, normal low oxygen saturation (SpO۲) levels (with intact lung tissue andadequate acid-base status) could be considered silent hypoxemia. Several factors influence a lower incidence of COVID-۱۹ at high altitude. At sea level, in COVID-۱۹, the silent hypoxemia starting at SpO۲ =< ۹۰% (comparable to a normal SPO۲ {۸۸-۹۲%} at ۳,۵۰۰m) suddenly evolves to critical hypoxemia. This, as a consequence of progressive pneumolysis + inflammation + overexpressed immunity + HAPE-type edema resulting in pulmonary shunting. The proposed treatment is based on the improvement of the Tolerance to Hypoxia (Hemoglobin factor), inflammation reduction, antibiotics, rehydration and anticoagulation if required. Understanding the pathophysiology of COVID-۱۹ may assist in this disease's management.

نویسندگان

Gustavo R. Zubieta-Calleja

High Altitude Pulmonary and Pathology Institute (HAPPI-IPPA), Av. Copacabana - Prolongación #۵۵, La Paz, Bolivia