
Hypoxia & Hyper-coagulability
Oxygen saturation:
- hemoglobin saturation, normal is 100%
- Measured via pulsoximeter (inaccurate in CO poisoning and with vasoconstriction of the fingers)
- partial pressure of oxygen in the arterial blood, normal is 90-100mmHg
- Measured via arterial blood gas measurement
- Poor ventilation: fluid and puss blocking the diffusion of oxygen from the alveoli to the capillaries
- Poor perfusion: vasoconstriction of the capillaries or blockage of the capillaries by a clot
- Defects in hemoglobin binding affinity due to low oxygen saturation or other unidentified defect (heme synthesis defect? Subclinical porphyria? methemoglobin?)



- Vasoconstriction:
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- Hypoxic pulmonary vasoconstriction (HPV): vasoconstriction of the pulmonary artery supplying a defective alveoli. Bypasses this part of the lung.

- High altitude, pulmonary edema (HAPE): If in a low oxygen environment, the pulmonary artery vasoconstricts globally, increasing pulmonary artery pressure. The increased pressure can cause rupture of the pulmonary artery capillaries allowing fluid to leak into the alveoli. Can this occur due to the severe hypoxia induced in COVID-19?
- High levels of Angiotensin-II, a potent vasoconstrictor. Is this due to the virus inhibiting ACE2?
- Microthrombi:

- Small clots blocking capillaries in the lungs leading to rupture and leaking of fluid into the lungs. These clots cause ischemia in other areas of the body including the brain, organs and extremities leading to stroke, organ failure and necrosis.
- 4% of patients who die of COVID-19 meet ISTH criteria for DIC
- Increased IL-6—> damage to endothelium—> consumption of platelets and Increased PAI-1 (inhibits fibrinolysis)—>micro (renal, cardiac, pulmonary) and macro (PE, DVT) thrombosis
- These are antibodies that attack the phospholipids of cell membranes. They form in response to the infection. We commonly see these antibodies triggered by the tick-born pathogen Bartonella.
- They bind to and lead to damage by immune attack of the endothelial cell membrane, stimulating clotting.
- D-dimer >1,500 ng/mL
- fibrinogen >800 mg/mL
- sepsis induced coagulopathy (SIC) criteria ≥4
- markedly elevated D-dimer (greater than six-fold at the upper limit of normal)
- IV unfractionated heparin: can be stopped easily, anti-inflammatory
- IV low molecular weight heparin (LMWH): 40 – 60mg/day, 0.6mg/kg per 12hrs for 7d or longer
- Enoxaparin: 1 mg kg s/c q 12 hours (dose adjust with Cr Cl < 30mls/min)
- Oral anticoagulants or vitamin K antagonists
- In patients with a history of heparin-induced thrombocytopenia (HIT) use fondaparinux
- Tissue plasminogen activator (Alteplase): 25mg of tPA over 2 hours followed by a 25mg tPA infusion administered over the subsequent 22 hours, with a dose not to exceed 0.9 mg/kg followed by full anticoagulation with heparin drip.
- Keep platelets count >50
- Fibrinogen> 2g/L
- Keep platelets count >20
- Fibrinogen> 2g/L
- PT ratio <1.5
- Active bleeding
- Platelet count <25×109/L
- Monitoring advised in severe renal impairment
- Abnormal PT or aPTT is not a contraindication
- Nattokinase or other proteolytic enzymes 60 minutes before meals
- The juice of one whole lemon (crushed by a juicer) in water daily
- Optimal hydration: 1/2 your body weight in ounces of water per day
- Minimize exposure to EMF (EMF is a possible promoter of clotting): unplug wifi at night, unplug lamps and other electronics at night, keep cell phone on airplane mode when not in use, consider grounding mats for your bed