Pathophysiology of COVID-19 Part 2 (SARS CoV 2) I Hypoxia in COVID-19 I Coagulopathy & MODS I The slides will be about the following: 1. Coagulopathy- intravascular microthrombi, pulmonary embolism & DVT 2. Acute respiratory distress syndrome (ARDS) 3. CT Scan of COVID-19 (Glass ground opacities) 4. Hypoxia in COVID-19 5. Causes and progression of hypoxia in COVID-19 6. Summary of COVID-19 pathophysiology You can also watch the same topic on HM Learnings Youtube channel. You can also follow HM Learnings on facebook, instagram and twitter for daily updates

3. Coagulopathy- intravascular microthrombi,
pulmonary embolism & DVT
• SARS-CoV-2 can directly affect endothelial cells and hence exhibit
widespread endothelitis characterized by EC dysfunction, lysis, and death,
• This leads to imbalance between the procoagulant activity and anticoagulant
activity
• Pro-coagulant activity is increased by complement system mediated
activation.
• Release of tissue factor from injured endothelial cell and activation of
clotting factor VII and XI causes diffuse DIC.
• This widespread systemic inflammation can lead to disseminated
intravascular coagulation and multi-organ dysfunction syndrome.

4. Acute respiratory distress
syndrome (ARDS)
• It is defined as an acute disorder that starts within 7 days of
inciting events and is characterized by bilateral lung infiltrates
and severe progressive hypoxemia without any evidence of
cardiogenic pulmonary edema.
• Clinical features- fever, cough, hypoxemia, dyspnea
• Pathophysiology- alveolar damage/collapse, surfactant
dysfunction, activation of immune system and dysregulation of
blood coagulation

5. CT Scan of COVID-19 (Glass
ground opacities)

6. Hypoxia
• The leading symptom of COVID-19 is hypoxemia (hypoxic
hypoxia: reduced PaO2 ) which can worsen or progress to
various stages of acute respiratory distress syndrome (ARDS).
• The hypoxia progresses as the infection spreads in the lungs.

7. How the hypoxia progresses?

9. 1. Compensatory response for hypoxia are
tachypnea, increase in depth of respiration,
cardiac output and pulmonary vasoconstriction.
With disease progression, these compensatory
mechanisms are lost.
2. Viral damage to type II pneumocytes →loss
of surfactant → alveolar collapse →
intrapulmonary shunting (right to left shunt)
3. Viral damage to alveolar wall → thickening
of alveolar wall → increased diffusion barrier
→ intrapulmonary shunting
4. Pulmonary edema → increased diffusion
barrier → intrapulmonary shunting
5. Hypercoagulable state → microthrombi
formation → dead space ventilation

10. SARS-CoV-2 entry into the respiratory tract
Alveolar damage, endothelial dysfunction
Cytokine storm
Loss of surfactant, thickening
of alveolar wall, vascular
integrity defect (leakage and
increased permeability)
Alveolar collapse, pulmonary
edema
Hypoxemia
ARDS
Hypercoagulable state
Microthrombi formation
Respiratory failure
DIC
MODS
Septic
shock/Cardiogenic
shock
Death

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