Professional Documents
Culture Documents
VQ MM Hypoxia Copd
VQ MM Hypoxia Copd
-chronic ↑↑ PaCO2 alters sensitivity of respiratory centers to CO2 (central chemo receptors
adapt) →
-O2 peripheral chemo receptors the main drive to breath.
-supplemental O2 →
-worsens V/Q mismatching (most important)
-redirects blood flow from alveolus with ↓ ventilation to alveolus with normal
-haldane effect
-in COPD patients, Hb exist in deoxy form (bound to CO2)
-supplemented O2 → ↓ Hb affinity for CO2 → ↑ CO2 offloading (Haldane effect) → ↑
hypercapnia
-↓ alveoli ventilation (not a major factor)
-normally, patients with chronic ↓↓ PaO2 have hypoxic ventilatory drive → ↑ alveoli
ventilation
-supplemented O2 → transient ↓ minute ventilation → sharp ↑ in PaCO2
-subsequently we see a rise in alveoli ventilation but with still rising PaCO2
(suggest there are other factors responsible for the continuous rise in PaCO2)
Altitude Sickness
-↓ PSNS
Acclimatization
-body acclimatize > 3 days
-kidneys
-↑ erythropoietin → ↑ RBC production (polycythemia) to help with ↓ CaO2 (arterial O2
content) → ↓ plasma volume
-↓ PaO2 → stimulates SM of blood vessels and macrophages to secret VEGF-A →
-angiogenesis → promotes formation of new capillaries → improve oxygenation
-endothelium
-hypoxia up-regulates the activity of nitric acid synthase → converts arginine to NO →
-via cGMP induces vasodilation → ↑ blood flow →↑ O2 delivery
Treatment
-acetazolamide (carbonic anhydrase inhibitor)
-as a diuretic will ↓ fluid hence ↓ pulmonary and cerebral edema
-will induce metabolic acidosis to combat the respiratory alkalosis