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Hypoxia and Hypercapnia

Hypoxia and Hypercapnia. Millis. -hypoxia - low oxygen delivery to the tissues -4 mechanisms of arterial hypoxemia 1)-sick lungs  hypoxic hypoxia (because it is within the lungs) 2)-alveolar hypoventilation  hypoxia due to increased dead space

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Hypoxia and Hypercapnia

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  1. Hypoxia and Hypercapnia Millis

  2. -hypoxia - low oxygen delivery to the tissues -4 mechanisms of arterial hypoxemia 1)-sick lungs  hypoxic hypoxia (because it is within the lungs) 2)-alveolar hypoventilation  hypoxia due to increased dead space -if dead space increase from 1800 to 2000 3) -shunt (V/Q = 0) 4) -diffusion defect -V/Q ratio  0 V with some Q -sick blood  anemic hypoxia

  3. HYPOXIC HYPOXIA • -dead space/tidal volume ratio is often measured with normal value as 0.3-0.4 • -anything that lowers the ratio will increase alveolar ventilation and vice versa • -tachypnea - increased rate with small tidal volume can be related to Vd/Vt ratio and is another form of alveoli hypoventilation • -greater portion of ventilation is going to the dead space when your tidal volume is smaller • -pulonary edema is most result of tachypnea  blood plasma leaks out from capillary and widens space between alveolus and capillary which will decrease the diffusion rate • -hyperpnea creates a lower Vd/Vt while tachnypnea does a higher

  4. -at normal heart rate, time of oxygen in capillary is sufficient -even during exercise when transit time decreases, there is no real problem unless you have an abnormal lung -DL = lung diffusion capacity measured by carbon monoxide diffusing capacity test -one breath of carbon monoxide is taken and the transfer of it is measured in the blood -factors decreasing diffusing capacity are: -going from supine to upright position, though it is not abnormal -lying down is better because there is a more even V/Q and more blood can take up carbon dioxide -goes down in interstitial (between capillaries and alveoli) fibrosis because capillary membrane is thickened

  5. -FiO2 is .21 every where on Earth, but barometric is low at high altitudes and you will have low pO2 -PaO2 can be used as an estimate for alveolar PO2 -central chemoreceptors are stimulated by CO2 -during hyperventilation, CO2 is going down so they will be inhibited, but peripheral will be stimulated -peripheral chemoreceptors can override the central chemoreceptors -A-aDO2 (alveolar-arterial DO2) = PAO2 – PaO2 -used as an index to see how sick the lung is  >5 = sick lung

  6. -breathing high oxygen mixtures cannot overcome shunt because there is no avenue to take up the oxygen -A-aDO2 has changes when the problems are diffusion, V/Q, and shunt because alveolar stays the same, but arterial value goes down -V/Q mismatching contributing to hypoxemia are low V/Q units -at the bottom of the lung there is low V/Q and low pO2 -increased pulmonary blood flow with no change in ventilation decreases V/Q -increase Q, not V, which causes the low V/Q and this is nor normal  both would increase in exercise so that V/Q will improve and increase a little -normoxia: normal % SaO2  high percentage of oxygen bound to hemoglobin (HbO2) and a low percentage of deoxygenated Hb (RHb) -hypoxia: %HbO2 is low and RHb is high

  7. ANEMIC HYPOXIAP50 & BOHR EFFECT

  8. ANEMIC HYPOXIA • -anemic hypoxia – Hb is sick • -can happen in sickle cell disease or anything that decreases Hb concentration (i.e. hemorrhage, P50 abnormal) • -P50 increases slightly in the lungs  negative Bohr shift • -P50 decreases in the tissues  positive Bohr shift • -decreased P50 in tissues and increase P50 in lungs would mean there is less loading in lungs, but also less unloading in the tissues

  9. -MetHb and CO poisoning -increased carbon monoxide can be a breakdown product of heme -overall effect is decrease in oxygen content compared to normal because CO has a higher affinity  % sat of O2 is reduced and curve will be shifted to the left -in anemia, Hb concentration is changing but % saturation is normal -PAO2 is also normal as long as the lungs are normal -CaO2 will be low because the Hb is low -hydroxyurea causes an increase in the production of HbF

  10. NORMOXIA: NORMAL SaO2 High %HbO2 Low %RHb

  11. -if PO2 decreases from 100 to 90, that is not hypoxic hypoxia since it is still on the flat portion of the dissociation curve -anything above 60 has relatively normal saturation -stagnant hypoxia – PaO2 is low due to low blood flow (Q is low) -leads to ischemia and infarction -lungs are sick during pulmonary embolism which affects the blood flow, but it is not stagnant hypoxia

  12. HYPOXIA: LOW O2 CONTENT Low PaO2, %HbO2 High %RHb

  13. -oxygen therapy adds oxygen to the plasma (only 3. mL/dL dissolved and normal oxygen content is 20) -most that can be added to oxygen content is 2-3 mL/dL out of 20

  14. Histotoxic hypoxia • -hypoxia in tissues • -venous PO2 is high and someone who dies of it will look cherry red • -shock=tissue hypoxia • -only purpose of delivering oxygen to the tissue is to make sure there is some oxygen at the end of the electron transport chain • -mitochondrial PO2 is maintained very low so a minor drop in arterial blood will cause a major drop in mitochondrial • -cyanide can be used as a chemical warfare agent and Met Hb scavenges cyanide and makes cyano-MetHb, removing the cyanide from the blood • -DeoxyHB scavenges nitrous oxide (vasodilator necessary to keep total peripheral resistance normal)

  15. a-vO2 DECREASED IN HISTOTOXIC HYPOXIA

  16. -Cushing Reflex – sending hypoxic blood to the brain increases brainstem sympathetic outflow -critical PO2  when you go below this value, oxygen consumption decreases -critical oxygen delivery  minimum oxygen delivery needed for maintenance of normal body function

  17. HYPERCAPNIA • -high alveolar PCO2, which means high arterial PCO2 • -you will almost never see one change and the other not change, but you cannot say that about O2 unless you are in a single alveolus (ventilation goes up, O2 goes up, CO2 goes up) • -FCO2 is proportional to PCO2, related by the barometric pressure • -FCO2 is the fraction = PCO2/barometric pressure) • -FACO2 = VCO2/VA • -normal alveolar ventilation  4200 for someone with total ventilation of 6000 mL/min • -PCO2 = 40 mmHg • -CO2 excretion rate = 200-250 ml/min

  18. MECHANISMS OF HYPERCAPNIA -alveolar hypoventilation • -respiratory failure • -cerebral blood vessels are the most sensitive to CO2, PCO2 • -adaptive value of increasing blood pressure  bring more blood to the brain • -bring more CO2 to the lungs and attempt to excrete more • -CO2 narcosis – when CO2 is above 80-90 mmHg, decrease ventilation by ½

  19. HYPOCAPNIA • -alveolar hyperventilation  PCO2 goes down because ventilation exceeds the amount needed to make it go down with CO2 excretion rate being kept normal • -lower CO2 by increasing ventilation at the same rate • -hyperpnea - even though more CO2 is made, ventilation goes up just enough to keep it normal • -decreases cerebral blood flow  if PCO2 goes below 30, then you will feel light-headed and below 20 you will lose consciousness, which depressed ventilation and returns PCO2 back to normal • -below 15 there is such intense of cerebral blood vessels that there is anaerobic metabolism in the brain  lactic acid production • -lowered PCO2  decrease chemoreceptors  decrease ventilation

  20. -when you go to high altitudes, peripheral chemoreceptors are working because you are getting histotoxic hypoxia -adaptive hyperventilation raises the alveolar PO2 by alveolar air equation -low O2 dilates cerebral blood vessels and there is no change in cerebral vascular resistance at high altitudes  it is a function of low PCO2, counteracted by low O2 at high altitudes -peripheral chemoreceptors are overriding the central

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