Physio Matching Ventilation & Perfusion (29)

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Physio Matching Ventilation & Perfusion (29)
2014-04-02 21:38:50
MBS Physiology
Exam 3
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  1. Hypoxia
    • a general term that refers to low PO2 levels
    • eg. a group of alveoli might exhibit hypoxia if their PO2 isn’t 104 mmHg
  2. Hypoxemia
    • specifically means low arterial PO2 (↓ PaO2)
    • is typically defined as a PaO2 < 85 mmHg
    • (-emia means something having to do with the blood)
  3. PAO2
    • calculated using the alveolar gas equation:
    • PAO2 = FIO2 (Patm–PH2O) – PACO2 / R
    • FIO2: fraction of oxygen in inspired air (0.21)
    • Patm: barometric pressure
    • PH2O: water vapor pressure at 100% saturation (37oC)
    • PACO2: alveolar PCO2 (determined by measuring PaCO2)
    • R: respiratory quotient (0.8)
    • PAO2 = 0.21 (760–47)–40/0.8 = 100 mmHg
    • (alveolar O2 is usually slightly higher than 100)
  4. Causes of Hypoxemia
    • 1. Alveolar Hypoventilation
    • 2. Reduced PIO2
    • 3. Reduced FIO2
    • all result in low blood oxygen however the A-aDO2 is not affected (difference between PAO2 & PaO2 would be in a normal range)
    • both alveolar & arterial PO2 decrease by the SAME amount
  5. Alveolar Hypoventilation
    • can result from pulmonary or neuromuscular disease (eg. myasthenia gravis) or CNS depression that decreases respiratory effort
    • as ventilation is reduced, CO2 accumulates in lungs → an increase in PACO2 & decreases the PAO2
    • (PAO2 = FIO2 (Patm–PH2O) – PACO2/R)
  6. Reduced PIO2
    • this can happen at a high altitude, where there is a decrease in the Patm
    • the fraction of inspired oxygen (FIO2) remains the same (0.21) but the PAO2 & therefore PaO2 decrease
  7. Reduced FIO2
    • if FIO2 (fraction of oxygen in inspired air) decreases (eg. in a person caught in a fire), PaO2 would decrease
    • fire selectively burns O2; longer you’re in room w/ a fire, the lower your fraction of inspired O2
  8. What would affect the A-aDO2 (difference between PAO2 & PaO2) resulting in a decreased PaO2?
    • a Shunt
    • shunts INCREASE the A-aDO2
    • this allows blood to pass through the pulmonary system without being ventilated
  9. Shunt
    • a passageway through which blood can pass from the right (mixed venous) side of the circulation directly to the left (arterial) w/o participating in gas exchange
    • b/c no gas exchange occurs in a shunt, shunted blood is = to mixed venous blood: PO2 = 40 mmHg, PCO2 = 46 mmHg
    • net result: O2 content of mixed arterial blood is reduced
  10. What contributes a 2% shunt in normal circulation?
    the bronchial circulation
  11. Right-to-left Shunts
    include cardiac defects such as atrial or ventricular Septal defects, Patent Ductus Arteriosus or Foramen Ovale, & Pulmonary Shunts in which alveoli DON’T exchange air w/ the atmosphere (eg. alveoli filed with blood, pus, etc)
  12. Diffusion Abnormalities
    • another cause of Hypoxemia that often involves a thickening of alveolar membranes
    • may result from interstitial lung disease like pulmonary fibrosis
    • produce a large A-aDO2 (A to a difference)
  13. What is true of diffusion abnormalities at rest vs. during exercise?
    they often DON’T cause hypoxemia at rest, but become worse w/ exercise when the transit time of the blood on pulmonary capillaries decreases
  14. So what would an increased A to a difference (A-aDO2) potentially indicate?
    either a Shunt or Diffusion Abnormalities
  15. What is the MAJOR cause of hypoxemia?
    • V/Q Mismatches
    • if ventilation & blood flow are not matched in various regions of the lung, impairment of BOTH O2 & CO2 exchange results
    • V/Q mismatches also result in hypercapnia (increased PACO2) & often lead to an A-aDO2
  16. Hypercapnia
    • defined as an increase in PaCO2 to > 45 mmHg
    • under normal conditions, PaCO2 ranges from 35–45 mmHg
    • principal effects of hypercapnea are on the CNS; can include headache, confusion, memory loss, & hypercapnic coma if severe enough
  17. This Relationship Defines the Causes of Hypercapnia
    • VA=K (VCO2 / PaCO2) or
    • PaCO2 = K (VCO2 / VA)
    • arterial PCO2 is proportional to the volume of CO2 produced by the tissues per minute divided by alveolar ventilation
  18. 4 Basic Causes of Hypercapnia
    • 1. Alveolar Hypoventilation (decreased VA): patient can’t (eg. spinal cord injury, ALS, polio, muscular dystrophy) or won’t breathe (eg. CVA, drug overdose, encephalitis)
    • 2. increased dead space ventilation due to shallow, rapid breathing (also decreases VA) or to increased VD/VT
    • 3. increased CO2 production (VCO2) in the setting of fixed ventilation
    • 4. severe V/Q mismatch: caused by diseases of the gas exchange system that lead to disproportionate amount of blood going to poorly ventilated alveoli
  19. How can an increase in dead space ventilation lead to Hypercapnia?
    • happens when respiration is depressed so you’re breathing shallow breaths
    • less air is getting into the alveoli, more is sitting in the dead space → less gas exchange
  20. In what setting would increased CO2 production be an issue?
    fever, anything that increases the metabolic rate (eg. hyperthyroidism)
  21. V/Q (Ventilation/Perfusion) Value
    • at rest normal alveolar ventilation (V) is 4.2 L/min & pulmonary blood flow (Q) is about 5 L/min
    • V/Q = 4.2/5.0 = 0.84
    • this ratio of air exchange to blood flow allows for optimal O2 & CO2 exchange in the lung
    • if minute ventilation (~5) is used for V instead of alveolar ventilation then the value of V/Q for the lung as a whole comes out a little over 1
  22. What is the ventilation/perfusion (V/Q) of each alveolus in an ideal lung?
    • the V/Q of every alveolus would be the same in an ideal lung
    • e/a alveolus represents a lung & receives 1/2 of the ventilation: 2.5 L/min
    • e/a lung also receives 1/2 of the perfusion: 2.5 L/min
    • therefore V/Q=1
    • gives us expected PaO2 = 100 mmHg & PaCO2 = 40 mmHg
  23. What is the ventilation/perfusion (V/Q) of REAL lungs?
    • lungs have regional distributions of both ventilation & perfusion
    • both of these parameters INCREASE from the apex to the base of the lungs, but not at equal rates
  24. Ventilation: Apex → Base
    • in an upright human ventilation decreases from the apex to the base of the lungs
    • Apex: intrapleural vacuum is greater because of the tendency of the lungs to “settle” on the diaphragm & pull away from the apical chest wall.
    • this distends the apical alveoli (makes them large & pulled open)
    • it also decreases their compliance
    • therefore they are difficult to distend further during inspiration
    • Basal: alveoli are less distended & more compliant; they receive MORE gas w/ each inspiration
    • how alveoli would look in upright lung
  25. During inhalation how does volume change differ in apex alveoli versus base alveoli of the lung?
    • volume change is greater in alveoli in the BASE of the lung
    • alveoli in the apex of the lung undergo little volume change
    • ventilation & compliance increases from apex → base
  26. Perfusion: Apex → Base
    • capillary perfusion pressure in the lungs is lowest in the apical region & increases as we move to the basal regions
    • this results from the gravitational effects on the hydrostatic pressure
    • therefore perfusion is HIGHEST in the lung base & LOWEST in the lung apex when upright
  27. How do the ventilation & perfusion gradients differ from each other as they decrease from the base to the apex of the lung?
    • their gradients are not equivalent
    • V/Q is > 3 at the lung apex but only ~0.6 at its base when upright
    • (when prone V/Q matching is more uniform)
  28. V/Q Graph
    • from the graph can see a steeper change in blood flow (perfusion, Q) than in ventilation
    • the ratio of these 2 values = V/Q
    • can see in the base of the lung the ratio is less than 1, ~0.6
    • ~ 3rd or 4th rib (corresponds to the central portion of the lung vertically) the V/Q = 1
    • as you go up into the apex V/Q tops out at over 3
  29. What does a HIGH V/Q indicate?
    • it means that in a given alveoli/area ventilation is happening but perfusion is not (or it’s low)
    • when blood flow is completely blocked as shown, Q = 0 & V/Q becomes infinite
    • affected alveoli become part of the dead space: they exchange air with the atmosphere but NOT with blood (wasted ventilation in alveolar dead space)
  30. What does “high V/Q” alveolar air look like?
    • high PO2, low PCO2
    • will be the same as air in the bronchi (PO2 = 150, PCO2 = 0 mmHg) when perfusion is COMPLETELY blocked
    • w/ limited perfusion (eg. a partial block) alveolar air will have a similar composition as bronchial/tracheal air b/c gas exchange isn’t occurring
  31. What will happen as a compensatory mechanism if you have no blood flow through part of the lungs?
    • blood flow that is blocked will be re-routed into other parts of the lung which, b/c Q is increased, will experience a decreased V/Q (there’ll be normal V but ↑Q)
    • increased blood flow through the non-blocked vessels will remove more O2 & add more CO2 to the over-perfused alveoli, causing them to have decreased PAO2 & increased PACO2
    • blood passing by these low V/Q alveoli will have LESS O2
  32. Hypocapnic Constriction
    • the lung will close off bronchi that lead to alveolar dead space (i.e. areas w/ a high V/Q b/c there is no perfusion due to a blockage)
    • this reduces airflow to unperfused alveoli & increases VA (alveolar ventilation) to functioning alveoli
    • this increased airflow partially compensates for a low V/Q value seen in functioning alveoli adjacent to dead ones
  33. Decreased V/Q
    • means there’s normal ventilation but a higher perfusion (Q increases at a fixed V, eg. b/c pulmonary capillary blood flow has been rerouted to a functional capillary)
    • or Alveoli become blocked so that V decreases
  34. Increased V/Q
    means there’s normal ventilation but low perfusion (eg. due to a blockage of blood flow)
  35. What happens as V/Q decreases due to a blocked alveoli?
    • PO2 in the affected alveoli will fall & the PCO2 will rise as the air supply isn’t renewed
    • if V goes to zero, the composition of alveolar gas & end-capillary blood (should be arterial) will be identical to mixed venous blood → alveolus will become a SHUNT b/c any blood that passes by it will fail to be oxygenated
    • hypoxic vasoconstriction will occur to re-route blood flow to an unblocked alveoli
  36. ↓ Air Flow
    • if you ↓ air flow to a region of the lung (↓ V/Q) → ↓ PO2 (alveolar then pulmonary venous) → hypoxic vasoconstriction of pulmonary vessels to that alveoli or area of the lung → ↓ blood flow
    • a ↓ in air flow ultimately causes a ↓ in blood flow in an effort to minimize a negative deviation of V/Q from 1
  37. ↓ Blood Flow
    • if you ↓ blood flow to a region of the lung (↑ V/Q) → ↓ alveolar PCO2 (less is being ‘dropped off’) → bronchoconstriction of structures to that alveoli or area of the lung → ↓ air flow
    • a ↓ in blood flow ultimately causes a ↓ in air flow in an effort to minimize a positive deviation of V/Q from 1
    • alveolar values for different lung states (V/Q values of 1 (normal), infinite (blocked vessel) & 0 (shunt))
    • ventilation blockage: PO2 = 40, PCO2 = 45
    • normal: PO2 = 100, PCO2 = 40
    • perfusion blockage: PO2 = 150, PCO2 = 0
  38. O2-CO2 diagram: V/Q line
    • changes in alveolar/end-capillary blood composition as the ventilation-perfusion ratio is either decreased below normal (point A) or increased above normal
    • ↓ V/Q: less O2, more CO2 (the same as mixed venous blood)
    • at A (V/Q=1): PO2 = 100 & PCO2 = 40
    • ↑ V/Q: more O2, less CO2 (the same as inspired air)
  39. Normal V/Q Variations
    • Apex alveoli are ventilated more than they’re perfused; their PO2 & PCO2 are more like those of the atmosphere
    • Base alveoli have a ↓ V/Q
    • PAO2 & PACO2 values = end-capillary PO2 & PCO2 at each lung level
    • PO2 & PCO2 in normal arterial blood result from an admixture of end capillary blood from all lung levels
  40. V/Q Mismatch
    when you have uneven ventilation or perfusion
  41. V/Q Mismatch: Uneven Perfusion
    • both lungs get = ventilation, but 1 receives more perfusion than the other

    • end capillary blood of under-perfused lung: PaO2 = 125, PaCO2 = 34

    • end capillary blood of over-perfused lung: PaO2 = 80, PaCO2 = 44 (less O2, more CO2)

    • mixed arterial blood: PaO2 = 83, PaCO2 = 40

    • • this patient is HYPOXEMIC
  42. Why doesn’t under-perfusion compensate for over-perfusion?
    • b/c the amount of end capillary blood w/ high PO2 & low CO2 (↑ V/Q) is LESS than the amount w/ low PO2 & high CO2
    • under-perfused flow is less than the flow that contributed to over-perfusion (↓ V/Q)
    • there is more “weight” toward blood that’s over perfused - contribute more mixed blood in pulmonary veins
  43. V/Q Mismatch: Uneven Ventilation
    • both lungs get = perfusion, but 1 receives more ventilation than the other

    • end capillary blood of the under-ventilated lung: PaO2 = 65, PaCO2 = 45

    • end capillary blood of the over-ventilated lung: PaO2 = 115, PaCO2 = 36

    • mixed arterial blood: PaO2 = 73, PaCO2 = 40

    • • this patient is also HYPOXEMIC
  44. Will a high V/Q in one part of the lung compensate for a low V/Q in another?
    • lung units w/ ↑ V/Q add relatively little O2 to the blood flow compared to the decreased O2 in alveoli w/ ↓ V/Q
    • increased ventilation increases PAO2 in the affected alveolus, but Hb saturation is minimally affected b/c Hb is essentially saturated at the normal PAO2 of 104 mmHg
  45. Shunt: An Extreme V/Q Mismatch
    • since NO gas exchange occurs w/ blood perfusing blocked alveoli, the end-capillary blood of the shunt = mixed venous blood (PaO2 = 40, PaCO2 = 45)

    • end capillary blood of the over-ventilated lung: PaO2 = 115, PaCO2 = 34

    • mixed arterial blood: PaO2 = 55, PaCO2 = 38

    • would see extreme hypoxemia b/c of the shunt
  46. What is the way to diagnose a shunt (besides the clinical symptoms of wheezing, difficulty breathing, etc.)?
    • if someone has a suspected shunt, give them 100% O2 to breathe
    • if you give pure O2 to someone w/ a shunt there won’t be a significant increase in arterial O2 content
    • b/c that O2 is ONLY going to already ventilated alveoli which are ALREADY fully saturating the Hb
  47. Diagnosing an Incomplete Shunt
    • for alveoli that are poorly ventilated but not shunted giving supplemental oxygen would significantly increase PAO2 in the affected alveoli & boost O2 content
    • the increase will occur even though the ventilation of the alveoli has not changed b/c of an increased diffusion gradient between the airway & the alveoli (more O2 in the air, means more will pass through into alveoli normally not exposed to that high of a content)
  48. Causes of Low V/Q
    • typically b/c of ventilatory problems

    • Mucus airway obstruction

    • Extreme broncho-constriction (can be caused by irritants)

    • Pulmonary edema (1. lowers compliance 2. water in alveoli = shunted)

    • Pulmonary fibrosis (↓ expansion)

    • Prolonged anesthesia (w/ atelectasis)

    • above causes either ↓ lung compliance or ↑ airway resistance, both of which → low V/Q
  49. Causes of High V/Q
    • Emphysema

    • Pulmonary embolism (flow is cut off downstream)

    • Hemorrhage

    • Positive pressure ventilation

    • Hypoxic vasoconstriction

    • • all of these can contribute to impaired
    • pulmonary circulation - most are due to low perfusion
  50. —————————————————————
    What is the ratio of shunted (Qs) to total (Qt) pulmonary blood flow?
    • Qs/Qt = (Cc–Ca)/(Cc–Cv)
    • Cc, Ca, & Cv are the contents of pulmonary capillary, artery & veins
    • Qs is essentially = to the amount of mixed venous blood that would have to be added to ideal blood to produce the observed lowering of PaO2
  51. Inefficient gas exchange will cause a decrease in what?
    • PaO2
    • it will also increase the A-aDO2, which can be used to implicate V/Q mismatching in hypoxemia
    • (PAO2 can be determined from the alveolar gas equation & PaO2 directly measured)
  52. Clinical effects of V/Q inequality
    • • reduces the efficiency of the lungs as a gas exchanger
    • • affects both O2 & CO2 but the effects on CO2 are more easily compensated for (increased PaCO2 results in increased ventilation which restores PaCO2 to normal)
    • • increased ventilation doesn’t add significantly to PaO2 b/c of the limitations of Hb binding
    • • V/Q mismatches typically present w/ hypoxemia w/o hypercapnia unless VERY severe
  53. How to Assess V/Q inequality
    • • using A-aDO2
    • • PaO2/FIO2 ratio
    • • Radiographic scans using inhalation of 81Kr or 133Xe (can use to scan for ventilation defects; 99Tc bound to albumin can be injected into the blood stream for a perfusion scan)
  54. PaO2/FIO2 Ratio
    • can be used an an index for patients w/ severe hypoxemia
    • normal ratio is 100/0.2 = 500
    • a ratio of < 300 seen w/ hypoxia despite increasing inspired O2 is consistent w/ V/Q mismatch