Case Studies

Case 6

Three men have been admitted with progressive breathlessness and all have an initial arterial P_aO₂ of 6.6 kPa when breathing air. The first patient is grossly obese and is complaining of a sore throat and an upper respiratory tract infection but has a normal chest CXR. Investigation has excluded pulmonary embolism. The second patient with non-specific interstitial pneumonitis has a reduced gas transfer (i.e. mainly diffusion defect), is on treatment with steroids and has developed a mild lower respiratory tract infection. The third patient has a true right-to-left shunt due to a longstanding atrial septal defect, and apart from a slightly enlarged heart has a normal CXR. Each patient is to be treated with oxygen.

• 1. Why is each patient hypoxaemic and what will happen when the FiO₂ is raised to 1.0 (i.e. 100% oxygen therapy)? Precise answers cannot be calculated but assume reasonable values for unknown data.

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  Correct answer:
  Patient 1:
  This patient has a mild upper respiratory tract infection and no significant low respiratory tract pathology. However, he is probably hypoventilating due to gross obesity restricting normal respiratory movement. Assuming his gas transfer and V/Q matching are normal, his PaCO2 can be calculated from the alveolar gas equation (Chapter 14):
  

  P_AO₂=P_IO₂–

  P_aCO₂ / R

  
  where P_AO₂≈P_aO₂ = 6.6 kPa (as measured); P_IO₂ = F_iO₂ × (barometric − water vapour pressure) = 0.21 × (101 − 6.2) = 19.9 kPa breathing air, and R, the respiratory quotient, is ~0.8. Thus, P_aCO2 = 10.6 kPa and if the arterial blood gas measurement confirms this, the patient has type 2 respiratory failure (Chapter 23). If the measured _aCO2 was much lower, it would suggest the assumptions were wrong and that another mechanism was causing or contributing to his respiratory failure.
  When the patient is given 100% O2 (F_iO₂ 1.0):
  P_IO₂=F_iO₂ × (barometric – water vapour pressure)
  =1 × (101–6.2)=95kPa
  So:
  

  P_aO₂ ≈ P_AO₂ = 95 –

  10.6 / 0.8

  =82kPa

  
  

  Patient 2
  This patient has a diffusion defect due to the interstitial lung disease (ILD, Chapter 30) although usually there is a significant contribution of ventilation/perfusion (V/Q) mismatch due to the hypoxaemia. His P_AO2 is thus greater than his P_aO2. Arterial blood gas (ABG) shows his P_aCO2 is low (4 kPa). The substantial increase in PAO2 when this patient is given 100% oxygen (F_iO₂ = 1) will more than overcome the partial diffusion defect associated with the ILD, and if this were a pure diffusion defect the P_aO2 could approach 90 kPa.

  P_aO₂ = 95 –

  4 / 0.8

  =90kPa

  
  Even allowing for a wider than normal range of V/Q ratios in this patient, there would still be a substantial increase in P_aO₂ on 100% oxygen.
  
  Figure 49 Effect of true shunt (Q_S/Q_T) on the arterial oxygen tension (P_aO₂) response to inspired oxygen fraction (F_iO₂).

  Hypoxaemia caused by true right–to–left shunt is refractory to supplemental O₂ when ‘shunt fraction’ exceeds 30%.

  Patient 3
  This patient is hypoxaemic due to true right–to–left shunting causing admixture of venous blood to systemic arterial blood (Chapter 13). As in the second case, the P_AO₂ will be 90 kPa with an F_iO₂ of 1.0. However, the saturation is already 100% in oxygenated blood passing through the lungs, and O₂ content will not be substantially increased by the high PAO2 apart from the small quantity of O2 dissolved in blood (90 × 0.023 mL; Chapter 8). The blood shunted from right to left through the atrial septal defect remains unaffected by the increased P_AO₂ and acts as venous admixture lowering oxygenation in the systemic circulation. Consequently, an FiO2 of 1.0 only fractionally increases systemic P_aO₂ perhaps to ~7.5 kPa in this case.

• 2. How will you ensure improved oxygenation in each patient?

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  Correct answer:
  

  Patient 1
  In some patients with chronic type 2 respiratory failure hypoxia drives ventilation rather than P_aO₂. As the patient’s P_aO₂ rises when he is given 100% O2, the drive to breath decreases, and this can lead to a further increase in P_aCO₂, progressive respiratory acidosis, confusion, coma and death. Consequently, this patient should be managed with low–dose (24–28%) O₂ therapy aiming for a saturation of 88–92% and regular measurement of arterial blood gases (Chapters 23 and 43). In this patient optimal treatment to improve oxygenation and reduce CO₂ retention would be non–invasive ventilation, which would improve ventilation and alveolar gas exchange (Chapter 42).

  Patient 2
  In this patient simply increasing the inspired oxygen concentration (F_iO₂ ~ 0.4–0.6) will correct the hypoxaemia. This patient probably has type 1 respiratory failure (Chapter 23) because CO₂ diffuses 20 times better than O₂ and consequently the diffusion defect does not impair CO₂ clearance. The hypoxaemia will cause hyperventilation, and the associated increase in minute ventilation ensures a low P_aCO₂ (∝ 1/alveolar ventilation). Consequently, there is little risk of hypercapnia during the use of high O₂ concentrations in this patient.

  Patient 3
  Only Patient 3 will not show a substantial increase in P_aO₂ when given 100% O₂. In this case oxygenation will only be improved by decreasing the shunt fraction and reducing left–sided venous admixture. Figure 47 illustrates the effect of true shunt on the response to increasing F_iO₂.