Emily’s main problem is a VQ mismatch due to bronchoconstriction and subsequently patchy alveolar ventilation. Some alveoli are ventilated well, many others very poorly.

1.How O2 and CO2 are carried by blood?

The shape of the oxyhaemoglobin dissociation curve is important here. A small change in PaO2 affects O2 saturation differently at different points on the curve. What would happen if Emily was anaemic? How would you know?

Carbon dioxide tansport is a very different process.


2.Why can Emily initially blow off excess CO2 (hyperventilate) but is still hypoxaemic?

Because adequately ventilated alveoli are doing all they can to exchange O2 and can’t do any more on the CO2 front except blow off more CO2 if respiratory drive increases. There's an workthough of this here. Basically, increasing ventilation of unobstructed alveoli only blows off more CO2; blood to these alveoli is already saturated with O2.


3.Why is she still hypoxaemic despite inhaling supplemental oxygen?

Because her alveolar ventilation is so poor that it’s bordering on a shunt. Too many alveoli are unventilated and too much blood is returning to the heart without taking on O2. Remember, Emily is having a life-threatening exacerbation.


4.Why would her blood pH would be alkaline during one ABG analysis and acid during the other? Which is which?

Her initial ABG should be alkaline because she is blowing off too much CO2. We haven’t provided pH values to make you think about what they should be like. Hers would probably be >7.45 as her PaCO2 is under 5 kPa.

Her second ABG should be acidic. Her condition has deteriorated (probably due to excess bronchoconstriction, inflammation or mucus plugging) to the point that she can neither take up O2 or get rid of CO2. The CO2 build up should produce acidaemia in an acute setting like this where the kidneys have not had time to compensate. In a COPD patient on the other hand, who may be chronically retaining CO2, you might see renal compensation and a normal arterial pH.


5.How would the oxyhaemoglobin-dissociation curve be shifted during different stages of the case?

In acidaemia, the curve is right-shifted, in alkalaemia it is left-shifted.


6.How do beta-agonists like salbutamol relieve bronchoconstriction?

By causing airway smooth muscle relaxation, thus functionally antagonising any bronchoconstrictor mediators present. What can salbutamol not do?


7.What would be different if Emily had blocked a main bronchus with an inhaled nut, rather than suffering from a severe asthma attack?

There are similarities and differences. If Emily was simply choking on a nut in one bronchus, that lung would be effectively shunted supplemental O2 would have little effect on her PaO2. Her condition would be static though, and shouldn’t worsen. In a sense, Emily’s condition is a bit like choking on lots of small fragments of nuts blocking many smaller bronchi. Overall, this has produced a pattern of responsiveness to supplemental O2 that is very like a simple shunt.

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