Lisa's symptoms relate to her hyperventilation, driven by psychological factors.


1. Why can we say with confidence that Lisa is hyperventilating?

Her low (<5 kPa) PaCO2 is all you need to confirm this. There's only one mechanism that leads to a low PaCO2, and that's to blow off CO2 excessively by hyperventilating.


2. Why has she fainted when her O2 levels are normal, or indeed slightly higher than normal?

Her high PaO2 also reflects her hyperventilation, but it's not the cause of her neurological symptoms; they relate to her low PaCO2. Cerebral blood vessels respond to the alkalosis associated with hypocapnia by constricting, reducing blood flow. This mechanism usually regulates blood flow in different parts of the brain according to metabolic demand, but the effect is global in alkalaemia.


3. How has the kidney compensated for Lisa’s hyperventilation? Is compensation complete?

Lisa's symptoms have occurred for several days, and her kidneys have had ample time to compensate for her persistent hyperventilation and subsequent alkalaemia. Remember, the regulation of blood pH is a collaboration between the lungs (CO2 excretion) and the kidneys (HCO3- excretion); the ratio of HCO3-/CO2 determines pH. In Lisa's case, HCO3- excretion by the kidneys has been reduced to compensate for the loss of CO2. Compensation isn't quite complete because her blood pH is still slightly alkaline (7.46; normal range 7.35-7.45).


4. Why might subarachnoid haemorrhage produce the same symptoms as we see in Lisa?

Damage to parts of the brain involved in the neural control of ventilation, or the impact of damage to higher centres probably accounts for the hyperventilation often seen in stroke and head trauma patients.

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