Hypercapnia will rapidly cause an intracellular acidosis in all cells in the body. The clinical picture will be affected by the arterial hypoxaemia that is usually present. The effects described below are the metabolic effects of hypercapnia rather than respiratory acidosis. Patients with respiratory acidosis can be hypocapnic if a severe metabolic acidosis is also present.
These effects are:
This can result in dyspnoea, disorientation, acute confusion, headache, mental obtundation or even focal neurologic signs. Patients with marked elevations of arterial pCO2 may be comatose but several factors contribute to this:
As a practical clinical example, the rise in intracranial pressure due to hypercapnia may be particularly marked in patients with intracranial pathology (eg tumours, head injury) as the usual compensatory mechanism of CSF translocation may be readily exhausted. Any associated hypoxaemia will contribute to an adverse outcome.
Typically, the patient is warm, flushed, sweaty, tachycardic and has a bouncing pulse.
The clinical picture may be modified by effects of hypoxaemia, other illnesses and the patient’s medication. Arrhythmias may be present particularly if significant hypoxaemia is present or sympathomimetics have been used.
Acutely the acidosis will cause a right shift of the oxygen dissociation curve. If the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left.
Why?
This is because of the obligatorily associated severe hypoxaemia. The alveolar gas equation predicts an alveolar pO2 of 37mmHg (and the arterial pOsub>2 would be lower than this) when the pCO2 is 90mmHg:
pAO2 = [0.21 x (760-47)] - 90 / 0.8 = 37 mmHg.
Higher values of paCO2 have been recorded in patients breathing an increased inspired oxygen concentration which prevents the hypoxaemia. Values up to about 260mmHg have been recorded with inadvertent administration of high inspired pCO2 but this is Guinness Book of Records stuff! High pCO2 levels also have an anaesthetic effect.
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