ICU · Respiratory / gas exchange
Hypercapnia & Ventilatory (Type-2) Respiratory Failure
Also known as Hypercapnia · Type 2 respiratory failure · Ventilatory failure · Carbon dioxide retention · CO2 narcosis · Hypercapnic respiratory failure · Haldane effect · Oxygen-induced hypercapnia · Respiratory acidosis
Hypercapnia (a raised PaCO2) is ventilatory, or type-2, respiratory failure. Because PaCO2 is proportional to CO2 production divided by alveolar ventilation, hypercapnia arises from increased CO2 production (fever, sepsis, overfeeding) or — far more commonly — reduced alveolar ventilation from a failure of the controller (opioids, brainstem), the pump and nerves (Guillain-Barre, myasthenia), the chest wall and load (obesity, kyphoscoliosis, COPD, asthma), or increased dead space. The effects are respiratory acidosis, cerebral vasodilation with raised intracranial pressure (headache, asterixis, drowsiness, CO2 narcosis), and sympathetic stimulation. Treatment is to ventilate the patient (non-invasive ventilation for COPD) and reverse the cause; controlled oxygen in COPD averts oxygen-induced hypercapnia (the Haldane effect and worsened V/Q mismatch).
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A 64-year-old with known COPD is brought to the ED at 4 am by his wife. He is drowsy, flushed, sweating, with a bounding pulse and a coarse flapping tremor of the outstretched hands — asterixis. The SpO2 reads 86 per cent on 15 L/min via non-rebreather, given by the ambulance crew. The ABG returns: pH 7.24, PaCO2 78, PaO2 56, HCO3 28. The team reaches for naloxone and BiPAP at the same time — and you ask them to use a Venturi mask at 24 per cent first.[2][9]
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