Respiratory Failure & Critical Care

type 2 respiratory failure

If type 1 failure is a delivery problem at the loading dock, type 2 failure is a problem with the whole bellows. Here the lungs are simply not moving enough air in and out, so carbon dioxide — the waste gas that breathing exists to clear — builds up in the blood while oxygen falls. The defining feature is a raised arterial carbon dioxide (hypercapnia), usually above about 50 millimetres of mercury, alongside the low oxygen.

The common thread is inadequate ventilation, which can fail anywhere along the chain that drives a breath: the brain's respiratory centre may be suppressed by drugs or stroke; the nerves or breathing muscles may be weakened; the chest wall may be stiff or deformed; or the airways and lungs themselves may be so obstructed, as in a severe COPD flare, that moving air costs more effort than the patient can supply. When carbon dioxide accumulates, it dissolves to form acid, so the blood pH drops — a key sign that the rise is acute and dangerous rather than long-standing and compensated.

Time changes the picture. In chronic type 2 failure the kidneys retain bicarbonate to buffer the acid, so a person can live with a high carbon dioxide and a near-normal pH for years. A useful and important caveat: in some of these chronically hypercapnic patients, giving too much oxygen can worsen carbon dioxide retention, so oxygen is titrated carefully to a target range rather than poured on.

A patient with a severe COPD exacerbation is drowsy with a PaCO2 of 78 millimetres of mercury and a pH of 7.25; non-invasive ventilation is started to support his failing breathing muscles and clear the carbon dioxide.

Rising carbon dioxide with a falling pH marks acute, decompensated type 2 failure.

Non-invasive ventilation is often the treatment of choice for acute type 2 failure, because it directly augments the volume of air moved and helps blow off carbon dioxide.

Also called
hypercapnic respiratory failure高碳酸血症性呼吸衰竭高碳酸血症性呼吸衰竭