Type 1 respiratory failure is hypoxaemia. The pO2 is low, the pCO2 may be low (due to hyper-ventilation to compensate for hypoxaemia) or normal.
Acute type 2 respiratory failure is hypoxaemia with hypercarbia. The pO2 is low, the pCO2 is high. pH is usually low. This follows type 1 failure, usually because of exhaustion, and consequent hypoventilation.
Chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation. The pO2 is low, the pCO2 is high, the HCO3 is high. pH is normal. This can occur in any disease that causes chronic hypoventilation.
Acute on chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation, and an acute event leading to a further hypercarbia, and consequently, acidaemia. The pO2 is low, the pCO2 is very high, HCO3 is high, the pH is low. Think acute exacerbation of any cause of chronic type 2 respiratory failure.
A common mistake is thinking that some diseases cause type 1 respiratory failure, and others cause type 2 failure – in OSCEs people frequently tell me that asthma causes type 1 failure, and COPD causes type 2 failure. It’s true that some disorders predispose to chronic type 2 respiratory failure, but acute type 1 and acute type 2 respiratory failure can occur in any respiratory condition. A few examples to illustrate my point.
Initially asthma causes an acute type 1 respiratory failure picture – patients become hypoxaemic due to gas trapping, and despite ventilating poorly, they hyperventilate to such an extent that they keep their pCO2 low. With a respiratory rate of up to 40 bpm, asthmatic patients in extremis will tire. As they do, the respiratory rate, and tidal volume, decrease, causing ventilatory failure, that is, type 2 respiratory failure.
When treating patients with acute-severe asthma, and particularly life threatening asthma, careful monitoring of pCO2 is essential: a rising pCO2 without obvious clinical improvement is an ominous sign.
Acute Heart Failure – Pulmonary Oedema
Pulmonary oedema causes hypoxaemia in the initial phase – this is type 1 respiratory failure. As the patient tires, ventilation becomes less effective, and acute type 2 failure ensues.
This is where it gets more confusing, but it’s really not complex. COPD is a heterogenous group of disease states under a single umbrella. Not all patients with COPD will retain CO2, indeed the majority will not. Most case series estimate that only 5 – 15 % of patients with COPD will retain CO2. Therefore most COPD patients you see will present with type 1 respiratory failure. Like the above cases, COPD patients with type 1 failure may tire, and develop acute type 2 failure.
Those COPD patients who do retain CO2 will present with acute on chronic type 2 respiratory failure. These patients are sensitive to high concentrations of inspired oxygen, and should have their oxygen therapy titrated to a SaO2 of 88 – 92 %. Although it was felt that the physiological rationale for CO2 retention was loss of “hypoxic drive” it is now recognised that V/Q mismatch is mostly responsible for the retention of CO2 in these patients.
Other patients at risk of Chronic Type 2 Respiratory Failure:
Obesity Hypoventilation Syndrome