There is no precise clinical definition of respiratory failure; the diagnosis rests on the interpretation of arterial blood gas measurements. A patient can be said to be in respiratory failure if the arterial oxygen tension (-Pao2) falls below 8.0 kPa/60 mmHg (normal range 11.3-13.3kPa or85-100mmHg) or if the arterial carbon dioxide tension(Paco2) rises above 6.6kPa/50mmHg (normal range4.6-6.0kPa or 35-45 mmHg), when the subject is at sealevel, awake and breathing air. The condition may be acuteor chronic; if the patient has arterial hypoxaemia with a normal or low Paco2 then he or she is said to have type Irespiratory failure; and if the Paco2 is elevated, type IIrespiratory failure. Arterial hypoxaemia does not alwaysimply respiratory failure: a low inspired O2 at altitude or ananatomical right-to-left shunt, as in congenital heart diseaseor arteriovenous malformation, can cause hypoxaemiadespite normal lung function.
In general, themain disturbance in type I failure is ventilation-perfusionmismatch, and in type II it is inadequate ventilation.Chronic respiratory failure in the UK is most commonlydue to chronic bronchitis and emphysema. Measurement of the alveolar-arterial (A-a) gradient isuseful in hypoxic patients, and may help to decide, forinstance, whether the patient’s hypoxaemia is secondary to central hypoventilation or to intrinsic lung disease. Bycalculating the A-a gradient the day-by-day progress ofpatients can be assessed even when they are being treatedwith varying concentrations of inspired oxygen. The A-agradient indicates the contribution of venous admixture(i.e. true shunt or V/Q abnormality) to hypoxaemia. It canbe calculated by using the concept of ‘ideal alveolar air PAO2 = FiO2 – Paco2/0.8
where FiO2 = inspired Po2 (20kPa in room air) and0.8 = respiratory exchange ratio. Thus the normal alveolaroxygen tension is approximately 14 kPa, the normal arterialoxygen tension approximately 12.5 kPa, and the normalA-a gradient is therefore 1-2 kPa.
In the management of the hypoxic patient it should beremembered that tissue O2 delivery depends not just onPao2 but also on the haemoglobin concentration andcardiac output. The most useful index of tissue oxygenationis the mixed venous (pulmonary arterial)/arterial O2content difference. The normal oxygen combining capacityis 1.4mL O2/g haemoglobin (approximately 0.06mmol/g).The oxygen content of blood is the oxygen combiningcapacity x haemoglobin concentration x saturation (plusa small amount of dissolved oxygen in plasma, which isnegligible at normal atmospheric pressure). Assuming thehaemoglobin concentration is 15g/100mL, and the oxygencontent of arterial blood is 1.4 x 15 x 0.95 = 20.58 mL/100 mL, and the oxygen content of mixed venous blood is1.4 x 15 x 0.75 = 15.75, the arterial/mixed venous oxygencontent difference is 4.83mL/100mL. If oxygen delivery isreduced (e.g. reduced cardiac output) the arterial/venouscontent difference widens.Type II hypercapnic ventilatory failure represents inadequacyof the respiratory muscle ‘pump’. The concept of’pump’ failure leading to hypercapnia is a useful one, focusingattention on the importance of CNS output, neuromuscularfunction and chest wall movement in themaintenance of adequate ventilation, althoughsevere impairment of gas exchange can contribute to anelevated CO2.
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