Respiratory failure is usually said to exist when arterial Po2 falls below 8 kPa (60 mmHg) when breathing air at sea level. In type 1 respiratory failure, the arterial hypoxia is accompanied by a normal or low arterial Pco2, whereas in type 2 or ventilatory failure, arterial Pco2 is increased above 6.7 kPa (50 mmHg). Respiratory failure may be acute or chronic. In chronic respiratory failure, there are permanent abnormalities in blood gases, which typically worsen periodically (acute on chronic). This strict definitio excludes some patients whose respiratory systems might otherwise be considered failing. Some patients have disabling dyspnoea (breathlessness) of respiratory origin but maintain Po2 more than 8 kPa.
Some of the many causes of respiratory failure are listed in Fig. 23a. Symptoms and signs clearly depend on the underlying cause. Dyspnoea and tachypnoea (increased respiratory rate) will be prominent in severe asthma but absent in conditions with reduced central drive.
Mechanisms leading to hypoxia and hypercapnia
Of the five causes of hypoxaemia (Fig. 23b), only hypoventilation
inevitably causes increased Paco2.
(Chapter 9) If hypoxia is out of proportion to the hypercapnia and the A–a Po2 gradient (Chapters 14) is increased, one of the other mechanisms (3-5 in Fig. 23b) must also be present. The primary effect of right-to-left shunts and ventilation–perfusion mismatching is to raise arterial CO2 content, but this is usually corrected or overcorrected by a reflex increase in ventilation (Chapters 13 and 14).
Thickening of the alveolar-capillary membrane in lung fibrosi may give rise to diffusion impairment, preventing equilibration of pulmonary capillary blood with alveolar gas, especially in exercise, when time in the capillary is reduced. However, in many conditions thought to cause diffusion impairment, there is also substantial VA/Q mismatching, and this is probably the main cause of the hypoxia.
Effects of hypoxia and hypercapnia
The direct effects of hypoxia and hypercapnia, together with the compensations and complications that occur in chronic respiratory failure, are shown in Fig. 23c.
Although hypoxia usually offers the greatest threat to vital organs, hypercapnia and especially acidosis are also important and they often accentuate the adverse effects of each other. Hypoxia and hypercapnia are better tolerated when they develop slowly in chronic respiratory failure because of adaptations such as polycythaemia and compensatory metabolic alkalosis.
Cyanosis is a greyish-blue tinge seen when the microcirculation of a tissue contains a high concentration of deoxygenated haemoglobin. It may occur with impaired blood fl w, for example in the hands and feet in circulatory shock, when it is known as peripheral cyanosis. When the arterial blood contains more than about 1.5-2 g/dL of deoxygenated haemoglobin, the concentration in the microcirculation reaches the critical level for cyanosis to be observable even in well-perfused tissues. This occurs with an arterial saturation of about 85% if haemoglobin concentration is normal (15 g/dL) and the resulting central cyanosis is visible in the tongue and mucous membranes of the mouth. It appears at higher oxygen saturations in polycythaemic patients, whereas in severe anaemia central cyanosis may be impossible, as it would require an O2 saturation incompatible with life.
Respiratory failure in asthma
Hypoxia in a severe asthma attack is primarily due to VA/Q mis- matching. Paco2 usually falls as the attack worsens, because peripheral chemoreceptor and pulmonary receptor stimulation produce a refl x in- crease in ventilation despite the increased work of breathing. A raised or even apparently normal Paco2 (e.g. 5.3 kPa, 40 mmHg) in a severe hypoxic asthma attack is a cause for concern, as it may indicate the onset of exhaustion and potentially life-threatening asthma.
Respiratory failure in chronic obstructive pulmonary disease
The clinical picture of severe chronic obstructive pulmonary disease (COPD) is variable (Chapter 26), but two extreme patterns-the pink puffer (dyspnoea, no cyanosis at rest) and the blue bloater (cyanosis at rest, cor pulmonale, oedema) are recognized. The blue bloater is associated with type 2 respiratory failure. He or she has a chronically low Pao2 and high Paco2, and these worsen with acute infections, which precipitate acute on chronic respiratory failure. Patients with chronic hypercapnia typically have a near-normal arterial pH owing to an efficien compensatory metabolic alkalosis via renal generation and retention of bicarbonate. During an acute exacerbation, Paco2 may increase further and pH then falls significantl, as renal adjustments are slow. Arterial pH can therefore indicate the proportions of acute and chronic hypercapnia. Patients with chronic hypercapnia are at risk of respiratory depression and a further, potentially fatal, increase in Paco2 if given high inspired oxygen (Chapter 43). This may be due to loss of hypoxic drive in the presence of reduced CO2 sensitivity, but other mechanisms may contribute to the rise in Paco2, including increased VA/Q mismatching by the removal of hypoxic vasoconstriction. As these patients are on the steep part of the oxyhaemoglobin dissociation curve, significan improvements in arterial oxygen content can usually be achieved by small increases in FIo2 (to 24 or 28%). The resulting small improvement in Pao2 does not cause respiratory depression (Chapter 12).
All patients suspected of having respiratory failure will need arterial blood gas measurement, as the severity is difficult to assess clinically. A chest X-ray helps detect possible causes and aggravating factors such as pneumonia or pneumothorax. Other investigations, including lung function tests, will depend on the clinical situation and likely underlying disease. Management will include airway maintenance, clearance of secretions, oxygen therapy (Chapter 43) and in some cases mechanical ventilation (Chapter 42). Specifi therapies, such as bronchodilators and antibiotics, are directed at the underlying cause or aggravating factors. Abnormalities in haemoglobin concentration, fluid balance and cardiac output should be treated to improve tissue oxygen delivery and increase mixed venous oxygen content, which in turn will also reduce the effects of venous admixture on arterial oxygenation.