Respiratory Failure
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.
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).
Management
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.
