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128 Chapter 3: Respiratory system

acute exacerbations of asthma or COPD, pulmonary Management
oedema, pneumonia, pulmonary embolus and fibros- Acute or acute on chronic respiratory failure
ing alveolitis. Hyperventilation frequently leads to a Treat any reversible underlying cause:
low pCO 2 . Oversedation or opiate overdose by stopping or re-
Type II failure, sometimes called ‘ventilatory failure’, versing sedation (e.g. flumazenil for benzodiazepines,

is due to alveolar hypoventilation such that the car- naloxone for opiates).
bon dioxide produced by tissue metabolism cannot Pulmonary oedema with diuretics.
be adequately removed and pCO 2 rises. If the failure Asthma by bronchodilators and corticosteroids.
is chronic the patient with a type II respiratory fail- Pneumonia with appropriate antibiotics.
ure will lose sensitivity to a raised carbon dioxide and Pneumothorax or pleural effusion by aspiration or
thereforerelysolelyonhypoxicrespiratorydrive.Ifag- drainage.
gressive oxygen therapy is initiated the level of oxygen COPD with bronchodilators, corticosteroids and an-
will rise and the respiratory drive is diminished, lead- tibiotics.
ingtofurtherdecreasedventilationwhichmaybefatal. Controlled oxygen therapy:
The most common cause of type II respiratory failure In patients who have a raised pCO 2 > 6kPa, oxygen
is chronic obstructive airway disease, other causes in- therapy can potentially worsen the situation, because
clude any severe respiratory disease, failure of respi- of the patient’s dependence on hypoxic drive. Con-
ratory effort, e.g. central drive depression, chest-wall trolled 24–28% oxygen is given by Venturi mask and
disease such as deformity and neuromuscular disease arterialbloodgasesarerepeatedtoensurethatthepO 2
such as myasthenia. is rising and the pCO 2 is not rising.
In patients with acute hypoxaemic failure and a nor-

mal or low pCO 2 , high-flow oxygen therapy can be
Clinical features used, but they must still be closely monitored with
Ina patient with a normal haemoglobin central cyanosis
regular arterial blood gases to ensure that they are not
is visible when the pO 2 falls below 6.7 kPa. Hypercap-
tiring and developing type II failure.
nia causes a flapping tremor of the outstretched hands, a
If pCO 2 continues to rise or pO 2 cannot be raised ade-
bounding pulse, vasodilation, increased agitation, then
quately with oxygen therapy then assisted ventilation is
confusion, drowsiness and coma. Other signs include
required, preferably before patients are completely ex-
the use of accessory muscles of respiration, tachypnoea,
hausted (see Table 3.17).
tachycardia, sweating and inability to speak in full sen-
tences. Chronic respiratory failure
Long-term oxygen therapy (LTOT) and in some cases
non-invasive ventilation, is indicated for chronic respi-
Complications
ratory failure. LTOT is indicated in patients with COPD
Pulmonary hypertension due to hypoxic pulmonary

who haveapO 2 < 7.3 kPa when stable or a pO 2 > 7.3
vasoconstriction. With time the arteries undergo a
and <8kPa when stable with polycythaemia, nocturnal
proliferative change leading to irreversible pulmonary
hypoxaemia, peripheral oedema or pulmonary hyper-
circulationchanges.Thereisincreasedafterloadonthe
tension. 19 hours/day of oxygen 1–3 L/minute has been
right side of the heart leading to cor pulmonale.
showntoincreasesurvivalinpatientswithchronicbron-
Polycythaemia results from hypoxia, it causes an

chitis or emphysema and respiratory failure. Patients
increase in blood viscosity and predisposes to
must have stopped smoking (for safety reasons), and an
thrombosis.
oxygen concentrator needs to be installed in their home.
Investigations Prognosis
Blood gas monitoring is the most important initial in- Fifty per cent of patients with severe chronic breathless-
vestigation to establish the type of failure and will dictate ness die within 5 years, but in all stopping smoking is the
the mode of oxygen therapy. most beneficial therapy.