parameters are not excessively abnormal)
may be able to be treated in primary care
and return home, but must be reviewed.
Patients experiencing severe symptoms
need prompt treatment. However, some
sort of assessment should be made so treatment
efficacy can be measured. Pulse rate
is easily measured; treatment that relieves
hypoxaemia will raise oxygen saturations
and reduce pulse rate, providing evidence
of a treatment’s effectiveness. Finding out
what has been done before presentation is
also important; patients who present with
features of acute severe asthma and say they
have self-administered a bronchodilator
without effect should be given further
bronchodilators and admitted to hospital.
Management
BTS and SIGN (2012) give detailed advice on
the management of acute exacerbations. A
beta2 agonist such as salbutamol should
always be given initially. These bronchodilators
bind to receptors on airway smooth
muscle and induce relaxation, which
increases airflow and reduces hypoxaemia.
An initial dose of four puffs of beta2 agonist
via a pressurised metered dose inhaler
(pMDI) should be administered as single
actuations (BTS and SIGN, 2012). This mode
of delivery is possible only with salbutamol;
terbutaline is available only in a dry-powder
inhaler so using a spacer is not possible.
Dry-powder devices need a greater inspiratory
flow on the part of the patient; this may
be limited by severe exacerbations so, if
using these devices, lung deposition of
beta2 agonists may be limited.
Patients can use either one or multiple
(ie 3-4) breaths. Beta2 agonists work rapidly,
usually within 3-4 minutes, and reach
peak activity after approximately 15 minutes.
Patients who do not respond in this
time should have further treatment of two