Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) describes the acute,
diffuse pulmonary inflammatory response to either direct (via
airway or chest trauma) or indirect blood-borne insults from
extrapulmonary pathology. It is characterised by:
●
Neutrophil sequestration in
pulmonary capillaries.
●
Increased capillary Permeability
● Protein-rich pulmonary oedema.
If this early phase does not resolve with treatment of the
underlying
cause, a fibroproliferative phase ensues and causes pulmonary
fibrosis. It is frequently associated with other organ dysfunction
as
part of multiple organ failure.
The term ARDS is often limited to patients requiring ventilatory
support on the ICU, but less severe forms, conventionally referred
to as acute lung injury (ALI) and having similar pathology, occur
on
acute medical and surgical wards. The clinical picture is
non-specific
and shares features with other conditions (diffuse bilateral
shadowing
on CXR in the absence of raised left atrial pressure, hypoxaemia,
impaired
lung compliance).
Management
Respiratory support is indicated to maintain the patency of the
airway, correct hypoxaemia and hypercapnia, and reduce the work
of breathing.
Oxygen therapy: Ensure adequate arterial oxygenation (SpO2
> 90%). If a patient remains hypoxaemic on high-flow
oxygen, other
measures are required.
Non-invasive respiratory support: If the patient has respiratory
failure associated with decreased lung volume, application of
continuous
positive airway pressure (CPAP) will improve oxygenation
by recruitment of under-ventilated alveoli and reduce the work of
breathing. CPAP is most successful when alveoli are readily
recruited
(e.g. pulmonary oedema, post-operative atelectasis). Patients
should
be cooperative, be able to protect their airway and have the
strength
to breathe spontaneously and cough effectively. In non-invasive
positive pressure ventilation (NIV), the patient’s spontaneous
breathing is supported by increased inspiratory and expiratory
pressures
delivered using a bi-level ventilator (BiPAP). For NIV to
succeed, the patient’s spontaneous breathing must be sufficient to
trigger the machine and they must be able to tolerate a
tight-fitting
facemask. NIV reduces the work of breathing, relieves
breathlessness
and is proven to reduce the need for endotracheal intubation
in patients with type 2 respiratory failure (e.g. exacerbations of
COPD;). It is also used during weaning from conventional
ventilation.
Endotracheal intubation and mechanical
ventilation: Many
patients admitted to ICU require intubation and mechanical
ventilation.
Indications for intubation are summarised in. The
various types of invasive ventilatory support are summarised in.
In the conscious patient, intubation requires induction of
anaesthesia
and muscle relaxation, while in more obtunded patients sedation
alone may be adequate. Hypotension commonly follows
sedation or anaesthesia because of direct cardiovascular effects
of the drugs and loss of sympathetic drive; positive pressure
ventila-27
tion
may compound this problem by increasing intrathoracic pressure,
which
reduces venous return.
The
selection of ventilator mode and settings for tidal volume,
respiratory
rate, positive end-expiratory pressure (PEEP) and inspiratory
to
expiratory ratio is dependent on the cause of the respiratory
failure.
Weaning from respiratory support: The majority of patients
require
mechanical ventilatory support for only a few days and do
not
need a process of weaning. In contrast, patients who have
required
long-term ventilatory support for severe lung disease, e.g.
ARDS,
may initially be unable to sustain even a modest degree of
respiratory
work due to reduced lung compliance and muscle weakness;
hence
they require a programme of gradual weaning from
ventilation.
Tracheostomy: This
is usually performed electively when endotracheal
intubation
is likely to be prolonged (> 14 days). Tracheostomies
help
patient comfort, aid weaning from ventilation, and allow access
for tracheal toilet and
intermittent respiratory support.
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