Ventilatory support - indications

Oxygenation failure (Type I respiratory failure)

Hypoxaemia is defi ned by PaO2 <11kPa on FIO2 ≥ 0.4. May be due to:

• Ventilation/perfusion mismatch (reduced ventilation in, or preferential perfusion of, some lung areas), e.g. pneumonia, pulmonary oedema, pulmonary vascular disease, very high cardiac output.

• Shunt (normal perfusion but absent ventilation in some lung zones), e.g. pneumonia, pulmonary oedema.

• Diffusion limitation (reduced alveolar surface area with normal ventilation), e.g. emphysema, or reduced inspired O2 tension,

e.g. altitude, suffocation.

• Acute ventilatory insufficiency (as above).

Acute ventilatory insufficiency (Type II respiratory failure)

Defined by an acute rise in PaCO2 and significant respiratory acidosis. PaCO2 is directly proportional to the body’s CO2 production and inversely proportional to alveolar ventilation (minute ventilation minus dead space ventilation). Causes include:

• Respiratory centre depression, e.g. drugs or intracranial pathology.

• Peripheral neuromuscular disease, e.g. Guillain-Barre syndrome, myasthenia gravis, or spinal cord pathology.

• Therapeutic muscle paralysis, e.g. as part of balanced anaesthesia, for management of tetanus or status epilepticus.

• Loss of chest wall integrity, e.g. chest trauma, diaphragm rupture.

• High CO2 production, e.g. burns, sepsis or severe agitation.

• Reduced alveolar ventilation, e.g. airways obstruction (asthma, acute bronchitis, foreign body), atelectasis, pneumonia, pulmonary oedema (ARDS, cardiac failure), pleural pathology, fi brotic lung disease, obesity.

• Pulmonary vascular disease (e.g. pulmonary embolus, ARDS).

To reduce intracranial pressure

Reduction of PaCO2 to approximately 4kPa causes cerebral vasoconstriction, and therefore, reduces intracranial pressure after brain injury. Studies suggest this effect is transient and may impair an already critical cerebral blood flow.

To reduce work of breathing

Assisted ventilation 9 sedation and muscle relaxation reduces respiratory

muscle activity and the work of breathing. In cardiac failure or noncardiogenic

pulmonary oedema, the resulting reduction in myocardial O2

demand is more easily matched to the supply of O2.

Indications for ventilatory support

Consider ventilatory support (invasive or non-invasive) if:

• Respiratory rate >30/min.

• Vital capacity <10–15mL/kg.

• PaO2 <11kPa on FIO2 ≥ 0.4.

• PaCO2 high with significant respiratory acidosis (e.g. pH <7.2).

• Vd/VT >60%.

• Qs/Qt >15–20%.

• Exhaustion.

• Confusion.

• Severe shock.

• Severe LVF.

• Raised ICP.