For medical students, ICU nurses and junior ICU trainees
Click here to download the accompanying Powerpoint tutorial with English
narration
Charles Gomersall, Gavin Joynt, Sarah Ramsay
Definitions
acute respiratory failure occurs when the pulmonary system is no longer
able to meet the metabolic demands of the body
hypoxaemic respiratory failure: arterial partial pressure of oxygen (PaO2)
less than or equal to 6.7 kPa when breathing room air
hypercapnic respiratory failure: arterial partial pressure of carbon
dioxide (PaCO2) more than or equal to 6.7 kPa
Basic respiratory physiology
The major function of the lung is to get oxygen into the body and carbon
dioxide out.
Gas exchange requires a pressure gradient between alveolar air and blood, a
short distance for diffusion of gases and intervening tissues which are
permeable to oxygen and carbon dioxide
Getting oxygen in
the alveolar partial pressure of oxygen (PAO2) is
dependent on the total alveolar pressure and the partial pressures of the
other gases in the alveolus
the sum of the partial pressures of all the gases is equal to the
total alveolar pressure
partial pressure of each gas in a mixture of gases is directly
related to the proportions in which they are present
therefore partial pressure of oxygen can be increased by:
increasing alveolar pressure or
increasing the proportion of oxygen in the mixture
increasing the inspired oxygen concentration increases the proportion
of oxygen in alveolar gas while reducing the proportion of nitrogen
the alveolar partial pressure of water vapour remains largely
constant and therefore does not contribute to changes in PAO2.
The proportion of carbon dioxide in alveolar gas does, however, change
and therefore factors which affect PACO2 also
affect PAO2
as carbon dioxide passes into the alveolus and oxygen passes into the
blood the PACO2 rises and the PAO2
falls. Ventilation is required replenish the alveolar gas with fresh
gas.
thus the factors that result in changes in PAO2
are:
PACO2
alveolar pressure
inspired oxygen concentration
ventilation
Getting carbon dioxide out
CO2 elimination is largely dependent on alveolar ventilation
(CO2 crosses the alveolar membrane very readily and so diffusion
abnormalities and shunting (see below) have little
effect on CO2 elimination).
Alveolar ventilation = Respiratory rate x (tidal volume-dead space)
Anatomical dead space is constant but physiological dead space depends on
the relationship between ventilation and perfusion.
form of ventilation-perfusion mismatch in which alveoli which are not
ventilated (eg due to collapse or pus or oedema fluid) but are still
perfused. As a result blood traversing these alveoli is not oxygenated. The
animation shows an alveolus with normal ventilation and perfusion and an
alveolus in which shunting is occurring.
this form of respiratory failure is relatively resistant to oxygen
therapy. Increasing the inspired oxygen concentration has little effect
because it can not reach alveoli where shunting is occurring and blood
leaving normal alveoli is already 100% saturated
commonest cause of hypoxaemic respiratory failure in critically ill
patients
hypoxic pulmonary vasoconstriction reduces the blood flow to
non-ventilated alveoli and reduces the severity of the hypoxaemia
causes of shunting:
intracardiac
any cause of a right to left shunt eg Fallot's tetralogy,
Eisenmenger's syndrome
pulmonary
pneumonia
pulmonary oedema
atelectasis
collapse
pulmonary haemorrhage
pulmonary contusion
Ventilation without perfusion
this is the opposite extreme of ventilation-perfusion mismatch
gas passes in and out of the alveoli but no gas exchange occurs because
the alveoli are not perfused. and the ventilation is ineffective. In this
respect these alveoli are behaving like other parts of the lung that are
ventilated but do not take part in gas exchange (eg the major airways) and
these alveoli therefore make up what is called physiological dead space
unless the patient is able to compensate for it the reduction in effective
ventilation results in an increase in PaCO2.
causes include:
low cardiac output
high intra-alveolar pressure leading to compression or stretching of
alveolar capillary (mechanically ventilated patients)
Diffusion abnormality
less common
may be due to an abnormality of the alveolar membrane or a reduction in
the number of alveoli resulting in a reduction in alveolar surface area
causes include:
Acute Respiratory Distress Syndrome
fibrotic lung disease
Alveolar hypoventilation
as carbon dioxide passes into the alveolus and oxygen passes into the
blood the pressure gradients between alveolar gas and blood are gradually
reduced. Ventilation is required to restore the pressure gradients
hypoventilation is marked by a rise in PaCO2 and a fall in PaO2
Causes of hypoventilation
Brainstem
brainstem injury due to trauma, haemorrhage, infarction, hypoxia,
infection etc
metabolic encephalopathy
depressant drugs
Spinal cord
trauma, tumour, transverse myelitis
Nerve root injury
Nerve
trauma
neuropathy eg Guillain Barre
motor neuron disease
Neuromuscular junction
myasthenia gravis
neuromuscular blockers
Respiratory muscles
fatigue
disuse atrophy
myopathy
malnutrition
Respiratory system
airway obstruction (upper or lower)
decreased lung, pleural or chest wall compliance
Respiratory monitoring
Clinical
The signs of respiratory failure are signs of respiratory compensation,
increased sympathetic tone, end-organ hypoxia, haemoglobin desaturation
Signs of respiratory compensation
tachypnoea
tachypnoea is a very good indicator of a severely ill patient
use of accessory muscles
nasal flaring
intercostal, suprasternal or supraclavicular recession
Increased sympathetic tone
tachycardia
hypertension
sweating
End-organ hypoxia
altered mental status
bradycardia and hypotension (late signs)
Haemoglobin desaturation
cyanosis
Pulse oximetry
estimates arterial saturation not PaO2 using absorption of two
different wavelengths of infrared light
the relationship between saturation and PaO2 is described by
the oxyhaemoglobin dissociation curve
a pulse oximetry saturation (SpO2) ~90% is a critical
threshold. Below this level a small fall in PaO2 produces a sharp
fall in SpO2
sources of error
poor peripheral perfusion. This will often lead to a discrepancy
between the heart rate displayed by the pulse oximeter and the heart
rate measured by other means (eg ECG). Look for any discrepancy when
assessing the SpO2
