Respiratory Failure
Respiratory Failure
Respiratory Failure
Type I = hypoxaemic
Type II = hypercapnic = ventilatory
failure = respiratory acidosis
Respiratory failure – Type I
Hypoxaemic
Alveolus
Respiratory failure – Type I
• Differentials
– Alveolar problem – fluid, pus,
destruction, collapse
– Circulation problem – V/Q mismatch,
PE, shunt, destruction
– Interstitial problem – fibrosis,
infiltration
Respiratory failure – Type I
By definition there is no problem with ventilation
• Options:
– High flow oxygen
– CPAP – for pulmonary oedema +/- atelectasis
– Bi-level – immunocompromised with LRTI
(ICU)
– Invasive ventilation – where above fails (and
failure can occur very quickly!)
Evaluating ventilatory (type 2) failure
Excess load or reduced Reduced drive
capacity (=won’t breathe)
(=can’t breathe) •Drugs
• Lung problem •Central pathology
• Chest wall problem •Sleep problem
(usually have
• Muscle problem
load/capacity
problem too)
Ventilatory failure (T2RF)
PaCO2>45mmHg
– Exacerbation of COPD
– Obesity hypoventilation syndrome
– Chest wall/neuromuscular – respiratory
muscle weakness
– Progression of Type I cause (prior to
respiratory arrest)
– Central – CNS depression/trauma/medications
(opioid/BZDs)
Respiratory failure – Type II
• Ventilatory failure → needs ventilation
Exclude reversible causes (particularly
drugs, oxygen)
Ventilate – invasive vs non-invasive
(Bi-level)
Bi-level
Limited (proven) indications
– COPD
– Neuromuscular disease
– Obesity hypoventilation
– Type I respiratory failure in
immunocompromised patients with LRTI or
pulmonary oedema
• Other uses are not proven
Traps
Asthma
– Classic temptation – evidence is generally
lacking
– Elevated PaCO2 due to asthma precedes
death by only a short period
– CO2 should generally be low in asthma
exacerbation
Traps
Altered conscious state
– Chicken or egg scenario
– Contraindication to non-invasive
therapy (no airway protection provided
+ theoretical aspiration risk from FFM)
– Exclusion of reversible causes and
airway protection are the priority
Settings, what settings?
• EPAP (and CPAP) = 1cmH2O for every 10kg of
body weight
– 70kg male – 7cmH2O
– if over 100kg - start at 10cmH2O
• IPAP = start 4-6cmH2O above the EPAP
• Repeat the ABG (1-2hrs) and titrate settings:
– increase EPAP if oxygen requirements high
– increase PS (IPAP-EPAP) if CO2 high/pH low
What is CPAP?
• Continuous PAP
–Fixed pressure applied via face mask
–Provides a constant/continuous pressure
throughout the respiratory cycle
–Does not provide ventilatory support
–Doesn’t offload respiratory muscles or lower
PaCO2
How does CPAP work?
• OSA
–Splints the upper airway during sleep
• APO
– increased intrathoracic pressure –
decreased venous return
– decreased atelectasis and alveolar collapse
does not affect ventilation/CO2
How to get CPAP or bilevel for your
patient:
1. Do an arterial blood gas
2. Think carefully about the underlying
diagnosis
3. Speak to the respiratory registrar
ABGs vs VBGs
Why venous?
• Venous blood gases (VBG) have been
considered as an alternative to arterial
(ABG) to assess breathless patients
• Why?
• Safer?
• Better?
• Easier?
Safer?
For the patient
- Up-to-date data demonstrating harm from ABG just
doesn’t exist
- Complication rate from arterial catheters 2.5%
(which is why we do punctures)
Do an ABG please!
Might be an excellent candidate for bilevel
Take home messages
• ABGs remain a vital component of the assessment of
a breathless patient and reliably monitoring their
response to therapy
• Differentiating hypoxaemic from hypercapnic
respiratory failure is useful both for diagnostic and
management purposes
• Evidence supports bilevel therapy predominantly for
hypercapnic respiratory failure – except in
immunocompromised and APO
• If you think your patient needs bilevel or CPAP, do an
ABG and speak to the Respiratory registrar
Questions?