Approach to Hypercapneic Respiratory Failure
Several past paper SAQs demand the candidate either generate a list of differentials or define a sensible approach to the assessment and management of acute hypercapneic respiratory failure.
- Question 16 from the first paper of 2014 (generate differentials)
- Question 14 from the second paper of 2011 and Question 1a from the second paper of 2000 are virually identical, and discuss a non-specific "approach" to the management of a comatose fat man with a PaCO2 in excess of 70mmHg.
Also related to this topic are past paper questions on the ventilation strategies in COPD, which include the following SAQs:
- Question 29 from the second paper of 2005
- Question 30 from the second paper of 2005
- Questions 1a, 1b, 1c and 1d from the first paper of 2001
|Decreased minute ventilation||
Central nervous system
Metabolic, endocrine and environmental
|Increased dead space||
Increased anatomical dead space
Increased alveolar dead space (i.e. ventilated but not perfused)
|Increased CO2 production||
Increased metabolic rate
Features of clinical examination that assist in making a diagnosis:
- Short fat neck of OSA
- Cushingoid appearance (OSA, but also suspicious of long term steroids for some sort of autoimmune condition, or COPD)
- Wasting and cachexia of severe CCF, end-stage COPD or cancer
- Abnormal breathig pattern (eg. the abdominal breathing of a C-spine quad)
Start with the hands.
- Clubbing (suggestive of chronicity)
- Unilateral small muscle wasting (lung mass invading brachial plexus)
- Pulse (collapsing pulse of AR?)
Axillae and neck
- Lymph nodes
- JVP (cardiac causes of ventilation failure)
- Dissection scars from lymph node clearance; radiotherapy tattoos
Face and cranial nerves
- Plethoric "mitral facies"
- Droop, cranial nerve signs of stroke
- Horner's syndrome (malignancy or stroke)
- Temporalis wasting (malnutrition)
- Abnormal chest wall movement (eg. flail segment or unilateral phrenic nerve paralysis)
- Subcutaneous emphysema on palpation, suggestive of pneumothorax
- Percussion findings (eg. dullness of an effusion)
- Auscultation findings of wheeze or creps (spasm or APO)
- Recent abdominal wounds (is pain or infection preventing diaphragm excursion?)
- Distension (Gas? Poop? Ascites?)
- Oedema of CCF or prolonged bed stay
- Muscle wasting of quads (another feature of malnutrition)
It would be nice to ignore the comatose fat man, but two SAQs have been repeated involving him. The college wanted an "approach" to his problem. The approach listed below is directly copied from those SAQs, with no modification.
- - Assess airway patency;
- - if airway is not protected, introduce simple airway devices and assess their effect on airway patency
- - if airway reflexes are intact, commence NIV paying attention to the dangers of the high pressures which will be required in an obese patient
- - if airway reflexes are intact, assess for intubation and solicit expert help for intubation.
- - assess any rapidly reversible causes of obtundation such as opioid intoxication and hypo/hyperglycaemia
- - if no rapidly reversible cause is found, mechanical ventilation must commence while the process of investigation continues
- - once airway patency is established and some form of mechanical ventilation is in progress, other causes for the reduced level of consciousness must be pursued and managed, including intracranial causes, thromboembolism, electrolyte abnormalities, cardiac failure, hypothyroidism etc.
- - at the same time, management of the possible causes of hypercapneic respiratory failure must commence (therapies specifically directed at COPD and OSA)
- - at the same time, standard management protocols for the care of an obese ICU patient must be followed, including thromboprophylaxis, pressure area care, the use of specialised bariatric equipment, and ulcer prophylaxis.