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:

Causes of Hypercapnia
Decreased minute ventilation

Central nervous system

  • Drugs affecting respiratory drive, eg. opiates
  • Brainstem or cortical lesion affecting consciousness
  • Central sleep apnoea
  • Spinal cord injury

Neuromuscular

    • Neuropathy, eg. Guillain-Barre
    • NMJ disorder, eg. myasthenia gravis
    • Myopathy

    Respiratory

    • Decreased lung compliance, eg. pulmonary oedema
    • Decreased chest wall compliance, eg. kyphosis or obesity
    • Increased airway resistance, eg. COPD or asthma

    Metabolic, endocrine and environmental

    • Metabolic alkalosis
    • Hypothyroidism
    • Hypothermia
    Increased dead space

    Increased anatomical dead space

    • Unusually long ventilator circuit (eg. while down in MRI)

    Increased alveolar dead space (i.e. ventilated but not perfused)

    • Bullous emphysema, COPD
    • Interstitial pulmonary fibrosis
    • Large pulmonary embolism
    Increased CO2 production

    Increased metabolic rate

    • Hyperthermia (including malignant hyperthermia)
    • Hyperalimentation
    • Hyperthyroidism
    • Seizures, status epilepticus
      

    Features of clinical examination that assist in making a diagnosis:

    Observation:

    • Obesity
    • 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)
    • Cyanosis
    • 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)

    Chest

    • 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)

    Abdomen

    • Recent abdominal wounds (is pain or infection preventing diaphragm excursion?)
    • Distension (Gas? Poop? Ascites?)

    Lower limbs

    • 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.

    1. - Assess airway patency;
    2. - if airway is not protected, introduce simple airway devices and assess their effect on airway patency
    3. - if airway reflexes are intact, commence NIV paying attention to the dangers of the high pressures which will be required in an obese patient
    4. - if airway reflexes are intact, assess for intubation and solicit expert help for intubation.
    5. - assess any rapidly reversible causes of obtundation such as opioid intoxication and hypo/hyperglycaemia
    6. - if no rapidly reversible cause is found, mechanical ventilation must commence while the process of investigation continues
    7. - 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.
    8. - at the same time, management of the possible causes of hypercapneic respiratory failure must commence (therapies specifically directed at COPD and OSA)
    9. - 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.

     

    References

    Khilnani, G. C., and C. Bammigatti. "Acute Respiratory Failure-Algorithmic Approach-Diagnosis and management." Medicine Update (2005): 548.

    UpToDate: Evaluation of the adult with dyspnea in the emergency department

    Rosen, Mark J. ". Hypercapnic Respiratory Failure." Medicine Board Review (2012).

    UpToDate: "Mechanisms, causes, and effects of hypercapnia"

    Williams, M. Henry, and Chang S. Shim. "Ventilatory failure: Etiology and clinical forms." The American journal of medicine 48.4 (1970): 477-483.