Question 21

College Answer

Candidates were expected to present a mechanistic description the neuro-cellular events 
following a rise in PaCO2 such as changes in H+ in CSF, stimulation of central and peripheral 
chemoreceptors and neural pathways that lead to stimulation of respiratory centre. A 
systematic approach to the question with in-depth details of direction and magnitude of 
physiologic changes were required. Most candidates presented graphs of cerebral blood 
flow and tidal volume changes with increasing PaCO2. Common omissions included other 
important points,such as the cardiovascular and respiratory effects of rising CO2 and the 
rightward shift of oxygen haemoglobin curve.

Discussion

The following is a short list of the physiological consequences of hypercapnia. Theoretically, it could be possible to graph all of these physiological changes along an axis of increasing CO₂, but these graphs would probably have little additional information to add to the statement "it gets worse". Acidosis gets worse, CNS depression gets worse, ICP gets worse, sympathetic overactivation gets ore overactivated, etc. 

The physiological consequences of hypercapnia are:

• Depressed airway reflexes with severe hypercapnia
• Changes in respiratory drive:
  • Increased respiratory drive with mild hypercapnia
  • Depressed respiratory drive with severe hypercapnia
  • These changes are controlled by central chemoreceptors
  • The chemoreceptors are sensitive to changes in the pH of CSF
  • Their output is maximal with a PaCO2 of 60-65 mmHg
  • With extremely high PaCO2, the neurodepressant effect of hypercapnia actually depresses the respiratory drive
• Changes in respiratory function:
  • Bronchodilation
  • Right shift of the oxygen-haemoglobin dissociation curve
• Cardiovascular stimulation:
  • Sympathetic overactivity, thus:
  • Hypertension
  • Tachycardia
  • Serum catecholamine excess
  • Increase in cardiac output
  • Prolonged QT interval
• Vasoactive effects:
  • Systemic arterial vasodilation
  • Pulmonary arterial vasoconstriction
• CNS effects
  • Progressively increasing sedation
  • Increased intracranial pressure
• Acid-base effects
  • Acidosis
  • Increased serum bicarbonate
• Other organ system effects
  • Increased renal vascular resistance
  • Decreased GFR
  • Decreased urine output
  • Increased portal venous pressure and vascular resistance

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