23A14: Exam Report

Describe the pharmacology of oxygen

51% of candidates passed this question.

Candidates who approached this question in a structured pharmacology approach were able to score well, outlining the pharmaceutics, pharmacodynamics, and pharmacokinetics.

Many candidates limited their pharmacodynamic discussion to adverse effects of oxygen only or listed effects without demonstrating understanding of their mechanism or consequences which limited their ability to score marks

14B17: Exam Report

Describe the pharmacology of oxygen.

35% of candidates passed this question.

Use of a general “pharmacology” structure to answer this question would help avoid significant omissions such as only discussing pharmacokinetics or only discussing pharmacodynamics. Oxygen has a well described list of pharmacodynamics effects that includes, cardiovascular, respiratory and central nervous system effects. Candidates’ knowledge of the pharmaceutics was limited for a routine drug. It was expected candidates would mention the potential for oxygen toxicity including a possible impact on respiratory drive in selected individuals, retrolental fibroplasia and seizures under some circumstances.

Many candidates did not answer the question asked, and instead focussed on the physiology of oxygen delivery and binding of oxygen to haemoglobin

F11i / 23A14 / 14B17: Describe the pharmacology of oxygen




Oxygen → chemical element, O = O, atomic number 8


  1. Treat hypoxia
  2. CO poisoning
  3. Decompression sickness
  4. Resorption of PTX


  • As a gas in black cylinders with white shoulders
  • Stored at 137 BAR @ 15°C
  • Colourless, tasteless, odourless gas
  • Supports combustion


FiO2 21 – 100% via inhalation


O2 is reduced via a series of electron transfers in the presence of cytochrome oxidase → Energy is released → used to form ATP


CNS – cerebral VC → ↓CBF

CVS – ↓HR, ↑coronary BF, ↓PVR

Resp – ↓vent drive (↓sensitivity of resp centre to CO2)

Metabolic – allows oxidative phosphorylation for the generation of ATP



Freely permeates BGB


Bound to Hb (majority) + dissolved


In mitochondria → CO2 + H2O


CO2 (exhaled) & H2O (urine, faeces, sweat)

Adverse Effects

Safety: supports combustion

  • O2 toxicity occurs due to excess production of O2 free radicals
  • At ↑PO2 → free radical production > scavenging mechanism

FiO2 safety:

  • 100% 12hrs
  • 80% 24hrs
  • 60% 36hrs

Toxicity depends on alveolar PAO2, not PaO­2


  • >2 ATM
  • Probability ↑with ↑time at ↑PaO2
  • N&V, numbness, twitching, dizziness
  • Seizures “Paul Bert effect”


  • Free radicals damage capillary membrane
  • Tracheobronchitis 2° abnormal ciliary transport
  • Absorption atelectasis
  • ARDS
  • Loss of hypoxic drive


  • Premature (<36weeks) at greatest risk
  • Vascularisation of foetal retina not until term
  • Constricts terminal vessels

Author: Krisoula Zahariou