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
Oxygen
Chemical
Oxygen → chemical element, O = O, atomic number 8
Use
- Treat hypoxia
- CO poisoning
- Decompression sickness
- Resorption of PTX
Presentation
- As a gas in black cylinders with white shoulders
- Stored at 137 BAR @ 15°C
- Colourless, tasteless, odourless gas
- Supports combustion
Route/Dose
FiO2 21 – 100% via inhalation
MoA
O2 is reduced via a series of electron transfers in the presence of cytochrome oxidase → Energy is released → used to form ATP
PD
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
PK
A
Freely permeates BGB
D
Bound to Hb (majority) + dissolved
M
In mitochondria → CO2 + H2O
E
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
CNS
- >2 ATM
- Probability ↑with ↑time at ↑PaO2
- N&V, numbness, twitching, dizziness
- Seizures “Paul Bert effect”
Lungs
- Free radicals damage capillary membrane
- Tracheobronchitis 2° abnormal ciliary transport
- Absorption atelectasis
- ARDS
- Loss of hypoxic drive
Neonate
- Premature (<36weeks) at greatest risk
- Vascularisation of foetal retina not until term
- Constricts terminal vessels
Author: Krisoula Zahariou