T/F oxygen and carbon dioxide are exchanged on a 1:1 basis across the alveolar-capillary membrane *
T/F the diffusion of oxygen from alveoli to blood occurs down an average partial pressure gradient of approximately 110 mmHg (150 – 40)
T/F the diffusion gradient for oxygen is greater in basal alveoli, compared with apical
T/F carbon dioxide diffuses less readily than oxygen through the alveolar-capillary membrane, because its molecular weight is higher
T/F at altitude, or with lung disease, the transfer of oxygen can become diffusion limited when the cardiac output increases
T/F If an aircraft at 36,000 ft depressurised, the alveolar PO2 would be below mixed venous PO2 (i.e. the diffusion gradient for O2 would be reversed), so breathing would actually excrete oxygen from the body. Therefore, you should hold your breath until your oxygen mask is on.
* this statement was confidently made by an SRMO at an ALS course I attended
Flowing on from yesterday’s post on lithium, I thought I would focus on another element today, fluorine, or in particular the fluoride ion.
This little guy comes into its own in anaesthesia when thinking about the metabolism of volatile anaesthetic agents, and their toxicity, hence the LO which I have given it.
There has been a bit of debate between the authors of this blog about how much current trainees should know about methoxyflurane, no longer used as an anaesthetic agent, but still widely used in pre-hospital settings as an analgesic.
Have you thought about why it is no longer used as an anaesthetic, given that it is both hypnotic and analgesic – a combination which is hard to find and highly sought after?
Miller’s Anaesthesia Ch 26 covers this topic well and I would think all the statements below could be examined.
BT_GS 1.26 Describe the toxicity of inhalational agents
All modern volatile anaesthetic agents contain fluorine atoms T/F
Approximately 70% of methoxyflurane is metabolised, with the kidney being a significant site of metabolism T/F
Plasma concentrations of fluoride ions following prolonged sevoflurane anaesthesia do not approach levels seen with methoxyflurane T/F
Peak plasma concentrations of fluoride ions following inhalational anesthesia correspond well with the risk of renal failure T/F
High intra-renal levels of fluoride due to renal metabolism are the likely reason for the high incidence of nephrotoxicity with methoyflurane T/F
The renal failure caused by fluoride ions is oliguric T/F
The risk of renal failure with methoxyflurane is negligible after 1MAC hour T/F
Did you know that the “Green Whistle” is actually an Australian development? (thanks to Slowlywaving, for pointing this out)
On the way to work today I listened to a fascinating podcast about an Australian psychiatrist, John Cade, who discovered the benefit of using Lithium in the treatment of bipolar mood disorder. Apparently Lithium was one of the three elements created in the Big Bang along with H and He
Lithium is not a drug we encounter commonly in our anaesthetic practice, although it is still the gold standard treatment for severe bipolar mood disorder and has some interesting toxic effects. As such, I thought it was worthy of a post. None of this is particularly examinable, but still good to know.
Lithium is covered well in Katzung Basic and Clinical Pharmacology (Ch 29)
BT_PO 1.99 Outline the pharmacology of anti-depressant, anti- psychotic, anti-convulsant, anti-parkinsonian and anti- migraine medication
Lithium can mimic the actions of sodium in the generation of membrane potentials T/F
Lithium produces a nephrogenic diabetes insipidus which does not respond to vasopressin T/F
Patients on lithium often exhibit T wave flattening on their ECG T/F
Lithium is completely renally cleared T/F
Leukocytosis is almost universal in patients receiving lithium therapy T/F
T/F methaemoglobin has the iron in the ferric (Fe3+) rather than the ferrous (Fe2+) state – this renders it completely unable to bind with oxygen
T/F methaemoglobin is normally present in trace amounts – but metHb can increase to toxic levels with certain drugs (e.g. prilocaine, nitrates) especially in people with methaemoglobin reductase deficiency
T/F carboxyhaemoglobin (COHb) has CO bound to the terminal amino groups on each of the 4 globin chains – this renders the Hb unable to bind O2
T/F CO binds to Hb with 250 times greater affinity than O2
T/F the binding of CO to Hb instead of O2 is the sole mechanism by which carbon monoxide leads to hypoxia
T/F sickle cell disease is a genetic disorder leading to a single nucleotide substitution on the B globin chain of Hb (valine instead of glutamic acid) – this reduces the affinity of HbS for O2
T/F a sickle cell crisis can be treated with IV methylene blue
BT_PM 1.25 Describe in detail pharmacology of paracetamol including mode of action, clinical utility, metabolism and toxicity, advantages and disadvantages of different routes of administration
T / F paracetamol inhibits both COX-1 and COX-2
T / F paracetamol is a prodrug – the active metabolite is para-aminophenol
T / F the oral biovavailability of paracetamol is about 90%
T / F paracetamol is metabolised by CYP2E1 to NAPQI (N-acetyl-p-benzoquinonamine) which is hepatotoxic – NAPQI is then further metabolised by conjugation with glutathione (this step renders NAPQI non-toxic)
T / F the above is the only metabolic pathway for paracetamol
T / F in paracetamol overdose, depletion of glutathione leads to NAPQI accumulation
1. Hemmings & Egan
2. Goodman & Gilman
Do you use IV paracetamol? Can you justify its use with reference to any good quality evidence, and/or any niche situations?