I mentioned that there have been posts on antiarrythmics in the past, but not one on these agents as far as I could see. They do appear in the tocolytic section of syllabus too, so you might find a few statements on them there.
I am going to focus on verapamil today as an agent with significant cardiac effects. It is not a benign drug, especially when other drugs are given with it.
BT_PO 1.57 Describe the pharmacology of antiarrhythmic agents and their clinical applications including calcium antagonists
Verapamil produces both bradycardia and negative ionotropy T/F
Verapamil is a good adjuvant to dantrolene in the treatment of MH as a means to control tachycardia T/F
The use of an intra-operative esmolol infusion, as part of a balanced anaesthetic, in a patient on verapamil may produce profound bradycardia T/F
Calcium channel antagonists enhance recovery from non-depolarising neuromuscular blockade T/F
*High dose insulin therapy can be used in the management of verapamil overdose T/F
*this one is not core, but quite interesting I thought
I had a look at the antiarrythmics page yesterday, when writing my post and saw specific mention of a drug I confess to never having heard of. Are you in the same boat?
How could this drug have escaped my attention? It seems to have become available around the time I finished medical school, so no real excuse there. Perhaps it is due to its specific indication for use…
I thought it was a good opportunity to learn something new and share it with you. All the statements below are true and are what I thought most noteworthy about this previously unknown (to me) drug…
BT_PO 1.57 Describe the pharmacology of antiarrhythmic agents and their clinical applications including ibutilide
Ibutilide is used for pharmacological cardioversion of atrial fibrillation and atrial flutter (but is more effective for the treatment of flutter)
It is a class III antiarrythmic which activates the late inward sodium current
It is administered by intravenous infusion
Over 80% of the dose excreted unchanged by the kidneys
It is more effective than sotalol at terminating the arrythmia
The main adverse effect is triggering of polymorphic VT which occurred in about 1.5% of trial patients
The risk of Torsades is dose dependent so tends to occur towards the end of the infusion but the risk is short lived due to the short t1/2 (3 hrs)
If you want further information, there are a few good review articles but they are all behind a paywall ( I find that very annoying, especially when over 20 yrs old…).
This is another of the “left over” LOs. There have actually been plenty of posts on anti arrhythmic drugs, you just need to search them individually.
The classic way of thinking of these drugs is using the Vaughan Williams classification. Miles Vaughan Williams died in 2016, just short of his 98th birthday. He is not to be confused with the other famous Vaughan Williams, Ralph, the composer, who was his father’s cousin. Perhaps you can put this rendition of The Lark Ascending on in the background whilst reading this post.
The Vaughan Williams classification has stood the test of time. A recent article published in Circulation helps place new drugs and understanding of electrophysiology in the context of the original classification (you do not need to know anywhere near this level of detail)
The answer to these statements should be found in most pharmacology texts
BT_PO 1.56 Describe the physiological and pharmacological basis of antiarrhythmic therapy including classification based on electro-physiological activity and mechanism of action
Individual antiarrythmic drugs work via a single class action T/F
Class Ib antiarrythmics reduce the peak Na+ current and shorten the action potential durationT/F
Class III antiarrythmics enhance potassium conductance in the heart T/F
Sotolol, as a beta blocker, has exclusively class II action T/F
Adenosine fits neatly within the Vaughan Williams classification *T/F
*you may change your mind on the answer to this one if you read the Circulation article
Describe the pharmacology of drugs used to manage acute or chronic cardiac failure, including: sympathomimetics, phosphodiesterase inhibitors, digoxin, diuretics, ACE inhibitors, nitrates and beta blockers
A guest post from an ex PEX chair :
Agatha Christie knew a lot about poisoning, probably as a result of working with a pathologist. (https://bookshop.theguardian.com/catalog/product/view/id/323440/). After reading this book, you would have to be brave to go into an English garden. One of her garden poisons was foxglove, which made me think of digoxin. As did the recent death of Miles Vaughan Williams, who classified anti arrhythmics. So often we see digoxin toxicity in clinical practice. An old drug, but one that continues to be used, and is loved by examiners because it allows for candidates to demonstrate an understanding of many different facets of pharmacology.
TRUE/FALSE Digoxin is highly protein bound, hence the introduction of another highly protein bound drug is likely to precipitate toxicity
TRUE/FALSE Digoxin is primarily excreted renally, and frequently patients who are prescribed digoxin may have borderline or impaired renal function which may precipitate toxicity
TRUE/FALSE Overdosage of digoxin may be treated using Digibind (R) which is an example of an immunoglobulin which binds to digoxin to cease its therapeutic effect
TRUE/FALSE Hypokalaemia is frequently seen in digoxin toxicity, reflecting digoxin’s inhibition of the Na/Ca pump
TRUE/FALSE The bioavailability of digoxin is reasonably high (approx 70%) allowing for oral loading doses to be only slightly slower in reaching therapeutic effects compared with intravenous loading doses