Vaughan williams arrhythmias

Still it remains a major reference for the people that write CICM exams. From this, we can conclude that it is intended to be committed to memory, and not to be understood. However, most normal people will probably agree that knowledge is not defined by data storage, and having a grasp of the underlying principles probably has some value for the intensivist in training.

Therefore, wherever possible, some of the sections that follow will go on deep tangents into the electrophysiological trickery that produces these antiarrhythmic effects listed in the Stoelting table. Class I agents are sodium channel blockers. They generally bind to a site inside the pore of the Nav1. All prefer to bind to open or inactivated sodium channels though the slowly dissociating Class Ic agents remain bound even when the channels return to their resting state.

Speaking of which, this class is further subdivided into subclasses according to what the drugs do to the action potential and what dissociation kinetics they have:.

Vaughan williams arrhythmias: Antiarrhythmic Drugs (Vaughan Williams Classification) Class

However, they do not need those effects. Beta blockade has a rather diverse and potent effect on multiple cardiac ion channels, as listed in this table paraphrased from Dorian :. All of this is due to the downscaling of the intracellular cAMP-mediated signalling that results from beta blockers competing with catecholamines. According to the the table from Stoeltingthe net electrophysiological effect of these ion channel current changes should be:.

How does any of this connect to the abovementioned ion channel effects? For a drug class which has been available for so many decades, the literature on the electrophysiological effects of beta blockers is surprisingly well hidden. Some material can be unearthed by dusting off studies like Venditti et alwho reported on the empirical findings of animal experiments for different beta blocker agents.

The original table of results is presented below. As you can see, the situation is a lot more complex than the Stoelting table will have you believe:. The weird lack of data for commonly used drugs like metoprolol, and the weird excess of data for rare exotic beta blockers like pindolol and nadolol, is due to the vintage of this study, which dates back to with metoprolol only having entered the market in Still, you can make out that broad trends really don't seem to exist across this group for example, to say that all beta blockers uniformly increase the duration of the action potential would be patently untrue.

Surely, by this point even the most loyal and patient reader will have sprayed profanities at their monitor, faced with this level of confusion and uncertainty. Who cares what happened to guinea pig myocytes in the eighties, they might ask. Tell me what CICM want me to write in my exam paper! Unfortunately, this absolutely reasonable request can only be answered with the Stoelting table.

This is probably what the First Part Exam question-writers will be referring to when they put together the SAQs for the written paper. You can bet that they won't be leafing through vaughan william arrhythmias copies of The American Journal of Cardiology from From this, it follows that Deranged Physiology would serve its readership best by trying to explain why the Stoelting table contains what it contains, and to find whatever evidence there is to support its assertions.

Amiodarone sotalol ibutilide and vernakalant are really the main contenders here, though worldwide there is an even larger selection of these agents available. This class prolongs repolarisation by interfering with the function of inward rectifier and outward delayed rectifier potassium currents, increasing the duration of the refractory period and of the action potential as a whole.

It is hard to discuss the Class III effects because the poster child for this class is amiodarone, and it acts promiscuously on all Class I-IV molecular targets. In fact, all Class III agents have some kind of extra weirdness sotalol is a beta-blocker, ibutilide acts on slow inward depolarising sodium currents, etc. A "pure" potassium channel blocker effect is therefore difficult to describe using an example.

Strictly speaking, they should only prolong repolarisation.

Vaughan williams arrhythmias: Antiarrhythmic agents, also known

The best resource to explain this would probably be the little fragment from Cardiac Electrophysiology: From Cell to Bedside p. In short, these drugs mainly block Ikr, Iks and Ik1 currents which are responsible for Phase 3 of the cardiac action potential. Class III drugs are not unique in the effect, as there are many other drugs which interfere with this current notably, macrolide antibiotics and antipsychotic drugs.

In the form of a diagram, one would express this like so:. Verapamil and diltiazem are the only real representatives here, as these are non-selective agents, whereas the dihydropyridine subclass tends to only affect the calcium channels in the vascular smooth muscle. In brief, their main effects are on pacemaker tissue, and on Phase 2 of the cardiac action potential.

The Stoelting table makes a number of statements about these drugs, which need to be memorised unquestioningly by CICM exam candidates, and should not be subjected to any further scrutiny. Our understanding of the control of cardiac rhythm has developed in that time and a group of cardiovascular scientists from Oxford, Cambridge and Beijing led by Associate Professor Ming Lei decided that the time was ripe to modernise the classification and to celebrate the centenary of the birth of Vaughan Williams.

Findings over the past 5 decades from studies of different molecular drug targets, their mechanisms of action, and consequent clinical effects have led to the need to revise the classification. The scheme then draws attention to multiple drug targets and actions and possible adverse, even pro-arrhythmic, effects. Therefore, attempts have been made to classify the different antiarrhythmic drugs by vaughan william arrhythmias.

Although different classification schemes have been proposed, the first scheme Vaughan-Williams is still the one that most physicians use when speaking of antiarrhythmic drugs. The following table shows the classic Vaughan-Williams classification and the basic mechanism of action associated with each class. Note that Class I drugs are further broken down into subclasses because of subtle, yet important differences in their effects on action potentials.

Vaughan williams arrhythmias: The following table shows the

This table includes a Class ID drug, although it is primarily used as an antianginal drug. Clicking on the "Class" or "Basic Mechanism" will take you to the page describing the drugs that comprise that class. The Vaughan-Williams classification has notable limitations. Pediatr Int. British Journal of Pharmacology. Progress in Cardiovascular Diseases.

A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. October J Clin Pharmacol. Antiarrhythmic drugs: a practical guide. Oxford: Blackwell Science. Emollients Cicatrizants Antipruritics Antipsoriatics Medicated dressings. Hormonal contraception Fertility agents Selective estrogen receptor modulators Sex hormones.

Anticancer agents Antimetabolites Alkylating Spindle poisons Antineoplastic Topoisomerase inhibitors. Immunomodulators Immunostimulants Immunosuppressants. Anabolic steroids Anti-inflammatories Non-steroidal anti-inflammatory drugs Antirheumatics Corticosteroids Muscle relaxants Bisphosphonates. Decongestants Bronchodilators Cough medicines H 1 antagonists.

Ophthalmologicals Otologicals. Antidotes Contrast media Radiopharmaceuticals Dressings Senotherapeutics. Antiarrhythmic agents C01B. Diltiazem Verapamil.

Vaughan williams arrhythmias: Antiarrhythmic medications play a pivotal role

Adenosine Benzodiazepines Barbiturates. Amiodarone Bretylium Quinidine Verapamil. Digitoxin Digoxin Ouabain. Categories : Antiarrhythmic agents Cardiac electrophysiology. Hidden categories: Pages with missing ISBNs Wikipedia articles needing page number citations from January All articles with dead external links Articles with dead external links from November Articles with short description Short description is different from Wikidata All articles with unsourced statements Articles with unsourced statements from March Toggle the table of contents.

Antiarrhythmic agent. Drug class. ArrhythmiaAtrial fibrillationVentricular tachycardiaetc. Drug Classes. In Wikidata. Ajmaline Disopyramide Procainamide Quinidine Sparteine. Increase QT interval Prevent paroxysmal recurrent atrial fibrillation triggered by vagal overactivity Treat ventricular arrhythmia Treat Wolff-Parkinson-White syndrome procainamide with caution.