Understanding Arrythmias & Action of Drugs on CVS Flashcards
What are arrhythmias? List the different types.
Arrhythmias/dysrhythmias are disturbances of cardiac rhythms. Abnormalities of heart rate/rhythm include: bradycardia (in context), atrial flutter, atrial fibrillation, tachycardia - ventricular or supra-ventricular, ventricular fibrillation.
What can be the cause of arrhythmias that count as tachycardic?
Ectopic pacemaker activity (dominates over the SAN), with damaged myocardium becoming depolarised and spontaneously active or latent pacemaker activity activated due to ischaemia. Or afterdepolarisations (triggered activity), atrial flutter / fibrillation, or a re-entry loop, with a conduction delay, perhaps with an accessory pathway.
What can be the cause of arrhythmias that count as bradycardic?
Sinus bradycardia from sick sinus syndrome (intrinsic dysfunction) or extrinsic factors (e.g. Drugs). Alternatively, conduction block problems at the AVN or BoH - at the AVN, it could be due to extrinsic factors.
Delayed afterdepolarisations (triggered activity), are more likely to happen if there’s a high intracellular ___________ concentration. Early afterdepolarisations can lead to ______________ and are more likely if the ________ _________ is prolonged - shown on an ECG by a longer QT interval.
Calcium
Oscillations
Action potentials
With normal excitation spread, impulses cancel when they meet, because the cell’s refractory period maintains direction; explain the idea of re-enterant mechanisms in the heart and how it can cause tachycardia.
There may be a block of conduction through a damaged area region, but in this case there’s incomplete conduction damage (unidirectional block), meaning that excitation can take the long route to spread the wrong way through the damaged area, setting up a circus of excitation.
How can mitral stenosis lead to atrial fibrillation (what’s the step in the middle)? Also, how would this be shown on an ECG?
The muscle could be overstretched and damaged over time, leading to several small entry loops in the left atria, which can lead to atrial fibrillation.
Wavy baseline, no discernible p waves and an irregular rhythm (at a higher rate).
How is an AVN RE-entry loop different from the mechanism of Ventricular pre-excitation?
Fast and slow pathways in the node create the AVN RE-entry loop, whereas Ventricular pre-excitation is from an accessory pathway between the atria and the ventricles, which creates a re-entry loop (e.g. In Wolff-Parkinson-White syndrome, where it corrects itself).
What are the 4 basic classes of anti-arrhythmic drugs?
I - block voltage sensitive sodium channels,
II - beta-adrenergic antagonists,
III - block potassium channels,
IV - block calcium channels.
Lidocaine is a class I anti-arrhythmic drug, used as a local anaesthetic, which exhibits use-dependent block, what does this mean and why is this the case?
It only blocks voltage-gated sodium channels in open/inactive state, so it preferentially blocks damaged depolarised tissue - blocks during depolarisation, but dissociates in time for the next AP, so little effect in normal cardiac tissue.
When might Lidocaine, a anti-arrhythmic Na+ channel blocker be used?
Intravenously post-MI if signs of ventricular tachycardia, as damaged areas of myocardium become depolarised and may fire automatically - more Na channels open in depolarised tissue. Not used prophylactically after an MI.
What is the effect on the Class II anti-arrhythmic drugs (e.g. Propranolol, atenolol etc), that are beta-blockers?
At beta-1 receptors in the heart, they b,of, sympathetic action, which decreases the pacemaker potential in the SAN and slows conduction at the AVN.
When is the use of anti-arrhythmic beta-adrenoreceptors most effective?
When there is more sympathetic drive as it can reduce the oxygen demand and so myocardial ischaemia. It’s beneficial following a MI, because they usually increase sympathetic activity - prevent ventricular arrhythmias.
What feature of beta-blocker action on the heart means that they can prevent supra-ventricular tachycardias and slow the ventricular rate in Atrial Fibrillation patients?
They slow conduction at the atrioventricular node.
Why do Class III anti-arrhythmic drugs, which block K+ channels, work more in theory than in practice?
They prolong the action potential, which is supposed to lengthen the absolute refractory period and stop the next action potential coming too soon, but they can be pro-arrhythmic as prolonged APs can cause early afterdepolarisations.
Although Class III anti-arrhythmic drugs, which block K+ channels aren’t generally used, there is the exception of Amiodarone, because it has other functions, what are these?
It slows the rise of the action potential, blocks calcium channels and is a beta blocker, so it can treat tachycardias associated with Wolff-Parkinson-White syndrome and is effective for suppressing ventricular arrhythmias post-MI.
