12. Arrhythmias And Drugs Flashcards
What are the 2 types of after depolarisations (triggered activity)? When is each more likely to happen?
Delayed after-depolarisations (return to resting membrane potential, then another spike) - intracellular Ca2+ high.
Early-after depolarisations (oscillations) - action potential prolonged, so longer QT.
What happens in normal spread of excitation at a branch point?
Excitation reaches branch point, spreads both ways, cancels out where meets.
What happens when excitation meets a branch point and there is a block of conduction through a damaged area?
Does not spread down damaged branch, doesn’t really cause any problems.
What happens when excitation reaches a branch with a unidirectional block (incomplete conduction damage)?
Excitation takes a long route to spread the wrong way through the damaged area, so as excitation never meets to cancel out, sets up a circus of excitation.
What arrhythmia is caused by multiple re-entrant circuits in the atria?
Atrial fibrillation
What happens in AV nodal re-entry?
Fast and slow pathways in the AV node create a re-entry loop leading to palpitations.
What happens in ventricular pre-excitation? Give an example of a syndrome this occurs in
Accessory pathway between atria and ventricles creates a re-entry loop eg Wolff-Parkinson White syndrome.
How do the anti-arrhythmic drugs, voltage-dependant Na+ channel blockers work?
Are a use-dependent block. Block voltage-gated Na+ channels in open or inactive state, so preferentially block damaged depolarised tissue.
What do drugs that block voltage-dependant Na+ channels have little effect in normal cardiac tissue?
Dissociates rapidly - blocks during depolarisation but dissociated in time for next AP, so has no effect on AP generation.
Why are drugs which block voltage-dependant Na+ channels sometimes given following an MI?
Given IV - if patient shows signs of ventricular tachycardia, as damaged areas of myocardium may be depolarised and fire automatically. There are more Na+ channels open in depolarised tissue, and so blocks those Na+ channels and prevent automatic firing.
How do the anti-arrhythmic drugs, beta-adrenoreceptor antagonists, work?
Block sympathetic action by acting on beta1-adrenoreceptors in the heart. Slow down pacemaker potential, and slow conduction at AV node.
When are beta-blockers used and why?
Prevent supraventricular tachycardia and slows ventricular rate in patients with AF - slows conduction in AV node.
Following MI - Mi causes increased sympathetic activity, arrhythmias partly due to increased sympathetic activity, so beta-blockers prevent ventricular arrhythmias. Also reduces O2 demand, reducing myocardial ischaemia.
How do the anti-arrhythmic drugs, K+ channel blockers, work?
Prolong the action potential by blocking K+ channels, lengthening the absolute refractory period. Prevents another action potential occurring too soon.
Why are K+ channel blockers not generally used?
In theory prevent another action potential occurring too soon, but can actually by pro-arrhythmic.
What type of anti-arrhythmic drug is amiodarone and what is it used clinically when other drugs of this type aren’t and why?
Blocks K+ channels, but also has other actions.
Used to treat tachycardia associated with Wolff-Parkinson-White syndrome.
Affective for suppressing ventricular arrhythmias post MI.
How do the anti-arrhythmic drugs, Ca2+ channel blockers, work?
Decrease slope of action potential at SA node and decreases AV nodal conduction, as well as force of contraction.
Where do dihydropyridine Ca2+ channel blockers work and not work?
Not effective in preventing arrhythmias but do act on vascular smooth muscle.
What antiarrhythmic drug can be administered IV, but is also already produced endogenously in the body? What does it do?
Adenosine - enhances K+ conductance, so hyperpolarises cells of conducting tissue. Is anti-arrhythmic and useful for terminating re-entrant supraventricular tachycardia (as cells take longer to be able to be depolarised again).
What do positive inotropes, eg cardiac glycosides and beta-adrenergic agonists, do and why are they not routinely used to treat heart failure?
Increase cardiac output. Improve symptoms but not long term survival.
What is the action of cardiac glycosides?
- ) Blocks Na+/K+ ATPase, yet Na+/Ca2+ exchanger still functioning, so leads to rise in Na+ concentration inside cells. Rise in Na+ concentration means left Na+ is moved in by Na+/Ca2+ exchanger, and so less Ca2+ moved out of cell, increasing force of contraction.
- ) Increase Vargas activity, slowing Av conduction and HR.
When are you most likely to use the positive inotrope cardiac glycosides?
In heart failure when there is an arrhythmia such as AF.
What do the positive inotropes, beta-adrenoreceptor agonists, act on and what does this cause?
Beta1-receptors, increase myocardial contractility.
When are the positive inotrope, beta-adrenoreceptor agonists, used?
Cardiogenic shock, and acute but reversible heart failure.
How do ACE-inhibitors work to reduce the workload of the heart in treatment of heart failure?
Decrease vasomotor tone, reduce afterload of heart. Decrease fluid retention, reduce preload of heart, reduce workload of heart.
