13. Cardiac arrhythmias and CVS drugs Flashcards
What is an arrhythmia?
An arrhythmia is an a abnormally/ irregular heart rate/rhythm.
Give 5 examples of types of arrhythmias
- Sinus Bradycardia
- sinus tachycardia
- atrial flutter
- atrial fibrillation
- tachycardia (ventricular tachycardia and supraventricular tachycardia)
- ventricular fibrillation
List 4 causes of tachycardia
Arrhythmias arise due to a disturbance of impulse generation, impulse conduction or both.
- Ectopic pacemaker activity
- After-depolarisations
- This is when you have abnormal depolarisations following the action potential. - Atrial flutter/ atrial fibrillation
- This is an abnormal heart rhythm which is characterised by rapid and irregular beating of the atrial chambers of the heart. - Re-entry loop
– conduction delay
– accessory pathway
What may lead to ectopic pacemaker activity?
This is when another (damaged) area of the myocardium becomes spontaneously active and it’s depolarisations dominate over the SA node. This leads to random and irregular depolarisations and heartbeats.
- latent pacemaker region activated due to ischaemia (dominates over SA node)
List and describe 2 causes of bradycardia
- Sinus bradycardia
This can be caused by a condition known as sick sinus syndrome. Here the SA node is malfunctioning and isn’t depolarising properly. This is a type of arrhythmia.
Another cause would be extrinsic factors such as drugs (e.g beta blockers, some Ca2+ channel blockers). These work to slow down conduction at the AV node.
- Conduction block:
Here there are problems at the AV node or the bundle of His, this means that there’s a block in conduction between the atria and the ventricles.
Another cause would be extrinsic factors (e.g beta blockers and some Ca2+ channel blockers). These cause slow conduction at the AV node.
Explain what a delayed after-depolarisation (DAD) is
DADs begin after repolarisation of the ventricles is completed but before another action potential would normally occur via the normal conduction systems of the heart.
They’re due to increased levels of intracellular calcium concentrations.
The overload in the SR of the cell causes spontaneous release of Ca2+ after repolarisation.
- thought to activate NCX channels
- sodium in causes slight depolarisation
- If threshold is reached an action potential is triggered before it should.
You get triggered activity.
If this happens routinely it can result in ventricular tachycardia.
Explain what an early after-depolarisation (EAD) is
This is when you get abnormal action potentials occurring before normal repolarisation is completed.
This can be due to random openings of sodium or calcium ion channels.
You’re more likely to get this if the action potential is prolonged.
If the AP is prolonged you get a longer QT interval.
This can suggest that the patient is more prone to arrhythmia.
Why are early after-depolarisations more likely to occur when there is prolonged AP?
If action potential is prolonged (e.g. in hypokalaemia)
- Ca++ channels recover from inactivation
- can lead to calcium spikes
- depolarising the membrane leading to oscillation
When does reentry occur?
When a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after expiration of the refractory period
Describe the reentrant mechanism in a unidirectional block.
A re-entry loop occurs when the normal spread of excitation across the heart is disrupted due to a damaged area.
In a normal spread of excitation without damage, the impulses will spread out from the point of diversion in opposite directions and impulses will also meet at a point and cancel out as all cells are in the refractory period.
If there’s an area of damage that blocks conduction through one diversion, it means that the impulse will spread the opposite way and continue as normal. This doesn’t create a problem.
However, where there’s an incomplete conduction damage, the damaged tissue will only conduct in one direction (unidirectional block)(but normally not in the right direction)
The excitation can’t get through the area of damage through one route so it’ll take the long route and spread the wrong way through the damaged area. This sets up a circuit of excitation where there is rapid depolarisation - setting up tachycardia
What effect can a reentry loop have on the atria?
Multiple small reentry loops can form in the atria, leading to atrial fibrillation. - tachycardia, irregular rhythm, wavy baseline
Explain what happens in AV nodal re-entry
AV nodal reentry is a type of tachycardia (supraventricular tachycardia).
It occurs when a re-entrant circuit forms within or next to the AVN, this causes the heart to beat prematurely as there is a circuit of depolarisation .
You get fast and slow pathways in the AVN to create a re-entry loop.
Explain what happens in ventricular pre-excitation
In ventricular pre-excitation part of the cardiac ventricles are activated too early.
Its caused by an abnormal electrical connection known as an accessory pathway between the atria and the ventricles - not the normal route.
This creates a re-entry loop such as in Wolff-Parkinson-White syndrome.
List the 4 basic classes of anti-arrhythmic drugs
I. Drugs that block voltage-sensitive sodium channels
II. Antagonists of β-adrenoreceptors
III. Drugs that block potassium channels
IV. Drugs that block calcium channels
Give an examples of a class I anti-arrhythmic drug?
Lidocaine (local anaethetic)
In which state of the Na+ channel does lidocaine block it?
Only blocks voltage gated Na+ channels in open or inactive state - therefore preferentially blocks damaged depolarised tissue.
Why does lidocaine have little effect in normal cardiac tissue?
Lidocaine has a rapid dissociation time meaning that it’ll block during depolarisation but dissociated in time for the next AP.
This means that it has little effect in normal tissue.
When and how might lidocaine be given following an MI?
Lidocaine is sometimes administered intravenously following an MI but only if the patient is showing signs of a ventricular tachycardia.
Why does lidocaine have a greater effect on damaged myocardium than normal myocardium?
• Damaged areas of myocardium may be depolarised and fire automatically
• More Na+ channels are open in depolarised tissue
- lidocaine blocks these Na+ channels (use-dependent)
- prevents automatic firing of depolarised ventricular tissue
What can lead to atrial fibrillation or flutter?
Atrial flutter or fibrillation may occur following conditions which put extra stretch and pressure on the atria (eg mitral valve stenosis)
Is lidocaine used prophylactically?
Not used prophylactically following MI
– Even in patients showing VT generally use other drugs
Give example of class II (Antagonists of β-adrenoreceptors) anti-arrhythmic drugs
propranolol, atenolol(Beta blockers)
What are the effects of class II anti-arrhythmic drugs?
They work by blocking sympathetic action and act on the β 1 -adrenoreceptors in the heart.
They carry out this action by decreasing the slope of the pacemaker potential in the SAN and slowing down conduction at the AV node.
What type of arrhythmias can beta blockers prevent and how?
Supraventricular arrhythmias
- β-blockers slow conduction in AV node
- Slows ventricular rate in patients with AF
Why are beta blockers (Antagonists of β-adrenoreceptors) given after a MI?
- MI often causes increased sympathetic activity (β-blockers block this activity - reduce the workload of the heart)
- Arrhythmias may be partly due to increased sympathetic activity
- β-blockers prevent ventricular arrhythmias
What effect do beta blockers have on oxygen demand for the heart and why is this important?
reduces O2 demand
- Reduces myocardial ischaemia
- Beneficial following MI
What is the main mechanism of Drugs that block K+ channels (class III)?
• Prolong the action potential
- mainly by blocking K+ channels
• This lengthens the absolute refractory period
