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Flashcards in Cardiac Arrythmias Deck (15):

Define cardiac arrhythmia

An abnormal rate of muscle contraction in the heart


What causes arrhythmia?

Acute MI, HF, hyperthyroidism, hypokalemia, autonomic dysfunction - too much Adr/NAdr, theraputic (digitalis) and abuse (Cocaine) drugs, inherited mutation of cardiac ion channel, fever


How do arrythmia intitiate? Potential treatments?

Normally heart beat begins in the SA node...if it originates elsewhere - abnormal peacemaking (automaticity) high B drive
Or caused by failure of conduction to stop at the end of the heart beat (reentry) - block conduction of reentry wave


What is the mechanism of reentry?

Caused by localised slow conduction. Wave front meanders and becomes ragged. Wave front may split in 2 and then may circle round and reenter it's original pathway (spiral wave front).

Slow conduction due to ischemia.


How are arrythmias maintained?



How can you directly block conduction in the damaged region?

Localised blocking of ion channels responsible in depolarisation in damaged areas...make them inecxcitable.

Block l type calcium channels in the av node
Block Na channels in the av node.

Those responsible for the upstroke.


How can you indirectly block reentrant pathways

Delay repolarisation anywhere in the reentrant pathways
Prolong refractory period
K+ channels mediate repolarisation therefore block them?


Explain Class 1 of the Vaghuan Williams Antiarrythmic classification.

Sodium channel blockers
Lidocaine, quinidine, flecainide
Block reentry in av and atria
MUST be selective to damaged region...but if decrease dose because it isn't slows abnormal conduction, not stops it, so causes reentry...PRO ARRYTHMIA.


Explain Class 2 of the Vaghuan Williams Antiarrythmic classification.

B1 antagonists


Explain Class 3 of the Vaghuan Williams Antiarrythmic classification.

Drugs that delay repolarisation
Amidodarone, sotalol
Block reentry in atria, by blocking potassium channels
Prolongs refractory period...fewer excitable cells encountered by ragged wave front...block reentry.
QT prolongation...but can cause Torsade de pointes.
Looks like VF...causes VF and death.


Explain Class 4 of the Vaghuan Williams Antiarrythmic classification.

Ca++ channel antagonist
Verapamil and diltiazem
Block reentry in the AV node
Must be selective damaged region

Iv bolus converts reentry in the av node to a sinus arrhythmia
High conc arrives at AV node blocking conduction in damaged section.
Vascular selective therefore must be given iv to reach av node
Diluted in ventricular blood therefore too low blood to cause side effects in rest of the body. Side effect is vasodilation


Explain Class 5 of the Vaghuan Williams Antiarrythmic classification.



Class 1b

No decrease in death
Use declining
Use after MI
Most selective for NaC


Class 1C

Good for supraventricular arrhythmia only
Blocks sodium channels throughout the heart
Cn be pro arrhythmia


Class 1a

Class III side effects
QT widening
Torsardes de points