Arrhythmias Flashcards
What is bradycardia?
Slower than normal heart rate (norm <60 but need to adjust for each pt)
In general how can drugs alter the CVS?
The rate and rhythm of the heart
The force of myocardial contraction
Peripheral resistance and blood flow
Blood volume
What can tachycardia lead to?
Fibrillation = no CO = medical emergency
Outline the 4 basic types 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
Explain how tachycardia can arise
Ectopic pacemaker = damaged area becomes depolarised and spontaneously active
After depolarisation = abnormal depolarisation following AP
Atrial flutter/AF
Re-entry loop = conduction delay or accessory pathway
Explain how bradycardia can arise
Sinus bradycardia = sinus rhythm but SAN dysfunction OR drugs slowing conduction
Conduction block = prob at AVN or bundle of His OR drugs slowing conduction
Why do delayed after-depolarisation occur?
Depolarisation after repolarisation but before another AP
Why = more likely to happen if intracellular Ca2+ high = activation of Na+/Ca2+ exchanger = brief inward current = delayed after depolarisation
What are early after-depolarisations and why do they occur?
Depolarisation occurring before the previous have finished
Occur during down stroke of AP
Why = likely in prolonged AP
How can a re-entrant mechanism generate arrhythmias?
Electrical signal completing alternative circuit and looping back on itself
Incomplete conduction damage = excitation takes longer to spread = proximal tissue has recovered = permits passage in loop
Multiple re-entrant circuits in the atria = atrial fibrillation
What is an example of re-entrant tachycardia?
Wolff-parkinson-white syndrom (WPW)
What is AV nodal re-entry?
Supraventricular tachycardia
Fast and slow pathways in the AV node create a re-entry loop
What is ventricular pre-excitation?
accessory pathway (pathway other then norm) between atria and ventricles creates a re-entry loop
such as in Wolff-Parkinson-White syndrome
Outline how class I: drugs which block voltage-dependent Na+ channels work
Damaged myocardium may be depolarised and fire automatically
Only blocks v-gated Na+ channels in open or inactive state = preferentially blocks damaged depolarised tissue
Little effect in normal cardiac tissue because it dissociates rapidly
E.g. Lidocaine
Sometimes used following MI
Describe the therapeutic uses of class II: β-adrenoreceptor antagonists (beta-blockers)
Block sympathetic action = decrease slope of AP in SA and slows conduction at AVN = slows HR
Reduced O2 demand
Used in angina, AF, following Mi to prevent ventricular arrhythmias
Outline how class III: drugs that block K+ channels, work
Prolong AP by blocking K+ channels = lengthens absolute refractory period = prevents another AP occurring too soon
Not generally used = can be pro-arrhythmic
