Arrhythmias Flashcards
(30 cards)
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
How do class IV: drugs that block Ca2+ channels, work?
Decreases slope of AP at SA
Decreases AV nodal conduction
Decreases force of contraction
E.g. Verapamil
How does adenosine work?
Acts on A1 receptors at AV node but has a very short half-life = requires flush
Enhances K+ conductance = hyperpolarises cells of conducting tissue (less likely to depolarise)
Anti-arrhythmic
What are the features of heart failure?
Reduces force of contraction or reduced filling
Reduced CO
Reduced tissue perfusion
Oedema
In general what drugs are used in the treatment of heart failure?
+ve inotropes = increase CO
Drugs which reduce work load of the heart
Define the term ‘inotropic’ drug and the circumstances under which these drugs can be used
= alters the force of contraction (+ve increase CO)
How do cardiac glycosides increase the force of contraction?
Block Na+/K+ ATPase = rise in [Na+]in = decrease in activity of Na+-Ca2+ exchanger = more Ca2+ stored in SR = increased force of contraction
How do cardiac glycosides slow HR?
Increase vagal activity = slow AV conduction = slows HR
Used in heart failure with AF
What drugs increase myocardial contractility?
Cardiac glycosides
Beta-adrenoreceptor agonist – act on beta1 receptors
Which drugs reduce the workload of the heart?
ACEI = inhibit action of angiotensin converting enzyme
1) Decreases vasomotor tone = fall in BP = Reduce afterload of heart
2) Decrease fluid retention = fall in BP = reduce preload = reduce work load
Diuretics = reduce vol
Ang II receptor blocker
Beta blocker = slows HR
