Arrhythmias and drugs Flashcards
Four things drugs can alter?
TPR
Inotropy
Heart rate and rhythm
Blood volume
Five abnormalities in cardiac rhythm?
Bradycardia Atrial flutter Atrial fib Tachycardia (Ventricular aand supraventricular tachycardia) Ventricular fibrillation
Causes of Tachycardia? 4. explain them
Ectopic Pacemaker activity- Damaged area of myocardium becomes depolarised and fires spontaneously, dominating over the SA node
Afterdepolarisation- Abnormal depolarisation following the AP
Atrial flutter or atrial fib
Re-entry loop (Either a conduction delay or accessory pathway
2 causes of bradycardia? explain them , with possible causes for each (2 each)
Sinus bradycardia- Intrinsic SA node dysfunction or some extrinsic factor (drugs)
Conduction block- Problems at AV node or buyndle of his
Extrinsic factors- drugs
When are delayed after-polarisations more likely to happen?
with high intracellular Ca2+
When are early afterdepolarisations more likely?
prolonged AP
Describe why re-entry loops can lead to tachycardia
there’s a partial block
when the wave of depolarisation comes down, it can only pass down one of the two pathways.
however, when it passes down and rounds, it can pass back up the pathway witb the partial block
since the pathway has had time to repolarise, this means no refractory period, so action potenials can fire again
Three examples of re-entry loops
Atrial fibrillation (multiple reentry loops in the atria
AV node has a fast and slow pathway–> it depolarisaing it (ie not the SA node)–>supraventricular tachycardia
Accessory pathway from the atria to the ventricles that can send a signal to the ventricles, bypassing the atria–>ventricles contracting too early
what are the 4 classes of drugs that affect rate and heart rhythm
Drugs that block VG Na+ channels
Antagonists for β-adrenoceptorss
drugs that block K+ channels
drugs that block Ca2+ channels
Example of a drug that blocks Na+ channels?
Lidocaine (Local anaesthetic)
Explain how drugs that block Na+ channels work to prevent arrhythmias
block open or inactive Na+ channels
in damaged myocardium, more Na+ channels open
so can depolarise spontaneously sends off a wave of depolarisation across the myocardium
Blocks these Na+ channels, so prevents arrhythmias
Why don’t Na+ channel blockers bloick the Na+ channels of normal myocytes?
these channels dissociate too quickly
Two example of β-adrenoceptor antagonists?
Propranolol and atenolol
What do β-adrenoceptor agonists do and to what effect?
blocks sympatyhetic activty to the heart by acting at the β 1 adrenoceptor
so decreases the slope of the pacemaker potential in the SA node and slows conduction at the AV node
Explain why blocking the sympathetic activity to the SA node will decrease the slope of the pacemaker potential?
Normally, noradrenaline binds to the β 1 receptors
these are GPCRs
G alpha s
so increases cAMP
cAMP activates HCN channels
so more Na+ can enter–> increased slope of pacemaker potential
blocking the sympathetic nervous decreases this effect