Arrhythmias Flashcards
PSNS opens which channel to cause hyperpolarisation of the SA node?
K channels
Explain the mechanism allowing PSNS to hyperpolarise the SA node
Acetylcholine acts on muscarinic receptors to decrease cAMP activity, which slows the closure of K channels, lengthening time between pacemaker potentials
SNS acts via noradrenaline to increase HR by what mechanism?
NA acts on beta receptors to increase cAMP activity, causing increased closure of K channels and opening of sodium channels
Most common cause of arrhythmia?
Ischemic heart disease
Arrhythmias can be classified by rate or..?
Site of abnormality
Define sinus tachycardia
Fast heart rate, but the SA node is still the primary pacemaker so waveform would be normal
Appearance of atrial fibrillation on ECG?
Normal looking but irregular QRS + random and chaotic P waves
Explain the consequences of atrial fibrillation that can lead to emboli formation
Irregular atrial contractions cause blood to pool in the atria, which can form a clot. The clot can then dislodge and travel to brain
Compare atrial flutter and atrial fibrillation
Flutter = regular ventricular contractions Fibrillation = irregular
HR in atrial fibrillation?
Atria = ~400 Ventricles= 160-180
2 different options for atrial fibrillation?
- rate control (e.g. BB or CCB) and anticoagulant
Name the arrhythmia responsible for sudden cardiac death
Ventricular tachycardia
Drug + other Tx for treatment and prevention of ventricular tachycardia?
Amiodarone
Electric shock / defibrillation
Symptoms of bradycardia?
Palpitations, syncope, fatigue, dizziness, heart failure
Compare intrinsic and extrinsic causes of bradycardia
Intrinsic = age, ischaemic heart disease, surgery Extrinsic = medications, electrolyte disturbances, metabolic rate
Define re-entry arrhythmias
Caused by an action potential that doesn’t die out like it is supposed to, but instead re-excites regions of myocardium right after the refractory period
Define heart block
Ventricular rate much slower than atria due to impairment of the AV node. Complete heart block = atria and ventricles beat independently of one another
Define pro-arrhythmic drugs
Drugs that prolong the QT interval
Drug used in bradycardia?
Atropine
Name 2 potential causes of dysrhymthias
- hypo or hyperthyroidism
- caffeine, sympathomimetic drugs
- heart disease
- electrolyte disturbances
Where do sodium channel blockers bind?
To the alpha subunit of the sodium channel, which prevents from being activated while at rest.
Explain the MOA of sodium channel blockers
They prevent action potentials by blocking the activation of sodium channels, meaning the cell does not depolarise. This slows the HR down
Name 3 sodium channel blockers (one from each class)
Disopyramide, lidocaine, flecainide
Which sodium channel blocker has the shortest DOA?
Lidocaine
Preferentially binds to frequently activating channels. Means the drug is more active when the HR is high
Compare lidocaine and flecainide
Flecainide has a longer duration of action
Do disopyramide and quinidine lengthen the refractory period?
Yes
Name 2 beta blockers that are selective for B1
Metoprolol and atenolol
Which class is most commonly used for for atrial fibrillation?
Class 1C (e.g. flecainide)
Which drug class is used to treat ventricular tachycardia?
Class 1B (lidocaine)
How do beta blockers slow HR?
Prevents the binding of noradrenaline to the beta receptor, meaning it reduces the impact of the SNS
Beta blockers reduce calcium influx. True or false?
True. Explains why they slow HR (authorhythmic AP) and are negative inotropes
Class 3 drugs are..?
Drugs that prolong the cardiac action potential
How do class 3 drugs work?
They block depolarisation by K channels which prolongs the action potential and lengthens the refractory period of the sodium channels
Drug class that can prevent re-entrant tachycardia?
Class 3
Name 1 class 3 drug
Amiodarone
Define PR interval
Time between atrial depolarisation and beginning of ventricular depolarisation. Relates to delay at AV node
Define QT interval
Depolarisation + contraction of ventricles
Class 4 drugs are also known as?
Calcium channel blockers
Name 2 calcium channel blockers
Verapamil and diltiazem
CCBs increase after-depolarisation arrhythmias. True or false?
False. They reduce this type of arrhythmia
MOA of adenosine?
Opens potassium channels, causing hyperpolarisation
Which drug can be administered to terminate re-entry tachycardia?
Adenosine.
MOA of digoxin?
Inhibits Na/K ATPase which increases intracellular sodium and calcium
Is digoxin a positive or negative inotrope?
Positive. Due to increased calcium
How is digoxin used for arrhythmias if it is a positive inotrope?
Slows conduction at AV node
2 drugs used for bradycardia?
Atropine and isoprenaline
MOA of atropine?
Muscarinic antagonist. Prevents PSNS activity
Prevents binding of acetylcholine
Isoprenaline MOA?
Beta agonist - sympathomimetic
Increases contractility and heart rate
Digoxin inhibition of Na/K ATPase pump causes what?
Increased intracellular calcium = increased contractile strength
What activates the funny channel causing it to open?
Hyperpolarisation of the previous action potential