Arrhythmias

Question 1

PSNS opens which channel to cause hyperpolarisation of the SA node?

Answer 1

K channels

Question 2

Explain the mechanism allowing PSNS to hyperpolarise the SA node

Answer 2

Acetylcholine acts on muscarinic receptors to decrease cAMP activity, which slows the closure of K channels, lengthening time between pacemaker potentials

Question 3

SNS acts via noradrenaline to increase HR by what mechanism?

Answer 3

NA acts on beta receptors to increase cAMP activity, causing increased closure of K channels and opening of sodium channels

Question 4

Most common cause of arrhythmia?

Answer 4

Ischemic heart disease

Question 5

Arrhythmias can be classified by rate or..?

Answer 5

Site of abnormality

Question 6

Define sinus tachycardia

Answer 6

Fast heart rate, but the SA node is still the primary pacemaker so waveform would be normal

Question 7

Appearance of atrial fibrillation on ECG?

Answer 7

Normal looking but irregular QRS + random and chaotic P waves

Question 8

Explain the consequences of atrial fibrillation that can lead to emboli formation

Answer 8

Irregular atrial contractions cause blood to pool in the atria, which can form a clot. The clot can then dislodge and travel to brain

Question 9

Compare atrial flutter and atrial fibrillation

Answer 9

Flutter = regular ventricular contractions 
Fibrillation = irregular

Question 10

HR in atrial fibrillation?

Answer 10

Atria = ~400 
Ventricles= 160-180

Question 11

2 different options for atrial fibrillation?

Answer 11

• rate control (e.g. BB or CCB) and anticoagulant

Question 12

Name the arrhythmia responsible for sudden cardiac death

Answer 12

Ventricular tachycardia

Question 13

Drug + other Tx for treatment and prevention of ventricular tachycardia?

Answer 13

Amiodarone

Electric shock / defibrillation

Question 14

Symptoms of bradycardia?

Answer 14

Palpitations, syncope, fatigue, dizziness, heart failure

Question 15

Compare intrinsic and extrinsic causes of bradycardia

Answer 15

Intrinsic = age, ischaemic heart disease, surgery 
Extrinsic = medications, electrolyte disturbances, metabolic rate

Question 16

Define re-entry arrhythmias

Answer 16

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

Question 17

Define heart block

Answer 17

Ventricular rate much slower than atria due to impairment of the AV node. Complete heart block = atria and ventricles beat independently of one another

Question 18

Define pro-arrhythmic drugs

Answer 18

Drugs that prolong the QT interval

Question 19

Drug used in bradycardia?

Answer 19

Atropine

Question 20

Name 2 potential causes of dysrhymthias

Answer 20

• hypo or hyperthyroidism
• caffeine, sympathomimetic drugs
• heart disease
• electrolyte disturbances

Question 21

Where do sodium channel blockers bind?

Answer 21

To the alpha subunit of the sodium channel, which prevents from being activated while at rest.

Question 22

Explain the MOA of sodium channel blockers

Answer 22

They prevent action potentials by blocking the activation of sodium channels, meaning the cell does not depolarise. This slows the HR down

Question 23

Name 3 sodium channel blockers (one from each class)

Answer 23

Disopyramide, lidocaine, flecainide

Question 24

Which sodium channel blocker has the shortest DOA?

Answer 24

Lidocaine

Preferentially binds to frequently activating channels. Means the drug is more active when the HR is high

Question 25

Compare lidocaine and flecainide

Answer 25

Flecainide has a longer duration of action

Question 26

Do disopyramide and quinidine lengthen the refractory period?

Answer 26

Yes

Question 27

Name 2 beta blockers that are selective for B1

Answer 27

Metoprolol and atenolol

Question 28

Which class is most commonly used for for atrial fibrillation?

Answer 28

Class 1C (e.g. flecainide)

Question 29

Which drug class is used to treat ventricular tachycardia?

Answer 29

Class 1B (lidocaine)

Question 30

How do beta blockers slow HR?

Answer 30

Prevents the binding of noradrenaline to the beta receptor, meaning it reduces the impact of the SNS

Question 31

Beta blockers reduce calcium influx. True or false?

Answer 31

True. Explains why they slow HR (authorhythmic AP) and are negative inotropes

Question 32

Class 3 drugs are..?

Answer 32

Drugs that prolong the cardiac action potential

Question 33

How do class 3 drugs work?

Answer 33

They block depolarisation by K channels which prolongs the action potential and lengthens the refractory period of the sodium channels

Question 34

Drug class that can prevent re-entrant tachycardia?

Answer 34

Class 3

Question 35

Name 1 class 3 drug

Answer 35

Amiodarone

Question 36

Define PR interval

Answer 36

Time between atrial depolarisation and beginning of ventricular depolarisation. Relates to delay at AV node

Question 37

Define QT interval

Answer 37

Depolarisation + contraction of ventricles

Question 38

Class 4 drugs are also known as?

Answer 38

Calcium channel blockers

Question 39

Name 2 calcium channel blockers

Answer 39

Verapamil and diltiazem

Question 40

CCBs increase after-depolarisation arrhythmias. True or false?

Answer 40

False. They reduce this type of arrhythmia

Question 41

MOA of adenosine?

Answer 41

Opens potassium channels, causing hyperpolarisation

Question 42

Which drug can be administered to terminate re-entry tachycardia?

Answer 42

Adenosine.

Question 43

MOA of digoxin?

Answer 43

Inhibits Na/K ATPase which increases intracellular sodium and calcium

Question 44

Is digoxin a positive or negative inotrope?

Answer 44

Positive. Due to increased calcium

Question 45

How is digoxin used for arrhythmias if it is a positive inotrope?

Answer 45

Slows conduction at AV node

Question 46

2 drugs used for bradycardia?

Answer 46

Atropine and isoprenaline

Question 47

MOA of atropine?

Answer 47

Muscarinic antagonist. Prevents PSNS activity | Prevents binding of acetylcholine

Question 48

Isoprenaline MOA?

Answer 48

Beta agonist - sympathomimetic | Increases contractility and heart rate

Question 49

Digoxin inhibition of Na/K ATPase pump causes what?

Answer 49

Increased intracellular calcium = increased contractile strength

Question 50

What activates the funny channel causing it to open?

Answer 50

Hyperpolarisation of the previous action potential