Anti-arrhythmic Drugs

Question 1

What are the different classifications for anti-arrythmic drugs?

Answer 1

1 = Na antagonists2 = B-blockers3 = K antagonists4 = Ca antagonists

Question 2

Describe class 1

Answer 2

Voltage gated Na+ blockers- decrease conduction velocity- decrease automaticity- increase depolarisation threshold

Question 3

Why are there different sub-classes of class 1 drugs?

Answer 3

Different effects on AP duration, effective refractory period and phase 0 slopeA = increase APD and ERP, moderate decrease in phase 0 slopeB = decrease APD and ERP, small reduction in phase 0 slopeC = no change in APD and ERP, large reduction in phase 0 slope

Question 4

Give a 1a drug

Answer 4

quinidine

Question 5

Give a 1b drug

Answer 5

Lidocaine

Question 6

Give a 1c drug

Answer 6

Flecainide

Question 7

Describe flecainide

Answer 7

Use for SVTsDon’t give in heart failure or with MI historyADRs = dizziness, vision disturbances and arrythmiasDDIs = CYP metabolism and renally excreted

Question 8

Describe lidocaine

Answer 8

Use for ventricular arrhythmias after MIDon’t give in AV block or heart failureADRs = hypotension, bradycardia, nystagmus and seizures

Question 9

Describe class 2

Answer 9

Beta-adrenoceptor blockers- block sympathetic action, decrease slope of pacemaker potential and decrease chronotropy- decreased automaticity- decrease phase 4 slope- increased threshold for activation in SAN and AVN- increase AVN conduction time and refractory period

Question 10

When would you give a bete blockers?

Answer 10

Post MIAnginaHypertension Arrythmias

Question 11

When would you not give a beta blocker?

Answer 11

AV blockHypotensionBradycardiaCongestive Heart Failure

Question 12

ADRs of beta blockers

Answer 12

BronchospasmFatigue and insomniaCold extremitiesBradycardiaHypotensionDecrease glucose tolerance in diabetic patients

Question 13

DDIs for beta blockers

Answer 13

Prevents salbutamol from working - antagonist overrides agonist actionsVerapamil - both are negative inotropes

Question 14

Describe class 3 drugs

Answer 14

Block K+ channels- increases the absolute refractory period and the AP duration- suppresses re-entry circuits by closing excitable gap

Question 15

Why are class 3 drugs not generally used?

Answer 15

Can be arrhythmic and increase the risk of torsades des points.

Question 16

Give some examples of class 3 drugs

Answer 16

AmiodaroneSotalol - high dose (low dose gives a class 2 action)

Question 17

Why would you give class 3?

Answer 17

SVT and other ventricular arrythmias

Question 18

When would you not give a class 3 drug?

Answer 18

AV block

Question 19

DDIs of class 3 drugs

Answer 19

Amiodarone inhibits CYP enzymes and P-glycoprotein- need to reduce other drugs (warfarin, flecainide and digoxin)

Question 20

Describe class 4 drugs

Answer 20

Block Ca2+ channels- decrease slope of pacemaker AP at SAN and AVN- increases refractory period and decreases chronotropy and inotropy

Question 21

Examples of class 4 drugs

Answer 21

Verapamil Diltiazem

Question 22

When would you give class 4 drugs?

Answer 22

SVTProphylaxis for angina and hypertension

Question 23

When would you not give class 4 drugs?

Answer 23

Heart failureBradycardiaAVN block

Question 24

ADRS of class 4 drugs

Answer 24

HypotensionBradycardiaHeart failureHeart block

Question 25

Describe adenosine

Answer 25

AVN blocker- decrease automaticity- increases AVN refractory period- short t1/2- diagnoses and treats SVT

Question 26

Describe the mechanism for digoxin

Answer 26

Inhibits Na/K/ATPase which also inhibits Na/Ca exchanger. - increased intracellular Ca2+ causing an increase in inotropy Increases AVN refractory period and decreases conduction velocity of AVN

Question 27

ADRs of digoxin

Answer 27

Narrow therapeutic index, can easily lead to digoxin toxicity- cardiac toxicity (bradycardia, AVN block, atrial tachycardia)- toxicity is enhance with hypokalaemia

Question 28

What are the main ways to improve ventricular stroke volume and therefore the cardiac output?

Answer 28

- Increase pre-load- Decrease after-load- Increase inotropy

Question 29

Why is increasing pre-load not a good option for someone in heart failure?

Answer 29

- Heart is on flat region of frank-starling curve- Can exacerbate pulmonary and systemic congestion or oedema

Question 30

Describe how decreasing afterload helps to increase ventricular stoke volume

Answer 30

An increased afterload will reduced ejection velocity. Treating this will hale to increase stroke volume and decrease the pre-load which will help in improving the ejection-fraction.

Question 31

How does increasing inotropy help to improve ventricular stroke volume?

Answer 31

Increases stroke volume and ejection fraction. - Should only be used for acute systolic failure/ end stage failure as prolonged use can worsen outcomes and increase mortality. - Increase oxygen demand in the long term which is bad in the long term- Good acutely, as they increase stroke volume and ejection fraction but also decrease preload.