Pharma9😍😍 anti arrhythmia

Question 1

Class I

Na + Channel Blockers

Answer 1

Ia Quinidine

Ib Lidocaine
Ic Flecainide

Question 2

B bolckers

Class2

Answer 2

Atenolol
Bisoprolol
Metoprolol

Question 3

Class3

Answer 3

Ap prolongers
Amiodarone
Sotalol

Question 4

Class 4

Answer 4

Ca blockers
Diltiazem
Verapamil

Question 5

Class 1👾👾generally

Answer 5

— 🌺Mainly block fast Na + channels —➡️ phase 0
🌺Weak K + channel block (1a) — 
🌺⬇️C onduction velocity — 
🌺⬇️D epolarisation amplitude — 
🌺⬇️automaticity — 
🌺⬇️ phase 4 slope — ­ 
🌺⬆️Depolarisation threshold — 
🌺Alter duration of action potential

Question 6

Class Ia e.g. Quinidine

Intermediate Na + Block
🤷🏻‍♀️حجي

Answer 6

­

⬆️Action Potential Duration
⬆️Effective Refractory Period

Question 7

Class Ib e.g. Lidocaine

Weak Na Block
🤷🏻‍♀️

Answer 7

⬇️Action Potential Duration
⬇️ffective Refractory Period
• Dissociates rapidly in time for next AP ,given by intravenously as high metabolism rate.

🤷🏻‍♀️ s sometimes used following MI if patient shows signs of ventricular tachycardia
💥 • Only blocks voltage gated Na + channels in open or inactive state

• Damaged areas of myocardium may be depolarised and fire automatically
• More Na + channels are open in depolarised tissue

– lidocaine blocks these Na + channels

– prevents automatic firing of depolarised ventricular tissue

• Not used prophylactically following MI

Question 8

Class Ic e.g. Flecainide

Strong Na Block
شوية حجي عنه

Answer 8

No changes in Action Potential Duration

No changes in Effective Refractory Period

Question 9

Lidocaine 🤮

Answer 9

Negatively ionotropic Seizures Nystagmus

Question 10

Flecainide 👾+🤷🏻‍♀️

Answer 10

Class 1c agent — Also blocks outward K + channels — Long dissociation half life ~ 10 s — Binds open Na + channels only
⬆️PR, QRS and QT intervals at normal rates
⬆️action potential in atrial tissue at fast rates

Question 11

Flecainide pk

Answer 11

Well absorbed orally Metabolised by CYP2D6 & renal elimination Elimination t 1/2 10-18 hours

Question 12

Flecainide use+🤮

Answer 12

Prophylaxis and treatment of SVT/PAF(paroxysmal AF)
Mean to maintain the sinus rhythm

Contraindicated with history of IHD/HF – Causes lethal dysrhythmias

Question 13

Class 2

Answer 13

— Thus β blockers 🔷⬇️intracellular Ca ++ levels
🔷⬇️ — automaticity —
🔷⬇️phase 4 slope —
🔷⬆️­ threshold for activation in SAN & AVN — ­
🔷⬆️AVN conduction time & refractory period —
💥Non-selective vs β 1 selective —
💥💥💥Negatively chronotropic & ionotropic

Question 14

Non-selective b blocker

Answer 14

Non-selective

Propranolol Sotalol

Question 15

b 1selective

Answer 15

b 1selective

Longer Acting Atenolol Bisoprolol

Shorter Acting Metoprolol Nebivolol Esmolol

Question 16

Mixedb 1 a1

Answer 16

Mixedb 1 a1

Carvedilol Labetalol

Question 17

B blocker 🤮🤮

Answer 17

Heart failure

Bradycardia,,Bronchospasm ,,Peripheral limb ischaemia ,,Loss of hypoglycaemic symptoms,, Fatigue

Question 18

B blocker use

Answer 18

Rate control of AF/Atrial flutter ,,Cardioversion AVRT/AVNRT ,,2°prevention VT/VF ,,💥Heart failure ,Hypertension ,💥Ischaemic Heart Disease
🌺 • Used following myocardial infarction
– MI causes increased sympathetic activity
• β-blockers prevent ventricular arrhythmias

– arrhythmias may be due to increased sympathetic activity
• also reduce O 2 demand

– reduce myocardial ischaemia

– beneficial following MI

Question 19

Class 3 🤷🏻‍♀️+💋

Answer 19

— ◾️⬆️­ action potential duration —
◾️Block slow outward K + channels

— ◾️⬆️refractory period — ­
◾️⬆️QT interval —
◾️Suppress re-entry circuits
◾️ However can ­ ⬆️risk of early after depolarisation leading to torsade de pointes
💥💥 Most commonly used are amiodarone & sotalol

Question 20

Amiodarone

Answer 20

All classes of action — Acute
◾️Blocks fast Na + and Ca 2+ channels – Class I & IV action Use dependent
◾️Blocks acetylcholine gated K + channels - Class II action
◾️Less negatively ionotropic than Class I/II/IV agents

— Chronic

🔸Blocks outward K + channels – Class III action
🔸Inhibits cell-cell coupling Prolongs action potential duration & refractory period Slows AV node conduction 🔸Prolongs QT interval

Question 21

Amiodarone 🤮🤮🤮

Answer 21

🔺short term
Phlebitis & hypotension with iv administration Requires central access when given iv
🔺long term
Pulmonary fibrosis ,Hypo/hyperthyroidism ,Hepatic dysfunction ,Corneal microdeposits ,Slate grey skin/photosensitivity, Peripheral neuropathy, Proximal myopathy ,Increases defibrillation threshold for ICDs
🔺drug interaction
Inhibits CYP Dose reductions of warfarin, digoxin and flecainide may be required

Question 22

Amiodarone use

Answer 22

🔸acute indication
Atrial Fibrillation Atrial Flutter Ventricular Tachycardia When other antiarrhythmics contraindicated
🔸chronic indication
2°prevention of VT/VF When other antiarrhythmics not tolerated
لكل الاريذيميا مال الاتريا والفنتريك ولمن البقية ما اكد استعملهن😁

Question 23

Sotalol 👾

Answer 23

— 🔺Racemate —
🔺d-sotalol pure class III agent —
🔺l-sotalol has b blocker and class III action —
Blocks outward K + channels —
Reverse use dependence —
Lowers defibrillation threshold for ICDs — 🔸Doses < 120mg bd has mainly b blocker action —
🔸Higher doses have class III action

Question 24

Sotalol 🤮🤮+use

Answer 24

b blocker adverse effects Torsades de pointes

— Clinical use

Paroxysmal AF

Question 25

Class 4 👾👾+🤷🏻‍♀️

Answer 25

— 🔺Diltiazem & verapamil 
🔺block slow inward Ca 
🔺— Slow phase 4 depolarization — 
🔺Slow conduction velocity — 
🔺Increase refractory period on AVN
They are non-dihydropyridine

Question 26

Verapamil🤷🏻‍♀️

Answer 26

iv or oral Sustained release preparations Negatively ionotropic Drug interactions with digoxin & amiodarone

Question 27

Diltiazem 🤷🏻‍♀️

Answer 27

Less negatively ionotropic than verapamil Sustained release preparations

Question 28

Class 4 use +🤮🤮

Answer 28

Bradycardia Heart failure Constipation
🔺use
Rate control of AF 
Cardioversion of AVRT/AVNRT 
Antianginal/antihypertensive

Question 29

Adenosine

Answer 29

🔸Main action as an AV node blocker

— 🔸Activates A 1 receptors in the heart — A 1 receptors are G i linked ➡️Inhibits adenylate cyclase ➡️⬇️cAMP levels
🔸 — Activates Ach K + channels in SAN and AVN ➡️Hyperpolarises cellsالخلية تنزل بالسالب

— 🔸Reduces automaticity, increases AVN refractory period —
🔸t 1/2 » few seconds —
🤮🤮Associated with transient chest tightness

— 💊Used as an iv bolus to diagnose/treat SVTs

Question 30

Digoxin effects😁😎

Answer 30

🔘direct cardiac effect
Inotropy and automaticity are subsequently increased while conduction velocity is reduced.

🔘cns effect
 ⬇️SNS outflow ­ 
⬆️PNS outflow (parasympathetic)
Sensitizes baroreceptor reflex 
🔘combined 
⬇️Automaticity of SAN and AVN 
⬆️­ Refractory period of AVN (like heart blook)
⬇️Conduction velocity of AVN

Question 31

Digoxin 🤮🤮

Answer 31

🔷 — Narrow therapeutic index
🔷Toxicity enhanced with ⬇️plasma K +

🔷cardiac toxicity
Bradycardia ,,Atrial/ventricular/junctional ectopics ,,AVN block ,,Atrial tachycardia with AVN block ,,Accelerated idioventricular tachycardia
🔷sx of toxity
Delerium, fatigue, confusion, nausea, vomiting anorexia, diarrhoea, blurred & yellow vision (xanthopsia)
🔷Severe toxicity can be treated with antibody fragment therapy (Digibind

Question 32

Digoxin use

Answer 32

— Main use is rate control in atrial fibrillation — ,,Heart failure — ,No mortality benefit

Question 33

Magnesium

Answer 33

Magnesium

— 🔘iv Mg 2+used to treat Torsades de Pointes

— 🔘Also digoxin toxicity —
🔘Mechanism of action unknown
— 🔘No benefit to chronic administration