Pharma9😍😍 anti arrhythmia Flashcards
Class I
Na + Channel Blockers
Ia Quinidine
Ib Lidocaine
Ic Flecainide
B bolckers
Class2
Atenolol
Bisoprolol
Metoprolol
Class3
Ap prolongers
Amiodarone
Sotalol
Class 4
Ca blockers
Diltiazem
Verapamil
Class 1👾👾generally
🌺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
Class Ia e.g. Quinidine
Intermediate Na + Block
🤷🏻♀️حجي
⬆️Action Potential Duration
⬆️Effective Refractory Period
Class Ib e.g. Lidocaine
Weak Na Block
🤷🏻♀️
⬇️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
Class Ic e.g. Flecainide
Strong Na Block
شوية حجي عنه
No changes in Action Potential Duration
No changes in Effective Refractory Period
Lidocaine 🤮
Negatively ionotropic Seizures Nystagmus
Flecainide 👾+🤷🏻♀️
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
Flecainide pk
Well absorbed orally Metabolised by CYP2D6 & renal elimination Elimination t 1/2 10-18 hours
Flecainide use+🤮
Prophylaxis and treatment of SVT/PAF(paroxysmal AF)
Mean to maintain the sinus rhythm
Contraindicated with history of IHD/HF – Causes lethal dysrhythmias
Class 2
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
Non-selective b blocker
Non-selective
Propranolol Sotalol
b 1selective
b 1selective
Longer Acting Atenolol Bisoprolol
Shorter Acting Metoprolol Nebivolol Esmolol
Mixedb 1 a1
Mixedb 1 a1
Carvedilol Labetalol
B blocker 🤮🤮
Heart failure
Bradycardia,,Bronchospasm ,,Peripheral limb ischaemia ,,Loss of hypoglycaemic symptoms,, Fatigue
B blocker use
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
Class 3 🤷🏻♀️+💋
◾️⬆️ 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
Amiodarone
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
Amiodarone 🤮🤮🤮
🔺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
Amiodarone use
🔸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😁
Sotalol 👾
🔺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
Sotalol 🤮🤮+use
b blocker adverse effects Torsades de pointes
Clinical use
Paroxysmal AF
Class 4 👾👾+🤷🏻♀️
🔺Diltiazem & verapamil 🔺block slow inward Ca 🔺 Slow phase 4 depolarization 🔺Slow conduction velocity 🔺Increase refractory period on AVN They are non-dihydropyridine
Verapamil🤷🏻♀️
iv or oral Sustained release preparations Negatively ionotropic Drug interactions with digoxin & amiodarone
Diltiazem 🤷🏻♀️
Less negatively ionotropic than verapamil Sustained release preparations
Class 4 use +🤮🤮
Bradycardia Heart failure Constipation 🔺use Rate control of AF Cardioversion of AVRT/AVNRT Antianginal/antihypertensive
Adenosine
🔸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
Digoxin effects😁😎
🔘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
Digoxin 🤮🤮
🔷 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
Digoxin use
Main use is rate control in atrial fibrillation ,,Heart failure ,No mortality benefit
Magnesium
Magnesium
🔘iv Mg 2+used to treat Torsades de Pointes
🔘Also digoxin toxicity
🔘Mechanism of action unknown
🔘No benefit to chronic administration
