cardio: arrhythmias Flashcards
antiarrythmic drugs: class 1a
sodium channel blockers - moderate:
procainamide, quinidine, disopyramide
antiarrythmic drugs: class 1b
sodium channel blockers - weak:
lidocaine, mexiletine
antiarrythmic drugs: class 1c
sodium channel blockers - strong:
flecainide, propafenone
antiarrythmic drugs: class 2
beta blockers, block sympathetic autonomic effects:
metoprolol
antiarrythmic drugs: class 3
potassium channel blockers, prolong effective refractory period:
amiodarone, sotalol
antiarrythmic drugs: class 4
ccb:
verapamil, diltiazem
antiarrythmic drugs: class 5
other MOA:
digoxin, adenosine, magnesium
normal cardiac rhythm
originates in SA node (frequency: 60-100bpm) -> spreads through the atria and enters the AV node -> AV conduction is low (~0.15s) -> impulse propagates through His-Purkinje system -> ventricular activation complete in <0.1s
arrhythmia
any cardiac depolarisation that deviates from normal rhythm
- abnormality in: site of origin of impulse, rate, regularity, conduction
likely triggers of arrhythmia
ischaemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, excessive catecholamine, autonomic influence, toxicity eg. digitalis, cardiac fibre overstretch, scarred/disease tissue
all arrhythmias result from disturbance in:
impulse formation/conduction, or both
amiodarone primarily class3, but shares
class 1,2,4 properties and additional actions
sotalol primarily class 3, but also
class 2
aim of antiarrhythmics pharmacology
- reduce ectopic pacemaker activity
- modify conduction/refractoriness in re-entry circuits to disable circus activity
MOA of sodium channel blockers
- local anesthesia action blocking sodium channels
- reduce sodium current, slows upstroke of action potential, hence slows conduction
flecainide moa
(class 1c) blocks sodium and potassium channels, no anti-muscarinic effects
flecanide use
pt w normal hearts with supraventricular arrhythmias
X aflutter, ihd, structural heart disease, hfref, liver disease, crcl<35
flecainide toxicity
may cause severe exacerbation of arrhythmia in patients with pre-existing ventricular tachyarrythmias or previous MI
disopyramide MOA
(class 1a)
- blocks sodium channels, slow upstroke of action potential
- nonspecifically blocks potassium channels, prolongs action potential
-> slows conduction
-> directly depresses sa and sv node
extracardiac effects:
- ganglion blocking activities, hence reduce peripheral vascular resistance -> produce hypoTN esp w iv use
amiodarone MOA
(class 3) prolongs action potentials
- usually by blocking K channels or
- sometimes by enhancing inward current eg. thru sodium channels (block sodium channels)
- also weak adrenergic and ccb
-> prolongs action potential duration
-> slow hr and av node conduction
extracardiac effects: produce peripheral vasodilation
dronedarone is a ____ of amiodarone
structural analogue, lacks iodine atoms
- less toxic but less effective alternative
- no thyroid and pulmonary toxicity
amiodarone use
treatment of serious ventricular arrhythmias, effective for supraventricular arrhythmias eg. AF
amiodarone toxicity
- bradycardia
- heart block in pt w existing SA/AV node disease
- fatal pulmonary fibrosis in 1% of pt
- hepatitis
- tissue accumulation: blue-grey skin discoloration, corneal microdeposits
- hypo/hyperthyroidism (source of inorganic iodine)
digoxin MOA
- positive inotropic effects: blocks Na-K ATPase, incr intracellular myocytes Na and hence Ca influx
- negative chronotropic effects: decreases conduction of electrical impulses through the av node inhibition and increases vagal activity
adenosine MOA
used iv for terminating SVT
- acts on adenosin receptors (GPCRs) -> influence potassium channels -> ca channels -> inhibit avail of ca in cells -> decr hyperexcitability and propagation of signals involved in AF
magnesium sulphate/trimagnesium dicitrate (anhydrous) used for
specific arrhythmias eg. torsades de pointes and digoxin-induced
moa of magnesium
exact unclear: Mg competes with Ca in terms of uptake and distribution of Ca within cells
arrhythmias, hr<60
Bradycardia: heart block, simple bradycardia
- atropine, adrenaline, dopamine
Arrhythmias, hr>100, QRS<120ms
Narrow complex (info propogated through AV node into purkinje complex = supraventricular issue):
- AF/flutter: class 3, 1c - or rate control by nodal blocking agents eg. Class 2/4
- Other SVTs: class 2/4
- Sinus tachycardia (MI or anxiety): class 2
Arrythmias, hr>100, qrs>120ms
Broad complex:
- VF: after 3x defibrillation attempts - vasopressin, adrenaline, amiodarone
- VT: amiodarone, class 1b
Supraventricular preexcitation tachycardias of the Wolff-Parkinson-White syndrome
AV node inhibitors (class 2/4) or by catheter ablation of the bypass tract
Arrhythmias of congestive heart failure
Class 2: carvediolol
Class 5: digoxin
Sustained ventricular tachycardia especially with infarcted or ischemic zone
Cardioversion if persistent or amiodarone
Drugs that can cause prolonged QT interval
Antiarrythmics: disopyramide, procainamide, quinidine, amiodarone, sotalol
Anaesthetics: halothane
Antibiotics: macrolides, metronidazole with alcohol, moxifloxacin
Antifungals: ketoconazole, fluconazole
Antivirals: nelfinavir
Antimalarials: chloroquine, mefloquine
Antipsychotics
Antihistamines: terfenadine, astemizole
Antidepressants: amitriptyline
