CPTP antiarrhyth Flashcards
Describe the cardiac action potential cycle
Phase 4 - spontaneous diastolic drift. Na+&Ca2+ entry. SAN, AVN and Purkinje
Phase 0 - Na+ channel opens at threshold potential. Fast Na+ entry. Na+ channel closes as potential less negative
Phase 1/2 - Slow Ca2+ entry
Phase 3 - K+ exit
Causes of arrhythmia
Abnormal impulse generation
- abnormal pacemaker activity
- triggered activity
Abnormal impulse conduction
- heart block
- re-entry phenomenon (re-excitation of a region of the heart by a single electrical impulse)
Types of bradyarrhythmia (slow HR)
Sinus bradycardia
Nodal/ junctional bradycardia (caused by the absence of the electrical impulse from the sinus node)
Heart block (1st, 2nd and 3rd)
Drugs to treat bradycardia
Atropine
Isoproterenol
Pacing
Atropine
mechanism of action
- Naturally occurring antimuscarinic alkaloid
- Blocks vagal inhibition of Sinus and AVN
- IV bolus administration
- Predominantly hepatic metabolism
- Short half-life
Atropine side effects
anticholinergic adverse effects
- dry mouth
- mydriasis
- postural hypotension
Isoproterenol (isoprenaline)
mechanisms of action
- B1/2 adrenoceptor agonist
- Positive chronotropic effect, esp. Sinus node
- Short half-life requiring IV infusion (also first pass metabolism)
Isorpoterenol side effects
Sympathomimetic adverse effects
- tachycardia
- arrhythmias
Types of tachyarrythmias (fast HR)
Supraventricular tachycardia (SVT)
Ventricular tachycardia (VT)
Describe SVT
- Sinus or nodal tachycardia
- Accessory pathway re-entrant tachycardias
- Atrial fibrillation or flutter
- Narrow complex
- Arise in SAN, atria or AVN
- Not usually life-threatening
Describe VT
-Can be monomorphic/ polymorphic
- Broad complex
- Arise in Purkinje fibres or ventricle
- Can cause cardiac arrest
Antiarrhythmic drugs classification
Class I
local anaesthetics/ sodium channel blockers/ membrane stabilisers/ inhibit phase 0 depolarisation
Class II; antisympathetic drugs
Class III; potassium channel blockers, inhibit phase III repolarisation
Class IV; Calcium channel blockers, inhibit Ca-dependent depolarisation
Class V
cardiac glycosides (vagolytic)
adenosine (antipurinergic)
magnesium sulphate
Class 1a
effect on action potential duration and examples
Lengthen action potential duration and refractory period
Quinidine, propafenone, disopyramide
Class Ib
effect on action potential duration and examples
Shorten action potential duration and refractory period
Lignocaine, lidocaine
Class Ic
effect on action potential duration and examples
no effect on action potential duration and refractory period.
Delay coinduction velocity in Purkinje fibres
Flecainide
Class Ib - lidocaine
actions
blocks fast sodium channels and slows phase 0 depolarisation
shortens action potential duration
specific effect on rapidly depolarising tissue (use-dependent effect)
lidocaine pharmacokinetics
- Short half-life (must be given IV)
- Not absorbed via oral route (hepatic first pass metabolism
- Hepatic clearance decreased in elderly, heart failure, liver disease
lidocaine side effects
hypotension, heart block
neurotoxicity, fits
Class II drugs
Beta blockers
- non-cardioselective; propranolol
- cardioselective (B2); Atenolol
Others
Bretyllium (BP lowering drugs)
Class III drug
e. g. amiodarone
- prolongs action potential duration and refractory period
- lengthened QT interval on ECG
- Long half-life
- Hepatic metabolism
Amiodraone side effects
- thyroid disturbances
- pulmonary fibrosis
- pro-arrhythmia and torsade de pointes
- peripheral neuropathy
- hepatitis
- blue-grey skin discolouration
CCB
Dihydropyridines
e.g. nifedipine, amlodipine
arterial vasodilation
Benzothiazepines
e.g. diltiazem
mixed vascular and cardiac effects
Phenylalkylamine
e.g. verapamil
negative inotrope and chronotrope, antiarrhythmic
cardiac glycoside
example
actions
indications
e. g. digoxin
- antiarrhythmic; vagotonic effect reduces rate and conduction velocity in sinus and AVN
- inotropic-increases intracellular Ca2+
