Arrhythmia Drugs Flashcards
Why do arrhythmias from?
Defects in impulse formation
Defects in impulse conduction
What are some defects in impulse formation?
Altered automacity
Triggered activity
What is physiological altered automacity?
Regulation of SA node activity by autonomic nevrous system
What is pathological altered automacity?
Latent pacemaker establishes HB instead of SA node (ectopic heart beat)
What are some causes of establishment of latent pacemaking?
If latent pacemaker fires at rate faster than SA node
If SA node firing frequency is pathologically low
What are some causes of latent pacemaker firing at rate FASTER than SA node?
Increased sympathetic acitvity, hypokalaemia and ischaemia trigger compensatory mechanisms in potential latent pacemakers i.e. cardiac myocytes
What are some causes of SA node firing frequency is pathologically low?
Ischaemia i.e. right coronary artery - no blood supply to SA node
Circulatory hormones i.e. hypothyroidism
Hypokalemia
What is triggered activity?
Afterdepolarizations triggered by normal action potential, two types
Early after depolarizations
Delayed after depolarizations
When do early after depolarisation occur?
Phase 2 (terminal plateau) - AD mediated by Ca2+ L type channels Phase 3 (repolarization) - AD mediated by K+ channel opening (usually closed at this stage)
TRUE/FALSE
Delayed after depolarizations are associated with drugs such as sotalol
FALSE
EADs associated with sotalol - drugs that lengthen QT interval (Ventricular systole) and prolonging AP
When do delayed after depolarisation occur?
Occurs after complete repolarization
Caused by transient inward current involving Na+ channels
TRUE/FALSE
Delayed after depolarizations are associated with drugs such as digoxin
TRUE
Digoxin reverses action of Na+/K+ pump, allowing Na+ to enter cell. This results in activation of Ca2+ channels which provokes DADs
What are some causes of defects in impulse CONDUCTION?
Re-entry
Conduction block
Accessory tracts
What is a re-entry circuit?
Defect in self sustaining electric circuit with parallel conduction, resulting in cyclical stimulation of myocardium.
Caused by unidirectional block or slowed retrograde conduction velocity
What is heart block?
Fault in heart’s natural pacemaker due to block in electrical conduction (can be due to ischaemia , fibrosis etc)
What is partial block?
Tissue conducts all impulses, but more slowly than usual. Example is first degree AV block
What is intermittent block?
Tissue conducts some impulses but not others. Example is second degree AV block
What is Mobitz T1?
Type of second degree heart block. PR interval (atrial systole) lengthens from cycle to cycle until AV node fails and VENTRICULAR beat is missed.
What is Mobitz T11?
Type of second degree heart block.
PR interval is CONSTANT but every nth ventricular depolarization missing
What is complete block?
No impulses are conducted through affected area. Example is third degree AV block.
Atria and ventricles beat independently, governed by separate pacemakers.
What is the significance of accessory tract pathways
Impulse conducted faster through accessory pathway than through AV node
predispose to reentrant loops and tachyarrhythmia
What is disopyramide?
Class IA anti-arrhythmic drug
What is lignocaine?
Class IB antiarrhythmic drug
What is flecainide
Class IC antiarrhythmic drug
What is the Vaughn Williams classification of antiarrhythmic drugs?
Class 1 stimulates Na+ channels Class 2 inhibits B-adrenoreceptors Class 3 stimulates K+ channels class 4 stimulates Ca2+ channels
What does Class IA anti-arrhythmic drug do?
Associates with disassociates with Na+ channels at MODERATE rate.
Slow rise of AP (velocity)
PROLONGS refractory period.
This works to PREVENT REENTRY
What does Class IB anti-arrhythmic drug do?
Associates with and disassociates with Na+ channels at FAST rate.
Depresses conduction velocity
This works to PREVENT PREMATURE BEATS and treat ventricular tachycardia
What does Class IC anti-arrhythmic drug do?
Associates with and disassociates with Na+ channels at SLOW rate.
STRONGLY depresses conduction velocity (phase 0)
This leads to -ve chrono and inotropic effects
TRUE/FALSE
Class I drugs bind preferentially to areas of the myocardium where AP firing frequency is highest
TRUE
During tachyarrhythmias Na+ channel spends most time in OPEN and ABSOLUTE inactivated state.
How does adenosine work?
Stimulates A1 (adenosine) receptors in AVN
Opens GIRK channels (G protein coupled inwardly rectifying K+ channels) in the atrioventricular node
This HYPERPOLARIZES cells and slows conduction in the AVN.
TRUE/FALSE
Adenosine is not used to terminate paroxysmal supraventricular tachycardia
FALSE
it is, slows conduction in AV node
TRUE/FALSE
Paroxysmal supraventricular tachycardia is caused by reentry
TRUE
What is the action of the Na+/K+ pump?
3 na+ pumped out of cell
2 K+ pumped into cell
What is the mechanism of digoxin?
Inhibits Na+/K+ pump which results in more intracellular sodium
This activates the Ca2+/Na+ exchanger which increases intracellular Ca2+ levels
SOMEHOW indirectly causes inc. vagal activity
TRUE/FALSE
Digoxin increases sympathetic activity to the heart and Is therefore contraindicated in the treatment of AF
FALSE
Digoxin actually increases vagal activity to the heart, the mechanism is unknown.
It IS used to treat AF
TRUE/FALSE
Adenosine and Digoxin BOTH slow conduction in the AVN node
TRUE
Digoxin through stimulating vagal activity
Adenosine due to stimulation of A1 receptors (adenosine receptors) and GIRK (causing efflux K+ and hyperpolarizing cell)
Why is digoxin used to treat atrial fibrillation & atrial flutter?
In AF&AF atria beats at such high rates that ventricles can only irregularily follow (chaotic reentry impulse)
Slowing the conduction of this impulse, slows and strengthens ventricular beat
What is the mechanism of Verapamil?
blocks L-type voltage-activated Ca2+ channels
Slows conduction and prolongs refractory period in AV node and bundle of His
TRUE/FALSE
Verapamil should be used with great caution in combination with other drugs that have a negative ionotropic effect
TRUE
can cause heart block in high dose - POWERFUL effect on AVN node conduction and already has negative inotropic effect - CAUTION with cumulative inotropic effects
Why has adenosine replaced verapamil in treatment of supraventricular arrhythmias ?
Its safer, adenosine used for acute treatment, but verapamil used for prophylaxis
What is lignocaine mainly used to treat?
Ventricular arrhythmias and premature beats - IV admin
What is flecainide mainly used for?
prophylaxis of paroxysmal atrial fibrillation
What is the main difference in pharm. use of disopyramide and procainamide?
Disopyramide is used (orally) to prevent recurrent ventricular arrhythmias,
procainamide (IV) to treat ventricular arrhythmias following myocardial infarction
What are some problems associated with beta blockers?
excessive supression sympathetic drive that may trigger VT
How do beta blockers work?
Control SVT by suppressing impulse conduction through the AV node
TRUE/FALSE
Sotolol is a beta blocker
FALSE
it is a Type 3 agent (K+ blocker)
How do class 3 drugs work?
block of voltage-activated K+ channels
slow repolarization of the AP =increase action potential
inc. duration the effective refractory period
TRUE/FALSE Amiodarone has class IA, II and IV actions and also blocks β-adrenoceptors
True it is a class 3 drug but does other stuff 2
Amiodarone is WAY more effective than other drugs, why is it not used in the long term?
Long term use side effects pulmonary fibrosis thyroid disorders photosensitivity reactions peripheral neuropathy
