Anti-arrythmics Flashcards
What are the possible underlying causes of arrhythmias?
Disorders of impulse formation:
Automaticity
Triggered activity
Disorder on impulse conduction:
reentry
Combination of both
What is automacity?
Ability of the cardiac cell to initiate an impulse without need a prior stimulation:
–> For sinus node and other focal pacemaker cells this is normal but can be enhanced and lead to an accelerated rate.
Cells that do not normally initiate an impulse can do so:
–> Multiple possible mechanisms (changes in K channels, increased Ca release from SR activating different Ca or N channels, etc)
What is triggered activity?
Impulse initiation in cardiac fibres caused by depolarizing oscillations within in membrane voltages (after depolarization). They are the consequence of preceeding action potential(s):
Early afterdepolarization (EAD) Delayed afterdepolarization (DAD)
When large enough to reach threshold, will trigger an action potential.
What are the classes in Vaughn-Williams classification?
Class 1: Na channel blockers
- Membrane stabilising. Slow the rate of depolarization and may inhibit the arrhythmia by decreasing the cells responsiveness to excitation
Class 2: Cathecholamine blockade (b-blockers)
Class 3: K channel blockers
- Increasing in refractory period
Class 4: Calcium channel blockade
-Depress inward Ca current, prolonging conduction and refractoriness.
Some block potassium channels
How many subgroups are there for Class 1?
Class 1A - quinidine, procainamide Class 1B - lidocaine, (being replaced by amiodarone ie. class 3) Class 1C - propafanone, fleicainide
What is procainamide?
Class 1A drug
How does procainamide work?
Prolongs the action potential duration and refractoriness of atrial and ventricular tissue.
What is procainamide used for?
Used in both supraventricular and ventricular arrhythmias.
–> Atrial fibrillation in WPW
What is a side effect of procainamide?
Prolonged QT/Torsades de pointes
Hemolytic anemia, thrombocytoepnia, neutropenia
Hypotension
SLE like syndrome
How does lidocaine work?
Increases the stimulation threshold and leads to suppression of automaticity (esp in Purkinje fibres)
Shortens the action potential duration and also can shorten QT in diseased tissues
- -> Used commonly for VF in ACS
- -> NOT GOOD FOR SUPRAVENTRICULAR
- -> good for post-MIs
What are side effects of lidocaine?
Hypotension, bradycardia
Neurological (confusion, headache, tremor, somnolence)
Seizure
What is Flecainide/Propafenone used in?
Used mainly for Atrial fibrillation. Also may have a use in PVCs.
What additional drud needs to be coadminitered with Flecainide/Propafenone?
Needs to be used with a B-blocker. (1:1 atrial flutter causing increased ventricular rate)
What are some risks using class 1C drugs?
Increases mortality in post MI patients, therefore not used in patients with ischemic heart disease. Also not used if any structural heart disease.
Increased risk of ventricular arrhythmias in chronic atrial fibrillation
What are class 2 drugs work?
Beta-blockers:
1) Blocks the sympathomimetic amine effects on Ifunny currents (phase 4) of nodal tissues. SA node: slowing HR AV node: prolonging refractory period. Terminating SVT (re-entry) Decrease ventricular response
2) Attenuation of sympathetic electrophysiological consequences Shortening of action potential duration Augmenting ventricular conduction Increasing vent. Automaticity Decreasing VF thresholds Reversal of anti-arrhytmic drugs
What are Class 3 drugs?
Potassium channel blockers
How do class 3 drugs work?
Action on phase 3 of AP waveform
–> Delays repolarization, lengthens APD
What is the drug of choice for ventricular arrythmias?
Amiodarone
Also used for: For A.fib/fl:
Ventricular rate control
Conversion to SR
Maintaining SR**
What is the first line antiarrythmic agent in cardiac arrest?
amiodarone
What are the effects of amiodarone?
Multiple actions
K, Na, Ca channels, B-blocker, CCB
What kind of monitoring should be done for amiodarone?
Pulmonary toxicity/infiltrates/hypersensitivity
–> Q3-6 month PFTs
Thyroid
–> Hypo and hyperthyrois
TSH at baseline and q 3-6 months
Liver cirrhosis is rare
–> Follow liver enzymes, stop if > 3x normal
Ocular
–> Microdeposits common and not required to discontinue
Optic neuritis/atrophy leading to vision loss
Blue skin pigmentation
Prolonged QT
What are class 3 drugs?
amiodarone and sotalol
What are effects of sotalol?
K channel and B-blocker effects
What is solatol used for?
Also used in Atrial fib and Ventricular tachycardias
T or F: sotalol has less side effects
T but…
Increased risk of torsades de pointes due to increased effect on QT (need to check QT on ECG 1 week after initiation)
Caution in EF< 40%
How does Adenosine work?
electrophysiological effects like ACh
decreases sinus rate; decreases A-V conduction
useful for supraventricular tachycardias
What is an example of cardiac glycoside?
Digoxin
How does digoxin work?
Direct action:
blocks Na/K atpase –> Increased intracellular Na –> decreased activity of Na/Ca exchanger (Na in for Ca out) –> increased intracellular Ca. More intracellular Ca for future muscle contractions.
- Increased contractility and excitability
Indirect action: increased vagal tone
Decreased impulse generation and propagation in nodal tissue
What is digoxin’s use?
occasionally used for atrial fibrillation
associated increases in contractility (CHF)
T or F: digoxin toxicity is common
T
What side effect may digoxin cause?
heart blocks, arrhythmias, enhancement of effects seen
with therapeutic dose and generation of
early and delayed afterdepolarizations
