Mechanistic approach to treatment of dysrhythmias Flashcards
How are bradydysrhythmias treated
Need to modify autonomic input
- anticholinergics
- beta blockers
- pacemakers
How are tachydysrhythmias treated
Increase automaticity
- decrease rate of depolarisation
- increase resting membrane potential (makes it more negative)
- make action potential threshold less negative
- treated by use of antidysrrhythnmic drugs
How are re-entrant rhythms treated
- increasing refractory period
- decreasing conduction velocity
How is triggered activity treated
- shorten action potential duration
- correct conditions of calcium overload
What are the signs of AF
- multiple re-entrant loops
- 350-600 action potentials per minute
- irregularly irregular pulse (fast or slow)
- loss of clear p waves on ECG
- thrombi
What are the different classes of antiarrhythmic drugs
- class 1- Na+ channel blockade
- Class 2- B-adrenergic receptor blockade
- class 3- K+ channel blockade
- Class 4- Ca2+ channel antagonists
when are voltage gated sodium channels closed
at resting potential
when are voltage gated sodium channels open
in response to a nerve impulse, the gate opens and sodium enters the cell
when are voltage gated sodium channels inactivated
for a brief period following activation, the channel does not open in response to a new signal
How do Class 1 antiarrhythmic drugs work
bind to open or inactivated Na+ channels
What category in class 1 drugs are mainly used to treat cardiac dysrhythmias
main drugs used are class 1C
What is the difference between class 1A, 1B, and 1C drugs
- 1A is a moderate Na+ channel block, with prolonged repolarisation
- 1B is a mild Na+ channel block with shortened repolarisation
- 1C is a marked Na+ channel block with no change in action potential duration
Explain how an Na+ channel blockade reduces re-entry
Decrease Phase 0 upstroke velocity and reduces conduction velocity, which decreases re-entry
What can trigger dysrhythmias
stress and emotion can trigger dysrhythmias (MI)
How do class 2 beta blockers decrease automaticity and re-entry
Decrease cardiac rate and increase refractory period in AV node
Reduce excitability in the ventricles
When are class 2 beta blockers used
- to control ventricular rate in AF or atrial flutter
- Post MI to reduce effects of adrenaline on damaged myocytes
- to treat re-entrant rhythms which use AV node
- eg. metoprolol, atenolol
what is the risk with class 2 beta blockers
Possible conduction block or bradycardia
Explain how class 3 Potassium channel blockers work
prolong the action potential and increase refractory period and therefore decrease re-entrant rhythms and return rhythm to a normal sinus rhythm
When are class 3 Potassium channel blockers used
Used to treat WPW and both atrial and ventricular fibrillation
Give examples of Class 3 potassium channel blockers
amiodarone, dronedarone, sotalol
What is the risk of using class 3 potassium channel blockers
may precipitate Torsades de Pointes
Describe the chemical structure of amiodarone
-Resembles thyroxine
- CYP3A4 main route for metabolism, metabolite active
- both amiodarone and metabolite have long half lives
how is amiodarone excreted
hepatic excretion
Describe the chemical structure of dronedarone
- No iodine so no thyroid side effects
- less lipophilic than amiodarone so its half life is shorter and so is the half life of its active metabolite
