Q2 antiarrhythmic drugs
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Most common arrhythmia
How many fascicles do the LBB and RBB have?
- LBB: 2 (anterior, posterior)
- RBB: 1
Is RBBB clinically significantly?
Is LBBB clinically significant?
- Yes - indicates that both fascicles knocked out --> extensive myocardial damage
- Often seen in advanced HF, coronary disease, MIs
What phases of the AP are repolarizing phases?
- 1 (K+ out)
- 3 (K+ out rapidly)
What phase of the AP is the depolarizing phase?
What phase of the AP is the plateau phase?
What is response for maintenance of phase 4?
- Na+/K+ ATPase pump
- Na+ out
- K+ in
What phases of the AP are associated with Ca2+ coming into the cell?
What ion enters the cell rapidly in phase 0 of AP?
Cause of early afterdepolarizations
QT prolonging drugs
Cause of late afterdepolarization
3 mechanisms of cardiac arrythmias
- Enhanced automaticity
Atrial re-entry arrhythmia associated with multiple reentry circuits and the one with one large big reentry circuit in atrium
- Multiple reentry circuits: atrial fibrillation
- One big circuit: atrial flutter
Early afterdepolarization affects what phase?
Late afterdepolarization affects what phase?
QT intervals begins where and ends where?
- Beginning of QRS complex
- End of T wave
3 mechanisms of anti-arrhythmic drugs
- Slowing or abolition of automatic rhythms
- Blocking of impulse propogation in re-entry
- Prevention or blocking of EADs and DADs
Vaughan Williams Classification of Antiarrhythmic Drugs
- I: Na+ channel blockade
- II: β blockade
- III: K+ channel blockade
- IV: Ca2+ channel blockade
Action of class I (Na+ channel blockade) on phase 0
Reduces phase 0 slope and peak of action potential
Action of class II (β blockade)
Block sympathetic activity --> reduction of rate and conduction
Action of class III (K+ channel blockade)
Delay phase 3 --> increase of action potential and increases refractory period (QT prolongation)
Action of class IV (Ca2+ channel blockade)
- Blocks L-type channels
- Reduces rate and conduction
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