Arrythmias (pathophysiology) Flashcards
Pacemaker cells (SA/AV node)
Specialized, non-contractile cells
Depolarized
High automaticity
Ca dependent spikes
Ventricular myocytes
Contractile cells
hyperpolarized
low automaticity
Na dependent spikes
PLATUE PHASE
Re-entry arrhythmia
ischemic damage on one of the sides causes no signal from that side leading to no cancellation
during the relative refractory period, this lack of cancellation can create another trigger signal to fire again without the SA/AV node
Re-entry requirements
multiple parallel pathways
unidirectional block
conduction time > than ERP
Class 2: BB
slow pacemaker and Ca currents in SA/AV node
increase refractories in SA/AV node
increase PR interval
Indications of BB
arrhythmias involving catecholamines
atrial arrhythmias–> protects ventricular rate
post MI prevention of ventricular arrhythmias
prophylaxis in long QT syndrome
Graphs for class 2 and 4
BB no reduction in peak shift to the right
CCB has a reduction in the peak
Class 4: CCB
Selective block for channels opening more frequently
Increase refractoriness of AV node
Increase PR interval
Block reentrant arrhythmias involving AV node
Atrial arrhythmias–>protect ventricular rate
Class 1A
Mix block of Na and K channels
Blocks open state
Moderate, incomplete dissociation
ECG effects: widen QRS, prolonged QT
Class 1A products
Quinidine: antimuscarinic activity, 2-8% risk of TdP
Procainamide: lupus-like syndrome, ganglionic block
Disopyramide: antimuscarinic activity
Class 1B
Na channel block
Blocks open state and inactivated state
Rapid, complete dissociation
Slight narrowing of action potential
ECG effects: no effects
Class 1B products
Lidocaine (IV): only ventricular arrhythmias (VF)
Phenytoin
Mexiletine
Tocainide
Class 1C
Strong Na block
Blocks open state
Very slow, incomplete dissociation
ECG effects: widens QRS
Class 1C products
Flecainide: ventricular and supraventricular
Propafenone: ventricular and supraventricular
SOME BB ACTIVITY
Moricizine
Class 3: K channel blockers
Blocks Ikr channel
Prolonged action potential duration
Increases ERP to prevent reentrant arrhythmias
Acts on the Ikr hERG channel resulting in increased risk of TdP by: inducing EADs and trigger upstrokes leading to multifocal and polymorphic VT
ECG effects: prolonged QT