Anti-Arrhythmias Flashcards
Phase 4 of SA nodal cells
slow, spontaneous depolarization caused by an inward pacemaker current; these channels are relatively nonselective cation channels; K+ moves out of cells
Phase 0 of SA nodal cells
more rapid depolarization mediated by highly selective voltage-gated Ca++ channels that open to allow Ca++ in
Phase 3 of SA nodal cells
Ca++ channels slowly close and K+-selective channels open (K+ out), resulting in membrane repolarization
(there is also some involvement of Na+ channels closing during this phase)
Which phase define SA nodal cell firing
phase 4 –> phase 0 –> phase 3 –> phase 4, and so on
Phase 4 of ventricular myocytes
resting membrane potential; established by activation of time-independent K+ currents, which drive membrane potential close to K+ equilibrium potential
Phase 0 of ventricular myocytes
rapid depolarization; inward Na+ through voltage-gated Na+ channels
Phase 1 of ventricular myocytes
early phase of repolarization; decrease in outward Na+ d/t voltage-gated inactivation of sodium channels; and efflux of K+ ion through transiently opened K+ channels
Phase 2 of ventricular myocytes
plateau; balance between inward Ca++ thru Ca++ channels - both transient (T-type) and long-lasting (L-type) - and outward K+ through K+ channels
During this phase the cardiac cells are insulated electrically, allowing rapid propagation of AP w/ little current dissipation
Phase 3 of ventricular myocytes
late phase of rapid repolarization; decrease in inward Ca++ current and large increase in outward K+ current
Sinus tachycardia
supraventricular
rapid, but regular rate
increased sympathetic tone cz heart to race (100-160 bpm); depolarization originates from SA node
Atrial fibrillation
supraventricular
irregular rhythm
multiple ectopic foci of atrial cells generate 350-450 impulse per min; the ventricle responds to an occasional impulse
What is the MC type of SV arrhythmia?
Afib
risk is that blood becomes stagnant at times can can form clots; tx with anticoagulants
Atrial flutter
supraventricular
regular rhythm
atrial impulse reenters and depolarizes atrium; generates 250-350 impulse per min; ventricle responds to every 2nd or 3rd impulse
Multifocal atrial tachycardia
supraventricular
rate is rapid and irregular
depolarization originates from several atrial foci at irregular intervals; 100-200 bpm
premature atrial depolarization (PAT)
supraventricular
irregular rhythm
heat beats prematurely b/c a focus of atrial cells fires spontaneously before the SA node is ready to fire
sinus bradycardia
supraventricular
slow, but regular rhythm
increased parasympathetic (vagal) tone cz heart to beat at < 60 bpm; depolarization originates from SA node
A-V reentry
involves A-V junction
(notes say supraventricular)
AV node is split into a pathway that conducts twd the ventricle and a pathway that conducts the impulse back to the atrium; atrium and ventricles contract simultaneously; rate is 150-250/min
Wolf-Parkinson-White
involves A-V junction
impulses reaching the ventricle via the AV node circle back to the atrium via an accessory pathway that also links atrium to ventricles; this circuit may also be reversed; rate can exceed 300 bpm
Premature Ventricular Contractions (PVCs)
ventricular
spontaneous depolarization of ectopic focus in ventricle; benign if fewer than 6 per min.
Ventricular tachycardia
ventricular (duh!)
usu. 2’ to reentry circuit (i.e. AV reentry of WPW can progress to this)
Ventricular fibrillation
…ventricular
completely erratic
many ectopic foci in ventricle; rate is 350-350 bpm
What are some sx of arrhythmias?
palpitations, dizziness, SOB, chest pain, fatigue
What are some concerns with arrhythmias?
stroke, heart failure, sudden cardiac death
Vaughan-Williams class I drugs
Na+ channel blockers
Vaughan-Williams class Ia
have little effect on SA node automaticity (most anti-arrhythmic drugs do effect SA); moderate block of both Na+ and K+ channels; slow phase 0 depolarization; prolong AP and slow conduction
Vaughan-Williams class Ib
Mild blocking or inactivating Na+ channels; shorten phase 3 repolarization; decrease duration of AP
Vaughan-Williams class Ic
Block open Na+ channels; markedly slow phase 0 depolarization
Vaughan-Williams class II
antagonize adrenergic receptors (block catecholamines at AV node); decrease slope of phase 4 depolarization; prolong repolarization in AV node (block reentry)
Vaughan-Williams class III
tend to prolong phase 3 repolarization without altering phase 0
Vaughan-Williams class IV
block slow inward (L-type calcium channels) current; decrease AV node conduction and increase refractory period
(similar action to class II, but does not block adrenergic sx)
Class Ia drugs
Double Quarter Pounder
Disopyramide
Quinidine
Procainamide