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
Which type of arrhythmias can you tx with class Ia drugs?
1) ventricular tachycardia
2) Paroxysmal recurrent Afib
3) Wolff-Parkinson-White (procainamide)
Class Ib drugs
Lettuce, Pickles, Mayo
Lidocaine
Phenytoin
Mexiletine
Which type of arrhythmias can you tx with class Ib drugs?
ventricular tachycardias
Class Ic drugs
Fries Please
Flecainide
Propafenone
Which type of arrhythmias can you tx with class Ic drugs?
paroxysmal Afib
Class II drugs
Propranolol (beta-blocker)
Which type of arrhythmias can you tx with class II drugs?
sinus (SV) tachycardia
Class III drugs
Amiodarone Sotalol Ibutilide Dofetilide Dronedarone
Which type of arrhythmias can you tx with class III drugs?
1) Wolff-Parkinson-White (sotalol)
2) Ventricular arrhyth.
3) Sinus tachycardia
What is the half-life of amiodarone?
2 months
**be mindful of this when adding other medications
Class IV drugs
Non-dihydropyridine
CCBs
Verapamil
Diltiazem
Which type of arrhythmias can you tx with class IV drugs?
1) prevent recurrence of paroxysmal SV tachycardias
2) control ventricular rate in afib
Which drugs work on rate control?
class II, class IV, and digoxin
**studies show that rate is a better way to target tx than rhythm
Which drugs work on rhythm control?
class Ia, class Ic, class III
Which drug is indicated for Afib, Aflutter, paroxysmal SVT, ventricular arrhythmias? Has drug interactions with warfarin and digoxin
Quinidine; Propafenone
Which drug is indicated only for paroxysmal SVT, and is C/I in glaucoma?
Disopyramide
Which drugs is indicated for ventricular arrhythmias and is commonly used as an add-on to amiodarone rather than as a sole agent. It is also C/I in 3rd degree AV block
Mexiletine
Which drug has been seen to increase digoxin and is increased by haloperidol, cimetidine, and fluoxetine?
Flecainide
Which drug is indicated for Afib, Aflutter, paroxysmal SVT, ventricular arrhythmias? C/I with severe sinus bradycardia or heart block?
Beta blockers
Which drug is indicated for supraventricular and ventricular arrhythmias, but is C/I in iodine hypersensitivity, hyperthyroidism, and 3rd degree AV heart block? Also has DI with warfarin, digoxin, and statins
Amiodarone
Which drug is indicated for paroxysmal or persistent Afib and Aflutter?
Dronedarone
Which drug is indicated for ventricular arrhythmias and maintenance of Afib and Aflutter? But has a increased risk of arrhythmias with other antiarrhythmics
Sotalol
Risk of proarrhythmia
- higher in Class I
- not in Class II
**dose-related with solatlol, Class IC, and N-acetyl procainamide (NAPA)
Class Ia s/e
Anticholinergic effects
Quinidine s/e
cardiac: negative inotropic, vagolytic, syncope, torsades
non-cardiac: cinchonism, GI, thrombocytopenia, DILE
Type of pro-arrhythmia that demonstrates twisting of the QRS complex; **can result in sudden cardiac death
Torsades de pointes
Procainamide s/e
cardiac: weak ganglionic blocking, NAPA metabolite
non-cardiac: DILE
What is DILE?
drug induced lupus erythematosus
Class Ib s/e
neurologic (stimulation or depression, convulsions)
Lidocaine s/e
Non-cardiac: CNS excitation and/or depression, nausea, tremor, vertigo, metallic taste, numb lips, visual and hearing disturbances
**high concentrations > 9 mcg/mL may cz convulsions, respiratory depression, seizures
Propafenone (Rhythmol) s/e
Cardiac: proarrhythmia in pt. with ischemic heart dz, beta-clocking leading to 1st or 2nd degree AVN blcok
Non-cardiac: metallic taste, dizziness
When is Propafenone (Rhythmol) C/I?
heart failure stage III-IV, liver dz, valvular dz (torsades), CAD, VTach
Propanolol s/e
bradycardia, hypotension, left ventricular HF, AVN block, bronchospasm
Amiodarone s/e
corneal microdeposits (pt. need to get eyes checked), peripheral neuropathy, pulmonary fibrosis (rare), disturbed thyroid fn, photosensitivity w/ blue-gray discoloration (d/t iodine content); may precipitate HF, vary rare incidence of torsades
Which drugs is similar to amiodarone but lacks iodine and thyroid s/e?
Dronedarone
Sotalol s/e
non-selective beta-blockade (one enantiomer is a beta-blocker but other blocks Ikr (K+ channel)
Torsades
Verapamil and Diltiazem s/e
Cardiac: negative inotropic, AVN block, sinus arrest
Non-cardiac: peripheral vasodilation, constipation, dizziness, flushing, HA, hypotension, gingival hyperplasia (benign but common)
Adenosine MOA
acts of adenosine receptors (GPCR) to decrease adenylyl cyclase to decrease cAMP –> INCREASE potassium efflux –> cell hyperpolarization –> transient heart block of AV node
(this medication works w/in 15 seconds)
Adenosine s/e
transient hypotension and chest pain
Type(s) of arrhythmia(s) that Adenosine tx
1) AV re-entrant tachy
2) AV nodal re-entrant tachy
Atropine MOA
competitive inhibitor of muscarinic acetylcholine receptors
Type(s) of arrhythmia(s) that Atropine tx
bradycardia
Atropine s/e
blurry vision, dry mouth, tachycardia
“dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter”
Atropine antidote
Physostigmine
given as slow IV injection of 1-4 mg (0.5-1 mg in kids) - rapidly abolishes delirium and coma cz by large doses of atropine
Digoxin MOA
inhibit the Na+/K+ ATPase in the myocardium
- decr. membrane sodium gradient
- decr. sodium-calcium xchange
- incr. intracellular Ca++
Type(s) of arrhythmia(s) that Digoxin tx
1) Afib
2) Aflutter with RVR heart failure
Digoxin s/e
bradycardia, partial or complete heart block, GI, drowsiness and fatigue, visual disturbances
