ICL 2.5: Antiarrhythmics Flashcards
what are the 4 classes of antiarrhythmics?
CLASS I: membrane stabilizers = Na channel blockers
CLASS II: B Blockers
CLASS III: K+ channel modifier (prolongs AP)
CLASS IV: Ca++ channel blockers
what are the subcategories of class I antiarrhythmics?
class I antiarrhythmics = membrane stabilizers = Na+ channel blockers
1(A) –> moderately decrease velocity of phase 0
1(B) –> little decrease in velocity of phase 0
1(C) –> marked decrease in velocity of phase 0
which drugs are class 1(A) antiarrhythmic drugs?
- quinidine
- procainamide
- disopyramide
moderately decrease velocity of phase 0 and prolongs action potential duration
which drugs are class 1(B) antiarrhythmic drugs?
- lidocaine
- mexiletine
little decrease in velocity of phase 0 and may shorten action potential duration
which drugs are class 1(C) antiarrhythmic drugs?
- propafenone
- flecainide
marked decrease in velocity of phase 0 and may prolong action potential duration n
which drugs are class II antiarrhythmic drugs?
B blockers!
- propranolol
- esmolol
- sotalol
which drugs are class III antiarrhythmic drugs?
K+ channel modifier agents that widen AP
- amiodarone
- dronedarone
- dofetilide
- ibutilide
which drugs are class IV antiarrhythmic drugs?
calcium channel blockers
- verapamil
- diltiazem
which drugs are used for PSVT?
- adenosine
2. digoxin
which drugs are used for AV block?
- isoprenaline and other sympathomimetics
2. atropine and other anticholinergics
which conditions is digoxin used for?
- Afib
- atrial flutter
- PSVT
used to control ventricular rate
adenosine is used more clinically for PSVT because digoxin is slower
what is triggered activity?
a normal AP is interrupted/followed by an abnormal depolarization aka a triggering rhythm
this can be due to either a delayed after depolarization or an early after depolarization
delayed after depolarization is due to Ca+2 overload and can be caused by digoxin toxicity, myocardial ischemia, adrenergic stress or heart failure
early after depolarization is due to interruption in phase 3 depolarization and can be caused by slow heart rate, hypokalemia and drugs prolonging the QT interval (quinidine, stall, procainamide)
what is tornado de pointes?
due to marked prolongation of AP depolarization
you’ll see long QT interval and frequent changing of QRS
seen in polymorphic ventricular tachycardia
what is reentry?
when the tachycardia is initiated by an ectopic beat but sustained by a closed loop or re-entry circuit
a multidirectional arrhythmia where there’s a scar area and the normal propagation of electricity is disrupted
most tachycardia-arrhythmias are due to re-entry around ischemic/scarred areas
which antiarrhythmic drug class is sotalol?
it’s a class III K+ channel blockade but it also has na+ channel blocking ability!!
so it’s great for atrial and ventricular arrhythmia treatment
it can effect repolarizaiton so it effects APD by increasing it similar to class III antiarrhythmics
what are the effects of class I antiarrhythmic drugs?
Na+ channel blockers
decrease in conduction velocity manifests as widening of WRS duration
increase action potential threshold = decreased automaticity/acing threshold
slight decrease in AP duration = QT interval
negative inotropy = lowers Na+ permeability through the channel which means less Na+ in the cell –> more Na/Ca exchange since the exchanger lets Na+ in and Ca+2 out –> less intracellular Ca+2 and less contractility
how do class IA antiarrhythmic drugs effect AP?
moderate Na+ channel blockers
increases AP duration
increases effective refractory period
IA are the only ones that prolong QT
effect atrial, perkinje and ventricular cardiomyocytes
how do class IB antiarrhythmic drugs effect AP?
weak Na+ channel blockers
decreases AP duration and effective refractory period
effect perkinje and ventricular cardiomyocytes; don’t effect atrial cells!
how do class IC antiarrhythmic drugs effect AP?
strong Na+ channel blockers
no effect on AP duration or effective refractory period
effect atrial, perkinje and ventricular cells
what are the adverse effects of class IA antiarrhythmic drugs?
- pro-arrhythmic
can cause tornado de pointes - negative inotropic effect (quinidine)
- systemic lupus erythematosus (procainamide)
- anticholinergic side effects (disopyramide) –>mad as hatter, dry as a bone
what are the adverse effects of class IB antiarrhythmic drugs?
- lidocaine –> seizures
2. mexilitine –> GI upset
what are the adverse effects of class IC antiarrhythmic drugs?
- proarrhythmic
2. propafenone –> metalic taste
what is the MOA of class II antiarrhythmic drugs?
decrease depressed SA node automaticity and prolong the refractoriness of the AV node
may prevent shortening of refractoriness at all levels in the heart
they also block adrenergic activation of Ca+2 channels = decreased force of contraciton
may suppress non-sustained ventricular arrhythmias especially in patients with an underlying adrenergic mechanism –> they’re the DOC in exercise-induced arrhythmias and in patients with long QT syndrome
B2 receptors are implicated in ischemia dependent ventricular fibrillation which may be prevented by nonselective blockade
what are the benefits of B blockers?
- anti-ischemic effects
2. decrease force of the contraction and HR = decreased oxygen demand!!
what are the clinical uses of B blockers?
- Afib
- atrial flutter
- atrial tachycardia
- PVCs
- recent MI
- adjunctive to NSVT an VT
what are the side effects of B blockers?
- sinus bradycardia
- heart pauses
- can block/pause AV node
- heart failure
- CNS = fatigue, sedation, sleep disturbance, sexual dysfunction
- dyspnea/bronchospasm from B2 blocking
- hypoglycemia unawareness; blocks the symptoms of low BG
when are B blockers contraindicated?
- cocaine toxicity
- pheochromocytoma
this would lead to unopposed alpha receptor stimulation = severe HTN, aortic dissection, coronary spasm or MI
what are the antidotes to B blockers?
- atropine
- glucagon
- fluids
how does glucagon act as an antidote to B blockers?
B blocker is blocking B receptor but glucagon can bypass that and still increase cAMP through activating a different receptor
how do class I vs. III antiarrhythmics effect QRS complex length?
class I = Na+ channel blocker –> effect phase 0 which directly effects depolarization and would increase QT interval and QRS complex
class III = K+ channel blockers = effects phase 3 –> this is the repolarization so it wouldn’t effect the QRS complex but it would prolong the QT interval
what is the MOA of class III antiarrhythmics?
increased APD = increased QT interval
many K+ channel blockers have a reverse use dependent effect and bind to resting channels –> AP prolongation is greater at slower rather than faster heart rates
there is increased risk of triggered activity due to prolonged phase 3 = early active depolarization
which drugs are mixed vs. pure class III antiarrhythmics?
MIXED
- amiodarone
- dronedarone
- sotalol
PURE
- ibutilide
- dofetilide
how does amiodarone work?
K+ channel blocker effects phase 3 and prolongs AP duration and refractory period in both atrial and ventricular cardiomyocytes
it has noncompetitive inhibition of alpha and B adrenergic receptors
reduces automaticity of automatic cells
what are the EKG changes you would see with amiodarone?
- eduction of Sinus rate only by 15-20%
- increased PR and QT duration (prolongs)
- U waves and NS (nonspecific) Twave changes
what are the clinical used of amiodarone?
- atrial flutter
- atrial fibrillation
- ventricular arrhythmias
how would you treat stable ventricular tachycardia?
- IV amiodarone
- cardioversion with moderate sedation
- post EKG
- expert an expert
what are the side effects of amiodarone?
- acute pulmonary toxicity = hypersensitivity pneumonitis
- long term toxicity = interstitial alveolar pneumonitis
- abnormal thyroid function test or thyrotoxicosis –> hypo or hyperthyroidism!
- abnormal liver function tests
- optic neurotis
- photosensitivity
- avoid grapefruit juice because prolonged QT
- caution with digoxin
how would you treat ventricular tachycardia after an MI?
amiodarone
if that doesn’t work, use lidocaine or procainamide
then DC cardioversion
chronic reaction use ICD with or w/o amiodarone
how would you treat ventricular tachycardia w/o structural heart disease?
- B blockers
- verapamil
chronically, use B blockers
how would you treat ventricular fibrillation?
treat with defibrillation 1st
amiodarone 2nd to prevent recurrence
then lidocaine and procainamide
what are class IV antiarrhythmic drugs?
they are effective in arrhythmias that must traverse Ca-dependent cardiac tissue like the AVN
they cause a use-dependent selective depression of calcium current in tissues that require the participation of L-type Ca channels
AV conduction velocity is decreased and effective refractory period increased by these drugs
PR interval is consistently increased
what are the effects of Ca+2 channel blockers?
- inhibit the SA and AVN and tissue with abnormal automaticity dependent on Ca+2 channels
- generally little effect on the APD
- stops triggered activity like EAD and DAD
- slows HR and decreases contractility
- EADs due to oscillatory depolarizations due to waves of Ca+2 channel reactivation
DADs result from Ca+2 overload of the cell
what are the clinical uses of Ca+2 channel blockers?
- SVTs
- atrial fibrillation
- certain ventricular arrhythmias
what are the side effects of Ca+2 channel blockers?
- AV blocks
2. heart failure
how does adenosine work?
binds to Adenosine receptors AV node
blocks Ca++ entry
blocks K+ channels –> hyperpolarizes cells
what are the clinical uses of adenosine?
diagnosing atrial arrhythmias
how does digoxin work?
blocks Na/K ATPase pump which allows more Ca+2 in the cell which increases force of contraction
it also increases vagal activity which decreases AV conduction and decreases HR –> decreases HR in both SA and AV nodes
toxicity = atrial tachycardias with AV node block
what are the antidotes to digoxin?
- digibind
2. magnesium
