Arrhytmia TX Flashcards
Arrhythmia define
Cardiac arrhythmias are accelerated, slowed, or irregular heart rates caused by abnormalities in the electrical impulses of the myocardium.
Bradyarrhythmias include sinus node dysfunction and atrioventricular block, and are characterized by a resting heart rate < 60/minutes.
Tachyarrhythmias (heart rates > 100/minute) are classified as supraventricular arrhythmias or ventricular arrhythmias.
Supraventricular arrhythmias originate between the sinus node and the atrioventricular node.
Ventricular arrhythmias originate below the atrioventricular node, on the ventricular level.
Arrhythmia TX What are antiarrythmic drugs
Antiarrhythmic drugs are used to prevent recurrent arrhythmias and restore sinus rhythm in patients with cardiac arrhythmias. These drugs are classified based on their electrophysiological effect on the myocardium.
Arrhythmia TX
Class I
Fast sodium channel blockers - Responsible for the rapid depolarization (phase 0) of fast-response cardiac action potentials
Class I drugs → Block Na channel
Block sodium channels → prolong QRS
* Some also affect K+ channels → prolong Qt
* Can prolong action potential duration
* Can prolong effective refractory period
Arrhythmia TX
Class IA Drugs
Quinidine, procainamide
They
* Prolong QRS
* Can also prolong Qt (↓K+ outflow)
Arrhythmia TX
Quinidine
- Oral drug
- Can decrease recurrence rate of atrial fibrillation
- Associated with increased mortality
Arrhythmia TX
Procainamide
- Intravenous drug
- Slows conduction in accessory pathways (WPW)
- Used in arrhythmias associated with bypass tracts
Associated with drug-induced lupus
* Classic drugs: INH, hydralazine, procainamide
* Often rash, arthritis, anemia
* Antinuclear antibody (ANA) can be positive
* Key features: anti-histone antibodies
* Resolves on stopping the drug
Arrhythmia TX
Class IB
Lidocaine
Mexiletine
Phenytoin
- Little/no effect on QRS at normal HR
- Slight decrease in Qt interval (minimal)
- Least effect on action potential of class 1 drugs
Most Na channel binding in depolarized state
* Ischemia → more depolarized myocytes
* Effective drugs in ischemic arrhythmias
Arrhythmia TX
Lidocaine
Mexiletine
Lidocaine also a local anesthetic
* Na channel nerve block
* May cause CNS stimulation
* Tremor, agitation
- Tremor in patient on Mexiletine = toxicity
- Cardiovascular side effects
- From excessive block of Na channels
- Bradycardia, heart block, hypotension
Arrhythmia TX
Class IC
Flecainide, Propafenone
- Block open Na channels
- Very slow unbinding
- Result: QRS can markedly prolong
- Limited use due to concern of toxicity
- Especially proarrhythmic effects
- Only used in patients with structurally normal hearts
- Effective in reducing recurrence of atrial fibrillation
- Must monitor for QRS prolongation
- Prolonged QRS → Risk of cardiac arrest
Arrhythmia TX
Class III
Potassium channel blockers
Amiodarone
Sotalol
Dofetilide
Ibutilide
Arrhythmia TX
Class III MOA
Inhibit delayed rectifier potassium currents
Prolong QT interval
Prolong AP duration (reverse use dependence) and ERP
+/-QRS ↑QT
↑AP ↑ERP
Arrhythmia TX
Amiodarone
- K channel blocker: Prolongs Qt interval
- Lowest incidence TDP of all class IIIs
Also has class I, II, and IV effects
* Class I: Prolongs QRS
* Class II, IV: Slow HR, delay AV conduction
* Very effective drug
* Suppresses atrial fibrillation
* Suppresses ventricular tachycardia
risks
* Many potential side effects related to accumulation
* Less likely at lower dosages
* Risk accumulates over time
* Young patients on indefinite therapy at greatest risk
* Often used in older patients
Hyper and hypothyroidism
* Contains iodine
* Increased LFTs
* Usually asymptomatic and mild
* Drug stopped if elevation is marked
* Skin sensitivity to sun
* Patients easily sunburn
Arrhythmia TX
Sotalol and Dofetilide
Both drugs block K channels (class III)
* Can prolong Qt interval → torsade de pointes
* Practical consideration:
* Patients often admitted to hospital to start therapy
* Rhythm monitored on telemetry
* Qt segment checked by EKG each day
* Sotalol: Also has beta blocking properties
* Can be used in patients with cardiomyopathy
* “Reverse use dependence”
Reverse use dependence: more binding slow rates
* Practical implication:
* Bradycardia in patient on sotalol/dofetilide
* Qt interval may prolong
* Increased risk of torsade de pointes
Commonly used in patients with atrial fibrillation
Arrhythmia TX
Ibutilide
Intravenous drug
* Half life of 2 to 12 hours
* Used for “chemical cardioversion”
Termination of arrhythmias
* Often atrial fibrillation or flutter
Arrhythmia TX
Class II
Beta Blockers : Metoprolol
Esmolol (short acting)
Propranolol
Atenolol
Timolol
Carvedilol
Class II Antiarrhythmics
* Main effect: Pacemaker cells (SA and AV node)
* Decrease slope of phase 4
* Prolong repolarization (phase 3)
Arrhythmia TX
Class IV
Calcium channel blockers
Verapamil
Diltiazem
Nifedipine
Inhibit slow calcium channels
Decrease slope of phase 0 and 4 → slower conduction velocity → increased ERP
Prolong AV node repolarization
Prolong PR interva
Arrhythmia TX
Class V
Adenosine
Magnesium sulfate
Digoxin
Ivabradine
Arrhythmia TX
Adenosine
Activates Gi protein → ↓ cAMP → deactivation of L-type Ca2+ channels → ↓ Ca2+ and ↑ K+ efflux → transient AV node block
Very short acting (∼ 15 sec)
Diagnosis and termination of certain forms of PSVT (e.g., AVNRT and orthodromic AVRT
Arrhythmia TX
Magnesium sulfate
Decreases calcium influx → prevents early afterdepolarizations (EAD
Used: TdP
Digoxin toxici
Arrhythmia TX
Digoxin
Inhibits Na+/K+-ATPases → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers → higher intracellular Ca2+ concentration → increased contractility and decreased heart rate
AFib
Atrial flutter
Chronic systolic heart failure
Arrhythmia TX
Ivabradine
Selectively inhibits If channel in the pacemaker cells of the SA node → prolongs slow depolarization (phase 4) → slows heart rate
TX:
Chronic stable coronary heart disease in patients who cannot tolerate beta blockers
Chronic HFrEF
