Anti-Arrhythmias (TBL) Flashcards
Quinidine
Class: 1A
MOA: blocks voltage-gated Na+ channels –> decrease conduction velocity in fast response fibers –> decrease reentry circuit
- Also blocks K+ channels, α1 receptors, muscarinic receptors
For: SVTs (“rhythm control”), VT
AEs: increase QTc interval (from K+ channel block) –> risk for TdP
- Diarrhea g hypokalemia –> risk for TdP
- N/V
- Hypotension
- Increase AV conduction –> increase rapid transmission of APs from an SVT
- Cinchonism (headache, tinnitus, deafness)
- Thrombocytopenia
***Inhibitors of CYP 2D6: DDI
Procainamide
Class: 1A
MOA: blocks voltage-gated Na+ channels –> decrease conduction velocity in fast response fibers –> decrease reentry circuit
- Also blocks K+ channels, Nn receptors
For: VT
AEs: increase QTc interval (from K+ channel block) –> risk for TdP
- Hypotension (from Nn block)
- Drug-induced lupus (rash, small joint arthalgias)
Lidocaine
Class: 1B
MOA: blocks voltage-gated Na+ channels –> decrease conduction velocity in fast response fibers –> decrease reentry circuit
For: VT, VF
AEs: CNS toxicity (DATS: drowsiness, agitation, tremors, seizures)
CV collapse/cardiac arrest
Felcainide
Class: 1C
MOA: blocks voltage-gated Na+ channels –> decrease conduction velocity in fast response fibers –> decrease reentry circuit
For: SVTs (“rhythm control”), VT
AEs: h mortality in patients w/ recent MI and premature
ventricular contractions (PVCs) shown in CAST
* Avoid in patients w/HF or history of MI or structural heart disease
Metoprolol
Class: II (B1 Beta-Blocker)
MOA: blocks β1 on AV node –> decreased conduction velocity (negative dromotropic effect) –> decreased APs reaching ventricle from an SVT
- Also blocks β1 on cardiac myocytes –> decrease Ca2+ overload –> decrease DADs
For: SVTs (“rate control”)
- decreased ischemia-related arrhythmias following an MI
AEs:
block beta-1: Heart failure, bradycardia, AV block, impairs cardiac stimulation from increased sympathetic tone during hypoglycemia (“hypoglycemic unawareness”), increased risk of sudden death if abruptly discontinue, hyperkalemia
block beta-2 on blood vessels, skeletal muscle, bronchiole smooth muscle:
- Exacerbation of asthma/COPD, impairment of peripheral circulation from vasoconstriction
- blocks skeletal muscle tremors from increased EPI release during hypoglycemia (“hypoglycemic unawareness”)
- hyperkalemia (decrease K+ uptake by skeletal muscle)
***Because of negative inotropic effect, need to titrate slowly up to therapeutic dose to avoid worsening HF
Propranolol
Class: II (Non-selective Beta-Blocker)
MOA: blocks β1 on AV node –> decreased conduction velocity (negative dromotropic effect) –> decreased APs reaching ventricle from an SVT
- Also blocks β1 on cardiac myocytes –> decrease Ca2+ overload –> decrease DADs
For: SVTs (“rate control”)
- decreased ischemia-related arrhythmias following an MI
AEs:
block beta-1: Heart failure, bradycardia, AV block, impairs cardiac stimulation from increased sympathetic tone during hypoglycemia (“hypoglycemic unawareness”), increased risk of sudden death if abruptly discontinue, hyperkalemia
block beta-2 on blood vessels, skeletal muscle, bronchiole smooth muscle:
- Exacerbation of asthma/COPD, impairment of peripheral circulation from vasoconstriction
- blocks skeletal muscle tremors from increased EPI release during hypoglycemia (“hypoglycemic unawareness”)
- hyperkalemia (decrease K+ uptake by skeletal muscle)
***Exaggerated effects if combined with non-DHP CCBs
***Because of negative inotropic effect, need to titrate slowly up to therapeutic dose to avoid worsening HF
Amiodarone
Class: III
MOA: blocks K+ channels g h refractory period g disrupts reentry circuits
- Also blocks Na+ channels, Ca2+ channels, adrenergic receptors
For: SVTs (“rhythm control”), VT, Ventricular fibrillation
AEs:
Hypotension
Pulmonary fibrosis (can be fatal!)
Corneal microdeposits
Blue/gray skin discoloration
Hepatotoxicity
Neurotoxicity
Hypo/Hyperthyroidism
Photosensitivity
Verapamil
Class: IV (non-DHP CCBs)
MOA: blocks LTCCs on AV node –> decrease conduction velocity (negative dromotropic effect) –> decrease APs reaching ventricle from an SVT
For: SVTs (“rate control”)
AEs:
Bradycardia/AV block
Hypotension
HF
Constipation
***Exaggerated effects if combined with beta blockers
Diltiazem
Class: IV (non-DHP CCBs)
MOA: blocks LTCCs on AV node –> decrease conduction velocity (negative dromotropic effect) –> decrease APs reaching ventricle from an SVT
For: SVTs (“rate control”)
AEs:
Bradycardia/AV block
Hypotension
HF
Constipation
***Exaggerated effects if combined with beta blockers
Adenosine
Class: V
MOA: stimulates A1 receptors (Gi-coupled) on AV node
–> decrease conduction velocity (negative dromotropic effect) –> disrupts reentry circuit involving the AV node
For: AVNRT ( aka: PSVT)
AEs:
transient asystole
dyspnea
flushing (vasodilation from stimulation of A2 receptors)
anxiety
**Caffeine and other methylxanthine drugs block adenosine
receptors –> require higher dose to get desired effect
**Vey rapid half-life so only used as I.V. bolus
Digoxin
Class: V
MOA: blocks Na+-K+ ATPase
- decreased parasympathetic tone & decreased sympathetic tone
For: Atrial fibrillation (AF) w/ HF (“rate control”)
AEs:
Cardiac arrhythmias (some due to increased cytosolic Ca2+
overload or increased parasympathetic tone)
GI- nausea
Visual distrubances (blurry yellow vision)
CNS (e.g., disorientation)
Atropine
Class: Muscarinic Antagonist
MOA: idk
For: Bradycardia/AV block; Anti-Che Toxicity
AEs: idk
