Class 1 Antiarrhythmic Drugs

Class 1 antiarrhythmics inhibit the fast Na channels in non-nodal myocardial tissues and are subdivided into 3 categories (A, B, and C) on the basis of their speed of dissociation from the Na channels and electrophysiologic effects. All drugs in class 1 reduce cardiac conduction velocity to some degree by slowing phase 0 depolarization. Indications vary between subgroups but generally include atrial and ventricular arrhythmias. Contraindications, adverse effects, and warnings are category- and drug-dependent factors.

Last update:

Editorial responsibility: Stanley Oiseth, Lindsay Jones, Evelin Maza

Table of Contents

Share this concept:

Share on facebook
Share on twitter
Share on linkedin
Share on reddit
Share on email
Share on whatsapp

Overview

Cardiac action potential

  • The trajectory followed by the action potential depends on the membrane potential Membrane potential The membrane potential is the difference in electric charge between the interior and the exterior of a cell. All living cells maintain a potential difference across the membrane thanks to the insulating properties of their plasma membranes (PMs) and the selective transport of ions across this membrane by transporters. Membrane Potential of cardiac cells, which varies between different parts of the heart.
  • Phase 4: resting potential
  • Phase 0: rapid depolarization phase that occurs because of the influx of Na ions through voltage-dependent Na channels
  • Phases 1‒3:
    • Represent repolarization
    • Prominent efflux of K
    • In Phase 2, the efflux of K is balanced by the transient influx of calcium → causes the action potential to plateau

Vaughan–Williams classification

  • The most commonly used classification for antiarrhythmic drugs
  • 5 classes based on the general effects of drugs (mechanisms of action):
    • Class 1: Na channel blockers (divided into 3 subgroups):
      • 1A: prolong the action potential
      • 1B: shorten the action potential
      • 1C: minimal effect on action potential duration
    • Class 2: beta-blockers
    • Class 3: K channel blockers
    • Class 4: calcium channel blockers Calcium Channel Blockers Calcium channel blockers (CCBs) are a class of medications that inhibit voltage-dependent L-type calcium channels of cardiac and vascular smooth muscle cells. The inhibition of these channels produces vasodilation and myocardial depression. There are 2 major classes of CCBs: dihydropyridines and non-dihydropyridines. Class 4 Antiarrhythmic Drugs (Calcium Channel Blockers)
    • Class 5: drugs that cannot be categorized into the above groups

Mechanism of action of Na channel blockers

Class 1 antiarrhythmics bind to and block the fast Na channels in non-nodal tissue (e.g., myocytes of the atria and ventricles, His-Purkinje system):

  • The slope of phase 0 depends on:
    • Activation of fast Na channels 
    • Rapid entry of Na ions into the cell
  • Blocking these channels:
    • ↓ Slope of phase 0 → ↓ in the amplitude of action potential
    • ↓ Velocity of action potential transmission within the heart (↓ conduction velocity; negative dromotropy)
      • Important mechanism for suppressing tachycardias caused by abnormal conduction (e.g., reentry mechanisms)
      • Reentry mechanisms can be interrupted by ↓ abnormal conduction
  • Note: Na channel blockers generally have no direct effect on nodal tissue, at least through the blockade of fast Na channels.
Cardiac action potential 1 antiarrhythmic drugs

Diagram demonstrating a cardiac action potential and the phases of action for different antiarrhythmic drug classes:
The cycle starts with phase 4, the resting potential. Phase 0 is when rapid depolarization occurs due to an influx of Na ions into the cell and where class 1 (Na channel blockers) antiarrhythmics work.
Repolarization follows, with an efflux of K through fast K channels in phase 1, Ca influx in phase 2, and efflux of K through delayed K channels in phase 3.

Image by Lecturio. License: CC BY-NC-SA 4.0

Differences among the class 1 subgroups

  • Each subgroup varies in the extent of Na channel blockade.
  • In addition to affecting phase 0 of the action potential, Na channel blockers may also alter:
    • Action potential duration
    • Effective refractory period (ERP): the period of time when a new action potential cannot be initiated
  • The table below summarizes a few of the distinguishing differences in physiologic effects between class 1 subgroups.

Electrophysiologic effects of class 1 antiarrhythmic drugs

Table: Electrophysiologic effects of the class 1 antiarrhythmic drugs
Class 1 subgroup Strength of Na channel blockade Effect on action potential duration Effect on ERP Effect seen on ECG ECG An electrocardiogram (ECG) is a graphic representation of the electrical activity of the heart plotted against time. Adhesive electrodes are affixed to the skin surface allowing measurement of cardiac impulses from many angles. The ECG provides 3-dimensional information about the conduction system of the heart, the myocardium, and other cardiac structures. Normal Electrocardiogram (ECG)
1A Intermediate
  • QT prolongation
  • QRS widening
1B Weak
  • QT shortening
  • ↑ PR duration
1C Strong Minimal to none Minimal to none*
  • No QT change
  • QRS widening
*Exception: ↑ ERP in the atrioventricular node
ERP: effective refractory period

Mnemonic

To recall all class I antiarrhythmic medications, think of ordering a burger at a restaurant: “Double Quarter Pounder with Lettuce, Mayo, Pickles, and Fries, Please!”

  • Disopyramide
  • Quinidine
  • Procainamide
  • Lidocaine
  • Mexiletine
  • Phenytoin
  • Flecainide
  • Propafenone

Class 1A

Overview

  • Medications:
    • Disopyramide
    • Quinidine
    • Procainamide
  • Mnemonic for class 1A agents: “Double Quarter Pounder”

Mechanism of action

  • Na channel effects:
    • Intermediate speed of binding and dissociation from voltage-gated Na channels
    • Slows the upstroke of action potential and conduction
  • K channel effects:
    • Blocks K channels → ↓ K efflux → slows repolarization
    • Leads to ↑ ERP and action potential duration → QT prolongation
  • Other effects:
    • Anticholinergic Anticholinergic Anticholinergic drugs block the effect of the neurotransmitter acetylcholine at the muscarinic receptors in the central and peripheral nervous systems. Anticholinergic agents inhibit the parasympathetic nervous system, resulting in effects on the smooth muscle in the respiratory tract, vascular system, urinary tract, GI tract, and pupils of the eyes. Anticholinergic Drugs activity → can ↑ sinoatrial rate and atrioventricular conduction
    • ↓ Myocardial contractility
  • Affects the following myocardial tissues:
    • Atria
    • Ventricular
    • Purkinje
Effect of 1a antiarrhythmics on cardiac action potential

Effect of group 1A antiarrhythmics on the cardiac action potential:
Notice the delayed phase 0 upstroke, as well as increased effective refractory period and action potential duration

Image by Lecturio. License: CC BY-NC-SA 4.0

Pharmacokinetics

  • Absorption:
    • Oral, IV, and IM routes
    • Rapid and significant absorption
  • Distribution:
    • Protein binding:
      • ↑ For quinidine
      • ↓ For procainamide
    • Widely distributed
  • Metabolism:
    • Disopyramide and quinidine: hepatic metabolism by cytochrome P450
    • Procainamide: hepatic metabolism to an active metabolite (N-acetylprocainamide, implicated in torsades de pointes)
  • Excretion: predominantly renal

Indications

Due to severe side effects, such as their proarrhythmic effect, class 1A medications are usually reserved for life-threatening arrhythmias such as:

  • Ventricular arrhythmias
  • Atrial arrhythmias
  • Specific indications:
    • Wolff-Parkinson-White syndrome (procainamide)
    • Brugada syndrome (quinidine)

Adverse effects

General:

  • Proarrhythmic
  • QT prolongation → torsades de pointes
  • Widening of the QRS complex
  • Hyperkalemia Hyperkalemia Hyperkalemia is defined as a serum potassium (K+) concentration >5.2 mEq/L. Homeostatic mechanisms maintain the serum K+ concentration between 3.5 and 5.2 mEq/L, despite marked variation in dietary intake. Hyperkalemia can be due to a variety of causes, which include transcellular shifts, tissue breakdown, inadequate renal excretion, and drugs. Hyperkalemia exacerbates cardiac toxicity.
  • ↑ Atrioventricular node conduction:
    • ↑ Ventricular rate in individuals with uncontrolled atrial fibrillation Atrial fibrillation Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. Atrial Fibrillation
    • Treatment with beta-blockers, digoxin, or calcium channel blockers Calcium Channel Blockers Calcium channel blockers (CCBs) are a class of medications that inhibit voltage-dependent L-type calcium channels of cardiac and vascular smooth muscle cells. The inhibition of these channels produces vasodilation and myocardial depression. There are 2 major classes of CCBs: dihydropyridines and non-dihydropyridines. Class 4 Antiarrhythmic Drugs (Calcium Channel Blockers) is required.
  • Hypotension Hypotension Hypotension is defined as low blood pressure, specifically < 90/60 mm Hg, and is most commonly a physiologic response. Hypotension may be mild, serious, or life threatening, depending on the cause. Hypotension
  • Negative inotropes → may exacerbate heart failure
  • ↓ Presynaptic acetylcholine release at the neuromuscular junction → prolonged activity of neuromuscular blocking agents
  • Use has been associated with ↑ mortality

Disopyramide:

  • Anticholinergic Anticholinergic Anticholinergic drugs block the effect of the neurotransmitter acetylcholine at the muscarinic receptors in the central and peripheral nervous systems. Anticholinergic agents inhibit the parasympathetic nervous system, resulting in effects on the smooth muscle in the respiratory tract, vascular system, urinary tract, GI tract, and pupils of the eyes. Anticholinergic Drugs side effects:
    • Xerostomia
    • Urinary retention
    • Blurred vision
    • Avoid in acute angle-closure glaucoma Glaucoma Glaucoma is an optic neuropathy characterized by typical visual field defects and optic nerve atrophy seen as optic disc cupping on examination. The acute form of glaucoma is a medical emergency. Glaucoma is often, but not always, caused by increased intraocular pressure (IOP). Glaucoma.
  • Numerous drug interactions

Quinidine:

  • Drug with the highest proarrhythmic effect in its class
  • GI upset
  • Cinchonism: tinnitus, hearing loss Hearing loss Hearing loss, also known as hearing impairment, is any degree of impairment in the ability to apprehend sound as determined by audiometry to be below normal hearing thresholds. Clinical presentation may occur at birth or as a gradual loss of hearing with age, including a short-term or sudden loss at any point. Hearing Loss, headache, and delirium Delirium Delirium is a medical condition characterized by acute disturbances in attention and awareness. Symptoms may fluctuate during the course of a day and involve memory deficits and disorientation. Delirium
  • Avoid in glucose-6-phosphate-dehydrogenase (G6PD) deficiency.
  • Avoid with monoamine oxidase inhibitors Monoamine oxidase inhibitors Monoamine oxidase inhibitors are a class of antidepressants that inhibit the activity of monoamine oxidase (MAO), thereby increasing the amount of monoamine neurotransmitters (particularly serotonin, norepinephrine, and dopamine). The increase of these neurotransmitters can help in alleviating the symptoms of depression. Monoamine Oxidase Inhibitors (MAOIs).

Procainamide:

  • Agranulocytosis and pancytopenia due to bone marrow Bone marrow Bone marrow, the primary site of hematopoiesis, is found in the cavities of cancellous bones and the medullary canals of long bones. There are 2 types: red marrow (hematopoietic with abundant blood cells) and yellow marrow (predominantly filled with adipocytes). Composition of Bone Marrow suppression
  • Reversible drug-induced lupus
  • Vasculitis

Contraindications

  • 2nd- and 3rd-degree heart block
  • Cardiogenic shock Shock Shock is a life-threatening condition associated with impaired circulation that results in tissue hypoxia. The different types of shock are based on the underlying cause: distributive (↑ cardiac output (CO), ↓ systemic vascular resistance (SVR)), cardiogenic (↓ CO, ↑ SVR), hypovolemic (↓ CO, ↑ SVR), obstructive (↓ CO), and mixed. Types of Shock
  • Congenital long QT syndrome Long QT syndrome Long QT syndrome (LQTS) is a disorder of ventricular myocardial repolarization that produces QT prolongation on electrocardiogram (ECG). Long QT syndrome is associated with an increased risk of developing life-threatening cardiac arrhythmias, specifically torsades de pointes. Long QT Syndrome
  • Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis: exacerbation due to anticholinergic effects
  • Avoid with fluoroquinolone antibiotics because of the risk of QT prolongation.

Class 1B

Overview

  • Medications:
    • Lidocaine
    • Mexiletine
    • Phenytoin
  • Mnemonic used for class 1B agents: “Lettuce, Mayo, Pickles”

Mechanism of action

  • Rapid binding and dissociation from voltage-gated Na channels → weakest effect on phase 0
  • ↓ ADP
  • Normal or ↓ ERP
  • Affects the following myocardial tissues:
    • Ventricular
    • Purkinje
    • Less effect on atrial tissue
    • Strongest binding in ischemic and depolarized tissues
Effect of 1b antiarrhythmics on cardiac action potential

Effect of Group 1B antiarrhythmics on the cardiac action potential. Notice the decrease in action potential duration

Image by Lecturio. License: CC BY-NC-SA 4.0

Pharmacokinetics

  • Absorption:
    • Lidocaine:
      • IV only
      • Immediate and complete absorption
    • Mexiletine:
      • Oral
      • Well absorbed
    • Phenytoin:
      • Oral, IM, and IV administration
      • Poor water solubility
  • Distribution:
    • Lidocaine:
      • Plasma protein binding is dependent on drug concentration.
      • Crosses the blood-brain and placental barriers by passive diffusion
    • Mexiletine: plasma protein binding: 50%‒60%
    • Phenytoin:
      • Extensively bound to plasma proteins
      • Prone to competitive displacement
  • Metabolism:
    • Metabolized by the cytochrome P450 system
    • Lidocaine: high 1st-pass metabolism
    • Mexiletine: low 1st-pass metabolism 
  • Excretion: Metabolites and unchanged drugs are renally excreted.

Indications

  • Ventricular arrhythmias
  • Lidocaine and mexiletine are useful in treating hemodynamically stable ventricular tachycardia Ventricular tachycardia Ventricular tachycardia is any heart rhythm faster than 100 beats/min, with 3 or more irregular beats in a row, arising distal to the bundle of His. Ventricular tachycardia is the most common form of wide-complex tachycardia, and it is associated with a high mortality rate. Ventricular Tachycardia.
  • Phenytoin:
    • Useful for reversal of digitalis-induced arrhythmias
    • Rarely used as an antiarrhythmic
    • More commonly used as an anticonvulsant Anticonvulsant Anticonvulsant drugs are pharmacological agents used to achieve seizure control and/or prevent seizure episodes. Anticonvulsants encompass various drugs with different mechanisms of action including ion-channel (Na+ and Ca+2) blocking and GABA reuptake inhibition. First-Generation Anticonvulsant Drugs

Adverse effects

  • CNS effects:
    • Lidocaine:
      • Tremors
      • Dysarthria
      • Insomnia Insomnia Insomnia is a sleep disorder characterized by difficulty in the initiation, maintenance, and consolidation of sleep, leading to impairment of function. Patients may exhibit symptoms such as difficulty falling asleep, disrupted sleep, trouble going back to sleep, early awakenings, and feeling tired upon waking. Insomnia or drowsiness
      • Confusion
      • Seizures Seizures A seizure is abnormal electrical activity of the neurons in the cerebral cortex that can manifest in numerous ways depending on the region of the brain affected. Seizures consist of a sudden imbalance that occurs between the excitatory and inhibitory signals in cortical neurons, creating a net excitation. The 2 major classes of seizures are focal and generalized. Seizures
    • Mexiletine:
      • Tremors
      • Dysphoria
      • Ataxia
      • Nystagmus
  • Cardiac effects:
    • Hypotension Hypotension Hypotension is defined as low blood pressure, specifically < 90/60 mm Hg, and is most commonly a physiologic response. Hypotension may be mild, serious, or life threatening, depending on the cause. Hypotension
    • Sinus slowing and bradycardia
    • Asystole
    • May precipitate arrhythmias
    • Hyperkalemia Hyperkalemia Hyperkalemia is defined as a serum potassium (K+) concentration >5.2 mEq/L. Homeostatic mechanisms maintain the serum K+ concentration between 3.5 and 5.2 mEq/L, despite marked variation in dietary intake. Hyperkalemia can be due to a variety of causes, which include transcellular shifts, tissue breakdown, inadequate renal excretion, and drugs. Hyperkalemia increases toxicity.
  • Phenytoin:
    • Gingival hyperplasia
    • Nystagmus
    • Ataxia
    • Nausea

Contraindications

  • 2nd- and 3rd-degree heart block
  • Wolff-Parkinson-White syndrome
  • Severe hepatic dysfunction (leads to restricted metabolism → ↑ toxicity)

Class 1C

Overview

  • Medications:
    • Flecainide
    • Propafenone
  • Mnemonic used for class 1C agents: “Fries, Please!”

Mechanism of action

  • Na channel effects:
    • Slows the speed of binding and dissociation from voltage-gated Na channels → ↑ effect
    • Prolongs the upstroke of the action potential (has the greatest ↓ in the slope of phase 0)
    • No (or minimal) impact on action potential duration and ERP, no effect on QT interval (exception: ↑ ERP in atrioventricular node)
  • Other effects:
    • ↓ Myocardial contractility
    • Propafenone is also used as a:
      • Beta-blocker
      • Calcium channel blocker
  • The following myocardial tissues are affected:
    • Atria
    • Ventricles
    • Purkinje fibres
Effect of 1c antiarrhythmics on cardiac action potential

Effect of group 1C antiarrhythmics on the cardiac action potential:
Notice that this group has the greatest effect on phase 0, while the action potential duration remains about the same.

Image by Lecturio. License: CC BY-NC-SA 4.0

Pharmacokinetics

  • Absorption:
    • Administered orally
    • Well absorbed
    • Flecainide: ↓ absorption when taken with milk
  • Distribution:
    • Flecainide: 40% protein bound
    • Propafenone: 95% protein bound
  • Metabolism:
    • Hepatic: cytochrome P450 system
    • Propafenone:
      • 2 active metabolites
      • 2 genetically distinct metabolic groups of individuals: poor and extensive metabolizers
  • Excretion: urine and feces

Indications

  • Paroxysmal atrial fibrillation Atrial fibrillation Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. Atrial Fibrillation/flutter
  • Prevention of paroxysmal supraventricular tachycardia Supraventricular tachycardia Supraventricular tachycardias are related disorders in which the elevation in heart rate is driven by pathophysiology in the atria. This group falls under the larger umbrella of tachyarrhythmias and includes paroxysmal supraventricular tachycardias (PSVTs), ventricular pre-excitation syndromes (i.e. Wolff-Parkinson-White syndrome), atrial flutter, multifocal atrial tachycardia, and atrial fibrillation. Supraventricular Tachycardias
  • Prevention of ventricular arrhythmias
  • Propafenone: treatment of life-threatening ventricular arrhythmias

Adverse effects

General:

  • Proarrhythmic effects:
    • Premature ventricular contractions
    • Ventricular tachycardia/fibrillation
    • Disturbances in K and magnesium levels can cause arrhythmias.
  • ↑ Risk of death in individuals with MI MI MI is ischemia and death of an area of myocardial tissue due to insufficient blood flow and oxygenation, usually from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is most commonly with chest pain, but women and patients with diabetes may have atypical symptoms. Myocardial Infarction
  • May aggravate or precipitate heart failure

Flecainide:

  • Headache
  • Dizziness
  • Dyspnea Dyspnea Dyspnea is the subjective sensation of breathing discomfort. Dyspnea is a normal manifestation of heavy physical or psychological exertion, but also may be caused by underlying conditions (both pulmonary and extrapulmonary). Dyspnea
  • Tremors

Propafenone:

  • Metallic taste
  • Dizziness
  • Bradycardia
  • Bronchospasm possible in individuals with asthma Asthma Asthma is a chronic inflammatory respiratory condition characterized by bronchial hyperresponsiveness and airflow obstruction. The disease is believed to result from the complex interaction of host and environmental factors that increase disease predisposition, with inflammation causing symptoms and structural changes. Patients typically present with wheezing, cough, and dyspnea. Asthma due to beta-blockade

Contraindications

  • 2nd- and 3rd-degree heart block
  • Brugada syndrome
  • Structural heart disease: ↑ mortality in individuals with heart failure and MI MI MI is ischemia and death of an area of myocardial tissue due to insufficient blood flow and oxygenation, usually from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is most commonly with chest pain, but women and patients with diabetes may have atypical symptoms. Myocardial Infarction
  • To be used with caution in individuals with hepatic and renal impairment → ↓ elimination

Comparison of Antiarrhythmic Drug Classes

Table: Comparison of antiarrhythmic drug classes 1‒4
Class Mechanism of action Effects Arrhythmia indications
1 1A
  • Block fast Na channels
  • ↓ Na entry into myocardial cells
  • Affect depolarization
  • ↓ Phase 0 slope
  • ↓ Conduction velocity in non-nodal tissues
  • Atrial and ventricular
  • WPW syndrome
1B Ventricular
1C Mostly atrial
2
  • Block beta receptors
  • ↓ Ca influx into myocardial cells
  • Affect refractory period
  • ↓ Phase 4 slope
  • ↑ Phase 4 duration
  • ↓ Conduction velocity in nodal and non-nodal tissues
Atrial and ventricular
3
  • Block K channels
  • ↓ K efflux from myocardial cells
  • Affect repolarization
  • ↑ Phase 3 duration
  • Most drugs ↓ impulse transmission in non-nodal tissues
  • Amiodarone and sotalol ↓ nodal conduction
Atrial and ventricular
4
  • Block Ca channels
  • ↓ Ca influx into myocardial cells
  • Affect phase 2 in non-nodal tissues
  • ↓ Phase 0 slope in nodal tissues
  • ↓ Conduction velocity in nodal tissues
Atrial
Ca: calcium
WPW: Wolff-Parkinson-White

References

  1. Kumar, K., Zimetbaum, P. (2021). Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials. In Knight, B. (Ed.), UpToDate. Retrieved June 19, 2021, from https://www.uptodate.com/contents/antiarrhythmic-drugs-to-maintain-sinus-rhythm-in-patients-with-atrial-fibrillation-clinical-trials
  2. Makielski, J., Eckhardt, L. (2021). Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs. In Levy, S. (Ed.), UpToDate. Retrieved June 19, 2021, from https://www.uptodate.com/contents/cardiac-excitability-mechanisms-of-arrhythmia-and-action-of-antiarrhythmic-drugs
  3. Kumar, K. (2021). Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations. In Zimetbaum, P, Knight, B. (Ed.), UpToDate. Retrieved June 19, 2021, from https://www.uptodate.com/contents/antiarrhythmic-drugs-to-maintain-sinus-rhythm-in-patients-with-atrial-fibrillation-recommendations
  4. Giardina, E.G. (2021). Major side effects of class I antiarrhythmic drugs. In Zimetbaum, P. (Ed.), UpToDate. Retrieved June 19, 2021, from https://www.uptodate.com/contents/major-side-effects-of-class-i-antiarrhythmic-drugs
  5. Wyse, D.G., Waldo, A.L., DiMarco, J.P., et al. (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med; 347, 1825. https://pubmed.ncbi.nlm.nih.gov/12466506/
  6. Falk, R.H. (2001). Atrial fibrillation. N Engl J Med; 344, 1067. https://pubmed.ncbi.nlm.nih.gov/11287978/
  7. Dan, G.A., Martinez-Rubio, A., Agewall, S., et al. (2018). Antiarrhythmic drugs-clinical use and clinical decision making: a consensus document from the European Heart Rhythm Association (EHRA) and European Society of Cardiology (ESC) Working Group on Cardiovascular Pharmacology, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and International Society of Cardiovascular Pharmacotherapy (ISCP). Europace; 20, 731. https://pubmed.ncbi.nlm.nih.gov/29438514/
  8. Mitchell, L.B. (2021). Drugs for arrhythmias. MSD Manual Professional Version. Retrieved July 11, 2021, from https://www.msdmanuals.com/professional/cardiovascular-disorders/arrhythmias-and-conduction-disorders/drugs-for-arrhythmias#v21365769
  9. King, S., et al. (2021). Antiarrhythmic medications. StatPearls. Retrieved July 11, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK482322/

Study on the Go

Lecturio Medical complements your studies with evidence-based learning strategies, video lectures, quiz questions, and more – all combined in one easy-to-use resource.

Learn even more with Lecturio:

Complement your med school studies with Lecturio’s all-in-one study companion, delivered with evidence-based learning strategies.

User Reviews

0.0

()

¡Hola!

Esta página está disponible en Español.

🍪 Lecturio is using cookies to improve your user experience. By continuing use of our service you agree upon our Data Privacy Statement.

Details