Class 5 Antiarrhythmic Drugs

Class 5 antiarrhythmic drugs are a miscellaneous group of medications that do not belong to a traditional class of antiarrhythmics. These drugs have varied mechanisms of action and uses. The medications in this class are digoxin, adenosine, Mg sulfate, and atropine. Digoxin’s antiarrhythmic effect comes from increased vagal tone and direct action on the atrioventricular node (AVN), resulting in decreased AVN conduction and sinoatrial (SA) automaticity. Digoxin can be used for 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 (AFib), atrial flutter Atrial flutter Atrial flutter is a regular supraventricular tachycardia characterized by an atrial heart rate between 240/min and 340/min (typically 300/min), atrioventricular (AV) node conduction block, and a "sawtooth" pattern on an electrocardiogram (ECG). Atrial Flutter (AFL), and 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 (SVT). Adenosine works on purinergic receptors to cause hyperpolarization, which causes decreased AVN velocity and increased refractoriness, making it a good choice for cardioversion of SVT. Magnesium’s mechanism of action is not well understood, but it does interact with multiple ion transport mechanisms and is helpful for patients with QT prolongation and torsades de pointes. Finally, atropine antagonizes muscarinic receptors and blocks vagal effects on the heart, making it useful in symptomatic and unstable bradyarrhythmias Bradyarrhythmias Bradyarrhythmia is a rhythm in which the heart rate is less than 60/min. Bradyarrhythmia can be physiologic, without symptoms or hemodynamic change. Pathologic bradyarrhythmia results in reduced cardiac output and hemodynamic instability causing syncope, dizziness, or dyspnea. Bradyarrhythmias.

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Editorial responsibility: Stanley Oiseth, Lindsay Jones, Evelin Maza

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Overview

Vaughan-Williams classification

This is the most commonly used classifications for antiarrhythmic drugs. There are 5 classes based on the drug class’s general effect (mechanism of action):

  • Class 1: sodium channel blockers (divided into 3 subgroups)
  • Class 2: beta-blockers
  • Class 3: potassium 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) (CCBs)
  • Class 5: miscellaneous agents that cannot be categorized into the above groups
    • They have no common mechanism of action.
    • Includes: 
      • Digoxin 
      • Adenosine 
      • Magnesium sulfate
      • Atropine

Digoxin

Mechanism of action

  • ↑ Vagal tone and direct action on the atrioventricular node (AVN): 
    • ↑ Refractory period → ↓ conduction velocity in the AVN
    • ↓ Sinoatrial (SA) node automaticity
    • Effect: ↓ ventricular rate in the setting of rapid supraventricular arrhythmias
  • Reversibly inhibits the Na/K-ATPase of myocytes, resulting in:
    • ↑ Intracellular Na → ↓ Na-calcium (Ca) antiporter exchange → ↓ Ca efflux 
    • ↑ intracellular Ca → ↑ Ca binding to contractile proteins → ↑ myocardial contractility 
  • May cause characteristic changes to a resting 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) (“digitalis effect”): 
    • ↑ PR interval (due to ↓ atrioventricular (AV) conduction)
    • ↓ QT interval
    • “Scooped” ST-segment depressions are the classic findings
    •  T wave flattening or inversions
Ecg typical “scooped” st-depression resulting from digoxin use

Typical “scooped” ST-segment depression resulting from digoxin use

Image: “Typical for digoxin intoxication is the oddly shaped ST-depression” by I.A.C. van der Bilt, MD. License: CC BY-NC-SA 3.0

Pharmacokinetics

  • Absorption: 
    • Routes of administration: 
      • Oral 
      • IV
    • Passive, nonsaturable absorption in the proximal small intestine Small intestine The small intestine is the longest part of the GI tract, extending from the pyloric orifice of the stomach to the ileocecal junction. The small intestine is the major organ responsible for chemical digestion and absorption of nutrients. It is divided into 3 segments: the duodenum, the jejunum, and the ileum. Small Intestine
    • Food delays absorption.
  • Distribution:
    • Higher concentrations in:
      • Heart
      • Liver Liver The liver is the largest gland in the human body. The liver is found in the superior right quadrant of the abdomen and weighs approximately 1.5 kilograms. Its main functions are detoxification, metabolism, nutrient storage (e.g., iron and vitamins), synthesis of coagulation factors, formation of bile, filtration, and storage of blood. Liver
      • Kidneys Kidneys The kidneys are a pair of bean-shaped organs located retroperitoneally against the posterior wall of the abdomen on either side of the spine. As part of the urinary tract, the kidneys are responsible for blood filtration and excretion of water-soluble waste in the urine. Kidneys
      • Skeletal muscle
    • Crosses the blood-brain barrier and placenta Placenta The placenta consists of a fetal side and a maternal side, and it provides a vascular communication between the mother and the fetus. This communication allows the mother to provide nutrients to the fetus and allows for removal of waste products from fetal blood. Placenta, Umbilical Cord, and Amniotic Cavity
  • Metabolism and excretion: 
    • Minimal hepatic metabolism:
      • Approximately 16% of an absorbed dose is metabolized to active metabolites.
      • Does not interact with the cytochrome P450 system
    • Predominantly excreted in the urine (50%–70% as an unchanged drug)

Indications

  • Arrhythmia (for HR control when other therapies are ineffective or contraindicated)
    • Atrial fibrillation (AFib) or atrial flutter Atrial flutter Atrial flutter is a regular supraventricular tachycardia characterized by an atrial heart rate between 240/min and 340/min (typically 300/min), atrioventricular (AV) node conduction block, and a "sawtooth" pattern on an electrocardiogram (ECG). Atrial Flutter (AFL)
    • Supraventricular tachycardia (SVT)
  • Systolic heart failure

Adverse effects

  • Cardiac conduction abnormalities and arrhythmia
    • Paroxysmal atrial tachycardia (PAT)
    • Premature atrial or ventricular contractions
    • AV block AV block Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. Atrioventricular Block
    • Ventricular arrhythmias
  • Other:
    • Nausea and vomiting
    • Skin Skin The skin, also referred to as the integumentary system, is the largest organ of the body. The skin is primarily composed of the epidermis (outer layer) and dermis (deep layer). The epidermis is primarily composed of keratinocytes that undergo rapid turnover, while the dermis contains dense layers of connective tissue. Structure and Function of the Skin rash
    • Blurred vision
    • Lethargy

Contraindications

  • Use should be avoided:
    • AV block AV block Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. Atrioventricular Block
    • Wolff-Parkinson-White (WPW) syndrome
    • Ventricular fibrillation Ventricular fibrillation Ventricular fibrillation (VF or V-fib) is a type of ventricular tachyarrhythmia (> 300/min) often preceded by ventricular tachycardia. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular Fibrillation ( V-fib V-fib Ventricular fibrillation (VF or V-fib) is a type of ventricular tachyarrhythmia (> 300/min) often preceded by ventricular tachycardia. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular Fibrillation)
    • Electrolyte abnormalities:
      • Hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia
      • Hypomagnesemia
      • Hypercalcemia Hypercalcemia Hypercalcemia (serum calcium > 10.5 mg/dL) can result from various conditions, the majority of which are due to hyperparathyroidism and malignancy. Other causes include disorders leading to vitamin D elevation, granulomatous diseases, and the use of certain pharmacological agents. Symptoms vary depending on calcium levels and the onset of hypercalcemia. Hypercalcemia 
  • Use with caution:
    • Renal failure
    • Elderly patients 
    • Thyroid disease 
    • Acute coronary syndrome (ACS): may ↑ myocardial oxygen demand → ischemia
    • Hypertrophic cardiomyopathy Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is the most commonly inherited cardiomyopathy, which is characterized by an asymmetric increase in thickness (hypertrophy) of the left ventricular wall, diastolic dysfunction, and often left ventricular outflow tract obstruction. Hypertrophic Cardiomyopathy (HCM) with left ventricular outflow tract obstruction
    • 2nd- or 3rd-degree heart block: unless a functioning pacemaker is placed

Drug interactions

  • ↑ AV blocking/bradycardic effect:
    • CCBs
    • Beta-blockers
    • Dronedarone
    • Lacosamide
  • ↑ Risk of toxicity due to:
    • ↑ Digoxin concentration:
      • Amiodarone
      • Quinidine
      • Spironolactone
    • Hypokalemia Hypokalemia Hypokalemia is defined as plasma potassium (K+) concentration < 3.5 mEq/L. Homeostatic mechanisms maintain plasma concentration between 3.5-5.2 mEq/L despite marked variation in dietary intake. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia and/or hypomagnesemia:
      • Loop diuretics Loop diuretics Loop diuretics are a group of diuretic medications primarily used to treat fluid overload in edematous conditions such as heart failure and cirrhosis. Loop diuretics also treat hypertension, but not as a 1st-line agent. Loop Diuretics
      • Thiazide diuretics Thiazide diuretics Thiazide and thiazide-like diuretics make up a group of highly important antihypertensive agents, with some drugs being 1st-line agents. The class includes hydrochlorothiazide, chlorothiazide, chlorthalidone, indapamide, and metolazone. Thiazide Diuretics

Adenosine

Chemistry

Adenosine is a naturally occurring purine nucleoside base.

Mechanism of action

Cardiac nodal cells:

  • Adenosine type 1 receptors → G-protein activation → blocks adenylyl cyclase
  • ↓ CAMP → L-type Ca channels are deactivated and K channels are activated
  • ↓ Ca influx and ↑ K efflux → hyperpolarization and action potential suppression
  • Antiarrhythmic effect:
    • ↓ AVN conduction velocity 
    • ↑ AVN refractory period
    • Reentry circuit through the AVN is interrupted. 
    • Normal sinus rhythm is restored.

Vascular smooth muscle cells:

  • Adenosine type 2 receptors → G-protein activation → adenylyl cyclase stimulation 
  • ↑ CAMP → protein kinase activation → stimulates K channels → hyperpolarization
  • Vascular smooth muscle relaxation → vasodilation

Pharmacokinetics

  • Absorption:
    • Route of administration: IV
    • Immediate onset
  • Metabolism and excretion: 
    • Half-life: < 10 seconds
    • Rapid cellular uptake by vascular endothelium and erythrocytes Erythrocytes Erythrocytes, or red blood cells (RBCs), are the most abundant cells in the blood. While erythrocytes in the fetus are initially produced in the yolk sac then the liver, the bone marrow eventually becomes the main site of production. Erythrocytes
    • Metabolized intracellularly to: 
      • AMP
      • Inosine → uric acid → excreted by kidneys

Indications

  • Arrhythmias:
    • Used in cardioversion of paroxysmal SVT (PSVT) to normal sinus rhythm
    • Transient AV blockade can aid in diagnosis of a tachyarrhythmia Tachyarrhythmia A tachyarrhythmia is a rapid heart rhythm, regular or irregular, with a rate > 100 beats/min. Tachyarrhythmia may or may not be accompanied by symptoms of hemodynamic change. Tachyarrhythmias caused by AFib or AFL.
    • Not effective for converting AFib or AFL
  • Diagnostic aid in myocardial perfusion scintigraphy:
    • Causes vasodilation of the coronary arteries Arteries Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Arteries → ↑ blood flow in the normal arteries Arteries Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Arteries but not in stenotic coronary arteries Arteries Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Arteries 
    • ↓ Thallium-201 uptake in stenotic arteries Arteries Arteries are tubular collections of cells that transport oxygenated blood and nutrients from the heart to the tissues of the body. The blood passes through the arteries in order of decreasing luminal diameter, starting in the largest artery (the aorta) and ending in the small arterioles. Arteries are classified into 3 types: large elastic arteries, medium muscular arteries, and small arteries and arterioles. Arteries → allows visualization of areas with insufficient blood flow
The use of adenosine in tachyarrhythmias 5 antiarrythmics

The use of adenosine in tachyarrhythmias:
A: Adenosine can be used to convert supraventricular tachycardias (SVTs), such as atrioventricular node (AVN) reentry tachycardia. Transient blockade of the AVN (noted by the long pause) terminates the reentry circuit, allowing for the resumption of normal sinus rhythm.
B: Sometimes, the underlying rhythm is not certain. Transient AVN blockade may allow for rhythm identification in these cases. This is demonstrated by the uncovering of “sawtooth” flutter waves due to atrial flutter Atrial flutter Atrial flutter is a regular supraventricular tachycardia characterized by an atrial heart rate between 240/min and 340/min (typically 300/min), atrioventricular (AV) node conduction block, and a "sawtooth" pattern on an electrocardiogram (ECG). Atrial Flutter (AFL).

Image by Lecturio.

Adverse effects

  • Common short-lived symptoms:
    • Flushing
    • Diaphoresis
    • Dizziness
    • Chest pain Chest Pain Chest pain is one of the most common and challenging complaints that may present in an inpatient and outpatient setting. The differential diagnosis of chest pain is large and includes cardiac, gastrointestinal, pulmonary, musculoskeletal, and psychiatric etiologies. Chest Pain 
    • Nausea
    • Anxiety 
    • Feeling of impending doom 
  • Cardiovascular events:
    • 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
    • Transient or new arrhythmias:
      • AFib/AFL
      • High-degree heart block
    • Cardiac arrest Cardiac arrest Cardiac arrest is the sudden, complete cessation of cardiac output with hemodynamic collapse. Patients present as pulseless, unresponsive, and apneic. Rhythms associated with cardiac arrest are ventricular fibrillation/tachycardia, asystole, or pulseless electrical activity. Cardiac Arrest
    • Myocardial ischemia
    • Cerebrovascular accident Cerebrovascular accident An ischemic stroke (also known as cerebrovascular accident) is an acute neurologic injury that occurs as a result of brain ischemia; this condition may be due to cerebral blood vessel occlusion by thrombosis or embolism, or rarely due to systemic hypoperfusion. Ischemic Stroke
  • Pulmonary events:
    • Dyspnea 
    • Bronchospasm

Contraindications

  • Hypersensitivity to adenosine
  • Clinically active bronchospasm
  • 2nd- or 3rd-degree AV block AV block Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. Atrioventricular Block
  • Sick sinus syndrome Sick Sinus Syndrome Sick sinus syndrome (SSS), also known as sinus node dysfunction, is characterized by degeneration of the sinoatrial (SA) node, the heart's primary pacemaker. Patients with SSS may be asymptomatic or may present with tachycardia or bradycardia. Sick Sinus Syndrome ( SSS SSS Sick sinus syndrome (SSS), also known as sinus node dysfunction, is characterized by degeneration of the sinoatrial (SA) node, the heart's primary pacemaker. Patients with SSS may be asymptomatic or may present with tachycardia or bradycardia. Sick Sinus Syndrome)
  • Symptomatic bradycardia
  • WPW with preexcitation AFib/AFL → can cause degeneration to V-fib V-fib Ventricular fibrillation (VF or V-fib) is a type of ventricular tachyarrhythmia (> 300/min) often preceded by ventricular tachycardia. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular Fibrillation

Drug interactions

  • ↓ Efficacy of adenosine (adenosine receptor antagonists):
    • Caffeine
    • Theophylline
  • ↑ Effect of adenosine (AVN blockade and/or adverse effects):
    • Carbamazepine
    • Dipyridamole
    • Nicotine
    • Digoxin
    • Verapamil

Magnesium (Mg) Sulfate

Mechanism of action

  • Mg plays an important role in cardiac conduction, since it affects multiple channels:
    • Na/K-ATPase (cofactor)
    • Ca channels (blocks)
    • Na channels 
    • Some K channels 
  • Effects:
    • ↓ Influx of Ca → suppresses early afterdepolarizations
    • Stabilization of the cardiac membrane
    • ↓ SA node impulse and ↑ conduction time

Pharmacokinetics

Magnesium supplementation for arrhythmias is usually administered IV as Mg sulfate.

  • Onset of action: immediate
  • Duration of action: 30 minutes
  • Excretion: renal

Indications

Magnesium is used as an antiarrhythmic for:

  • QT prolongation and torsades de pointes
  • Digoxin toxicity
  • Other hypomagnesemia-induced arrhythmias 
    • SVT 
    • AFib/AFL
    • Ventricular tachycardia/ V-fib V-fib Ventricular fibrillation (VF or V-fib) is a type of ventricular tachyarrhythmia (> 300/min) often preceded by ventricular tachycardia. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular Fibrillation

Adverse effects

  • Facial flushing
  • 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
  • Diminished reflexes
  • Respiratory depression
  • Asystole

Warnings and precautions

Magnesium should be used with caution in patients with:

  • Neuromuscular disorders, especially 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 (MG) → worsened symptoms
  • Renal impairment → hypermagnesemia

Drug interactions

  • Gabapentin: ↑ depressive effect 
  • Neuromuscular blocking agents: ↑ neuromuscular blocking effect
  • Dihydropyridine CCBs: ↑ risk of hypotension or muscle weakness

Atropine

Mechanism of action

  • Competitive antagonist of acetylcholine at muscarinic receptors → blocks vagal effect on the heart 
  • This leads to:
    • ↑ AVN conduction velocity
    • ↑ SA node automaticity
    • ↑ HR

Pharmacokinetics

  • Absorption:
    • Rapid
    • Well absorbed
    • Onset of action:
      • IV: almost immediate
      • IM: 15–30 minutes
  • Distribution:
    • Widely throughout the body
    • Crosses the blood-brain barrier
    • Protein binding: 14%–44%
  • Metabolism: hepatic via enzymatic hydrolysis
  • Excretion: urine

Indications

  • Arrhythmia: 
    • Symptomatic or unstable bradyarrhythmias Bradyarrhythmias Bradyarrhythmia is a rhythm in which the heart rate is less than 60/min. Bradyarrhythmia can be physiologic, without symptoms or hemodynamic change. Pathologic bradyarrhythmia results in reduced cardiac output and hemodynamic instability causing syncope, dizziness, or dyspnea. Bradyarrhythmias
    • Not usually effective for:
      • 2nd-degree AV block AV block Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. Atrioventricular Block, Mobitz type 2
      • 3rd-degree AV block AV block Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. Atrioventricular Block
  • Other indications:
    • Muscarine-containing mushroom poisoning
    • Organophosphate poisoning
    • ↓ Salivation and respiratory secretions

Adverse 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 effects:
    • Tachycardia
    • Pupil Pupil The pupil is the space within the eye that permits light to project onto the retina. Anatomically located in front of the lens, the pupil's size is controlled by the surrounding iris. The pupil provides insight into the function of the central and autonomic nervous systems. Physiology and Abnormalities of the Pupil dilation and blurred vision
    • Dry mouth
    • Constipation Constipation Constipation is common and may be due to a variety of causes. Constipation is generally defined as bowel movement frequency < 3 times per week. Patients who are constipated often strain to pass hard stools. The condition is classified as primary (also known as idiopathic or functional constipation) or secondary, and as acute or chronic. Constipation
    • Urinary retention
    • Anhidrosis
    • Hallucinations and behavioral changes
  • Hypersensitivity, including anaphylactic reactions

Contraindications

  • Narrow-angle 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: may precipitate acute 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
  • MG: may precipitate a myasthenic crisis

Drug interactions

  • The following medications may enhance the anticholinergic effects of atropine:
    • Amantadine
    • Botulinum toxin
    • Glycopyrrolate
    • Mirabegron
  • Atropine may: 
    • ↓ The absorption of nitroglycerin
    • ↓ Therapeutic effect of acetylcholinesterase (AChE) inhibitors
    • ↑ Constipating and/or urinary retention side effects of:
      • Clozapine
      • Opioid agonists

References

  1. Levine, E. (2019). Classification of arrhythmic agents. Medscape. Retrieved August 12, 2021, from https://emedicine.medscape.com/article/2172024-overview
  2. Makielski, JC, & Eckhardt, LL. (2019). Cardiac excitability, mechanisms of arrhythmias, and action of antiarrhythmic drugs. UpToDate. Retrieved July 22, 2021, from https://www.uptodate.com/contents/cardiac-excitability-mechanisms-of-arrhythmia-and-action-of-antiarrhythmic-drugs
  3. Digoxin: Drug information. UpToDate. Retrieved July 22, 2021, from https://www.uptodate.com/contents/digoxin-drug-information
  4. Magnesium sulfate: Drug information. UpToDate. Retrieved July 22, 2021, from https://www.uptodate.com/contents/magnesium-sulfate-drug-information
  5. Adenosine: Drug information.  UpToDate. Retrieved July 22, 2021, from https://www.uptodate.com/contents/adenosine-drug-information
  6. Atropine: Drug information.  UpToDate. Retrieved July 22, 2021, from https://www.uptodate.com/contents/atropine-systemic-drug-information
  7. Hume, JR, & Grant, AO. (2012). Agents used in cardiac arrhythmias. In Katzung, BG, Masters, SB, & Trevor, AJ. (Eds.), Basic & clinical pharmacology (12th edition, pp. 227–250). https://pharmacomedicale.org/images/cnpm/CNPM_2016/katzung-pharmacology.pdf
  8. David, MNV, & Shetty, M. (2021). Digoxin. StatPearls. Retrieved August 26, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK556025/
  9. Singh, S, & McKintosh, R. (2021). Adenosine. StatPearls. Retrieved August 26, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK519049/
  10. Hicks, MA, & Tyagi, A. (2021). Magnesium sulfate. StatPearls. Retrieved August 26, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK554553/
  11. Voster, A. (2017). The pharmacology of amiodarone and digoxin as antiarrhythmic agents. Part I Anesthesia Refresher Course. University of Cape Town. http://www.anaesthesia.uct.ac.za/sites/default/files/image_tool/images/93/2017-29-Digoxin%20and%20Amiodarone%20%28A%20Vorster%29.pdf

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