An arrhythmia occurs when the electrical impulses that direct and regulate heartbeats do not function properly. This can lead to the heart beating:
Too fast (known as tachycardia)
Too slow (referred to as bradycardia)
Too early (premature contraction)
Too erratically (fibrillation)
Types of Arrhythmia:
Arrhythmias are categorized based on three factors:
Rate: Whether it’s too slow or too fast.
Origin: Whether it begins in the ventricles (lower chambers) or the atria (upper chambers).
Regularity: In a normally functioning heart, electrical impulses follow precise pathways. Interruptions in these pathways can cause abnormal heartbeats.
Specific types include:
Bradycardia: Heart rate slows to under 60 beats per minute. Causes can include heart block and sick sinus syndrome.
Tachycardia: Heart rate speeds up to more than 100 beats per minute. If brief, it may not be serious, but prolonged tachycardia may require medical attention.
Ventricular Arrhythmias: Begin in the ventricles and can be serious.
Remember, while some arrhythmias are common and harmless, others can be problematic. When an arrhythmia affects blood flow to vital organs, it can become life-threatening. Seek medical attention if you experience persistent irregular heartbeats or associated symptoms.
2. INTRODUCTION
“CHANGE IN RHYTHM”
• Abnormal electrical conduction or automaticity changes heart rate and
rhythm. Arrhythmias vary in severity—from mild, producing no symptoms,
and requiring no treatment (such as sinus arrhythmia, in which heart rate
increases and decreases with respiration) to catastrophic ventricular
fibrillation, which mandates immediate resuscitation.
• Normal blood pressure 60-100/min
• Brady arrhythmia < 60/min
• Tachyarrhythmia > 100/min
• Simple tachyarrhythmia 100-150/min
• Paroxysmal supraventricular tachycardia 150-200/min (Wolff-
Parkinson-White syndrome)
• Flutter 250-300
• Fibrillation >350
3. DEFINATION
Cardiac arrhythmia is a disorder of rate, rhythm ,origin or conduction
of impulses with heart.
Person’s heart may beat too quickly, too slowly, too early, or with an
irregular rhythm.
Arrhythmias occur when the electrical signals that coordinate
heartbeats are not working correctly.
8. TYPES OF CARDIAC ARRHYTHMIAS
1. Extra systole: Premature beats due to abnormal automaticity or after
depolarization , arising from atrioventricular (AV) node, atrium, or
ventricle.
2. Paroxysmal supra ventricular tachycardia: Sudden onset of atrial
tachycardia mostly due to circus re-entry type within or around the
AV node.
3. Atrial flutter: Higher impulse and the arterial beat up to 200–
350/min.
4. Atrial fibrillation: Arterial fibres are activated asynchronously at the
rate of 300–550/min.
9. 5. Ventricular tachycardia: It is a run of four consecutive ventricular
extra systoles. It may be sustained or un sustained arrhythmia due to
discharge from ectopic focus.
6. Torsades de pointes: Twisting of valves leads to polymorphic
ventricular charge and produces asynchronous complexes.
7. Ventricular fibrillation: Fractional activation of ventricles resulting in
in coordinated concentration of fibres with loss of pumping
function.
8. Atrio-ventricular block: It is due to depression of the impulse
conduction through AV node and bundle of his due to vagal
influence and ischaemias.
10. Mechanism of cardiac arrhythmia
1.Defects in Impulse Formation (SA Node)
i ) Altered Automaticity: In pathologic conditions, automaticity can be altered
when latent pacemaker cells take over the SA node's role as the pacemaker
of the heart.
ii) An escape beat may occur as a latent pacemaker initiates an impulse. A
series of escape beats, known as an escape rhythm, may result from
prolonged SA nodal dysfunction.
iii) On the other hand, an ectopic beat occurs when latent pacemaker cells
develop an intrinsic rate of firing that is faster than the SA nodal rate.
iv) A series of ectopic beats, termed an ectopic rhythm, can result from
ischemia, electrolyte abnormalities, or heightened sympathetic tone.
v) Direct tissue damage (such as can occur after a myocardial infarction) also
results in altered automaticity
12. ii) Conduction Block Conduction block occurs when an impulse fails to
propagate because of the presence of an area of in excitable cardiac tissue.
iii) Accessory Tract Pathways: Some individuals possess accessory electrical
pathways that bypass the AV node.
13. ETIOLOGY
• Alcohol abuse
• Diabetes
• Heart disease, such as congestive heart failure
• High blood pressure
• Hyperthyroidism, or an overactive thyroid gland
• Stress
• Scarring of the heart, often due to a heart attack
• Smoking
• Certain dietary and herbal supplements
• some medications
14. Pathophysiology
Altered automaticity, reentry, or conduction disturbances may cause
cardiac arrhythmias. Enhanced automaticity is the result of partial
depolarization, which may increase the intrinsic rate of the sino
atrial node or latent pacemakers, or may induce ectopic pacemakers
to reach threshold and depolarize.
Ischemia or deformation causes an abnormal circuit to develop
within conductive fibers. Although current flow is blocked in one
direction within the circuit, the descending impulse can travel in the
other direction. By the time the impulse completes the circuit, the
previously depolarized tissue within the circuit is no longer
refractory to stimulation; therefore, arrhythmias occur.
15. Symptoms of Arrhythmia
Symptoms of tachycardia
• Breathlessness
• Dizziness
• Fainting or nearly fainting
• Fluttering in the chest
• Chest pain
• Sudden weakness
16. Symptoms of bradycardia
• Angina, or chest pain
• Trouble concentrating
• Confusion
• Dizziness
• Tiredness
• Palpitations
• Shortness of breath
• Fainting or nearly fainting
17. Symptoms of atrial fibrillation
• Angina
• Breathlessness
• Dizziness
• Palpitations
• Fainting or nearly fainting
• Weakness
18. Class Known as Examples Mechanism
ia Na Quinidine Intermediate
channel Procanamide association
blockers Disopyramide
ib Lidocaine Fast association
phenytoin
mexiletine
ic Flecainide, slow association
Propafenone,
19. Class known as Example(s) Mechanism
ii Beta-blockers Propranolol β-Adrenoceptor
Esmolol antagonism
Sotalol
iii Potassium Amiodarone k+ channel blockers
channel Bretylium
blocker Dofetilide
Ibutilide
Dronederon
iv Calcium Verapamil Calcium channel blockers
channel Diltiazem
blockers
v Others Adenosine
Digitalis For PSVT
Isoprenaline For A-V block
Atropine AF, AFI and PSVT
Digitalis
20. MECHANISM OFACTION OF Na+ CHANNEL BLOCKERS
Bind to and block fast sodium channels
Rapid depolarization
Phase 0
Slope of phase 0 depends on the activation of fast sodium-channels and the rapid
entry of sodium ions into the cell
Blocking these channels decreases the slope of phase
Which also leads to a decrease in the amplitude of the action potential
21. Class 1a: Delaying depolarization resulting in prolonged action potential
duration
Class 1b: shorten the APD and reduce refractoriness (because of the opening of
K+ channels) Used only for ventricular arrhythmia
Class 1c: These agents have the most potent sodium channel blocking effects
with negligible effect on K+ channels (therefore no effect on APD)
22. Quinidine
Mechanism of action
acts on sodium channels on the neuronal cell membrane
limiting the spread of seizure activity and reducing seizure propagation
The anti arrhythmic actions are mediated through effects on sodium channels
in Purkinje fibers
Contraindications: Contraindicated in patients who are known to beallergic to
it, myasthenia gravis , intolerance or idiosyncracy to quinine, heart block,
coronary heart failure, hypotensive state, H/O embolism, prolonged QT
inter digitalis intoxication.
Pregnancy: Contraindicate. Lactation: Contraindicate
Severe side effect: Abnormal ECG, Tremor, Cerebral ischemia
23. Procainamide
Mechanism of action
Procainamide is sodium channel blocker
It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the
initiation and conduction of impulses
Thereby affecting local anesthetic action
Contraindications: Contraindicated in patients with hypersensitivity to the drug,
complete heart block, lupus erythematosus (cell mediated inflammation of
tissueorgan), torsades de pointes and prolonged Q-T interval.
Lactation: Contraindicated
Severe side effect: Agranulocytosis, SLE, pancytopenia, complete heart block, MI,
renal failure, hypotension (when given IV), Q-T prolongation, hallucination,
psychosis
24. Disopyramide
Mechanism of action
It inhibits the fast sodium channels
In animal studies disopyramide decreases the rate of diastolic
depolarization(phase 4) in cells with augmented automaticity
decreases the upstroke velocity (phase 0) and increases the action potential
duration of normal cardiac cells
decreases the disparity in refractoriness between infracted and adjacent
normally perfused myocardium, and has no effect on alpha or beta
adrenergic receptors
25. Contraindications: Contraindicated in the presence of cardiogenic shock ,
preexisting second- or third-degree AV block (if no pacemaker is present),
congenital Q-T prolongation known or hypersensitivity to the drug.
Pregnancy: Use with caution. Safety not established. Lactation: Use with
caution. Elderly: May be used. Pediatric: Use with caution
Severe side effect: Urinary frequency and urgency, blurred vision, urinary
hesitancy
26. Lidocaine
Mechanism of action
Lidocaine exerts its anti arrhythmic effect by depressing ventricular
excitability, and increasing the stimulation threshold of the ventricle during
diastole.
Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes
required for the initiation and conduction of impulses there by effecting
local anesthetic action
Contraindications: Contraindicated in patients with hypersensitivity to any of
the components of the formulation.
Pregnancy: Use with caution. Lactation: Use with caution.
Severe side effect: euphoria, tremors, convulsion, bradycardia, hypotension
27. Phenytoin
Mechanism of action
Acts on the sodium channel on both neuronal and cardiac tissue
Cause SA and SA nodal blocks as well as dysrhythmias
Also used in digoxin toxicity
Inhibits digitalis binding to the sodium potassium ATPase pump
Antagonizes digitalis induced delayed after depolarization
Contraindications: Contraindicated in patients with hypersensitivity to the
drug, sinus bradycardia and AV block. Rapid IV administration of the drug
is contraindicated. Pregnancy: Contraindicated. Lactation: Contraindicated
28. Severe side effect: On prolonged therapy gingival hypertrophy, Megaloblastic
anemia, neutropenia, lymphadenopathy, osteomalacia may occur.
Psychiatric changes
Gingival hypertrophy
29. Mexiletine
Mechanism of action
Mexiletine inhibits the inward sodium current required for the initiation and
conduction of impulses
Thus reducing the rate of rise of the action potential in phase 0
It decreases the effective refractory period (ERP) in Purkinje fibers in the heart
Increase in the ERP/APD ratio
It shortens the action potential duration
reduces refractoriness, and decreases Vmax in partially depolarized cells with
fast response action potentials
30. Contraindications: Contraindicated in the presence of cardiogenic shock or
preexisting second- or third-degree AV block (if no pacemaker is present)
Severe side effect: Tremor
Flecainide
Mechanism of action
Flecainide acetate is a class IC anti arrhythmic drug that possesses local
anesthetic and electrophysiologic activity
which markedly delays Na+ channel recovery
It suppresses VES,VT,WPW tachycardia and prevents recurrence of AV and
PSTV
32. Contraindication: Cardiogenic shock Hypersensitivity to flecainide Right
bundle branch block, with left hemi block and without pacemaker Second-
or third-degree atrio ventricular block, without pacemaker
Severe side effect : Cardiac arrest, Cardiac dysrhythmia, Cardiogenic shock,
Congestive heart failure, New onset or worsening , Disorder of pacing
function, Electrocardiogram abnormal, Heart block, Prolonged QT interval,
Sinus node dysfunction, Syncope , Torsades de pointes , Ventricular
fibrillation, Ventricular tachycardia
33. Propafenon
Mechanism of action
Blocking Na+ channels
Considerably depresses impulse transmission
Profound effect on His-Purkinje as well as accessory pathway conduction
Anterograde as well as retrograde conduction in the bypass tract of WPW
syndrome is retarted
Contraindication: Bradycardia Bronchospastic disorders or severe obstructive
pulmonary disease Brugada syndrome Cardiogenic shock Heart failure
Marked electrolyte imbalance Marked hypotension Sinoatrial,
atrioventricular, and intraventricular disorders of impulse generation or
conduction (e.g., sick sinus node syndrome, AV block) in the absence of an
artificial pacemaker
35. Class II: Beta blockers
Not all beta blockers is used in arrhythmia only beta 1 blockers and some non
selective beta blockers are used.
Mechanism of action
Beta-1 blockers results in inotropy
Decreased heart rate
Increased relaxation
Decreased cardiac conduction times
E.g.: Atenolol, Betaxolol, Bisoprolol, Esmolol
36. Atenolol
Contraindication: Cardiogenic shock Hypersensitivity to atenolol or any
component of the product Overt cardiac failure Second and third degree
heart block Sinus bradycardia
Severe side effect: Heart failure, Myocardial infarction, Ventricular arrhythmia
Endocrine Thyrotoxicosis Anaphylaxis, Systemic lupus erythematosus
Pulmonary embolism Withdrawal symptom
Esmolol
Contraindication: Cardiogenic shock Decompensated heart failure
Hypersensitivity reactions (e.g., anaphylaxis) to esmolol or any component
of the product (possibility of cross sensitivity between beta blockers)IV
administration of cardio depressant calcium-channel antagonists (e.g.,
verapamil) in close proximity to esmolol hydrochloride (i.e., while cardiac
effects are still present) Pulmonary hypertension Second- or third-degree
atrioventricular block Severe sinus bradycardia Sick sinus syndrome
37. Severe side effect: Myocardial infarction, Seizure, Bronchospasm
Non selective beta blockers
Mechanism of action
Stimulation of beta receptors can lead to the release of adrenaline
which causes the constriction of blood vessels
Nonselective beta-blockers inhibit all beta receptors
Contraction of heart muscles
resulting in decreased Heart rate
E.g. Propranalol, Sotalol
38. Propranolol
Contraindication: Blood pressure less than 50/30 mmHg Bronchial asthma
or bronchospasm, history of Cardiogenic shock or Decompensated heart
failure Heart rate less than 80 beats/min Hypersensitivity to propranolol
hydrochloride or any component of the product Pheochromocytoma
Premature infants with corrected age less than 5 weeks Second or third
degree heart block (if no pacemaker is present) Sick sinus syndrome (if no
pacemaker is present) Sinus bradycardia (if no pacemaker is present)
Infants weighing less than
Severe side effect: Brady arrhythmia, Cardiogenic shock, Congestive heart
failure, Heart block, Heart failure, Hypotension, Prolonged PR interval,
Shortened QT interval Erythroderma, Stevens-Johnson syndrome, Toxic
epidermal necrolysis Hypoglycemia Anaphylaxis Cerebrovascular accident
Bronchospasm
Other: Withdrawal symptom
39. Sotalol
Contraindication: Bronchial asthma or related bronchospastic conditions
Uncontrolled cardiogenic shock or decompensated heart failure Congenital
or acquired long QT syndromes or a baseline QT interval greater than 450
milliseconds for treatment of atrial fibrillation or flutter For treatment of
atrial fibrillation or flutter, the oral liquid and IV formulations are
contraindicated with CrCl less than 40 mL/min Hypersensitivity to sotalol
Serum potassium less than 4 mEq/L Sinus bradycardia (less than 50
beats/min during waking hours) sick sinus syndrome, or second or third
degree atrioventricular block without a functioning pacemaker
Severe side effect: Atrioventricular block, Brady arrhythmia , Cardiac
dysrhythmia , Congestive heart failure , Prolonged QT interval, Torsades de
pointes Disorder of glucose regulation Cerebrovascular accident
40. Class III
Potassium channel blockers
Class III agents predominantly block the potassium channels, thereby
prolonging repolarization (prolongation of APD). These drugs may precipitate
torsades de’ pointes due to prolongation of QT interval.
41. Amiodarone
Mechanism of action
Amiodarone also blocks myocardial potassium channels
which contributes to slowing of conduction and prolongation of refractoriness
The antisympathetic action and the block of calcium and potassium channels
responsible for the negative dromotropic effects on the sinus node and for the
slowing of conduction and prolongation of refractoriness in the
atrioventricular node
Its vasodilatory action can decrease cardiac workload and consequently
myocardial oxygen consumption
42. Contraindication: Cardiogenic shock ,Hypersensitivity to amiodarone or to
any of its components, including iodine Sick sinus syndrome, second- or
third-degree atrioventricular block, bradycardia leading to syncope without
a functioning pacemaker Severe sinus bradycardia or second or third
degree atrioventricular block, if no pacemaker is present
Severe side effect: Bradyarrhythmia, Cardiac dysrhythmia, Congestive heart
failure, High threshold for implanted defibrillator, Prolonged QT interval,
Sinus arrest, Torsades de pointes , Vacuities, Ventricular
arrhythmia Injection site extravasation, Stevens-Johnson syndrome, Toxic
epidermal necrolysis Hyperthyroidism , Hypothyroidism , Thyroid cancer,
Thyrotoxicosis Thrombocytopenia Hepatotoxicity Anaphylaxis,
Hypersensitivity reaction, Lupus erythematosus Low back pain, acute,
Rhabdomyolysis Pseudotumor cerebri, Raised intracranial pressure
Blindness AND/OR vision impairment level, Optic neuritis, Toxic optic
neuropathy Renal impairment Acute respiratory distress syndrome ,
Pulmonary fibrosis, Pulmonary toxicity
43. Dronedarone
Mechanism of action
Dronedarone is multichannel blocker
Inhibits delayed rectifier and other potassium channels and L type of calcium
channel
The non competitive beta adrenergic blocking activity is more marked compare to
amiodarone
Contraindication: atrial fibrillation, permanent (when normal sinus rhythm will
not or cannot be restored) Atrioventricular block, second- or third-degree, or
sick sinus syndrome (except when used in conjunction with a functioning
pacemaker) Bradycardia of less than 50 beats per minute Concomitant use of
QT-prolonging drugs or herbal products that might increase the risk of Torsade
de Pointes Concomitant use of strong CYP3A inhibitors Heart failure,
symptomatic, with NYHA Class IV symptoms or recent decomposition
requiring hospitalization Hepatic impairment, severe Hypersensitivity to
dronedarone or any of its excipients Liver or lung toxicity due to previous use
of amiodarone Pregnancy or nursing QTc Bazett interval of 500 msec or
greater or PR interval greater than 280 msec
44. Severe side effect : Congestive heart failure, Prolonged QT interval
Hepatotoxicity, Liver failure Acute renal failure, Renal failure Interstitial
lung disease
Dofetilide
Contraindication: Concomitant use of cimetidine, dolutegravir,
hydrochlorothiazide (alone or with triamterene), ketoconazole, megestrol,
prochlorperazine, trimethoprim (alone or with sulfamethoxazole), or
verapamil; increased risk of QT-interval prolongation Congenital or
acquired long QT syndromes (QTc interval greater than 440 msec or
500 msec for patients with ventricular conduction
abnormalities) Hypersensitivity to dofetilide Severe renal impairment (CrCl
less than 20 mL/min)
Severe side effect: Heart block , Prolonged QT interval, Torsades de pointes ,
Ventricular arrhythmia, Ventricular fibrillation , Ventricular tachycardia
45. Ibutilide
Contraindication: Hypersensitivity to ibutilide or any other component of the
product
Severe side effect: Bradyarrhythmia, Heart block , Prolonged QT interval ,
Torsades de pointes, Ventricular arrhythmia Cerebrovascular accident
Renal failure Pulmonary edema
46. Class IV
Calcium channel blockers
Mechanism of action
Class IV agents are the blockers of L-type voltage gated calcium channels
They decrease the rate of phase 4 depolarization in SA and AV nodes
This results in decreased automaticity of SA node
decreased conduction through the AV node
E.g. Verapamil, Diltiazem
47. Verapamil
Mechanism of action
Verapamil hydrochloride is an L-type calcium channel inhibitor (slow-channel
blocker)
that selectively blocks the transmembrane influx of calcium ions into arterial
smooth muscles including conductile and contractile myocardial cells
without affecting the concentration of serum calcium
Its hypertensive effect is attributed to the reduction of systemic vascular
resistance and selective vasodilation of peripheral arteries
Its antianginal effect is related to inhibition of coronary spasm, and relaxation
of main coronary artery and coronary arterioles
48. Verapamil is drug of choice for the treatment of supra ventricular
tachycardia (SVT) and for the prophylaxis of PSVT.
Contraindication : atrial fibrillation/flutter associated with accessory bypass
tract (e.g., Wolff-Parkinson-White)cardiogenic shock hypersensitivity to
verapamil hydrochloride hypotension (less than 90 mmHg systolic
pressure) left ventricular dysfunction, severe second- or third-degree
atrioventricular block (without functioning artificial pacemaker) sick sinus
syndrome (without functioning artificial pacemaker)
Severe side effect: Atrioventricular block, Myocardial infarction ,Pulmonary
edema
49. Diltiazem
Mechanism of action
Diltiazem hydrochloride is a slow calcium channel blocker
that blocks calcium ion influx during depolarization of cardiac and vascular
smooth muscle
It decreases peripheral vascular resistance and causes relaxation of the
vascular smooth muscle resulting in a decrease of both systolic and
diastolic blood pressure
Diltiazem slows calcium entry through membranes in vascular myocardial
muscle fibre and smooth muscle fibre and thus decreases the quantity of
intracellular calcium reaching contractile proteins.
It increases coronary flow by reducing resistance.
Due to its moderate bradycardiac action and its moderate reduction in systemic
arterial resistance, diltiazem reduces the cardiac workload.
50. No negative inotropic effect has been demonstrated on a healthy myocardium.
Diltiazem induces a moderate slowing in heart rate and can have a
depressant effect on a diseased sinus node
Contraindication: Acute MI with pulmonary congestion on x-
ray Administration of IV beta-blockers within a few hours of IV
diltiazem Atrial fibrillation or flutter associated with an accessory bypass
tract (Wolff-Parkinson-White or short PR syndromes); risk of potentially
fatal heart rate fluctuations Cardiogenic shock Heart block, second or third-
degree atrioventricular without a functioning ventricular
pacemaker Hypersensitivity to diltiazem Newborns; some IV injections
contain benzyl alcohol Sick sinus syndrome without a functioning
ventricular pacemaker Symptomatic hypotension, systolic blood pressure
90 mmHg or less Ventricular tachycardia; may lead to hemodynamic
deterioration and ventricular fibrillation
51. Severe side effect: Congestive heart failure , Heart block, Myocardial
infarction Hepatotoxicity
Class V
Other drugs
Class V agents include digoxin, adenosine, magnesium, atropine and
potassium
Adenosine
Adenosine Administered by rapid i.v. injection
adenosine terminates within 30 sec. more than 90% episodes of PSVT
involving the A-V node
It activates ACh sensitive K+ channels and causes membrane hyper
polarization through interaction with Al type of adenosine GPCRs on SA
node (pacemaker depression brady-pro30secmathehashascardia), A-V node
(prolongation of ERP →slowing of conduction)
52. and atrium (shortening of AP, reduced excitability).
It indirectly reduces Ca²+ current in A-V node
Depression of the reentrant circuit through A-V node is responsible for
termination of majority of PSVTs.
Adrenergically induced DADs in ventricle are also suppressed.
Coronary dilatation occurs transiently
53. Contraindication: Known or suspected bronchoconstrictive or bronchospastic
lung disease (e.g., asthma) Second- or third-degree atrioventricular block
(if no pacemaker is present) Sinus node disease, such as sick sinus
syndrome or symptomatic bradycardia
Severe side effect: Cardiac arrest, Cardiac dysrhythmia, Complete
atrioventricular block , Heart failure, Ventricular arrhythmia , Ventricular
tachycardia Bronchospasm, In asthmatic
54. Atropine
When AV block is due to vagal overactivity e.g. digitalis toxicity, some cases
of MI ; it can be improved by Atropine (i.m)
Magnesium
Magnesium is used for treatment of both congenital and acquired
long QT syndrome
Newer drug
Tocainide
55. Tocainide
class ib drug
Sodium channel blockers
Contraindication: hypersensitivity to tocainide or amide type anesthetics
,second or third degree AV block
Severe side effect : Cardiac dysrhythmia, Scaling eczema, Stevens-Johnson
syndrome Agranulocytosis , Anemia , Thrombocytopenia Hepatotoxicity
,Lupus erythematosus ,Seizure Disorder of respiratory system
56. References
• K D TRIPATHI Books seventh edition page 526-538 . (n.d.).
Https://www.jainbookdepot.com/. from
http://www.jainbookdepot.com/servlet/jbdispinfo?offset=0&searchtype=Au
thor&text1=K%20D%20Tripathi
• MedlinePlus - health information from the National Library of Medicine.
(n.d.). Medlineplus.gov. Retrieved, from https://medlineplus.gov/
• (N.d.). Mypustak.com. from https://www.mypustak.com/product/DRUGS-
AND-DOSAGES-A-QUICK-GLANCE-None?1516041
• Micromedex Products: Please Login. (n.d.). Micromedexsolutions.com.
Retrieved October 31, 2023, from https://www.micromedexsolutions.com
• "Drugs.com - prescription drug information. (n.d.). Drugs.com. from
https://www.drugs.com/“
