Anti-arrhythmics pharmacology 2023.pptx

DR KTD PRIYADARSHANI
REGISTRAR IN EMERGENCY MEDICINE
2024/01/03

ANTI ARRHYTHMIC DRUGS
OBJECTIVES
▸ Physiology
▸ Classification
▸ Perioperative considerations
▸ Use of antiarrhythmics

PERI OPERATIVE APPROACH
▸ Arrhythmias are common in perioperative period, most are relatively benign
▸ Due to transient changes in physiology, surgical stimuli, or the effect of anesthetic agents.
▸ Perioperative factors that facilitate cardiac arrhythmias
▸ Hypoxemia, electrolyte imbalance, acid base,
▸ MI
▸ Altered sympathetic activity
▸ Administration of drugs

PRE OP OPTIMISATION
▸ “Once the causes are treated- arrhythmia typically resolve”
▸ Alleviation of symptoms
▸ To improve cardiac function (result of tachycardia or dys-synchrony)
▸ To prevent progression into a life-threatening arrhythmia
▸ To reduce the need for electrical cardio-version

THE RISK?
▸ Narrow therapeutic window
▸ Inter-patient variability in efficacy
▸ Association between antiarrhythmic drugs and mortality in patients with structural
heart disease, MI or both (Cardiac Arrhythmia Suppression Trial (CAST), Survival with Oral D-sotalol
(SWORD), and Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) )
▸ Should be closely monitored for drug-induced proarrhythmias

0-IVABRADINE
▸ Reducing the ‘funny current’ during phase 4
▸ Hyperpolarization-Activated Cyclic-Nucleotide-Gated Channel Blocker
▸ Ivabradine is the only drug ( oral )
▸ Negative chronotropic actions
▸ No other hemodynamic effects
▸ Useful in patients with impaired cardiac function who have suboptimal HR control despite treatment with
b-blockers
▸ “ Clinical trial- a single dose of ivabradine before surgery - attenuated HR response to intubation and
surgical incision without causing hypotension- role in myocardial protection in selected patients

CLASS I: VOLTAGE-GATED SODIUM CHANNEL BLOCKERS
▸ Reduce excitability / increase the threshold potential
▸ Class Ia: Intermediate dissociation kinetics
▸ Kinetics intermediate between class Ib and Ic
▸ Demonstrate use dependency - enhanced channel blocking properties at high heart rates
▸ Reduce the slope of phase 0 - decrease conduction speed
▸ Also block delayed rectifier K+ channels - prolongation of the AP (class III activity).

1A- QUINIDINE
▸ class IA drug
▸ in the treatment of acute and chronic supraventricular arrhythmia
▸ SVT associated with WPW, atrial fibrillation & flutter
▸ Ventricular ectopic beats
▸ rarely used because of its side effects
▸ MOA- Quinidine decreases the slope of phase 4 depolarization, which explains its
effectiveness in suppressing cardiac arrhythmias caused by enhanced automaticity

▸ Metabolism and Excretion
▸ Quinidine is hydroxylated in the liver to inactive metabolites, which are excreted
in the urine.
▸ The concurrent administration of phenytoin or rifampin may lower blood levels of
quinidine by enhancing liver clearance.
▸ Side Effects.
▸ Quinidine has a low therapeutic ratio, with heart block, hypotension, and
proarrhythmic being potential adverse side effects.

1A- PROCAINAMIDE
▸ Effective for treatment of ventricular tachyarrhythmia but less effective in
abolishing atrial tachyarrhythmias.
▸ Premature ventricular contractions and paroxysmal ventricular tachycardia are
suppressed in most patients within a few minutes after intravenous (IV)
administration, which is better tolerated than IV quinidine but may still cause
hypotension.

▸ Mechanism of Action
▸ Procainamide is an analogue of the local anesthetic procaine.
▸ Procainamide possesses an electrophysiologic action similar to that of quinidine
but produces less prolongation of the QTc interval on the ECG (paradoxical
ventricular tachycardia is a rare feature of procainamide therapy).
▸ Procainamide has no vagolytic effect and can be used in patients with atrial
fibrillation to suppress ventricular irritability without increasing the ventricular rate.

▸ Metabolism and Excretion - Procainamide is eliminated by renal excretion and
hepatic metabolism (dose of procainamide must be decreased when renal
function is abnormal).
▸ Side Effects
▸ Similar to quinidine, use of procainamide has dramatically decreased due to its
side effect profile and availability of newer agents.
▸ Hypotension that results from procainamide is more likely to be caused by
direct myocardial depression than peripheral vasodilation.
▸ Chronic administration of procainamide may be associated with a syndrome
that resembles systemic lupus erythematosus

1A- DISOPYRAMIDE
▸ comparable to quinidine in effectively suppressing atrial and ventricular tachyarrhythmias.
About 50% of the drug is excreted unchanged by the kidneys.
▸ Side Effects
▸ The most common side effects of disopyramide are dry mouth and urinary hesitancy, both
of which are caused by the drug’s anticholinergic activity.
▸ Prolongation of the QTc interval on the ECG and paradoxical ventricular tachycardia
(similar to quinidine) may occur.
▸ Disopyramide has significant myocardial depressant effects and can precipitate congestive
heart failure and hypotension.

1A- MORICIZINE
▸ phenothiazine derivative that is reserved for the treatment of life-threatening
ventricular arrhythmias when other drugs such as amiodarone are not available
or contraindicated (e.g., allergy).
▸ Side Effects.
▸ Proarrhythmic effects occur in 3% to 15% of patients treated chronically with
moricizine.

CLASS IB: RAPID DISSOCIATION KINETICS
▸ Preferentially bind to partially depolarised cells (MI)
▸ Na+ channels are in an inactivated state
▸ Dissociation is rapid- most Na+ channels ready for the next AP
▸ Shorter AP - fast recovery of Na channels & effect on K channels
▸ Accelerated conduction in regions of slow conduction
▸ Phase 0 unaffected

1B- LIDOCAINE
▸ principally for suppression of ventricular arrhythmias, having minimal if any effect on
supraventricular tachyarrhythmias.
▸ The efficacy of prophylactic lidocaine therapy for preventing early ventricular fibrillation after
acute myocardial infarction has not been documented and is no longer recommended.
▸ Advantages of lidocaine over quinidine or procainamide are the more rapid onset and prompt
disappearance of effects when the continuous infusion is terminated, greater therapeutic index,
and a much reduced side effect profile.
▸ Lidocaine for IV administration differs from that used for local anesthesia because it does not
contain a preservative.

▸ The effectiveness of lidocaine in suppressing premature ventricular
contractions reflects its ability to decrease the rate of spontaneous phase 4
depolarization
▸ The ineffectiveness of lidocaine against supraventricular tachyarrhythmias
presumably reflects its inability to alter the rate of spontaneous phase 4
depolarization in atrial cardiac cells.
▸ Metabolism and Excretion.
▸ Lidocaine is metabolized in the liver, and resulting metabolites may possess
cardiac antiarrhythmic activity.

▸ Side Effects
▸ Lidocaine is essentially devoid of effects on the ECG or cardiovascular system when the plasma
concentration remains less than 5 g/mL (does not alter the duration of the QRS complex on the ECG,
and activity of the sympathetic nervous system is not changed).
▸ Toxic plasma concentrations of lidocaine ( 5 to 10 g/mL) produce peripheral vasodilation and direct
myocardial depression, resulting in hypotension.
▸ Stimulation of the central nervous system (CNS) occurs in a dose-related manner, with symptoms
appearing when plasma concentrations of lidocaine are greater than 5 g/mL. Seizures are possible at
plasma concentrations of 5 to 10 g/mL.
▸ CNS depression, apnea, and cardiac arrest are possible when plasma lidocaine concentrations are
greater than 10 g/mL.
▸ The convulsive threshold for lidocaine is decreased during arterial hypoxemia, hyperkalemia, or
acidosis (importance of monitoring these parameters during continuous infusion of lidocaine to patients
for suppression of ventricular arrhythmias).

1B- MEXILETINE
▸ orally effective amine analogue of lidocaine that is used for the chronic suppression of
ventricular cardiac tachyarrhythmias.
▸ As it is a lidocaine analog, mexiletine may be effective in decreasing neuropathic pain for
patients in whom alternative pain medications have been unsatisfactory.
▸ Side Effects
▸ Neurologic side effects include tremulousness, diplopia, vertigo, and occasionally slurred
speech.
▸ Increases in liver enzymes may occur especially in patients manifesting congestive heart
failure.

1B- PHENYTOIN
▸ effective in suppression of ventricular arrhythmias associated with digitalis
toxicity and may be useful in the treatment of paradoxical ventricular tachycardia
or torsades de pointes.
▸ The IV dose is 100 mg (1.5 mg/kg) every 5 minutes until the cardiac arrhythmia is
controlled or 10 to 15 mg/kg (maximum 1,000 mg) has been administered.
▸ Because phenytoin can precipitate in 5% dextrose in water, it is preferable to give
the drug via a delivery tubing containing normal saline.

▸ Phenytoin exerts a greater effect on the electrocardiographic QTc interval than does
lidocaine and shortens the QTc interval more than any of the other antiarrhythmic drugs.
▸ The ability of some volatile anesthetics to depress the sinoatrial node is a consideration if
administration of phenytoin during general anesthesia is planned.
▸ Phenytoin is hydroxylated and then conjugated with glucuronic acid for excretion in the
urine (impaired hepatic function may result in higher than normal blood levels of the drug).
▸ Warfarin, phenylbutazone, and isoniazid may inhibit metabolism and increase phenytoin
blood levels.

▸ Side Effects
▸ Phenytoin toxicity most commonly manifests as CNS disturbances, especially
cerebellar disturbances (ataxia, nystagmus, vertigo, slurred speech, sedation,
mental confusion).
▸ Phenytoin partially inhibits insulin secretion and may lead to increased blood
glucose levels in patients who are hyperglycemic.
▸ Leukopenia, granulocytopenia, and thrombocytopenia may occur as a
manifestation of drug-induced bone marrow depression.

CLASS IC: SLOW DISSOCIATION KINETICS
▸ Bind to inactivated Na+ channels and dissociate very slowly
▸ The slope of phase 0 of the action potential and conduction speed are reduced

1C- FLECAINIDE
▸ fluorinated local anesthetic analogue of procainamide that is more effective in suppressing
ventricular premature beats and ventricular tachycardia than quinidine and disopyramide.
▸ Flecainide is also effective for the treatment of atrial tachyarrhythmias (effective for the treatment of
tachyarrhythmias).
▸ Oral absorption of flecainide is excellent, and a prolonged elimination half-time (about 20 hours)
makes a twice daily dose of 100 to 200 mg acceptable (not available in an IV formulation).
▸ Elimination of flecainide is decreased in patients with congestive heart failure or renal failure and
decreased left ventricular function.

▸ Side Effects
▸ Proarrhythmic effects occur in a significant number of treated patients
especially in the presence of left ventricular dysfunction.
▸ Flecainide prolongs the QRS complex and may depress sinoatrial node
function as do -adrenergic antagonists and calcium channel blockers (not
administered to patients with second- and third-degree atrioventricular heart
block).
▸ The most common noncardiac adverse effect of flecainide is dose-related
blurred vision.
▸ Flecainide increases the capture thresholds of pacemakers.

1C- PROPAFENONE
▸ effective oral antiarrhythmic drug for suppression of ventricular and atrial tachyarrhythmias.
▸ The rate of metabolism is genetically determined with about 90% of patients able to metabolize
propafenone efficiently in the liver (availability of propafenone increases significantly in the presence
of liver disease).
▸ Side Effects
▸ Propafenone depresses the myocardium and may cause conduction abnormalities such as
sinoatrial node slowing, atrioventricular block, and bundle branch block.
▸ Propafenone interferes with the metabolism of propranolol and metoprolol resulting in increased
plasma concentrations of these blockers. This drug also increases the plasma concentration of
warfarin and may prolong the prothrombin time.

1D- RANOLAZINE
▸ in treatment of atrial arrhythmias and suppression of no sustained ventricular tachycardia and for the adjunctive
treatment of chronic stable angina.
▸ Inhibits late Na+ (INaL) and delayed rectifier K+ (IKr) channels
▸ blocks late sodium currents found during phase 2, which leads to a delay in the activation of repolarizing potassium
channels in phase 3.
▸ increases the APD and ERP
▸ Increases refractoriness and reducing intracellular Ca2+
▸ Approved for treating chronic stable angina pectoris
▸ Emerging evidence for a role in preventing and treating AF after cardiac surgery
▸ CI in patients with creatinine clearance <30 ml/min

2- BETA ADRENERGIC ANTAGONISTS
▸ effective for treatment of cardiac arrhythmias related to enhanced activity of the sympathetic
nervous system (perioperative stress).
▸ Their use as an anti-arrhythmic is limited to rate control in the treatment of paroxysmal SVT,
AF and sinus tachycardia due to increased levels of catecholamines.
▸ Acebutolol is effective in the treatment of frequent premature ventricular contractions.
▸ Adrenergic antagonists, especially propranolol, may be effective in controlling torsades de
pointes for patients with prolonged QTc intervals.
▸ Acebutolol, propranolol, and metoprolol are approved for prevention of sudden death
following myocardial infarction.

▸ The antiarrhythmic effects of -adrenergic antagonists most likely reflect blockade of the
responses of receptors in the heart to sympathetic nervous system stimulation, as well
as the effects of circulating catecholamines (rate of spontaneous phase 4 depolarization
is decreased and the rate of sinoatrial node discharge is decreased).
▸ Adrenergic antagonists can depress the myocardium not only by blockade but also by
direct depressant effects on cardiac muscle.
▸ The usual oral dose of propranolol for chronic suppression of ventricular arrhythmias is
10 to 80 mg every 6 to 8 hours. Effective blockade is usually achieved in an otherwise
normal person when the resting heart rate is 55 to 60 beats per minute. For emergency
suppression of cardiac arrhythmias in an adult, propranolol may be administered IV in a
dose of 1 mg per minute (3 to 6 mg)

▸ Orally administered propranolol is extensively metabolized in the liver, and a hepatic first-pass effect is
responsible for the variation in plasma concentration.
▸ Propranolol readily crosses the blood–brain barrier.
▸ The principal metabolite of propranolol is 4-hydroxypropranolol, which possesses weak -adrenergic
antagonist activity.
▸ Side Effects
▸ Bradycardia, hypotension, myocardial depression, and bronchospasm are side effects of beta adrenergic
antagonists that reflect the ability of these drugs to inhibit sympathetic nervous system activity. The use of
propranolol in patients with preexisting atrioventricular heart block is not recommended.
▸ Interference with glucose metabolism may manifest as hypoglycemia in patients being treated for diabetes
mellitus.
▸ Upregulation of -adrenergic receptors occurs with chronic administration of -adrenergic antagonists such
that abrupt discontinuation of treatment may lead to supraventricular tachycardia.

2- DIGITALIS
▸ Digitalis preparations such as digoxin are effective cardiac antiarrhythmics for stabilization of atrial electrical activity
and the treatment and prevention of atrial tachyarrhythmias.
▸ MOA
▸ Direct- bind and inhibit cardiac Na/K ATPase> increased intracellular Na+ and decreased intracellular K+
concentrations > exchange Na with extracellular Ca > positive inotropy
▸ Indirect- the release of acetylcholine at cardiac muscarinic receptors is enhanced > slows conduction & prolongs
refractory period in AV node and bundle of His
▸ Because of their vagolytic effects, these drugs can also slow conduction of cardiac impulses through the
atrioventricular node and thus slow the ventricular response rate in patients with atrial fibrillation. Conversely,
digitalis preparations enhance conduction of cardiac impulses through accessory bypass tracts and can
dangerously increase the ventricular response rate in patients with Wolff -Parkinson-White syndrome.

▸ The usual oral dose of digoxin is 0.5 to 1.0 mg in divided doses over 12 to 24 hours followed by
a maintenance dose of 125–500 µg per day. The therapeutic range is 1–2 µg.l-1.
▸ Digitalis toxicity is a risk and may manifest as virtually any cardiac arrhythmia premature
ventricular contractions, bigeminy, all forms of AV block including third-degree block, junctional
rhythm and atrial or ventricular tachycardia. Hypokalaemia, hypercalcaemia or altered pH may
precipitate side effects.
▸ anorexia, nausea and vomiting, diarrhoea and lethargy. Visual disturbances, headache,
gynaecomastia occurs during long-term administration, Skin rashes
▸ Drug interactions

3- ADENOSINE
▸ an endogenous nucleoside that slows conduction of cardiac
impulses through the atrioventricular node, making it an
effective alternative to calcium channel blockers (verapamil) for
the acute treatment of paroxysmal supraventricular
tachycardia, including that due to conduction through accessory
pathways in patients with Wolff -Parkinson-White syndrome.
▸ This drug is not effective in the treatment of atrial fibrillation,
atrial flutter, or ventricular tachycardia. The usual dose of
adenosine is 6 mg IV followed, if necessary, by a repeat
injection of 6 to 12 mg IV about 3 minutes later. Adenosine
receptors represent a logical target for treatment of pain.

▸ Adenosine stimulates cardiac adenosine1 receptors to increase potassium ion currents, shorten the action
potential duration, and hyperpolarize cardiac cell membranes.
▸ Its short-lived cardiac effects (elimination half-time 10 seconds) are due to carrier-mediated cellular uptake and
metabolism to inosine by adenosine deaminase.
▸ Methylxanthines inhibit the actions of adenosine by binding to adenosine1 receptors. Conversely, dipyridamole
(adenosine uptake inhibitor) and cardiac transplantation (denervation hypersensitivity) potentiate the effects of
adenosine.
▸ Side Effects
▸ Adenosine may produce transient atrioventricular heart block.
▸ Bronchospasm, although an uncommon complication, has been observed after the IV administration of adenosine,
even in the absence of preexisting symptoms (use with caution, if at all, in patients known to have active
wheezing).
▸ The pharmacologic effects of adenosine are antagonized by methylxanthines (theophylline, caffeine) and
potentiated by dipyridamole.

3- AMIODARONE
▸ potent antiarrhythmic drug with a wide spectrum of activity against refractory supraventricular and
ventricular tachyarrhythmias. In the presence of ventricular tachycardia or fibrillation that is
resistant to electrical defibrillation, amiodarone 300 mg IV is recommended.
▸ Preoperative oral administration of amiodarone decreases the incidence of atrial fibrillation after
cardiac surgery.
▸ It is also effective for suppression of tachyarrhythmias associated with Wolff -Parkinson-White
syndrome. Similar to blockers and unlike class I drugs, amiodarone decreases mortality after
myocardial infarction.
▸ After initiation of oral therapy, a decrease in ventricular tachyarrhythmias occurs within 72 hours.
After discontinuation of chronic oral therapy, the pharmacologic effect of amiodarone lasts for a
prolonged period (up to 60 days), reflecting the prolonged elimination half-time of this drug

▸ Amiodarone prolongs the effective refractory period in all
cardiac tissues and also has an antiadrenergic effect
(noncompetitive blockade of and receptors).
▸ Amiodarone acts as an antianginal drug by dilating
coronary arteries and increasing coronary blood flow.
▸ Amiodarone has a prolonged elimination half-time (29
days) and is minimally dependent on renal excretion.
▸ The principal metabolite, desethylamiodarone, is
pharmacologically active and has a longer elimination half-
time than the parent drug, resulting in accumulation of this
metabolite with chronic therapy.

▸ Side effects- chronic Rx- daily maintenance >400 mg
▸ Pulmonary toxicity- pulmonary alveolitis (5-15%)
▸ CVS- prolong QTc interval on the ECG- increased incidence of ventricular
tachyarrhythmias. HR is often slow and resistant to treatment with atropine
▸ Ocular, dermatologic, neurologic and hepatic- corneal microdeposits, optic
neuropathy, neurologic toxicity- peripheral neuropathy, tremors, sleep disturbance,
headache, or proximal skeletal muscle weakness, Transient, mild increase in plasma
transaminases, fatty liver infiltration
▸ Pharmacokinetic- inhibit P450, displace digoxin from binding site, potentiate
anticoagulant effect of warfarin
▸ Endocrine- hypo or hyperthyroidism

3- SOTALOL
▸ nonselective beta adrenergic antagonist drug that is
usually restricted for use in patients with life-
threatening ventricular tachycardia or fibrillation.
▸ Side Effects-The most dangerous side effect of
sotalol is torsades de pointes. Th e blocking effects
of sotalol result in decreased myocardial contractility,
bradycardia, and delayed conduction of cardiac
impulses through the atrioventricular node.

3- IBUTILIDE
▸ effective for the conversion of recent onset atrial
fibrillation or atrial flutter to normal sinus rhythm.
▸ Polymorphic ventricular tachycardia may occur
during ibutilide treatment, especially in patients
with predisposing factors (impaired left
ventricular function, preexisting prolonged QTc
intervals, hypokalemia, hypomagnesemia)

3- VERNAKALANT
▸ Blocks multiple ion channels including Na+ channels (INaL) and various delayed rectifier K+ channels
▸ Prolongation of the AP and effective refractory period
▸ Atrium specific and only causes mild QT prolongation without increasing the risk of torsade de pointes
VT
▸ Used for terminating acute AF, which typically occurs within 90 min

4- VERAPAMIL & DILTIAZEM
▸ Verapamil is highly effective in terminating paroxysmal supraventricular tachycardia, controls reentrant tachycardia,
and effectively controls the ventricular rate in most patients who develop atrial fibrillation or flutter.
▸ Verapamil does not have a depressant effect on accessory tracts and thus will not slow the ventricular response rate
in patients with Wolff -Parkinson-White syndrome. Verapamil has little efficacy in the therapy for ventricular ectopic
beats.
▸ The usual dose of verapamil for suppression of paroxysmal supraventricular tachycardia is 5 to 10 mg IV (75 to 150
g/kg) over 1 to 3 minutes followed by a continuous infusion of about 5 g/kg/minute to maintain a sustained effect. Th
e administration of calcium gluconate, 1 g IV, approximately 5 minutes before administration of verapamil may
decrease verapamil-induced hypotension without altering the drug’s antiarrhythmic effects.
▸ Diltiazem, 20 mg IV, produces antiarrhythmic effects similar to those of diazepam, and the potential side effects are
similar.

▸ Verapamil and the other calcium channel blockers inhibit the flux of calcium ions across the slow
channels of vascular smooth muscle and cardiac cells (manifests as a decreased rate of spontaneous
phase 4 depolarization).
▸ Verapamil has a substantial depressant effect on the atrioventricular node and a negative
chronotropic effect on the sinoatrial node. Th is drug exerts a negative inotropic effect on cardiac
muscle and produces a moderate degree of vasodilation of the coronary arteries and systemic
arteries.
▸ An estimated 70% of an injected dose of verapamil is eliminated by the kidneys, whereas up to 15%
may be present in the bile.
▸ Th e need for a large oral dose is related to the extensive hepatic first-pass effect that occurs with the
oral route of administration

▸ Side Effects
▸ Atrioventricular heart block is more likely in patients with preexisting defects in
the conduction of cardiac impulses.
▸ Direct myocardial depression and decreased cardiac output are likely to be
exaggerated in patients with poor left ventricular function.
▸ Peripheral vasodilation may contribute to hypotension.
▸ There may be potentiation of anesthetic-produced myocardial depression, and
the effects of neuromuscular blocking drugs may be exaggerated.

MAGNESIUM
▸ Preventing and treating torsade de pointes VT
▸ Mechanism of its antiarrhythmic effect is unknown (Membrane-stabilising effect as
a result of blocking Ca2+ and K+ channels )
▸ Does not shorten the QT interval
▸ Treating arrhythmias associated with digoxin toxicity
▸ Controlling the ventricular response in patients with AF – (Patients with AF have been
shown to have a lower serum Mg2+ concentration than healthy individuals)

CHOICE OF DRUG- CONTRAINDICATIONS
▸ Amiodarone in patients with severe pulmonary disease
▸ B-blockers in patients with asthma
▸ CCB in patients with acute decompensated heart failure
▸ Flecainide should be avoided in patients with MI or structural heart disease
▸ Sotalol should be avoided in patients with prolonged QT d

REFERENCES
▸ Stoelting’s hand book of pharmacology & physiology in anesthetic practice-3rd edition
▸ Kim, C.J., Lever, N. and Cooper, J.O. (2023). Antiarrhythmic drugs and anaesthesia:
part 1. mechanisms of cardiac arrhythmias. BJA Education, [online] 23(1), pp.8–16.
doi:https://doi.org/10.1016/j.bjae.2022.11.001.
▸ Kim, C.J., Lever, N. and Cooper, J.O. (2022). Antiarrhythmic drugs and anaesthesia.
Part 2: pharmacotherapy. BJA Education, 23(2), pp.52–
60.doi:https://doi.org/10.1016/j.bjae.2022.11.005
▸ https://cvpharmacology.com/antiarrhy/sodium-blockers

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