Antiarrhythmic drugs Flashcards by Aidyl XXX

Q

What are the class 1A Sodium channel blocker?

A

Disopyramide
Procainamide
Quinidine

Slows phase 0 depolarization in ventricular muscle fibers

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Q

What is class 1b sodium channel blocker?

A

Lidocaine
Mexiletine

Shortens phase 3 repolarization in ventricular muscle fibers

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Q

What is class 1c sodium blocker?

A

Flecainide
Propafenone

Markedly slows phase 0 depolarization in ventricular muscle fibers

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Q

What are class 2 beta blockers?

A

Atenolol
Esmolol
Metoprolol

Inhibits phase 4 depolarization in SA and AV node

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Q

What are class 3 potassium channel blockers?

A

Amiodarone
Dofetilide
Dronedarone
Ibutilide
Sotalol

Prolongs phase 3 repolarization in ventricular muscle fibers

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Q

What are the other anti-anginas?

A

Adenosine
Digoxin
Mg sulphate

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Q

What is class 4 calcium channel anti anginals?

A

Diltiazem
Verapamil

Inhibits action potential in SA and AV nodes

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Q

What is the moa of class 1a antiarrhythmic drugs?

A

Class IA antiarrhythmic drugs: Quinidine, procainamide,
and disopyramide
Quinidine [KWIN-i-deen] is the prototype class IA drug. Other agents
in this class include procainamide [proe-KANE-a-mide] and disopyra-
mide [dye-soe-PEER-a-mide]. Because of their concomitant class III
activity, they can precipitate arrhythmias that can progress to ven-
tricular fibrillation.
1. Mechanism of action: Quinidine binds to open and inactivated
sodium channels and prevents sodium influx, thus slowing the
rapid upstroke during phase 0 (Figure 20.5). It decreases the
slope of phase 4 spontaneous depolarization, inhibits potas-
sium channels, and blocks calcium channels. Because of these
actions, it slows conduction velocity and increases refractoriness.
Quinidine also has mild α-adrenergic blocking and anticholinergic
actions. Procainamide and disopyramide have actions similar to
those of quinidine. However, there is less anticholinergic activ-
ity associated with procainamide and more with disopyramide.
Neither procainamide nor disopyramide has α-blocking activity.
Disopyramide produces a negative inotropic effect that is greater
than the weak effect exerted by quinidine and procainamide, and
unlike the other drugs, it causes peripheral vasoconstriction. The
drug may produce a clinically important decrease in myocardial
contractility in patients with systolic heart failure.
Class IA drugs slow Phase 0
depolarization. In addition,
because of their Class III
activity, these drugs prolong
the action potential.

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Q

What are the therapeutic uses of class 1a sodium blockers?

A

Therapeutic uses: Quinidine is used in the treatment of a wide
variety of arrhythmias, including atrial, AV junctional, and ventricu-
lar tachyarrhythmias. Procainamide is available in an intravenous
formulation only and may be used to treat acute atrial and ventricu-
lar arrhythmias. However, electrical cardioversion or defibrillation
and amiodarone have mostly replaced procainamide in clinical use.
Disopyramide is used in the treatment of ventricular arrhythmias as
an alternative to procainamide or quinidine and may also be used
for maintenance of sinus rhythm in atrial fibrillation or flutter.

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Q

What are the pharmacokinetics of class 1a sodium channels?

A

Pharmacokinetics: Quinidine sulfate or gluconate is rapidly and
almost completely absorbed after oral administration. It undergoes
extensive metabolism primarily by the hepatic cytochrome P450 3A4
(CYP3A4) isoenzyme, forming active metabolites. Procainamide has
a relatively short duration of action of 2 to 3 hours. A portion of pro-
cainamide is acetylated in the liver to N-acetylprocainamide (NAPA),
which prolongs the duration of the action potential. Thus, NAPA has
properties and side effects of a class III drug. NAPA is eliminated via
the kidney, and dosages of procainamide may need to be adjusted
in patients with renal failure. Disopyramide is well absorbed after oral
administration. It is metabolized in the liver to a less active metabo-
lite and several inactive metabolites. Disopyramide is a substrate of
CYP3A4. About half of the drug is excreted unchanged by the kidneys.

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Q

What are the adverse reactions of class 1a sodium channels?

A

Adverse effects: Large doses of quinidine may induce the symp-
toms of cinchonism (for example, blurred vision, tinnitus, headache,
disorientation, and psychosis). Drug interactions are common with
quinidine since it is an inhibitor of both CYP2D6 and P-glycoprotein.
Intravenous administration of procainamide may cause hypotension.
Disopyramide has the most anticholinergic adverse effects of the
class IA drugs (for example, dry mouth, urinary retention, blurred
vision, and constipation). Both quinidine and disopyramide should
be used with caution with potent inhibitors of CYP3A4.

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Q

What are the moa of class 1b sodium channel blockers?

A

The class IB agents rapidly associate and dissociate from sodium
channels. Thus, the actions of class IB agents are manifested when
the cardiac cell is depolarized or firing rapidly. The class IB drugs
lidocaine [LYE-doe-kane] and mexiletine [MEX-i-le-teen] are useful in
treating ventricular arrhythmias.

Mechanism of action: In addition to sodium channel blockade,
lidocaine and mexiletine shorten phase 3 repolarization and
decrease the duration of the action potential

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Q

What are the therapeutic uses of class IB antiarrythmic drugs lidocaine & mexiletine

A

Therapeutic uses: Although amiodarone has supplanted lidocaine
for use in ventricular fibrillation or pulseless ventricular
tachycardia (VT), lidocaine may be useful as an alternative.
Lidocaine may also be used in polymorphic VT or in combination with amiodarone
for VT storm. The drug does not markedly slow
conduction
and, thus, has little effect on atrial or AV junction
arrhythmias. Mexiletine is used for chronic treatment of ventricular
arrhythmias, often in combination with amiodarone.

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Q

What is the PK activity of class IB antiarrhythmic drugs: Lidocaine and mexiletine

A

Pharmacokinetics: Lidocaine is given intravenously because
of extensive first-pass transformation by the liver, which precludes
oral administration. The drug is dealkylated to two less
active metabolites, primarily by CYP1A2 with a minor role by
CYP3A4. Lidocaine should be monitored closely when given
in combination with drugs affecting these CYP isoenzymes.
As lidocaine is a high extraction drug, drugs that lower hepatic
blood flow (β-blockers) may require lidocaine dose adjustment.
Mexiletine is well absorbed after oral administration. It is metabolized
in the liver primarily by CYP2D6 to inactive metabolites
and excreted mainly via the biliary route.

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Q

What are the adverse effects of Class IB antiarrhythmic drugs: Lidocaine and mexiletine?

A

Adverse effects: Lidocaine has a fairly wide therapeutic index. It
shows little impairment of left ventricular function and has no negative
inotropic effect. Central nervous system (CNS) effects include
nystagmus (early indicator of toxicity), drowsiness, slurred speech,
paresthesia, agitation, confusion, and convulsions, which often
limit the duration of continuous infusions. Mexiletine has a narrow
therapeutic index and caution should be used when administering
the drug with inhibitors of CYP2D6. Nausea, vomiting, and dyspepsia
are the most common
adverse effects

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Q

Class IC antiarrhythmic drugs: Flecainide and propafenone mechanism of action

A

Class IC antiarrhythmic drugs: Flecainide and propafenone
These drugs slowly dissociate from resting sodium channels and
show prominent effects even at normal heart rates. Several studies
have cast serious doubts on the safety of the class IC drugs, particularly
in patients with structural heart disease.
1. Mechanism of action: Flecainide [FLEK-a-nide] suppresses phase
0 upstroke in Purkinje and myocardial fibers (Figure 20.7). This
causes marked slowing of conduction in all cardiac tissue, with a
minor effect on the duration of the action potential and refractoriness.
Automaticity is reduced by an increase in the threshold potential,
rather than a decrease in slope of phase 4 depolarization. Flecainide
also blocks potassium channels leading to increased action potential
duration, even more so than propafenone. Propafenone [proe-
PA-fen-one], like flecainide, slows conduction in all cardiac tissues
but does not block potassium channels.

Q

what are therapeutic effects of

A

Therapeutic uses: Flecainide is useful in the maintenance of
sinus rhythm in atrial flutter or fibrillation in patients without structural
heart disease (left ventricular hypertrophy, heart failure, atherosclerotic
heart disease) and in treating refractory ventricular
arrhythmias. Flecainide has a negative inotropic effect and can
aggravate chronic heart failure. Use of propafenone is restricted
mostly to atrial arrhythmias: rhythm control of atrial fibrillation or
flutter and paroxysmal supraventricular tachycardia prophylaxis in
patients with AV reentrant tachycardias. The latter indication takes
advantage of the β-blocking properties of propafenone.

Q

What is the PK for flecainine and propafenone?

A

Pharmacokinetics: Flecainide is absorbed orally and is metabolized
by CYP2D6 to multiple metabolites. The parent drug and metabolites
are mostly eliminated renally, and dosage adjustment may be required
in renal disease. Propafenone is metabolized to active metabolites
primarily via CYP2D6, and also by CYP1A2 and CYP3A4. The
metabolites are excreted in the urine and the feces

Q

What are flecainide and propafenone adverse effects?

A

Adverse effects: Flecainide is generally well tolerated, with
blurred vision, dizziness, and nausea occurring most frequently.
Propafenone has a similar side effect profile, but it may also
cause bronchospasm due to its β-blocking effects. It should be
avoided in patients with asthma. Propafenone is also an inhibitor
of P-glycoprotein. Both drugs should be used with caution with
potent inhibitors of CYP2D6.

Q

What are the class 2 antiarrythmic drugs?

A

Class II agents are β-adrenergic antagonists, or β-blockers. These drugs
diminish phase 4 depolarization and, thus, depress automaticity, prolong
AV conduction, and decrease heart rate and contractility. Class II agents
are useful in treating tachyarrhythmias caused by increased sympathetic
activity. They are also used for atrial flutter and fibrillation and for AV nodal
reentrant tachycardia. In addition, β-blockers prevent life-threatening ventricular
arrhythmias following a myocardial infarction. [Note: In contrast to
the sodium channel blockers, β-blockers and class III compounds, such
as sotalol and amiodarone, are increasing in use.]
Metoprolol [me-TOE-pro-lol] is the β-blocker most widely used in the
treatment of cardiac arrhythmias. Compared to nonselective β-blockers,
such as propranolol [pro-PRAN-oh-lol], it reduces the risk of bronchospasm.
It is extensively metabolized in the liver primarily by CYP2D6
and has CNS penetration (less than propranolol, but more than atenolol
[a-TEN-oh-lol]). Esmolol [ESS-moe-lol] is a very-short-acting β-blocker
used for intravenous administration in acute arrhythmias that occur during
surgery or emergency situations. It has a fast onset of action and
a short half-life, making it ideal for acute situations and also limiting its
adverse effect profile. Esmolol is rapidly metabolized by esterases in red
blood cells. As such, there are no pharmacokinetic drug interactions.

Q

What are class 3 antiarrythmics?

A

Class III agents block potassium channels and, thus, diminish the outward
potassium current during repolarization of cardiac cells. These agents
prolong the duration of the action potential without altering phase 0 of
depolarization or the resting membrane potential (Figure 20.8). Instead,
they prolong the effective refractory period, increasing refractoriness. All
class III drugs have the potential to induce arrhythmias.

Q

what is class 3 amiodarone moa?

A

Mechanism of action: Amiodarone [a-MEE-oh-da-rone] contains
iodine and is related structurally to thyroxine. It has complex effects, showing class I, II, III, and IV actions, as well as α-blocking
activity. Its dominant effect is prolongation of the action potential
duration and the refractory period by blocking K+ channels.

Q

What are the therapeutic uses of amiodarone?

A

Therapeutic uses: Amiodarone is effective in the treatment of
severe refractory supraventricular and ventricular tachyarrhythmias.
Amiodarone has been a mainstay of therapy for the rhythm
management of atrial fibrillation or flutter. Despite its adverse effect
profile, amiodarone is the most commonly employed antiarrhythmic
and thought to be the least proarrhythmic of the class I and III
antiarrhythmic drugs.

Q

What is the PK of amiodarone?

A

Pharmacokinetics: Amiodarone is incompletely absorbed after
oral administration. The drug is unusual in having a prolonged
half-life of several weeks, and it distributes extensively in adipose
tissue.
Full clinical effects may not be achieved until months after
initiation of treatment, unless loading doses are employed.

What is the adverse effects of amiodarone?

Adverse effects: Amiodarone shows a variety of toxic effects, including pulmonary fibrosis, neuropathy, hepatotoxicity, corneal deposits, optic neuritis, blue-gray skin discoloration, and hypo- or hyperthyroidism. However, use of low doses and close monitoring reduce toxicity, while retaining clinical efficacy. Amiodarone is subject to numerous drug interactions, since it is metabolized by CYP3A4 and serves as an inhibitor of CYP1A2, CYP2C9, CYP2D6, and P-glycoprotein.

What is Dronedarone?

Dronedarone Dronedarone [droe-NE-da-rone] is a benzofuran amiodarone derivative, which is less lipophilic, has lower tissue accumulation, and has a shorter serum half-life than amiodarone. It does not have the iodine moieties that are responsible for thyroid dysfunction associated with amiodarone. Like amiodarone, it has class I, II, III, and IV actions. Dronedarone has a better adverse effect profile than amiodarone but may still cause liver failure. The drug is contraindicated in those with symptomatic heart failure or permanent atrial fibrillation due to an increased risk of death. Currently, dronedarone is used to maintain sinus rhythm in atrial fibrillation or flutter, but it is less effective than amiodarone.

What is dronedarone according to bcps?

d) Dronedarone: 21%–25% efficacy (1) Amiodarone analog lacking the iodine moiety that contributes to the thyroid toxicity of amiodarone (2) Has electrophysiologic properties of classes I–IV (3) Dose: 400 mg twice daily with morning and evening meal (4) Hepatically metabolized; CYP3A4 substrate; CYP3A4, CYP2D6, and P-gp inhibitor (5) Half-life is 13–19 hours. (6) Small increase in SCr by 0.1 mg/dL probably a result of inhibition of creatinine’s tubular secretion; rapid onset, will plateau after 7 days, and is reversible. Monitor SCr periodically. (7) Acute kidney injury has also been reported, and it is usually reversible with drug discontinuation. (8) Contraindicated in permanent AF; NYHA class II or III HF with recent decompensation necessitating hospitalization; NYHA class IV HF; second- or third-degree AV block or sick sinus syndrome (in absence of pacemaker); severe liver impairment, HR less than 50 beats/minute; concurrent use of strong CYP3A4 inhibitors or QTc interval–prolonging agents; history of amiodarone-induced hepatotoxicity or pulmonary toxicity; pregnancy; or QTc interval 500 milliseconds or greater. 9) One trial found dronedarone less effective than amiodarone for the maintenance of SR, but with fewer adverse effects. (10) Drug interactions (A) Digoxin: Increased digoxin exposure; lower digoxin dose by 50% (B) β-Blockers, non-DHP CCBs, and clonidine: Excessive bradycardia; initiate these drugs at lowest dose. Diltiazem and verapamil can increase dronedarone exposure; therefore, monitor ECG. (C) Statins: Increased statin exposure. Limit dose of simvastatin to 10 mg/day and lovastatin to 20 mg/day. (D) Dabigatran: In patients with moderate renal impairment (CrCl 30–50 mL/minute), dronedarone increases dabigatran exposure; decrease dabigatran dose to 75 mg twice daily. (E) Strong CYP3A4 inhibitors and inducers: Avoid. (F) Cyclosporine, tacrolimus, sirolimus: Increased exposure of these agents; monitor serum concentrations closely (11) Other safety issues (A) Liver injury: According to postmarketing surveillance, dronedarone has been associated with rare but severe hepatic liver injury. Hepatic enzymes should be monitored, especially during the first 6 months of treatment. (B) Pulmonary toxicity: In postmarketing surveillance, cases of interstitial lung disease, including pneumonitis and pulmonary fibrosis, have been reported. Patients should report any new signs of dyspnea or nonproductive cough.

What is amiodarone according to bcps?

Amiodarone: 85%–95% efficacy (1) Has electrophysiologic properties of classes I–IV (2) Oral loading dose required (e.g., 400 mg 2 or 3 times per day for 2 weeks and then 400 mg/day for 4 weeks, followed by a 200-mg/day maintenance dose). Achieving a loading dose of 10 g is desirable. Many different regimens exist. (3) Long half-life of about 60 days (4) In addition, has AV nodal blocking properties, which may help to control HR if AF recurs (5) May use in patients with HF (6) Hepatically metabolized: Cytochrome P450 (CYP) 3A4 substrate; inhibitor of CYP3A4, CYP1A2, CYP2C9, CYP2D6, and P-glycoprotein (P-gp) (7) Minimal incidence of ventricular arrhythmias (8) Drug interactions (many) (A) Digoxin: Increased digoxin exposure. Lower digoxin dose by 50%. (B) Warfarin: Increased warfarin exposure. Lower warfarin dose by 33%–50%. (C) Simvastatin: Increased simvastatin exposure. Do not exceed dose of 20 mg/day. (D) Lovastatin: Increased lovastatin exposure. Do not exceed dose of 40 mg/day. (E) β-Blockers, non-DHP CCBs, clonidine, ivabradine: Additive bradycardia (9) Extensive monitoring for noncardiac adverse effects (A) Liver function tests (LFTs): Baseline and every 6 months (B) Thyroid function tests: Baseline and every 6 months (C) Chest radiography: Baseline and annually (D) ECG: Periodically (E) Pulmonary function tests (including DLCO [carbon dioxide diffusion in the lungs]): Baseline and for unexplained cough/dyspnea, chest radiographic abnormalities or clinical suspicion. Discontinue if pulmonary fibrosis occurs. (F) Ophthalmologic examination: Baseline (if visual impairment) and if patient has symptoms of visual impairment. Discontinue if optic neuritis occurs. (G) Skin toxicities: “Blue skin” syndrome and sunburn (H) Neurologic toxicity: Tremor, neuropathy (I) Nausea, vomiting (J) Adverse effects may require increased monitoring, dose reduction, or drug discontinuation

What is sotalol?

C. Sotalol Sotalol [SOE-ta-lol], although a class III antiarrhythmic agent, also has potent nonselective β-blocker activity. The levorotatory isomer (l-sotalol) has β-blocking activity, and d-sotalol has class III antiarrhythmic action. Sotalol blocks a rapid outward potassium current, known as the delayed rectifier. This blockade prolongs both repolarization and duration of the action potential, thus lengthening the effective refractory period. Sotalol is used for maintenance of normal sinus rhythm in patients with atrial fibrillation, atrial flutter, or refractory paroxysmal supraventricular tachycardia and in the treatment of ventricular arrhythmias. Since sotalol has β-blocking properties, it is commonly used for these indications in patients with left ventricular hypertrophy or atherosclerotic heart disease. This drug can cause the typical adverse effects associated with β-blockers but has a low rate of adverse effects when compared to other antiarrhythmic agents. The dosing interval should be extended in patients with renal disease, since the drug is renally eliminated. To reduce the risk of proarrhythmic effects, sotalol is most often initiated in the hospital to monitor QT interval.

What is satolol in bcps?

Sotalol: 50%–60% efficacy (1) Renal excretion. Dose adjustment and vigilant corrected QT (QTc) interval monitoring necessary in renal impairment. Recommended starting dose is 80 mg twice daily (unless creatinine clearance [CrCl] less than 60 mL/minute, then once daily). (2) Should be initiated in the hospital (minimum of 3-day stay), where QTc interval, serum electrolytes (e.g., K and magnesium), and renal function can be monitored (3) Contraindicated in patients with HF (stable or unstable); CrCl less than 40 mL/minute; QTc interval greater than 450 milliseconds; and second- or third-degree AV block or sick sinus syndrome (in absence of pacemaker) (4) Possesses nonselective β-blocking properties; may result in additive bradycardia with β-blockers, non-DHP CCBs, clonidine, ivabradine, and digoxin (5) Sotalol is ineffective for cardioversion but may be used for maintenance of NSR (normal SR).

What is dofetilide?

D. Dofetilide Dofetilide [doh-FET-il-ide] is a pure potassium channel blocker. It can be used as a first-line antiarrhythmic agent in patients with persistent atrial fibrillation and heart failure or in those with coronary artery disease. Because of the risk of proarrhythmia, dofetilide initiation is limited to the inpatient setting. The half-life of this oral drug is 10 hours. The drug is mainly excreted unchanged in the urine. Drugs that inhibit active tubular secretion are contraindicated.

What is dofetilide in bcps?

c) Dofetilide: 50%–60% efficacy (1) Should be initiated in the hospital (minimum of 3-day stay) so that QTc interval, serum electrolytes (e.g., K and magnesium), and renal function can be monitored (2) Starting dose is selected based on renal function (A) CrCl greater than 60 mL/minute: 500 mcg twice daily (B) CrCl 40–60 mL/minute: 250 mcg twice daily (C) CrCl 20–39 mL/minute: 125 mcg twice daily (D) CrCl less than 20 mL/minute: Contraindicated (3) Modification of subsequent doses is based on QTc interval measured 2–3 hours after initial dose: QTc > 500 milliseconds (or 550 milliseconds in ventricular conduction abnormalities) OR QTc increased greater than 15% above baseline: reduce dose by 50% (4) If QTc is greater than 500 milliseconds (or 550 milliseconds in ventricular conduction abnormalities) at any point after in-hospital doses 2–5, discontinue dofetilide (5) Hepatically metabolized by CYP3A4 (6) Renal elimination through renal cationic secretion; check QTc interval if renal function declines (7) Contraindicated in patients with CrCl less than 20 mL/minute or QTc interval greater than 440 milliseconds (or 500 milliseconds for patients with ventricular conduction abnormalities) (8) May use in patients with HF (9) Drug interactions (A) Avoid concomitant use of the following drugs: cimetidine, verapamil, itraconazole, ketoconazole, hydrochlorothiazide, prochlorperazine, megestrol, dolutegravir, and trimethoprim alone or in combination with sulfamethoxazole (B) Use CYP3A4 inhibitors, triamterene, metformin, and amiloride with caution: increased dofetilide exposure

What is ibutilide?

Ibutilide Ibutilide [eye-BYOO-tih-lide] is a potassium channel blocker that also activates the inward sodium current (mixed class III and IA action). Ibutilide is the drug of choice for chemical conversion of atrial flutter, but electrical cardioversion has supplanted its use. Ibutilide undergoes extensive first-pass metabolism and is not used orally. Because of the risk of QT prolongation and proarrhythmia, ibutilide initiation is limited to the inpatient setting.

What are class 4 antiarrythmic agents?

Class IV drugs are the nondihydropyridine calcium channel blockers verapamil [ver-AP-a-mil] and diltiazem [dil-TYE-a-zem]. Although voltage- sensitive calcium channels occur in many different tissues, the major effect of calcium channel blockers is on vascular smooth muscle and the heart. Verapamil shows greater action on the heart than on vascular smooth muscle, and diltiazem is intermediate in its actions. In the heart, verapamil and diltiazem bind only to open depolarized voltage-sensitive channels, thus decreasing the inward current carried by calcium. They prevent repolarization until the drug dissociates from the channel, resulting in a decreased rate of phase 4 spontaneous depolarization. These drugs are therefore use-dependent. They also slow conduction in tissues that are dependent on calcium currents, such as the AV and SA nodes (Figure 20.9). These agents are more effective against atrial than against ventricular arrhythmias. They are useful in treating reentrant supraventricular tachycardia and in reducing the ventricular rate in atrial flutter and fibrillation. Both drugs are metabolized in the liver by CYP3A4. Dosage adjustments may be needed in patients with hepatic dysfunction. Both agents are also inhibitors of CYP3A4, as well as substrates and inhibitors of P-glycoprotein. As such, they are subject to many drug interactions.

What is digoxin?

Digoxin [di-JOX-in] inhibits the Na+/K+-ATPase pump, ultimately shortening the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in the AV node. Digoxin is used to control ventricular response rate in atrial fibrillation and flutter; however, sympathetic stimulation easily overcomes the inhibitory effects of digoxin. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in VT and fibrillation. [Note: Serum trough concentrations of 1.0 to 2.0 ng/mL are desirable for atrial fibrillation or flutter, whereas lower concentrations of 0.5 to 0.8 ng/mL are targeted for systolic heart failure.]

What is adenosine?

Adenosine [ah-DEN-oh-zeen] is a naturally occurring nucleoside, but at high doses, the drug decreases conduction velocity, prolongs the refractory period, and decreases automaticity in the AV node. Intravenous adenosine is the drug of choice for abolishing acute supraventricular tachycardia. It has low toxicity but causes flushing, chest pain, and hypotension. Adenosine has an extremely short duration of action (approximately 10 to 15 seconds) due to rapid uptake by erythrocytes and endothelial cells.

What is mg sulphate?

Magnesium is necessary for the transport of sodium, calcium, and potassium across cell membranes. It slows the rate of SA node impulse formation and prolongs conduction time along the myocardial tissue. Intravenous magnesium sulfate is the salt used to treat arrhythmias, as oral magnesium is not effective in the setting of arrhythmia. Most notably, magnesium is the drug of choice for treating the potentially fatal arrhythmia torsades de pointes and digoxin-induced arrhythmias