Sodium channel blockers:

These drugs inhibit the flow of sodium ions into cardiac cells, slowing down the electrical conduction in the heart.

Examples:

• Procainamide
• Lidocaine
• Flecainide

Beta blockers:

These drugs block the effects of adrenaline (epinephrine) on the heart, reducing the heart rate and the force of contractions.

Examples:

• Propranolol
• Metoprolol
• Atenolol

Potassium channel blockers:

These drugs prolong the repolarisation phase of the cardiac action potential, helping to stabilise the heart’s electrical activity.

Examples:

• Amiodarone
• Sotalol
• Dofetilide

Calcium channel blockers:

These drugs block the influx of calcium ions into cardiac cells, slowing down the heart rate and reducing the force of contractions.

Examples:

• Verapamil
• Diltiazem

Some medications don’t fit into the above classes but still have antiarrhythmic properties.

Example:

• Adenosine is used to treat supraventricular tachycardia by slowing down the electrical conduction in the heart.
• Adenosine is also used for diagnostic purposes in cardiology. It is administered intravenously to induce a temporary heart block, which can help identify the underlying cause of certain arrhythmias.

Some medications don’t fit into the above classes but still have antiarrhythmic properties

Examples:

• Digoxin is a medication that has both positive inotropic (increases the force of heart contractions) and negative chronotropic (slows down the heart rate) effects.
• It is used in the treatment of certain types of arrhythmias, particularly atrial fibrillation and atrial flutter. It is also used in heart failure management.

Mode of action:

Amiodarone is a primarily a class III antiarrhythmic. Like other antiarrhythmic drugs of this class, amiodarone works primarily by blocking potassium rectifier currents that are responsible for the repolarisation of the heart during phase 3 of the cardiac action potential.

Indication: 

• Tachyarrhythmias associated with Wolff-Parkinson-White syndrome
• Atrial flutter and fibrillation when other drugs cannot be used
• All types of tachyarrhythmias of paroxysmal nature;when other drugs cannot be used

Dosing (Initial loading dose: 

• 200mg TDS for 7 days
• 200mg BD for 7 days
• 200 mg OD maintenance 

Side effects: 

• Corneal microdeposits: reversible on withdrawal of treatment, however, if vision is impaired amiodarone must be stopped to prevent blindness and expert advice acquired. 
  

1. Signs to look out for: Glaring, difficulty driving at night

• Hepatotoxicity: Treatment should be discontinued if severe liver function abnormalities or clinical signs of liver disease develop.

1. Signs to look out for: Jaundice, nausea, de-ranged LFTs, abdominal pain, itching

• Skin: Phototoxic reactions during treatment even several months after discontinuing amiodarone can occur;

1. Signs to look out for: Slate grey skin, erythema, burning (a wide- spectrum sunscreen to protect against both long-wave ultraviolet and visible light should be used even several months after stopping the drug)

• Pulmonary toxicity: Pneumonitis should always be suspected if new or progressive shortness of breath or cough develops in a patient taking amiodarone.

1. Signs to look out for: Dry cough, chesty, shortness of breath

• Thyroid function Amiodarone contains iodine and can cause disorders of thyroid function; both hypothyroidism and hyperthyroidism can occur. 

1. Signs to look out for:

• Hyperparathyroidism: (weight loss, fast heart rate, heat intolerance- Can give carbimazole
• Hypothyroidism: Weight gain, slower heart rate, cold intolerance- Can give levothyroxine

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• Pregnancy: Possible risk of neonatal goitre; use only if no alternative is available
• Breastfeeding: Significant presence in milk; theoretical risk of neonatal hypothyroidism from iodine release

• Amiodarone is an enzyme inhibitor (specifically CYP3A4) therefore increasing concentrations of: Digoxin (half dose), Verapamil and Diltiazem; 
• Increased concentration of amiodarone when taken with grapefruit juice (enzyme inhibitor)
• Amiodarone together with beta blockers or CCB’s like Diltiazem and Verapamil can cause; bradycardia, AV block and heart failure
• QT prolongation: Quinolone, Lithium, Tricyclic antidepressants, Macrolides

Note: 

Amiodarone has a long half-life; there is potential for drug interactions to occur for several weeks or months) after treatment with it has been discontinued.

Mode of action:

Digoxin is a cardiac glycoside, exhibits positive ionotropic effects by enhancing the force of myocardial contraction. Additionally, it exerts negative chronotropic effects by decreasing conductivity in the atrioventricular (AV) node, thereby reducing the ventricular rate.

Indications and dose: 

• Maintenance, for atrial fibrillation or flutter: Dose 125–
  250 micrograms daily, dose according to renal function and initial loading dose. Reduce dose in the elderly
• Heart failure for patients in sinus rhythm: Dose 62.5-125 micrograms daily. Reduce dose in the elderly

• Plasma-digoxin concentration: After initial dosing or dose change, levels should be checked after 7 days once steady state is achieved. Bloods should be taken at least 6 hours after maintenance dosing begins Patients symptoms, heart rate and ECG should also be monitored
• Renal function (renal main route of excretion). Monitor serum electrolytes; toxicity increased by electrolyte disturbances (hypokalaemia, hypomagnesaemia and hypercalcaemia).

Toxicity symptoms include; nausea, vomiting, diarrhoea, abdominal pain confusion and yellow vision.

• Digoxin toxicity can occur even within the therapeutic always interpret results in the clinical context of the patients condition.
  
  
• The likelihood of toxicity depends on the serum concentration of digoxin.
• Levels less than 1.5 nanograms/mL with no hypokalaemia indicate that digoxin toxicity is unlikely.
• With levels between 1.5 nanograms/mL and 3.0 nanograms/mL, digoxin toxicity should be considered a possibility.
• Levels higher than 3.0 nanograms/mL indicate digoxin toxicity is likely.

Pregnancy: May need dosage adjustments

Breastfeeding: Small amounts in milk- not significant enough to be harmful

Hypokalaemia causes digoxin toxicity, drugs that causes this: Loop/ thiazide diuretics, steroids, theophylline  

Enzyme inhibitors cause higher levels of digoxin: Amiodarone, diltiazem/ verapamil (rate limiting CCBs), Macrloides

Enzyme inducers cause lower levels of digoxin: St Johns Wart, Rifampicin

Renal: Reduced renal excretion due to drugs such as