Miscellaneous Antiarrhythmic Agents: Adenosine and others


Adenosine is an antiarrhythmic agent that is widely used for the investigation and management of both narrow complex and, less often, broad complex tachycardias. It produces a transient block in the atrioventricular node. This effect is mediated by interaction with A1 receptors (reducing cyclic adenosine monophosphate) present on myocytes, thereby activating potassium channels, which increase K+ efflux, causing cell hyperpolarization.

Adenosine is considered first-line therapy for the investigation and termination of supraventricular tachycardias because of its efficacy and safety. It is also being used in some areas to aid in the diagnosis of broad complex tachycardias, usually if they have not responded to lignocaine (lidocaine).

Mechanism & Clinical Use

  • Naturally occurring nucleoside with a half-life of less than 10 seconds.
  • Activates inward rectifier K+ current and inhibits calcium current.
  • Highly effective (90–95%) for converting paroxysmal supraventricular tachycardia to sinus rhythm.


  • Causes flushing, shortness of breath, or chest burning in some patients.
  • May induce high-grade AV block or atrial fibrillation, but the effects are short-lived.


Digoxin is a cardiac glycoside that has been used for many years in the treatment of heart failure and arrhythmias. It is derived from the foxglove plant, Digitalis lanata. While its primary indication is for the treatment of heart failure, it also has antiarrhythmic properties that make it useful in managing certain types of cardiac arrhythmias, particularly atrial fibrillation and atrial flutter.

Mechanism of Action

Digoxin works by inhibiting the sodium-potassium ATPase pump in the myocardial (heart muscle) cells. This action raises the amount of sodium inside cells, which then makes it easier for the sodium-calcium exchanger to trade intracellular sodium for extracellular calcium. The net effect is an increase in intracellular calcium, which enhances cardiac contractility.

Digoxin slows down the flow of electrical impulses through the atrioventricular (AV) node, which is one of its antiarrhythmic effects. This is particularly useful in conditions like atrial fibrillation or atrial flutter, where electrical impulses can bombard the AV node at a very high rate. By slowing down AV nodal conduction, digoxin helps to control the ventricular rate, making it more regular and often slower.


Digoxin has a narrow therapeutic index, meaning that the difference between an effective dose and a toxic dose is small. In patients with renal impairment, dose adjustments are necessary because the kidneys are the main organs responsible for excreting it.

Adverse Effects

The narrow therapeutic index also means that digoxin has a high potential for toxicity. Symptoms of digoxin toxicity can include nausea, vomiting, diarrhea, confusion, and visual disturbances. More seriously, digoxin toxicity can lead to life-threatening arrhythmias, including ventricular tachycardia and ventricular fibrillation.

Clinical Use

In the modern era, the use of digoxin for arrhythmias has declined due to the development of other antiarrhythmic drugs that are more effective and have better safety profiles. However, it is still used in specific cases where other treatments are not suitable or have failed.


Due to its narrow therapeutic window, patients on digoxin are closely monitored. Serum levels of the drug, as well as renal function, are regularly checked. Electrocardiograms may also be performed to monitor the drug’s effects on the heart’s electrical activity.

In summary, while digoxin is primarily used for heart failure, its ability to slow down AV nodal conduction makes it useful as an antiarrhythmic agent in specific cases. However, its narrow therapeutic index and potential for serious adverse effects mean that it must be used cautiously with regular monitoring.


Mechanism & Clinical Use

  • Selective blocker of the “funny” current (If) in the SA node.
  • Slows pacemaker activity without affecting myocardial contractility or ventricular repolarization.
  • Used for heart rate control in coronary artery disease and congestive heart failure.


  • Visual disturbances have been described.


Mechanism & Clinical Use

  • Multi-ion channel blocker.
  • Effective for rapid termination of atrial fibrillation in patients with minimal structural heart disease.


  • Sinus bradycardia and hypotension are the main cardiovascular adverse effects.


Mechanism & Clinical Use

  • Influences Na+/K+-ATPase, sodium channels, certain potassium channels, and calcium channels
  • Used in digitalis-induced arrhythmias and torsades de pointes.


  • Further investigation is needed to fully understand its actions and indications.


These miscellaneous agents offer a range of mechanisms and clinical uses for treating arrhythmias. While some are well established in clinical practice, others are still under investigation. Each comes with its own set of benefits and risks, making it crucial to tailor the choice of antiarrhythmic agent to the individual patient’s needs.

Note: This article is intended for educational purposes and should not be considered as medical advice. Always consult with a healthcare professional for medical advice and treatment.

Disclaimer: This article is for informational purposes only and does not constitute medical advice. Always seek the advice of a healthcare provider with any questions regarding a medical condition.

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