Adenosine: ultrashort action
Adenosine (Adenosine) is a natural (endogenous) nucleoside acting as an agonist of adenosine $A_1$ receptors. Its main pharmacokinetic feature is an extremely short half-life of about 10 seconds. The total duration of action does not exceed one minute. This is because the substance is instantly taken up by erythrocytes via a specific nucleoside transporter and rapidly degraded by vascular endothelial enzymes. For this reason, the drug is administered exclusively via intravenous bolus.
At the molecular level, stimulation of $A_1$ receptors leads to the opening of coupled potassium channels. $K^+$ ions flow out of the cell, causing membrane hyperpolarization. Electrophysiologically, this manifests as suppression of sinus node automaticity, decreased myocardial contractility, and sharp inhibition of conduction in the atrioventricular (AV) node.
The drug causes transient AV block, which breaks the re-entry excitation wave circuit (re-entry) between the atria and ventricles. Therefore, adenosine is used exclusively for the termination of supraventricular tachyarrhythmias, including Wolff-Parkinson-White (WPW) syndrome. Due to the specifics of its mechanism of action, side effects are possible, such as transient asystole and breathing difficulties (dyspnea).
Cardiac glycosides in arrhythmias
A prominent representative of the group is digoxin (a foxglove preparation). Its main indication in antiarrhythmic therapy is the tachy-form of atrial fibrillation.
In atrial fibrillation, their automaticity increases pathologically, chaotic re-entry circulation of excitation occurs (re-entry), and the atrial rate reaches 300 beats per minute. Natural AV node conduction acts as a filter, passing only every second or fourth impulse. However, without treatment, the ventricular rate remains high—about 150 beats per minute—which requires medical correction.
Digoxin has a negative dromotropic effect, meaning it decreases atrioventricular conduction. By creating incomplete conduction block, it converts tachy-form atrial fibrillation into normosystolic form. The clinical outcome is the normalization of the ventricular rate.
In case of overdose or high doses, complete transverse block occurs. At the atrial level, fibrillation may transition into flutter. The ventricles then switch to an autonomous (idioventricular) rhythm. The pacemaker becomes the cardiomyocytes of the bundle of His, setting a rate of 40–60 impulses per minute. Hemodynamically, the rhythm becomes slower but coordinated, which improves the heart's pumping function.
Potassium and magnesium preparations
Electrolytes play a critical role in maintaining the stability of cardiomyocyte cell membranes. Clinical practice utilizes potassium chloride (most effective in intravenous polarizing mixtures) and combination agents such as potassium and magnesium asparaginate (Panangin, Asparkam).
They are indicated for tachyarrhythmias and extrasystoles, but under one key condition: the rhythm disorders must be caused by hypokalemia or hypomagnesemia (decreased concentration of these ions in the blood). The drugs are administered both orally (per os) and intravenously. Reported side effects include neurological (paresthesias), gastrointestinal (dyspepsia), and cardiac (conduction suppression up to AV block) effects.
A special place in resuscitation practice is held by magnesium sulfate. When administered intravenously, it is a specific agent for terminating life-threatening polymorphic ventricular tachycardia—the specific arrhythmia type known as Torsades de Pointes (Torsades de Pointes).
Briefly: answers to topical questions
What are the contraindications to the use of adenosine?
Contraindications to the use of adenosine include severe bronchial asthma, angina pectoris, and the combination of Wolff-Parkinson-White (WPW) syndrome with atrial fibrillation (AF).
- Severe bronchial asthma is a direct contraindication.
- Angina pectoris is a direct contraindication.
- WPW syndrome combined with AF — use is contraindicated because the impulse will travel via accessory pathways, which can lead to ventricular fibrillation.
What extracardiac symptoms are characteristic of cardiac glycoside intoxication?
Cardiac glycoside intoxication is characterized by the following extracardiac manifestations:
- Nausea and vomiting may be a sign of digitalis intoxication in digoxin overdose.
- Visual disturbances are listed among the side effects of digoxin.
- Hyperkalemia is listed among the side effects of digoxin.
Which drugs have clinically significant interactions with digoxin?
Digoxin has clinically significant interactions with the following drugs and groups:
- Quinidine inhibits P-glycoprotein, thereby increasing blood concentrations of digoxin and raising the risk of digitalis intoxication.
- Verapamil is a P-glycoprotein inhibitor; the combination of digoxin and verapamil increases the risk of digitalis intoxication.
- Amiodarone combined with digoxin increases the risk of digitalis intoxication.
- Phenobarbital, rifampicin, phenytoin are hepatic microsomal enzyme inducers; they accelerate the metabolism and inactivation of drug substances, which may weaken the therapeutic effect of digoxin.
- Ivabradine requires caution when used concomitantly with digoxin.
Class and exam questions
Why is adenosine administered only via intravenous bolus?
Due to its pharmacokinetics: the drug is instantly taken up by erythrocytes and degraded by endothelial enzymes. Its half-life is about 10 seconds, so if administered slowly, it will be destroyed before reaching the heart.
How does digoxin help in atrial fibrillation?
It exerts a negative dromotropic effect—inhibiting conduction in the AV node. This allows filtering out extra impulses coming from the atria and reducing the ventricular rate to normal values.
In which case will potassium and magnesium preparations be effective against arrhythmias?
Only if the rhythm disorder is directly related to a decreased concentration of these ions in the blood (hypokalemia or hypomagnesemia).
What else to study on this topic
- The molecular mechanism of $A_1$ receptor coupling with potassium channels.
- Pathophysiology of Wolff-Parkinson-White (WPW) syndrome.
- Electrophysiological differences between atrial fibrillation and atrial flutter.
- Mechanism of idioventricular rhythm development in complete AV block.
- The nature of polymorphic ventricular tachycardia (Torsades de Pointes).
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