Medications used to treat various health conditions can inadvertently affect the heart’s electrical system. The heart relies on a precise sequence of electrical impulses to maintain a steady rhythm, and certain therapeutic agents can disrupt the speed and efficiency of this process. This interference leads to changes in the heart’s conduction pathway, which are visible as abnormalities on an electrocardiogram, such as Right Bundle Branch Block.
What is Right Bundle Branch Block?
The heart’s rhythm is governed by a specialized network of cells known as the cardiac conduction system. This system includes the sinoatrial (SA) node, the atrioventricular (AV) node, the Bundle of His, and the left and right bundle branches. After the electrical signal passes through the AV node, it splits to travel down the two main bundle branches, which deliver the impulse to the left and right ventricles, causing them to contract.
Right Bundle Branch Block (RBBB) occurs when the electrical signal is slowed or blocked as it travels down the right bundle branch. The impulse must detour through the surrounding muscle tissue of the left ventricle before finally reaching the right ventricle. This indirect route causes the right ventricle to contract later than the left, creating a slight delay in the heart’s overall electrical sequence. While RBBB is often discovered incidentally, it signifies a defect in the conduction system that can be chemically induced by certain drugs.
How Medications Interfere with Cardiac Conduction
The electrical impulse that drives each heartbeat is generated by the rapid movement of ions, primarily sodium (\(\text{Na}^+\)), potassium (\(\text{K}^+\)), and calcium (\(\text{Ca}^{2+}\)), across the membranes of heart cells. This movement creates an action potential, which propagates the electrical signal. The speed of conduction through the specialized His-Purkinje network is determined largely by the swift initial influx of sodium ions, known as Phase 0 depolarization.
Many medications that cause RBBB do so by binding to and blocking these voltage-gated cardiac sodium channels. This blockade slows the rate of Phase 0 depolarization, decreasing the velocity at which the electrical signal is transmitted through the ventricles. This cellular mechanism causes a measurable widening of the QRS complex on an electrocardiogram, which is the electrical signature of ventricular depolarization. If this slowing of conduction is significant, it can functionally mimic or create a blockage along the right bundle branch pathway.
Primary Drug Classes Associated with RBBB
The medications most commonly associated with inducing or exacerbating RBBB are those that possess strong sodium channel blocking properties. This effect, often termed a “quinidine-like” action, is the direct cause of the conduction delay seen on the electrocardiogram. These drugs are generally grouped into categories based on their primary therapeutic use, but their shared cardiac side effect stems from this common interference with sodium channels.
Class I Antiarrhythmics
The Class I antiarrhythmic drugs are specifically designed to manage abnormal heart rhythms, and their entire mechanism of action relies on sodium channel blockade. These agents are categorized into subclasses (Ia, Ib, and Ic) based on the degree and kinetics of this blockade. Subclasses Ia and Ic are the most potent in slowing conduction velocity, directly leading to the potential for a bundle branch block.
Drugs like flecainide and propafenone, which are Class Ic agents, exhibit a strong and prolonged blockade of the sodium channel. This high-affinity binding significantly slows the speed of electrical transmission through the His-Purkinje system and ventricular muscle. Class Ia agents, such as procainamide, also exert this effect, combining sodium and potassium channel blockade to slow both conduction and repolarization.
Tricyclic Antidepressants
Tricyclic Antidepressants (TCAs), a class of older antidepressant medications, are notorious for their cardiovascular side effects due to their powerful action as sodium channel blockers. This effect is often magnified in cases of overdose, but it can also occur at therapeutic doses, especially in patients with pre-existing heart disease. The TCAs, including drugs like amitriptyline and imipramine, directly impair the Phase 0 depolarization of cardiac cells.
The resulting cardiotoxicity is marked by a prolonged QRS duration on an ECG, indicating delayed ventricular conduction. This sodium channel blockade can create an electrocardiographic pattern that includes RBBB morphology and ST-segment elevation, known as a Brugada syndrome phenotype. This specific pattern is highly concerning because it indicates a risk for severe, life-threatening ventricular arrhythmias.
Antipsychotic Medications
Certain antipsychotic drugs, particularly some of the older, lower-potency typical agents and a few atypical agents, possess significant sodium channel blocking properties that contribute to cardiotoxicity. Medications like olanzapine, risperidone, and phenothiazine-derived antipsychotics have been documented to cause or be associated with bundle branch blocks.
Like the TCAs, these agents can trigger the Brugada-like ECG pattern. The sodium channel block is the primary mechanism responsible for the delayed conduction through the bundle branches. This adverse effect is a major consideration when prescribing these medications, particularly in individuals with existing cardiac risk factors.
Other Drug Classes
The potential for drug-induced conduction delay is not limited only to psychotropic or antiarrhythmic medications. Other classes of drugs possess sodium channel blocking activity sufficient to cause RBBB. Chemotherapy agents, such as anthracyclines (e.g., doxorubicin), are known to cause cardiotoxicity that can manifest as conduction system abnormalities. Some selective serotonin reuptake inhibitors (SSRIs) like citalopram and fluoxetine have also been linked to bundle branch block, especially at higher doses, due to a lesser effect on cardiac ion channels.
When to Seek Medical Attention
If you are taking any medication and receive a diagnosis of RBBB, communicate this information to your prescribing healthcare provider immediately. While RBBB is often asymptomatic and may not require direct treatment, a new diagnosis warrants a review of your current medication regimen. This is especially true if the RBBB is associated with the start of a new drug or a change in dosage.
You should seek prompt medical evaluation if you experience new symptoms such as unexplained fainting (syncope), near-fainting (presyncope), or lightheadedness. Severe symptoms like chest pain, pronounced shortness of breath, or sudden, severe palpitations also require urgent medical attention. These symptoms can suggest the conduction delay is progressing or is combined with a more serious underlying heart rhythm disorder.