Cardiac ConductionEdit

Note: This article provides a neutral, evidence-based overview of cardiac conduction and its clinical implications. It does not adopt any political viewpoint and focuses on physiology, diagnosis, and management.

Cardiac conduction refers to the heart’s intrinsic electrical system that initiates and coordinates the sequence of atrial and ventricular activation. This system ensures orderly atrial contraction followed by ventricular contraction, optimizing filling, stroke volume, and cardiac output. When conduction is disrupted, the heart may beat too slowly (bradycardia), too quickly or irregularly (tachyarrhythmias), or lose synchrony between chambers, with potential consequences for hemodynamics and overall health.

Anatomy and physiology

The conducting system

The heart’s electrical activity begins with the sinoatrial node sinoatrial node in the right atrium, which sets the pace for the heart. The impulse then travels through atrial myocardium to the atrioventricular node, which introduces a critical delay to allow complete ventricular filling. From the AV node, impulses pass into the bundle of His and split into the left bundle branch and right bundle branch, distributing rapidly via the Purkinje fibers to synchronize ventricular contraction.

Conduction velocity and refractoriness

Conduction velocity is highest in the Purkinje system and slower in nodal tissue. The AV node’s deliberate delay (often about 100–200 milliseconds) coordinates atrial and ventricular rhythms and prevents retrograde conduction from causing rapid ventricular rates. Nodal tissue relies more on calcium currents for upstroke, while working myocytes use fast sodium currents; these differences underlie distinct action potential shapes and refractory properties that help maintain orderly propagation.

Autonomic regulation

Conduction and heart rate are modulated by the autonomic nervous system. Sympathetic input tends to increase heart rate and conduction velocity, while parasympathetic input (principally via the vagus nerve) slows the rate and can slow AV conduction. Baroreflexes and hormonal influences also contribute to short- and long-term regulation of conduction and rhythm.

Electrocardiography and interpretation

The surface electrocardiogram (electrocardiography) is a noninvasive record of the heart’s electrical activity. The P wave corresponds to atrial depolarization, the PR interval reflects conduction from the SA node through the AV node, the QRS complex represents ventricular depolarization, and the T wave reflects ventricular repolarization. Normal ranges help identify deviations in conduction:

PR interval: typically 120–200 milliseconds.
QRS duration: generally less than 120 milliseconds.
QT interval: adjusted for heart rate, reflecting repolarization time.

Clinical features and disorders

Common conduction disturbances

Sick sinus syndrome (sinus node dysfunction) involves impaired automaticity or recovery of the SA node, leading to bradycardia, pauses, or chronotropic incompetence.
Atrioventricular (AV) block comprises impaired conduction from atria to ventricles and is classified by degree (first-degree, second-degree, third-degree). First-degree AV block lengthens the PR interval without dropped beats; second-degree blocks intermittently fail to conduct every atrial impulse; third-degree (complete) block disconnects atrial and ventricular activity.
Bundle branch blocks (BBB) reflect delayed activation of one ventricle, producing characteristic QRS widening and axis changes. Left bundle branch block (LBBB) and right bundle branch block (RBBB) have distinct ECG patterns and implications for diagnosis and therapy.
Preexcitation syndromes, such as Wolff-Parkinson-White syndrome, involve an accessory pathway that creates abnormal conduction and can predispose to tachyarrhythmias.

Diagnostic approaches

Evaluation typically includes resting and ambulatory ECG recording (Holter or event monitors), exercise testing, and, when indicated, invasive electrophysiology studies to map conduction properties and provoke arrhythmias. Imaging modalities such as echocardiography assess structural correlates that influence conduction (e.g., atrial enlargement, ventricular dilation).

Therapeutics and management

Device therapy

Pacemakers are indicated for symptomatic bradycardia, high-grade AV block, or certain conduction-system diseases where the heart cannot maintain adequate rate or rhythm. They restore reliable chronotropic support and improve perfusion while reducing syncope risk.
Cardiac resynchronization therapy (CRT) combines pacing of the right and left ventricles to improve synchronization in select patients with heart failure and dyssynchronous conduction.

Ablation and rhythm control

Catheter ablation targets specific circuits or foci responsible for tachyarrhythmias arising from the conduction system or adjacent tissue (e.g., AV nodal reentrant tachycardia, WPW-related tachycardias). Electrophysiology-guided ablation can reduce or eliminate reliance on antiarrhythmic medications and, in some cases, obviate the need for ongoing device therapy.

Medical therapy and lifestyle considerations

Drug therapies may influence conduction (e.g., certain antiarrhythmic agents can slow AV conduction or ventricular conduction). Management also emphasizes treating underlying diseases such as ischemia, electrolyte disturbances, or hypothyroidism, which can affect conduction. Lifestyle factors, comorbidities, and patient preferences all shape the selection among monitoring, pharmacology, pacing, or ablation strategies.

Controversies and debates

When to implant a pacemaker in elderly patients or those with comorbidities remains debated, balancing symptomatic relief and procedural risks against quality of life and longevity.
The relative merits of right ventricular apical pacing versus more physiological pacing (such as His bundle pacing or left bundle branch area pacing) continue to be discussed. Physiologic pacing aims to preserve synchrony and may reduce long-term heart failure risk, but broader long-term data and practical considerations drive current practice.
In some cases, ablation and device therapy are weighed against long-term medical management. Patient values, anticipated symptom burden, and risk of procedure-related complications all influence decisions.
Access to advanced therapies and disparities in care can shape outcomes; ongoing debates focus on how guidelines, reimbursement, and clinician judgment interact to optimize population health while avoiding overtreatment.

Research and future directions

Advances in conduction-system pacing (including His bundle pacing and left bundle branch area pacing) seek to preserve physiologic activation of the ventricles and improve outcomes in patients requiring pacing. Enhanced imaging and electrophysiology mapping, improved device algorithms, and personalized approaches to cardiac resynchronization therapy continue to refine diagnosis and treatment. Investigations into genetic contributions to congenital conduction disorders also hold promise for earlier identification and targeted management.