Pathophysiology Foundations: How Conduction Abnormalities Arise

Why Arrhythmias Happen: Three Core Mechanisms

Before you can recognize an abnormal rhythm on a 12-lead EKG strip, you need to understand why the heart beats irregularly in the first place. Almost every clinically significant arrhythmia arises from one of three physiological mechanisms: re-entry, enhanced automaticity, or triggered activity. Understanding these mechanisms will help you connect what you see on the strip to what is happening inside the heart's conduction system.

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The Normal Foundation

In a healthy heart, the sinoatrial (SA) node fires spontaneously at a regular rate, sending an impulse down a predictable path: SA node → internodal pathways → atrioventricular (AV) node → Bundle of His → right and left bundle branches → Purkinje fibers → ventricular muscle. This orderly sequence produces the P wave, PR interval, and QRS complex you will learn to measure. Any disruption to impulse formation or conduction along this route can produce an arrhythmia.

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Mechanism 1: Re-Entry

Re-entry is the most common mechanism behind sustained arrhythmias, including atrial flutter, atrial fibrillation (AFib), supraventricular tachycardia (SVT), and many ventricular tachycardias.

Three conditions must all be present for re-entry to occur:

1. Two distinct conduction pathways that share a common entry and exit point — forming a loop.

2. Unidirectional block in one limb of the loop — the impulse can travel in only one direction through that pathway.

3. Sufficiently slow conduction in the unblocked limb — slow enough that the blocked limb has time to recover its excitability before the impulse returns.

When these three conditions exist, an impulse travels down the open limb, exits, and then curves back up through the previously blocked limb (which has now recovered). It finds the open limb excitable again and goes around the loop repeatedly — a circus movement. Each lap around the circuit generates another depolarization, producing a rapid, often regular, tachycardia.

Common clinical examples: AV nodal re-entrant tachycardia (AVNRT) uses two pathways within or near the AV node. Wolff-Parkinson-White (WPW) syndrome uses an accessory pathway (Bundle of Kent) as the second limb. Atrial flutter uses a large re-entry loop within the right atrium.

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Mechanism 2: Enhanced Automaticity

Automaticity is the ability of certain cardiac cells to depolarize spontaneously without an external stimulus. Normally, the SA node has the highest rate of automaticity and therefore controls the heart rate. Cells in the AV node, bundle branches, and Purkinje fibers also have automaticity, but at slower rates — they are latent pacemakers.

Enhanced automaticity occurs when a focus outside the SA node develops an abnormally rapid rate of spontaneous depolarization and "outpaces" the SA node, or when an ectopic focus fires at a rate faster than normal for its location. Contributing factors include:

• Electrolyte imbalances (notably low potassium or magnesium)
• Ischemia or hypoxia, which can destabilize resting membrane potential
• Elevated catecholamines (stress, stimulant medications)
• Digitalis toxicity

Common clinical examples: Premature atrial contractions (PACs) and premature ventricular contractions (PVCs) often reflect enhanced automaticity in an ectopic focus. Accelerated junctional rhythm and some forms of atrial tachycardia also involve enhanced automaticity. Sinus tachycardia itself is a physiologically appropriate increase in SA node automaticity.

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Mechanism 3: Triggered Activity

Triggered activity arises from afterdepolarizations — abnormal secondary oscillations in membrane voltage that occur after the main action potential. There are two types:

• Early afterdepolarizations (EADs) happen before the cell has fully repolarized (during phase 2 or 3 of the action potential). EADs are associated with prolonged QT interval and can trigger the dangerous ventricular arrhythmia Torsades de pointes.
• Delayed afterdepolarizations (DADs) happen after full repolarization (phase 4). DADs are associated with calcium overload inside the cell, which can occur with digitalis toxicity or severe ischemia. DADs can produce PVCs or, if they reach threshold repeatedly, ventricular tachycardia.

Triggered activity is distinct from enhanced automaticity because the abnormal impulse requires a preceding action potential to "trigger" it — it cannot start on its own.

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Conduction Structures Implicated in Common Disturbances

| Rhythm Disturbance | Primary Structure(s) Implicated | Dominant Mechanism |

|---|---|---|

| Sinus bradycardia / tachycardia | SA node | Altered automaticity |

| PACs | Atrial ectopic focus | Enhanced automaticity |

| Atrial flutter | Right atrial tissue (tricuspid isthmus) | Re-entry |

| Atrial fibrillation | Pulmonary vein foci + atrial tissue | Re-entry / enhanced automaticity |

| AVNRT / SVT | AV node dual pathways | Re-entry |

| AV block (1°, 2°, 3°) | AV node / Bundle of His | Conduction delay or block |

| PVCs | Ventricular ectopic focus | Enhanced automaticity or triggered activity |

| Torsades de pointes | Ventricular myocardium | Triggered activity (EADs) |

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Safety and Scope of Practice Notes

As an EKG technician, your role is to acquire and report rhythm strips accurately — not to diagnose or treat arrhythmias. However, understanding these mechanisms helps you recognize when a strip may reflect a life-threatening condition that requires you to notify clinical staff immediately. If a patient shows signs of hemodynamic compromise (loss of consciousness, no palpable pulse, extreme distress) while you are recording, activate your facility's emergency response without delay. Accurate, artifact-free recordings are essential: a noisy strip can obscure the very features that allow clinicians to identify the mechanism driving an arrhythmia and choose appropriate treatment.