Treating Cardiac Arrhythmias: Physiology of Initiation and Conduction

Treating cardiac arrhythmias involves targeting the underlying physiological disturbances in the heart's impulse initiation and impulse propagation. 

Step-by-step approach to the physiological basis of treatment:

1. Identify the Type of Arrhythmia and Underlying Physiological Problem:

Determine if the arrhythmia is primarily due to a problem with impulse initiation (altered automaticity) or impulse propagation (conduction abnormality). ECG analysis is a key tool for this, allowing assessment of rate, rhythm, and conduction patterns like P waves, QRS complexes, and intervals. For example, a prolonged P-R interval indicates delayed AV conduction, while an intermittently wide QRS might suggest bundle branch block.

Pinpoint the specific location and nature of the abnormality (e.g., SA node, AV node, Purkinje fibers, accessory pathway, re-entrant circuit, ectopic focus).

2. Address Disturbances of Impulse Initiation (Altered Automaticity):

Physiological Basis of Disease: Normally, the SA node is the primary pacemaker due to its fastest intrinsic firing rate. Other areas like the AV node and Purkinje fibers also have intrinsic automaticity. Arrhythmias can arise from changes in SA nodal rate (sinus tachycardia/bradycardia, often due to autonomic modulation) or from ectopic foci firing abnormally. Abnormal automaticity can occur even in non-pacemaker cells under certain conditions, such as prolonged action potentials leading to early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs).

Physiological Basis of Treatment: The goal is often to suppress abnormal pacemakers or correct the rate of the normal pacemaker if it is inappropriate.

For bradycardias (slow rates), especially those due to failed normal pacemakers (like profound bradycardia from complete AV block where slow Purkinje pacemakers take over), treatment may involve increasing the heart rate. If the intrinsic system is permanently unreliable, an artificial ventricular pacemaker can be implanted to maintain adequate cardiac output. Autonomic modulation can also change SA node rate (sympathetic increases, parasympathetic decreases).

For tachycardias (fast rates), treatment aims to decrease the firing rate of the SA node (if sinus tachycardia) or suppress the activity of ectopic foci or abnormal automaticity. This can involve drugs that affect the ionic currents underlying pacemaker activity or abnormal depolarizations (e.g., affecting Na+, K+, or Ca2+ channels). For example, in Long QT Syndrome (LQTS), where prolonged action potentials lead to EADs and triggered activity12, treatment strategies include restoring extracellular K+ levels and increasing heart rate, which can help mitigate the propensity for arrhythmias like torsades de pointes.

Drugs that target the autonomic nervous system can modulate heart rate (e.g., blocking vagal effects with atropine can increase heart rate19..., blocking beta-adrenergic receptors can decrease heart rate).

3. Address Disturbances of Impulse Propagation (Conduction Abnormalities):

Physiological Basis of the Disease: The electrical impulse normally propagates through the conduction system in a specific, timed manner. Disturbances include conduction blocks (partial or complete failure of propagation) and re-entry (impulse travels in a loop and re-excites tissue). Blocks can be caused by structural damage (ischemia, disease) or functional changes (altered ionic currents, depolarization)5. Re-entry requires a closed loop, a region of unidirectional block, and sufficiently slow conduction. Aberrant/accessory pathways are anatomical abnormalities that bypass normal conduction and can be substrates for re-entry.

Physiological Basis of Treatment: The goal is to restore normal conduction where possible, bypass permanent blocks, or disrupt re-entrant circuits.

For conduction blocks that are significant and cause symptoms (e.g., third-degree AV block leading to profound bradycardia)5, the physiological problem is that the impulse cannot pass through the blocked region. The treatment is to bypass the block using an artificial pacemaker to directly stimulate the ventricle at an adequate rate.

For re-entry, the physiological problem is a self-perpetuating electrical loop. Treatment aims to break the re-entry circuit by altering conduction or refractoriness within the loop. This can be achieved by:

Slowing conduction in a part of the loop further, making the tissue still refractory when the impulse arrives5. Drugs that block calcium channels (e.g., diltiazem) can slow conduction, particularly in the AV node where conduction depends heavily on calcium currents (slow response tissue). Drugs that block sodium channels can slow conduction in fast-response tissues (atria, ventricles, Purkinje fibers).

Prolonging refractoriness in a part of the loop, so that the tissue is unable to be re-excited when the impulse returns. Drugs that affect potassium channels can prolong the action potential duration and thus the refractory period.

In cases of aberrant/accessory pathways, the anatomical substrate for re-entry exists. Treatment may involve disrupting this pathway, often through catheter ablation (a procedure not detailed in the sources but implied by targeting "abnormal anatomy").

In essence, the physiological approach to treating cardiac arrhythmias involves understanding whether the problem is with the spark (initiation) or the wire (conduction), and then applying therapies that physiologically correct the rate of the spark or alter the properties of the wire to prevent abnormal propagation or looping.