Cardiac Conduction System Anatomy

<aside> <img src="/icons/defibrillator_red.svg" alt="/icons/defibrillator_red.svg" width="40px" /> The sinoatrial node is the main pacemaker of the cardiac conduction system, typically initiating electrical impulses at a rate of 60-100/min.  Other parts of the conduction system (eg, atrioventricular node, His bundle) have their own intrinsic pacemakers, and they initiate impulses at a slower rate when impulses from the sinoatrial node are blocked.

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• The electrical impulses in the myocardial conduction system are normally initiated by the sinoatrial (SA) node at a rate of 60-100/min.  These impulses are then transmitted through the atria to the atrioventricular (AV) node, then on to the His bundle, bundle branches, Purkinje fibers, and ventricular myocardium.  Most of the conduction system has its own intrinsic pacemaker, which is normally suppressed by the more rapid SA node pacemaker but triggers when a signal from further up the conduction system is not received.

• When the SA node is initiating impulses through a normal conduction system, the heart rate is 60-100/min. ECG shows P waves quickly followed by a narrow QRS complex, representing normal atrial depolarization followed by normal ventricular depolarization (normal sinus rhythm).
• When electrical impulses are initiated below the AV node and His bundle, the heart rate typically slows to 25-40/min (based on the intrinsic pacemaker rate of the bundle branches and Purkinje system). On ECG, the QRS complexes are typically wide compared to the narrow QRS complexes initiated by the AV node and His bundle.

Cardiac Conduction System Physiology

<aside> 🐢 Adenosine slows phase 4 and phase 0 (causes hyperpolarization) of the cardiac pacemaker action potential.  The summative result of these effects is a decreased rate of sinus node firing, slowed atrioventricular node conduction, and increased refractoriness in pacemaker tissue.

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The action potential (AP) in cardiac cells consists of the "slow" AP in pacemaker cells (located primarily in the sinoatrial and atrioventricular [AV] nodes) and the "fast" AP in nonpacemaker cells.  Pacemaker cells demonstrate spontaneous depolarization (automaticity), and their AP is divided into 3 phases.

• Phase 4 (pacemaker potential): Slow influx of cations (mostly Na+) when hyperpolarization-activated cyclic nucleotide-gated (HCN) channels open (funny current)
• Phase 0 (upstroke): Rapid influx of Ca2+ when voltage-gated L-type Ca2+ channels open
• Phase 3 (repolarization): Rapid efflux of K+ ions when K+ channels open

By activating the A1 receptor, adenosine slows the pacemaker AP, largely through effects on the G protein/cyclic AMP (cAMP) pathway.

• Adenosine slows Na+ influx by reducing levels of cAMP, which decreases activity of the HCN channels (slowed phase 4)
• Lower cAMP levels delaying Ca2+ influx due to decreased conductance through L-type Ca2+ channels (slowed phase 0)
• Adenosine also enhances K+ efflux (by directly stimulating inward rectifier channels) to make the resting membrane potential more negative (ie, hyperpolarization)

The summative result of these effects is a slowed rate of sinus node discharge (negative chronotropy), decreased conduction velocity through the atrioventricular node (negative dromotropy), and increased refractoriness in pacemaker tissue.  The rapid onset and offset of adenosine combined with its near-complete suppression of AV node conduction make it useful in terminating certain supraventricular tachycardias.