The conducting system of the heart consists of cardiac muscle cells and conducting fibers (not nervous tissue) that are specialized for initiating impulses and conducting them rapidly through the heart (see the image below). They initiate the normal cardiac cycle and coordinate the contractions of cardiac chambers. Both atria contract together, as do the ventricles, but atrial contraction occurs first.
The conducting system provides the heart its automatic rhythmic beat. For the heart to pump efficiently and the systemic and pulmonary circulations to operate in synchrony, the events in the cardiac cycle must be coordinated. [1, 2]
Schematic illustration of the cardiac conduction system.
Innervation of the AV node, His bundle, and ventricular myocardium
The AV node and His bundle are innervated by a rich supply of cholinergic and adrenergic fibers with higher densities as compared with the ventricular myocardium. Parasympathetic nerves to the AV node region enter the heart at the junction of the IVC and the inferior aspect of the LA, adjacent to the coronary sinus ostium.
The autonomic neural input to the heart demonstrates some degree of “sidedness,” with the right sympathetic and vagal nerves affecting the SA node more than the AV node and the left sympathetic and vagal nerves affecting the AV node more than the SA node. The distribution of the neural input to the SA and AV nodes is complex because of substantial overlapping innervation.
Stimulation of the right stellate ganglion produces sinus tachycardia with less effect on AV nodal conduction, whereas stimulation of the left stellate ganglion generally produces a shift in the sinus pacemaker to an ectopic site and consistently shortens AV nodal conduction time and refractoriness, but it inconsistently speeds the SA node discharge rate. However, stimulation of the right cervical vagus nerve slows the SA node discharge rate, and stimulation of the left vagus primarily prolongs AV nodal conduction time and refractoriness when sidedness is present. Neither sympathetic nor vagal stimulation affects normal conduction in the His bundle.
The right vagus nerve primarily innervates the sinoatrial (SA) node, whereas the left vagus innervates the atrioventricular (AV) node; however, significant overlap can exist in the anatomic distribution.
Effects of sympathetic stimulation
Stimulation of sympathetic ganglia shortens the refractory period equally in the epicardium and underlying endocardium of the left ventricular free wall, although dispersion of recovery properties occurs (ie, different degrees of shortening of refractoriness occur) when measured at different epicardial sites. Nonuniform distribution of norepinephrine (NE) may, in part, contribute to some of the nonuniform electrophysiologic effects, because the ventricular content of NE is greater at the base than at the apex of the heart, with greater distribution to muscle than to Purkinje fibers. Afferent vagal activity appears to be higher in the posterior ventricular myocardium, which may account for the vagomimetic effects of inferior myocardial infarction. [4, 8]
Effects of vagal stimulation
The vagus modulates cardiac sympathetic activity at prejunctional and postjunctional sites by regulating the amount of NE released and by inhibiting cyclic adenosine monophosphate (cAMP) – induced phosphorylation of cardiac proteins. Tonic vagal stimulation results in a greater absolute reduction in sinus rate in the presence of tonic background sympathetic stimulation. In contrast, changes in AV conduction during concomitant sympathetic and vagal stimulation are essentially the algebraic sum of the individual AV conduction responses to tonic vagal and sympathetic stimulation alone.
Cardiac responses to brief vagal bursts commence after a short latency and dissipate quickly; conversely, cardiac responses to sympathetic stimulation begin and dissipate slowly. The rapid onset and offset of responses to vagal stimulation allow dynamic beat-to-beat vagal modulation of heart rate and AV conduction, whereas the slow temporal response to sympathetic stimulation precludes any beat-to-beat regulation by sympathetic activity. Because the peak vagal effects on sinus rate and AV nodal conduction occur at different times in the cardiac cycle, a brief vagal burst can slow the sinus rate without affecting AV nodal conduction or can prolong AV nodal conduction time and not slow the sinus rate. [3]
Arrhythmias
The normal sinus rate of 60-100 beat/min at rest is affected by several factors including autonomic nervous system input, medications, metabolic and electrolyte status, and pathological conditions. [9]
Etiologies of sinus node and atrioventricular node dysfunction are as follows:
Enhanced automaticity
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Fever
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Catecholamine release
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Stimulants
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Medications
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Hyperthyroid states
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Idiopathic
Decreased automaticity
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Increased vagal tone
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Medications
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Electrolyte abnormalities
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Obstructive sleep apnea (OSA)
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Myocarditis (inflammatory, infectious, infiltrative)
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Endocarditis
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After cardiac surgery
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Degeneration
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Fibrosis
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Valvular heart disease
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Rheumatologic
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Genetic (channelopathies, neuromuscular disorders)
Inherited forms of cardiac conduction disease are rare, however, the discovery of causative genetic mutations has enhanced our understanding of the processes underlying impulse generation and propagation.
The circadian pattern of normal heart rates widely varies; enhanced vagal tone during sleep can result in heart rates < 40 beats/min, pauses, and Wenckebach conduction block in normal individuals. However, pauses greater than 3 sec are rarely seen in normal individuals and should prompt further evaluation. Exercise conditioning can also result in a physiologically normal slow sinus rate at rest. [10]
Alterations in vagal and sympathetic innervation can influence the development of arrhythmias and sudden cardiac death due to ventricular tachyarrhythmias. Cardioneuropathy may develop due to damage to the nerves extrinsic to the heart, such as the stellate ganglia, as well as to intrinsic cardiac nerves from diseases that may affect primarily nerves, such as viral infections or, secondarily, from diseases that cause cardiac damage. Such neural changes may create electrical instability through various electrophysiologic mechanisms. For example, myocardial infarctioncan interrupt afferent and efferent neural transmission and create areas of sympathetic supersensitivity that may be conducive to the development of arrhythmias. [4