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Natural pacemaker

The sinoatrial node (SA node), commonly known as the heart's natural pacemaker, is a specialized cluster of cardiac cells located at the junction of the crista terminalis and the superior vena cava in the wall of the right atrium.^[1] It functions as the primary initiator of the heartbeat by spontaneously generating electrical impulses at a rate of 60 to 100 beats per minute in a resting adult, which propagate through the cardiac conduction system to coordinate atrial and ventricular contractions.^[1] This automaticity ensures rhythmic pumping of blood throughout the body without external stimulation.^[2] Composed of pacemaker cells (P cells) interspersed with transitional cells and connective tissue, the SA node exhibits unique electrophysiological properties that enable its pacemaker role.^[1] These cells undergo spontaneous depolarization through mechanisms involving the "funny current" (I_f) and intracellular calcium handling, creating a pacemaker potential that triggers action potentials.^[1] Under normal conditions, the SA node dominates over subsidiary pacemakers like the atrioventricular node, maintaining sinus rhythm as the default cardiac pattern.^[1] The SA node's activity is finely regulated by the autonomic nervous system to adapt heart rate to physiological needs.^[1] Sympathetic stimulation via beta-1 adrenergic receptors increases the firing rate by enhancing ion channel activity, accelerating the heart during stress or exercise, while parasympathetic input through the vagus nerve slows it by hyperpolarizing cells, promoting rest.^[1] Hormonal influences, such as thyroid hormones, can also modulate its function.^[3] Clinically, SA node dysfunction—often due to aging, fibrosis, or ischemia—can result in bradyarrhythmias, sinus pauses, or sick sinus syndrome, where the node fails to generate or conduct impulses reliably.^[1] In such cases, the heart may rely on slower backup pacemakers, leading to symptoms like fatigue or syncope, and artificial pacemakers may be implanted to restore normal rhythm.^[4] Research continues to explore SA node cellular dynamics to improve treatments for conduction disorders.^[5]

Anatomy

Sinoatrial Node

The sinoatrial node (SA node), also known as the sinus node, is a small cluster of specialized cardiomyocytes situated at the junction of the superior vena cava and the right atrium, specifically along the crest of the crista terminalis. This structure functions as the heart's primary natural pacemaker, initiating electrical impulses that coordinate cardiac contraction. Composed of a crescent-shaped mass of cells embedded in connective tissue, the SA node spans a compact area beneath the epicardium in the upper posterior wall of the right atrium.^[1]^[6] The cellular makeup of the SA node includes a heterogeneous population of pacemaker cells, referred to as P cells, which are characterized by sparse myofibrils and a lack of well-organized sarcomeres, enabling their automaticity. These P cells are interspersed with transitional cells, which exhibit intermediate features between nodal and atrial myocytes and facilitate the conduction of impulses from the node to the surrounding atrial myocardium. The node also contains supporting non-myocytic elements, such as fibroblasts and extracellular matrix components, that contribute to its structural integrity.^[7]^[8]^[9] Histologically, the SA node is distinguished by its rich innervation from autonomic nerve fibers and a robust vascular supply essential for its function. Blood supply is provided by the SA nodal artery, which originates as a branch of the right coronary artery in approximately 60% of individuals and from the left circumflex artery in 40% of cases; in 5-10% of hearts, dual supply from both is present.^[10]^[11]^[12] The node's dimensions typically range from 10-20 mm in length, 2-3 mm in width, and 1-3 mm in thickness, encompassing a relatively small volume that houses thousands of specialized cells.^[10]^[11]^[12] During embryogenesis, the SA node develops from mesodermal progenitor cells in the sinus venosus region, the embryonic venous inflow tract that incorporates into the right atrium as the heart tube loops and remodels. This origin reflects the evolutionary conservation of pacemaker tissue at the venous pole of the heart, with molecular markers such as Tbx18 and Shox2 guiding its specification from second heart field and sinus venosus contributions.^[13]^[14]

Atrioventricular Node

The atrioventricular (AV) node, serving as the heart's secondary pacemaker, is situated in the right atrium within the triangle of Koch, a region bounded by the tendon of Todaro superiorly, the coronary sinus ostium posteriorly, and the septal leaflet of the tricuspid valve inferiorly, positioning it near the interatrial septum and just above the tricuspid valve annulus.^[15]^[16] This strategic location allows it to receive electrical impulses from the atria while bridging conduction to the ventricles. In cases of sinoatrial node failure, the AV node can assume pacemaker function as an escape rhythm generator, typically at rates of 40-60 beats per minute. Structurally, the AV node is smaller than the sinoatrial node, measuring approximately 1-3 mm in length and 1-2 mm in width, and comprises a small number of specialized nodal cells.^[17]^[18] Its cellular composition includes slow-conducting nodal cardiomyocytes, which are smaller and paler than typical working myocardial cells due to sparse myofibrils and abundant glycogen, transitioning distally to faster-conducting transitional cells at the His bundle interface.^[19]^[20] These nodal cells exhibit automaticity but at a slower intrinsic rate than the sinoatrial node, underscoring the AV node's subsidiary role. The AV node's blood supply derives primarily from the AV nodal artery, which originates as a branch of the right coronary artery in about 90% of individuals, with the remainder supplied by the left circumflex artery in cases of left coronary dominance.^[21]^[22] This arterial branch penetrates the node from its central fibrous body, ensuring nutrient delivery critical for its conduction properties. Preferential conduction to the AV node occurs through the atrial myocardium, primarily via faster-conducting regions such as the anterior pathway along the crista terminalis and Bachmann's bundle, and the posterior pathway near the coronary sinus. The concept of discrete internodal tracts remains debated and is not supported by histological evidence.^[23]^[24]^[25]

Electrophysiology

Pacemaker Potential

The pacemaker potential refers to the spontaneous phase 4 diastolic depolarization observed in cardiac pacemaker cells, such as those in the sinoatrial node, which gradually raises the membrane potential to initiate rhythmic action potentials.^[26] This process lacks a stable resting potential, distinguishing it from contractile myocytes, and relies on the interplay of several ionic currents to achieve automaticity.^[26] During phase 4, the membrane potential in sinoatrial node cells starts from a maximum diastolic potential of approximately -60 to -65 mV and slowly depolarizes to around -40 mV.^[26] The primary driver is the funny current (I_f), an inward current activated by hyperpolarization below -40 to -45 mV and mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, predominantly the HCN4 isoform in pacemaker tissues.^[26]^[27] I_f carries mainly Na⁺ ions inward at diastolic potentials, with a reversal potential near -10 to -20 mV, contributing to the initial slope of depolarization.^[26] Additional contributions include inward Ca²⁺ currents through T-type (Ca_v3.1/3.2) channels, which activate around -60 mV and accelerate depolarization in the mid-to-late phase, as well as the progressive decay of outward K⁺ currents that reduces hyperpolarizing influences.^[28]^[26] Unlike ventricular myocytes, which maintain a stable resting potential near -90 mV via strong inward rectifier K⁺ current (I_{K1}), pacemaker cells express minimal I_{K1}, allowing unchecked spontaneous depolarization driven by HCN channels.^[26] Upon reaching the threshold of approximately -40 mV, the pacemaker potential triggers the opening of voltage-gated Ca²⁺ channels, initiating phase 0 depolarization.^[26] Mathematically, the rate of change in membrane potential during early phase 4 can be approximated by the contribution of I_f as:

\frac{dV}{dt} \approx g_f (E_f - V) + I_{\text{other}}

where g_f is the funny conductance, E_f \approx -10 mV is the reversal potential of I_f, V is the membrane potential, and I_{\text{other}} represents additional currents.^[26] This model highlights I_f's role in setting the depolarization slope and firing rate.^[26]

Action Potential Phases

The action potential in natural pacemaker cells, such as those in the sinoatrial node, differs markedly from that in ventricular myocytes, featuring a rapid upstroke followed by repolarization without the characteristic notch or plateau phases. Upon reaching the threshold potential during phase 4 (as detailed in the pacemaker potential section), the membrane undergoes phase 0 depolarization primarily driven by influx of Ca²⁺ through L-type voltage-gated calcium channels, rather than the fast Na⁺ currents dominant in working myocardium.^[29]^[30] These channels, predominantly Cav1.2 isoforms, activate more slowly, resulting in a conduction velocity of approximately 0.05 m/s within the node, which ensures coordinated but delayed propagation to atrial tissue.^[31]^[32] The upstroke peaks at around +10 mV, reflecting the limited amplitude due to the reliance on Ca²⁺ dynamics and sparse expression of voltage-gated Na⁺ channels in pacemaker cells.^[31]^[29] Unlike ventricular action potentials, pacemaker potentials lack phases 1 and 2, avoiding the early repolarization notch and prolonged plateau; this absence stems from the minimal density of fast Na⁺ channels and reduced transient outward K⁺ currents, with greater dependence on Ca²⁺-mediated depolarization for excitability.^[32]^[33] A transient outward K⁺ current, mediated by Kv4.3 channels, is present but plays a minor role in these cells, contributing little to shaping the upstroke or early recovery.^[34] Repolarization occurs during phase 3, where outward K⁺ currents predominate to restore the membrane potential to approximately -60 mV over a duration of 100-200 ms.^[29]^[31] The rapid delayed rectifier current (I_{Kr}, via hERG channels) and slow delayed rectifier current (I_{Ks}, via KCNQ1/KCNE1 complexes) are key contributors, activating after inactivation of L-type Ca²⁺ channels to drive K⁺ efflux and terminate the action potential efficiently.^[32]^[35] This brief repolarization supports the high-frequency firing characteristic of pacemakers. A notable phenomenon associated with these phases is overdrive suppression, where pacing at rates faster than the intrinsic rhythm induces a transient hyperpolarization beyond -60 mV, delaying subsequent spontaneous activity. This arises from elevated intracellular Na⁺ accumulation during rapid depolarizations, which activates the electrogenic Na⁺/K⁺-ATPase pump to extrude Na⁺ in exchange for K⁺, generating a net outward (hyperpolarizing) current.^[36]^[37]

Regulation

Autonomic Influences

The autonomic nervous system plays a central role in modulating the activity of the sinoatrial node (SAN), the heart's primary natural pacemaker, to dynamically adjust heart rate in response to physiological demands. The sympathetic and parasympathetic branches exert opposing influences: sympathetic activation accelerates the firing rate of SAN pacemaker cells, while parasympathetic input decelerates it. This neural control enables rapid adjustments to maintain hemodynamic stability, with the balance between the two systems determining the sinus rhythm under normal conditions.^[38] Sympathetic innervation of the SAN arises from postganglionic fibers of the cardiac sympathetic nerves, which release norepinephrine that binds to β1-adrenergic receptors on pacemaker cells. This binding activates Gs proteins, stimulating adenylyl cyclase to increase cyclic AMP (cAMP) levels, which in turn activates protein kinase A (PKA). PKA phosphorylates key ion channels, including hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that conduct the funny current (If), thereby enhancing If and steepening the slope of the diastolic depolarization (phase 4) in SAN cells. Additionally, PKA increases L-type calcium (Ca²⁺) currents, further accelerating the rate of spontaneous depolarization and elevating heart rate, often up to 150 beats per minute (bpm) during heightened sympathetic activity such as exercise.^[39]^[38] In contrast, parasympathetic innervation is provided by vagal nerve fibers that release acetylcholine, which binds to M2 muscarinic receptors on SAN cells. This activates Gi proteins, inhibiting adenylyl cyclase to reduce cAMP levels and also directly opening G-protein inwardly rectifying potassium (GIRK) channels via the IK,ACh current. The resulting potassium efflux hyperpolarizes the membrane potential, slowing the phase 4 depolarization slope and reducing the spontaneous firing rate of pacemaker cells, which can lower heart rate to 40-60 bpm during states of rest or high vagal tone.^[39]^[40] Under normal physiological conditions, the intrinsic firing rate of the isolated SAN is approximately 100 bpm, but in vivo, the resting heart rate is modulated to 60-100 bpm primarily due to dominant parasympathetic (vagal) tone that suppresses the intrinsic rate, with sympathetic input providing baseline acceleration. This balance is evident in sinus rhythm, where tonic vagal activity maintains a lower heart rate at rest, while sympathetic surges override it during stress. Reflex arcs, such as the baroreceptor reflex, further fine-tune this regulation: increased arterial pressure stimulates baroreceptors in the carotid sinus and aortic arch, leading to enhanced vagal outflow and reduced sympathetic activity to slow heart rate and lower blood pressure.^[41]^[42]^[43] Cardiac denervation, as occurs in heart transplantation, disrupts this autonomic balance by eliminating both sympathetic and parasympathetic inputs, resulting in a higher resting heart rate of 90-110 bpm due to the loss of inhibitory vagal dominance and reliance on the unmodulated intrinsic SAN rate. Over time, partial reinnervation may occur, but the initial denervated state highlights the critical role of parasympathetic tone in suppressing heart rate below intrinsic levels.^[44]^[45]

Hormonal Modulation

Thyroid hormones, particularly triiodothyronine (T3) and thyroxine (T4), exert a significant influence on the sinoatrial node by upregulating the expression and conductance of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, which carry the funny current (If) responsible for phase 4 depolarization.^[46] This enhancement accelerates the pacemaker potential, elevating the basal heart rate over prolonged periods.^[47] In conditions of hyperthyroidism, where circulating T3 and T4 levels are elevated, this manifests as sinus tachycardia, with resting heart rates often exceeding 100 beats per minute and reaching up to 120 beats per minute or higher.^[48] Circulating catecholamines, such as epinephrine released from the adrenal medulla during stress, provide systemic modulation of pacemaker activity through β-adrenergic receptors on sinoatrial node cells, distinct from rapid neural inputs.^[39] Epinephrine binds primarily to β1-receptors, activating adenylyl cyclase to increase cyclic AMP levels, which in turn phosphorylates HCN channels and enhances the funny current (If), steepening the slope of phase 4 depolarization and thereby increasing the firing rate.^[49] This systemic effect sustains elevated heart rates during prolonged stress, contributing to chronotropic responses on timescales longer than acute sympathetic bursts.^[39] Electrolyte imbalances, as endocrine-influenced factors, also modulate pacemaker function by altering ion channel availability and membrane excitability. Hyperkalemia depolarizes the maximum diastolic potential in sinoatrial node cells, inactivating sodium channels and reducing overall excitability, which slows the slope of phase 4 depolarization and diminishes spontaneous firing rates.^[50] Conversely, hypocalcemia attenuates L-type calcium currents (ICaL), which are critical for the upstroke of phase 0 in pacemaker action potentials, leading to prolonged depolarization phases and overall slowing of sinoatrial node activity.^[51] The renin-angiotensin system contributes to tonic modulation of heart rate via angiotensin II, which binds to AT1 receptors expressed on sinoatrial node cells, eliciting a mild positive chronotropic effect by enhancing calcium influx and pacemaker current activation.^[52] This interaction supports sustained increases in firing rate during states of volume expansion or hypotension, independent of acute neural reflexes.^[53] Aging progressively impairs the sinoatrial node's responsiveness to hormonal modulators, including thyroid hormones and catecholamines, through downregulation of receptor density and signaling pathways like β-adrenergic responsiveness, leading to diminished chronotropic effects.^[54] This reduced sensitivity, combined with intrinsic declines in pacemaker cell automaticity, contributes to bradycardia in the elderly, where the intrinsic heart rate—unaffected by autonomic influences—drops to approximately 60 beats per minute in older adults (mean age 65 years).^[55]

Clinical Aspects

SA Node Dysfunction

SA node dysfunction, also known as sinus node dysfunction, refers to a spectrum of abnormalities in the sinoatrial (SA) node's ability to generate and conduct electrical impulses, leading to inappropriate heart rhythms.^[56] The primary clinical manifestation is sick sinus syndrome, characterized by alternating bradyarrhythmias and tachyarrhythmias due to progressive fibrosis and scarring of the SA node and surrounding atrial tissue.^[57] This condition often results from age-related degenerative changes, with prevalence estimated at about 0.2% (1 in 600) among individuals over 65 years and higher in those over 70.^[56]^[58] Common causes include ischemia from occlusion of the SA nodal artery, which supplies blood to the node and can lead to ischemic necrosis; inflammatory processes such as post-viral myocarditis that damage nodal cells; and infiltrative diseases like amyloidosis, where amyloid deposits impair nodal function.^[57]^[59]^[60] Idiopathic fibrosis remains the most frequent etiology, particularly in older adults, often without a identifiable precipitant.^[56] Patients typically present with symptoms related to reduced cardiac output, including syncope, fatigue, and palpitations, which may be intermittent and worsen over time.^[61] Electrocardiographic findings include sinus bradycardia with heart rates below 50 beats per minute or sinus pauses exceeding 3 seconds, reflecting impaired impulse generation.^[57] In severe cases, these pauses can lead to hemodynamic instability, though the atrioventricular node may occasionally provide subsidiary pacemaking as a backup mechanism.^[62] Diagnosis relies on ambulatory monitoring such as Holter electrocardiography to capture episodic bradycardias or pauses during daily activities, with electrophysiological studies confirming dysfunction by measuring the sinus node recovery time—the interval from cessation of atrial pacing to the first spontaneous sinus beat—which exceeds 1.5 seconds in abnormal cases.^[63]^[64] These tests help differentiate SA node issues from other conduction disorders.^[65] Treatment for symptomatic SA node dysfunction primarily involves implantation of a permanent pacemaker to maintain appropriate heart rate and rhythm, particularly in cases of severe bradycardia or pauses. Dual-chamber pacemakers are often preferred to preserve atrioventricular synchrony. As of 2025, leadless pacemakers, including atrial-only devices, are emerging as safe alternatives for select patients with sick sinus syndrome, reducing risks associated with traditional leads.^[66]^[67]^[68] Asymptomatic cases may require only monitoring. The term "sick sinus syndrome" was first described by Bernard Lown in 1967, initially in the context of arrhythmias following electrical cardioversion.^[69]

Ectopic Pacemakers

Ectopic pacemakers refer to focal regions within the heart exhibiting enhanced automaticity outside the sinoatrial (SA) node, primarily in the atria, atrioventricular (AV) junction, or Purkinje fibers, where they generate spontaneous depolarizations at rates typically ranging from 60 to 150 beats per minute under pathological conditions.^[70] These sites normally remain dormant due to suppression by the dominant SA node rhythm but can activate when their intrinsic firing rate exceeds that of the primary pacemaker, leading to premature beats or escape rhythms.^[71] The primary types of ectopic pacemakers include atrial ectopic foci, often originating from myocardial sleeves in the pulmonary veins, which are implicated in initiating atrial fibrillation (AF) through rapid bursts of impulses, and junctional escapes from the AV junction that emerge at rates of 40 to 60 beats per minute when SA node function falters.^[72] Atrial foci in the pulmonary veins, for instance, can produce high-frequency ectopic beats that trigger AF paroxysms, while junctional rhythms serve as protective escapes but may accelerate pathologically.^[73] Ventricular ectopic sites in the His-Purkinje system contribute to premature ventricular contractions, altering the QRS complex duration beyond 0.10 seconds.^[71] Mechanistically, ectopic pacemakers arise from triggered activity involving afterdepolarizations, such as early afterdepolarizations (EADs) during the plateau phase or delayed afterdepolarizations (DADs) in diastole, both driven by intracellular calcium overload that activates the sodium-calcium exchanger, generating inward currents sufficient to reach threshold potential.^[74] Additionally, abnormal upregulation of the funny current (I_f), a hyperpolarization-activated cyclic nucleotide-gated channel current, steepens the diastolic depolarization slope in these foci, enhancing spontaneous firing akin to primary pacemaker physiology but in aberrant locations.^[75] These processes are exacerbated by factors like ischemia or sympathetic stimulation, promoting calcium accumulation and membrane instability.^[70] Clinically, ectopic pacemakers manifest as premature atrial contractions (PACs) originating from sites like the crista terminalis, which can propagate to induce supraventricular tachycardias, or as ventricular ectopy from Purkinje fibers, potentially escalating to ventricular tachycardia via reentry.^[71] In the context of SA node suppression, junctional ectopic foci provide a backup rhythm but at slower rates, around 40 to 60 beats per minute for escapes, though acceleration to over 60 beats per minute signals dysfunction.^[76] Normally, the SA node's overdrive pacing prevents ectopic dominance by hyperpolarizing these sites post-activation, restoring suppression.^[71] Pharmacologically, β-blockers mitigate ectopic rates by attenuating sympathetic-driven automaticity and reducing calcium overload, thereby stabilizing membrane potential in susceptible foci.^[72]

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Cardiac Pacemaker Activity and Aging - PMC - PubMed Central
Decreased maximal heart rate with aging is related to reduced β-adrenergic responsiveness but is largely explained by a reduction in intrinsic heart rate. J ...Missing: hormones | Show results with:hormones
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A decrease in maximal exercise heart rate (HR max ) is a key contributor to reductions in aerobic exercise capacity with aging.
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Sick Sinus Syndrome - StatPearls - NCBI Bookshelf - NIH
Sick sinus syndrome, also known as sinus node dysfunction, is a disorder of the sinoatrial node caused by impaired pacemaker function and impulse transmission.Continuing Education Activity · Etiology · Evaluation · Treatment / Management
[57]
Sinus Node Dysfunction - AAFP
The incidence of sinus node dysfunction is 0.8 per 1,000 person-years and is expected to double by 2060 due to the aging population.
[58]
Sick Sinus Syndrome - DynaMed
Mar 7, 2022 · Sick sinus syndrome (SSS) represents a spectrum of symptoms and heart rhythm abnormalities related to abnormalities in sinus node and atrial impulse formation.
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Sinus Node Dysfunction: Background, Etiology, Pathophysiology
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[60]
Electrophysiological Manifestations of Cardiac Amyloidosis: JACC
Oct 19, 2021 · ... disease course. Sinus Node Dysfunction. Sinus node dysfunction (SND) is defined as an inability of the sinoatrial node to generate a heart ...
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Sick sinus syndrome - Symptoms & causes - Mayo Clinic
Sick sinus syndrome causes slow heartbeats, pauses (long periods between heartbeats) or irregular heartbeats (arrhythmias). Sick sinus syndrome is relatively ...Missing: prevalence | Show results with:prevalence
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Sinus Node Dysfunction - StatPearls - NCBI Bookshelf
Sinus node dysfunction is a disease that is characterized by the inability of the sinoatrial node of producing an adequate heart rate that meets the physiologic ...
[63]
Electrophysiologic Study Interpretation - StatPearls - NCBI Bookshelf
Mar 28, 2025 · The EP evaluation of sinus node dysfunction includes measuring the sinus node recovery time (SNRT) and the sinoatrial conduction time (SACT).Continuing Education Activity · Anatomy and Physiology · Technique or Treatment
[64]
Sinus Node Dysfunction Workup - Medscape Reference
Jul 8, 2025 · In most patients, ambulatory ECG monitoring for an extended period of time (typically 2-4 weeks but potentially longer) has the greatest yield and allows for ...
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Diagnosis and Treatment of Sick Sinus Syndrome - AAFP
Apr 15, 2003 · Causes of Sick Sinus Syndrome Symptoms, which may have been present for months or years, can include syncope, palpitations, and dizziness, as ...Abstract · Clinical Manifestations · Diagnosis · Treatment
[66]
Entry - #608567 - SICK SINUS SYNDROME 1; SSS1 - (OMIM.ORG)
History. The sick sinus syndrome was originally described by Lown (1967) as a complicating arrhythmia following cardioversion.
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Ectopic Pacemaker - an overview | ScienceDirect Topics
An ectopic pacemaker is defined as a subsidiary pacemaker that discharges impulses at a rate faster than the sinus node due to enhanced automaticity, ...
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Ectopic Foci - CV Physiology
Ectopic foci are abnormal pacemaker sites within the heart (outside the SA node) that display automaticity. Their pacemaker activity, however, is normally ...Missing: mechanisms types clinical review
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Initiation of Atrial Fibrillation by Ectopic Beats Originating From the ...
Ectopic beats from PVs can initiate AF, and β-adrenergic receptor blocker, calcium channel blockers, and sodium channel blockers can suppress these ectopic ...
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Sep 3, 1998 · The pulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation. These foci respond to treatment with radio- ...
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Calcium Signaling and Cardiac Arrhythmias | Circulation Research
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Circulation Research Thematic Synopsis: Cardiac Arrhythmias
... afterdepolarizations (EADs), triggered activity and recurrent SVF. ... The Role of the Funny Current in Pacemaker Activity [Review]; DiFrancesco.
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Junctional Rhythm - StatPearls - NCBI Bookshelf - NIH
Jul 7, 2025 · Junctional escape rhythm: Heart rate between 40 and 60 bpm. Accelerated junctional rhythm: Heart rate between 60 and 100 bpm. Junctional ...Continuing Education Activity · Introduction · Evaluation · Treatment / Management