Electrical Conduction System and ECG Basics - Anatomy and Physiology

SECTION 1

Historical Context & Motivation

The realization that the heart generates its own electrical signals — and that those signals can be captured at the body surface — ranks among the most consequential discoveries in clinical medicine. Before the invention of the electrocardiogram (ECG or EKG), physicians relied on auscultation and pulse palpation to evaluate cardiac rhythm, tools that could detect gross abnormalities but offered no insight into the electrical events underlying each heartbeat. The quest to understand cardiac electricity unfolded across roughly a century, drawing on advances in electrophysiology, instrument design, and clinical cardiology. Each milestone below represents a turning point that moved the field closer to the twelve-lead ECG tracing that medical students learn to interpret today.

1842 • Matteucci Detects Cardiac Electricity

Carlo Matteucci demonstrated that each heartbeat in a frog was accompanied by a measurable electrical current, providing the first empirical evidence that the heart's contraction was an electrical event rather than a purely mechanical one.

1893 • His Describes the Bundle of His

Wilhelm His Jr. identified a muscular bridge connecting the atrial and ventricular septa, later named the bundle of His. This discovery revealed the anatomical pathway by which electrical impulses travel from the atria to the ventricles.

1903 • Einthoven's String Galvanometer

Willem Einthoven constructed a highly sensitive string galvanometer capable of recording the heart's electrical activity from the body surface. He labeled the waveforms P, Q, R, S, and T — nomenclature that endures unchanged to the present day.

1906 • Tawara Maps the Conduction Network

Sunao Tawara published detailed histological descriptions of the atrioventricular (AV) node and Purkinje fibers, completing the anatomical picture of the cardiac conduction system.

1942 • Goldberger Completes the 12-Lead System

Emanuel Goldberger augmented the existing limb leads by introducing aVR, aVL, and aVF, which, combined with Einthoven's three standard leads and Wilson's six precordial leads, yielded the standard 12-lead ECG used universally in clinical practice.

The central question that emerged from this history — and the one this lesson addresses — is deceptively simple: how does a mass of cardiac muscle cells coordinate millions of individual contractions into a rhythmic, efficient pump, and how does the ECG translate that coordination into a diagnostic waveform? Answering that question requires an understanding of both the anatomy of the conduction system and the biophysics that generates the electrical signals detectable at the skin surface.

SECTION 2

Core Principles of Cardiac Conduction

Cardiac conduction rests on a set of foundational principles that distinguish the heart from skeletal and smooth muscle. Unlike skeletal muscle, which depends on motor neuron stimulation, the heart is autorhythmic — specialized cells within the conduction system spontaneously generate action potentials without any external neural input. This intrinsic automaticity ensures that the heart continues to beat even when severed from all nervous connections, a property exploited in cardiac transplantation. The following grid organizes the key concepts that govern how the conduction system initiates, propagates, and coordinates the electrical signal that triggers each heartbeat.

Automaticity

Pacemaker cells in the SA node possess unstable resting membrane potentials that gradually depolarize (the pacemaker potential), primarily driven by I_f ('funny current') — a slow influx of Na⁺ and K⁺ through HCN channels that eliminates the need for nervous stimulation.

Sequential Conduction

The impulse follows a fixed anatomical pathway: SA node → atrial myocardium → AV node → bundle of His → right and left bundle branches → Purkinje fibers. This sequence ensures that atria contract before ventricles, optimizing ventricular filling.

AV Nodal Delay

The AV node deliberately slows conduction (≈ 0.1 s), creating a critical pause between atrial and ventricular systole. This physiological delay allows complete atrial emptying before the ventricles begin to contract, a function reflected in the PR interval on the ECG.

Rapid Ventricular Conduction

Once past the AV node, the impulse races through the bundle branches and Purkinje network at speeds up to 4 m/s. This rapid, simultaneous activation of the ventricular myocardium from endocardium to epicardium produces the synchronized contraction needed for efficient blood ejection.

Hierarchy of Pacemakers

If the SA node fails, the AV node can assume pacemaker function at a slower rate (40–60 bpm); if the AV node also fails, ventricular Purkinje fibers fire at 20–40 bpm. This built-in redundancy — the escape rhythm hierarchy — serves as a life-preserving failsafe.

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KEY TAKEAWAY

Think of the cardiac conduction system as a corporate relay chain of command with built-in redundancy. The CEO (SA node) sets the pace; middle management (AV node) deliberately pauses to make sure upstream work is complete before authorizing the next phase; and the front-line workers (Purkinje fibers) execute simultaneously across the entire factory floor. If the CEO is incapacitated, the vice-president (AV node) takes over at a reduced tempo, and if even that person fails, a floor supervisor (Purkinje cells) keeps minimal operations running. The ECG is essentially the company-wide activity report, capturing each stage of this chain in real time.

SECTION 3

Anatomy of the Cardiac Conduction System

The diagram below illustrates the spatial arrangement of the conduction system within the heart and the approximate conduction velocities at each level. Understanding this anatomy is essential for interpreting the ECG, because each waveform corresponds to electrical activation of a specific cardiac region. Follow the numbered pathway from the SA node through the AV node, down the bundle of His, and into the Purkinje fiber network that spreads across the ventricular endocardium.

Numbered steps trace the impulse from the SA node (①) through atrial muscle, the AV node (②) with its critical 0.1-second delay, the bundle of His (③), the bundle branches (④), and the Purkinje fibers (⑤). Note the dramatic acceleration of conduction velocity from 0.05 m/s at the AV node to 4 m/s in the Purkinje system.

Several features of this anatomy deserve emphasis. First, the fibrous skeleton of the heart — a dense connective tissue plane separating the atria from the ventricles — acts as an electrical insulator. Without it, impulses could cross haphazardly from atrial to ventricular tissue, bypassing the AV node and eliminating the delay essential for sequential contraction. The AV node and bundle of His represent the only normal electrical bridge across this insulating layer, which is why pathological 'accessory pathways' (as seen in Wolff-Parkinson-White syndrome) produce clinically significant arrhythmias. Second, the Purkinje fibers ramify from the ventricular apex upward, ensuring that contraction begins at the bottom of the ventricles and progresses toward the outflow tracts — a pattern that wrings blood upward toward the pulmonary artery and aorta with maximal hemodynamic efficiency.

SECTION 4

Electrophysiology of Pacemaker and Contractile Cells

Two fundamentally different action potential shapes exist in the heart, and understanding their ionic basis is critical for interpreting the ECG. Pacemaker cells (found in the SA node, AV node, and parts of the conduction system) lack a stable resting membrane potential; instead, they exhibit a gradual Phase 4 depolarization driven by the funny current (I_f) and T-type Ca²⁺ channels. When threshold is reached, L-type Ca²⁺ channels open (Phase 0), producing a relatively slow upstroke compared to ventricular muscle. Repolarization (Phase 3) is mediated by K⁺ efflux. In contrast, contractile (working) myocytes have a stable resting potential near −90 mV and display a fast Phase 0 (rapid Na⁺ influx), a characteristic plateau phase (Phase 2) sustained by L-type Ca²⁺ influx balanced against K⁺ efflux, and a Phase 3 repolarization driven by delayed-rectifier K⁺ channels.

Key Ionic Currents and Phases

Phase	Pacemaker Cell	Contractile Myocyte
Phase 4	Slow spontaneous depolarization via I_f (funny current) + T-type Ca²⁺	Stable resting potential ≈ −90 mV; inward-rectifier K⁺ (I_K1) maintains potential
Phase 0	Slow depolarization via L-type Ca²⁺ channels (no fast Na⁺ channels)	Rapid depolarization via fast Na⁺ channels → sharp upstroke to +30 mV
Phase 1	Absent (no initial repolarization)	Brief repolarization; transient outward K⁺ current (I_to)
Phase 2	Absent (no plateau)	Plateau: L-type Ca²⁺ influx balanced by K⁺ efflux; lasts ≈ 200 ms
Phase 3	Repolarization via delayed-rectifier K⁺ channels	Repolarization: rapid K⁺ efflux (I_Kr, I_Ks) returns membrane to −90 mV

Comparison of action potential phases in pacemaker vs. contractile cardiac cells

HEART RATE FROM SA NODE AUTOMATICITY

HR (bpm) = 60 / cycle length (s)

If the SA node pacemaker potential reaches threshold every 0.8 s, then HR = 60 / 0.8 = 75 bpm. Sympathetic stimulation increases I_f, steepening Phase 4 and shortening the cycle length; parasympathetic stimulation does the opposite.

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Clinical Note

Drugs that block the funny current (e.g., ivabradine) slow the heart rate by reducing the slope of Phase 4 depolarization in SA nodal cells. This pharmacological principle demonstrates the clinical relevance of understanding pacemaker electrophysiology at the ionic-channel level.

SECTION 5

ECG Waveform Anatomy and Intervals

The surface ECG captures the summed electrical activity of millions of cardiac cells as detected by electrodes placed on the limbs and chest wall. Each deflection on the tracing corresponds to a distinct phase of the cardiac electrical cycle. The diagram below illustrates a normal PQRST complex with its key intervals and segments labeled. Mastering this waveform anatomy is the gateway to systematic ECG interpretation, because virtually every arrhythmia and conduction disorder manifests as a change in the morphology, duration, or relationship among these components.

A single cardiac cycle recorded on a standard ECG. The P wave reflects atrial depolarization; the QRS complex represents ventricular depolarization (atrial repolarization is hidden within it); and the T wave corresponds to ventricular repolarization. The PR interval captures the time from the onset of atrial depolarization to the beginning of ventricular depolarization, encompassing AV nodal delay.

ECG Component	Electrophysiological Event	Normal Duration / Amplitude	Clinical Significance of Abnormality
P wave	Atrial depolarization (SA node → atrial muscle)	< 0.12 s; < 2.5 mm tall	Absent P: atrial fibrillation. Peaked P: right atrial enlargement. Notched P: left atrial enlargement
PR interval	Onset of P to onset of QRS; includes AV nodal delay	0.12–0.20 s	> 0.20 s: 1st-degree AV block. < 0.12 s with delta wave: WPW pre-excitation
QRS complex	Ventricular depolarization (septum → apex → base)	0.06–0.10 s	> 0.12 s: bundle branch block or ventricular origin. Pathological Q waves: prior myocardial infarction
ST segment	Plateau phase of ventricular action potential; ventricles uniformly depolarized	Isoelectric (at baseline)	Elevation: acute MI (STEMI) or pericarditis. Depression: ischemia or digitalis effect
T wave	Ventricular repolarization (epicardium → endocardium)	Upright in most leads; concordant with QRS	Inverted T: ischemia, strain, or electrolyte abnormality. Tall peaked T: hyperkalemia
QT interval	Total ventricular electrical activity (depol. + repol.)	≤ 0.44 s (rate-corrected: QTc)	Prolonged QTc: risk of torsades de pointes; caused by drugs, congenital channelopathies, or electrolyte imbalances

ECG waveform components and their electrophysiological correlates

SECTION 6

Worked Example — Calculating Heart Rate and Identifying Intervals on an ECG Strip

ECG paper runs at a standard speed of 25 mm/s and is divided into small boxes (1 mm = 0.04 s) and large boxes (5 mm = 0.20 s). Understanding these calibration constants allows you to derive heart rate and evaluate interval durations directly from the tracing. The following worked example walks through a systematic analysis of a regular-rhythm ECG strip.

ECG Strip Analysis — Regular Sinus Rhythm

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Step 1 — Determine Rhythm Regularity

Examine the R-R intervals across the strip. In this example, the R-R intervals are constant, measuring 4 large boxes (20 small boxes) between consecutive R waves. Constant R-R intervals indicate a regular rhythm.

R-R interval = 4 large boxes = 20 small boxes
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Step 2 — Calculate Heart Rate (Large-Box Method)

For regular rhythms, divide 300 by the number of large boxes between consecutive R waves. Since each large box equals 0.20 s, 300 large boxes span exactly 60 seconds (one minute). Therefore: HR = 300 / 4 = 75 bpm. An alternative small-box method divides 1500 by the number of small boxes: HR = 1500 / 20 = 75 bpm, confirming the result.

Heart Rate = 75 bpm
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Step 3 — Measure the PR Interval

Identify the onset of the P wave and the onset of the QRS complex. In this strip, the PR interval spans 4 small boxes. Since each small box = 0.04 s, the PR interval = 4 × 0.04 = 0.16 s. This value falls within the normal range (0.12–0.20 s), indicating normal AV conduction without first-degree block.

PR interval = 0.16 s — Normal
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Step 4 — Measure the QRS Duration

The QRS complex in this strip spans 2 small boxes: QRS duration = 2 × 0.04 = 0.08 s. A value under 0.12 s indicates that ventricular depolarization is proceeding normally through the His-Purkinje system without bundle branch block.

QRS duration = 0.08 s — Normal
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Step 5 — Evaluate the QT Interval and Calculate QTc

The QT interval (onset of QRS to end of T wave) measures 9 small boxes = 0.36 s. Because QT varies with heart rate, we correct it using Bazett's formula: QTc = QT / √(R-R interval in seconds). The R-R interval = 20 × 0.04 = 0.80 s, so √0.80 ≈ 0.894. QTc = 0.36 / 0.894 ≈ 0.403 s. Since 0.403 s < 0.44 s, the corrected QT is within normal limits.

QTc ≈ 0.403 s — Normal
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Step 6 — Final Interpretation

Upright P waves precede each QRS in a 1:1 ratio, the PR interval is constant and within normal limits, the QRS is narrow, the ST segment is isoelectric, and the T waves are upright and concordant with the QRS. The overall interpretation is normal sinus rhythm at 75 bpm with no evidence of conduction delay, ischemia, or hypertrophy.

Normal Sinus Rhythm, 75 bpm, normal intervals

BAZETT'S FORMULA FOR CORRECTED QT

QTc = QT / √(RR)

Where QT is the measured QT interval (s), RR is the R-R interval (s), and QTc is the rate-corrected QT. Normal QTc is ≤ 0.44 s (some sources use ≤ 0.45 s for females). Prolonged QTc raises the risk of potentially fatal ventricular arrhythmias.

SECTION 7

ECG Strengths, Limitations, and Common Arrhythmias

The 12-lead ECG remains one of the most widely used diagnostic tests in medicine, but like any tool it has both remarkable strengths and notable limitations. Understanding these helps clinicians integrate ECG findings with history, physical examination, and other diagnostic modalities rather than relying on the tracing in isolation.

Strengths	Limitations
Non-invasive, inexpensive, rapid (< 5 min), and universally available at the bedside	Provides only a snapshot; may miss intermittent arrhythmias (requires Holter or loop monitoring for paroxysmal events)
Exquisitely sensitive for detecting acute myocardial ischemia and infarction (ST changes, Q waves)	Poor sensitivity for structural abnormalities (e.g., valvular disease, small septal defects) — echocardiography is needed
Directly reveals conduction abnormalities (AV blocks, bundle branch blocks, accessory pathways)	Normal ECG does not exclude coronary artery disease; patients may have significant stenoses without resting ECG changes
Highly reproducible and standardized across institutions worldwide	Artifacts from muscle tremor, patient movement, and poor electrode contact can mimic arrhythmias and confound interpretation

Strengths and limitations of the standard 12-lead ECG

Common Rhythm Disturbances Detectable by ECG

Sinus bradycardia — normal P-QRS-T morphology with rate < 60 bpm; common in trained athletes and during sleep.
Sinus tachycardia — normal morphology with rate > 100 bpm; a physiological response to exercise, fever, or sympathetic activation.
Atrial fibrillation (AFib) — absent P waves replaced by irregular fibrillatory baseline; irregularly irregular ventricular response.
First-degree AV block — PR interval > 0.20 s with every P wave followed by a QRS; indicates delayed but not blocked AV conduction.
Ventricular tachycardia (VT) — wide QRS complexes (> 0.12 s) at rates of 100–250 bpm; a life-threatening arrhythmia requiring urgent intervention.

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CLINICAL PERSPECTIVE

The ECG is analogous to a seismograph for the heart: it is extraordinarily sensitive to the electrical tremors of the myocardium and can reveal the timing, direction, and magnitude of those tremors with remarkable fidelity. However, just as a seismograph cannot tell you about the chemical composition of the rocks beneath it, the ECG cannot directly visualize structural pathology. A normal ECG tracing does not guarantee a structurally normal heart, and conversely, minor ECG variants (such as early repolarization in young adults) may be entirely benign. The art of clinical medicine lies in integrating the electrical data from the ECG with anatomical imaging, hemodynamic assessment, and the patient's clinical presentation.

SECTION 8

Connection to Advanced Electrophysiology and Cardiac Imaging

The surface ECG introduced in this lesson represents the foundation upon which an entire subspecialty of medicine — clinical cardiac electrophysiology (EP) — has been built. Advanced EP studies involve inserting catheters into the heart chambers to record intracardiac electrograms from specific sites, map arrhythmia circuits, and deliver targeted radiofrequency ablation to disrupt reentrant pathways. The table below contrasts the basic ECG concepts covered here with their advanced counterparts.

Concept (This Lesson)	Advanced Extension
Surface ECG waveform analysis	Intracardiac electrograms (His bundle recording, coronary sinus electrograms) with millisecond-resolution timing
PR interval as index of AV conduction	Decomposition into AH interval (AV node) and HV interval (His-Purkinje) to localize conduction block
Qualitative understanding of automaticity	Hodgkin-Huxley formalism and computational models of ion channel kinetics for pacemaker cells
12-lead ECG as a 2-D representation	3-D electroanatomical mapping (CARTO, EnSite) fused with cardiac MRI for arrhythmia substrate identification
Escape rhythm hierarchy as a failsafe	Cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillators (ICDs) for managing conduction failure

From basic ECG to advanced electrophysiology

Students who pursue cardiology or cardiac surgery will encounter these advanced topics in clinical rotations and fellowship training. For now, a solid command of the conduction system anatomy, pacemaker electrophysiology, and systematic ECG waveform interpretation provides the essential framework upon which all subsequent learning is built. Courses in pathophysiology will extend this foundation to arrhythmia mechanisms (reentry, triggered activity, abnormal automaticity), and pharmacology courses will connect specific antiarrhythmic drug classes to the ion channels and phases of the cardiac action potential discussed in Section 4.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

Explain why the AV node's slow conduction velocity is physiologically advantageous rather than simply an imperfection. What would happen to cardiac output if the AV node conducted impulses at the same speed as Purkinje fibers?

Show answer

The AV node's conduction velocity of approximately 0.05 m/s produces a ~0.1-second delay between atrial and ventricular depolarization. This delay ensures that the atria have completed their contraction and fully emptied blood into the ventricles before the ventricles begin to contract. If the AV node conducted at Purkinje-fiber speeds (4 m/s), atrial and ventricular systole would occur nearly simultaneously, eliminating the 'atrial kick' that contributes roughly 15–25% of ventricular filling. The result would be a significant decrease in stroke volume and cardiac output, particularly during exercise when filling time is already reduced by high heart rates.

Question 2: BASIC CALCULATION

An ECG strip shows a regular rhythm with R-R intervals of 5 large boxes. What is the heart rate? If the PR interval measures 6 small boxes, is AV conduction normal?

Show answer

Using the large-box method: HR = 300 / 5 = 60 bpm. This is at the lower end of the normal sinus rate (60–100 bpm), so this is normal sinus rhythm (or sinus bradycardia at exactly 60 bpm depending on the source). For the PR interval: 6 small boxes × 0.04 s/box = 0.24 s. The normal PR interval range is 0.12–0.20 s, so 0.24 s exceeds the upper limit. This indicates first-degree AV block — a condition in which every P wave is followed by a QRS (conduction is not dropped), but the AV nodal transit time is pathologically prolonged.

Question 3: INTERMEDIATE

A patient's ECG shows an R-R interval of 15 small boxes and a measured QT interval of 10 small boxes. Using Bazett's formula (QTc = QT / √RR), calculate the corrected QT interval and determine whether it is within normal limits (≤ 0.44 s).

Show answer

First, convert to seconds: R-R = 15 × 0.04 = 0.60 s; QT = 10 × 0.04 = 0.40 s. Applying Bazett's formula: QTc = 0.40 / √0.60 = 0.40 / 0.7746 ≈ 0.516 s. Since 0.516 s exceeds the 0.44 s threshold, this patient has a prolonged QTc interval. Clinically, a QTc above 0.50 s is associated with a substantially increased risk of torsades de pointes, a polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation. The clinician should review the patient's medication list for QT-prolonging drugs and check serum potassium and magnesium levels.

Question 4: APPLIED

A 65-year-old patient presents with fatigue. The ECG shows P waves occurring at a regular rate of 80 bpm, but only every third P wave is followed by a QRS complex. The QRS complexes are narrow (0.08 s). Identify the rhythm, determine the ventricular rate, and explain which component of the conduction system is likely dysfunctional.

Show answer

The pattern of P waves at a regular atrial rate with a fixed ratio of non-conducted beats (3:1 P-to-QRS ratio) is consistent with high-grade (advanced) second-degree AV block or third-degree (complete) heart block with a consistent escape rhythm. If every third P wave conducts, the ventricular rate = 80 / 3 ≈ 27 bpm. However, the narrow QRS (0.08 s) suggests that the escape pacemaker is junctional (AV junction or proximal His bundle) rather than ventricular, because ventricular escape rhythms typically produce wide QRS complexes > 0.12 s. The site of block is most likely at the AV node itself. This patient's ventricular rate of ~27 bpm explains the fatigue and may warrant urgent temporary pacing followed by permanent pacemaker implantation.

Question 5: CRITICAL THINKING

During cardiac transplantation, all nervous connections to the donor heart are severed. Despite this, the transplanted heart beats rhythmically immediately upon reperfusion. Explain the electrophysiological basis for this phenomenon, discuss how the transplanted heart's rate regulation differs from a normally innervated heart, and predict the resting heart rate of a transplant recipient compared to a healthy individual of the same age.

Show answer

The transplanted heart beats because the SA node's automaticity is intrinsic — it does not require neural input. The pacemaker potential (Phase 4 depolarization driven by the funny current

I_f

, T-type Ca²⁺ channels, and the Na⁺/Ca²⁺ exchanger) spontaneously brings the membrane to threshold, generating rhythmic action potentials. In a denervated heart, the resting rate is higher than in a normally innervated heart (typically 90–110 bpm vs. 60–80 bpm) because the dominant resting tone on the SA node in healthy individuals is parasympathetic (vagal), which slows the heart. Without vagal tone, the SA node fires at its intrinsic rate, which is faster. Furthermore, the transplanted heart cannot respond to acute sympathetic or parasympathetic neural signals — rate increases during exercise depend entirely on circulating catecholamines (epinephrine from the adrenal medulla), producing a delayed and blunted chronotropic response. This is why transplant recipients experience slower heart rate acceleration at the onset of exercise and reduced peak heart rates compared to healthy individuals.

SUMMARY

Lesson Summary

Summary

The heart's electrical conduction system orchestrates cardiac contraction through a precisely timed relay of depolarization. The SA node serves as the primary pacemaker (60–100 bpm), generating spontaneous action potentials via automaticity (Phase 4 depolarization driven by the funny current). The impulse spreads through atrial muscle, then encounters the AV node, which introduces a critical ~0.1-second delay to ensure complete atrial emptying before ventricular systole. From the AV node, the signal accelerates through the bundle of His, splits into right and left bundle branches, and fans out via Purkinje fibers (at up to 4 m/s) to produce synchronized ventricular contraction from apex to base.

The electrocardiogram (ECG) translates this electrical activity into a diagnostic tracing. The P wave represents atrial depolarization, the QRS complex reflects ventricular depolarization (normal duration 0.06–0.10 s), and the T wave corresponds to ventricular repolarization. The PR interval (0.12–0.20 s) measures AV conduction time, and the QT interval (corrected by Bazett's formula: QTc = QT / √RR, normal ≤ 0.44 s) captures total ventricular electrical activity. Heart rate is calculated from the R-R interval using the 300-divided-by-large-boxes method. A built-in escape rhythm hierarchy (AV node at 40–60 bpm, Purkinje fibers at 20–40 bpm) provides life-preserving redundancy should the SA node fail.