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Human Physiology · Cardiovascular system

Cardiac Electrophysiology and the ECG

The heart sets its own rhythm and carries each impulse along a dedicated wiring system. The ECG lets you watch that electrical activity from the outside. This page explains both, and what a physiotherapist needs to recognise on a monitor.

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Part 3 · Cardiovascular System · Chapter 11 of 47

Learning objectives

By the end of this page you should be able to:

  • Describe the conducting system and the order in which the heart is activated.
  • Explain the pacemaker potential and how the autonomic nervous system changes heart rate.
  • Name the ECG waves and intervals and state their normal values.
  • Calculate heart rate from an ECG strip.
  • Describe the limb and chest leads of a 12-lead ECG.
  • Recognise the rhythms a physiotherapist must act on, and apply exercise evidence in atrial fibrillation.

Why it matters

Physiotherapists exercise patients on cardiac monitors in intensive care, on wards and in rehabilitation. You will see sudden changes in rhythm, and you may be the first to notice them.

You do not need to interpret ECGs like a cardiologist. You do need to know what a normal trace looks like, how to count the rate, and which changes mean stop, call for help, or start resuscitation.

The conducting system

Figure 1 · The conducting system

The conducting system of the heart from the sinoatrial node to the Purkinje fibres A schematic heart. The sinoatrial node at the top of the right atrium starts each beat; the impulse spreads across the atria to the atrioventricular node, which delays it, then passes down the bundle of His, the left and right bundle branches and the Purkinje fibres into the ventricular walls. SA node — pacemakerAtria — impulse spreadsAV node — delay about 0.1 sBundle of HisLeft and right bundle branchesPurkinje fibresIntrinsic rates: SA node 60–100, AV junction 40–60, ventricles 20–40 per minute
Fast where speed matters, slow where timing matters. The AV node delay lets the atria finish emptying before the ventricles contract.

Each beat begins in the sinoatrial (SA) node, a small cluster of specialised cells in the wall of the right atrium. The impulse spreads across both atria, which contract together.

It then reaches the atrioventricular (AV) node, the only normal electrical connection between atria and ventricles. The AV node conducts slowly, delaying the impulse by about a tenth of a second. This lets the atria finish emptying into the ventricles.

From the AV node the impulse races down the bundle of His, the left and right bundle branches and the Purkinje fibres. These conduct very fast, so the whole ventricular muscle is activated almost at once, from the inside outwards and from the apex upwards.

SiteIntrinsic rate if it takes overConduction speed
SA node60–100 per minuteSlow
AV junction40–60 per minuteVery slow in the node
Ventricular Purkinje and muscle20–40 per minutePurkinje very fast

Because the SA node fires fastest, it normally sets the rate. If it fails, slower sites take over. This back-up explains why complete heart block produces a slow but often survivable ventricular rhythm.

The pacemaker potential

Figure 2 · The pacemaker potential

Sinoatrial node action potentials showing the slow diastolic depolarisation Repeating voltage trace from a sinoatrial node cell. Instead of a flat resting potential, the voltage drifts slowly upward from about minus 60 millivolts to a threshold near minus 40, then rises in a calcium-driven upstroke and falls back as potassium leaves. A note explains that sympathetic activity steepens the drift and vagal activity flattens it. threshold about −40 mV-60-400+20Slow depolarisationfunny current, then Ca²⁺Upstroke: Ca²⁺ inK⁺ outSympathetic: steeper slope → fasterVagal: flatter slope, lower start → slowerTime (s) — no stable resting potential
Built to fire on its own. The slow drift towards threshold depends largely on the ‘funny’ current carried by HCN4 channels [2]. Schematic trace.

SA node cells have no stable resting potential. After each impulse the voltage drifts slowly upward towards threshold. A major contributor is an inward current called the funny current, carried by HCN4 channels, which unusually opens on hyperpolarisation [2]. Calcium channels then complete the drift and produce the upstroke.

Loss-of-function changes in these channels are associated with slow heart rates and other rhythm problems [2]. Drugs that block the funny current are used clinically to slow the heart.

Autonomic control of heart rate

SympatheticParasympathetic (vagus)
TransmitterNoradrenalineAcetylcholine
Effect on pacemaker slopeSteeper; threshold reached soonerFlatter, and the starting voltage is more negative
Heart rateRisesFalls
AV conductionFasterSlower
At restLow toneDominant; resting rate is below the SA node’s own rate

At rest the vagus holds the heart rate below the SA node’s intrinsic rate of about 100. At the start of exercise, heart rate first rises as vagal tone is withdrawn; sympathetic drive takes over as exercise intensifies.

The electrocardiogram

As waves of depolarisation and repolarisation sweep through the heart, they create small currents that reach the skin. The electrocardiogram (ECG) records them as voltage over time. The American Heart Association and partner societies publish standards for how ECGs are recorded and measured [1].

Figure 3 · The ECG waveform

A labelled ECG complex with P wave, QRS complex, T wave and the main intervals One heartbeat on an ECG: a small P wave for atrial depolarisation, a sharp QRS complex for ventricular depolarisation, and a broad T wave for ventricular repolarisation. Brackets mark the PR interval, the QRS duration and the QT interval. PRQSTPR interval 0.12–0.20 sQRS under 0.12 sQT intervalAtrial depolarisationVentricular depolarisationVentricular repolarisation
Electrical events, not contraction. Each wave records depolarisation or repolarisation spreading through the heart; contraction follows a fraction of a second later.
FeatureWhat it representsNormal value
P waveAtrial depolarisationUpright in lead II, under 0.12 s
PR intervalStart of atrial depolarisation to start of ventricular depolarisation, mostly AV node delay0.12–0.20 s
QRS complexVentricular depolarisationUnder 0.12 s
ST segmentVentricles fully depolarisedLevel with the baseline
T waveVentricular repolarisationUsually upright where QRS is upright
QT intervalTotal ventricular depolarisation and repolarisationVaries with heart rate; corrected value (QTc) used

Atrial repolarisation is hidden within the QRS complex. Note that the ECG shows electrical events only: a normal ECG does not guarantee that the heart is pumping well.

Reading the paper

Figure 4 · Reading ECG paper

ECG grid paper with a rhythm strip and a heart rate calculation Pink ECG grid with small and large squares and a regular rhythm strip. The interval from one R wave to the next spans four large squares, giving a heart rate of 300 divided by 4, or 75 beats per minute. R to R = 4 large squaresAt 25 mm/s: 1 small square = 0.04 s; 1 large square = 0.20 sHeart rate ≈ 300 ÷ large squares between R waves = 300 ÷ 4 = 75 per minute
The quick method works only for regular rhythms. For irregular rhythms, count the QRS complexes in a six-second strip and multiply by ten.

Standard paper runs at 25 mm per second, so each small square is 0.04 s and each large square 0.20 s [1]. For a regular rhythm, heart rate is 300 divided by the number of large squares between R waves, or 1500 divided by the number of small squares.

The leads

Figure 5 · Einthoven’s triangle

The three standard limb leads forming Einthoven's triangle Electrodes on the right arm, left arm and left leg form a triangle around the heart. Lead I runs from right arm to left arm, lead II from right arm to left leg, and lead III from left arm to left leg. A side panel lists the twelve leads of a standard ECG. Right armLeft armLeft legLead ILead IILead IIIHeart12-lead ECGLimb leads I, II, IIIaVR, aVL, aVF:frontal planeChest leads V1–V6:horizontal plane
Each lead is a viewpoint. Twelve leads look at the heart’s electrical activity from twelve directions; correct electrode placement matters [1].

A standard ECG uses ten electrodes to produce twelve leads. Six limb leads view the heart in the frontal plane; six chest leads, V1 to V6, view it in the horizontal plane. Electrode position affects the trace, so standards specify where each goes [1]. A bedside monitor usually shows only one or two leads, often lead II.

Rhythms a physiotherapist must recognise

RhythmWhat you seeWhat to do
Sinus rhythmP before every QRS, regular, rate 60–100Normal
Sinus tachycardiaNormal pattern, rate over 100Expected with exercise; at rest, look for pain, fever, dehydration, anxiety
Sinus bradycardiaNormal pattern, rate under 60Normal in fit people and on beta-blockers; report if symptomatic
Atrial fibrillationNo clear P waves; irregularly irregular QRSCheck rate and symptoms; new AF should be reported
Ectopic beatsEarly beats, occasionalCommon; report if frequent or increasing with exercise
Heart blockLong PR, dropped beats or dissociated P and QRSReport; high-degree block needs urgent review
Ventricular tachycardia or fibrillationWide fast complexes, or chaotic traceCheck the patient: if unresponsive and not breathing normally, call for help and start CPR

Always look at the patient, not just the monitor. A flat or chaotic trace with a talking patient is usually a loose electrode.

Clinical relevance for the physiotherapist

  • Exercise in atrial fibrillation. A 2024 Cochrane review of 20 trials found that exercise-based rehabilitation likely reduces AF recurrence, symptom burden and episode duration. Effects on mortality and serious adverse events were uncertain [3].
  • Beta-blockers and rate. Patients on beta-blockers or rate-limiting drugs may not reach predicted exercise heart rates; use perceived exertion as well.
  • Pacemakers and defibrillators. Know the programmed rate limits, avoid strong electrotherapy near the device, and follow local guidance on arm movement after implantation.
  • Exercise ECG. ST depression during exercise can indicate myocardial ischaemia; patients with known findings need agreed intensity limits.
  • Electrolytes. Abnormal potassium alters cardiac excitability and the ECG (Chapter 5).

Assessment and application

Before a session with a monitored patientWhy
Note the baseline rhythm and rateSo that you can recognise change
Check the latest ECG report and medicationsRate-limiting drugs and known arrhythmias change targets
Agree stop criteria with the teamNew arrhythmia, symptomatic changes, excessive rate rise or fall
Check electrode contactMovement artefact can mimic arrhythmia

Practical skill · counting heart rate from a strip

For a regular rhythm, count the large squares between two R waves and divide into 300. For an irregular rhythm, count the QRS complexes in a 6-second strip (30 large squares) and multiply by 10. Then compare with the palpated pulse, because some beats may not produce a pulse.

Common mistakes

  • Thinking the ECG measures contraction. It measures electrical activity only.
  • Placing the AV node delay in the QRS. It is in the PR interval.
  • Using the 300 rule on an irregular rhythm.
  • Reacting to the monitor before looking at the patient.
  • Assuming a low heart rate is abnormal in a trained athlete or a patient on beta-blockers.

Exam preparation

Long answer

Describe the origin and spread of the cardiac impulse. Add a note on the normal ECG.

  • Conducting system and sequence of activation (Figure 1).
  • Pacemaker potential and its ionic basis; funny current (Figure 2) [2].
  • Autonomic control of rate.
  • Normal ECG: waves, intervals and normal values (Figure 3, table) [1].
  • Leads and paper speed (Figures 4 and 5) [1].

Short notes

  • Pacemaker potential [2].
  • Einthoven’s triangle [1].
  • Heart block.
  • Exercise-based rehabilitation in atrial fibrillation [3].

Viva and practical

  • “Why does the SA node set the rate?” — it has the fastest intrinsic rate [2].
  • “What does the PR interval represent?” — mostly AV nodal delay [1].
  • “Is exercise safe in atrial fibrillation?” — trials suggest benefit for recurrence and symptoms; mortality effects are uncertain [3].
  • OSCE: calculate the heart rate from a printed strip and identify sinus rhythm.

Current evidence

Exam and traditional teaching

Atrial fibrillation is often taught as a reason to limit exercise, and the pacemaker potential is described simply as a sodium leak.

What the evidence adds

The pacemaker drift depends substantially on the funny current through HCN4 channels, and defects in it cause bradycardia and other arrhythmias [2].

Exercise-based rehabilitation in atrial fibrillation likely reduces recurrence and symptom burden, although longer and larger trials are still needed [3].

What the student should understand

Know the normal ECG and the stop signals by heart. With those in place, exercise is a treatment for many patients with rhythm disorders, not something to avoid.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. The normal pacemaker of the heart is the:
  1. (A) AV node
  2. (B) SA node
  3. (C) Bundle of His
  4. (D) Purkinje system

Answer: (B) SA node cells depolarise spontaneously, driven largely by the funny current through HCN4 channels [2].

Q2. The slow diastolic depolarisation of SA node cells depends substantially on:
  1. (A) Fast sodium channels
  2. (B) The ‘funny’ current through HCN channels
  3. (C) Chloride entry
  4. (D) The sodium–potassium pump

Answer: (B) DiFrancesco describes the funny current as central to spontaneous activity and to loss-of-function bradycardia [2].

Q3. The main purpose of the AV node delay is to:
  1. (A) Speed up the heart
  2. (B) Let the atria finish emptying before the ventricles contract
  3. (C) Protect the SA node
  4. (D) Shorten the QRS

Answer: (B) Slow AV conduction appears on the ECG as the PR interval, standardised in ECG recommendations [1].

Q4. On a standard ECG at 25 mm/s, one large square represents:
  1. (A) 0.04 s
  2. (B) 0.20 s
  3. (C) 1 s
  4. (D) 0.5 s

Answer: (B) Standard paper speed is 25 mm/s, so each 5 mm large square is 0.20 s [1].

Q5. If there are 4 large squares between consecutive R waves in a regular rhythm, the heart rate is about:
  1. (A) 50
  2. (B) 75
  3. (C) 100
  4. (D) 150

Answer: (B) 300 ÷ 4 = 75 beats per minute at standard paper speed [1].

Q6. The QRS complex represents:
  1. (A) Atrial depolarisation
  2. (B) Ventricular depolarisation
  3. (C) Ventricular repolarisation
  4. (D) AV node conduction only

Answer: (B) QRS is ventricular depolarisation; ECG standards define how its duration is measured [1].

Q7. A normal PR interval is about:
  1. (A) 0.04–0.08 s
  2. (B) 0.12–0.20 s
  3. (C) 0.30–0.40 s
  4. (D) Over 0.5 s

Answer: (B) A PR interval beyond 0.20 s suggests first-degree AV block; measurement is standardised [1].

Q8. Lead II records the potential difference between:
  1. (A) Left arm and left leg
  2. (B) Right arm and left leg
  3. (C) Right arm and left arm
  4. (D) V1 and V6

Answer: (B) The standard limb leads form Einthoven’s triangle; correct placement is part of ECG standards [1].

Q9. A Cochrane review of exercise-based rehabilitation in atrial fibrillation found that it likely:
  1. (A) Increases AF recurrence
  2. (B) Reduces AF recurrence and symptom burden
  3. (C) Has no effect on any outcome
  4. (D) Always reduces mortality

Answer: (B) Buckley and colleagues found likely reductions in AF recurrence and symptom burden; mortality effects were uncertain [3].

Q10. Sympathetic stimulation increases heart rate mainly by:
  1. (A) Flattening the pacemaker slope
  2. (B) Steepening the slow depolarisation of SA node cells
  3. (C) Blocking the AV node
  4. (D) Lengthening the QRS

Answer: (B) The funny current is modulated by autonomic signals that change the slope of diastolic depolarisation [2].

Quick review

Key takeaways

  • SA node → atria → AV node (delay) → His → bundle branches → Purkinje.
  • Pacemaker cells drift to threshold; the funny current through HCN4 channels is central [2].
  • Sympathetic steepens the drift and speeds the heart; the vagus slows it.
  • P = atrial depolarisation; QRS = ventricular depolarisation; T = ventricular repolarisation. PR 0.12–0.20 s, QRS under 0.12 s [1].
  • At 25 mm/s: rate = 300 ÷ large squares between R waves (regular rhythm) [1].
  • Exercise-based rehabilitation in AF likely reduces recurrence and symptoms [3].

Further reading

SourceWhy it earns its place
Hampton JR — The ECG Made EasyThe classic short introduction to ECG reading
Kligfield P et al. — JACC, 2007The standards for recording and measuring ECGs [1]
Hall JE, Hall ME — Guyton and Hall Textbook of Medical PhysiologyPhysiology of rhythm and conduction
Buckley BJR et al. — Cochrane Review, 2024Exercise evidence in atrial fibrillation [3]

References

  1. Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and interpretation of the electrocardiogram: part I: the electrocardiogram and its technology. Journal of the American College of Cardiology. 2007 Mar 13;49(10):1109–1127. doi:10.1016/j.jacc.2007.01.024 PMID 17349896 Scientific statement
  2. DiFrancesco D. HCN4, sinus bradycardia and atrial fibrillation. Arrhythmia & Electrophysiology Review. 2015;4(1):9–13. doi:10.15420/aer.2015.4.1.9 PMID 26835093 Review
  3. Buckley BJR, Long L, Risom SS, et al. Exercise-based cardiac rehabilitation for adults with atrial fibrillation. Cochrane Database of Systematic Reviews. 2024 Sep 17;9(9):CD011197. doi:10.1002/14651858.CD011197.pub3 PMID 39287086 Cochrane systematic review

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Reviewed by the Physiotherapist India Team. · Human Physiology contents