The Heart’s Electrical Conduction System: From the SA Node to the ECG

You are looking at an ECG and somebody asks, “What is actually happening in the heart here?”

It is a much better question than it sounds.

Most of us first meet the ECG as a collection of shapes: P wave, QRS complex, T wave. Then come the boxes, intervals and rhythm names. It is possible to memorise all of that and still not really understand what the trace is showing.

So for this blog, we are going underneath the ECG paper.

We are going to follow one electrical impulse through one heartbeat, from the sinoatrial node to the ventricular myocardium, and keep stopping to look at what that part of the journey produces on the ECG. Once the physiology is clear, conduction blocks and broad complexes become much easier to reason through rather than recognise from a memorised picture.

Watch the electrical journey

Follow the electrical impulse through the heart, then use the sections below to connect each stage to the ECG trace.

Before the ECG: what makes a cardiac cell electrical?

Cardiac cells maintain different concentrations of charged ions across their cell membranes. Sodium, potassium and calcium are particularly important. Because charged particles are not distributed equally across the membrane, there is an electrical potential difference between the inside and outside of the cell.

When ion channels open and close, ions move across that membrane and the membrane potential changes. A sufficiently large change can produce an action potential: the electrical event that allows excitation to travel through cardiac tissue.

There is an important distinction here. The heart contains working myocardial cells, which produce the force of contraction, and specialised cells involved in generating or conducting the electrical impulse. They do not all behave electrically in exactly the same way.

Working atrial and ventricular myocytes have a relatively stable resting membrane potential between action potentials. Pacemaker cells are different. Their membrane potential gradually drifts towards threshold, allowing them to depolarise spontaneously. This property is automaticity.

That is the first reason the heart can beat without the brain sending a separate command for every contraction.

The sinoatrial node starts the rhythm, but it does not make the P wave

In normal sinus rhythm, the dominant pacemaker is the sinoatrial (SA) node, a specialised region of tissue high in the right atrium near the junction with the superior vena cava. Its pacemaker cells normally reach threshold more rapidly than subsidiary pacemaker sites elsewhere in the conduction system, so the SA node sets the rhythm.

The autonomic nervous system modifies that rate. Sympathetic stimulation tends to increase pacemaker activity and heart rate, while parasympathetic activity, predominantly through the vagus nerve, slows it. The important point is that autonomic input modulates the heart's intrinsic pacemaker activity; it does not have to initiate every beat.

Now follow the impulse.

The SA node depolarises. That tiny nodal electrical event is not what you see as a P wave. The surface ECG is not sensitive enough to display the SA node's action potential as its own recognisable deflection.

Instead, the impulse spreads from the SA nodal region through the atrial myocardium. Activation also reaches the left atrium, with Bachmann's bundle providing an important route of interatrial conduction. It is tempting to draw the atria as though they contain a set of neat insulated electrical cables. Human atrial conduction is more complex than that, so it is safer to think of the impulse spreading through atrial myocardium along preferential routes rather than imagining fixed 'wires' connecting every structure.

As millions of atrial myocardial cells depolarise, their combined electrical activity becomes large enough to be detected at the body surface.

That produces the P wave.

P wave = atrial depolarisation.

Not atrial contraction.

The distinction matters because electrical activation and mechanical contraction are linked, but they are not the same event. Depolarisation changes the electrical state of the myocardial cell. That electrical event triggers intracellular calcium handling and excitation–contraction coupling, which then allows the contractile proteins to generate force. In other words, the atria depolarise first and atrial contraction follows.

So when you see a P wave, you are looking at the surface electrical consequence of atrial myocardium depolarising. You can infer that atrial contraction should follow, but the ECG has not directly recorded the squeeze.

Why does the impulse slow down at the atrioventricular node?

After travelling across the atria, the impulse reaches the atrioventricular (AV) junction and AV node.

This is not just another stop on a diagram. The timing here is essential to effective pumping.

The atria and ventricles need to activate in sequence. If the ventricles were electrically activated immediately after the atria began to depolarise, atrial systole would have less opportunity to contribute to ventricular filling before ventricular contraction began. Slow conduction through the AV nodal region creates a physiological delay between atrial and ventricular activation.

The anatomy also helps control the route. The fibrous skeleton around the atrioventricular junction electrically insulates most atrial myocardium from ventricular myocardium. Under normal circumstances, the specialised atrioventricular conduction axis provides the route by which the impulse passes from atria to ventricles.

That makes the AV node rather more interesting than a simple 'pause button'. It is part of a specialised conduction system that delays transmission, protects the timing of ventricular activation and also has decremental conduction properties that help limit how rapidly some atrial impulses reach the ventricles.

Now look back at the ECG.

The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. In adults, it is generally 0.12–0.20 seconds, or about three to five small squares when the ECG is recorded at the standard paper speed of 25 mm/s.

Students are often taught that 'the PR interval is the AV-node delay'. That is useful as an early shortcut, but physiologically it is incomplete.

The PR interval begins when atrial depolarisation begins. It therefore includes conduction through the atrial myocardium, the important slowing through the AV nodal region and conduction into the His system up to the point at which ventricular depolarisation begins. The AV node contributes substantially to the delay, but the entire PR interval is not a direct measurement of the AV node alone.

That gives you a much more useful way to interpret an abnormal PR interval: it tells you that the journey from the beginning of atrial activation to the beginning of ventricular activation is taking an unusual amount of time.

The His–Purkinje system: why the ventricles can activate so quickly

Once the impulse leaves the AV nodal region, it enters the bundle of His. The His bundle penetrates the fibrous tissue and carries the impulse into the interventricular septum, where conduction continues into the right and left bundle branch systems and then through the Purkinje network.

The purpose of this system becomes obvious when you remember the size of the ventricles.

Ventricular myocardium is a large three-dimensional muscle mass. If activation had to crawl slowly from one ventricular myocyte to the next from a single starting point, different regions would contract at very different times. Instead, the His–Purkinje network distributes excitation rapidly through the ventricles, allowing ventricular myocardium to depolarise in a coordinated sequence.

The left bundle is itself anatomically complex and divides into fascicular pathways. For basic ECG interpretation, however, the central principle is more useful than memorising every branch: the specialised ventricular conduction system gets the electrical impulse to large areas of ventricular myocardium quickly.

As ventricular myocardium depolarises, the combined electrical activity produces the QRS complex.

QRS = ventricular depolarisation.

Again, it is not ventricular contraction. Mechanical systole follows electrical activation.

There is another useful detail hiding here. Atrial repolarisation also occurs, but its electrical signal is small and normally coincides with the much larger electrical activity of ventricular depolarisation. It is therefore usually buried within the QRS complex rather than appearing as a separate obvious wave.

Why is a normal QRS narrow, and why can it become broad?

This is where conduction physiology starts paying you back clinically.

When the impulse reaches both ventricles through the normal His–Purkinje system, ventricular activation is rapid. The resulting QRS is therefore relatively narrow.

If part of that rapid pathway is unavailable, the impulse may still reach ventricular myocardium, but activation has to spread differently. A bundle branch block is the classic example. One ventricle is activated normally through its functioning branch, while activation of the other is delayed and spreads through myocardium by a slower route. Ventricular depolarisation takes longer, so the QRS widens.

For complete right or left bundle branch block, a QRS duration of 120 ms or more is commonly used as part of the diagnostic criteria in adults. But width alone does not diagnose a bundle branch block; the QRS morphology and clinical context matter too.

This is why 'broad QRS = bundle branch block' is a poor rule to learn. Ventricular rhythms, pacing, pre-excitation, electrolyte disturbance and other intraventricular conduction abnormalities can also produce broad complexes.

A better question is: what has made ventricular depolarisation take longer?

That question forces you back to the physiology instead of asking the ECG to behave like a flashcard.

The ST segment and T wave: the ventricles have to recover

Depolarisation cannot simply continue indefinitely. Cardiac cells need to restore the electrical conditions that allow them to respond appropriately to the next impulse.

Ventricular action potentials have a prolonged plateau phase, influenced importantly by calcium entry and potassium movement. At the body surface, the ST segment corresponds broadly to a period when much of the ventricular myocardium is depolarised. Because large regions are in a similar electrical state, there is normally little net voltage difference for the surface ECG to record, so the ST segment sits close to the isoelectric baseline.

The ventricular myocardium then repolarises. The summed electrical activity of ventricular repolarisation produces the T wave.

T wave = ventricular repolarisation.

Repolarisation is not simply depolarisation running backwards. Different ventricular regions have different action-potential durations, and the sequence of recovery helps determine the direction and shape of the T wave. For a student learning the normal trace, the essential point is that the T wave represents electrical recovery of the ventricles, preparing myocardial cells for subsequent activation.

The QT interval and the small wave you may see afterwards

We have followed the P wave, QRS complex and T wave, but there is another measurement worth knowing. The QT interval runs from the start of the QRS complex to the end of the T wave. It covers ventricular depolarisation and repolarisation together: how long the ventricles take to become electrically activated and then recover.

The QT changes with heart rate, which is why you will often see QTc on an ECG report. This is the QT interval corrected for heart rate. The correction is not perfect, particularly at unusual rates or with a broad QRS. A prolonged QTc can increase the risk of dangerous ventricular arrhythmias. Some medicines and low potassium, magnesium or calcium levels can contribute. Interpretation belongs with the clinical team, not a diagnosis made from one number on the printout (NHS Specialist Pharmacy Service, 2026).

Occasionally, a small U wave appears after the T wave. It is not always present or easy to see. A small U wave can occur in an otherwise normal trace, particularly at a slower heart rate, while a prominent U wave can be associated with hypokalaemia. Its presence on its own does not establish a diagnosis.

Now one heartbeat has travelled all the way through:

SA node initiates the rhythm → atrial myocardium depolarises → P wave → AV conduction slows → PR interval → His–Purkinje system distributes the impulse → ventricular myocardium depolarises → QRS complex → ventricular myocardium repolarises → T wave.

That single sequence is the foundation underneath a large part of ECG interpretation.

Now break the pathway: understanding AV block instead of memorising it

Heart block becomes much easier when you stop treating each degree as an unrelated ECG pattern.

Start with normal conduction. One atrial impulse produces atrial depolarisation, travels through the AV conduction system and successfully reaches the ventricles. On the ECG, each P wave therefore has a corresponding QRS complex.

Now make conduction progressively less reliable.

First-degree AV block

Every atrial impulse still reaches the ventricles, so there is still 1:1 AV conduction. The problem is time: conduction from atrial activation to ventricular activation is prolonged.

On the ECG, every P wave is followed by a QRS, but the PR interval is consistently greater than 200 ms in an adult.

Calling it a 'block' can initially feel strange because nothing is actually dropped. Think of it as delayed AV conduction.

Second-degree AV block: some impulses get through and some do not

Now conduction fails intermittently.

In Mobitz I, or Wenckebach, conduction progressively slows until an atrial impulse fails to conduct. The ECG shows progressive PR prolongation followed by a P wave that is not followed by a QRS. After the dropped ventricular beat, the sequence starts again.

In Mobitz II, the behaviour is different. Conducted beats usually retain a similar PR interval, but an atrial impulse suddenly fails to reach the ventricles. You therefore see a P wave without the QRS complex you expected after it.

The distinction is not just an ECG naming exercise. Mobitz II often reflects disease lower in the His–Purkinje conduction system and carries a greater risk of progression to high-grade or complete AV block, so recognising and escalating significant bradycardia or conduction disturbance matters.

What about 2:1 AV block?

Sometimes every other atrial impulse is blocked, leaving two P waves for each QRS complex. This is 2:1 AV block. You can see that some impulses are not reaching the ventricles, but there are not enough consecutive conducted beats to see whether the PR interval lengthens before a dropped beat. A 2:1 pattern on its own cannot be called Mobitz I or Mobitz II. The level of block and its significance require further assessment, especially if the patient is symptomatic (Barold and Herweg, 2024).

Complete AV block: the atria and ventricles stop listening to each other

In third-degree, or complete, AV block, atrial impulses no longer control ventricular activation.

The SA node may continue to drive the atria, so P waves can remain regular. But those impulses are not being conducted to the ventricles. If ventricular activity is to continue, a subsidiary pacemaker below the level of block must generate an escape rhythm.

You now have two electrical clocks running independently: an atrial rhythm and a ventricular escape rhythm.

That produces atrioventricular dissociation. P waves and QRS complexes have no fixed relationship, so there is no consistent PR interval. The ventricular rate is usually slower than the atrial rate. The QRS may be narrow or broad depending on where the escape rhythm originates; a broad complex is not required for the diagnosis.

You may also hear approximate rates quoted for escape rhythms: a junctional escape is often around 40–60 beats per minute, whereas a ventricular escape may be around 20–40. These are useful tendencies rather than rules. The rate and QRS appearance vary, and a slow or unreliable escape rhythm can leave the patient poorly perfused. Never judge a patient's safety from an escape rate alone.

Bring it back to the patient

You are looking after a patient who says they feel light-headed when they sit up. They look pale. Their pulse is 38 beats per minute.

The monitor is showing a slow rhythm, so a 12-lead ECG is obtained. You can see P waves occurring regularly. QRS complexes are also present, but much more slowly. Sometimes a P wave appears before a QRS, sometimes inside the ST–T portion, sometimes after it. There is no repeating PR relationship.

Do not start by hunting through pictures of heart block.

Start with the electrical journey.

The presence of regular P waves tells you that atrial depolarisation is continuing. The presence of QRS complexes tells you that the ventricles are still depolarising. But the lack of a consistent relationship between them tells you that atrial impulses are no longer determining when the ventricles activate.

That is the physiology of complete AV block.

Now the patient's symptoms make sense too. A ventricular rate of 38 beats per minute may substantially reduce cardiac output. Remember the simple relationship: cardiac output = heart rate × stroke volume. Stroke volume may compensate to a degree, but a marked bradycardia can still reduce systemic and cerebral perfusion. The patient may therefore develop dizziness, presyncope, syncope, hypotension, chest discomfort, breathlessness or other signs of haemodynamic compromise.

For a student nurse, recognising that the patient and rhythm may represent significant deterioration is more important than trying to prove an electrophysiological diagnosis independently. Assess the patient, obtain a full set of observations, recognise features of poor perfusion or instability, and escalate promptly according to local policy and your level of competence.

What does escalation look like in practice? With a pulse of 38 and symptoms of poor perfusion, call for your supervising registered nurse and request urgent clinical review immediately. Begin an ABCDE assessment within your competence. Check blood pressure, oxygen saturation, respiratory rate, temperature and consciousness, and repeat observations as the situation changes. Do not leave the patient alone while you arrange help. Follow local arrangements for cardiac monitoring and a 12-lead ECG. Chest pain, collapse, severe breathlessness, hypotension or reduced consciousness warrant an emergency response rather than routine review.

Calculate and record NEWS2 where it is used, but do not delay raising concern while waiting for the total. The Resuscitation Council UK's adult bradycardia guidance asks the trained team to consider adverse features and risk of deterioration alongside the rhythm. Students are not expected to independently choose medicines or pacing. Recognise, communicate, assist and document what happened (Resuscitation Council UK, 2025; Royal College of Physicians, 2017).

For an SBAR handover you might say: “I'm concerned about this patient's slow pulse and light-headedness. Their heart rate is 38. The ECG appears to show P waves and QRS complexes without a fixed relationship, suggesting possible complete AV block. I've started observations and need an urgent review.” Add the actual blood pressure, oxygen saturation and other findings, plus relevant medical or medicine history, as soon as known. For someone who has experienced a blackout, NICE guidance treats heart block and other conduction abnormalities on a 12-lead ECG as red flags requiring appropriate assessment (NICE, 2010).

The ECG should always come back to the person attached to it.

One last thing: what the ECG can and cannot tell you

A surface ECG records differences in electrical potential detected at electrodes on the skin. It does not directly photograph an electrical impulse moving through the heart.

It also does not directly display the electrical activity of the SA node, AV node, His bundle or individual Purkinje fibres. Those structures are too small for their electrical activity to create the major surface deflections you recognise. Instead, we use the timing and pattern of atrial and ventricular myocardial activity to infer how the conduction system is behaving.

That is why physiology matters.

A prolonged PR interval suggests that atrial-to-ventricular conduction is taking longer. A dropped QRS after a P wave tells you that an atrial impulse has not successfully produced ventricular depolarisation. A broad QRS tells you ventricular activation is taking longer or travelling differently. P waves and QRS complexes marching independently tell you atrial and ventricular activation have become dissociated.

The ECG is therefore not just a set of lines to name. It is the surface evidence left behind by electrical events occurring inside the heart.

Once you learn to read it that way, you are no longer memorising a trace. You are following the heartbeat.

Next, use 12-Lead ECG Explained: Why 10 Electrodes Create 12 Leads to understand how electrodes turn this electrical activity into different views of the heart, then work through ECG Interpretation for Student Nurses for rate, rhythm and common ECG patterns.

References

Akhtar, M. (2016) 'Human His-Purkinje system: normal electrophysiologic behavior', Cardiac Electrophysiology Clinics, 8(4), pp. 641–682. doi:10.1016/j.ccep.2016.07.003.

Barold, S.S. and Herweg, B. (2024) 'Mobitz type II second-degree atrioventricular block: a commonly overdiagnosed and misinterpreted arrhythmia', Frontiers in Cardiovascular Medicine, 11, article 1450705. doi:10.3389/fcvm.2024.1450705.

Kennedy, A., Finlay, D.D., Guldenring, D., Bond, R.R., Moran, K. and McLaughlin, J. (2016) 'The cardiac conduction system: generation and conduction of the cardiac impulse', Critical Care Nursing Clinics of North America, 28(3), pp. 269–279. doi:10.1016/j.cnc.2016.04.001.

National Institute for Health and Care Excellence (NICE) (2010) Transient loss of consciousness ('blackouts') in over 16s, CG109. NICE recommendations.

NHS Specialist Pharmacy Service (2026) Managing medicines associated with QT interval prolongation. NHS SPS guidance.

Park, D.S. and Fishman, G.I. (2017) 'Development and function of the cardiac conduction system in health and disease', Journal of Cardiovascular Development and Disease, 4(2), article 7. doi:10.3390/jcdd4020007.

Park, D.S. and Fishman, G.I. (2026) 'The cardiac conduction system: development, function and therapeutic targets', Nature Reviews Cardiology, 23(5), pp. 303–323. doi:10.1038/s41569-025-01227-x.

Resuscitation Council UK (2025) Adult advanced life support guidelines. Resuscitation Council UK guidance.

Royal College of Physicians (2017) National Early Warning Score (NEWS) 2: Standardising the assessment of acute-illness severity in the NHS. London: RCP. RCP NEWS2.

van Weerd, J.H. and Christoffels, V.M. (2016) 'The formation and function of the cardiac conduction system', Development, 143(2), pp. 197–210. doi:10.1242/dev.124883.