Cardiac Conduction System
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Direct answer
The sinoatrial node, the heart's dominant pacemaker at 60-100 discharges per minute, sits at the junction of the superior vena cava and right atrium and drives the rest of the hierarchy by overdrive suppression: the atrioventricular node fires at 40-60 per minute and Purkinje fibres at 15-40. Impulse spread relies on gap junctions, reaching ventricular muscle at 0.3-0.5 m/s but racing through Purkinje fibres at up to 4 m/s — the fastest tissue — while the AV node deliberately crawls at 0.05 m/s, the slowest, imposing the 0.09-second delay that lets atrial systole precede ventricular contraction. Pacemaker cells owe their automaticity to the funny current (If), an inward sodium flux through channels opened by repolarisation, which drifts the membrane from -55 to -60 mV up to threshold. On the surface ECG the P wave lasts under 0.12 s, the PR interval spans 0.12-0.20 s, the QRS under 0.11 s, and the QT about 0.35-0.44 s.
What you must remember
- Pacemaker hierarchy: SA node 60-100 per minute (intrinsic 70-80), AV node 40-60, His-Purkinje 15-40; the fastest pacemaker rules by overdrive suppression.
- Conduction velocities: Purkinje fibres 4 m/s (fastest, largest diameter, most gap junctions); atrial and ventricular working myocardium 0.3-0.5 m/s; AV node 0.05 m/s (slowest — the source of AV delay).
- AV nodal delay: 0.09 s in the node itself, totalling with the penetrating bundle the PR interval of 0.12-0.20 s; the delay is calcium-channel dependent and vagally sensitive.
- Pacemaker mechanism: prepotential from the funny current If (sodium inward, activated by negative potentials) plus T-type calcium influx; no stable resting potential — the membrane drifts from -55 to -60 mV to threshold at -40 mV.
- ECG calibration: paper speed 25 mm/s so 1 mm = 0.04 s and 10 mm = 1 mV; the P wave 0.08 s, QRS 0.06-0.11 s, QT corrected less than 0.44 s.
- Escape rhythms: when the SA node fails, a junctional escape at 40-60 or an idioventricular rhythm at 15-40 takes over; Stokes-Adams attacks are transient complete block with a pause and syncope.
- Accessory pathways: Wolff-Parkinson-White syndrome uses the bundle of Kent, giving a short PR, wide QRS and delta wave, with risk of re-entry tachycardia.
Reading the conduction cascade on an ECG
Trace one normal beat. Depolarisation of the SA node is invisible on the surface — too small a mass. The atria depolarise over about 0.08 s, writing the P wave, and the impulse then wades through the slow, calcium-dependent AV node: this hidden interval is most of the PR segment's 0.16 s. Below the node the impulse accelerates explosively — the bundle branches and Purkinje network carry it at up to 4 m/s, so the entire ventricular mass is activated within the 0.08 s of the QRS, ensuring synchronous contraction. Repolarisation follows over the ST segment and T wave. Now break the chain: digoxin or ischaemia delays the node and lengthens PR; complete block separates P waves from QRS complexes, and a Stokes-Adams episode occurs when the escape pacemaker is slow to wake. In Wolff-Parkinson-White the Kent bundle bypasses the gatekeeper node, pre-exciting the ventricle — a slur into the QRS, the delta wave — and creates a two-way highway around which a re-entrant circuit can spin.
The classic confusion
Candidates mix up two different "slow". The AV node's 0.05 m/s velocity is a structural slowness (thin fibres, few gap junctions, calcium-dependent action potentials) and it is physiological — it buys the atrium its 0.09-second head start and protects the ventricle from atrial fibrillation's chaotic bombardment. Purkinje slowness does not exist; the bundle of His and its branches are the fastest tissue in the heart, which is why a ventricular beat is narrow when it arises below a functioning conduction system but broad when muscle-to-muscle spread must carry it. The second confusion is pacemaker automaticity with the fast sodium action potential: nodal cells have no stable phase 4, no phase 1, and depend on If and calcium — the exact reason verapamil and digoxin slow the node while leaving His-Purkinje conduction to sodium channels.
Frequently asked questions
Which is the fastest conducting tissue in the heart?
Purkinje fibres, at up to 4 m/s, ensuring near-simultaneous activation of both ventricles; the AV node is the slowest at 0.05 m/s.
Why is the AV nodal delay physiologically necessary?
The roughly 0.09-second delay allows atrial systole to complete ventricular filling before contraction, and screens the ventricle from rapid atrial rates.
What current generates the SA node pacemaker potential?
The funny current If, an inward sodium current activated during repolarisation, aided by T-type calcium influx, drifts the membrane from about -55 to -60 mV to threshold.
What are the normal PR and QRS intervals?
PR 0.12-0.20 s and QRS 0.06-0.11 s at the standard paper speed of 25 mm/s, where 1 mm equals 0.04 s.
What causes a Stokes-Adams attack?
A sudden transient complete heart block with a slow idioventricular escape, dropping cardiac output enough to cause syncope — classically in the elderly with infranodal disease.