AV node and conducting system
The electrical gate between atria and ventricles — normally the only route through the insulating fibrous skeleton — which holds each beat up for a fraction of a second and then hands it to a fast wiring system that makes both ventricles squeeze together.
What it normally does
The atria and ventricles are electrically insulated from each other by the fibrous ring of the cardiac skeleton, and in a normally formed heart the AV node is the only route across it. The node is richly supplied by both limbs of the autonomic nervous system: vagal tone slows conduction through it and lengthens its refractory period, sympathetic tone speeds conduction up. Note what this gate does and does not control — the sinus node sets the heart rate; autonomic tone at the AV node sets how readily impulses get across to the ventricles, which becomes the rate-determining step when the atria are firing very fast. Its blood supply comes from the AV nodal artery, a branch of the right coronary artery in most people (right dominance, roughly 85 to 90 per cent).
If an extra strand of muscle bridges that insulation, the node's protective filtering can be bypassed altogether — the basis of accessory pathway tachycardia and of pre-excited atrial fibrillation. It also explains why inferior (right coronary) infarction is the infarct that blocks the node.
Nodal cells depolarise using calcium rather than sodium, so conduction through the node is slow — roughly 0.1 second. That nodal delay is the largest part of the PR interval (normally 120 to 200 ms, which also contains atrial depolarisation and conduction through the His-Purkinje system). The delay lets the atria finish topping up the ventricles (the atrial kick), and it makes the node a decremental filter: bombard it faster and it blocks more impulses instead of passing them on. In many people the node is functionally split into a fast limb and a slow limb with different conduction speeds and different recovery times.
This is the single fact behind most of the rest: slow it further and you get first degree and Mobitz I block; exploit the filter and you get rate control in atrial fibrillation; let the two limbs set up a circuit and you get AVNRT. Every drug in this topic works on this calcium-dependent, vagally modulated step.
Below the node the wiring is fast: the bundle of His splits into a right and a left bundle branch, and Purkinje fibres spread the impulse through both ventricles in under 120 ms — the narrow QRS. Both ventricles contract as one coordinated squeeze from the apex up.
Lose one branch and activation has to travel muscle cell to muscle cell instead, which is slow and out of step — the wide QRS of bundle branch block, and the reason a wide escape complex tells you the block is below the node.
Subsidiary pacemakers below the sinus node can take over if the impulse from above stops, but they are slower and less reliable the further down you go: junctional escape at 40 to 60 beats per minute with a narrow QRS, ventricular (His-Purkinje) escape at 20 to 40 with a wide QRS.
In complete heart block the escape rhythm is the whole prognosis — a narrow junctional escape is comparatively stable, a wide ventricular escape is slow, unreliable and can stop altogether.
What goes wrong
- Slow conduction through the node (first degree block and Mobitz I second degree block)← from “Nodal cells depolarise using calcium rather th…”
High vagal tone, drugs that act on the node, ischaemia or inflammation make the calcium-dependent conduction even slower. In first degree block every impulse still gets through, just late, so the PR interval is longer than 200 ms. In Mobitz I the node conducts progressively worse beat by beat — the PR interval stretches a little further each cycle until one impulse fails completely, then the node recovers and the pattern restarts (Wenckebach).
Block at the node: narrow QRS, PR lengthens before the drop, better with exercise or atropine, usually benign and usually needs no pacemaker — but check the drug chart and, in a young patient with a sore joint or a murmur, check for acute rheumatic fever.
You would find: A long PR interval, or progressively lengthening PR with a dropped QRS, on an otherwise narrow-complex ECG. Often asymptomatic, and it commonly improves with exercise because sympathetic drive opens the gate. A newly prolonged PR interval is a minor criterion for acute rheumatic fever — worth looking for in Aboriginal and Torres Strait Islander patients, who carry most of Australia's acute rheumatic fever and rheumatic heart disease burden.
- Block below the node (Mobitz II and complete heart block)← from “Subsidiary pacemakers below the sinus node can…”
In Mobitz II the failure is in the His bundle or the bundle branches rather than the node: diseased conducting tissue fails without warning, so beats drop with no PR lengthening first. When conduction fails completely (third degree block) the atria and ventricles uncouple entirely and the ventricles depend on whatever escape pacemaker survives below the block — and where the block sits decides how safe that is. Block at the node itself (high vagal tone, AV nodal blocking drugs, inferior infarction, congenital block) usually leaves a junctional escape at 40 to 60 with a narrow QRS, which is relatively stable. Block below the node leaves a ventricular escape at 20 to 40 — slow, wide and unreliable, and it can stop altogether.
The escape complex is the answer: wide and around 20 to 40 means dead His-Purkinje wiring, atropine will not help, and the treatment is pacing. Mobitz II and complete heart block are pacemaker territory regardless of symptoms.
You would find: Bradycardia with P waves marching through the tracing bearing no relationship to the QRS complexes (AV dissociation), and blackouts with no warning (Stokes-Adams attacks). Read the escape: a wide escape at 20 to 40 places the block below the node, a narrow escape at 40 to 60 places it at the node. Infranodal block typically worsens rather than improves with exercise or atropine, and that is the pacemaker end of heart block.
- Bundle branch block← from “Below the node the wiring is fast: the bundle …”
One branch stops conducting, so that ventricle is no longer activated by its own fast wiring. The impulse crosses from the other side muscle cell to muscle cell, which is slow. The two ventricles contract out of step instead of together.
QRS 120 ms or more with the appropriate morphology. LBBB makes the ST segments uninterpretable for ischaemia by ordinary rules; new LBBB with ongoing ischaemic pain is a high-risk ACS needing urgent assessment, not a rhythm curiosity. Wide split S2 in RBBB, reversed split in LBBB.
You would find: QRS 120 ms or wider. Left bundle branch block changes the whole sequence of ventricular activation, so the ST segments and T waves are secondarily abnormal and cannot be read for ischaemia in the ordinary way — a new or presumed-new left bundle branch block with ischaemic chest pain marks a high-risk presentation needing urgent assessment for infarction (it is no longer treated as a STEMI on the ECG appearance alone). The second heart sound also splits abnormally, because the two ventricles no longer finish together: widened splitting in right bundle branch block, reversed (paradoxical) splitting in left.
- AV nodal re-entrant tachycardia (AVNRT)← from “Nodal cells depolarise using calcium rather th…”
The node's two limbs conduct and recover at different speeds. An early atrial beat finds the fast limb still refractory, goes down the slow limb, and by the time it arrives the fast limb has recovered — so it travels back up it and re-enters the slow limb. A self-sustaining circuit now spins inside the node and drives the ventricles, typically at 150 to 250 beats per minute.
Regular, narrow, abrupt on and abrupt off, young patient. The node is part of the circuit, so anything that blocks the node — vagal manoeuvres, adenosine, verapamil — can terminate it; definitive cure is slow pathway ablation.
You would find: A regular narrow-complex tachycardia around 180, starting and stopping abruptly, typically in a young otherwise well patient. Palpitations, neck pounding, sometimes light-headedness. Vagal manoeuvres can stop it dead because the circuit depends on the node.
- Accessory pathway tachycardia (AVRT, Wolff-Parkinson-White)← from “The atria and ventricles are electrically insu…”
An extra strand of muscle bridges the fibrous ring, so there is a second route between atria and ventricles that lacks the node's slow, protective, decremental conduction. Impulses can run down one route and back up the other, creating a larger circuit that includes atrium, node, ventricle and pathway. It also means the node's filtering can be bypassed.
Irregular, broad and very fast means pre-excited AF until proved otherwise: AV nodal blockers (verapamil, diltiazem, digoxin, adenosine, and beta blockers) can accelerate conduction down the pathway and are avoided — the treatment is electrical cardioversion, or an agent that acts on the pathway itself.
You would find: Between attacks: a short PR interval and a slurred upstroke into the QRS (delta wave). The dangerous version is atrial fibrillation in someone with an accessory pathway — an irregular, fast, broad-complex tachycardia, because the fibrillating atrium is firing straight down the unfiltered pathway, and it can degenerate into ventricular fibrillation.
- Atrial fibrillation with a rapid ventricular response (the node as filter)← from “Nodal cells depolarise using calcium rather th…”
The atria fire at 400 to 600 impulses per minute in fibrillation (about 300 in typical flutter), far faster than the ventricles could tolerate. Because the node conducts decrementally, most of those impulses arrive while it is still refractory and are blocked; only a variable minority get through, which is why the ventricular response is irregular. The ventricular rate is therefore set by the node's refractory period and the autonomic tone acting on it, not by the atrial rate.
Rate control means deliberately worsening the node's conduction: beta blocker or non-dihydropyridine calcium channel blocker first line, digoxin as an add-on or for the sedentary patient. The exception is the pre-excited, broad, irregular AF of Wolff-Parkinson-White, where blocking the node makes things worse.
You would find: An irregularly irregular narrow-complex tachycardia, often 100 to 160 at rest, with loss of the atrial kick and of a discrete P wave. High sympathetic tone (sepsis, pain, thyrotoxicosis, alcohol) shortens the nodal refractory period and drives the ventricular rate up.
What we give, and how it works
Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.
- Binds
- β₁ adrenoceptors (Gs-coupled) on sinoatrial and AV nodal cells and on working myocardium.
- Which does
- Less Gs signalling means less adenylyl cyclase activity, lower cyclic AMP and less protein kinase A phosphorylation of L-type calcium channels and the funny current — so the nodal upstroke is slower and the refractory period longer.
- So you see
- Fewer atrial impulses cross to the ventricles: the ventricular rate in atrial fibrillation falls, the PR interval lengthens, and re-entry that depends on the node is harder to sustain.
- And the same mechanism causes
- The same lengthening of nodal refractoriness that produces rate control produces symptomatic bradycardia and higher-degree AV block when the node is already diseased or a second nodal blocker is on board.
- Handling
- Metoprolol, bisoprolol and atenolol are the usual Australian agents; atenolol is renally cleared and accumulates in renal impairment, whereas metoprolol is hepatically metabolised. Avoid pairing an intravenous beta blocker with intravenous verapamil.
Catches people out: They exaggerate the node's normal filtering, so in someone whose node is already diseased they can tip a long PR interval into frank block. Combining them with verapamil or diltiazem stacks two brakes on the same gate and can produce profound bradycardia or asystole, particularly if either is given intravenously.
- Binds
- L-type (Cav1.2) voltage-gated calcium channels in nodal tissue, working myocardium and vascular smooth muscle — verapamil most cardioselective, diltiazem intermediate.
- Which does
- Blocks calcium entry in a use-dependent way, so the faster the node is driven the more it is blocked: the phase 0 upstroke of nodal cells is slowed and the refractory period lengthened.
- So you see
- Slower ventricular rate in atrial fibrillation, and termination of node-dependent re-entry; some arteriolar vasodilatation as well.
- And the same mechanism causes
- The same L-type block in working myocardium is negatively inotropic, so it can precipitate decompensation in a failing ventricle; and in pre-excited atrial fibrillation, blocking the node diverts conduction down the accessory pathway, accelerating the ventricular rate and risking ventricular fibrillation.
- Handling
- Avoid in reduced ejection fraction heart failure and in combination with beta blockers, especially intravenously. Verapamil inhibits P-glycoprotein and raises digoxin levels.
Catches people out: They also weaken the ventricle's contraction, so they are avoided in heart failure with reduced ejection fraction. They must not be used for a broad-complex irregular tachycardia in suspected Wolff-Parkinson-White: closing the node pushes conduction down the accessory pathway and the ventricular rate can accelerate dangerously.
- Binds
- A1 adenosine receptors (Gi-coupled) on AV nodal, sinus nodal and atrial cells.
- Which does
- Gi opens the acetylcholine-sensitive inward-rectifier potassium current and inhibits adenylyl cyclase, hyperpolarising nodal cells and cutting the calcium current — transient complete AV nodal block.
- So you see
- A few seconds of AV block that either terminates node-dependent re-entry or strips away the QRS complexes so the atrial rhythm can be seen.
- And the same mechanism causes
- Adenosine receptors sit elsewhere too, so the same brief agonism gives flushing, chest tightness, dyspnoea and a sense of doom, bronchospasm in asthma, and a transient sinus pause; it can also provoke atrial fibrillation, which is why it is hazardous when an accessory pathway is present.
- Handling
- Its plasma half-life is under 10 seconds, so the effect is over in seconds; it is exaggerated in the denervated transplanted heart and in patients taking dipyridamole, and blunted by theophylline and caffeine.
Catches people out: It terminates a tachycardia only when the node is part of the circuit — it will not stop atrial fibrillation or flutter, though it will transiently reveal the atrial activity (a few adenosine-sensitive tachycardias, such as some outflow tract ventricular tachycardias, are the exception to that rule). Warn the patient first: flushing, chest tightness and a sense of impending doom are very common but last only seconds. Ask about asthma, since it can provoke bronchospasm, and avoid it in a broad irregular pre-excited tachycardia.
- Binds
- The Na⁺/K⁺-ATPase of the myocyte; the AV nodal slowing is chiefly an indirect, centrally and reflexly mediated increase in vagal tone acting through M2 receptors at the node.
- Which does
- At the node, vagal stimulation raises potassium conductance and reduces the calcium current, slowing conduction and prolonging refractoriness. In the working myocyte, pump inhibition raises intracellular sodium, the sodium-calcium exchanger extrudes less calcium, and stored calcium rises — positive inotropy.
- So you see
- Fewer atrial impulses cross in atrial fibrillation, so the resting ventricular rate falls, with a modest increase in contractility rather than the negative inotropy of the other rate-control drugs.
- And the same mechanism causes
- Excess pump inhibition, worsened by hypokalaemia, leaves calcium-overloaded and abnormally automatic myocardium on top of a vagally blocked node — the characteristic toxicity of nausea and vomiting, xanthopsia and confusion, with the combination of AV block and increased ventricular automaticity.
- Handling
- Renally cleared with a narrow therapeutic index, so dose is governed by renal function and lean body mass; hypokalaemia potentiates it because potassium and digoxin compete at the pump, and amiodarone, verapamil and clarithromycin raise its concentration.
Catches people out: Because the nodal effect is vagally mediated, exercise overrides it — good rate control at rest, poor with activity, so it is not the agent for an active patient. It is cleared by the kidneys and has a narrow margin between working and toxic; low potassium makes toxicity worse. It is avoided in pre-excited atrial fibrillation.
- Binds
- M2 muscarinic acetylcholine receptors (Gi-coupled) on sinoatrial and AV nodal cells — a competitive antagonist.
- Which does
- Removing vagal Gi signalling closes the acetylcholine-sensitive potassium current and restores cyclic AMP and the calcium current, so nodal cells depolarise faster and recover sooner.
- So you see
- Faster sinus rate and improved AV nodal conduction, with shortening of a vagally prolonged PR interval.
- And the same mechanism causes
- The same muscarinic blockade elsewhere gives dry mouth, blurred vision, urinary retention, and confusion or delirium in older patients; and at the heart, speeding the atria while a diseased His-Purkinje system cannot follow can worsen the block in infranodal disease and paradoxically drop the ventricular rate.
- Handling
- Its site of action is the node, so its usefulness is a diagnostic clue as well as a treatment: a response points to nodal disease, no response points below the node and towards pacing.
Catches people out: It works on the node, so it helps first degree and Mobitz I block. It does not help block below the node — in Mobitz II or infranodal complete block it can speed the atrial rate without improving conduction, and may worsen the conducted ratio; the answer there is pacing.
Ask one question of every block: is it in the node or below it? Narrow QRS, PR lengthening before the dropped beat, better with exercise or atropine — that is the node being lazy, and it is usually benign. Wide QRS, beats dropping without warning, worse with exercise, an escape at 20 to 40 — that is dead wiring in the His-Purkinje system, the escape rhythm cannot be trusted, and it needs a pacemaker. The same node is the problem in block and the solution in atrial fibrillation: rate control works by deliberately making the gate slower — which is exactly why it backfires when an accessory pathway is carrying the beats instead.
Now test whether it stuck
Reading this through is not the same as being able to reconstruct it. Every question in the bank is free, with a full debrief on each option.