The Conducting System: The Heart's Own Wiring

Muscle that gave up contracting to become a wire

The conducting system is not nerve tissue. It is cardiac muscle with a different job. Every element of the system — the sinoatrial node, the atrioventricular node, the bundle of His, the bundle branches, the Purkinje fibres — is made of modified cardiac myocytes, not neurons. These cells are pale and poor in myofibrils, because they traded contractile machinery for two other properties. The first is automaticity: unlike ordinary working myocardium, they never sit still at a stable resting membrane potential but drift steadily upwards until they reach threshold and fire, entirely on their own. The second is a conduction velocity tuned to the job — deliberately crawling in the nodes, spectacularly fast in the Purkinje network. Because they are muscle, they are joined to their neighbours by gap junctions in intercalated discs, so the whole heart behaves as a functional syncytium: one cell's decision to fire becomes every cell's decision. This is what makes a heart different from a skeletal muscle, which waits politely for a nerve, and it is the reason the chambers described in the heart's four chambers contract in an order rather than all at once.

The sinoatrial node: the pacemaker and where to find it

A crescent of pale cells, about a centimetre and a half long, hidden in the wall of the right atrium. The sinoatrial (SA) node lies subepicardially in the upper part of the right atrium, precisely at the junction of the superior vena cava with the atrium, at the superior end of the crista terminalis — the smooth muscular ridge inside the atrium that separates the smooth-walled sinus venarum behind from the rough, pectinate-muscled atrium in front. Externally that same ridge is marked by a shallow groove, the sulcus terminalis, and this is the surgeon's landmark: cannulate or cut carelessly near the cavoatrial junction and you can destroy the pacemaker of a living human being. The node is the fastest automatic tissue in the heart, drifting to threshold roughly sixty to a hundred times a minute at rest, and by the simple law that the fastest oscillator sets the pace for everything coupled to it, the SA node rules. Its blood supply is worth memorising because it explains a whole clinical syndrome: the SA nodal artery arises from the right coronary artery in about sixty per cent of people and from the circumflex in about forty, and both of those vessels are traced in the coronary arteries and cardiac veins.

From the node the impulse spreads through the atrial myocardium in every direction at once, cell to cell through gap junctions, like a ripple from a stone. Anatomists also describe three preferential internodal pathways — anterior, middle and posterior — bands of myocardium arranged so that conduction reaches the atrioventricular node faster than the general wavefront would. Their status as discrete tracts is argued over; their functional effect is not. One branch, however, is undisputed and clinically important: Bachmann's bundle, a broad band leaving the anterior internodal pathway and crossing the interatrial groove to the left atrium. It is the main electrical bridge between the two atria, and it is why the left atrium contracts only a few tens of milliseconds behind the right rather than waiting for the impulse to seep across. Damage or stretch it — as a chronically dilated left atrium does — and the atria begin to depolarise out of step, one of the substrates on which atrial fibrillation is built.

The atrioventricular node: a delay built on purpose

Everywhere else in the body, slow conduction is a fault. Here it is the entire point. The atrioventricular (AV) node sits in the lower part of the interatrial septum, immediately above and slightly in front of the opening of the coronary sinus, on the right atrial side of the septum. Its address has a formal name that every electrophysiologist and every examiner knows: the triangle of Koch, bounded by the tendon of Todaro behind, the attachment of the septal cusp of the tricuspid valve below and in front, and the orifice of the coronary sinus below and behind. The AV node lies at the apex of that triangle, where the first two boundaries converge. And what it does there is extraordinary: it conducts badly on purpose. Its cells are small, poorly coupled and slow, and the impulse crawls through the node at a fraction of the speed it travelled through the atria, so that roughly one tenth of a second is spent going nowhere. That pause is not an imperfection to be engineered away. It is the reason the atria have time to finish emptying their last twenty per cent of blood into the ventricles before the ventricles begin to squeeze. Remove the delay and atrial contraction would collide with ventricular contraction, and the atria would empty backwards into the veins.

The node has a second job that is arguably even more valuable: it is a filter. Its cells recover slowly — they have a long refractory period — so when an impulse arrives too soon after the last one, the node simply refuses to pass it. In atrial flutter the atria may be firing three hundred times a minute; in atrial fibrillation, four to six hundred, chaotically. If those impulses reached the ventricles unchecked the patient would die within seconds of ventricular fibrillation. Instead the AV node passes only a fraction of them, and the ventricles respond at a survivable, if irregular, hundred and forty. This is the gate that separates a frightening arrhythmia from a fatal one, and it is exactly the gate that rate-control drugs push further shut in atrial fibrillation and SVT. The AV node is also automatic in its own right, at a slower intrinsic rate of about forty to sixty a minute — an understudy waiting silently in the wings. Its artery comes from the right coronary artery in around eighty per cent of hearts.

The fibrous skeleton: an insulator with one door

Between the atria and the ventricles lies a continuous plate of dense fibrous tissue — the fibrous skeleton — made of the four fibrous rings that encircle the valve orifices, the right and left fibrous trigones that join them, and the membranous part of the interventricular septum. Its mechanical roles are described alongside the valves in the heart valves and heart sounds: it anchors the valve cusps, gives the myocardium something to pull against, and prevents the orifices stretching. But it has an electrical role that is just as important, and students routinely miss it. Fibrous tissue does not conduct. The skeleton therefore forms a complete insulating partition between atrial and ventricular muscle, so that the wave sweeping across the atria cannot leak directly into the ventricles anywhere along that plane. There is exactly one normal opening in the barrier, and the atrioventricular bundle passes through it. The whole architecture of the heartbeat depends on this: one delay, in one node, feeding one door.

The bundle of His, the branches and the Purkinje net

From here on, the system's only concern is speed. The atrioventricular bundle — the bundle of His — leaves the AV node, pierces the fibrous skeleton, and runs forward along the posterior border of the membranous part of the interventricular septum. After a centimetre or two it divides at the junction of the membranous and muscular septum into two bundle branches that run down either side of the muscular septum beneath the endocardium. The right bundle branch is a single slender cord that descends the right side of the septum and, near the apex, sends a large portion of its fibres across the cavity of the right ventricle inside the moderator band — the septomarginal trabecula — to reach the base of the anterior papillary muscle. That is not decoration: it means the papillary muscle is excited early, tightens the chordae tendineae, and holds the tricuspid valve shut before the full force of ventricular contraction arrives. The left bundle branch is broader and fans out on the left side of the septum, dividing into an anterior and a posterior fascicle, so that the left ventricle is served by two semi-independent cables — which is why a single fascicle can fail on its own and produce a hemiblock.

Both branches end by breaking up into the Purkinje fibres, a dense subendocardial plexus that spreads over the inner surface of both ventricles, into the papillary muscles and up the walls towards the base. Purkinje cells are large, rich in gap junctions and almost devoid of myofibrils, and they conduct at around four metres per second — some four to six times faster than ordinary ventricular muscle, and roughly a hundred times faster than the AV node. The consequence is the whole purpose of the design: the ventricles do not contract in a slow wave from one end to the other, they contract almost as a single unit. And because the Purkinje fibres reach the apex first and the outflow tracts last, the squeeze begins at the bottom and travels upwards, wringing blood towards the aortic and pulmonary orifices rather than sloshing it around the cavity. If the ventricles are ever left to their own devices — cut off from everything above — their intrinsic rate is a bleak twenty to forty a minute, enough to keep a patient conscious lying down and not much more.

Reading the anatomy off an ECG

The trace is not a picture of the heartbeat. It is a picture of this pathway. Map the structures onto the trace and the ECG stops being a set of shapes to memorise. The SA node's own discharge is far too small to register, so the first thing that appears is the P wave — atrial depolarisation spreading from the node across both atria. The flat PR segment that follows is the impulse crawling through the AV node and the bundle: electrically almost silent, but the most consequential tenth of a second in the cycle, and the PR interval measures it. The QRS complex is ventricular depolarisation through the His–Purkinje system; because that system is so fast, the complex is narrow — under 0.12 seconds. Anything that forces the ventricles to depolarise through ordinary muscle instead, cell by cell, widens it: a bundle branch block, a ventricular ectopic, a paced beat. Finally the T wave is ventricular repolarisation. Atrial repolarisation is there too, but it is buried inside the QRS and never seen. Narrow QRS therefore means the impulse came down the normal wiring; wide QRS means it did not.

The autonomic dial: turning it up and turning it down

The heart's nerves modulate a rhythm they did not create. Sympathetic fibres begin in the lateral horn of the upper thoracic spinal cord, roughly T1 to T4 or T5, synapse in the cervical and upper thoracic sympathetic ganglia, and reach the heart as cardiac nerves that join the cardiac plexus around the arch of the aorta and the tracheal bifurcation, described with the rest of the thoracic innervation in the nerves of the thorax. Their effect is threefold: they make the SA node drift to threshold faster (chronotropic), they speed conduction through the AV node (dromotropic), and they increase the force of contraction of the working myocardium (inotropic). Parasympathetic supply is carried by the vagus nerve, whose preganglionic fibres synapse in small ganglia within the atrial wall itself. Its distribution is deliberately lopsided: the vagus richly supplies the SA and AV nodes and the atrial muscle, slowing the pacemaker and slowing conduction through the gate, but it barely reaches ventricular myocardium at all. The receptor pharmacology of that push and pull is set out in fight-or-flight versus rest-and-digest. At rest the vagus is winning: a healthy adult's heart rate of seventy is a sinus node that would otherwise run at a hundred, held back on a leash.

The grades of block are simply a description of how badly the one door is working. In first-degree block every impulse gets through, but late: a PR interval longer than 0.20 seconds, usually harmless. In second-degree block some impulses fail. Mobitz type I — Wenckebach — shows a PR interval that lengthens beat by beat until one P wave is not followed by a QRS at all, and it is typically a fatigued AV node, often benign and sometimes simply high vagal tone in an athlete. Mobitz type II drops beats without warning and usually reflects disease below the node, in the bundle or the branches; it is far more dangerous because the escape rhythm beneath it is slow and unreliable. In third-degree block nothing crosses at all, the atria and ventricles beat independently, and survival depends entirely on whatever tissue below the block wakes up. That is where the hierarchy of intrinsic rates becomes visible in a single patient: a junctional escape near the node gives a narrow QRS at forty to sixty; a ventricular escape from the Purkinje network gives a wide QRS at twenty to forty and a patient who faints. The lower the escape, the slower and the worse — the anatomy of the system, written out as a rhythm strip.