Sinoatrial Node

The sinoatrial node is a crescent of specialized muscle roughly 10 to 20 mm long, 3 to 7 mm wide, and only 1 to 2 mm thick, lying just under the epicardium of the right atrium at the junction with the superior vena cava. On the outside of the heart this spot is the sulcus terminalis; on the inside it is the ridge of the crista terminalis. It is high, posterior, and to the right of almost everything else in the atria, and that position is the first fact you need for reading a P wave.

The node is not a nerve. It is cardiac muscle that has given up contracting in order to keep time. Its cells are small, pale, and poor in contractile fibrils. They are joined to each other by gap junctions.

Blood arrives by the sinoatrial nodal artery, which comes off the right coronary artery in about two thirds of people and the left circumflex in most of the rest. The node is also densely wired with both sympathetic and parasympathetic nerve endings, which is why autonomic tone reaches it so quickly and so strongly.

A ventricular muscle cell sits at about -90 mV between beats, held there by potassium channels, and fires only when a neighbor pushes it past threshold. It then depolarizes with a fast sodium current, in a fraction of a millisecond, and holds a long plateau before repolarizing.

A sinoatrial cell has no stable resting voltage. At the end of a beat it reaches its most negative point, around -60 mV, and immediately begins to drift upward. This slow rise is the pacemaker potential, phase 4, and it is where heart rate is decided. Three things drive it:

• The funny current (I_f). HCN channels open when the cell is hyperpolarized, which is exactly the moment a beat ends. They let sodium leak in, so the very act of finishing one beat starts the next.

• Decaying potassium current. The potassium channels that repolarized the last beat close gradually, removing the brake.

• Calcium. T-type calcium channels open in the last stretch of the drift, and the sarcoplasmic reticulum releases small puffs of calcium that the sodium-calcium exchanger converts into inward current. This is sometimes called the calcium clock, working alongside the membrane clock above.

At about -40 mV the L-type calcium channels open and the cell fires. Notice what is missing: there are no fast sodium channels to speak of at these voltages. The upstroke is carried by calcium, so it is slow, and the action potential is small and rounded rather than spiked. That slow upstroke is why conduction inside the node crawls at about 0.05 m/s while atrial muscle conducts at close to 1 m/s, and why drugs that block L-type calcium channels slow the sinus rate.

Left alone, the human node fires at a little over 100 beats per minute in a young adult, falling by about half a beat per year of age. A transplanted heart, which has lost its nerve supply, runs close to that intrinsic rate. A resting adult sits nearer 60 to 80 because the vagus nerve is holding the node back all the time. So the resting heart rate is not the node's natural pace; it is the node's pace minus a standing vagal brake.

Sympathetic input releases noradrenaline onto beta-1 receptors, which raises cyclic AMP inside the cell. Cyclic AMP binds directly to the HCN channels and opens more of them, so the funny current is larger and the phase 4 climb is steeper. It also boosts the calcium currents. The cell reaches threshold sooner and the rate rises.

Vagal input releases acetylcholine onto M2 receptors and does two things at once. It lowers cyclic AMP, flattening the climb, and it opens a separate potassium channel (I_K,ACh) that pulls the cell further from threshold at the end of each beat. A flatter climb from a lower start is a much longer interval. This is why vagal tone can slow the node dramatically within a single beat, while sympathetic effects build over several seconds.

Because vagal tone waxes and wanes with breathing, so does the sinus rate: faster on inspiration, slower on expiration. In people this respiratory sinus arrhythmia is subtle. In dogs, whose resting vagal tone is high, it is pronounced and normal, and it often comes with a P wave that changes shape as the pacemaker site shifts within the node.

The node itself is invisible on a surface ECG. It is a few milligrams of tissue firing a small, slow action potential, far too little to register through the chest. The ECG records the consequence: the wave of depolarization moving across the atrial muscle, which is the P wave.

Because the node sits high and to the right, the atria activate from that corner outward: downward, leftward, and slightly forward. The right atrium goes first and makes the first half of the P wave; the impulse then crosses to the left atrium, largely through Bachmann's bundle, and the left atrium makes the second half. That geometry fixes the P wave's direction. In the frontal plane the atrial vector points between 0 and +75 degrees, so the P wave is upright in leads I, II, and aVF, and inverted in aVR, which looks at the heart from the right shoulder. In V1, which sits over the right atrium, the P wave is often biphasic: an early positive bump as the right atrium comes toward the electrode, then a small negative dip as the left atrium moves away from it.

Two things stay hidden. The interval between the node firing and the first atrial muscle depolarizing, the sinoatrial conduction time, is normally 45 to 125 ms and cannot be read off a surface tracing. And the node's cycle is only visible as the interval between successive P waves, which is why the P-P interval is the honest measure of sinus rate, not the R-R interval.

Put together, these give the working definition of sinus rhythm: a P wave before every QRS, every P wave the same shape, upright in lead II and inverted in aVR, at a rate appropriate for the patient. Each criterion is a statement about where the impulse started, not a pattern to memorize.

When the node fails, the heart does not stop, because every part of the conduction system below it can pace too, just more slowly: the atrioventricular junction at roughly 40 to 60 beats per minute, the ventricular Purkinje network at 20 to 40. These backups are silent while the node is working, and the reason is mechanical rather than mysterious. Being driven faster than its own pace makes a cell admit more sodium per minute, so its sodium-potassium pump works harder, and that pump is electrogenic: it pushes out three sodium for every two potassium it brings in, leaving the cell a little more negative. The faster pacemaker literally holds the slower ones below threshold. This is overdrive suppression.

It also explains the pause after a sinus arrest. When the node stops, the junction is still hyperpolarized by its own overworked pump and needs a few seconds to drift back up to threshold. That gap, between the node quitting and the backup waking, is the dangerous part of sinus node disease.

Go deeper. See the node's output as a rhythm in normal sinus rhythm, then the two ends of the autonomic range in sinus bradycardia and sinus tachycardia. The wave it produces has its own page at P wave. Next on this path: the structure that receives the impulse and deliberately slows it, the atrioventricular node.