Physiology chapters
Properties of cardiac tissue and the conduction pathway
The four properties of heart muscle (automaticity, excitability, conductivity and contractility), the route of the cardiac impulse from SA node to Purkinje fibres with its speeds and delays, and how the autonomic nerves change heart rate and conduction.
- Cardiac muscle has automaticity, excitability, conductivity and contractility; it works as a functional syncytium and cannot be tetanised.
- The impulse starts in the SA node (about 70–80/min), is delayed at the AV node (about 0.1 s) so the atria can empty, then races through the His-Purkinje system.
- Vagal stimulation slows rate and AV conduction; sympathetic stimulation speeds rate, conduction and force.
On this page
Overview
The heart beats on its own. Each beat starts in a small group of specialised cells and spreads through a conduction system in a fixed order, so that the atria contract before the ventricles.
This page covers the special properties of heart muscle and the conduction pathway. The ionic basis of the beat is on cardiac action potentials.
Structure of cardiac muscle
Cardiac muscle is striated like skeletal muscle, but its cells are branched and joined end to end by intercalated discs.
- Desmosomes in the discs hold the cells together.
- Gap junctions let ions pass freely, so the action potential spreads from cell to cell.
The atria and the ventricles each behave as a functional syncytium: when one cell is excited, all are. The atrial and ventricular syncytia are separated by fibrous tissue, and the only normal link between them is the AV bundle.
Properties of cardiac muscle
Automaticity and rhythmicity
Some cardiac cells can generate impulses on their own, without nerve input (automaticity), at a regular rate (rhythmicity). This is due to a slow, spontaneous depolarisation between beats (the pacemaker potential).
| Tissue | Intrinsic rate (per minute) |
|---|---|
| SA node | About 70–80 |
| AV node | About 40–60 |
| Purkinje fibres | About 15–40 |
The SA node fires fastest, so it sets the rate for the whole heart: it is the normal pacemaker. Each beat resets the slower tissues before they reach threshold (overdrive suppression).
If the SA node fails, the AV node usually takes over at about 40–60 beats per minute. In complete heart block, the ventricles beat at the Purkinje rate of about 15–40.
Excitability
Cardiac muscle responds to a stimulus with an action potential. Its excitability changes through the cardiac cycle because of the refractory periods.
Conductivity
The impulse spreads through the conduction system and from cell to cell through gap junctions. Speeds differ greatly (see below).
Contractility
Cardiac muscle contracts in response to the action potential.
- It follows the all-or-none law as a syncytium.
- Its force rises with stretch: the Frank-Starling law (more filling → stronger contraction).
- Its force rises with sympathetic stimulation and with more Ca2+ (positive inotropy).
Long refractory period: no tetanus
The ventricular action potential lasts about 0.25–0.3 seconds, and the refractory period lasts nearly as long as the contraction itself. A new beat cannot start until the muscle has started to relax.
Because of its long refractory period, cardiac muscle cannot be tetanised. This lets the heart fill between beats.
The conduction pathway
- SA node: a small strip of tissue in the upper right atrial wall, just where the superior vena cava enters. The impulse starts here.
- Atrial muscle and internodal pathways: carry the impulse across the atria to the AV node.
- AV node: in the lower part of the atrial septum. The impulse is delayed here.
- AV (His) bundle: passes through the fibrous skeleton into the ventricular septum.
- Right and left bundle branches: run down each side of the septum.
- Purkinje fibres: spread through the ventricular walls from the inside (endocardium) outwards.
Conduction speeds
| Tissue | Approximate velocity |
|---|---|
| Atrial muscle | About 0.3 m/s |
| Internodal pathways | About 1 m/s |
| AV node | About 0.05 m/s (slowest) |
| Ventricular muscle | About 0.3–0.5 m/s |
| Purkinje fibres | About 1.5–4 m/s (fastest) |
The AV nodal delay
The total delay from the SA node to the ventricles is about 0.16 seconds, mostly in the AV node and bundle. The delay lets the atria finish contracting and fill the ventricles before the ventricles contract. It also protects the ventricles from very fast atrial rhythms.
The delay is caused by small fibres, fewer gap junctions and a less negative resting potential in the AV nodal cells.
Slowest conduction: AV node. Fastest: Purkinje fibres.
The fast Purkinje system means all parts of the ventricles contract almost together, which makes pumping efficient.
Autonomic control of the heart
| Effect | Parasympathetic (vagus, ACh, muscarinic M2) | Sympathetic (noradrenaline, β1) |
|---|---|---|
| Heart rate (chronotropy) | Decreases | Increases |
| AV conduction (dromotropy) | Slows; strong stimulation can block it | Speeds |
| Force (inotropy) | Small decrease (mainly atria) | Strong increase |
How the vagus slows the heart: ACh opens extra K+ channels, which hyperpolarises the SA nodal cells and makes the pacemaker potential take longer to reach threshold.
How sympathetic nerves speed it: noradrenaline increases Na+ and Ca2+ permeability, making the pacemaker potential rise faster, and increases Ca2+ entry in muscle, making contraction stronger.
The right vagus mainly supplies the SA node; the left vagus mainly the AV node.
Vagal escape
Very strong vagal stimulation can stop the SA node for a few seconds. Then the Purkinje fibres take over at a slow rate. This is ventricular escape.
Clinical relevance
Heart block
How it happens: damage to the AV node or bundle (ischaemia, fibrosis, drugs such as beta-blockers or digoxin).
What you see: first degree: a long PR interval. Second degree: some beats fail to conduct. Third degree (complete): atria and ventricles beat independently, with a slow ventricular rate; may cause fainting (Stokes-Adams attacks). A pacemaker may be needed.
Ectopic pacemaker
How it happens: another part of the heart fires faster than the SA node, often due to ischaemia, caffeine, low potassium or stretch.
What you see: extra beats (ectopics) or abnormal rhythms.
Expect: the intrinsic rates of each pacemaker tissue, slowest and fastest conduction, the purpose and cause of the AV nodal delay, why the heart cannot be tetanised, the functional syncytium, and how vagal and sympathetic stimulation change rate, conduction and force.
Quick revision
- Properties: automaticity, excitability, conductivity, contractility.
- SA node 70–80/min; AV node 40–60; Purkinje 15–40.
- AV node slowest (about 0.05 m/s); Purkinje fastest (about 1.5–4 m/s).
- AV delay lets the atria fill the ventricles.
- Long refractory period: no tetanus.
- Vagus: slower rate and AV conduction (K+ channels). Sympathetic: faster and stronger (β1).
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
Why is the SA node the pacemaker of the heart?
It has the fastest rate of spontaneous depolarisation, so it reaches threshold first and drives the rest of the heart.
Why is there a delay at the AV node?
To let the atria contract and fill the ventricles before ventricular contraction begins.
Where is conduction fastest in the heart?
In the Purkinje fibres.
Why can cardiac muscle not be tetanised?
Its refractory period lasts almost as long as the contraction, so a new contraction cannot start until the muscle relaxes.