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Action Potential of the Heart

The action potential in the myocardium of the heart is similar to that in skeletal muscle, for example, like skeletal myocytes, a myocyte has a negative membrane potential when at rest which becomes positive when its membrane is depolarised. However, there are some fundamental differences. One of the main differences between skeletal and cardiac myocytes is how they increase the cytoplasmic calcium concentration in order to induce a contraction. When skeletal muscle is stimulated by motor axons, influx of Na+ quickly depolarizes the skeletal muscle cell causing the action potential to continue down the T-tubules causing release of calcium ions from the sarcoplasmic reticulum. In cardiac myocytes, calcium ion release from the sarcoplasmic reticulum is brought about by an influx of the calcium ions into the cell through voltage-gated calcium channels on the sarcolemma. This is called calcium-induced calcium release and increases the concentration of free calcium ions in the cytoplasm, thus causing muscle contraction. In both muscle types, after the absolute refractory period, potassium channels open once again and the efflux of potassium ions repolarises the membrane bringing it back to the resting state. The voltage-gated calcium channels in the cardiac sarcolemma are normally due to an influx of sodium ions during the resting phase of the action potential In the heart we can distinguish both physiologically and anatomically several types of action potentials in the:

• SAN
• Atria
• AV node
• Purkyně fibres
• Ventricles

Sinoatrial Node

The SAN has an autoregulated action potential in that it does not require an external stimulus and can self-excitate. One of the reasons that allows this self-excitation is that it is has a resting membrane potential of -55 to -60mV as opposed to -85 to -90mV in the ventricles. Therefore it is more easily depolarised as the threshold potential is only -40mV. However, the main reason is due to sodium funny channels. These channels make the cells in the SAN more leaky to sodium and calcium ions, so there is a constant influx of these ions into the cell which initiates the action potential. These channels are always open allowing a fast depolarisation, and fast repolarisation. The sinoatrial node does not have a resting stage.

Atria

The atria action potential has four stages:

1. resting membrane potential from voltage gated sodium channels
2. rapid depolarisation of the membrane from the opening of fast sodium and calcium channels
3. initial repolarisation from potassium channels
4. plateau phase where there is a balance between influx of calcium ions and efflux of potassium ions
5. repolarisation from the sodium-potassium pump

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The diagram above actually shows the action potential of a ventricular myocyte. However, the shape is similar for atrial myocytes. (nb. the numbers in the diagram are one below the ones noted above e.g. 0 on the diagram, is the resting membrane potential from voltage gated sodium channels)

Atrioventricular node

The AVN has the same principle as the SAN but does not have as many sodium funny channels. This means that the cycle of its autorhythmicity is longer. It also has resting phase and its repolarisation is more rapid.

Purkyně Fibres

These fibres transmit the action potential from the SAN to the ventricles. It is similar to that of the atria except that the plateau phase is much longer which allows a stronger contraction and prevents a tetanic contraction.

Ventricles

The ventricles also have a similar action potential curve to that of the atria and purkyně fibres. Its plateau phase is longer than in the atria but not as long as in the purkyně network.

Links

http://en.wikipedia.org/wiki/Cardiac_action_potential http://commons.wikimedia.org/wiki/File:Action_potential.png

Bibliography

GUYTON, Arthur – HALL, John. Textbook of Medical Physiology. 12th edition. 2011. ISBN 9781416054528.