Physiology for MRCEM Primary

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Cardiovascular physiology

Sinoatrial node

[box type=”download”]  Absence of fast Na channels and implications of this  Physiological basis of the pacemaker potential  Effects of chronotropes upon potassium currents hence rate of contraction [/box]

The sinoatrial node and origin of the heart beat

The sinoatrial node (SAN) resting potential starts at approximately −60 mV and gains steadily with time until it reaches a threshold of around −40 mV, when an AP is initiated (pacemaker potential).
The SAN lacks fast Na+ channels, so the upstroke of the AP is slow via L-type Ca2+ channels.
This means that SAN to myocyte conduction is slow; this is particularly important in the AV node, which has a similar AP.
The pacemaker potential occurs because of a slowly reducing outward K+ current set against inward currents, specifically the “funny” current, IF.
Factors that affect IF alter the rate of decay and time to reach threshold, and hence the heart rate, and are called chronotropic agents.
The sympathetic transmitter, noradrenaline (norepinephrine), is a positive chronotrope that increases IF.
The parasympathetic transmitter, acetylcholine, decreases IF, lengthens the time to reach threshold and decreases heart rate.

Action potentials elsewhere in the heart.

Purkinje fibres have a larger Na+ current that contributes to their fast conduction velocity.
Other atrial cells, AVN, bundle of His and Purkinje system may also exhibit decaying resting potentials that can act as pacemakers.
The SAN is normally fastest and predominates. This is called dominance or overdrive suppression.