Autorhythmicity [aw-toh-rith-miss-uh-tee], or automaticity, refers to the heart’s ability to spontaneously generate an electric charge without outside help. Cardiac electrical activity originates in the sinoatrial node (SAN) and is propagated via the ‘His-Purkinje’ network, the fastest conduction pathway within the heart. This pathway is known as the electrical conduction system of the heart.

The electrical signal travels from the SAN, which stimulates the atria to contract, to the atrioventricular node (AVN), which slows down conduction of the action potential from the atria to the ventricles. This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibers called the ‘bundle of His,’ located between the ventricles, and then to the ‘purkinje’ fibers at the bottom (apex) of the heart, causing ventricular contraction.

Other than the SAN, the AVN and purkinje fibers also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because, action potential production in the SAN is faster. This means that before the AVN or purkinje fibres reach the threshold potential for an action potential, they are depolarized by the oncoming impulse from the SAN. This is called ‘overdrive suppression.’

Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute, purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives. An example of premature ventricular contraction, is the classic ‘athletic heart syndrome.’ Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block, where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death.

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