Cardiac action potential 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
Cardiac excitation-contraction coupling a neurotransmitter called acetylcholine (ACh) which binds to specific receptor (M2 muscarinic receptor) on the sarcolemma of both SAN cells and ventricular cells. This again activates a G-protein. However this G-protein works by inhibiting, the cAMP pathway, therefore, preventing the sympathetic nervous system from increasing heart rate. As well as this, in the SAN, the G-protein activates specific potassium channel, that opposes action potential initiation (see SAN for more details), thus slowing heart rate. Cardiac excitation-contraction coupling Cardiac excitation-contraction coupling (Cardiac EC coupling) describes the series of events, from the production of an electrical impulse (action potential) to the contraction