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 action potential membrane potential Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost the contraction stops and myocytic cells relax, which in turn relaxes the heart muscle. During this phase, the action potential fatefully commits to repolarisation. This begins with the closing of the L-type Cachannels, while the K channels (from phase 2) remain open. The main potassium channels involved in repolarization are the delayed rectifiers (I) and (I)