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 Ca Uniport system, which pumps Ca into the mitochondia. Heart rate is affected by nerves. Sympathetic nerves, coming from the spinal cord, increase heart rate, whereas parasympathetic nerves (for example the vagus nerves) work to decrease it. Sympathetic nerves work by releasing a protein (neurotransmitter) called noradrenaline which binds to a specific receptor (beta 1 adrenoceptor) located in the sarcolemma and the t-tubule membrane of cardiac cells. This activates a protein, called a G-protein and results in a series of reactions (known as a cyclic AMP pathway) that leads to the production of a molecule called cAMP (cyclic adenosine monophosphate).