However, in coronary artery blood the a-vO2 difference is 65 – 70 % at rest
This wide a-vO2 difference of demonstrates how extremely efficient the heart muscle is at extracting and utilising O2
Even at rest the coronary venous blood is almost desaturated – and there is only a little O2 reserve that the myocardium could “tap into” if required
Myocardium & Intermittence - cardiac muscle pt2:
Since cardiac muscle routinely extracts most of the oxygen available to it even at rest, there is little more for it to extract if it needs to
This means that when the heart needs greater O2 supplies (e.g. on exercise) the blood flow in the coronary system must be substantially increased
This increased blood flow is primarily achieved by vasodilation of the coronary arteries
Myocardium & Intermittence - cardiac muscle pt3:
The trigger for coronary arteryvasodilation is primarily an O2 deficiency and CO2 excess, i.e. when the activity of the heartincreases there is a temporary oxygen lack in the myocardial tissues and an increase in metabolic waste products
This O2 lack plus a host of vasodilator substances (NO, H+, K+, adenosine and CO2 etc..) released by the myocardial and coronary artery endothelial cells cause coronary artery vasodilation and increased blood flow
Myocardium & Intermittence - cardiac muscle pt4:
In health, coronary artery blood flow is matched to the metabolic needs of the heart i.e. supply = metabolic demand
This matching of O2 need and O2 supply is absolutely critical to cardiac function, because as an entirely aerobic organ, the heart depends entirely on oxidative processes to produce ATP
Myocardium & Intermittence - cardiac muscle pt5:
A temporary inadequacy of blood (O2) supply quickly results in a loss of cardiac muscle function and dysfunction within the intrinsic conducting system
A more sustained decoupling of supply and demand can result in permanentcardiac tissue damage and a permanentloss of function
Certain pathologies e.g. atherosclerosis may impair the supply of blood to the myocardium