In accordance with the
Frank–Starling law of the heart, the
myocardium contracts more powerfully as the
end-diastolic volume increases. Stretching of the
myofibrils in cardiac muscle causes them to contract more powerfully due to a greater number of cross-bridges being formed between the
myofibrils within
cardiac myocytes. This is true up to a point, however beyond this there is a loss of contractile ability due to loss of connection between myofibrils; see figure. Various pathologies, listed below, can lead to volume overload. Different mechanisms are involved depending on the cause, however the common theme is that of a high cardiac output with a low or normal
afterload. The output may be high due to the inefficiency in
valve disease, or it may be high due to
shunting of blood in left-to-right shunts and
arteriovenous malformations. Left ventricular volume overload may produce inverted
u waves on the
electrocardiogram. ==Causes==