Volume overload

Pathophysiology

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.