End-diastolic volume
| Cardiology Network |
 Discuss End-diastolic volume further in the WikiDoc Cardiology Network |
| Adult Congenital |
|---|
| Biomarkers |
| Cardiac Rehabilitation |
| Congestive Heart Failure |
| CT Angiography |
| Echocardiography |
| Electrophysiology |
| Cardiology General |
| Genetics |
| Health Economics |
| Hypertension |
| Interventional Cardiology |
| MRI |
| Nuclear Cardiology |
| Peripheral Arterial Disease |
| Prevention |
| Public Policy |
| Pulmonary Embolism |
| Stable Angina |
| Valvular Heart Disease |
| Vascular Medicine |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in a ventricle at the end of filling (diastole). Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload, which refers to the length of the sarcomeres in cardiac muscle prior to contraction (systole). An increase in EDV increases the preload on the heart and, through the Frank-Starling mechanism of the heart, increases the amount of blood ejected from the ventricle during systole (stroke volume).
Because nearly two-thirds of the blood in the systemic circulation is stored in the venous system, end-diastolic volume is closely related to venous compliance. Increasing venous compliance elevates the capacitance of the veins, reducing venous return and therefore end-diastolic volume. Decreasing venous compliance has the opposite effect. For example, activation of the baroreceptor reflex (occurring, for instance, in acute hemorrhage) causes venoconstriction, which decreases venous compliance, improves venous return, and therefore increases end-diastolic volume.
See also