Assume you are 45 minutes on the supine position. Furthermore: you stand all of a sudden and fast and without sympaticus activity. The venous return (smooth musculature of vessels) accommodates faster to the change (decrease of venous return) so returns blood to the heart before the sympaticus has accommodated for increased cardiac output. This creates a significant increase in the blood volume entering the heart. In pathological situation where systemic vasoconstriction not occurring normally, the heart is not capable of handling the overdistension; resulting in a pain during the second cardiac cycle.
I am interested in knowing which phase the heart is most vulnerable:
- isovolumetric contraction
- isovelumetric relaxation
or more explicitly (from my answer here)
- Atrial systole
- Isovolumetric ventricular contraction
- Rapid ventricular ejection
- Reduced ventricular ejection
- Isovolumetric ventricular relaxation
- Rapid ventricular filling
I think filling can happen normally, but not with the sudden isovolumetric contraction (most sympathetic innervations here, so therefore I think this is the weak link). When there is too much blood in the ventricles, some of the blood is reflected back from the ventricles into the atria causing a painful sensation and possibly tachycardia (as well as an possible increased risk of atrial fibrillation if such events happen regularly).
Is the isovolumetric contraction (systole of ventricles) of the cardiac cycle the possible weak link in accommodating a sudden increased venous return?