when does isovolumetric relaxation and ventricular filling take place
Cardiac cycle "Ventricular diastole," begins when the ventricles starts to relax. At this point, some blood of the previous cycle's systole is still flowing out of the ventricles through the semilunar valves, due to the inertia of the moving blood column, which overcomes the higher pressure in the aorta/pulmonary trunk with respect to the pressure in the ventricles. This short lasting phase, called "protodiastole" ends with the closure of the semilunar valves, producing the second heart sound (S2). Now that both the AV valves and the semilunar valves are closed, the ventricles are now closed chambers. Hence, this phase is known as isovolumetric (also called isovolumic, isometric) relaxation phase. Then the atrioventricular (AV) valves (the mitral valve and the tricuspid valve) open, allowing blood to fill the ventricles. This ventricular inflow phase can be sub-divided into the 'first rapid filling phase' as blood rushes in from the atria as a result of ventricular dilation; a phase of slow ventricular filling called 'Diastasis', and the 'last rapid filling phase' due to atrial contraction (systole).
Diastolic heart failure Diastolic failure is characterized by an elevated diastolic pressure in the left ventricle, despite an essentially normal/physiologic end diastolic volume (EDV). Histological evidence supporting diastolic dysfunction demonstrates ventricular hypertrophy, increased interstitial collagen deposition and infiltration of the myocardium. These influences collectively lead to a decrease in distensibility and elasticity (ability to stretch) of the myocardium. As a consequence, cardiac output becomes diminished. When the left ventricular diastolic pressure is elevated, venous pressure in lungs must also become elevated too: left ventricular stiffness makes it more difficult for blood to enter it from the left atrium. As a result, pressure rises in the atrium and is transmitted back to the pulmonary venous system, thereby increasing its hydrostatic pressure and promoting pulmonary edema.[1]