A topic in the Open Knowledge Graph — a free, open map of 15,290 topics and the order to learn them in.
The cardiac cycle alternates between isovolumetric contraction, ejection, isovolumetric relaxation, and filling phases. Ventricular pressure changes relative to atrial and aortic pressure determine valve opening and closure. The Frank-Starling law shows that increased preload (ventricular stretch) increases contractile force due to optimal calcium-myofilament interaction at longer muscle length.
Trace the cardiac cycle on a pressure-volume diagram while listening to actual heart sounds. Correlate chamber pressure changes with valve function and blood flow direction.
The cardiac cycle is a pressure-management system. From your study of hemodynamics, you know that blood flows down pressure gradients—from high pressure to low—and that valves enforce one-way flow. The heart exploits this by generating pressure changes that sequentially open and close four valves, shuttling blood through the pulmonary and systemic circuits. The cycle has four phases, and the key to understanding each is asking: what are the relative pressures on either side of each valve?
Isovolumetric contraction begins when the action potential triggers ventricular contraction. The ventricle starts to squeeze, but all four valves are initially closed—inflow valves (mitral and tricuspid) shut because ventricular pressure exceeds atrial pressure, and outflow valves (aortic and pulmonic) are still shut because aortic pressure exceeds the rising ventricular pressure. Volume stays constant (hence "isovolumetric") while pressure climbs rapidly. Once ventricular pressure exceeds aortic pressure, the aortic valve snaps open and ejection begins: the ventricle ejects its stroke volume into the aorta. At peak systole, ventricular pressure is slightly above aortic pressure; when the ventricle starts to relax, flow reverses momentarily and slams the aortic valve shut. Then isovolumetric relaxation begins—again all valves closed, volume constant, pressure dropping. Finally, when ventricular pressure falls below atrial pressure, the mitral valve opens and filling begins, both passively (blood flows in by pressure gradient) and actively (atrial contraction contributes roughly 20% at rest). The cycle then repeats.
The Frank-Starling law links your knowledge of muscle mechanics to cardiac output. Recall that sarcomere length affects the number of cross-bridge interactions: there is an optimal length at which actin and myosin filaments overlap maximally. In the heart, increased preload—the ventricular volume at end-diastole—stretches sarcomeres toward this optimum, increasing the sensitivity of troponin to calcium and enabling stronger contraction. The practical consequence: if venous return suddenly increases (you stand up quickly and blood pools momentarily, or you exercise and venous return increases), the heart automatically generates more force and ejects a larger stroke volume without any change in heart rate or neural input. This intrinsic mechanism makes each ventricle's output match its input beat-by-beat.
The pressure-volume (PV) loop is the most compact representation of all this information. On a PV diagram, the x-axis is ventricular volume and the y-axis is ventricular pressure. As you trace the cycle clockwise, you move through: filling (volume increases, pressure rises slightly) → isovolumetric contraction (volume constant, pressure climbs steeply) → ejection (volume decreases, pressure peaks then falls) → isovolumetric relaxation (volume constant, pressure drops). The width of the loop is stroke volume; the area inside it is the stroke work performed by the ventricle. Increased contractility tilts the end-systolic pressure-volume relationship (ESPVR) line steeper, producing a taller, wider loop and greater stroke work. Changes in afterload shift the loop rightward or change its shape. Reading PV loops lets you immediately diagnose what changed—preload, afterload, or contractility—from a single diagram.