Contraction Mechanism and Atrial Systole
Myocardial contraction occurs through the interaction of actin and myosin proteins in the presence of calcium ions. Unlike skeletal muscle, cardiomyocytes receive $Ca^{2+}$ not only from the sarcoplasmic reticulum but also from the extracellular environment, a phenomenon known as the calcium-induced calcium release.
The cycle begins with atrial systole, lasting 110 ms on the right and 100 ms on the left. At this moment, blood is ejected into the ventricles. The auricles (atrial appendages) play an important role by providing necessary atrial distension and acting as an auxiliary pump. The right and left halves of the heart contract almost simultaneously, with minimal asynchrony due to the propagation pattern of excitation.
Period of Tension and Blood Ejection
Ventricular systole begins with the period of tension, which consists of two stages:
- Asynchronous contraction.
- Isovolumetric contraction: cardiomyocytes tense up without shortening. Chamber volumes do not change because blood is incompressible and all valves are closed.
As soon as the pressure in the right ventricle reaches 15 mm Hg and in the left ventricle 80 mm Hg, the semilunar valves open, and blood rushes into the great vessels.
At this time, the atrioventricular (mitral and tricuspid) valves are shut. To prevent the cusps from everting back into the atria (prolapse), they are anchored by chordae tendineae attached to contracting papillary muscles. These cords also act as shock absorbers, mitigating hydraulic shock.
Relaxation and Diastole
When the ventricles begin to relax, the pressure within them falls below that in the aorta and pulmonary trunk. Blood flows backward, filling the pockets of the semilunar valves and snapping them shut. The aortic wall contains elastic and collagen fibers that cushion the hydraulic impact and return the valves to their baseline position (a principle considered when designing prosthetic heart valves).
Next comes the isovolumetric relaxation phase (60 ms for the right ventricle and 80 ms for the left ventricle). Muscle fiber length remains constant, all valves are closed, and pressure drops to 5–10 mm Hg.
Ventricular Filling
Blood enters the heart from the veins exclusively during diastole. Ventricular filling is divided into several phases:
- Rapid filling (80 ms). The atrioventricular valves open. Blood rapidly fills the chambers due to the pressure gradient and the sharp relaxation of the walls. Perfusion of the coronary arteries creates a so-called hydraulic scaffold that physically helps the ventricles expand. Pressure drops close to zero.
- Reduced filling / diastasis (160–170 ms). Blood flow velocity decreases due to a diminishing pressure gradient and the elastic resistance of the ventricular walls.
Filling is completed by the next atrial systole.
Cardiac Work and Hemodynamics
External cardiac work is equal to the product of the change in pressure and the change in volume ($\Delta P \times \Delta V$). On a pressure-volume loop, this work is represented by the area of the loop.
- Increased venous return (Frank-Starling law): leads to an increase in stroke volume and cardiac work without elevating arterial blood pressure.
- Increased vascular resistance (afterload): forces the heart to perform more work and increases arterial blood pressure, while stroke volume remains unchanged.