Systole (/ˈsɪstəli/ SIST-ə-lee) is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.
[3] Atrial systole occurs late in ventricular diastole and represents the contraction of myocardium of the left and right atria.
At the start of atrial systole, during ventricular diastole, the ventricles are normally filled to about 70–80 percent of capacity by inflow from the atria.
Cardiac rate control via pharmacology is common today; for example, the therapeutic use of digoxin, beta adrenoceptor antagonists, or calcium channel blockers are important historical interventions in this condition.
Both valves are pressed open during the late stages of ventricular diastole; see Wiggers diagram at the P/QRS phase (at right margin).
The compromised load caused by atrial fibrillation detracts from the overall performance of the heart, but the ventricles continue to work as an effective pump.
If this rate can be slowed to a normal range, say about 80 bpm, the resultant longer fill-time within the cardiac cycle restores or improves the pumping capability of the heart.
The labored breathing, for example, of individuals with uncontrolled atrial fibrillation, can often be returned to normal by (electrical or medical) cardioversion.
Ventricular systole induces self-contraction such that pressure in both left and right ventricles rises to a level above that in the two atrial chambers, thereby closing the tricuspid and mitral valves—which are prevented from inverting by the chordae tendineae and the papillary muscles.
In the left ventricle, the aortic valve opens into the aorta which divides and re-divides into the several branch arteries that connect to all body organs and systems except the lungs.
[7] Intact, the SA node provides continual electrical discharge known as sinus rhythm through the atrial mass, the signals of which then coalesce at the atrioventricular node, there to be organized to provide a rhythmic electrical pulse into and across the ventricles through sodium-, potassium- or calcium-gated ion channels.
As the pulse moves out of the (upper) atria into the (lower) ventricles, it is distributed throughout a muscular network to cause systolic contraction of both ventricular chambers simultaneously.
The actual pace of the cycle—just how fast or slowly the heart beats—is cued by messages from the brain, reflecting the brain's responses to conditions of the body, such as pain, emotional stress, level of activity, and to ambient conditions including external temperature, time of day, etc.
[8] Electrical systole opens voltage-gated sodium, potassium and calcium channels in cells of myocardium tissue.
The mechanical forces of systole cause rotation of the muscle mass around the long and short axes, a process that can be observed as a "wringing" of the ventricles.
The cardiac action potential spreads distally (or outwardly) to the small branches of the Purkinje tree via the flux of cations through gap junctions that connect the sarcoplasms of adjacent myocytes.
It is often shown followed by a third number, the value of the heart rate (in beats per minute), which typically is measured jointly with blood pressure readings.