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Ventricular systole
The parts of a QRS complex. Ventricular systole begins at the QRS, Atrial systole begins at P

Systole (pronounced /ˈsɪstɒli/) is a phase of the cardiac cycle where the myocardium is contracting in a coordinated manner in response to an endogenous electrical stimulus, and pressure is being generated within the chambers of the heart driving blood flow. Experimental and clinical measurements of systolic contraction are often based on ejection fraction and cardiac output. All four chambers of a human heart undergo systole and diastole in a timed fashion so that blood is propelled forward through the cardiovascular system.




Electrical systole

Electrical systole is first derived from sympathetic discharge from the sinoatrial node.

Mechanical systole

Electrical systole initiates gating of sodium, potassium and calcium channels triggering the essential binding of actin and myosin in the work of ATP (see Physiological mechanism below). The contraction of myocardium thus allowed induces conformational change of the muscle mass enabling expedient ejection of blood mass or mechanical systole. Mechanical systole is the origin of the pulse. The pulse is readily palpated at many points on the body and represents a universally accepted tactile (and sometimes visual) method of observing peak or systolic blood pressure. Mechanical forces enabled by electrical systole further allow movement of the muscle mass around long and short axes. It is well understood that the mass rotates clockwise through systole on the long axis, a process understood as "wringing" of the ventricles.

Atrial systole

Atrial systole is the contraction of myocardium of the left and right atria. Although atrial systole occurs in late part of ventricular diastole, the main force driving blood from the atria to the ventricles is the decrease in ventricular pressure that occurs during ventricular diastole. The drop in ventricular pressure that occurs during ventricular diastole allows the atrioventricular valve to open, emptying the contents of the atrium into the ventricle. Contraction of the atrium confers a relatively minor, additive effect toward ventricular filling; atrial contraction becomes significant in left ventricular hypertrophy, in which the ventricle does not fully relax during ventricular diastole. Loss of normal electrical conduction in the heart, as seen during atrial fibrillation, atrial flutter, and complete heart block, may abolish atrial systole. The aortic valve and pulmonary valve remain closed, while the atrioventricular mitral and tricuspid valves remain open because the pressure gradient between the atrium and ventricle is preserved during late ventricular diastole.

Atrial fibrillation represents a common electrical malady apparent during the time period of atrial systole. Ordered sinoatrial control of atrial electrical activity is lost, as a result coordinated pressure generation does not occur in the upper cardiac chambers. Atrial fibrillation represents an electrically disordered but well blood perfused atrial mass working in an uncoordinated fashion.

The ventricles are electrically isolated from the atria by the unique and electrically impermeable collagen layers of connective tissue known as cardiac skeleton. The bulwarks of this entity stem from the central body to form the four valve rings. Collagen extensions from the valve rings seal and limit atrial electrical influence from ventricular electrical influence to the SA/AV/Purkinje fibers. The compromised load of atrial fibrillation detracts from overall performance but the ventricles continue work as a physiologically effective pump. Given this pathology, ejection fraction may deteriorate by ten to thirty percent. Pharmacological manipulation of rate control, for example, by beta adrenoceptor antagonists is an important intervention in this condition. Titration of desirable heart rate in atrial fibrillation is now a fairly straightforward clinical intervention better served by beta blockade and occasionally backed up by calcium channel blocker or digoxin. Individuals prone to a hypercoagulable state are at variable risk of thrombus, thus requiring therapy with warfarin for life if the defined pathology cannot be corrected.

Right atrial systole

Right atrial systole coincides with right ventricular diastole, driving blood the through the tricuspid valve into the right ventricle. The time variable of right atrial systole is tricuspid valve (TV) open to (TV) close.

Left atrial systole

Left atrial systole coincides with left ventricular diastole, driving blood through the mitral valve (MV) into the left ventricle. The time variable of left atrial systole is mitral valve (MV) open to (MV) close.

Ventricular systole

Ventricular systole is the contraction of the myocardium of the left and right ventricles. Ventricular systole induces increased pressure in the left and right ventricles. Pressure in the ventricles rises to a level above that of the atria, thus closing the tricuspid and mitral valves, which are prevented from inverting by chordae tendineae and associated papillary muscles. Ventricular pressure continues to rise in isovolumetric contraction with maximal pressure generation (max dP/dt) occurring during this phase, until the pulmonary and aortic valves open in the ejection phase. In the ejection phase, blood flows down its pressure gradient through the aorta and pulmonary artery from left and right ventricles respectively. It is important to note that cardiac muscle perfusion through coronary vessels does not occur during ventricular systole, but occurs during ventricular diastole.

Ventricular systole is the origin of the pulse.

Right ventricular systole

Right ventricular systole drives blood through the pulmonary valve (PV) into the lungs. Right heart systole is volumetrically defined as right ventricular ejection fraction (RVEF). The time variable of right ventricular systole is PV open to PV close. Increased RVEF is indicative of Pulmonary Hypertension.

Left ventricular systole

Left ventricular systole drives blood through the aortic valve (AoV) to the body. Left ventricular systole is volumetrically defined as left ventricular ejection fraction (LVEF). The time variable of left ventricular systole is AoV open to AoV close.

Physiological mechanism

Systole of the heart is initiated by the electrically excitable cells of the sinoatrial node. These cells are activated spontaneously by depolarization of their membranes beyond a given threshold for excitation. At this point, voltage-gated calcium channels on the cell membrane open and allow calcium ions to pass through, into the sarcoplasm of muscle cell. Calcium ions bind to ryanodine receptors on the sarcoplasmic reticulum causing a flux of calcium ions to the sarcoplasm.

Calcium ions bind to troponin C, causing a conformational change in the troponin-tropomyosin complex, and thus allowing myosin head binding sites on F-Actin to be exposed. This transition allows cross bridge cycling to occur. The cardiac action potential spreads distally to the small branches of the Purkinge tree via the flux of cations through gap junctions that connect the sarcoplasm of adjacent myocytes. The electrical activity of ventricular systole is coordinated by the atrioventricular node, this discrete collection of cells receives electrical stimulation from the atrium, but also has a slower intrinsic pacemaker activity. The cardiac action potential is propagated down the bundle of His to Purkinje fibres which rapidly causes coordinated depolarisation, and excitation-contraction coupling from the apex of the heart up.

See also

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