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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.

[edit] Types

[edit] Electrical systole

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

[edit] 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 and counterclockwise through systole and diastole on the long axis, a process understood as "wringing" of the ventricles.

[edit] Atrial systole

Atrial systole is the contraction of myocardium of the left and right atria. Atrial systole occurs in late part of ventricular diastole, but it is important to note that the main force driving blood from the atria to the ventricles is not atrial contraction, but decreased ventricular pressure in ventricular diastole, atrial systole plays a minor, and additive role in forcing blood into the ventricles. In left ventricular hypertrophy, where relaxation of the left ventricle in diastole does not occur sufficiently, the contraction of the left atrium becomes important for ventricular filling. Atrial systole is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation, atrial flutter, and complete heart block. Aortic and pulmonary valves are closed. Mitral and tricuspid valves are open due to the pressure gradient between the atria and ventricles in 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.

[edit] Right atrial systole

Right atrial systole drives blood through the tricuspid valve into the right ventricle. The time variable of right atrial systole is tricuspid valve (TV) open to (TV) close.

[edit] Left atrial systole

Left atrial systole drives 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.

[edit] 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.

[edit] Right ventricular systole

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

[edit] 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 aortic valve (AoV) open to (AoV) close.

[edit] 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 an 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.

[edit] See also

• Wiggers diagram
• Systole (mathematics)

[edit] External links

• systole at eMedicine Dictionary
• Systole at Dorland's Medical Dictionary