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Systole // is an ancient medical term first understood as a gathering and later contraction of the heart. More recently it is understood as a force that drives blood out of the heart. Without qualifiers, it usually means the contraction of the left ventricle. The term "systole" originates from New Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν (sustellein, “to contract”), from σύν (sun, “together”) + στέλλειν (stellein, “send”).
When the smaller, upper atria chambers contract in the first phase of systole, they send blood down to the larger, lower ventricle chambers. When the lower chambers are filled and the valves to the atria are closed, the ventricles contract in the second phase, sending blood from the left ventricle to the aorta and body, and from the right ventricle to the lungs. Thus, the atria and ventricles contract in sequence (the atria feeding blood into the ventricles), while the left and right ventricles contract at the same time.
Cardiac systole is the contraction of the specialized muscle tissue of the heart in response to an electrochemical stimulus to the heart's cells (cardiomyocytes).
The cardiac output (CO) is the volume of blood pumped by the left ventricle in 1 minute. The ejection fraction (EF) is the volume of blood pumped divided by the total volume of blood in the left ventricle.
Cardiac electrical systole is staged and first derived from sympathetic charge from the sinoatrial node (SA node). Subsequent physiologic discharge from the SA node then finds it way through the atrial mass, eventually meeting at the atrioventicular node to be gated through the available channels from the atria to the ventricles to allow ventricular systole or [LVEF] + [RVEF].
Electrical systole opens voltage-gated sodium, potassium and calcium channels. A rise in intracellular calcium triggers the interaction of actin and myosin in the presence of ATP that generates force (see Physiological mechanism below). The muscular contraction of myocardium generates an active stress that increases intra-ventricular pressure and when intra-ventricular pressure exceeds aortic pressure there is ejection of blood. Mechanical systole is the origin of the pulse. The pulse is readily palpated (felt) 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 resulting from electrical systole cause rotation of the muscle mass around the long and short axes; a process envisaged as "wringing" of the ventricles.
Atrial systole represents the contraction of myocardium of the left and right atria. Atrial systole occurs late in ventricular diastole. One 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 valves to open, emptying the contents of the atria into the ventricles. 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 interval of atrial systole. Theory suggests that an ectopic focus, usually within the pulmonary trunks, competes with the sinoatrial node for electrical control of the atrial chambers to the detriment of atrial myocardial performance. 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 with an electrically (comparatively) healthy ventricle.
The ventricles are histologically and electrically isolated from the atria by the unique and electrically impermeable Collagen layers of connective tissue known as the 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 pathways. Exceptions such as accessory pathways may occur in this firewall between atrial and ventricular electrical influence but are rare. The compromised load of atrial fibrillation detracts from overall performance but the ventricles continue to work as a physiologically effective pump. Given this pathology, Ejection Fraction may deteriorate by ten to thirty percent. Uncorrected atrial fibrillation can lead to heart rates approaching 200 beats per minute. If one can slow this rate down to a normal range of approximately 80 beats per minute, the filling time of the heart cycle is longer and confers additional benefit to the pumping ability of the heart. Breathless individuals with uncontrolled atrial fibrillation can be rapidly returned to normal breathing when conversion with medication or electrical Cardioversion is attempted. Pharmacological manipulation of rate control, for example, by beta blocker|beta adrenoceptor antagonists, non-dyhydropyridine calcium channel blockers and digoxin are important historical interventions in this condition. Individuals prone to a hypercoagulable state are at a decided risk of Thromboembolism, 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 the blood 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. The atria contains two valves named as Bicuspid and Tricuspid valves which open during late stages of Diastole.
Ventricular systole is a written description of 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 and representative end organs excluding the lungs Pulmonary system. 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.
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 Purkinje 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 to the roots of the great vessels.
When blood pressure is stated for medical purposes, it is usually written as a Ratio of systolic to diastolic pressure; for example: 120/80 mmHg. This is not intended to be read as a ratio and cannot be legitimately read as a ratio. It is not a display of a numerator over a denominator but rather a medical notation used for quickly showing the two clinically significant pressures involved and cannot be reduced into lower terms.
- February 10, 2011 Systole has been mathematically interpreted in encyclopedic terms such as Ejection Fraction, Cardiac Output and Q. "Systole definition - Medical Dictionary definitions of popular medical terms easily defined on MedTerms". Medterms.com. Retrieved 2011-02-10.
- Lang RM, Bierig M, Devereux RB, et al. (March 2006). "Recommendations for chamber quantification". Eur J Echocardiogr 7 (2): 79–108. doi:10.1016/j.euje.2005.12.014. PMID 16458610.