Systole

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Systolic
)
For other uses, see Systolic geometry.
pulmonic (pulmonary) valve
en route to the lungs for reoxygenation.

Systole (/ˈsɪstəli/ SIST-ə-lee) is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.[1]

Etymology

The term originates, via Neo-Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν (sustéllein 'to contract'; from σύν sun 'together' + στέλλειν stéllein 'to send'), and is similar to the use of the English term to squeeze.

Terminology, general explanation

Electrical waves track a systole (a contraction) of the heart. The end-point of the P wave depolarization is the start-point of the atrial stage of systole. The ventricular stage of systole begins at the R peak of the QRS wave complex; the T wave indicates the end of ventricular contraction, after which ventricular relaxation (ventricular diastole) begins.[2]

The mammalian

mitral (or bicuspid) valve; and the right atrium above the right ventricle (lighter blue), connected through the tricuspid valve
. The atria are the receiving blood chambers for the circulation of blood and the ventricles are the discharging chambers.

In late ventricular

lungs
. Thus, the pairs of chambers (upper atria and lower ventricles) contract in alternating sequence to each other. First, atrial contraction feeds blood into the ventricles, then ventricular contraction pumps blood out of the heart to the body systems, including the lungs for resupply of oxygen.

Cardiac systole is the contraction of the

cardiomyocytes
).

Cardiac output is the volume of blood pumped by the ventricles in one minute. The ejection fraction is the volume of blood pumped divided by the total volume of blood in the left ventricle.[3]

Types of systole

Atrial systole

ECG
, the two atria begin contracting (systole), pulsing blood under pressure into the ventricles.

Atrial systole occurs late in

complete heart block
—may eliminate atrial systole completely.

Contraction of the atria follows depolarization, represented by the P wave of the ECG. As both atrial chambers contract—from the superior region of the atria toward the atrioventricular septum—pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular valves. 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. Atrial contraction also referred to as the "atrial kick," contributes the remaining 20–30 percent of ventricular filling. Atrial systole lasts approximately 100 ms and ends prior to ventricular systole, as the atrial muscle returns to diastole.[4]

The two ventricles are isolated electrically and

histologically (tissue-wise) from the two atrial chambers by electrically impermeable collagen layers of connective tissue known as the cardiac skeleton. The cardiac skeleton is made of dense connective tissue which gives structure to the heart by forming the atrioventricular septum—which separates the atria from the ventricles—and the fibrous rings which serve as bases for the four heart valves.[5] Collagen extensions from the valve rings seal and limit electrical activity of the atria from influencing electrical pathways that cross the ventricles. These electrical pathways contain the sinoatrial node, the atrioventricular node, and the Purkinje fibers
. (Exceptions such as accessory pathways may occur in this firewall between atrial and ventricular electrical influence but are rare.)

Cardiac rate control via pharmacology is common today; for example, the therapeutic use of digoxin,

blood coagulation) are at decided risk of blood clotting, a very serious pathology requiring therapy for life with an anticoagulant
if it cannot be corrected.

Right and left atrial systoles

The atrial chambers each contains one valve: the tricuspid valve in the right atrium opens into the right ventricle, and the mitral (or bicuspid) valve in the left atrium opens into the left ventricle. Both valves are pressed open during the late stages of ventricular diastole; see Wiggers diagram at the P/QRS phase (at right margin). Then the contractions of atrial systole cause the right ventricle to fill with oxygen-depleted blood through the tricuspid valve. When the right atrium is emptied—or prematurely closed—right atrial systole ends, and this stage signals the end of ventricular diastole and the beginning of ventricular systole (see Wiggers diagram). The time variable for the right systolic cycle is measured from (tricuspid) valve-open to valve-closed.

The contractions of atrial systole fill the left ventricle with oxygen-enriched blood through the mitral valve; when the left atrium is emptied or closed, left atrial systole is ended and ventricular systole is about to begin. The time variable for the left systolic cycle is measured from (mitral) valve-open to valve-closed.

Atrial fibrillation

Main article: Atrial fibrillation

sinoatrial
control of atrial electrical activity is disrupted, causing the loss of coordinated generation of pressure in the two atrial chambers. Atrial fibrillation represents an electrically-disordered but well perfused atrial mass working (in an uncoordinated fashion) with a (comparatively) electrically-healthy ventricular systole.

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. Given this pathology, the ejection fraction may deteriorate by ten to thirty percent. Uncorrected atrial fibrillation can lead to heart rates approaching 200 beats per minute (bpm). 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 and Wiggers diagram

A Wiggers diagram, showing various events during systole (here primarily displayed as ventricular systole, or ventricular contraction). The very short interval (about 0.03 second) of isovolumetric, or fixed-volume, contraction begins (see upper left) at the R peak of the QRS complex on the electrocardiogram graph-line. + Ejection phase begins immediately after isovolumetric contraction—ventricular volume (red graph-line) begins to decrease as ventricular pressure (light blue graph-line) continues to increase; then pressure drops as it enters diastole.

A

pulmonary trunk respectively. Notably, cardiac muscle perfusion
through the heart's coronary vessels does not happen during ventricular systole; rather, it occurs during ventricular diastole.

Ventricular systole is the origin of the pulse.

Right and left ventricular systoles

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.

By its contractions, right ventricular (RV) systole pulses oxygen-depleted blood through the pulmonary valve through the pulmonary arteries to the lungs, providing

systemic circulation of oxygenated blood to all body systems. The left ventricular systole enables blood pressure
to be routinely measured in the larger arteries of the left ventricle of the heart.

LV systole is volumetrically defined as the left ventricular ejection fraction (LVEF). Similarly, RV systole is defined as the right ventricular ejection fraction (RVEF). Higher than normal RVEF is indicative of pulmonary hypertension. The time variables of the ventricular systoles are: right ventricle, pulmonary valve-open to valve-closed; left ventricle, aortic valve-open to valve-closed.

Electrical systole

Main article:
Electrical conduction system of the heart

The

right atrium adjacent to the junction with the superior vena cava.[6] The S-A Node is a pale yellow structure. For humans, it is approximately 25 mm long, 3–4 mm wide and 2 mm thick. It contains two types of cells: (a) the small, round P cells which have very few organelles and myofibrils, and (b) the slender elongated transitional cells, which are intermediate in appearance between the P and the ordinary myocardial cells.[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
.

The continual rhythmic discharge generates a wavelike movement of electrical ripples that stimulate the smooth muscles of the myocardium and cause rhythmic contractions to progress from top to bottom of the heart. 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]

Mechanical systole

Electrical systole opens voltage-gated sodium, potassium and calcium channels in cells of myocardium tissue. Subsequently, a rise in intracellular calcium triggers the interaction of

aortic circulation systems.[9]

Mechanical systole causes the pulse, which itself is readily palpated (felt) or seen at several points on the body, enabling universally adopted methods—by touch or by eye—for observing systolic blood pressure. 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.

Physiological mechanism

Systole of the heart is initiated by

calcium ions to pass through into the sarcoplasm (cytoplasm) of cardiac muscle cells. Calcium ions bind to molecular receptors on the sarcoplasmic reticulum (see graphic), which causes a flux (flow) of calcium ions into the sarcoplasm
.

Calcium ions bind to troponin C, causing a conformational (i.e., structural) change in the troponin-tropomyosin protein complex, causing the myosin head (binding) sites on F-actin filamentous proteins to be exposed, which causes muscle contraction to occur. The

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.

The electrical activity of ventricular systole is coordinated by the

apex of the heart
up to the roots of the great vessels.

Clinical notation

When blood pressure is stated for medical purposes, it is usually written with the systolic and diastolic pressures separated by a slash, for example, 120/80 mmHg. This clinical notation is not a mathematical figure for a fraction or ratio, nor a display of a numerator over a denominator. Rather, it is a medical notation showing the two clinically significant pressures involved (systole followed by diastole). 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.

Pathology

Systolic malfunction.

See also

References

  1. ISBN 9781401811280
    .
  2. ISBN 0-7868-6495-8
    .
  3. PMID 16458610
    .
  4. ISBN 978-1938168130
    . Retrieved 11 August 2014.
  5. ISBN 978-0-19-856878-0
    .
  6. ISBN 978-0-19-856878-0
    .
  7. OCLC 752495251
    .
  8. ISBN 0-7868-6495-8
    .
  9. ISBN 0-7868-6495-8
    .

External links
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