Editing Heart (section)

===Blood flow===
[[File:Latidos.gif|thumb|left|Blood flow through the valves]]
[[File:Flow through the Heart.webm|thumb|Blood flow through the heart]]
[[File:Schematic 3D illustration of blood flow through the heart.ogg|thumb|Video explanation of blood flow through the heart]]
The heart functions as a pump in the [[circulatory system]] to provide a continuous [[blood flow|flow of blood]] throughout the body. This circulation consists of the [[systemic circulation]] to and from the body and the [[pulmonary circulation]] to and from the lungs. Blood in the pulmonary circulation exchanges [[carbon dioxide]] for oxygen in the lungs through the process of [[breathing|respiration]]. The systemic circulation then transports oxygen to the body and returns carbon dioxide and relatively deoxygenated blood to the heart for transfer to the lungs.<ref name="CNX2014"/>

The [[#Right heart|right heart]] collects deoxygenated blood from two large veins, the [[superior vena cava|superior]] and [[inferior vena cava|inferior]] [[venae cavae]]. Blood collects in the right and left atrium continuously.<ref name="CNX2014"/> The superior vena cava drains blood from above the [[thoracic diaphragm|diaphragm]] and empties into the upper back part of the right atrium. The inferior vena cava drains the blood from below the diaphragm and empties into the back part of the atrium below the opening for the superior vena cava. Immediately above and to the middle of the opening of the inferior vena cava is the opening of the thin-walled coronary sinus.<ref name="CNX2014"/> Additionally, the [[coronary sinus]] returns deoxygenated blood from the myocardium to the right atrium. The blood collects in the right atrium. When the right atrium contracts, the blood is pumped through the [[tricuspid valve]] into the right ventricle. As the right ventricle contracts, the tricuspid valve closes and the blood is pumped into the pulmonary trunk through the pulmonary valve. The pulmonary trunk divides into pulmonary arteries and progressively smaller arteries throughout the lungs, until it reaches [[capillaries]]. As these pass by [[Pulmonary alveolus|alveoli]] carbon dioxide is [[gas exchange|exchanged]] for oxygen. This happens through the passive process of [[diffusion]].

In the [[#Left heart|left heart]], oxygenated blood is returned to the left atrium via the pulmonary veins. It is then pumped into the left ventricle through the [[mitral valve]] and into the aorta through the aortic valve for systemic circulation. The aorta is a large artery that branches into many smaller arteries, [[arteriole]]s, and ultimately capillaries. In the capillaries, oxygen and nutrients from blood are supplied to body cells for metabolism, and exchanged for carbon dioxide and waste products.<ref name="CNX2014"/> Capillary blood, now deoxygenated, travels into [[venule]]s and veins that ultimately collect in the superior and inferior vena cavae, and into the right heart.

====Cardiac cycle====
{{main|Cardiac cycle|Systole|Diastole}}
[[File:2027 Phases of the Cardiac Cycle.jpg|thumb|The cardiac cycle as correlated to the ECG]]

The cardiac cycle is the sequence of events in which the heart contracts and relaxes with every heartbeat.{{sfn|Guyton & Hall|2011|pp=105–107}} The period of time during which the ventricles contract, forcing blood out into the aorta and main pulmonary artery, is known as [[systole]], while the period during which the ventricles relax and refill with blood is known as [[diastole]]. The atria and ventricles work in concert, so in systole when the ventricles are contracting, the atria are relaxed and collecting blood. When the ventricles are relaxed in diastole, the atria contract to pump blood to the ventricles. This coordination ensures blood is pumped efficiently to the body.<ref name="CNX2014"/>

At the beginning of the cardiac cycle, the ventricles are relaxing. As they do so, they are filled by blood passing through the open [[Mitral valve|mitral]] and [[Tricuspid valve|tricuspid]] valves. After the ventricles have completed most of their filling, the atria contract, forcing further blood into the ventricles and priming the pump. Next, the ventricles start to contract. As the pressure rises within the cavities of the ventricles, the mitral and tricuspid valves are forced shut. As the pressure within the ventricles rises further, exceeding the pressure with the aorta and pulmonary arteries, the aortic and pulmonary valves open. Blood is ejected from the heart, causing the pressure within the ventricles to fall. Simultaneously, the atria refill as blood flows into the right atrium through the superior and [[inferior vena cava]]e, and into the left atrium through the pulmonary veins. Finally, when the pressure within the ventricles falls below the pressure within the aorta and pulmonary arteries, the aortic and pulmonary valves close. The ventricles start to relax, the mitral and tricuspid valves open, and the cycle begins again.{{sfn|Guyton & Hall|2011|pp=105–107}}

====Cardiac output====
{{main|Cardiac output}}
[[File:2029 Cardiac Cycle vs Heart Sounds.jpg|thumb|The x-axis reflects time with a recording of the heart sounds. The y-axis represents pressure.<ref name="CNX2014"/>]]
Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle (stroke volume) in one minute. This is calculated by multiplying the stroke volume (SV) by the beats per minute of the heart rate (HR). So that: CO = SV x HR.<ref name="CNX2014"/>
The cardiac output is normalized to body size through [[body surface area]] and is called the [[cardiac index]].

The average cardiac output, using an average stroke volume of about 70mL, is 5.25 L/min, with a normal range of 4.0–8.0 L/min.<ref name="CNX2014"/> The stroke volume is normally measured using an [[echocardiogram]] and can be influenced by the size of the heart, physical and mental condition of the individual, [[sex]], [[Myocardial contractility|contractility]], duration of contraction, [[preload (cardiology)|preload]] and [[afterload]].<ref name="CNX2014"/>

[[Preload (cardiology)|Preload]] refers to the filling pressure of the atria at the end of diastole, when the ventricles are at their fullest. A main factor is how long it takes the ventricles to fill: if the ventricles contract more frequently, then there is less time to fill and the preload will be less.<ref name="CNX2014"/> Preload can also be affected by a person's blood volume. The force of each contraction of the heart muscle is proportional to the preload, described as the [[Frank-Starling mechanism]]. This states that the force of contraction is directly proportional to the initial length of muscle fiber, meaning a ventricle will contract more forcefully, the more it is stretched.<ref name="CNX2014" />{{sfn|Guyton & Hall|2011|pp=110–113}}

[[Afterload]], or how much pressure the heart must generate to eject blood at systole, is influenced by [[vascular resistance]]. It can be influenced by narrowing of the heart valves ([[stenosis]]) or contraction or relaxation of the peripheral blood vessels.<ref name="CNX2014"/>

The strength of heart muscle contractions controls the stroke volume. This can be influenced positively or negatively by agents termed [[inotropes]].<ref name="BERRY2010">{{cite journal|last1=Berry|first1=William|last2=McKenzie|first2=Catherine|title=Use of inotropes in critical care|journal=Clinical Pharmacist|date=1 January 2010|volume=2|page=395|url=http://www.pharmaceutical-journal.com/learning/learning-article/use-of-inotropes-in-critical-care/11049283.article|url-status=live|archive-url=https://web.archive.org/web/20161128052534/http://www.pharmaceutical-journal.com/learning/learning-article/use-of-inotropes-in-critical-care/11049283.article|archive-date=28 November 2016}}</ref> These agents can be a result of changes within the body, or be given as drugs as part of treatment for a medical disorder, or as a form of [[life support]], particularly in [[intensive care unit]]s. Inotropes that increase the force of contraction are "positive" inotropes, and include [[sympathetic nervous system|sympathetic]] agents such as [[adrenaline]], [[noradrenaline]] and [[dopamine]].<ref name=OH2010>{{cite book|author= Bersten, Andrew|title=Oh's Intensive Care Manual|date=2013|publisher=Elsevier Health Sciences|location=London|isbn=978-0-7020-4762-6|pages=912–922|edition=7th}}</ref> "Negative" inotropes decrease the force of contraction and include [[calcium channel blocker]]s.<ref name=BERRY2010 />