Editing Cardiac output (section)

==Factors influencing cardiac output==
{{See also|Heart rate|Stroke volume|Ejection fraction}}
{{Anchor|2036SummaryOfFactorsInCardiacOutput}}
[[File:2036 Summary of Factors in Cardiac Output.jpg|thumb|Hierarchical summary of major factors influencing cardiac output.|alt=Hierarchical summary of major factors influencing cardiac output.]]

Cardiac output is primarily controlled by the oxygen requirement of tissues in the body. In contrast to [[pump|other pump systems]], the heart is a demand pump that does not regulate its own output.<ref name="Sircar2008">{{cite book|last=Sircar|first=Sabyasachi|name-list-style=vanc|title=Principles of Medical Physiology|url=https://books.google.com/books?id=zFl7y5xqHj4C&pg=PA237|year=2008|publisher=Thieme|isbn=978-1-58890-572-7|page=237|access-date=13 March 2016|archive-date=27 July 2020|archive-url=https://web.archive.org/web/20200727180537/https://books.google.com/books?id=zFl7y5xqHj4C&pg=PA237|url-status=live}}</ref> When the body has a high metabolic oxygen demand, the metabolically controlled flow through the tissues is increased, leading to a greater flow of blood back to the heart, leading to higher cardiac output.

The capacitance, also known as compliance, of the arterio-vascular channels that carry the blood also controls cardiac output. As the body's blood vessels actively expand and contract, the resistance to blood flow decreases and increases respectively. Thin-walled veins have about eighteen times the capacitance of thick-walled arteries because they are able to carry more blood by virtue of being more distensible.<ref name="Young2010">{{cite book|last=Young|first=David B.|name-list-style=vanc|title=Control of Cardiac Output|url=https://books.google.com/books?id=R7b_5XMhffcC|year=2010|publisher=Morgan & Claypool Publishers|isbn=978-1-61504-021-6|page=4|access-date=13 March 2016|archive-date=27 July 2020|archive-url=https://web.archive.org/web/20200727171333/https://books.google.com/books?id=R7b_5XMhffcC|url-status=live}}</ref>

From this formula, it is clear the factors affecting stroke volume and heart rate also affect cardiac output. The figure to the right illustrates this dependency and lists a few of these factors. A more detailed hierarchical illustration is provided in [[#2036SummaryOfFactorsInCardiacOutput|a subsequent figure]].

Equation ({{EquationNote|1}}) reveals HR and SV to be the primary determinants of cardiac output Q. A detailed representation of these factors is illustrated in the figure to the right. The primary factors that influence HR are autonomic [[innervation]] plus [[Endocrine system|endocrine]] control. Environmental factors, such as electrolytes, metabolic products, and temperature are not shown. The determinants of SV during the cardiac cycle are the contractility of the heart muscle, the degree of [[Preload (cardiology)|preload]] of myocardial distention prior to shortening and the afterload during ejection.<ref name="pmid18771592" /> Other factors such as electrolytes may be classified as either positive or negative inotropic agents.<ref name="CNX20142">{{cite book|last1 = Betts|first1 = J. Gordon|name-list-style = vanc|title = Anatomy & physiology|date = 2013|isbn = 978-1938168130|url = https://cnx.org/content/m46676/latest/?collection=col11496/latest|access-date = 11 August 2014|pages = 787–846| publisher=OpenStax College, Rice University |archive-date = 23 February 2022|archive-url = https://web.archive.org/web/20220223063018/https://openstax.org/books/anatomy-and-physiology/pages/19-1-heart-anatomy|url-status = live}}</ref>

=== Cardiac response ===
{| align=center
|-
|
{| border="1" class="wikitable"
|+ Table 3: Cardiac response to decreasing blood flow and pressure due to decreasing cardiac output<ref name="CNX2014"/>
!
!  Baroreceptors (aorta, carotid arteries, venae cavae, and atria)
! Chemoreceptors (both central nervous system and in proximity to baroreceptors)
|-
! Sensitive to
| Decreasing stretch<ref name="CNX2014"/> || Decreasing O<sub>2</sub> and increasing CO<sub>2</sub>, H<sup>+</sup>, and lactic acid<ref name="CNX2014"/>
|-
! Target
| Parasympathetic stimulation suppressed<ref name="CNX2014"/>
| Sympathetic stimulation increased<ref name="CNX2014"/>
|-
! Response of heart
| Increasing heart rate and increasing stroke volume<ref name="CNX2014"/>
| Increasing heart rate and increasing stroke volume<ref name="CNX2014"/>
|-
! Overall effect
| Increasing blood flow and pressure due to increasing cardiac output; haemostasis restored<ref name="CNX2014"/>
| Increasing blood flow and pressure due to increasing cardiac output; haemostasis restored<ref name="CNX2014"/>
|}
|-
|
{| border="1" class="wikitable"
|+ Table 4: Cardiac response to increasing blood flow and pressure due to increasing cardiac output<ref name="CNX2014"/>
!
! Baroreceptors (aorta, carotid arteries, venae cavae, and atria)
! Chemoreceptors (both central nervous system and in proximity to baroreceptors)
|-
! Sensitive to
| Increasing stretch<ref name="CNX2014"/> ||  Increasing O<sub>2</sub> and decreasing CO<sub>2</sub>, H<sup>+</sup>, and lactic acid<ref name="CNX2014"/>
|-
! Target
| Parasympathetic stimulation increased<ref name="CNX2014"/> ||  Sympathetic stimulation suppressed<ref name="CNX2014"/>
|-
! Response of heart
| Decreasing heart rate and decreasing stroke volume<ref name="CNX2014"/> ||  Decreasing heart rate and decreasing stroke volume<ref name="CNX2014"/>
|-
! Overall effect
| Decreasing blood flow and pressure due to decreasing cardiac output; haemostasis restored<ref name="CNX2014"/>
| Decreasing blood flow and pressure due to decreasing cardiac output; haemostasis restored<ref name="CNX2014"/>
|}
|}