Module 14: The Cardiovascular System: The Heart

Lesson 8: Cardiac Output: Factors Influencing Stroke Volume

Cung Lượng Tim: Yếu Tố Ảnh Hưởng Đến Thể Tích Nhát Bóp

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Dưới đây là danh sách những thuật ngữ Y khoa của module The Cardiovascular System: The Heart.
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Medical Terminology: The Cardiovascular System: The Heart

afterload
force the ventricles must develop to effectively pump blood against the resistance in the vessels
anastomosis
(plural = anastomoses) area where vessels unite to allow blood to circulate even if there may be partial blockage in another branch
anterior cardiac veins
vessels that parallel the small cardiac arteries and drain the anterior surface of the right ventricle; bypass the coronary sinus and drain directly into the right atrium
anterior interventricular artery
(also, left anterior descending artery or LAD) major branch of the left coronary artery that follows the anterior interventricular sulcus
anterior interventricular sulcus
sulcus located between the left and right ventricles on the anterior surface of the heart
aortic valve
(also, aortic semilunar valve) valve located at the base of the aorta
artificial pacemaker
medical device that transmits electrical signals to the heart to ensure that it contracts and pumps blood to the body
atrial reflex
(also, called Bainbridge reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases
atrioventricular (AV) node
clump of myocardial cells located in the inferior portion of the right atrium within the atrioventricular septum; receives the impulse from the SA node, pauses, and then transmits it into specialized conducting cells within the interventricular septum
atrioventricular bundle
(also, bundle of His) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches
atrioventricular bundle branches
(also, left or right bundle branches) specialized myocardial conductile cells that arise from the bifurcation of the atrioventricular bundle and pass through the interventricular septum; lead to the Purkinje fibers and also to the right papillary muscle via the moderator band
atrioventricular septum
cardiac septum located between the atria and ventricles; atrioventricular valves are located here
atrioventricular valves
one-way valves located between the atria and ventricles; the valve on the right is called the tricuspid valve, and the one on the left is the mitral or bicuspid valve
atrium
(plural = atria) upper or receiving chamber of the heart that pumps blood into the lower chambers just prior to their contraction; the right atrium receives blood from the systemic circuit that flows into the right ventricle; the left atrium receives blood from the pulmonary circuit that flows into the left ventricle
auricle
extension of an atrium visible on the superior surface of the heart
autonomic tone
contractile state during resting cardiac activity produced by mild sympathetic and parasympathetic stimulation
autorhythmicity
ability of cardiac muscle to initiate its own electrical impulse that triggers the mechanical contraction that pumps blood at a fixed pace without nervous or endocrine control
Bachmann’s bundle
(also, interatrial band) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium
Bainbridge reflex
(also, called atrial reflex) autonomic reflex that responds to stretch receptors in the atria that send impulses to the cardioaccelerator area to increase HR when venous flow into the atria increases
baroreceptor reflex
autonomic reflex in which the cardiac centers monitor signals from the baroreceptor stretch receptors and regulate heart function based on blood flow
bicuspid valve
(also, mitral valve or left atrioventricular valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
bulbus cordis
portion of the primitive heart tube that will eventually develop into the right ventricle
bundle of His
(also, atrioventricular bundle) group of specialized myocardial conductile cells that transmit the impulse from the AV node through the interventricular septum; form the left and right atrioventricular bundle branches
cardiac cycle
period of time between the onset of atrial contraction (atrial systole) and ventricular relaxation (ventricular diastole)
cardiac notch
depression in the medial surface of the superior lobe of the left lung where the apex of the heart is located
cardiac output (CO)
amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV
cardiac plexus
paired complex network of nerve fibers near the base of the heart that receive sympathetic and parasympathetic stimulations to regulate HR
cardiac reflexes
series of autonomic reflexes that enable the cardiovascular centers to regulate heart function based upon sensory information from a variety of visceral sensors
cardiac reserve
difference between maximum and resting CO
cardiac skeleton
(also, skeleton of the heart) reinforced connective tissue located within the atrioventricular septum; includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta; the point of attachment for the heart valves
cardiogenic area
area near the head of the embryo where the heart begins to develop 18–19 days after fertilization
cardiogenic cords
two strands of tissue that form within the cardiogenic area
cardiomyocyte
muscle cell of the heart
chordae tendineae
string-like extensions of tough connective tissue that extend from the flaps of the atrioventricular valves to the papillary muscles
circumflex artery
branch of the left coronary artery that follows coronary sulcus
coronary arteries
branches of the ascending aorta that supply blood to the heart; the left coronary artery feeds the left side of the heart, the left atrium and ventricle, and the interventricular septum; the right coronary artery feeds the right atrium, portions of both ventricles, and the heart conduction system
coronary sinus
large, thin-walled vein on the posterior surface of the heart that lies within the atrioventricular sulcus and drains the heart myocardium directly into the right atrium
coronary sulcus
sulcus that marks the boundary between the atria and ventricles
coronary veins
vessels that drain the heart and generally parallel the large surface arteries
diastole
period of time when the heart muscle is relaxed and the chambers fill with blood
ejection fraction
portion of the blood that is pumped or ejected from the heart with each contraction; mathematically represented by SV divided by EDV
electrocardiogram (ECG)
surface recording of the electrical activity of the heart that can be used for diagnosis of irregular heart function; also abbreviated as EKG
end diastolic volume (EDV)
(also, preload) the amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction
end systolic volume (ESV)
amount of blood remaining in each ventricle following systole
endocardial tubes
stage in which lumens form within the expanding cardiogenic cords, forming hollow structures
endocardium
innermost layer of the heart lining the heart chambers and heart valves; composed of endothelium reinforced with a thin layer of connective tissue that binds to the myocardium
endothelium
layer of smooth, simple squamous epithelium that lines the endocardium and blood vessels
epicardial coronary arteries
surface arteries of the heart that generally follow the sulci
epicardium
innermost layer of the serous pericardium and the outermost layer of the heart wall
filling time
duration of ventricular diastole during which filling occurs
foramen ovale
opening in the fetal heart that allows blood to flow directly from the right atrium to the left atrium, bypassing the fetal pulmonary circuit
fossa ovalis
oval-shaped depression in the interatrial septum that marks the former location of the foramen ovale
Frank-Starling mechanism
relationship between ventricular stretch and contraction in which the force of heart contraction is directly proportional to the initial length of the muscle fiber
great cardiac vein
vessel that follows the interventricular sulcus on the anterior surface of the heart and flows along the coronary sulcus into the coronary sinus on the posterior surface; parallels the anterior interventricular artery and drains the areas supplied by this vessel
heart block
interruption in the normal conduction pathway
heart bulge
prominent feature on the anterior surface of the heart, reflecting early cardiac development
heart rate (HR)
number of times the heart contracts (beats) per minute
heart sounds
sounds heard via auscultation with a stethoscope of the closing of the atrioventricular valves (“lub”) and semilunar valves (“dub”)
hypertrophic cardiomyopathy
pathological enlargement of the heart, generally for no known reason
inferior vena cava
large systemic vein that returns blood to the heart from the inferior portion of the body
interatrial band
(also, Bachmann’s bundle) group of specialized conducting cells that transmit the impulse directly from the SA node in the right atrium to the left atrium
interatrial septum
cardiac septum located between the two atria; contains the fossa ovalis after birth
intercalated disc
physical junction between adjacent cardiac muscle cells; consisting of desmosomes, specialized linking proteoglycans, and gap junctions that allow passage of ions between the two cells
internodal pathways
specialized conductile cells within the atria that transmit the impulse from the SA node throughout the myocardial cells of the atrium and to the AV node
interventricular septum
cardiac septum located between the two ventricles
isovolumic contraction
(also, isovolumetric contraction) initial phase of ventricular contraction in which tension and pressure in the ventricle increase, but no blood is pumped or ejected from the heart
isovolumic ventricular relaxation phase
initial phase of the ventricular diastole when pressure in the ventricles drops below pressure in the two major arteries, the pulmonary trunk, and the aorta, and blood attempts to flow back into the ventricles, producing the dicrotic notch of the ECG and closing the two semilunar valves
left atrioventricular valve
(also, mitral valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
marginal arteries
branches of the right coronary artery that supply blood to the superficial portions of the right ventricle
mesoderm
one of the three primary germ layers that differentiate early in embryonic development
mesothelium
simple squamous epithelial portion of serous membranes, such as the superficial portion of the epicardium (the visceral pericardium) and the deepest portion of the pericardium (the parietal pericardium)
middle cardiac vein
vessel that parallels and drains the areas supplied by the posterior interventricular artery; drains into the great cardiac vein
mitral valve
(also, left atrioventricular valve or bicuspid valve) valve located between the left atrium and ventricle; consists of two flaps of tissue
moderator band
band of myocardium covered by endocardium that arises from the inferior portion of the interventricular septum in the right ventricle and crosses to the anterior papillary muscle; contains conductile fibers that carry electrical signals followed by contraction of the heart
murmur
unusual heart sound detected by auscultation; typically related to septal or valve defects
myocardial conducting cells
specialized cells that transmit electrical impulses throughout the heart and trigger contraction by the myocardial contractile cells
myocardial contractile cells
bulk of the cardiac muscle cells in the atria and ventricles that conduct impulses and contract to propel blood
myocardium
thickest layer of the heart composed of cardiac muscle cells built upon a framework of primarily collagenous fibers and blood vessels that supply it and the nervous fibers that help to regulate it
negative inotropic factors
factors that negatively impact or lower heart contractility
P wave
component of the electrocardiogram that represents the depolarization of the atria
pacemaker
cluster of specialized myocardial cells known as the SA node that initiates the sinus rhythm
papillary muscle
extension of the myocardium in the ventricles to which the chordae tendineae attach
pectinate muscles
muscular ridges seen on the anterior surface of the right atrium
pericardial cavity
cavity surrounding the heart filled with a lubricating serous fluid that reduces friction as the heart contracts
pericardial sac
(also, pericardium) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium
pericardium
(also, pericardial sac) membrane that separates the heart from other mediastinal structures; consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium
positive inotropic factors
factors that positively impact or increase heart contractility
posterior cardiac vein
vessel that parallels and drains the areas supplied by the marginal artery branch of the circumflex artery; drains into the great cardiac vein
posterior interventricular artery
(also, posterior descending artery) branch of the right coronary artery that runs along the posterior portion of the interventricular sulcus toward the apex of the heart and gives rise to branches that supply the interventricular septum and portions of both ventricles
posterior interventricular sulcus
sulcus located between the left and right ventricles on the posterior surface of the heart
preload
(also, end diastolic volume) amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction
prepotential depolarization
(also, spontaneous depolarization) mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise
primitive atrium
portion of the primitive heart tube that eventually becomes the anterior portions of both the right and left atria, and the two auricles
primitive heart tube
singular tubular structure that forms from the fusion of the two endocardial tubes
primitive ventricle
portion of the primitive heart tube that eventually forms the left ventricle
pulmonary arteries
left and right branches of the pulmonary trunk that carry deoxygenated blood from the heart to each of the lungs
pulmonary capillaries
capillaries surrounding the alveoli of the lungs where gas exchange occurs: carbon dioxide exits the blood and oxygen enters
pulmonary circuit
blood flow to and from the lungs
pulmonary trunk
large arterial vessel that carries blood ejected from the right ventricle; divides into the left and right pulmonary arteries
pulmonary valve
(also, pulmonary semilunar valve, the pulmonic valve, or the right semilunar valve) valve at the base of the pulmonary trunk that prevents backflow of blood into the right ventricle; consists of three flaps
pulmonary veins
veins that carry highly oxygenated blood into the left atrium, which pumps the blood into the left ventricle, which in turn pumps oxygenated blood into the aorta and to the many branches of the systemic circuit
Purkinje fibers
specialized myocardial conduction fibers that arise from the bundle branches and spread the impulse to the myocardial contraction fibers of the ventricles
QRS complex
component of the electrocardiogram that represents the depolarization of the ventricles and includes, as a component, the repolarization of the atria
right atrioventricular valve
(also, tricuspid valve) valve located between the right atrium and ventricle; consists of three flaps of tissue
semilunar valves
valves located at the base of the pulmonary trunk and at the base of the aorta
septum
(plural = septa) walls or partitions that divide the heart into chambers
septum primum
flap of tissue in the fetus that covers the foramen ovale within a few seconds after birth
sinoatrial (SA) node
known as the pacemaker, a specialized clump of myocardial conducting cells located in the superior portion of the right atrium that has the highest inherent rate of depolarization that then spreads throughout the heart
sinus rhythm
normal contractile pattern of the heart
sinus venosus
develops into the posterior portion of the right atrium, the SA node, and the coronary sinus
small cardiac vein
parallels the right coronary artery and drains blood from the posterior surfaces of the right atrium and ventricle; drains into the coronary sinus, middle cardiac vein, or right atrium
spontaneous depolarization
(also, prepotential depolarization) the mechanism that accounts for the autorhythmic property of cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-open sodium ion channels and causes the electrical potential to rise
stroke volume (SV)
amount of blood pumped by each ventricle per contraction; also, the difference between EDV and ESV
sulcus
(plural = sulci) fat-filled groove visible on the surface of the heart; coronary vessels are also located in these areas
superior vena cava
large systemic vein that returns blood to the heart from the superior portion of the body
systemic circuit
blood flow to and from virtually all of the tissues of the body
systole
period of time when the heart muscle is contracting
T wave
component of the electrocardiogram that represents the repolarization of the ventricles
target heart rate
range in which both the heart and lungs receive the maximum benefit from an aerobic workout
trabeculae carneae
ridges of muscle covered by endocardium located in the ventricles
tricuspid valve
term used most often in clinical settings for the right atrioventricular valve
truncus arteriosus
portion of the primitive heart that will eventually divide and give rise to the ascending aorta and pulmonary trunk
valve
in the cardiovascular system, a specialized structure located within the heart or vessels that ensures one-way flow of blood
ventricle
one of the primary pumping chambers of the heart located in the lower portion of the heart; the left ventricle is the major pumping chamber on the lower left side of the heart that ejects blood into the systemic circuit via the aorta and receives blood from the left atrium; the right ventricle is the major pumping chamber on the lower right side of the heart that ejects blood into the pulmonary circuit via the pulmonary trunk and receives blood from the right atrium
ventricular ejection phase
second phase of ventricular systole during which blood is pumped from the ventricle
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Many of the same factors that regulate HR also impact cardiac function by altering SV. While a number of variables are involved, SV is ultimately dependent upon the difference between EDV and ESV. The three primary factors to consider are preload, or the stretch on the ventricles prior to contraction; the contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels. These factors are summarized in Table 1 and Table 2.
Preload is another way of expressing EDV. Therefore, the greater the EDV is, the greater the preload is. One of the primary factors to consider is filling time, or the duration of ventricular diastole during which filling occurs. The more rapidly the heart contracts, the shorter the filling time becomes, and the lower the EDV and preload are. This effect can be partially overcome by increasing the second variable, contractility, and raising SV, but over time, the heart is unable to compensate for decreased filling time, and preload also decreases.

With increasing ventricular filling, both EDV or preload increase, and the cardiac muscle itself is stretched to a greater degree. At rest, there is little stretch of the ventricular muscle, and the sarcomeres remain short. With increased ventricular filling, the ventricular muscle is increasingly stretched and the sarcomere length increases. As the sarcomeres reach their optimal lengths, they will contract more powerfully, because more of the myosin heads can bind to the actin on the thin filaments, forming cross bridges and increasing the strength of contraction and SV. If this process were to continue and the sarcomeres stretched beyond their optimal lengths, the force of contraction would decrease. However, due to the physical constraints of the location of the heart, this excessive stretch is not a concern.

The relationship between ventricular stretch and contraction has been stated in the well-known Frank-Starling mechanism or simply Starling’s Law of the Heart. This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. This means that the greater the stretch of the ventricular muscle (within limits), the more powerful the contraction is, which in turn increases SV. Therefore, by increasing preload, you increase the second variable, contractility.

Otto Frank (1865–1944) was a German physiologist; among his many published works are detailed studies of this important heart relationship. Ernest Starling (1866–1927) was an important English physiologist who also studied the heart. Although they worked largely independently, their combined efforts and similar conclusions have been recognized in the name “Frank-Starling mechanism.”

Any sympathetic stimulation to the venous system will increase venous return to the heart, which contributes to ventricular filling, and EDV and preload. While much of the ventricular filling occurs while both atria and ventricles are in diastole, the contraction of the atria, the atrial kick, plays a crucial role by providing the last 20–30 percent of ventricular filling.
It is virtually impossible to consider preload or ESV without including an early mention of the concept of contractility. Indeed, the two parameters are intimately linked. Contractility refers to the force of the contraction of the heart muscle, which controls SV, and is the primary parameter for impacting ESV. The more forceful the contraction is, the greater the SV and smaller the ESV are. Less forceful contractions result in smaller SVs and larger ESVs. Factors that increase contractility are described as positive inotropic factors, and those that decrease contractility are described as negative inotropic factors (ino- = “fiber;” -tropic = “turning toward”).

Not surprisingly, sympathetic stimulation is a positive inotrope, whereas parasympathetic stimulation is a negative inotrope. Sympathetic stimulation triggers the release of NE at the neuromuscular junction from the cardiac nerves and also stimulates the adrenal cortex to secrete epinephrine and NE. In addition to their stimulatory effects on HR, they also bind to both alpha and beta receptors on the cardiac muscle cell membrane to increase metabolic rate and the force of contraction. This combination of actions has the net effect of increasing SV and leaving a smaller residual ESV in the ventricles. In comparison, parasympathetic stimulation releases ACh at the neuromuscular junction from the vagus nerve. The membrane hyperpolarizes and inhibits contraction to decrease the strength of contraction and SV, and to raise ESV. Since parasympathetic fibers are more widespread in the atria than in the ventricles, the primary site of action is in the upper chambers. Parasympathetic stimulation in the atria decreases the atrial kick and reduces EDV, which decreases ventricular stretch and preload, thereby further limiting the force of ventricular contraction. Stronger parasympathetic stimulation also directly decreases the force of contraction of the ventricles.

Several synthetic drugs, including dopamine and isoproterenol, have been developed that mimic the effects of epinephrine and NE by stimulating the influx of calcium ions from the extracellular fluid. Higher concentrations of intracellular calcium ions increase the strength of contraction. Excess calcium (hypercalcemia) also acts as a positive inotropic agent. The drug digitalis lowers HR and increases the strength of the contraction, acting as a positive inotropic agent by blocking the sequestering of calcium ions into the sarcoplasmic reticulum. This leads to higher intracellular calcium levels and greater strength of contraction. In addition to the catecholamines from the adrenal medulla, other hormones also demonstrate positive inotropic effects. These include thyroid hormones and glucagon from the pancreas.

Negative inotropic agents include hypoxia, acidosis, hyperkalemia, and a variety of synthetic drugs. These include numerous beta blockers and calcium channel blockers. Early beta blocker drugs include propranolol and pronethalol, and are credited with revolutionizing treatment of cardiac patients experiencing angina pectoris. There is also a large class of dihydropyridine, phenylalkylamine, and benzothiazepine calcium channel blockers that may be administered decreasing the strength of contraction and SV.
Afterload refers to the tension that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood. Damage to the valves, such as stenosis, which makes them harder to open will also increase afterload. Any decrease in resistance decreases the afterload. Figure 1 summarizes the major factors influencing SV, Figure 2 summarizes the major factors influencing CO, and Table 3 and Table 4 summarize cardiac responses to increased and decreased blood flow and pressure in order to restore homeostasis.

OpenStax. (2022). Anatomy and Physiology 2e. Rice University. Retrieved June 15, 2023. ISBN-13: 978-1-711494-06-7 (Hardcover) ISBN-13: 978-1-711494-05-0 (Paperback) ISBN-13: 978-1-951693-42-8 (Digital). License: Attribution 4.0 International (CC BY 4.0). Access for free at openstax.org.

FactorEffect
Cardioaccelerator nervesRelease of norepinephrine by cardioaccelerator nerves
ProprioreceptorsIncreased firing rates of proprioreceptors (e.g. during exercise)
ChemoreceptorsChemoreceptors sensing decreased levels of O2 or increased levels of H+, CO2 and lactic acid
BaroreceptorsDecreased firing rates of baroreceptors (indicating falling blood volume/pressure)
Limbic systemAnticipation of physical exercise or strong emotions by the limbic system
CatecholaminesDecreased epinephrine and norepinephrine release by the adrenal glands
Thyroid hormonesIncreased T3 and T4 in the blood (released by thyroid)
CalciumIncrease in calcium ions in the blood
PotassiumDecrease in potassium ions in the blood
SodiumDecrease in sodium ions in the blood
Body temperatureIncrease in body temperature
Nicotine and caffeinePresence of nicotine, caffeine or other stimulants
FactorEffect
Cardioinhibitor nerves (vagus)Release of acetylcholine by cardioinhibitor nerves
ProprioreceptorsDecreased firing rates of proprioreceptors (e.g. during rest)
ChemoreceptorsChemoreceptors sensing increased levels of O2 or decreased levels of H+, CO2 and lactic acid
BaroreceptorsIncreased firing rates of baroreceptors (indicating rising blood volume/pressure)
Limbic systemAnticipation of relaxation by the limbic system
CatecholaminesDecreased epinephrine and norepinephrine release by the adrenal glands
Thyroid hormonesDecreased T3 and T4 in the blood (released by thyroid)
CalciumDecrease in calcium ions in the blood
PotassiumIncrease in potassium ions in the blood
SodiumIncrease in sodium ions in the blood
Body temperatureDecrease in body temperature
Opiates and tranquilizersPresence of opiates (heroin), tranquilizers or other depressants

Multiple factors impact preload, afterload, and contractility, and are the major considerations influencing SV.

The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents.


Baroreceptors (aorta, carotid arteries, venae cavae, and atria)Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive toDecreasing stretchDecreasing O2 and increasing CO2, H+, and lactic acid
TargetParasympathetic stimulation suppressedSympathetic stimulation increased
Response of heartIncreasing heart rate and increasing stroke volumeIncreasing heart rate and increasing stroke volume
Overall effectIncreasing blood flow and pressure due to increasing cardiac output; homeostasis restoredIncreasing blood flow and pressure due to increasing cardiac output; homeostasis restored

Baroreceptors (aorta, carotid arteries, venae cavae, and atria)Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive toIncreasing stretchIncreasing O2 and decreasing CO2, H+, and lactic acid
TargetParasympathetic stimulation increasedSympathetic stimulation suppressed
Response of heartDecreasing heart rate and decreasing stroke volumeDecreasing heart rate and decreasing stroke volume
Overall effectDecreasing blood flow and pressure due to decreasing cardiac output; homeostasis restoredDecreasing blood flow and pressure due to decreasing cardiac output; homeostasis restored
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Script:
  1. Many factors affect heart rate and stroke volume, and together, they contribute to cardiac function.
  2. Heart rate is largely determined and regulated by autonomic stimulation and hormones.
  3. There are several feedback loops that contribute to maintaining homeostasis dependent upon activity levels, such as the atrial reflex, which is determined by venous return.
  4. Stroke volume is regulated by autonomic innervation and hormones, but also by filling time and venous return.
  5. Venous return is determined by activity of the skeletal muscles, blood volume, and changes in peripheral circulation.
  6. Venous return determines preload and the atrial reflex.
  7. Filling time directly related to heart rate also determines preload.
  8. Preload then impacts both end diastolic volume and end systolic volume.
  9. Autonomic innervation and hormones largely regulate contractility.
  10. Contractility impacts end diastolic volume as does afterload.
  11. Cardiac output is the product of heart rate multiplied by stroke volume.
  12. Stroke volume is the difference between end diastolic volume and end systolic volume.
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