This system consists of the heart and the blood vessels. Vessels that carry blood away from the heart are called arteries and those that carry blood toward the heart are called veins. Capillaries, short, thin-walled vessels, lie within the various organs and connect arteries to veins.
The cardiovascular system consists of the heart (box at left) and blood vessels. Vessels leaving the heart are called arteries (curved tube at upper left corner) which give rise to smaller vessels called arterioles (curved tube at upper right corner). These give rise to capillaries (lower right corner) that recombine to form veins (lower left corner) which return blood to the heart.
The central nervous system (box in center) has two cardiac centers (CA and CI circles) and two centers that control blood vessels (VI and VD circles). Nerves (solid and dashed lines) enter and leave the central nervous system.
Interstitial fluid that surrounds tissues is represented as the area inside the circle of vessels beside the capillary.
The block arrow (top of heart box) represents blood flowing from the heart into the arterial system; CO is cardiac output, the volume of blood leaving the heart each minute. The block arrow (bottom of heart box) represents blood flowing from the venous system into the heart; VR is venous return, the volume of blood returning to the heart each minute. The block arrows along the vessels represent the flow of blood along its pressure gradient. The donut structure at the beginning of the capillary represents the precapillary sphincter muscles that open and close to regulate the flow of blood into capillary beds.
Blood entering the heart, venous return, plays an important role in regulating the volume that will be ejected with each beat--stroke volume. The volume ejected each minute, cardiac output, is also dependent on heart rate.
The box represents the heart. The block arrow leaving the top of the box represents cardiac output (CO), the volume of blood that is ejected from the heart each minute. The block arrow entering the bottom of the heart represents venous return (VR), the volume of blood that is returned to the heart each minute.
Stretch receptors (SR) in the heart wall are stimulated by venous return; the solid arrow between VR and SR represents this direct relationship. Sensory neurons send this information to the brain via the glossopharyngeal (GP) nerve, a stimulatory nerve represented by the solid line. The brain responds by sending stimulatory signals--solid line--back to the heart via the cardiac nerves (CN). This stimulatory nerve (solid line) innervates the pacemaker region that controls heart rate (HR) and the ventricles which are responsible for contractility (C).
The pacemaker (HR) of the heart has 'dual innervation.' This means that it is innervated by both stimulatory and inhibitory nerves. The vagus nerve (VN) is an inhibitory nerve as indicated by the dashed arrow. It originates in the brain and its signals reduce the heart rate (HR).
Contractility (C) has to do with the force of contraction that is due to the availability of calcium ions; more calcium ions cause a greater force of contraction. The neurotransmitter from the cardiac nerves causes more calcium to be available for cells in the ventricles.(See tutorial on 'Cardiac Contractile Cells'.)
The heart does not fully empty with each contraction but more forceful contractions do eject more blood (i.e., stroke volume, SV). Accordingly, less blood is left behind; this remaining volume is called the (end systolic volume, ESV). Systole means 'contraction.' The dashed arrow from C to ESV represents this inverse relationship; greater contractility results in reduced end systolic volume. Likewise, the dashed arrow from ESV to SV represents the inverse relationship between these two factors; greater end systolic volume means less was ejected--stroke volume.
End diastolic volume (EDV)--'diastole' means relaxation-- is the volume of blood in the heart the instant before contraction. If the heart rate is slow there is more time for filling and the EDV of each contraction will be greater. Also, if the venous return (VR) is increased there will be more blood entering the heart prior to each contraction. The direct relationship between VR and EDV is represented by the solid arrow--greater venous return (VR) will lead to greater end diastolic volume (EDV).
Starling's Law of the Heart states, "the more the heart muscle is stretched when it is filling (greater EDV), the more forcefully it will contract".--ejecting more blood (SV). In the model, the direct relationship between end diastolic volume (EDV) and stroke volume (SV) is shown by the solid arrow. Venous return (VR) and end diastolic volume (EDV) are also directly related as indicated by the solid arrow.
The two factors that control cardiac output (CO) are stroke volume (SV) and heart rate (HR). Both relationships are direct (solid arrows); an increase in either, or both, will increase cardiac output.
Two factors also control stroke volume; end diastolic volume (EDV) and end systolic volume (ESV). The first relationship is direct (solid arrow) and the second is inverse (dashed arrow.) End diastolic volume (EDV) increases when venous return (VR) increases--a direct relationship (solid arrow). However, end systolic volume (ESV) is inversely related (dashed arrow) to the availability of calcium ions--contractility (C). This will be discussed in the tutorial on 'Neural Controls.'
High upstream blood pressure (BP) not only causes the forward movement of blood (flow arrow) but also presses outward on the vessel walls. This force is called hydrostatic pressure (HP) (HP block arrow). The great arteries are elastic and stretch (dashed outline of vessel) under this high blood pressure. However, they then recoil (RC block arrow) and prevent pressure from dropping too much.
Blood pressure drops as it flows through vessels. The drop is due to the work done in stretching the vessels and frictional drag on the vessel walls (not shown here). The drop in pressure is important because blood moves (i.e., flows) along a pressure gradient, that is, from high pressure to lower pressure. The gradient is represented by the difference in the size of the BP acronyms at the two ends of the flow arrow.
With the decrease in pressure due to the forward flow of blood, the previously stretched elastic walls of these vessels recoil (RC block arrow). This returns the vessel to its original diameter (solid vessel outline). This recoil helps counteract the drop in blood pressure and acts as a 'squeeze' to assist continued blood flow (block flow arrow entering next vessel).
A carotid sinus (CS) is located in the walls of the carotid arteries. It contains stimulatory neurons (solid line) that increase their signals to the brain as blood pressure increases. The relationship between carotid blood pressure (BP) and activation of the carotid sinus (CS) is direct (solid line).
Blood flow is directly affected by the pressure gradient and inversely affected by the peripheral resistance. The muscular arterioles are the primary sites where peripheral resistance (PR), which affects blood pressure, is regulated.
Flow, driven by a pressure gradient, is depicted as the labeled block arrow between a large 'BP' and a smaller 'BP'. If the downstream blood pressure increases the gradient will be reduced and flow will decrease. The dashed arrow pointing back to the flow arrow shows this inverse relationship. Decreased flow into this vessel will 'back up' blood in feeder vessels and increase 'upstream' pressure. This inverse relationship is shown by the dashed arrow pointing from the flow arrow to the larger 'BP' acronym.
The diameter of a vessel is the determining factor in how rapidly the pressure will drop as well as how easily blood will flow. As blood is flowing through a vessel some of the blood is in direct contact with the vessel's wall and loses energy through friction. This concept is referred to as peripheral resistance (PR). The energy loss decreases the blood pressure as flow continues through the vessel.
In a small diameter vessel, a large proportion of the blood would experience this resistance and the pressure drop would be great; in a large diameter vessel, a small proportion of blood would experience resistance and the pressure drop would be small. In other words, small diameter vessels offer high resistance and large diameter vessels offer low resistance. This causes an inverse relationship between peripheral resistance and the downstream blood pressure shown by the dashed arrow in the map.
Arterioles are the primary type of vessels whose diameter is highly variable. This is accomplished by changing the degree of contraction of the abundant circular smooth muscles in their walls. The greater the degree of vasoconstriction (VCN) --the smaller their diameter--the greater the peripheral resistance encountered by blood flowing through them. This is shown as the solid arrow (direct relationship) between VCN and PR.
The sympathetic division of the autonomic nervous system can exert generalized control of most arterioles in the body. This is accomplished by wide-ranging vasomotor nerves (VM) that secrete norepinephrine and cause vasoconstriction. These stimulatory nerves are shown as a solid line.
Individual arterioles are also responsive to 'local controls' such as the concentration of oxygen (O2) and carbon dioxide (CO2) in the interstitial fluid surrounding them. The relationship between oxygen concentration and the extent of vasoconstriction is direct (solid arrow)--the greater the oxygen (O2)concentration the greater the extent of vasoconstriction (VCN). In other words, if there is sufficient oxygen in the tissue then the blood flow--which would bring in more oxygen--is reduced. Also, the relationship between carbon dioxide (a waste product of cellular activity) concentration and vasoconstriction is inverse (dashed arrow); the greater the carbon dioxide (CO2) concentration the less the extent of vasoconstriction (VCN). In other words, if there is a lot of carbon dioxide in the tissue a greater blood flow is needed to allow its diffusion into, and removal by, the blood.
Capillaries are the sites of diffusion of respiratory gases--among other things-- between the blood and interstitial fluid. Interstitial fluid in active tissues becomes oxygen poor and carbon dioxide rich; the reverse is true of inactive tissues. Also, fluid shifts, due to an interplay between hydrostatic and osmotic pressures, play a major role in water balance.
Capillaries are not always open; flow through them is controlled by precapillary sphincters shown as a donut in the map. The relationship between vasoconstriction and flow is inverse (dashed arrow); an increase in vasoconstriction causes a decrease in flow into the capillary.
Vasoconstriction is under the control of carbon dioxide (CO2) and oxygen (O2) in the surrounding interstitial fluid. The relationship between carbon dioxide concentration and vasoconstriction is inverse (dashed arrow). An increase in carbon dioxide (CO2) causes a decrease in vasoconstriction (VCN). The reverse is true for oxygen concentration; the relationship is direct (solid arrow). An increase in oxygen (O2) causes an increase in vasoconstriction (VCN).
When blood enters porous capillaries, hydrostatic pressure (HP) forces fluid (HP block arrow) into the interstitial space leaving larger plasma proteins (PP) in the vessel. This direct relationship is shown by a solid arrow pointing from the HP block arrow to PP in the capillary. If hydrostatic pressure was the only force at work, the interstitial fluid would become increasingly dilute and the volume of plasma would decrease while becoming increasingly concentrated.
The force that prevents this from happening is called osmotic pressure (OP). A clear understanding of diffusion is necessary to understand how this force works.
If a substance is concentrated in one place it will tend to 'spread out' into adjacent regions where it is less abundant. This is because of its random motion. Eventually, the concentration of the substance will be uniform throughout the region. While it is 'spreading out' it is said to be diffusing. Once the concentration is uniform throughout random motion is still occurring but diffusion is not.
Blood flows through capillaries passing through oxygen poor tissues; oxygen diffuses from the blood into the interstitial fluid (block arrow labeled D). Oxygen poor tissues have a high concentration of carbon dioxide; carbon dioxide diffuses from this fluid into the blood (block arrow labeled D).
If the substance under consideration happens to be water it will behave just like any other substance. It will spread out (i.e., diffuse), along its gradient, away from a place where it is highly concentrated into adjacent regions where it is less abundant. This will continue until the concentration of water is uniform throughout the region. Because water is so abundant and its diffusion is so critical to life the diffusion of water is given a special name...osmosis.
Increasing plasma proteins (PP) in the capillaries means there is a shortage of water there; water was forced out by hydrostatic pressure. A water gradient now exists between these two adjacent fluid compartments and is symbolized by the solid arrow pointing from PP to the OP block arrow. Accordingly, water will diffuse--osmosis-- back into the capillaries. This return of water prevents a significant decrease in blood volume or pressure indicated by the OP block arrow pointing to the blood pressure acronym, BP. It is helpful to think of osmotic pressure (OP) as the re-established blood pressure due to this return of water to the blood.
Veins return blood to the heart. Over the course of a minute this volume is called the venous return (VR). By the time blood has reached the veins its pressure has been reduced to practically nothing. Because blood flows along its pressure gradient there are several mechanisms that assist the flow.
Veins are compliant (COM), that is, they stretch when filling with blood but, unlike elastic arteries, recoil is minimal. Compliance (COM) is shown as the dashed outline around the vein. The stretch is caused by the hydrostatic pressure ( HP block arrow) resulting from blood pressure (BP) entering veins.
Compliant vessels (COM) have large diameters which means they have low peripheral resistance (PR). This inverse relationship is shown by the dashed arrow between these two factors. Also, low peripheral resistance is inversely related to flow as indicated by the dashed arrow.
High compliance favors flow by providing little loss of pressure due to friction; the peripheral resistance is small. However, compliance simultaneously does not favor flow because the pressure gradient--flow arrow between the two BP acronyms--is kept small. In other words, since less energy is lost to friction, the pressure at the downstream end of the vessel will not have dropped much.
Many veins have one way valves that prevent the backflow of blood; a handy mechanism especially in light of the low pressure gradient in veins. These are not shown on the model.
Deep veins pass between skeletal muscles in the extremities. Contraction of these muscles (Csm) presses on the veins causing forward movement of blood through the one way valves. This is shown by the solid arrow (direct relationship) between Csm (i.e., contraction of skeletal muscles) and venous return (VR).
During inhalation, the pressure in the pleural cavities decreases causing the lungs to expand. The veins entering the heart are affected by this pressure drop in the same manner as the lungs; they expand. This pressure drop, due to decreased pleural pressure (Pp) at the end of the great veins, decreases blood pressure (BP) at this location. This direct relationship is shown by the solid arrow between these two factors. The term 'thoracic pump' is often applied to this phenomenon.
The medullary vascular centers work in tandem to regulate generalized peripheral resistance. Peripheral resistance, by impeding flow, increases upstream blood pressure in elastic arteries.
Vasoconstrictor (VC) centers are located in the medulla of the brain stem. They are associated with the sympathetic nervous system. Neural pathways travel through the spinal cord to synapse with vasomotor nerves (VM)-- solid lines are stimulatory nerves--leading to muscular arteries throughout the body.
The vasoconstrictor centers maintain a baseline muscle tone (i.e., VCN) in these vessels. If this neural control ceased the precipitous drop in blood pressure would be life threatening. Likewise, if this stimulation was suddenly increased the rapid rise in blood pressure would also be life threatening. Blood pressure must be monitored to prevent either extreme. Follow the interactions that begin with high arterial blood pressure.
A carotid sinus (CS) is located at the bifurcation of each carotid artery. The carotid sinus is stimulated by increasing blood pressure (BP); this direct relationship is indicated by the solid arrow between BP and CS. Neurons travel to the brain travel in the glossopharyngeal nerve (GP); this nerve stimulates the vasodilator center (VD).
The vasodilator center (VD) sends inhibitory signals to the vasoconstrictor center as represented by the dashed line. The vasoconstrictor center (VC) communicates with muscular arteries throughout the body via stimulatory vasomotor (VM) nerves shown as a solid line. The overall result of increased vasodilator activity, by inhibiting the vasoconstrictor center, is generalized vasodilation throughout the body.
Vasodilation is the same as low vasoconstriction. Low vasoconstriction (VCN)--resulting in large diameter vessels--causes low peripheral resistance (PR)--a direct relationship (solid arrow)--throughout the arterioles. Generalized low peripheral resistance (PR) drops the blood pressure (BP) within the arterioles-- a direct relationship indicated by the solid arrow.
Consider the flow of blood from the arteries into the dilated arterioles as shown at the top of the map. The reduced blood pressure (BP) in the arterioles favors flow into them-- an inverse relationship (dashed arrow). This increased flow will decrease the upstream blood pressure (BP)--another inverse relationship (dashed arrow). The increase in flow from the arteries will reduce arterial blood pressure (BP)
The cardioinhibitor and cardioaccelerator centers in the medulla control the heart rate and the force of contraction. These centers are regulated by signals from the carotid sinus as well as from stretch receptors in the heart. Follow the interactions beginning with increased arterial blood pressure.
The carotid sinus (CS) is stimulated as blood pressure (BP) increases --a direct relationship (solid arrow). Stimulatory impulses (solid line) from the sinus lead to the cardioinhibitor centers (CI). This center sends simultaneous inhibitory signals (dashed lines) to two locations: to the pacemaker (heart rate (HR)) via the vagus nerve (V) and to the medullary cardioaccelerator center (CA).
Notice that the pacemaker (HR) has dual innervation. It has inhibitory neurons (dashed line) from the cardioinhibitor center (CI) via the vagus nerve(V). It also has stimulatory neurons (solid line) from the cardioaccelerator center (CA)via the cardiac nerves (CN).
Simultaneous stimulation does indeed occur but they do not rise and fall together; this could stop the heart! Instead, as the carotid sinus (CS) increases heart rate (HR) it simultaneously decreases impulses from the cardioaccelerator center (CA). When the cardioinhibitor center is decreasing heart rate it is also decreasing the ability of the cardioaccelerator center to increase heart rate!
Decreased heart rate leads to deceased cardiac output which then leads to decreased arterial blood pressure. We've returned to the beginning where arterial blood pressure was increasing-- negative feedback, homeostasis at work.
Stimulatory neurons (solid lines) simultaneously increase the heart rate (HR) and the contractility (C). The neurons involved run from the cardioaccelerator center (CA) via the cardiac nerves (CN) .
The number of cross-bridges that can form within myofilaments in cardiac contractile cells is dependent on the concentration of calcium ions. About 80% of cytoplasmic calcium is pumped into the sarcoplasmic reticulum between each contraction. The actual amount stored is increased by allowing more calcium into the cell from the interstitial fluid. (This is discussed in detail in the 'Cardiac Contractile Cell Tutorial'.) The end effect is that increased contractility (C) empties the heart more completely leaving less residual blood-- end systolic volume (ESV) behind.
Increased venous return (VR) stretches the heart causing stretch receptors to send stimulatory signals to the cardioaccelerator center (CA) via the glossopharyngeal nerve (GP) (solid line). This results in increased activity of this center resulting in increased heart rate and force of contraction (contractility).