coronary anatomy and blood flow

8/12/2019 Coronary Anatomy and Blood Flow

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of a major organ (10-13 ml/100 ml). In non-diseased coronary vessels, whenever cardiac

activity and oxygen consumption increases, there is an increase in coronary blood flow

(active hyperemia)that is nearly proportionate to the increase in oxygen consumption.

Goodautoregulationbetween 60 and 200 mmHg perfusion pressure helps to maintain

normal coronary blood flow whenever coronary perfusion pressure changes due to

changes in aortic pressure. Adenosineis an important mediator of active hyperemia and autoregulation. It serves as

a metabolic coupler between oxygen consumption and coronary blood flow. Nitric oxide

is also an important regulator of coronary blood flow.

Activation of sympathetic nerves innervating the coronary vasculature causes onlytransient vasoconstriction mediated by1-adrenoceptors. This brief (and small)

vasoconstrictor response is followed by vasodilation caused by enhanced production of

vasodilator metabolites(active hyperemia)due to increased mechanical and metabolic

activity of the heart resulting from1-adrenoceptoractivation of the myocardium.Therefore, sympathetic activation to the heart results in coronary vasodilation and

increased coronary flow due to increased metabolic activity (increased heart rate,

contractility) despite direct vasoconstrictor effects of sympathetic activation on thecoronaries. This is termed "functional sympatholysis."

Parasympathetic stimulation of the heart(i.e., vagal nerve activation) elicits modest

coronary vasodilation (due to the direct effects of released acetylcholine on the

coronaries). However, if parasympathetic activation of the heart results in a significantdecrease inmyocardial oxygen demanddue to a reduction in heart rate, then intrinsic

metabolic mechanismswill increase coronary vascular resistance by constricting the

vessels.

Progressive ischemic coronary artery disease results in the growth of new vessels (termed

angiogenesis) andcollateralizationwithin the myocardium. Collateralization increases

myocardial blood supply by increasing the number of parallel vessels, thereby reducing

vascular resistance within the myocardium.
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Extravascular compression (shown to the right) during systole markedly affects coronary

flow; therefore, most of the coronary flow occurs during diastole. Because of

extravascular compression, the endocardium is more susceptible toischemiaespecially atlower perfusion pressures. Furthermore, with tachycardia there is relatively less time

available for coronary flow during diastole to occurthis is particularly significant in

patients with coronary artery disease wherecoronary flow reserve(maximal flowcapacity) is reduced.

In the presence ofcoronary artery disease,coronary blood flow may be reduced. This willincreaseoxygen extractionfrom the coronary blood and decrease the venous oxygen content.

This leads to tissuehypoxiaandangina.If the lack of blood flow is due to a fixedstenotic lesion

in the coronary artery (because of atherosclerosis), blood flow can be improved within that

vessel by 1) placing a stent within the vessel to expand the lumen, 2) using an intracoronaryangioplasty balloon to stretch the vessel open, or 3) bypassing the diseased vessel with a vascular

graft. If the insufficient blood flow is caused by a blood clot (thrombosis), a thrombolytic drug

that dissolves clots may be administered. Anti-platelet drugs and aspirin are commonly used to

prevent the reoccurrence of clots. If the reduced flow is due to coronaryvasospasm,thencoronary vasodilators can be given (e.g.,nitrodilators,calcium-channel blockers)to reverse and

prevent vasospasm.

Coronary circulationis the circulation of blood in theblood vesselsof theheartmuscle

(myocardium). The vessels that deliver oxygen-rich blood to the myocardium are known as

coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle areknown as cardiac veins. These include thegreat cardiac vein,themiddle cardiac vein,thesmall

cardiac veinand theanterior cardiac veins.

As the left and right coronary arteries run on the surface of the heart, they can be called

epicardial coronary arteries. These arteries, when healthy, are capable of autoregulation tomaintain coronary blood flow at levels appropriate to the needs of theheart muscle.Theserelatively narrow vessels are commonly affected byatherosclerosisand can become blocked,

causinganginaor aheart attack.(See also:circulatory system.) The coronary arteries that run

deep within the myocardium are referred to as subendocardial.

The coronary arteries are classified as "end circulation", since they represent the only source of

blood supply to the myocardium; there is very little redundant blood supply, which is whyblockage of these vessels can be so critical.

Contents

1 Structure

o 1.1 Anastomoses

o 1.2 Variation

1.2.1 Coronary artery dominance

2 Function

o 2.1 Supply to papillary muscles

o 2.2 Changes in diastole
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o 2.3 Changes in oxygen demand

3 See also

4 Additional images

5 References

Structure

Schematic diagram of the coronary arteries and veins.

Schematic view of the heart
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An anteriorleft coronary artery.

Base and diaphragmatic surface of heart.

The two coronary arteries originate from the left side of the heart at the beginning (root) of the

aorta,just after the aorta exits theleft ventricle.Theleft coronary arteryoriginates from the left

aortic sinus,while theright coronary arteryoriginates from the right aortic sinus. No artery arisesfrom the posterior aortic sinus.
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Anastomoses

Cast of coronary arteries (right = yellow, left = red)

There are some anastomoses between branches of the two coronary arteries. However thecoronary arteries are functionally end arteries and so these meetings are referred to as anatomical

anastamoses,which lack function, as opposed to functional or physiological anastomoses like

that in the palm of the hand. This is as blockage of one coronary artery generally results in death

of the heart tissue due to lack of sufficient blood supply from the other branch. When twoarteries or their branches join, the area of the myocardium receives dual blood supply. These

junctions are called anastomoses. If one coronary artery is obstructed by anatheroma,the secondartery is still able to supply oxygenated blood to the myocardium. However this can only occur ifthe atheroma progresses slowly, giving the anastomoses a chance to proliferate. Under the most

common configuration of coronary arteries, there are three areas of anastomoses. Small branches

of the LAD (left anterior descending/anterior interventricular) branch of the left coronary joinwith branches of the posterior interventricular branch of the right coronary in the interventricular

groove. More superiorly, there is an anastomosis between the circumflex artery (a branch of the

left coronary artery) and the right coronary artery in the atrioventricular groove. There is also an

anastomosis between the septal branches of the two coronary arteries in the interventricular

septum. The photograph shows area of heart supplied by the right and the left coronary arteries.

Variation

The left and right coronary arteries occasionally arise by a common trunk, or their number may

be increased to three; the additional branch being the posterior coronary artery (which is smallerin size). In rare cases, a person will have the third coronary artery run around the root of the

aorta.
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Occasionally, a coronary artery will exist as a double structure (i.e. there are two arteries, parallel

to each other, where ordinarily there would be one).

Coronary artery dominance

The artery that supplies theposterior descending artery(PDA)[1]

determines the coronarydominance.

[2]

If the posterior descending artery is supplied by theright coronary artery(RCA), then the

coronary circulation can be classified as "right-dominant".

If the posterior descending artery is supplied by thecircumflex artery(CX), a branch of the left

artery, then the coronary circulation can be classified as "left-dominant".

If the posterior descending artery is supplied by both the right coronary artery and the

circumflex artery, then the coronary circulation can be classified as "co-dominant".

Approximately 70% of the general population are right-dominant, 20% are co-dominant, and

10% are left-dominant.

[2]

A precise anatomic definition of dominance would be the artery whichgives off supply to the AV node i.e. the AV nodal artery. Most of the time this is the rightcoronary artery.

Function

Supply to papillary muscles

Thepapillary musclesattach themitral valve(the valve between theleft atriumand theleft

ventricle)and thetricuspid valve(the valve between theright atriumand theright ventricle)to

the wall of the heart. If the papillary muscles are not functioning properly, the mitral valve may

leak during contraction of the left ventricle. This causes some of the blood to travel "in reverse",from the left ventricle to the left atrium, instead of forward to the aorta and the rest of the body.

This leaking of blood to the left atrium is known asmitral regurgitation.Similarly, the leaking of

blood from the right ventricle through the tricuspid valve and into the right atrium can alsooccur, and this is described astricuspid insufficiencyor tricuspid regurgitation.

The anterolateral papillary muscle more frequently receives two blood supplies:left anteriordescending(LAD) artery and theleft circumflex artery(LCX).

[3]It is therefore more frequently

resistant to coronaryischemia(insufficiency of oxygen-rich blood). On the other hand, the

posteromedial papillary muscle is usually supplied only by the PDA.[3]

This makes the

posteromedial papillary muscle significantly more susceptible to ischemia. The clinicalsignificance of this is that amyocardial infarctioninvolving the PDA is more likely to cause

mitral regurgitation.

Changes in diastole

During contraction of theventricularmyocardium (systole), the subendocardial coronary vessels(the vessels that enter the myocardium) are compressed due to the high intraventricular

pressures. However, the epicardial coronary vessels (the vessels that run along the outer surface
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of the heart) remain patent. Because of this, blood flow in the subendocardium stops. As a result

most myocardial perfusion occurs during heart relaxation (diastole)when the subendocardial

coronary vessels are patent and under low pressure. Flow never comes to zero in the rightcoronary artery, since the right ventricular pressure is less than the left ventricular pressure.

Changes in oxygen demand

The heart regulates the amount ofvasodilationor vasoconstriction of the coronary arteries based

upon the oxygen requirements of the heart. This contributes to the filling difficulties of thecoronary arteries. Compression remains the same. Failure of oxygen delivery caused by a

decrease in blood flow in front of increased oxygen demand of the heart results in tissue

ischemia, a condition of oxygen deficiency. Brief ischemia is associated with intense chest pain,known asangina.Severe ischemia can cause the heart muscle to die from hypoxia, such as

during amyocardial infarction.Chronic moderate ischemia causes contraction of the heart to

weaken, known as myocardial hibernation.

In addition to metabolism, the coronary circulation possesses unique pharmacologiccharacteristics. Prominent among these is its reactivity to adrenergic stimulation. The majority of

vasculature in the body constricts tonorepinephrine,a sympathetic neurotransmitter the bodyuses to increase blood pressure. In the coronary circulation, norepinephrine elicits

vasoconstriction, due to the predominance of beta-adrenergic receptors in the coronary

circulation, however metabolic control factors will increase as a result of increased oxygendemand in the heart and will more greatly influence vasodilation. Thus sympathetic innervation

to the coronary arteries ultimately causes vasodilation.

Cerebral circulation

From Wikipedia, the free encyclopedia

Cerebral circulationis the movement ofbloodthrough the network ofblood vesselssupplyingthebrain.Thearteriesdeliver oxygenated blood,glucoseand other nutrients to the brain and theveinscarry deoxygenated blood back to theheart,removingcarbon dioxide,lactic acid,and

other metabolic products. Since the brain is very vulnerable to compromises in its blood supply,

the cerebral circulatory system has many safeguards. Failure of these safeguards results incerebrovascular accidents,commonly known asstrokes. The amount of blood that the cerebral

circulation carries is known ascerebral blood flow.The presence of gravitational fields or

accelerations also determine variations in the movement and distribution of blood in the brain,

such as when suspended upside-down.

The following description is based on idealized human cerebral circulation. The pattern of

circulation and itsnomenclaturevary between organisms.

Contents

1 Arterial cerebral circulation
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o 1.1 Anterior cerebral circulation

o 1.2 Posterior cerebral circulation

2 Cerebral venous drainage

3 See also

4 External links

Arterial cerebral circulation

Artery: Cerebral circulation

Schematic representation of the Circle of Willis,arteriesof

thebrainandbrain stem.

Gray's p.574
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Cortical areas and their arterial blood supply

The arterial cerebral circulation is normally divided into anterior cerebral circulation andposterior cerebral circulation. There are two main pairs ofarteriesthat supply thecerebral

arteriesand thecerebrum:Internal carotid arteriesandvertebral arteries.

The anterior and posterior cerebral circulations are interconnected via bilateralposterior

communicating arteries.They are part of theCircle of Willis,which provides backup circulation

to the brain. In case one of the supply arteries is occluded, the Circle of Willis provides

interconnections between the anterior and the posterior cerebral circulation along the floor of thecerebral vault, providing blood to tissues that would otherwise becomeischemic.

Anterior cerebral circulation

The anterior cerebral circulationis the blood supply to the anterior portion of the brain. It is

supplied by the following arteries:

Internal carotid arteries:These large arteries are the left and right branches of thecommon

carotid arteriesin the neck which enter the skull, as opposed to theexternal carotidbranches
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which supply the facial tissues. The internal carotid artery branches into theanterior cerebral

arteryand continues to form themiddle cerebral artery

Anterior cerebral artery(ACA)

o Anterior communicating artery:Connects both anterior cerebral arteries, within and

along the floor of the cerebral vault.

Middle cerebral artery(MCA)

Posterior cerebral circulation

The posterior cerebral circulationis the blood supply to the posterior portion of the brain,including theoccipital lobes,cerebellumandbrainstem.It is supplied by the following arteries:

Vertebral arteries:These smaller arteries branch from thesubclavian arterieswhich primarily

supply the shoulders, lateral chest and arms. Within thecraniumthe two vertebral arteries fuse

into thebasilar artery.

o Posterior inferior cerebellar artery(PICA)

Basilar artery:Supplies themidbrain,cerebellum,and usually branches into theposterior

cerebral artery

o Anterior inferior cerebellar artery(AICA)

o Pontine branches

o

Superior cerebellar artery(SCA)

Posterior cerebral artery(PCA)

Posterior communicating artery

Cerebral venous drainage

Vein: Cerebral venous drainage

Dural veins

The venous drainage of the cerebrum can be separated into two subdivisions: superficial anddeep.
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The superficial system is composed ofdural venous sinuses,which have wall composed of dura

mater as opposed to a traditional vein. The dural sinuses are, therefore located on the surface of

the cerebrum. The most prominent of these sinuses is thesuperior sagittal sinuswhich flows inthe sagittal plane under the midline of the cerebral vault, posteriorly and inferiorly to thetorcula,

forming theconfluence of sinuses,where the superficial drainage joins with the sinus that

primarily drains the deep venous system. From here, twotransverse sinusesbifurcate and travellaterally and inferiorly in an S-shaped curve that form thesigmoid sinuseswhich go on to formthe twojugular veins.In the neck, thejugular veinsparallel the upward course of thecarotid

arteriesand drain blood into thesuperior vena cava.

The deep venous drainage is primarily composed of traditional veins inside the deep structures of

the brain, which join behind the midbrain to form thevein of Galen.This vein merges with the

inferior sagittal sinusto form thestraight sinuswhich then joins the superficial venous systemmentioned above at theconfluence of sinuses.

Placental Blood CirculationThe placenta is a unique vascular organ that receives blood supplies from both the maternal andthe fetal systems and thus has two separate circulatory systems for blood: (1) the maternal-

placental (uteroplacental) blood circulation, and (2) the fetal-placental (fetoplacental) blood

circulation. The uteroplacental circulation starts with the maternal blood flow into theintervillous space through decidual spiral arteries. Exchange of oxygen and nutrients take place

as the maternal blood flows around terminal villi in the intervillous space. The in-flowing

maternal arterial blood pushes deoxygenated blood into the endometrial and then uterine veins

back to the maternal circulation. The fetal-placental circulation allows the umbilical arteries tocarry deoxygenated and nutrient-depleted fetal blood from the fetus to the villous core fetal

vessels. After the exchange of oxygen and nutrients, the umbilical vein carries fresh oxygenatedand nutrient-rich blood circulating back to the fetal systemic circulation. At term, maternal bloodflow to the placenta is approximately 600700 ml/minute. It is estimated that the surface area of

syncytiotrophoblasts is approximately 12m2[1]and the length of fetal capillaries of a fully

developed placenta is approximately 320 kilometers at term [2,3]. The functional unit ofmaternal-fetal exchange of oxygen and nutrients occur in the terminal villi. No intermingling of

maternal and fetal blood occurs in the placenta.Figure 2.1illustrates (1) the relationship of the

uterus, placenta, and the fetus, and (2) the directions of blood flow from mother to the placenta

as well as fetal blood flow from the placenta to the fetus.
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Figure 2.1

An illustration of human pregnancy and directions of the placenta blood flow. The right panelshows the relationship of the uterus, placenta, and fetus during pregnancy. The left panel shows

the directions of blood flow from mother to the placenta and(more...)

Go to:

2.1. Maternal-placental blood circulation

Uteroplacental circulation is not fully established until the end of the first trimester. Although the

exact mechanism of how the uteroplacental circulation is established is not completely

understood, two theories have been proposed. The first theory is that in the first trimester,

endovascular trophoblasts migrate along the decidual spiral arteries, invade the vessel walls, andcreate a path for maternal blood to perfuse the placenta intervillous space. This theory is

supported by the presence of endovascular trophoblasts in the decidual spiral arteries of the first

trimester placenta [4,5]. The second theory proposes that trophoblasts invade decidual spiralarteries and form trophoblastic plugs. These trophoblastic plugs obstruct maternal blood flow

into the intervillous space and prevent flow until the end of first trimester of pregnancy (1012

weeks). The plugs then loosen and permit continuous maternal blood flow into the intervillousspace. This theory is based on the observations of ex vivohistologic analysis of hysterectomy

specimens of first-trimester placentas, in which plugs of trophoblasts were found either partially

or fully obstructing or filling the vessel lumen of decidual spiral arteries [6]. Although the twotheories diverge as to whether or not invading trophoblasts plug the arteries to prevent bloodflow into the intervillous space, it is clear that the genesis of uteroplacental (maternal-placental)

blood flow during the first trimester is a dynamic and progressive process.

Normal early placental development results in transformation of spiral arteries that extend fromthe decidua (the layer of tissue lining the uterus) to the muscle layer. Most textbooks provide the

classic description of the placenta circulation based on studies of second-, or third-trimesterplacentas. As shown inFigure 2.2,maternal blood enters the placenta through the basal plate

endometrial arteries (spiral arteries), perfuses intervillous spaces, and flows around the villi

where exchange of oxygen and nutrients occurs with fetal blood. It has been estimated that thereare about 120 spiral arterial entries into the intervillous space at term [7]. Maternal blood

traverses through the placenta intervillous space and drains back through venous orifices in the

basal plate, then returns the maternal systemic circulation via uterine veins. Maternal-placental

blood flow is propelled by maternal arterial pressure because of the unique nature of low-resistance uteroplacental vessels, which accommodate the massive increase in uterine perfusion

over the course of gestation [7]. During pregnancy, maternal blood volume increasesprogressively from 68 weeks of gestation and reaches a maximum approximately at 3234

weeks and then keeps relatively constant until term. In general, maternal blood (plasma) volumeis increased up to 4050% near term compared to the nonpregnant state. Gowland et al. studied

maternal blood perfusion in human placenta from 20 weeks of gestational age until term using

echo planar imaging (EPI) [8]. They found that in normal pregnancies the average perfusion ratewas about 176 24 ml/100 gram/minute.
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Figure 2.2

A schematic drawing of a section through a fullterm placenta. Upper panel: (1) The relation ofthe villous chorion (C) to the decidua basalis (D) and the fetal-placental circulation; (2) The

maternal blood flows into the intervillous spaces in(more...)

Spir al artery remodeli ng:Remodeling of the uterine arteries is a key event in early pregnancy

that begins after implantation. The trophoblast differentiates into villous trophoblasts and

extravillous trophoblasts. These trophoblasts have distinct functions when in contact with

maternal tissues. Vil lous trophoblastsgive rise to the chorionic villi, the major structure ofplacental cotyledon. Chorionic villi primarily transport oxygen and nutrients between fetus and

mother. Extr avil lous tr ophoblastsmigrate into the decidua and myometrium and penetrate the

maternal vasculature. The extravillous trophoblasts can be classified as interstitial trophoblastsand endovascular trophoblasts. Interstitial trophoblasts invade the decidua and surround spiral

arteries. Endovascular trophoblasts invade spiral arteries. In the uterine spiral arteries,

endovascular trophoblasts interdigitate between the endothelial cells, replacing the endotheliallining and most of the musculoelastic tissue in the vessel walls, thereby creating a high-flow,

low-resistance placental circulation. High flow and low resistance is the description usually

given for the normal uteroplacental vasculature as a result of physiological remodeling of

decidual spiral arteries.Figure 2.3illustrates the process of spiral artery remodeling during

pregnancy.

Figure 2.3

The process of spiral artery remodeling during pregnancy. In early pregnancy, two types of

extravillous trophoblasts are found outside the villous, endovascular and interstitial trophoblasts.

Endovascular trophoblasts invade and transform spiral arteries(more...)

Placental blood flow is increased throughout pregnancy. The volume of placental blood flow isabout 600700 ml/minute (80% of the uterine perfusion) at term. Steep falls in the pressure occur

in the transition from uterine arteries to intervillous spaces. The pressure is about 80100 mmHg

in uterine arteries, 70 mmHg in spiral arteries, and only 10 mmHg within intervillous space. Thelow-resistance of uteroplacental vessels and the gradient of blood pressure between uterinearteries and placental intervillous space allow the maternal blood to perfuse the intervillous space

efficiently and effectively. The blood in the intervillous space is therefore completely exchanged

two to three times per minute. In general, the spiral arteries are perpendicular to the uterine wall,
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while the veins are parallel to the uterine wall. This arrangement facilitates closure of the veins

during uterine contractions and prevents squeezing of maternal blood from the intervillous space.

Go to:

2.2. Fetal-placental circulation

Umbil ical cord:The umbilical cord is the lifeline that attaches the placenta to the fetus. Duringprenatal development, the umbilical cord comes from the same zygote as the fetus. The umbilical

cord in a full-term human neonate averages ~5070 centimeters (20 inches) long and ~2centimeters (0.75 inches) in diameter. It extends from the fetal umbilicus to the fetal surface of

the placenta or chorionic plates. The cord is not directly connected to the mothers circulatory

system. Instead it joins the placenta, which transfers materials to and from the mothers blood

without allowing direct mixing. The umbilical cord contains one vein (the umbilical vein) andtwo arteries (the umbilical arteries) buried within Whartons jelly. The umbilical vein carries

oxygenated, nutrient-rich blood from the placenta to the fetus, and the umbilical arteries carry

deoxygenated, nutrient-depleted blood from the fetus to the placenta (Figure 2.2). Anyimpairment in blood flow within the cord can be a catastrophic event for the fetus.

Umbilical vessels are sensitive to various vasoactivators, such as serotonin, angiotensin II, andoxytocin. The contractility of smooth muscles in vessel walls is also influenced by substances

produced by the neighboring endothelial cells in a paracrine manner [9]. Umbilical cord vessels

produce several potent vasodilators. For example, an in vitrostudy has shown that the

endothelium from umbilical vein (HUVECs) produces far more prostaglandins than theendothelium from umbilical arteries (HUAECs) [10]. Interestingly, the synthesis and production

of prostacyclin (PGI2) and PGE2are significantly less by HUVECs from smoking and diabetic

pregnant women than in normal pregnant women [11]. Both PGI2and PGE2are potent

vasodilators and inhibitors for platelet aggregation. Nitric oxide (NO) and atrial natriureticpeptide (ANP) are also present in umbilical vessels. Giles et al. studied the correlation of nitric

oxide synthase (NOS) activity in placentas with Doppler ultrasound umbilical artery flow

velocity wave-forms. They found that placentas from women with abnormal umbilical arteryflow velocity waveforms showed significantly lower mean NOS activity than did placentas from

women with normal umbilical artery flow velocity wave-forms [12].

Placental vi ll ous capil lar ies:At the junction of umbilical cord and placenta, the umbilical

arteries branch to form chorionic arteries and traverse the fetal surface of the placenta in the

chorionic plate and branch further before they enter into the villi. The chorionic arteries are

easily recognized because they always cross over the chorionic veins. These vessels are

responsive to vasoactive substances as mentioned above. About two thirds of the chorionicarteries form networks supplying the cotyledons in apattern of disperse-type branching. The rest

of the chorionic arteries radiate to the edge of the placenta and down to a network.Figure 2.4shows the maternal and fetal surfaces of a placenta; note the disperse-type branching pattern of

fetal vessels (fetal surface) in the chorionic plate.
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Figure 2.4

Maternal and fetal surface of the placenta. Please note the pattern of disperse-type branching of

fetal vessels (fetal surface) in the chorionic plate. (Fromhttp://www.walgreens.com/marketing/library/graphics//images/en/17010.jpg). Used with

permission(more...)

Each umbilical cord artery generally provides eight or more terminal chorionic plate arteries,which are referred to as stem arteries of the peripheral trunci chorii to the fetal villous

cytyledons. The first order branches have an average length of 510 mm; the artery is an average

of 1.5 mm in diameter with the accompanying vein being about 2 mm. These truncal vesselsdivide into four to eight horizontal cotyledonary vessels of the secondary order, with an average

diameter of 1 mm. The horizontal distance varies with the size of the cotyledon, and as they

curve toward the basal plate, they begin branching into the third-order villous branches. Thereare about 3060 branches in each cotyledon, with calibers of 0.10.6 mm and lengths of 1525

mm. In the villi, the third-order villous branches form an extensive arteriocapillary venous

system, vill ous capill aries, bringing the fetal blood extremely close to the maternal blood; but nointermingling between fetal and maternal blood occurs. There are about 1528 cotyledons per

placenta.

The villous capillaries are branches of the umbilical vessels, and the capillary networks are the

functional unit of maternal-fetal exchange. The blood pressure in the umbilical arteries averagesabout 50 mmHg, and the blood flows through smaller vessels that penetrate the chorionic plate to

the capillaries in the villi where arterial blood pressure falls to 30 mmHg. In the umbilical veinthe pressure is 20 mmHg. The pressure in the fetal vessels and their villous branches is always

greater than that within the intervillous space. This protects the fetal vessels against collapse.

Assessment of fetal blood f low:Ultrasound and Doppler flow measurements provide means to

visualize the umbilical cord and to evaluate the fetal blood flow.Figure 2.5shows an example of

an ultrasound color image of umbilical cord arteries and vein. By measuring the amount offorward blood flow through the umbilical artery during both fetal systole and diastole, an overall

measure of fetal health can be obtained. In general, the more forward blood flow from the fetus

to the placenta through the umbilical artery, the healthier the fetus.Table 2.1summarizesmeasurements and vessel blood flow characteristics accessed by ultrasound and Doppler devices.The mean absolute vein blood flow is about 443 92 ml/min in normal umbilical cord between

24 and 29 weeks of gestation, and reduced absolute vein blood flow is associated with low fetal

birthweight [13]. Therefore, an assessment of fetal blood flow through the umbilical cord byultrasound color Doppler sonography has proven to be a valuable noninvasive procedure for

assessing fetal well-being during pregnancy.
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http://www.ncbi.nlm.nih.gov/books/NBK53254/

http://en.wikipedia.org/wiki/Cerebral_circulation

http://www.netterimages.com/image/21426.htm

Switching over at birth Circulatory system situation

Circulatory system situationQuiz

Quiz 08

At time of birth, two events are responsible for the functional adaptation

of the body to postnatal life:

Disruption of the placental circulation system

Unfolding of the lungs with the first breaths

The supply of blood from the placenta via the venous duct into thebaby's body is disrupted with the cutting through of the umbilical cord.

Thereby the blood supply in the right cardiac atrium is decreased and

the pressure in the right atrium is reduced. At the same time, through the

first couple of breaths of the newborn, the pressure in the smallcirculatory system is massively attenuated (compareDilation of the

muscular arteries of the small circulation system). The result of thesepressure changesin the body is a reduction of the blood flow via thearterial duct and through the foramen ovale and an increase of the blood

flow through the lungs. The reflex closure of the arterial ductafter the

first breaths of the newborn and the elevation of the pressure in the large

circulation system are subsidiary mechanisms.With the cutting of the umbilical cord, the placental low pressurearea

falls away.

Quiz

Quiz 15

Circulation system before / after birth Navigation
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Circulation

system at the

end of the

pregnancy

Circulation

system after

birth

Immediately after birth the newborn must begin to breathe regularly. The first breaths are

difficult because the lungs are still filled with fluid (ca. 50 ml) and at birth the alveoli are

collapsed. Half (50%)of this fluid is resorbed via the lymph vessels, a quarteris pressed outby the birth process (not true in births by caesarian section) and the rest gets into the blood

circulation system via the capillaries. The pulmonary alveoli unfold with the first breaths.

This process is supported by the presence of the surfactantthat reduces the tension of thealveolar surface.

Blood Circulation in the Fetus andNewborn

How does the fetal circulatory system work?
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During pregnancy, the fetal circulatory system works differently than after birth:

The fetus is connected by the umbilical cord to the placenta, the organ that develops

and implants in the mother's uterus during pregnancy.

Through the blood vessels in the umbilical cord, the fetus receives all the necessarynutrition, oxygen, and life support from the mother through the placenta.

Waste products and carbon dioxide from the fetus are sent back through the umbilical

cord and placenta to the mother's circulation to be eliminated.

Click to Enlarge

The fetal circulatory system uses two right to left shunts, which are small passages that directblood that needs to be oxygenated. The purpose of these shunts is to bypass certain body

partsin particular, the lungs and liverthat are not fully developed while the fetus is still in

the womb. The shunts that bypass the lungs are called the foramen ovale, which moves bloodfrom the right atrium of the heart to the left atrium, and the ductus arteriosus, which moves

blood from the pulmonary artery to the aorta.

Oxygen and nutrients from the mother's blood are transferred across the placenta to the fetus.

The enriched blood flows through the umbilical cord to the liver and splits into three

branches. The blood then reaches the inferior vena cava, a major vein connected to the heart.Most of this blood is sent through the ductus venosus, also a shunt that passes highly

oxygenated blood through the liver to the inferior vena cava and then to the right atrium of the

heart. A small amount of this blood goes directly to the liver to give it the oxygen and

nutrients it needs.

Waste products from the fetal blood are transferred back across the placenta to the mother's

blood.

Inside the fetal heart:

Blood enters the right atrium, the chamber on the upper right side of the heart. When

the blood enters the right atrium, most of it flows through the foramen ovale into the
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left atrium.

Blood then passes into the left ventricle (lower chamber of the heart) and then to the

aorta, (the large artery coming from the heart).

From the aorta, blood is sent to the heart muscle itself in addition to the brain. After

circulating there, the blood returns to the right atrium of the heart through the superior

vena cava. About two thirds of the blood will pass through the foramen ovale asdescribed above, but the remaining one third will pass into the right ventricle, towardthe lungs.

In the fetus, the placenta does the work of breathing instead of the lungs. As a result,

only a small amount of the blood continues on to the lungs. Most of this blood isbypassed or shunted away from the lungs through the ductus arteriosus to the aorta.

Most of the circulation to the lower body is supplied by blood passing through the

ductus arteriosus.

This blood then enters the umbilical arteries and flows into the placenta. In theplacenta, carbon dioxide and waste products are released into the mother's circulatory

system, and oxygen and nutrients from the mother's blood are released into the fetus'

blood.

At birth, the umbilical cord is clamped and the baby no longer receives oxygen and nutrientsfrom the mother. With the first breaths of life, the lungs begin to expand. As the lungs expand,the alveoli in the lungs are cleared of fluid. An increase in the baby's blood pressure and a

significant reduction in the pulmonary pressures reduces the need for the ductus arteriosus to

shunt blood. These changes promote the closure of the shunt. These changes increase thepressure in the left atrium of the heart, which decrease the pressure in the right atrium. The

shift in pressure stimulates the foramen ovale to close.

The closure of the ductus arteriosus and foramen ovale completes the transition of fetal

circulation to newborn circulation.

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coronary anatomy and blood flow

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