Transcript Fetal circulation

Regulation of the heart and
vessel activities
Romana Šlamberová, MD PhD
Department of Normal, Pathological and
Clinical Physiology
Distribution of blood
circulation
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Total volume of blood in all vessels
(intravascular volume):
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man: 5.4 l (77 ml / kg)
woman: 4.5 l (65 ml / kg)
Distribution:
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Heart 7%
Pulmonary circulation 9%
Systemic circulation 84%
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from that veins 75%
large arteries 15%
small arteries 3%
capilaries: 7%
Resistance of blood circulation
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Total peripheral resistance:  of all paralel
restistance in the body
Actual resistance is given based on the lumen of
vessels and viscosity of blood
Percentage portion of resistance in different types of
vessels:
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large arteries 19%
small arteries 47%
capillaries 27%
veins 7%
Resistance depends not only on type of vessel, but
also on the actual situation of blood need in organs
Regulation of blood circulation
Mechanisms of regulation:
 Local
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Humoral (chemical) – O2, CO2, H+
Nervous
Enzymatic and hormonal
General
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Fast = short-term (regulate blood pressure)
Slow = long-term (regulate blood volume) – several
days
Local chemical regulatory
mechanisms
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The most obvious in the heart and the brain
Goal: autonomic regulation of resistance by
organ based on its metabolic needs
Principal: accumulation of products of
metabolism (CO2, H+, lactacid ) or
consumption of substances necessary for
proper function (O2) directly affects smooth
muscles of vessels and induce vasodilatation
Local nervous regulatory
mechanisms
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The most obvious in the skin and mucous
Goal: central regulation of blood distribution
Principal: Autonomic nervous system
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Sympaticus
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Vasoconstriction – activation of α receptors in vesselsnoradrenalin (glands, GIT, skin, mucous, kidneys, other inner organs)
Vasodilatation – activation of β receptors in vessels – adrenalin
(heart, brain, skeletal muscles)
Parasympaticus - Acetylcholin
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Vasoconstriction – heart
Vasodilatation – salivatory glands, GIT, external genitals
Local enzymatic and hormonal
regulatory mechanisms
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Kinin ↑ = vasodilatation
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Cells of GIT glands contain kallikrein – changes kininogen to
kinin → kallidin → bradykinin (vasodilatation)
Kinins are any of various structurally related polypeptides,
such as bradykinin and kallikrein, that act locally to induce
vasodilation and contraction of smooth muscle.
A role in inflammation, blood pressure control, coagulation
and pain.
Hormones of adrenal medula: adrenalin
(vasodilatation), noradrenalin (vasoconstriction)
General fast (short-term)
regulatory mechanisms (1)
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Nervous autonomic reflexes
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Baroreflex
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glomus caroticum, glomus aorticum
Afferentation: IX and X spinal nerve
Centre: medulla oblongata, nucleus tracti solitarii
Efferentation: X spinal nerve, sympatetic fibres
Effector: heart (atriums), vessels
Effect: After acute increase of blood pressure –
activation of receptors – decrease of blood pressure
(vasodilatation, decrease of effect of sympaticus)
Baroreceptor sensitivity
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The sensitivity of baroreceptor reflex
corresponds with good prognosis of life length
(lower probability of heart attack)
Depends on the
tonus of n. vagus
People with low
vagotonus have
higher incidence of
unexpected death
Association between baroreceptor
sensitivity and
hypercholesterolemia
Persons with higher level
of LDL cholesterol have
lower baroreceptor
sensitivity
Koskinen et al. 1995
General fast (short-term)
regulatory mechanisms (2)
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Receptors in the heart
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Reflex of atrial receptors – mechano- and volumoreceptors
– activated by increased blood flow through the heart
 A receptors – sensitive to ↑ of wall tension after systole of
atriums
 B receptors – sensitive to ↑ of wall tension after systole of
ventricles
Ventricular receptors – mechano- and chemical receptors activated in pathological cases
 Hypoxia of myocardium → decrease of heart rate
(Bezold-Jarisch reflex) → protection of myocardium of
larger damage
General fast (short-term)
regulatory mechanisms (3)
Humoral mechanisms
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Adrenalin – β receptors →
vasodilatation → ↓ peripheral
resistance → blood from skin and
GIT to skeletal muscles, heart and
brain → ↑ minute heart volume
Noradrenalin – α receptors →
vasoconstriction → ↑ blood
pressure
Renin-angiotensin – activated
by ↓ pressure in vas afferens
General slow (long-term)
regulatory mechanisms
Regulatory mechanisms of water and electrolytes
exchanges
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Regulation of total blood volume by kidneys
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Increase of ADH (vasopressin)
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When ↑ blood pressure → ↑ of filtration pressure in glomeruli → ↑
production of urine → ↓ volume of circulating blood → ↓ blood
pressure
↑ ADH → ↑ of the permeability of collecting ductus for the water →
water is reabsorbed → ↑ volume of circulating blood → ↑ blood
pressure
Increase of Aldosterone
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↑ aldosterone → ↑ reabsorbtion Na+ and water → ↓ volume of urine
→ ↑ volume of circulating blood → ↑ blood pressure
Intracardial regulatory
mechanisms (1)
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Frank-Starling’s law =
initial length of the fibers is
determined by the degree
of diastolic filling of the
heart, and the pressure
developed in the ventricle is
proportionate to the total
tension developed.
The developed tension
increases as the diastolic
volume increases until it
reaches a maximum, then
tends to decrease.
Ganong: Review of Medical Physiology
Intracardial regulatory
mechanisms (2)
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Inotrophy = ability of muscle
contraction and its dependency on other
factors, e.g. initial tension of muscle fiber.
Ionotropic effect of heart rhythm
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↑ heart frequency → ↑ amount of Ca2+ that
goes into heart cells → ↑ Ca2+ available for
tubules of sarkoplasmatic reticulum → ↑ Ca2+
that is freed by each contraction → ↑ strength
of contraction
Extracardial regulatory
mechanisms
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Cardiomotoric centers
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Inhibition – ncl. Ambiguus (beginning of n. vagus in
medulla oblongata)
Excitation - Th1-3 beginning of sympathetic fibres
Vasomotoric centers
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In brain stem (medulla oblongata, Pons Varoli)
In the hypothalamus (controls activity of vasomotoric
centers in brain stem)
Brain cortex – control both the hypothalamus and the
brain stem
Midbrain regions of CV control
Rostral
ventrolateral
medulla
Cardiac accelerator
center
Vasoconstrictor center
Area postrema
Nucleus tractus
solitarius
Nucleus ambiguous
Cardiac decelerator center
Caudal ventrolateral
Medulla
Fibers from this neurons project
to the vasoconstrictor area and
inhibit it
Ackermann
Cerebral chemoreceptors
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Chemoreceptors in the medulla are most sensitive to
pCO2 and pH and less sensitive to pO2
Reflex during decreased cerebral blood flow:
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increase in pCO2 and decrease in pH activates
chemoreceptors
Increase in both sympathetic and parasympathetic outflow
Increased contractility, increased total physical response,
but decreased heart rate
Intense arteriolar vasoconstriction redirects blood flow to the
brain
Sympathetic nerve activity and
arterial pressure
•Decreasing blood pressure is followed
with increasing sympathetic nerve activity
•Vasoconstriction increases blood pressure
Respiration arytmia
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Heard frequency = 72 pulses/min, = pulse interval
0.83 s
During relaxation the frequency changes based of
the respiration (RESPIRATION ARYTMIA)
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inspiration - increased frequency
expiration – decreased frequency
Bradycardia = fysiological = deep long-term
inspiration, deep forward bend and knee band =
reflex changes of vagal tonus.
Tachycardia = fysiological = swallow (decrease
of vagal tonus), change of position from lying or
sitting to standing (ORTHOSTATIC REACTION).
Orthostatic reaction
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Changes in posture from supine position to standing
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Mechanisms
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Blood pools in the veins of lower extremities
Venous return to the heart decreases, cardiac
output decreases (Frank-Starling law)
Mean arterial pressure decreases
Decreased activation of baroreceptors
Increased sympathetic outflow to the heart and
blood vessels and decreased parasympathetic
outflow
Specific circulatory systems
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Pulmonary and systemic circulation differs
in their pressure and resistence. Pressure in
pulmonary circulation is about 4 – 5 times
lower than in systemic one.
Different organs have
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Differences in vascular resistance
Differences in metabolic demands
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Local control (intrinsic)
Hormonal control (extrinsic)
Cerebral circulation
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15 % of cardiac output
Is controlled by local metabolites
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pCO2 (H+) is the most important vasodilator
CO2 diffuses to vascular cells, forms H2CO3 (H+)
Intracellular H+causes vasodilatation
Increase in blood flow, removal of excess CO2
Decrease in pO2 increases cerebral blood flow
Many vasoactive substances do not affect cerebral
circulation, do not cross the blood-brain barrier
Coronary circulation
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5 % of cardiac output
Local metabolic factors
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Hypoxia: increase in myocardial contractility – increased O2
consumption – local hypoxia
Hypoxia causes vasodilatation of the coronary arterioles –
compensatory increase in blood flow and O2 delivery
Adenosine (from ATP) causes vasodilatation
Mechanical compression of the blood vessels during
systole in the cardiac cycle – brief period of occlusion
and reduction of blood flow
Pulmonary circulation
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100% of cardiac output
Lower pressure and low resistance
Controlled by local metabolites, primarily by pO2
(bellow 70 mm Hg)
Opposite effect than in other tissue – hypoxia causes
vasoconstriction
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Mechanism – inhibition of NO production in endothelial cells
of blood vessel walls
Redistribution of blood from poorly ventilated areas to wellventilated areas
Renal circulation
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25 % of cardiac output
Renal blood flow is autoregulated
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Constant blood flow even when renal perfusion pressure
changes (80-200 mmHg)
Renal autoregulation is independent of sympathetic
innervation (transplanted kidney)
Angiotensin II – vasoconstrictor for both afferent and
efferent arterioles, but efferent arteriole is more sensitive
Prostaglandins (E2, I2 – produced locally) – vasodilatation of
both arterioles
Skeletal muscle circulation
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25 % of cardiac output
Sympathetic innervation
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At rest: activation of a1 (noradrenaline) receptors causes
vasoconstriction, increased resistance and decreased blood
flow
Activation of b2 (adrenaline) receptors causes vasodilatation
Local metabolites
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During exercise: local vasodilator – lactate, adenosine, K+
Skin circulation
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5 % of cardiac output
Dense sympathetic innervation – regulates blood flow
for regulation of body temperature
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Increase core body temperature – decrease sympathetic
tone to the smooth muscle sphincters controlling A-V
anastomoses - increase skin blood flow
Arteriovenous anastomoses – permit bypass of the
capillary vessels
Fetal circulation (1)
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The circulatory system of a
human fetus works differently
from that of born humans,
mainly because the lungs are
not in use: the fetus obtains
oxygen and nutrients from
mother through the placenta
and the umbilical cord.
Blood from the placenta is
carried by the umbilical vein.
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About half of this enters the
ductus venosus and is carried to
the inferior vena cava,
while the other half enters the
liver proper from the inferior
border of the liver.
Fetal circulation (2)
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The blood then moves to the right atrium of the heart. In the fetus, there is
an opening between the right and left atrium (the foramen ovale), and most
of the blood flows from the right into the left atrium, thus bypassing
pulmonary circulation (which aren't being used for respiration at this point
as the fetus is suspended in amniotic fluid).
The majority of blood flow is into the left ventricle from where it is pumped
through the aorta into the body.
Some of the blood moves from the aorta through the internal iliac arteries
to the umbilical arteries, and re-enters the placenta, where carbon
dioxide and other waste products from the fetus are taken up and enter the
mother's circulation.
Some of the blood from the right atrium does not enter the left atrium, but
enters the right ventricle and is pumped into the pulmonary artery.
In the fetus, there is a special connection between the pulmonary artery and
the aorta, called the ductus arteriosus, which directs most of this blood
away from the lungs.
Postnatal development of
circulation
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With the first breath after birth, the pulmonary
resistance is dramatically reduced. More blood moves
from the right atrium to the right ventricle and into the
pulmonary arteries, and less flows through the
foramen ovale to the left atrium.
The blood from the lungs travels through the pulmonary
veins to the left atrium, increasing the pressure there.
The decreased right atrial pressure and the increased left
atrial pressure pushes the septum primum against the
septum secundum, closing the foramen ovale, which now
becomes the fosse ovalis. This completes the
separation of the circulatory system into the left and the
right.
The ductus arteriosus normally closes off within one
or two days of birth, leaving behind the ligamentum
arteriosum.
The umbilical vein and the ductus venosus closes off
within two to five days after birth, leaving behind the
ligamentum teres and the ligamentum venosus of the
liver respectively.
Differences between fetal and
adult circulatory systems
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The fetal foramen ovale - the adult fosse ovalis.
The fetal ductus arteriosus - the adult ligamentum arteriosum.
The extra-hepatic portion of the fetal left umbilical vein - the
adult ligamentum teres hepatis (the "round ligament of the
liver").
The intra-hepatic portion of the fetal left umbilical vein (the
ductus venosus) - the adult ligamentum venosum.
The proximal portions of the fetal left and right umbilical
arteries - the adult umbilical branches of the internal iliac
arteries.
The distal portions of the fetal left and right umbilical arteries the adult medial umbilical ligaments.
Fetal hemoglobin differs from adult hemoglobin.
Fetal hemoglobin (1)
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Fetal hemoglobin differs most
from adult hemoglobin in that
it is able to bind oxygen
with greater affinity than
the adult form, giving the
developing fetus better access
to oxygen from the mother's
bloodstream.
The P50 value for fetal
hemoglobin (i.e., the partial
pressure of oxygen at which
the protein is 50% saturated;
lower values indicate greater
affinity) is roughly 19 mmHg,
whereas adult hemoglobin has
a value of approximately
26.8 mmHg.
Fetal hemoglobin (2)
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At birth, fetal hemoglobin comprises 50-95% of the child's
hemoglobin.
These levels decline after six months as adult hemoglobin
synthesis is activated, while fetal hemoglobin synthesis is
deactivated.
Soon after, adult hemoglobin (hemoglobin A) takes over as the
predominant form of hemoglobin in normal children.
Neonatal jaundice tends to develop because of two factors
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Decrease of the number of erythrocytes.
The breakdown of fetal hemoglobin as it is replaced with adult
hemoglobin
The relatively immature hepatic metabolic pathways, which are
unable to conjugate bilirubin as fast as an adult.