Transcript REGULATION OF HEARTBEAT AND BLOOD PRESSURE

REGULATION OF HEARTBEAT
AND BLOOD PRESSURE
MUC – IB TRANSPORT
NOVEMBER 24, 2009
REGULATION OF HEART RATE
• Basic rate of heart beat is controlled by the
activity of the SAN.
• However since heart rate is constantly
changing as the body goes through different
activities, the heart rate is controlled by two
control systems:
– Nervous
– Chemical (hormonal)
REGULATION OF HEART RATE
• These two systems ensure that constant
conditions are maintained within the
bloodstream even though external conditions
are constantly changing.
CARDIAC OUTPUT
• This is the amount of blood flowing from the
heart over a given period of time.
• Cardiac output = stroke volume x heart rate
• Stroke volume is the volume of blood pumped
out of the heart at each beat and the heart
rate is number of beats per minute.
• One way of controlling cardiac output is to
control the heart rate.
QUESTION
NERVOUS CONTROL OF HEART RATE
• First let us look at the divisions of the nervous
system of the human body.
NERVOUS CONTROL OF HEART RATE
• Centre for control of heart rate in the brain is
in the medulla.
• The medulla has two regions affecting heart
rate:
– Cardiac inhibitory center (reduces heart rate)
– Cardiac accelerator centre (increases heart rate)
NERVOUS CONTROL OF HEART RATE
• Two parasympathetic nerves called the vagus
nerves, leave the inhibitory center and run,
one on either side of the trachea to the heart.
• Nerve fibres lead to the SAN, AVN and bundle
of His (which branch into the pair of Purkinje
fibres) to trigger a release of neurotransmitter
acetylcholine.
• This substance reduces the heart rate.
VAGUS NERVES
NERVOUS CONTROL OF HEART RATE
• Other nerves, part of the sympathetic nervous
system, originate in the cardiac accelerator
region.
• These run parallel to the spinal cord and enter
the SAN and cardiac cells to cause a release of
neurotransmitter substance norepinephrine.
• The substance results in an increase in the
heart rate.
NERVOUS CONTROL OF HEART RATE
• These two sets of nerves from the inhibitory
and acceleratory regions in the medulla coordinate to control the heart rate.
NERVOUS CONTROL OF HEART RATE
• The aorta, carotid arteries and vena cava have
stretch receptors that respond to the
stretching of the tissue.
• Sensory nerve fibres from these recptors run
to the cardiac inhibitory centre in the medulla.
NERVOUS CONTROL OF HEART RATE
• As the volume of blood flowing through these
vessels fluctuate, the stretch receptors
register the changes.
• Impulses received from the aorta and carotids
decrease the heart rate (a fail-safe mechanism
so that the heart does not work too hard).
• Those from the vena cava stimulate the
accelerator center which increases the heart
rate.
STRETCH RECEPTORS FROM THE
VESSELS TO THE MEDULLA
HORMONAL CONTROL OF HEART RATE
• Adrenaline and noradrenaline /
norepinephrine (secreted by the
adrenal glands) stimulate the heart
rate.
• Cardiac output and blood pressure are
increased by increasing the heart rate.
HORMONAL CONTROL OF HEART RATE
• The hormone thyroxine (secreted by the
thyroid gland) raises basal metabolic rate.
This is the rate at which energy is used by an
organism at complete rest.
• This leads to greater metabolic activity with
greater demand for oxygen and production of
more heat.
HORMONAL CONTROL OF HEART RATE
• Vasodilation increases.
• Blood flow then increases.
• Hence cardiac output increases.
• Thyroxine therefore can indirectly or directly
stimulate heart rate.
OTHER FACTORS THAT CONTROL
HEART RATE
• High pH decelerates heart rate.
• Low pH accelerates the heart rate.
• Emotions, sights and sounds can increase the
heart rate by increasing sympathetic activity.
• Low temperature decelerates heart rate.
• High temperature accelerates heart rate.
LONG TERM EFFECTS OF EXERCISE ON
HEART RATE
• Heart gets stronger with exercise because
muscles are worked out.
• Heart chambers get larger and there is a 40%
increase in cardiac output.
MEASURING BLOOD PRESSURE
• Blood pressure is the force developed by the
blood pushing against the walls of the blood
vessels.
• Usually measured in the brachial artery in the
arm using a sphygmomanometer.
• Systolic pressure is high and is placed at top
• Diastolic pressure is low and placed at bottom.
• Normal pressure is around 120mmHg / 80mmHg.
REGULATION OF BLOOD PRESSURE
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Blood pressure depends on several factors:
Heart rate
Stroke volume
Resistance to blood flow by the blood vessels
(peripheral resistance)
• Strength of heartbeat
REGULATION OF BLOOD PRESSURE
• Resistance altered by vasodilation and
vasoconstriction.
• Controlled by vasomotor centre in the medulla
• Nerve fibres run from this centre all over the
body.
• Vasomotor centre activity is regulated by
impulses coming from pressure receptors in the
walls of the aorta and carotids.
BLOOD CLOTTING
• Blood clotting serves
two main purposes:
– It prevents the body
from losing too much
blood from a wound
– It keeps invading
organisms from
entering a wound and
causing infection.
Blood disorders
• Thrombosis: A blood clot in a blood vessel or within
the heart.
• Embolism: When an object migrates from one part of
the body and blocks a blood vessel at another part of
the body.
• Haemophilias: bleeding disorders that arise from a
missing or mutant blood clotting protein/factor.
BLOOD GROUPS
• There are four blood groups: A, B, AB and O.
BLOOD GROUP INTERACTIONS
Deficiency Anemia
Iron Deficiency (helps make haemoglobin)
Folate Deficiency (helps make DNA)
Pernicious (lack of Vitamin B12) (helps make folate)
Copper Deficiency (iron absorption decreases)
Vitamin C Deficiency (iron absorption decreases)
Sickle Cell Anemia
• Genetic disorder so cannot be cured as
deficiency anemia.
• A base glutamic acid is replaced by valine in
the beta-proteins that helps make up
heamoglobin.
• The red blood cells adopt a sickle shape and
lodge in the blood vessels instead of flowing
through freely.
OXYGEN TRANSPORT,
DISSOCIATION CURVES AND THE
BOHR EFFECT
DECEMBER 1, 2011
OXYGEN DISSOCIATION CURVES
• Release of oxygen from haemoglobin is
dissociation.
• The amount of oxygen that can combine with
haemoglobin is determined by the oxygen
concentration or partial pressure.
• The more oxygen in the air the higher the
partial pressure.
OXYGEN DISSOCIATION CURVES
• The higher the partial pressure of
oxygen, the more saturated
haemoglobin becomes with
oxygen.
• The degree to which
haemoglobin is
saturated is
illustrated by a
sigmoid curve.
• Over the steep part
of the curve a small
decrease in the
oxygen partial
pressure of the
environment will
bring about a large
fall in the
percentage
saturation of
haemoglobin.
• The oxygen given up by the pigment in such a
situation is available to the tissue.
FOETAL AND MATERNAL
HAEMOGLOBIN
• Foetal haemoglobin (HbF) is structurally
different from normal haemoglobin (Hb).
• The foetal dissociation curve is shifted to the
left relative to the curve for the normal adult.
FOETAL AND MATERNAL
HAEMOGLOBIN
• At the placenta there is a higher concentration of a
certain chemical compound (2,3-DPG) is formed.
• This binds more readily to adult haemoglobin but not
to foetal haemoglobin.
• This causes the adult Hb to release more oxygen at
the placenta to be taken up by the foetus.
• Foetal Hb is made up of gamma chains not beta
ones, and 2,3-DPG does not bind readily to gamma
chains, hence it does not give up its oxygen.
• The foetal haemoglobin
saturates more readily
than that of the mother
under the same
conditions of partial
pressure.
• This saturation also falls
less rapidly than for the
mother when oxygen
levels decrease.
• This is because,
typically, fetal arterial
oxygen pressures are
low, and hence the
leftward shift enhances
the placental uptake of
oxygen.
FOETAL AND MATERNAL
HAEMOGLOBIN
THE BOHR EFFECT
• This states that at lower pH, haemoglobin will bind to
oxygen with less affinity.
• Since high carbon dioxide levels in the blood form
carbonic acid, this effect has its roots in carbon
dioxide concentration.
• Hence high respiratory levels are associated with
high carbon dioxide levels.
THE BOHR EFFECT
• In regions with an increased partial pressure
of carbon dioxide, the oxygen dissociation
curve is shifted to the right.
• This is the Bohr effect and has a physiological
advantage.
• Increasing the carbon dioxide concentration
results in oxygen being released from
haemoglobin.
THE BOHR EFFECT
• Vertical line represent
29 mmHg or the partial
pressure which gives
50% oxygen saturation
in red blood cells.
MYOGLOBIN
• Red pigment similar to one of ht epolypeptide chains in
haemoglobin.
• Found in skeletal muscles and gives meat its red
colouration.
• Shows a great affinity for oxygen and oxygen
dissociation curve is displaced well to the left of
haemoglobin.
MYOGLOBIN
• It will only release its oxygen when oxygen
in the environment is below 20mm Hg.
• Hence myoglobin is a store of oxygen in
resting muscle.
MEAT CHEMISTRY
• When meat is cooked, some of the proteins in it denature and
become opaque, turning red meat pink. At 60 degrees C, the
myoglobin itself denatures and becomes tan-coloured, giving
well done meat a brownish-grey colour. Freezing for long
periods of time can also denature the myoglobin.
• At lower partial
pressures of oxygen,
the saturation of
myoglobin with oxygen
still remains relatively
high.
CARBON MONOXIDE AND
HAEMOGLOBIN
• The iron in Hb has an affinity for carbon monoxide
250 times greater than that for oxygen.
• Carboxyhaemoglobin is formed and is stable.
• 0.1% CO in air can be fatal.
• Asphyxiation occurs readily.
• Treatment is removal from the source and
administering of almost pure oxygen with a little
carbon dioxide to stimulate the respiratory centre in
the medulla causing faster breathing and heart rate.
CARBON DIOXIDE TRANSPORT
• Carbon dioxide carried in blood three ways:
• In the plasma (5%)
• Combined with haemoglobin (10-20%)
• As hydrogencarbonate (85%) leading to
chloride shift.
CHLORIDE SHIFT
• CO2 enters red blood cells, dissolves in water
to form carbonic acid.
• This acid dissociates into hydrogen and
hydrogencarbonate ions.
• CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-
• The hydrogen ions displace oxygen from
haemoglobin and when the heamoglobin
accepts the hydrogen, haemoglobinic acid is
formed.
• H+ + HCO3- + Hb  HHb + HCO3-
CHLORIDE SHIFT
• In this way haemoglobin buffers the blood.
• Most of the hydrogencarbonate ions
formed in the red cells diffuse into the
plasma and combine with sodium ions to
form sodium hydrogencarbonate.
• Loss of this negatively charged ion from the red cells
leaves the red cells positively charged.
• They attract negatively charge chloride ions from the
plasma.
• This is the chloride shift.
• Carbonic anhydrase enzyme important in this
equilibrium.