cardio Flashcards
(98 cards)
1
Q
Explain which and how intermediate control mechanism of arterial blood pressure can
increase blood pressure back to normal if it was too low!
A
Renin- angiotensin system:
The liver will produce angiotensinogen and release it into
blood. When blood pressure decreases, the kidneys release renin which converts
angiotensinogen in the blood into angiotensin I. Blood will be delivered to the
pulmonary circulation where endothelial cells contain high concentrations of
angiotensin converting enzymes that convert angiotensin I into angiotensin II.
Angiotensin II reaches all blood vessels in the body and causes vasoconstriction.
Angiotensin II is one of the strongest vasoconstrictors in our body, which in
nanogram concentration can increase arterial blood pressure by 20-40 mmHg.
- Fluid reabsorption: With low blood pressure there will be a reabsorption of interstitial
fluid into the capillaries and a smaller filtration out. When pressure in the interstitium
is higher than the pressure inside the capillary → reabsorption takes place. This will
restore the blood pressure.
- Stress relaxation: (Stress refers to stress of the smooth muscle cells in the blood
vessel wall. Stress of the smooth muscle cell is caused by the stretch of the cell).
Sudden stress of smooth muscle cells causes deformation Ca2+ channels to open
which leads to contraction of smooth muscle cells. If the stress goes on for several
minutes or hours, the smooth muscle cell will adapt to the stretch. This will lead to
deformation Ca2+ channels closing and the calcium concentration in the cell will
decrease, leading to relaxation of the smooth muscle cells. Relaxation of the smooth
muscle cells causes less tension of the blood vessel wall which might decrease the
blood pressure. Stress relaxation due to continuous stretching of the blood vessel wall
causes relaxation of smooth muscle cells in its wall.
Meaning:
If the blood vessel wall is subjected to high pressure over a long time,
the muscle cells will relax and accept the high blood pressure instead of working
against it.
2
Q
Characterize sympathetic nervous system effects in the cardiovascular (heart and
different blood vessels) and urogenital system!
A
The sympathetic nervous system will cause an increase in heart rate, force of
contraction, excitability, velocity of conduction and increased speed of relaxation
- For the urogenital system in males there will be an ejaculation and for women that are
pregnant there will be a contraction and for non pregnant women there will be a
relaxation in the uterus.
3
Q
Explain the role of different types of calcium channels in the cardiac muscle (name a
type, location and explain its function)!
A
In cardiac tissues, the two types of calcium channels are the L type and the T type.
L-type channels are found in all cardiac cells and T-type are expressed in Purkinje
cells, pacemaker and atrial cells. Both these types of channels contribute to
atrioventricular conduction as well as pacemaker activity.
4
Q
A
5
Q
Explain pressure of volume changes in the left atrium and left ventricle during
the filling phase!
A
During the filling phase in the left ventricle the pressure is much lower than
the pressure in the aorta which means that the semilunar valves will still be
closed. The filling phase is divided into two phases: the passive and active
filling phase. The blood will flow from the veins through the atria into the
ventricles, the ventricle will receive about 80% of the blood. The active
filling phase also known as the atrial systole will push the remaining 20% of
the blood into the ventricle for the next atrial systole. Pressure in the atria and
ventricle will rise.
- During the filling phase in the left atrium the pressure in the ventricle is lower
than the pressure in the atrium. This means that the atrioventricular valves are
open and the blood will enter the ventricles. For the passive phase the blood
will flow passively from the veins through the atrium into the ventricles,
filling the ventricles with about 80%. In the active filling phase (atrial
systole) the next atrial systole will begin and the atrial muscle contraction
will push the remaining 20% of the blood into the ventricle to fill its maximal
volume.
6
Q
. Name and give a size of volume of the left ventricle at the beginning and at the
end of filling phase
A
At the beginning of the filling phase the volume is called end systolic volume
(residual volume + reserve volume) (30-60 depending on person &
contraction strength), after the filling the volume is called end diastolic
volume (110-150ml) (residual volume + stroke volume + reserve volume)
7
Q
Indicate the blood volume delivered to the skeletal muscle. Indicate its changes during
exercise
A
- The skeletal muscles receive 21% from the cardiac output. This is 3-5 ml/min/100g.
During exercise the percentage they receive may reach 85% of the CO and 50-80
ml/min/100g
8
Q
Explain the cause of the QRS complex (each wave if possible) and QT interval in
the electrocardiogram and provide normal values!
A
- QRS complex starts at the beginning of Q to the end of S. It shows the
depolarization of the ventricles, normal values are 0,06-0,1s. R is always
present and positive, it represents the depolarization of the main mass of the
ventricle. Q and S waves are not always present in an ECG but they are
normally always negative. The Q wave corresponds to depolarization of the
interventricular septum. The S wave signifies the final depolarization of the
ventricles, at the base of the heart - QT interval is shown from the beginning of the Q wave to the end of the T
wave. It represents depolarization and repolarization of the ventricles.
Normal values are 0,30-0,45s.
9
Q
Measure and evaluate the duration of QRS complex and QT interval in this
electrocardiogram!
A
- QRS ––> 3*0,02= 0,06s which is normal value
- QT interval ––> 45= 20
200,02=0,4s which is normal value
10
Q
Indicate the blood volume delivered to the lungs. Indicate its changes during exercise.
A
- The lung circulation is divided into the bronchial circulation and the pulmonary
circulation. The pulmonary circulation receives 100% of the cardiac output (from the
right atrium, venous blood) to oxygenate it for it to be later sent to the rest of the
body. The bronchial circulation receives 1 to 2 % of the cardiac output.
11
Q
Explain differences in reflex arch between somatic and autonomic nervous system!
A
The afferent part is the same in somatic and autonomic systems but the efferent part of the reflex arch
has multiple differences.
- Higher centers: SNS has its highest center in the cerebral cortex and ANS has its highest
center in the hypothalamus.
- Lower centers: SNS lowest center are all segments of the spinal cord while the ANS has the
lowest centers in the thoracic, lumbar and sacral part of the spinal cord.
- Conscious/ Subconscious: The SNS is conscious because the cerebral cortex controls the
consciousness. The ANS is subconscious.
- Reflex center: meaning the location of the neuron cell body, the SNS has it located in the
anterior horn and in the ANS its located in the lateral horn of the spinal cord.
- Efferent pathway: in the somatic reflex arch the efferent pathway is made up from one neuron
while in the autonomic its made from two neurons preganglionic and postganglionic neurons.
The preganglionic neuron leaves the spinal cord and synapses with the postganglionic one
that is located outside of the spinal cord.
- Nerve fiber types: The somatic will have well myelinated A alpha or A gamma nerve fibers,
they will have a fast speed of impulse conduction. In the autonomic preganglionic neuron
there are B group fibers and the postganglionic belongs to the C group, the B group fiber is
less myelinated while the C group fibers are unmyelinated.
- Conductor (effector): In the somatic reflex arch it is skeletal muscle while the autonomic has
three possible effectors; cardiac muscle cells, smooth muscle cells and secretory cells
- Neurotransmitter & the receptors in the synapse with the effector: Somatic reflex arch has a
Acetylcholine neurotransmitter that binds to a nicotinic receptor. While the autonomic
nervous system has several options. The neurotransmitter can be acetylcholine but it will bind
to the muscarinic receptor. The neurotransmitter can also be epinephrine or norepinephrine
and it will bind to either alpha or beta adrenergic receptors.
- Reflex time: The autonomic reflex arch has a longer reflex time, it’s because of three reasons.
The first reason is because it has at least one more synapse compared to the somatic reflex
arch. The second reason is because it has ANS has slow conducting fibers while SNS has fast.
- Co-transmission: Happens only in the ANS. Co-transmission means that together with the
already existing neurotransmitters additional neurotransmitters can be packed together in
vesicles. The neurotransmitter that can be packed together with AcH is VIP. NE is usually
released together with ATP and NPY
12
Q
Explain the local regulation mechanisms that can lead to dilation of cerebral
blood vessels
A
Metabolic regulation: results in vasodilation when the partial pressure of carbon
dioxide increases and partial pressure of oxygen decreases. The blood vessels will
dilate to compensate for the lack of oxygen.
- Humoral regulation: vasodilation happens when the release of nitric oxide is done.
Nitric oxide will activate cAMP which activates kinase which leads to less calcium
which means it will affect the diameter.
- Myogenic regulation: there will not be a stretch which means there will be a
relaxation of the smooth muscle cells.
13
Q
. Explain venous blood flow differences from arterial
A
- Low blood pressure – veins are less elastic than arteries, and because of that
they have a very large capacity to hold blood. 15 – 0 mmHg. - Low pressure difference – only 15 mmHg, while in arteries the difference is
approximately 65 mmHg. The low pressure difference leads to slow blood
flow. - Bigger cross-sectional area – decreases the blood flow.
- Slower linear velocity – the velocity is constant. In arteries the velocity is
high, and decreases when the blood reaches the capillaries. 0.15 – 0.2 m/s - Blood flow in one direction with the help of valves- They work passively. If
the pressure before the valve is greater than the pressure after the valve, they
will open. If the pressure before the valve is lower than the pressure after
valve, they will close. - Greater compliance – Stretch well, can hold more blood and work as a blood
depot
14
Q
Explain mechanisms that facilitate venous blood return (muscle pump,
respiratory pump, heart pump)
A
- Muscle pump:
- When the skeletal muscles contract, the upper valve will open and
the lower valve will close leading to increased blood pressure
because blood is pushed up. When the skeletal muscle relaxes, the
upper valve will close because of greater pressure from above, this
also prevents backflow. The lower valve opens and the vein is filled
again. This describes why there is greater venous return when
standing up. - Respiratory pump:
- During inspiration, the diaphragm moves down → increased
pressure in the abdominal cavity → compresses the veins in this area.
At the same time, the pressure in the thoracic cavity decreases. This
process leads to decreased pressure in the veins of the thoracic cavity,
but increased pressure in the abdominal veins, so the abdominal veins
push blood into the thoracic veins. - During expiration, the pressure in the thoracic cavity increases, so
thoracic veins are compressed, and more blood is pushed in the
direction of the heart. - Heart pump:
- Works during systole, especially ejection phase.
- During the ejection phase, the AV plane moves down towards the
ventricles, which stretches the atria and decreases pressure in them.
Because of the decreased pressure, the atria is able to “suck” blood
from the great veins.
15
Q
a. Indicate the blood volume that is delivered to coronary circulatory
A
about 200 ml/min and 4% cardiac output. During exercise it rises up to
250mL/min/100g.
16
Q
. Explain mechanisms that can lead to dilation of coronary arterioles
Central: neuronal, hormonal
A
- Central neural regulation activates sympathetic fibers, from T1 to L3;
Acetylcholine binds to M3 cholinoreceptors. - Central hormonal regulation releases epinephrine binding to B2, ANP & BNP
are also released as vasodilators but they are weak.
Peripheral: metabolic, humoral, myogenic - Peripheral metabolic regulation has increased partial pressure of carbon
dioxide and K+ and adenosine while having decreased oxygen levels and pH
levels. - Peripheral humoral regulation releases PGI2, histamine, NO, kinins, EDHF to
cause a vasodilation - Peripheral myogenic regulation will have no stretch in the smooth muscles
causing a relaxation
17
Q
Measure the duration of P wave, PQ segment and PQ interval in the
electrocardiogram. Speed of recording 50 mm/s, amplification 10 mm/mV.
A
P wave duration: 4 x 0,02= 0,08s
- PQ segment duration: 2,5 x 0,02= 0,05s
- PQ interval duration: 7 x 0,02= 0,14s
18
Q
Explain the cause of P wave, PQ segment and PQ interval in the
electrocardiogram and give their normal values!
A
- P wave: shows the depolarization of the atria. Normal values are 0,06-0.1s
- PQ segment: shows the impulses that are spread through the atrioventricular
node. Normal values are 0,04-0,1 s - PQ interval: shows the impulse spread through the atria to the ventricle.
Normal value are 0,12-0,20 s - The patient showed all normal values
19
Q
- Name phases of the action potential of the working myocardium cell. Explain changes of
ion permeability in the cell membrane during the different phases of this action
potential
A
The working myocardium has no automaticity, they are dependent on pacemaker cells
and external electrical stimuli. They have resting membrane potential at -90 mV.
- Fast depolarization (phase 0): impulse comes that opens the voltage gated sodium
channels. When the sodium ions rush into the cell it causes a fast depolarization.
- Initial fast repolarization (phase 1): The voltage gated sodium channels close and the
voltage gated potassium channels open causing an outflux of potassium. At the same
time a small amount of chloride ions goes in.
- Slow repolarization/plateau (phase 2): L- calcium channels open leading to a calcium
influx and outflux of potassium. The exchange is equal meaning that the membrane
potential does not change much causing the “plateau look”. This goes on for about
100 ms.
- End fast repolarization (phase 3): The L-calcium channels close. But additional
potassium channels open which leads to a potassium outflux that decreases the action
potential rapidly back to the initial resting membrane (-90mV).
20
Q
. Explain the effect of epinephrine on the heart including the effect on a cellular level (also
mention the site of production of epinephrine and the receptors it binds to)
A
- The effect of epinephrine in the heart is started from the sympathetic nervous system
being triggered (fight or flight). Epinephrine will bind to β1-receptor and stimulate Gprotein which will activate adenosine cyclase (AC). AC will convert ATP to cAMP.
cAMP increases permeability of sodium and calcium-channels in the cardiac muscle
cell membrane. With the sodium and calcium influx in the cell there will be a rapid
depolarization which leads to the increase of heart rate of the person. Since more
calcium ions come into the cell, it binds to the troponin to activate contractile
filaments which increase the force of contraction. The increased permeability to
sodium and calcium ions can cause and increase excitability of the cardiac muscle
cells. It can also increase the speed of conduction and increase relaxation rate (all
positive effects on the heart)
21
Q
20 years old female person has blood pressure 120/95 mmHg and heart rate 84 x/min
a) Give normal range of arterial blood pressures and indicate if blood pressure for
this person is normal!
A
Normal blood pressure should be lower than 120/80, for systolic it should be
90-120 mmHg and for diastolic it should be 60-80 mmHg. The systolic blood
pressure is normal but the diastolic is a bit higher than normal. Normal heart
rate: 60-100 x/min
22
Q
State at which moment the systolic/diastolic blood pressure is read:
A
in the auscultatory method: the first sound that is hearable after we deflate
the cuff is the systolic and after that we will hear a turbulent blood flow, once
the blood flow is not hearable anymore the diastolic pressure is determined.
- in the palpatory method: the diastolic pressure cannot be measured since
there is no stethoscope, but when placing the fingers on the artery it will
allow us to register systolic pressure, this method can be used when the
surroundings are loud.
23
Q
Calculate the mean arterial pressure for this person! Provide the calculation
formula!
A
- ⅓(PS) + ⅔ (PD) ––>⅓ (120) + ⅔ (95) ––> 40 + 63= approximately
103mmHg
24
Q
Calculate the pulse pressure of this person! Provide the calculation formula!
A
Pulse pressure: Ps-Pd= 120-95= 25 mmHg
25
Evaluate the elastic and peripheral resistance for the circulatory system from the
given data; indicate parameters on which your conclusions are based on!
- The peripheral resistance is high for this individual, because the diastolic
pressure is above normal ranges (60-80 mmHg). The high peripheral
resistance = decreased overall compliance = high diastolic BP. The elastic
resistance is normal or (low), meaning that the aorta is elastic and can expand
during ejection, which keeps systolic blood pressure within normal values
(90-120 mmHg).
26
Explain the innervation and function (including effects) of the adrenal medulla.
- The adrenal medulla is innervated by the sympathetic nervous system. The adrenal
medulla produces mostly epinephrine (80%) and it causes different functions. such as;
increased metabolic intensity like fat breakdown in adipose tissues, increasing
glucose levels in blood. Increase heart activity by having positive effects. Decrease
motility and secretion in gastrointestinal tract. Dilate bronchi, dilate pupils and relax
ciliary muscle to widen and adapt to the far vision. Increase sweating secretion.
Stimulate platelet aggregation to speed up clot formation.
27
Characterize the sympathetic nervous system effects in the respiratory system
and eyes.
Respiratory: The diameter: There will be bronchodilation. The bronchial glands:
Less secretion
Eyes: M. dilatator pupillae: The pupils will dilate. M. ciliaris: The ciliary muscle will
relax
28
Indicate centers of the sympathetic nervous system, indicate neurotransmitters
and receptors in synapse with the effector.
- The highest center of the SNS is the hypothalamus and the lower centers are
in the T1-L3 segments. The neurotransmitter that is released in the
preganglion is Acetylcholine and it will bind to the nicotinic receptors. In the
postganglion the neurotransmitters that are released and synapsing with the
effector are Norepinephrine or Epinephrine and they will bind to either alpha
or beta receptors. In sweat glands, some blood vessels of skeletal muscles,
coronary circulation and in the brain there is Acetylcholine and it will bind to
muscarinic receptors.
29
What effects in the respiratory system will be caused by propranolol? Explain it!
- Propranolol blocks beta receptors and b2 receptors exist in the respiratory
tract, the stimulation will lead to bronchoconstriction, leading to breathing
problems to people with already pre- existing breathing diseases such as
asthma.
30
Explain when during the cardiac cycle extrasystole can be triggered:
- When a stimulus is given after the ARP but before the end of the diastole, and
the stimulus is strong enough to cause a contraction, an extra-systole
(=extracontraction) can be observed
31
Explain why it cannot be triggered in the other part of the cardiac cycle
- It cannot be triggered before the ARP because excitability is 0%, and after the
diastole then a stimulus would just cause normal systole, and heart wouldn’t
skip a beat.
32
Explain the cause of compensatory pause after extrasystole
- Because a new stimulus is needed to cause a new contraction, but the natural
stimulus (of the pacemaker) falls into the ARP of the extrasystole → it
doesn’t cause a contraction. It compensates for the arrhythmia caused by the
extrasystole & ensures that the heart beats in its normal rhythm again.
33
Indicate the volume of blood that adult persons brain receives during rest and
physical exercise:
- 14% of cardiac output and 700ml/min for the resting cerebral blood flow.
During physical activity the brain receives more blood , up to 750 ml/min
34
. Explain the peripheral (local) regulation mechanisms that can lead to dilation of
cerebral blood vessels
- Metabolic regulation: results in vasodilation when the partial pressure of
carbon dioxide increases and partial pressure of oxygen decreases. The blood
vessels will dilate to compensate for the lack of oxygen.
- Humoral regulation: vasodilation happens when the release of nitric oxide is
done. nitric oxide will activate cAMP which activates kinase which leads to
less calcium which means it will affect the diameter.
- Myogenic regulation: there will not be a stretch which means there will be a
relaxation of the smooth muscle cells.
35
Name elements of the electrocardiogram that indicate electrical events in
ventricles, explain their cause and give normal values.
- QRS complex shows the depolarization the ventricles: 0,06-0,1s
- T wave shows the repolarization of the ventricles: 0,2-0,4 mV
- QT interval shows the depolarization and repolarization of the ventricles:
0,3-0,45s
36
Explain changes of blood pressure in the left ventricle and left atrium during the
isovolumetric relaxation phase; indicate the state of valves during it!
- Blood pressure in left ventricle will drop rapidly in isovolumetric relaxation
since the surface expands and it increases in left atrium since the ventricle
previously pulled it with when it contracted. Now that it can go back, it
decreases the surface and heightens the pressure. During isovolumetric
relaxation, both AV and SL valves are closed.
37
How do we call the blood volume in ventricle at the beginning of
isovolumetric relaxation phase? How much is it?
End-systolic volume. Reserve volume 20-40 ml + Residual volume 10-20 ml
38
Which heart sound we can record at the beginning of the isovolumetric
relaxation? What is the cause of it?
Second heart sound. This sound is caused by the SL valves closing.
39
Characterize the parasympathetic nervous system effects in the cardiovascular
( heart and different blood vessels) and urogenital system.
- The parasympathetic nervous system will cause an decrease in heart rate,
force of contraction, excitability, velocity of conduction and decreased speed
of relaxation.
- For the urogenital system the wall of the bladder will contract while the
sphincters will relax.
40
Give the localization of the highest and lowest centers of the parasympathetic
nervous system, indicate neurotransmitters and their corresponding receptors in
the synapse with the effector.
Highest center: hypothalamus but anterior part
- Lowest center: in spinal cord from sacral 2-4 and cranial nerves
- Neurotransmitters: Neurotransmitter that is released by preganglionic
parasympathetic neurons and the corresponding receptor:ACh → N-receptor
- Neurotransmitter that is released by postganglionic parasympathetic neurons
and the corresponding receptors:ACh → M-receptor.
- In the synapse with the effector there is only one option and that is
acetylcholine and muscarinic receptor.
41
Specify the type of receptor that is located in the synapse with the cardiac muscle
- In the synapse with the effector there is only one option and that is
acetylcholine and muscarinic receptor, M2 receptor.
42
Explain pressure in the aorta during the ejection phase; indicate the state of the heart
valves during this phase!
- Beginning of ejection phase: Pressure in ventricle becomes greater than pressure in
aorta ––> semilunar valves open and blood is ejected from the ventricle into the large
arteries. Blood flow into the aorta is greater than outflow from the aorta ––> blood
volume in aorta increases, raising pressure
- End of ejection phase: Blood pressure in aorta decreases. Ventricles gets emptier and
less blood will flow into the aorta than what flows out of the aorta to the peripheral
arteries ––> blood pressure decreases
- After ejection: Pressure in ventricles becomes lower than pressure in aorta ––> SL
valves close. Immediately after closure, pressure in aorta increases because of
backflow of blood and reflection from the closed semilunar valve.
42
Explain changes of blood pressure in left ventricle and left atrium during the
ejection phase, indicate the state of valves during it!
- The ventricular pressure is higher than the pressure in the atrium and this
leads to the opening of the SL valves, which marks the beginning of the
ejection phase. The ventricle starts rapid ejection, and the contraction leads to
rapidly increased pressure. The pressure reaches 120 mmHg (systolic
pressure). When the contraction is over, the pressures slowly decreases. SL
valves are still open, so the blood still flows out. But the atrioventricular
valve is closed.
- During ejection, ventricular muscle cells shorten and pull down the
atrioventricular plane. This stretches the atrium and decreases pressure ––>
facilitates venous blood return to the atrium. Rapid ejection is most important
when pressure in atrium decreases.
43
What effects in the heart should be caused by the atropine? Explain the action of
atropine!
Since Atropine is a parasympathetic blocker, it will increase heart rate.
44
How do we call blood volume that leaves the ventricle during the ejection phase?
How much is it?
-It is called stroke volume and it is 60-100 ml
45
Define the stroke volume and give its normal value.
- The stroke volume is the volume of blood that is pumped in the large arteries
in 1 cardiac cycle, normal values are 60-100ml
46
Which heart sound we can record at the end of the ejection phase? What is the
cause of it?p+x
Second heart sound. This sound is caused by the SL valves closing.
47
Explain how and why does stroke volume change if afterload increases
With an increased afterload we get an increased resistance in aorta and that
leads to a decrease in stroke volume because the heart needs to work harder
to eject the blood out.
48
Characterize changes of work of the heart if afterload is increased.
-The heart needs to work harder since there is an resistance from the aorta
49
. Explain regulatory mechanisms that can increase coronary blood flow!
Peripheral:
- Metabolic regulation: The coronary blood flow is mostly dependent on metabolic
regulation. Partial pressure of carbon dioxide, adenosine and potassium ions will
increase while pH and partial pressure of oxygen will decrease causing vasodilation.
- Humoral regulation: These substances will be secreted; Histamine, kinins, nitric oxide
and PGI2 & PGE2 will cause vasodilation
- Myogenic regulation: No stretch
Central:
- Neutral: Sympathetic and parasympathetic will secrete acetylcholine that will bind to
M3 causing nitric oxide to be released and vasodilation will happen
- Hormonal: Epinephrine will bind to b2.
50
Explain pressure that stimulate filtration through the wall of capillaries, explain
factors that determine them and give their average values
- Filtration and reabsorption are dependent on pressure gradient across the
capillary wall, the substances will flow from higher pressure region → lower
pressure region
- Factors that determine the filtration and reabsorption: Hydrostatic pressure
and Colloid osmotic pressure.
- Hydrostatic pressure, Pc (blood hydrostatic pressure): 30-40 mmHg
- Colloid osmotic pressure: πc (plasma colloid osmotic pressure): 10-20 mmHg.
51
Explain the role of glycocalyx in filtration
- It will not let proteins filtrate
52
What will happen with filtration through the wall of capillaries if plasma protein
concentration decreases?
Explain your choice.
- If blood plasma volume decreases then the blood pressure will decrease. The
blood plasma protein decreases because there is too high blood pressure from
the beginning, it will decrease the blood pressure. It will also increase
filtration and decrease reabsorption.
53
8. Explain which and how intermediate and slow control mechanisms of arterial blood
pressure can decrease blood pressure back to normal if it was too high?
Intermediate control mechanisms:
Renin- angiotensin system: The liver will produce angiotensinogen and release it into
blood which decreases the blood pressure.
- Fluid filtration: With high blood pressure there will be a filtration increase to the
capillaries into the interstitial fluid and a smaller amount of reabsorption in. When
pressure inside the capillary is greater than the pressure in the interstitium ––>
filtration takes place and this will restore the blood pressure
- Stress relaxation: (Stress refers to stress of the smooth muscle cells in the blood
vessel wall. Stress of the smooth muscle cell is caused by the stretch of the cell).
Sudden stress of smooth muscle cells causes deformation Ca2+ channels to open
which leads to contraction of smooth muscle cells. If the stress goes on for several
minutes or hours, the smooth muscle cell will adapt to the stretch. This will lead to
deformation Ca2+ channels closing and the calcium concentration in the cell will
decrease, leading to relaxation of the smooth muscle cells. Relaxation of the smooth
muscle cells causes less tension of the blood vessel wall which might decrease the
blood pressure.
Slow control mechanisms:
- Renal blood volume pressure regulation: With high arterial blood pressure (> 160
mmHg) means that there will be more blood delivered to the glomerular blood vessel
from the renal artery. Which increases filtration rate and decreases absorption due to
greater pressure in the capillaries. This will lead to a greater amount of urine being
excreted. People with high blood pressure go to the bathroom more often
- Hormones that decrease blood pressure: ANP, BNP (Atrial natriuretic peptide, B
natriuretic peptide) In case of increased blood pressure, cardiac endocrine myocytes
release ANP and BNP due to stretching of the wall of the heart. ANP and BNP block
to tubular epithelial cells in the kidneys and block Na+ reabsorption. Since Na+ ions
cannot go into the bloodstream, water also stays in the nephron. With more Na+ and
H2O they will be excreted with urine which leads to a plasma volume decrease, and
blood pressure decreases.
54
. Explain the humoral regulation of the heart function (name substances that regulate,
place and conditions when they are produced, explain the effect on cardiac cells)
Substances that increase heart activity
- Epinephrine and Norepinephrine from the adrenal medulla, Ep will bind to β1 and NE
will bind to α1 receptor causing all positive effects on the heart
- Iodine containing hormones T3 and T4, produced in the thyroid gland. These
hormones will upregulate number of β1-receptor in the cardiac muscle cells, increase
β1 sensitivity to NE and E, Increased thyroid gland function ––> high resting heart
rate and high contractility, it can also decreased thyroid gland function ––> lower
heart rate and lower contractility
- Angiotensin II, is secreted in case if blood pressure is low. Its functions: are
vasoconstriction (major effect) and contraction of cardiac muscle (minor effect).
- Glucocorticoids are produced in the adrenal cortex, cortisol. Upregulates α1-receptor
leading to higher force of contraction in cardiac muscle cells
- Calcium ions: with high extracellular calcium concentration more will be transported
into cardiac muscles during excitation leads to stronger contraction. Calcium
concentration increase can lead to cardiac arrest. If calcium concentration is is too
high calcium cannot be pumped out of the cell to provide relaxation making the heart
stop during systole. Intravenous calcium preparations is injected slowly to avoid this
Substances that decrease force of contraction
- Potassium ions: If extracellular potassium concentration increases → full
repolarization cannot happen and voltage gated sodium channels inactivation gate
open. The sodium channels becomes unexcitable, and the cell cannot respond to
stimuli given → this will lead to cardiac arrest during diastole
- Adenosine: normally we have a low adenosine concentration in the body. In case of
supraventricular tachycardia, the heart rate increases tremendously, and adenosine is
infused into the central veins to stop the tachycardia attack. Adenosine stimulates
potassium outflux → hyperpolarization.
55
Evaluate blood pressures according their normal values!
- Normal blood pressure is 120/80 and here both in supine and standing
position it is too low.
56
Calculate pulse pressure in both positions and explain its change from supine to
standing position
systolic-diastolic= pulse pressure
- supine: 110-70= 40 mmHg
- standing: 100-75= 25 mmHg
- The heart does not have to work as hard in supine position to pump blood to
the body as it does in standing posture. There is a drop in pulse pressure
because of gravity.
57
Explain diastolic blood pressure change from supine to standing position.
- Diastolic blood pressure increases. Blood Pressure decreases and with the
help of baroreceptors the blood vessels will constrict leading to an increase in
diastolic pressure (Pd).
58
Explain the effect of epinephrine on the heart muscle:
- Indicate the nervous system which effects it stimulates: Epinephrine is a
sympathetic nervous system neurotransmitter. The sympathetic nervous system is
responsible for the fight or flight response, therefore its intention will be to raise heart
rate and cardiac output, having a positive effect on the cardiac muscle.
- Name the receptor type that binds it and explain in the heart until the cellular
level: Epinephrine can act on the nodal cells and the contractile myocardium. On both
there are beta 1 adrenergic receptors that work through Gs coupled protein. The Gs
coupled protein stimulates adenyl cyclase (AC) that will turn ATP into CAMP.
CAMP activates PKA that will be able to stimulate proteins, enzymes (in this case
calcium channels). More action potentials will be generated in the nodal cells (SA
node, AV node, bundle of His,...) and the contractility of the myocardium increases.
Both of these will result in a greater heart rate and cardiac output. The resting
membrane potential for the nodal cell is about -60 although it isn't stable. For the
myocardium cell it is -85 mV. The nodal cell is depolarized by the opening of the
funny Na+ channels and T-type Ca channels, and later L type Ca channels and the
myocardium cell is depolarized with the opening of the L-type Ca channels. PKA can
phosphorylate all those channels to be more active.
59
Explain the change of effect of epinephrine if it is infused after the propranolol!
- Epinephrine acts on both alpha-adrenergic and beta-adrenergic receptors in the body.
Propranolol is a beta-blocker that blocks the effects of epinephrine on both
beta1-adrenergic receptors and beta 2.
- If epinephrine is infused after propranolol, the effects of epinephrine will be altered
due to the blockage of beta-adrenergic receptors by propranolol. Epinephrine causes a
positive effect on the heart, this will be blocked by propranolol. Because propranolol
binds to the same beta-adrenergic receptors that epinephrine would normally bind to,
thereby preventing epinephrine from exerting its effects.
60
Explain the changes of work in the heart (preload, afterload, contractility)
- Preload: Increased preload means greater venous return and that will lead to greater
stroke volume, the work of the heart will increase and the heart will work effectively.
- Afterload: Increased afterload means increased resistance of aorta, this increase will
decrease the stroke volume. The heart has to work harder but it's ineffective.
- Contractility: If contractility increases there will be an increase in stroke volume and
the work of the heart will increase. The heart will work effectively.
61
Characterize alpha adrenergic receptors, explain their location and functions.
- All alpha adrenergic receptors bind to NE and E. a1 will activate IP3 and
DAG in the effector cell leading to smooth muscle cells contracting and
glands will inhibit secretion. a2 will decrease cAMP concentration in the
cells. Alpha 2 is found presynaptically and will inhibit NE release and also
stimulate platelet aggregation with the help of epinephrine.
62
Explain consequences of alpha-adrenergic receptor block in urinary and
gastrointestinal system!
- Alpha adrenergic receptors provide a sympathetic effect.
- Gastrointestinal system: the motility decreases and the sphincters will relax,
glands will decrease secretion.
- Urinary tract: the wall will relax and the sphincters will relax.
63
Explain mechanisms that facilitate blood flow in veins (muscle pump, respiratory pump,
heart pump)
Muscle pump: when the skeletal muscles contract the upper valves will open and the
lower ones will close, leading to the increased blood pressure because the blood will
be pushed up. When the skeletal muscle will relax the upper valve will close because
of greater pressure from above and this will prevent backflow. The lower valve opens
and the vein will be filled again. This is why we have greater pressure in veins while
standing up.
- Respiratory pump:
- During inspiration the diaphragm moves down which will increase the
pressure in the abdominal cavity that compresses the veins. At the same time
the thoracic cavity will have a decrease in pressure. This process leads to
decreased pressure in the veins of the thoracic cavity, but increased pressure
in the abdominal veins, so the abdominal veins push blood into the thoracic
veins.
- During expiration the pressure in the thoracic cavity increases, so thoracic
veins are compressed, and more blood is pushed in the direction of the heart.
- Heart pump: Works during systole, especially ejection phase. During the ejection
phase, the AV plane moves down towards the ventricles, which stretches the atria and
decreases pressure in them. Because of the decreased pressure, the atria is able to
“suck” blood from the great veins.
64
Indicate the volume of blood that skeletal muscles receive during rest and
physical exercise!
The skeletal muscle receives 21% of cardiac output during rest but up to 85%
during exercise. At rest the skeletal muscle will receive 3-5 ml/min/100g and
during physical activity the skeletal muscle will receive 50-80 ml/min/100g.
65
Explain mechanisms that can lead to the blood vessel dilation in leg muscles
during exercise!
Peripheral:
- Metabolic: For the vasodilation there will be an increased PCO2,
increased adenosine concentration, increased K+ outflux. Decreased
PO2 and pH.
- Myogenic: Absence of stretch causing an skeletal muscle relaxation
- Humoral: Histamine, Kinins, Nitric oxide, PGI2, PGE2, EDHF
Central:
- Neural: Sympathetic and Parasympathetic vasodilator fibers (AcH →
M3 receptor)
- Hormonal: Epinephrine binds to beta 2, ANP & BNP but they cause
a weak vasodilation.
66
Characterize the sympathetic nervous system effects in the respiratory system
and digestive system!
Respiratory:
- The diameter: There will be bronchodilation
- The bronchial glands: Less secretion
Digestive system:
- The wall: Decrease in the motility
- The sphincters: The sphincters will contract
- The GI glands: The secretion will decrease.
67
Indicate neurotransmitters and their receptors in the synapse with the effector in
the sympathetic nervous system!
- The neurotransmitters that are released and synapsing with the effector are
Norepinephrine or Epinephrine and Acetylcholine. NE and E will bind to
either alpha or beta adrenergic receptors. In sweat glands, some blood vessels
of skeletal muscles, coronary circulation and in the brain there is
Acetylcholine and it will bind to muscarinic receptors.
68
Explain which and how rapid control mechanism of arterial blood pressure can increase
or decrease blood pressure back to normal?
Rapid control mechanisms work within less than 10 seconds and have an effect for
some minutes.
Baroreceptors: senses changes in stretch and tension in blood vessels. It also senses
both an increase and decrease in blood pressure.
With increased blood pressure the baroreceptors are activated and send impulses to
the sensory area. The sensory area will:
- Stimulates the cardioinhibitory center → suppresses the heart activity.
- Inhibit the cardioacceleratory center → heart activity not stimulated
- Inhibit vasomotor area → vasodilation
- → the increased blood pressure will decrease back to normal.
With decreased blood pressure the baroreceptor will send less signals to the sensory
area so that it will not be stimulated.
- Cardioinhibitory center will not be stimulated → parasympathetic effect on
heart is removed
- Cardioacceleratory center is not inhibited → sympathetic effect on heart
increases
- Vasomotor area is not inhibited → vasoconstriction
- → the decreased blood pressure will increase and return to normal
Chemoreceptor: These chemoreceptors sense: Decreased PO2 (mostly) and pH but
also increased PCO2. These changes can occur if blood pressure is less than 80
mmHg. Activated chemoreceptors sends impulses to sensory center, the sensory
center activates vasomotor center causing a vasoconstriction and such stimulation of
chemoreceptors leads to increase of blood pressure
CNS ischemic response: Triggered from within the vasomotor center and is activated
by an increased PCO2 (mostly), decreased pH and decreased PO2. These changes can
occur if the blood pressure is below 40 mmHg. The vasomotor center activates within
itself due to changes within it and stimulates sympathetic centers T1-L3 →
vasoconstriction. The vasoconstriction increases blood pressure in the circulation.
- If the vasomotor center raises blood pressure sufficiently → the person can
survive.
- If the vasomotor center does not raise the blood pressure sufficiently→ the
vasomotor center dies and within 5 minutes of oxygen deprivation nerve cells
go into irreversible changes which might lead to death of neurons. If the
cardiovascular control center dies which can cause circulatory arrest and
death.
69
Explain events that begin and end each phase, characterise pressure in the
ventricle in respect to aortic and atrial pressure at the time of closure and
opening of valves!
1. Atrial systole: pressure in ventricle is 5 times lower than in atrium, AV valves are
open. The blood from atrium enters the ventricle and the pressure in ventricle is
lower than pressure in aorta, SL are closed and no blood leaves the ventricle
2. Isovolumetric contraction (ventricular systole): At the beginning: pressure in
ventricle is greater than pressure in atrium so AV valve closed, the ventricle becomes
a closed space since both valves are closed which leads to the length of cardiac
muscle and the volume not changing.
3. Ejection (ventricular systole): AV valve is closed since pressure is higher in the
ventricle than in the atrium. SL opens because pressure in the ventricle is greater than
pressure in the artery, blood from ventricles is ejected into large arteries. rapid
ejection: ventricular muscle contraction raises pressure until maximal. Slow ejection:
when ventricle gets emptied out och pressure in ventricle starts decreasing
4. Isovolumetric relaxation: AV valve is closed since pressure is higher in the ventricle
than in the atrium. SL closes since pressure in the ventricle becomes lower than in the
aorta- blood outflow from ventricle stops. The length and volume does not change.
ventricle relaxes and the pressure will drop
5. Filling phase (common diastol): AV valve opens since pressure in the ventricle is
lower than in atrium- blood flows into the ventricle. SL are closed since there is no
outflux from ventricles. Passive: 80% of the blood, blood flows down the pressure
gradient. Active: atrium pushes the last 20% of blood, pressure in atrium and
ventricle rises.
70
. Name, measure and evaluate the duration of all elements of an
electrocardiogram that are caused by electrical activity of atria. Speed of
recording 50 mm/s, amplification 10 mm/mV.
1/50= 0,02
- P wave: 5 x 0,02= 0,1, normal
- PQ segment: 2 x 0,02= 0,04, normal
- PQ interval: 7 x 0,02 = 0,14, normal
71
. Explain the cause of all elements of an electrocardiogram that are caused by
electrical activity of atria and give their normal values!
- P wave: Represents depolarization of right and left atria. The upgoing part
shows right atrium and the downgoing part shows the left atrium. Normal
value is from 0,06-0,1s.
- PQ segment: Represents the impulse spread through atrioventricular node.
Normal value is from 0,04-0,1s.
- PQ interval: Represents the impulse spread through atria to ventricle.
Normal value is 0,12-0,20s.
72
20 years old female person has blood pressure 150/80 mmHg and heart rate 84 x/min
a) Give normal range of arterial blood pressures and indicate if blood pressure for
this person is normal!
Normal blood pressure should be lower than 120/80, for systolic it should be
90-120 mmHg and for diastolic it should be 60-80 mmHg. The systolic is a
bit high and diastolic blood pressure is normal. Normal heart rate: 60-100
x/min, this patient has normal heart rate.
73
State at which moment the systolic/diastolic blood pressure is read:
In the auscultatory method: the first sound that is hearable after we deflate
the cuff is the systolic and after that we will hear a turbulent blood flow, once
the blood flow is not hearable anymore the diastolic pressure is determined.
- in the palpatory method: the diastolic pressure cannot be measured since
there is no stethoscope, but when placing the fingers on the artery it will
allow us to register systolic pressure, this method can be used when the
surroundings are loud.
74
Calculate the pulse pressure of this person! Provide the calculation formula!
Pulse pressure: Ps-Pd= 150-80= 70 mmHg.
75
20 years old female person has blood pressure 143/96 mmHg and heart rate 74 x/min
a) Give normal range of arterial blood pressures and indicate if blood pressure for
this person is normal!
Normal blood pressure should be lower than 120/80, for systolic it should be
90-120 mmHg and for diastolic it should be 60-80 mmHg. The systolic and
diastolic are higher than normal. Normal heart rate: 60-100 x/min, this patient
has normal heart rate.
76
Calculate the mean pressure of this person! Provide the calculation formula!
mean arterial pressure = ⅓ systolic + ⅔ diastolic
- 71,5 + 64 = 135,5 mmHg.
77
Name phases of cardiac pacemaker cell action potential and explain ion
permeability changes during them!
Funny voltage gated sodium channels open due to hyperpolarization (when
membrane potential decreases below -40 mV
1. When membrane potential reaches -55 to -60 mV, sodium influx will trigger
pacemaker potential or slow diastolic depolarization
2. At -50 mV, T-calcium channels (transient) opens, and calcium influx helps
funny sodium channels to depolarize the membrane until threshold is reached
3. At threshold (-40mV), L-calcium channels open and calcium influx triggers
fast depolarization
4. When L-calcium channels close, voltage gated potassium channels open, and
potassium outflux causes repolarization, bringing the membrane potential to
lower values
5. When membrane potential again reaches below -40 mV, funny sodium
channels start opening and from about -55 to -60 mV the next pacemaker
potential or slow diastolic depolarization begins.
78
Which phase of the action potential is affected by the sympathetic nervous
system? Name the neurotransmitter and receptor in the pacemaker cells!
The phase of the action potential affected by the sympathetic nervous system
is the depolarization phase in the pacemaker cells of the heart.
- The neurotransmitter released by sympathetic nerves is norepinephrine,
which binds to beta-1 adrenergic receptors on the surface of pacemaker cells
in the sinoatrial (SA) node, increasing the rate of depolarization and resulting
in an increase in heart rate.
79
Explain changes of blood pressure in the left ventricle and left atrium during
isovolumetric relaxation phase; indicate the state of valves during it!
Left ventricle:
- The ventricular pressure falls below the aortic pressure which closes the
semilunar valves this starts the isovolumetric relaxation. The ventricular
muscles relax, and the pressure rapidly decreases since no new blood flows
into the ventricle but the walls will try to expand. The blood volume stays the
same but pressure decreases. Due to no volume change, and no change in
length of cardiac muscle cells → pressure rapidly drops. At the end of
isovolumetric relaxation, when pressure in the ventricle is lower than
pressure in atrium → atrioventricular valves open and the filing phase begins.
Left atrium:
- Ventricular muscle has relaxed, and the atrioventricular plane is moved back
to initial position. At the same time, the atrium is almost maximally filled
with blood, thus the small movement of the atrioventricular plane raises
pressure in the atrium.
80
How do we call blood volume in the ventricle at the end of isovolumetric
contraction phase? How much is it?
The volume of blood in the ventricle at the end of the isovolumetric
contraction phase is called end-diastolic volume (EDV). The EDV is the
amount of blood remaining in the ventricle after it has contracted and before
it begins to fill with blood again.
- The exact value of ESV can vary but the average ESV for a healthy adult is
around 50-60 milliliters for the left ventricle and 60-70 milliliters for the right
ventricle.
81
Explain pressures that stimulate filtration through the wall of capillaries;
explain factors that determine them and give their average values!
Hydrostatic pressure describes pressure of fluid against the wall of
capillaries. Blood hydrostatic pressure is pressure exerted by the blood in the
capillary wall It tries to push blood out of the capillary stimulating filtration.
The average value is 30-40 mmHg in the arterial end and 10-20 mmHg in the
venous end.
- Colloid osmotic pressure is determined by the number of proteins that cannot
pass the wall of the capillary. Interstitial colloid osmotic pressure, proteins in
interstitium, attracts water to the interstitium which stimulates filtration. The
average value is 0-10 mmHg.
- If net hydrostatic pressure is greater than net colloid osmotic pressure →
filtration occurs: Fluid from the capillary will be filtered to the sub
glycocalyx space and from there the fluid will get out to the interstitial space.
The colloid pressure in the sub glycocalyx space decreases to 0 mmHg which
decreases the concentration of proteins in the sub glycocalyx space. The
decrease of sub glycocalyx colloid osmotic pressure will lead to a decrease
in filtration. The Average value of the net hydrostatic pressure when filtration
occurs is about 32 mmHg in the arterial end and about 12 mmHg in the
venous end.
82
Explain principles of calculation of filtration pressure through the wall of
capillaries!
In the arterial end we have a hydrostatic pressure of 35 mmHg while in the
venous end we have a pressure of 15 mmHg. In the interstitial space we have
a hydrostatic pressure of 3 mmHg in both ends of the capillary.
- The colloid pressure is 25 mmHg through the capillary and in the interstitial
space we have a pressure of 5 mmHg.
- To find out the arterial end net hydrostatic pressure we take the blood
hydrostatic blood - interstitial hydrostatic pressure, 35- 3= 32 mmHg and for
the venous end we take 15-3= 12 mmHg
- To find out the net colloid osmotic pressure we take plasma colloid osmotic
pressure- interstitial colloid osmotic pressure, 25-5= 20mmHg
- In order to find out which force out of filtration or reabsorption is greater we
use the effective filtration pressure. If the pressure value is negative then the
reabsorption will happen but if it is positive then filtration will happen. To
calculate the effective filtration pressure value: Net hydrostatic pressure - net
colloid osmotic pressure. 32- 20 = 12 which indicates a filtration happening
and 12-20 = -8 mmHg which indicates reabsorption.
83
Explain what’s going with rhesus disease in the second pregnancy!
During the second pregnancy, anti-D antibodies from the mother (that were produced
from the first pregnancy) can penetrate the placenta wall causing agglutination of
fetal erythrocytes leading to hemolysis which can cause harm or death of the fetus in
the uterus. Nowadays this is prevented by a shot.
84
Explain the extrinsic pathway of hemostasis until the production of clot!
The extrinsic pathway begins in damaged tissue and proceeds in blood. It is
activated within several seconds.
- In the prothrombin activator complex, the Xa factor and the Va factor are
present. The formation of this complex leads to clot formation by converting
prothrombin into thrombin, then fibrinogen into fibrin. First the mesh of the
fibrin is loose, then it becomes stabilized. This results in a blood clot.
85
Name the test that can be used to check the extrinsic pathway function, give its
normal value!
The test is called prothrombin time and the international normalized ratio is
70-100%.
86
Explain the role of thrombomodulin in hemostasis!
Reduces blood coagulation by activating plasma protein C that stimulates the
breakdown of blood clotting factors.
87
What is the normal number of blood platelets?
150,000 to 300,000 platelets per microliter of blood.
88
How is platelet plug formed?
Platelets, at the site of injury will stick to the the subendothelial tissue with the help
of receptors.
- Ia receptor ––> Sticks platelets directly to the subendothelial tissues (meaning
collagen fibers)
- Ib receptor ––> Uses von Willebrand factor, which sticks platelet tighter to
the subendothelial tissue
- Third receptor expressed on activated platelets: IIb/IIIa ––> binds and
concentrate fibrinogen at the site of clot formation, and later it will be
converted into fibrin.
89
What inhibits platelet plug formation outside the blood vessel damage site?
Prostaglandin I2 and Nitric oxide. These substances inhibit platelet adhesion
and aggregation outside the damage area. This prevents clot formation in all
cardiovascular blood vessels.
90
Give the normal number of erythrocytes, explain their functions!
The number of erythrocytes is different in women and men. In males it is
4,5-5,5 million per microliters and in females it is 4,0-5,0 million per
microliters. The function is to transport hemoglobin.
91
Explain factors that are needed for normal erythrocyte development!
The erythrocytes develop in the red bone marrow. It develops to
erythropoiesis. Vitamin B12 and folic acid is needed to multiply erythrocytes.
Also Iron is needed because it synthesizes hemoglobin and hemoglobin is the
main substance in erythrocytes.
92
Explain all effects of thrombin in the blood clotting regulation (in stimulation and
inhibition)!
The secondary haemostasis comes after the primary and forms fibrin meshwork. It
has 3 stages: formation of prothrombin activator complex, prothrombin ––> thrombin,
and fibrinogen ––> fibrin. Fibrin traps blood cells making a secondary red clot. There
is an intrinsic and an extrinsic pathway to get to the production of prothrombin (1
stage) that activate at different rates but are both necessary. All these stages use 12
coagulating cofactors to be executed. Thrombin is necessary for the triggering of the
fibrin meshwork in the 3rd stage. It also gives positive feedback to a lot of cofactors
necessary for the other stages (V5, XIII13, VIII8 and XI11) and it binds to the
platelets stimulating their aggregation.
93
Explain consequences after the first rhesus incompatible pregnancy!
Rh incompatibility usually isn't a problem during the first pregnancy. That's
because the baby's blood does not normally enter the mother's circulatory
system during the pregnancy. During the birth, though, the mother's and
baby's blood can mix. This leads to complications for the second pregnancy.
94
Explain consequences after the second rhesus incompatible pregnancy!
The mothers antibodies that were developed after the first birth will recognize
the D antigens on the surface of the baby's blood cells as foreign. Her
antibodies will pass into the baby's bloodstream and attack those cells,
causing hemolysis.
95
Explain events in the primary hemostasis!
The hemostasis is divided into 3 stages but two of them are primary
hemostasis. First there will be a vasoconstrictor in the site of the injury which
will decrease blood flow through the injured part to decrease blood loss.
Second is the platelet plug formation, here the different platelets will stick
together on the injured blood vessel wall which will decrease the bleeding.
96
Explain factors that inhibit platelet plug formation!
Substances like prostacyclin I2 and NO (nitric oxide) decrease the stickiness
of the platelet which escapes the clot formation site and inhibits platelet
adhesion and aggregation outside the damaged area.
97
Explain tests that can be used to evaluate primary hemostasis; give their normal
values!
(Duke) 1-5 min: The first test is related to the bleeding time which according to the
Dukes method is about 1-5 minutes
1. We make a small cut in the fingertip, or more often in the earlobe
2. Every 30 seconds we touch the wound with a filter paper to check if the
bleeding has stopped or not
3. We take the time from the cut of the finger/earlobe until the bleeding has
completely stopped
(Ivy) 1-9 min: Since bleeding time depends on the circulation of skin of earlobe,
finger, lower arm, and blood pressure of the circulation it is also standardized
1. In the standardize method, also called Ivy method, the cuff is wrapped around
the upper arm and inflated until 40 mmHg
2. Small scratches are then made on the middle side of the lower arm
3. By using a filter paper is again the time until the bleeding stopped measured
4. The bleeding time can extend from 1-9 minutes
* Since these tests are dependent on the skills of the doctor and on the blood flow of
the skin, which might be changed due to temperature of body and outer environment
* These tests are not considered precise
- Platelet function analysis
1. Venous blood is taken from the person, and it is drawn through thin glass
tubes which either is covered by: Collagen/epinephrine (<180 s) &
Collagen/ADP (<120 s)
2. We the measure the time it takes to make the platelet clot and stop blood from
flowing through this small tube is taken.
3. In case of collagen/epinephrine coated glass tube ––> lesser than 180s
4. In the collagen/ADP coated glass tube ––> lesser than 120 seconds
5. In the case if platelet count or function is weaker these functional tests are
longer.
