Test One Flashcards

1
Q

Signals from bio208

A

Signals can be:
Chemical messages: different ions (Ca); neurotransmitters (acethylcholine); different hormones (which ones did you mention in BIO208? - see
slide 10 if you forgot or my last point in the notes here)
or Electrical messages, such as
- messages for communication - transport: different ions involved in membrane potential changes (Na, K)
- Action potential travelling through a neuron (fast)
- Events at the synaptic cleft or a neuromuscular junction (a bit slower as multiple cells involved)
- Transport of PTH or calcitonin through blood (slowest)

more on a slower response system in the body - your endocrine system and introduce hormones as
chemical signals. Hormones can be proteins, peptides, steroids, amines and glycoproteins that travel through the body via blood stream to
“affect the activity only of its target cells; that is, cells with receptors for that particular hormone. Once the hormone binds to the receptor, a
chain of events is initiated that leads to the target cell’s response. Hormones play a critical role in the regulation of physiological processes
because of the target cell responses they regulate” (From Open Stax Anatomy & Physiology).

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2
Q

Monitoring blood calcium levels

A

Signals: Calcium, Calcitonin, PTH, Osteoclast, Osteoblast
Transported to: From thyroid/parathyroid to osseous tissues / renal tissues (kidneys) / digestive tissue (intestine)
From Open Stax Anatomy & Physiology:
“Figure 17.16 Parathyroid Hormone in Maintaining Blood Calcium Homeostasis Parathyroid hormone increases blood calcium levels when
they drop too low. Conversely, calcitonin, which is released from the thyroid gland, decreases blood calcium levels when they become too
high. These two mechanisms constantly maintain blood calcium concentration at homeostasis.” What is figure 17.16 an example of? An
endocrine system response related to parathyroid/thyroid gland role in calcium balance as a negative feedback loop. The negative feedback
loops are the basis of homeostatic balance or physiological regulation in the body. In addition to continually including endocrine system and
hormones, we will always discuss negative feedback loops as they play a key role in balance in the body (and endocrine system). Part 3a is
what you have focused on in BIO208 - we will talk more about 3b in unary system lectures in BIO209.
What we can use this figure for, is to illustrate how or why an endocrine system can involve a slower response - the signals are transported via
blood, which circulate through the body, which take more time than transport between neurons and other cells, for example (direct
communication or link)

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3
Q

What is blood

A

Blood is composed of plasma and formed elements. Plasma contains mostly water, proteins, and other solutes. Formed
elements contain red blood cells (erythrocytes), white blood cells (leukocytes), and platelets. Hormones are secreted into the blood and
circulate in the plasma mostly via transport proteins (or freely).
Figure 18.2 illustrates normal composition of blood on the left, anemic blood (with low composition of hematocrit of % of erythrocytes), and
plychetemic blood (elevated composition of hematocrit).
“Figure 18.2: The cellular elements of blood include a vast number of erythrocytes and comparatively fewer leukocytes and platelets. Plasma
is the fluid in which the formed elements are suspended. A sample of blood spun in a centrifuge reveals that plasma is the lightest
component. It floats at the top of the tube separated from the heaviest elements, the erythrocytes, by a buffy coat of leukocytes and platelets.
Hematocrit is the percentage of the total sample that is comprised of erythrocytes. Depressed and elevated hematocrit levels are shown for
comparison.

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4
Q

What’s in a blood vessel

A

water, proteins, nutrients, blood cells (erythrocytes and leukocytes), platelets, hormones, ions/solutes

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5
Q

Lymphatic system transport

A

Another type of transport system that we will focus less on is the lymphatic system (lymph vessels, lymph nodes and organs, such as thymus
and spleen). Lymph contains a fluid (interstitial fluid) and white blood cells. Blood and lymph both circulate through the body and depending
on the distance needed to travel can represent a slow signal and slow response. In Figure 21.2 on the left, you can see the main vessels and
nodes of the lymphatic system in green but what should be also visible is the connection between the lymphatic system and the blood
vessels (example of the capillary network where exchange of nutrients, oxygen, carbon dioxide and other solutes happens). In Figure 21.4 on
the right, you can also seen that the lymphatic system drains into the circular system via thoracic duct on the left and the lymphatic duct on
the right into some of the main large veins (which we will cover in more details in a few lectures)

Blood/Lymph Connection: Lymph enters the venous section of the cardiovascular system through thoracic duct and right lymphatic duct.
Why the connection? Return the fluid to the blood (lymph = fluid and white blood cells,“recycled blood plasma”) - the fluids is rich in white
blood cells for immune system response and protection of the body

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6
Q

Lymphocytes and their functions

A

Where do the white blood cells that exist in lymph and blood develop?
There are two different developmental origin of different types of white blood cells that play a role in defence against foreign bodies in your
body (one origin leads to the development of red and white blood cells and the other to the development of different lymphocytes).
From Open Stax Anatomy & Physiology:
Figure 21.5 Hematopoietic System of the Bone Marrow All the cells of the immune response as well as of the blood arise by differentiation
from hematopoietic stem cells. Platelets are cell fragments involved in the clotting of blood.”

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7
Q

Compare and contrast nervous and endocrine
system signal.

A

Nervous system
Speed: fast
Distance: short
Organ system connections: nervous to any other system
Endocrine
Speed: slowest
Distance: long
Organ system connections: endocrine to any other system
Blood
Speed: slower (cycles of circulation)
Distance: long
Organ system connections: Involved in transport of signals/nutrients and messages for all systems
Lymph:
Speed: slower (cycles of circulation)
Distance: long
Organ system connections: Drainage into cardiovascular system (venous system)

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8
Q

locate your heart! How big is it?

A

In thoracic
cavity
• Medially
between the
lungs (rather
central than to
the left)

The heart is positioned above the diaphragm, posterior to the sternum, and between the lungs in the thoracic cavity (medially but slightly to
the left of the body in the thoracic cavity.
Do you remember what saggital view refers to? views in sagittal plane split the body in right and left views. In videos, I will be using Visible
Body but here I will use Complete Anatomy. You may have used other 3D viewing software or apps in BIO208 and you can use whatever
works best for you but please note that we will use 3D visualization aids less in BIO209 as I will just occasionally use them to help you
understand the positioning of a structure or different views of a structure.

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9
Q

How is your heart protected in the thorax?

A

Heart is protected by the pericardium in the pericardial cavity. In addition to the most outer fibrous pericardium, beneath this layer the heart is
further lined with serous pericardium, which consists of two layers: the outer parietal serous layer and the inner visceral (viscera - closer to
organ) serous layer, also known as epicardium. Below the epicardium if the muscle layer of the heart or the myocardium and the inner lining of
the heart (the lining outlining all the chambers) is the endocardium.
Protected by
pericardium in
pericardial cavity
• Layers: fibrous
pericardium,
parietal & visceral
layers of serous
pericardium,
myocardium and
endocardium

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10
Q

What are some key external heart features?

A

In the anterior view of the heart you can see the apex, right and some of the left atria (auricles are the muscular pouches of atria), you also see
mostly right ventricle but also a large part of the right ventricle. Of the major vessels associated with the heart, you can see the superior and
inferior vena cava (the major vein bringing blood to the heart from the body) and aorta divided into ascended aorta, aortic arch, descending
aorta (the major artery sending blood from the heart to the body), You also see pulmonary arteries and veins which are heart’s connections to
the lungs. You also see coronary arteries and veins which are smaller vessels that provide blood supply to the hard working cardiac muscle.

In the posterior view of the heart you can see the apex, left atria and right atria, complete left ventricle and most of the right ventricle .Of the
major vessels associated with the heart, you also see superior and inferior vena cava, and aorta and the pulmonary veins and arteries. You
also see coronary sinus, which is a larger blood vessel that divides into coronary arteries and veins.

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11
Q

What are some key internal heart features?

A

To view internal heart structures, we are looking at the anterior view with some of the heart chambers in frontal sections. Between right atrium
and ventricle you see the tricuspid valve with chord tendinae attaching this valve to the inferior part of the right ventricle. On the left side, we
see the bicuspid valve between the left atrium and left ventricle. You also see the valves in the major blood vessels connected with the
ventricles that send the blood towards the body or the lungs. On the left side is the aorta with the aortic valve and on the right side is the
pulmonary artery with the pulmonary valve. These are all one-way valves, meaning that they only allow blood from from atria to ventricles or
from ventricles to major blood vessels.

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12
Q

How does the blood flow through the heart?

A

To help us discuss blood flow, we can also look at the transfers section of the heart, right at the level between the atria and ventricles.
Blood flow through both sides of the heart happening simultaneously (check some of the animations I included in the video lecturette page for
Module 2 to help you visualize how heart’s left and right side work together at the same time.
Blood flow through the heart on the R side:
- from the body via superior/inferior vena cava into right atrium (blood low in oxygen)
- from the right atrium through the tricuspid valve into right ventricle
- from the right ventricle through the pulmonary valve into pulmonary arteries to the lungs (to be oxygenated)
Blood flow of the heart on the L side:
- from the lungs via pulmonary veins into left atrium (blood rich in oxygen)
- from the left atrium through the bicuspid valve into left ventricle
- from the left ventricle through the aortic valve into aorta to the rest of the body

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13
Q

What is special about cardiac muscle?

A

Striated,
shorter, thinner
• Less t-tubules
and low
calcium stores
• Rich in
mitochondria
and intercalated
discs Myocardium or cardiac muscle is similar in striated appearance to the skeletal muscle, but there are some structural differences that also
result in differences in electrical conductivity through the muscle. Because of lower amount of t-tubules in cardiac muscles, there are less
calcium stores so supply is needed and this muscle is rich in mitochondria because of constant and hard work of the muscle tissue. You can
also see intercalated disks rich in desmosomes and gap junctions, which ensure that all sections of the muscle are well connected with each
other and signal (ions) can move fast through different muscle sections so that cardiac contraction can be synchronous.

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14
Q

What is special about cardiac muscle electric potential

A

Slow influx,
prepotential
• Rapid influx of
calcium,
depolarization
• Outflux of
potassium,
repolarization

The electrical potential of the heart takes place in conductive heart cells (which result in electrical conduction cause a contraction in
contractile cells of the heart). You are looking at how an action potential moves through the electrical conducting cells. We see a slow influx
of sodium, which depolarizes the membrane to a threshold (movement os sodium inside the cells to increase the positive polarity of the
membrane by influx of positive ions). What speeds up this depolarization is the calcium, which does so rapidly and then it is the outflow of
potassium, just like in the action potential in the neurons that repolarizes the membrane.
The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization. The
prepotential accounts for the membrane reaching threshold and initiates the spontaneous depolarization and contraction of the cell. Note the
lack of a longer resting potential.
Here, we are looking at action potential through the contractile cells of the heart, which result in cardiac muscle contraction. Note the plateau
as the calcium cahnnels open and influx of calcium is slower so that depolarization of the cardiac muscle is longer and therefore the resulting
contraction is longer in duration.

Its own
conduction
system
• Sinoatrial (SA)
node
• Atrioventricular
node (AV)
• AV and bundle
branches
• Purkinje fibers

We mentioned that the electrical potential of the heart takes place in conductive heart cells. In this slide, you are now viewing, the electrical
conducting cells and pathways in the heart. Note the two nodes, the sinoatrial (SA) and atrioventricular (AV) nodes. SA node is self-pacing
centre of the heart, while the AV node controls the electrical conduction to the ventricles. The signal starts at the SA node and is sent to AV
node via intermodal conducting pathways. From AV node, signal is sent via AV bundle (or bindle of His) to the wall between right and left
ventricle, specifically to the right and left bundle branches, which then branch off throughout the ventricle wall and also branch off into smaller
conducting pathways in the ventricles, the Purkinje fibers.

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15
Q

How does cardiac conduction work

A

Rest
• 2: Action potential
(AP) at SA node
and across atria
• 3: AP at AV node,
atria contract
• 4: AP through AV
bundles
• 5: AP though ventricles
Heart
Module 2
• 6: ventricles contract
(repolarization)
(1) The sinoatrial (SA) node and the remainder of the conduction system are at rest (moment of closure of potassium channels). (2) The SA
node initiates the action potential, which sweeps across the atria. (3) After reaching the atrioventricular node, there is a delay of approximately
100 ms that allows the atria to complete pumping blood before the impulse is transmitted to the atrioventricular bundle. (4) Following the
delay, the impulse travels through the atrioventricular bundle and bundle branches to the Purkinje fibers, and also reaches the right papillary
muscle via the moderator band. (5) The impulse spreads to the contractile fibers of the ventricle. (6) Ventricular contraction begins.

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16
Q

How do we assess cardiac function?

A

P wave - atrial depolarization
QRS - ventricular depolarization
T wave - ventricular repolarization
PR interval - events at the atria
QT interval - events at the ventricles
P-R segment - time during which atria contract (no line deflection - no ion movements)
S-T segment - time during which ventricles contract (no line deflection - no ion movements)

(1) The sinoatrial (SA) node and the remainder of the conduction system are at rest (moment of closure of potassium channels). (2) The SA
node initiates the action potential, which sweeps across the atria; P wave - atrial depolarization
(3) After reaching the atrioventricular node, there is a delay of approximately 100 ms that allows the atria to complete pumping blood before
the impulse is transmitted to the atrioventricular bundle; P-R segment - time during which atria contract (no line deflection - no ion
movements); (4) Following the delay, the impulse travels through the atrioventricular bundle and bundle branches to the Purkinje fibers, and
also reaches the right papillary muscle via the moderator band; QRS - ventricular depolarization (5) The impulse spreads to the contractile
fibers of the ventricle; S-T segment - time during which ventricles start contracting (no line deflection - no ion movements)
(6) Ventricular depolarization begins

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17
Q

What is a cardiac cycle

A

• Time between
atrial contraction
and ventricular
relaxation
• Contraction:
systole
• Relaxation:
diastole

The period of time that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle (Figure 19.27).
The period of contraction that the heart undergoes while it pumps blood into circulation is called systole.
The period of relaxation that occurs as the chambers fill with blood is called diastole. Both the atria and ventricles undergo systole and
diastole, and it is essential that these components be carefully regulated and coordinated to ensure blood is pumped efficiently to the body

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18
Q

How else do we assess cardiac function?(sounds)

A

Lub (S1) is the sound that the closure of the atrioventricular (tricuspid and bicuspid) valves makes. Dub (S2) is the sound of semilunar(aortic
and pulmonary) valve closures. Semilunar valves close (dub or S2) as the cardiac cycle ends and ventricles complete ejection of the blood
from the ventricles into the blood vessels carrying the blood away from the heart. Atrioventricular valves close (Lub or S1) as the first phase of
ventricular contraction begins and the ventricles have completely filled with blood.

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19
Q

What is cardiac output

A

Cardiac output
(CO) is the amount
of blood pumped
by each ventricle
in one minute
• CO depends on
heart rate and
stroke volume
(SV)

We assess or measure cardiac function through cardiac output. Specifically cardiac output (amount of blood pumped through the heart in a
minute) depends on heart rate and stroke volume. Heart rate is affected by autonomic innervation, hormones (see Slide 19) as well as fitness
level and age. Stroke volume (how much volume of blood can the heart pump) is determined by heart size, fitness levels, gender, contractility
of the heart muscles, duration of contraction, how much blood did the heart receive (preload) and how much resistance is there to sending
blood out of the heart (after load). You will discuss cardiac output in relation to exercise in much more detail in next case study in tutorials (just
before your first term test)

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20
Q

What factors affect heart rate

A

What factors affect heart rate (HR)?
Figure 19.33
Heart structures Blood flow Cardiac conduction
Figure 19.32
Sympathetic nervous system; release of
norepinephrine; increased levels of CO2, low
blood pressure; exercise or anticipation of
physical exercise; increased thyroid
hormones; decrease in sodium, potassium
and/or calcium; increase in body
temperature; stimulants

Here you are seeing how heart rate is affected by autonomic innervation. Vagus nerve has a parasympathetic signal to the heart to slow down
the heart rate, while the sympathetic cardiac nerves send a signal to increase the heart rate. You can see some examples of when
parasympathetic and sympathetic nerves can be activated in the slide but you don’t have to remember all the details yet - we will come back
to this when we talk about regulation of heart function in more details.

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21
Q

What factors affect stroke volume

A

SV = EDV-ESV
• Increase in EDV
increases SV
• Decrease in EDV
decreases SV
• Increase in ESV
decreases SV
• Decrease in ESV
increases SV

We mentioned that cardiac output (amount of blood pumped through the heart in a minute) depends on stroke volume and this slides defines
stroke volume and how it can be affected. First of all, stroke volume is end diastolic volume minus the end systolic volume or on other words
how much blood enters the heart before the cardiac cycle and how much is left in the heart at the end of the cardiac cycle. The higher the
EDV (more blood enters the heart), the higher the stroke volume. The lower the amount of blood left in the heart (ESV), the higher the stroke
volume.
EDV depends on preload, which is how fast and how much venous blood is returning to the heart (more blood or faster return increases EDV,
thus increasing SV). ESV depends on resistance too flow (after load) and contractility of the heart . The higher the resistance or afterload, the
more blood is left in the heart or higher the ESV, which therefore reduces SV. The higher the contractility, the less blood stays in the heart so
the ESV is lower, meaning that SV is higher.
The bottom row of this table discusses regulation of cardiac output,

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22
Q

How do HR & SV affect cardiac output?

A

HR affected by
autonomic
innervation,
hormones and
input by venous
return
• SV affected by
preload,
contractility, and
afterload
• CO affected by
HR and SV

his slide summarizes how heart rate and stroke volume affect cardiac output again.
Heart rate is affected by autonomic regulation and hormones as seen on Slide 19. Factors that affect stroke volume (SV) are venous return
and filling time of the atria (which is related to preload). If venous return is large and filling time is fast, preload is high and therefore end
diastolic volume (EDV) is high. Because SV is EDV mini end systolic volume (ESV), when EDV is increased so is SV. Autonomic innervation,
hormones affect the contracitility of the heart. The higher the contractility, the less blood stays in the heart so the ESV is lower, meaning that
SV is higher. How vasodilated or vasoconstricted vessels are affects the resistance (afterload). The higher the resistance or afterload, the more
blood is left in the heart or higher the ESV, which therefore reduces SV. We will come back to in Module 4 in more details when we discuss
regulation of heart function.

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23
Q

Blood flow

A

Pulmonary: carries blood from and to gas exchange areas in lungs
Systemic: carries blood from and to areas of the body (other than the lungs)
Blood enters left atrium, left ventricle, rest of body
Right side from systemic circuit to right atrium, right ventricle to pulmonary
Pulmonary carries blood to and from gas exchange areas in lungs- capillary beds surround respite ray strictures
Blood leaving left atrium via aorta into smaller arteries
Through capillaries to exchange oxygen, nutrients collect waste, sent back to heart
Blood sent to systemic circuit first goes back through pulmonary circuit before sent to heart
More complex circuits, has communication with heart receives material from blood removes waste- hepatic

What are the major structures
Aorta vs artery

Lecture
The heart and two circuits
Pulmonary- lung and circuit that exists around alveola
Communication of heart to lung

Colouration of the blood, blue- deoxygenated, red- oxygen-
The space is capillaries
Two circuits dependent on one another blood reaching systemic goes through pulmonary before – need it to be oxygenated

One more type of system- hepatic
The liver receives and sends blood by systemic circuits, liver is connected to blood around different systems to help liver, receives from hepatic artery rom systemic and organs via hepatic veins important to regulation of hormones

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24
Q

What are arteries

A

Away from the heart
Elastic
Thick walls with small lumens

Three tissue layers, tunics:
intima, wavy, with elastic membrane in larger arteries media, thick, muscular, with elastic membrane in larger arteries
externa, thin in all but largest arteries, with elastic fibers and nerves
A- away from heart
Arteries carry blood away from heart
Elastic with thick walls
Lumen- space in blood vessel
Larger artery different from elastic
Creates pressure- larger ones
Three tissue layers- tunic
Intima- closest to lumen, wavy wide, elastic membranes
Media- thick elastic ape range, wav, most smooth muscle sport
External- most outer, thin, elastic fiber, nerve endings

Lecture

Arteries- away from heart
Elastic and muscular- bigger
Aorta, artery
Return back to original sgaoe wth ease
Have thick walls an small lumens
Darker pin– walls and layers of vessel, the space is the lumen- inside space
In histological- no colour difference between vein and artery

Tunica
Intima- inner thinnest layer, wavy, closest to lumen
Media layer, extensive in bigger arteries
External- outer layer – biggest layer in large arteries, gives signals if it is increasing or Dec in diameter

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25
Q

What are veins

A

Toward the heart Compliant Thin walls with large lumens Valves in limbs and inferior to the heart

Three tissue layers, tunics:
intima, smooth, no elastic membrane media, thin, with collagenous fibers and nerves, no elastic membrane
externa, thick, with collagenous fibers, smooth fibers, smooth muscle and nerves
Carry blood toward heart
More compliant
Thin vessel wall, irregularly shaped, larger lumen
Medium- positioned inferior have valves correct blood flow
Tunic
Intima- thinner

Opposite direction of blood flow
Compliant- stretches easily, extends

Thinner walled, lumen is irregular shaped
Not wavy
Intima, smooth, no elastic membrane
Media- collagen
External- thickest, smooth muscle appearance

Venule- closest to capillary

Vein are resevoir of blood- 60%, processing more blood than arteries

Valves help push the blood flow towards the heart

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26
Q

What are capillaries

A

Continuous: water, small solutes and lipid- soluble material

Fenestrated: rapid exchange of water and large solutes peptides

Sinusoid (rarest): exchange of largest molecules (plasma, cells) in bone marrow, liver and glands
Other vessel
Capillary bed
Arteriole and venule empty into smaller vessels- capillary, network= bed
Have different openings in the layers
Sinusoid- many openings, let cell through support infiltration of cells, lymph glands
Continuous- small solutes fee started- middle
Have full membrane but can allow for rapid exchange of water and large solutes

Lecture
Mesh network- capillary bed- vessel circuits connect to cappilary on either side
Venule- receives from capillary

Filtration or exchange, here need higher chance for exchange, need to exhange many things- extra peatrive layers allow for molecules to go through

Most perforated , exchanges largest

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27
Q

How does diameter change in vessels?

A

Elastic arteries and venae cavae have the largest diametiencfralusdt(ecsdt.?losest
to the heart) Arterioles and venules have the
smallest diameter (closest to the capillary beds)
Different properties and factors of changes of blood vessels
They have different diamanter
Aorta and artery- larger so are veins
Higher diameter, more blood flow
Larger diameter, lower resistance
Increasing diameter Dec resistanxce

Lecture
Blood vessel types and diameter
Largest vessel, largest diameter
Order of vessel in closest to farthest from heart
Dimatater, directly proportional to blood flow, inversely related to resistance, higher diameter, lower resistance

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28
Q

How does area change in vessels?

A

Areas with vessels that have small diameter have the highestincfcalusdrteosdt.?ss-
sectional area Increase in cross- sectional area
increases surface available for exchange Cross sectional area
Area with vessels that have smal diameter have large area
What it to be larger so more elements can be exchanged through the tissues and body, not getting diameter , maximize space

Small diameter- highest area
Increases exhange of elements

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29
Q

How does velocity change in vessels?

A

Blood flows fastest in the
arteriesI with large diameter

Blood flows slowest in vessels with small diameters
High blood flow in the largest diameter
Connected to some of the layers lowest in small diameters
Veins have s larger diameter, why not as fast as arteries, they are more compliant and brings it toward heart, have harder time

As get closer to cappiliary want it to slow down, allows for exchange
High elastic pressure= artery
Venous- more compliance, less muscle
Artery work at higher speeds and pressures
Veins- don’t reach speed, more compliant and agianst gravity

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30
Q

How does velocity change in vessels?

A

There is a lot more blood
volumeI that needs to be supported
In large part, this blood volume needs to be circulated againts gravity

One-way valves to ensure unidirection al flow of blood (in limbs and vessels inferior to the heart)
The valves help the velocity inc, blood pushes through valve closes so there’s no backflip, helps push good up towards eart
Veins have more challenges, upport more blood volume
Artery can help take away
Blood needs to be circulated against gravity
One way vta;be help push blood up
Valves open one at a time, needs to pass through for valve to open first

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31
Q

How pressure changes in vessel

A

Pressure is the highest in arteries with the largest diameter and most elastic/muscular tunics

Pressure is the lowest in the largest veins
Blood pressure changes relates to large musculature tunic, thicker walled (muscular system veins

Related to resistance
Tunica media- thickest= highest power

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32
Q

How pressure changes

A

Blood pressure: peak systolic over peak diastolic
Arterial pressure is higher during ventricular systole (walls contract) and lower during diastole (walls stretch and recoil)
There is a pressure difference between the vessels, peace vessels in systole and lowest pressure in diastole
Arterial pressure is the average of the two contractile systems
Systolic- walls contracting
Lowest when diastole- walls of ventricles in stretch and recoil
Measuring this pressure- good presssure
Can help tell about heart health

Pressure during contraction and relaxation
Mean of presssure= average between relation and contraction

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33
Q

What happens in capillary beds

A

Bulk flow: fluid moves I from
pressure area (capillary bed) lower pressure area (tissues) via filtration

Net filtration pressure is the interaction of the hydrostatic (the force exerted by the blood in a vessel - forces fluids out of capillary) and osmotic pressures (the movement of fluid from the interstitial fluid - forces fluids into the capillary)
Filtration Hydrostatic pressure > osmotic pressure Positive net filtration (fluid exits capillary, filtration)
No net movement ydrostatic pressure = osmotic pressure
0 net filtration
(no fluid movements)
Reabsorption Hydrostatic pressure < osmotic pressure Negative net filtration (fluid enters capillary, reabsorption)
Surface area exchange and increase- exchange of blood and materials in tissue
Exchange in capillary beed
Fluid moves fom higher pressure(in blood vessel
To lower pressure area- tissue
Done via filtration
Can tell which direction it’s going out or in
Out- filtration
In- venous end- becomes venule drains into veins and back to heart
Return of the fluid- reabsorptiuon
Direction of bulk flow- can determine through the filtration pressure-NFP
Interaction of two pressures(hydrostatic- by blood vessel) osmotc(movement of fluid from interstitial fluid- moves back into capillary bed)
Higher pressure in capillary bed or higher osmotic pressure- positive net filtration- fluids moving from high to low, exiting capillary bed- filtration

Hydrostatic Lower than osmotic- negative net filtration
The fluid is moving bac- higher to lower pressure - reabsoprion
Equalized- zero movement

Bulk flow- fluid moves from high to low pressure via filtration
Hydrostatic- pressure in blood vessels
Osmotic pressure outside space
Are they moving from high to low- hydrostatic high and osmotic low- move from high to low
Hydrostatic pressure is low and osmotic is high, allows material into blood to be sent back

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34
Q

Different roles of blood

A

Cells, tissues, organs and organ systems of the body are impacted by or depend on the cardiovascular system

Delivering hormones

Transports white blood cells, antibodies and excess fluids from lymphatic

Transport for oxygen and carbon dioxide

Sexual arousal and erection, delivery of sex hormones

Delivers resting circulation to kidneys for filtering
Connections between blood and different body systems
These are the key riles
Major vessels- connect back to heart

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35
Q

Major pulmonary vessels

A

Pulmonary veins- right vs left- from and to lung
Aortic arch- ascending and descending aorta
Branches into 3 main arteries- brachiceohlaic trunk, common carotid artery
Most to left- subclavia atery’
Bring blood into right atriria

Right
Inferior and superior vena cava
Pulmonary trunk branches into pulmonary artery

Aortic arch
Coming from left atrium

You should be able to locate:
- aorta (ascending and descending)
- aortic arch
- vena cave (inferior and superior)
- pulmonary arteries (and pulmonary trunk - the base leaving the right
ventricle)
- pulmonary veins

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36
Q

Major systemic vessels

A

Brachiocephlaic branch
Scamming carotid artery descending aorta beach SES into ilia and femoral artery - into legs
Braciocheplaic trunk and sublavian, auxiliary artery connect to upper limb

Veins
Systemic veins bringing back to hart- right side

Brachiocephalic vein, axillary and cephalic vein

Iliac vein and femoral vein

Jugular vein]
Subclaviean
You should be able to locate:
- common carotid artery
- brachiocephalic trunk
- internal and external jugular vein
- subclavian artery and vein
- axillary vein and artery
- brachial artery and vein
- radial and ulnar artery and vein
- renal artery and vein
- iliac artery and vein
- femoral artery and vein
- tibial and fibular artery and vein

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37
Q

What is cardiac output

A

Amount of blood pumped by each ventricle in one minute

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38
Q

What does cardiac output depend on

A

Heart rate and stroke volume

We assess or measure cardiac function through cardiac output.
Specifically cardiac output (amount of blood pumped through the heart in
a minute) depends on heart rate and stroke volume. Heart rate is affected
by autonomic innervation, hormones (see Slide 4) as well as fitness level
and age

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39
Q

Heart rate

A

contractions per
minute or beats
per minute
• Affected by
sympathetic and
parasympathetic
innervation. Here you are seeing how heart rate is affected by autonomic innervation.
Vagus nerve has a parasympathetic signal to the heart to slow down the
heart rate, while the sympathetic cardiac nerves send a signal to increase
the heart rate. You can see some examples of when parasympathetic
and sympathetic nerves can be activated in the slide but you don’t have
to remember all the details yet - we will come back to this when we talk
about regulation of heart function in more details. We already discussed
the regular action potential signal through the conducting cells of the
heart.

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40
Q

Stroke volume

A

Stroke volume
(SV): how much
volume of blood
can the heart
pump
• SV = end-diastolic
volume (EDV) -
end-systolic
volume (ESV)

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41
Q

What does stroke volume depend on

A

Stroke volume (how much volume of blood can the heart pump) is
determined by heart size, fitness levels, gender, contractility of the heart
muscles, duration of contraction, how much blood did the heart receive
(preload) and how much resistance is there to sending blood out of the
heart (after load). You will discuss cardiac output in relation to exercise in
much more detail in next case study in tutorials (just before your first term
test).

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42
Q

What affects stroke volume

A

The higher the EDV (more blood enters the heart), the higher the stroke
volume. The lower the amount of blood left in the heart (ESV), the higher
the stroke volume. EDV depends on preload, which is how fast and how
much venous blood is returning to the heart (more blood or faster return
increases EDV, thus increasing SV). ESV depends on resistance too flow
(after load) and contractility of the heart . The higher the resistance or
afterload, the more blood is left in the heart or higher the ESV, which
therefore reduces SV. The higher the contractility, the less blood stays in
the heart so the ESV is lower, meaning that SV is higher

Increase in EDV increases SV
. Decrease in EDV =
decreases SV
• Increase in ESV decreases SV
• Decrease in ESV increases SV

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43
Q

How do HR & SV affect cardiac output?

A

• HR affected by autonomic innervation, hormones and input by venous return
• SV affected by preload, contractility, and afterload

The higher the EDV (more blood enters the heart), the higher the stroke
volume. The lower the amount of blood left in the heart (ESV), the higher
the stroke volume. EDV depends on preload, which is how fast and how
much venous blood is returning to the heart (more blood or faster return
increases EDV, thus increasing SV). ESV depends on resistance too flow
(after load) and contractility of the heart . The higher the resistance or
afterload, the more blood is left in the heart or higher the ESV, which
therefore reduces SV. The higher the contractility, the less blood stays in
the heart so the ESV is lower, meaning that SV is higher.

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44
Q

Neural regulation of heart rate

A

Parasympathetic nervous system; release of
acetylcholine; decreased levels of CO2, high
blood pressure; rest; decreased thyroid
hormones; decrease in calcium; increase in
sodium and/or potassium; decrease in body
temperature; opiates and depressants Sympathetic nervous system; release of
norepinephrine; increased levels of CO2, low
blood pressure; exercise or anticipation of
physical exercise; increased thyroid
hormones; decrease in sodium, potassium
and/or calcium; increase in body
temperature; stimulants (nicotine,

Here you are seeing how heart rate is affected by autonomic innervation.
Vagus nerve has a parasympathetic signal to the heart to slow down the
heart rate, while the sympathetic cardiac nerves send a signal to increase
the heart rate. You can see some examples of when parasympathetic
and sympathetic nerves can be activated in the slide but you don’t have
to remember all the details yet - we will come back to this when we talk
about regulation of heart function in more details.
Parasympathetic nervous system; release of acetylcholine; decreased
levels of CO2, high blood pressure; rest; decreased thyroid hormones;
decrease in calcium; increase in sodium and/or potassium; decrease in
body temperature; opiates and depressants.
Sympathetic nervous system; release of norepinephrine; increased levels
of CO2, low blood pressure; exercise or anticipation of physical exercise;
increased thyroid hormones; decrease in sodium, potassium and/or
calcium; increase in body temperature; stimulants (nicotine, caffeine)

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45
Q

Auto regulation of cardiovascular systems

A

Vascular resistance: friction between blood and vessel walls; depends on
diameter and length of vessel, ΔP represents the difference in pressure,
r4 is the radius (one-half of the diameter) of the vessel to the fourth
power, η is the Greek letter eta and represents the viscosity of the blood,
λ is the Greek letter lambda and represents the length of a blood vessel.
By examining this equation, you can see that there are only three
variables: viscosity, vessel length, and radius, since 8 and π are both
constants. The important thing to remember is this: Two of these
variables, viscosity and vessel length, will change slowly in the body. Only
one of these factors, the radius, can be changed rapidly by
vasoconstriction and vasodilation, thus dramatically impacting resistance
and flow. Resistance is inversely proportional to the radius of the blood
vessel and a slight increase or decrease in diameter causes a huge
decrease or increase in resistance. Most of the time and in the summary
diagram above, we are talking about arteriole vasoconstriction or
vasodilation but it does happen elsewhere, like in the veins.
Venoconstriction increases the return of blood to the heart or increases
the preload of the cardiac muscle

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46
Q

Neural regulation of cardiovascular systems

A

Neural mechanisms that regulate blood chemistry and pressure are:
sympathetic/parasympathatic innervation as well as overall radius of
peripheral vessels (vasconstriction/vasodilation)
Neural mechanisms
Blood pressure- cardiac centre, vasomotor centers
Sympathetic stimulation:
increasing cardiac output and increasing blood flow
Parasympathetic
sumulation. decreasing cardiac output and decreasing blood flow
Blood chemistry
Cardiac
Vasomotor centers
Vasoconstriction of most peripheral vessels - norepinephrine (NE):
decreasing flow, veins increasing flow
Vasodilation of select peripheral vessels - primarily acetylcholine
and nitric oxide (NO)

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47
Q

Increased blood pressure neural regulation

A

Inc blood pressure
Increased baroeexeptor firing

Increased inhibition
of cardiac and
decrease in activity
of accelerator and
vasomotor centres

Inc cardiac inhibitor centres
Lower cardiac accelerator centres
Decrease vasomotor centre
Decrease cardiac output HR and SV
(decrease in
venous return)
decreases CO
Inc vasodilation Increase in diameter
decreases resistance
Blood pressure drops
When blood pressure rises too high, the baroreceptors fire at a higher
rate and trigger parasympathetic stimulation of the heart. As a result,
cardiac output falls. Paraympathetic stimulation of the peripheral arterioles
will also decrease, resulting in vasodilation. Combined, these activities
cause blood pressure to fall.”
Blood Pressure (BP)=Cardiac Output (CO)×Peripheral Resistance

Here, peripheral resistance refers to the resistance the blood encounters as it flows through the arteries. If blood pressure increases and peripheral resistance remains constant, it may impact cardiac output.

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48
Q

DecreaSed blood pressure

A

Dec blood pressure
Dec baroreceptor firing
Dec cardiac inhibitors centers
Inc cardiac accelerators
Inc vasomotor centers
Inc cardiac output
Inc vasodilation
Blood pressure increase
When blood pressure decreases, the baroreceptors fire at a slower rate
and trigger sympathetic stimulation of the heart. As a result, cardiac
output rises Sympathetic stimulation of the peripheral arterioles will also
decrease, resulting in vasoconstriction. Combined, these activities cause
blood pressure to raise.”

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49
Q

Endocrine regulation of cardiovascular systems

A

Endocrine mechanisms that regulate blood volume and pressure are
related to hormones from renal, adrenal system, such as EPO, ADH,
Aldestorone and others help regulate the radius of peripheral vessels
(vasconstriction/vasodilation), which affects blood pressure and its
regulation

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50
Q

Endocrine regulation Dec blood pressure

A

For example, when blood pressure and blood volume is low, renin
(angiotensin II) and EPO secretion increases, which together increase
thirst and RBC formation, which together increase blood volume. Blood
volume increases while also sympathetic NS increases cardiac output
and peripheral vasoconstriction, which ultimately increases blood
pressure as well

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51
Q

Afterload

A

force the ventricles must develop to effectively pump blood against the resistance in the
vessels

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52
Q

Blood flow

A

movement of blood through a vessel, tissue, or organ that is usually expressed in terms of
volume per unit of time

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53
Q

Blood pressures

A

force exerted by the blood against the wall of a vessel or heart chamber; can be described with
the more generic term hydrostatic pressure

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54
Q

Cardiac output

A

cardiac output (CO)
amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV

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55
Q

Cardiac plexus

A

cardiac plexus
paired complex network of nerve fibers near the base of the heart that receive sympathetic and
parasympathetic stimulations to regulate HR

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56
Q

Cardiac reflexes

A

cardiac reflexes
series of autonomic reflexes that enable the cardiovascular centers to regulate heart function
based upon sensory information from a variety of visceral sensors

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57
Q

End diastolic volume

A

also, preload) the amount of blood in the ventricles at the end of atrial systole just prior to
ventricular contraction

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58
Q

End systolic volume

A

amount of blood remaining in each ventricle following systole

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59
Q

Filling time

A

filling time
duration of ventricular diastole during which filling occurs

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60
Q

Heart rate

A

number of times the heart contracts (beats) per minute

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61
Q

Preload

A

also, end diastolic volume) amount of blood in the ventricles at the end of atrial systole just
prior to ventricular contraction

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62
Q

Stroke volume

A

stroke volume (SV)
amount of blood pumped by each ventricle per contraction; also, the difference between EDV
and ESV

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63
Q

Systolic pressure

A

larger number recorded when measuring arterial blood pressure; represents the maximum value
following ventricular contraction

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64
Q

Vasodilation

A

relaxation of the smooth muscle in the wall of a blood vessel, resulting in an increased vascular
diameter

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65
Q

Vasomotion

A

irregular, pulsating flow of blood through capillaries and related structures

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66
Q

Venous reserve

A

volume of blood contained within systemic veins in the integument, bone marrow, and liver that
can be returned to the heart for circulation, if needed

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67
Q

Aorta

A

largest artery in the body, originating from the left ventricle and descending to the abdominal
region where it bifurcates into the common iliac arteries at the level of the fourth lumbar
vertebra; arteries originating from the aorta distribute blood to virtually all tissues of the body

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68
Q

Aortic arch

A

arc that connects the ascending aorta to the descending aorta; ends at the intervertebral disk
between the fourth and fifth thoracic vertebrae

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69
Q

Arteriole

A

arteriole
(also, resistance vessel) very small artery that leads to a capillary

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70
Q

Artery

A

artery
blood vessel that conducts blood away from the heart; may be a conducting or distributing
vessel

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71
Q

Ascending aorta

A

initial portion of the aorta, rising from the left ventricle for a distance of approximately 5 cm

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72
Q

Axillary artery

A

axillary artery
continuation of the subclavian artery as it penetrates the body wall and enters the axillary
region; supplies blood to the region near the head of the humerus (humeral circumflex arteries);
the majority of the vessel continues into the brachium and becomes the brachial artery

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73
Q

Axillary vein

A

axillary vein
major vein in the axillary region; drains the upper limb and becomes the subclavian vein

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74
Q

blood colloidal osmotic pressure (BCOP)

A

blood colloidal osmotic pressure (BCOP)
pressure exerted by colloids suspended in blood within a vessel; a primary determinant is the
presence of plasma proteins

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75
Q

Blood flow

A

movement of blood through a vessel, tissue, or organ that is usually expressed in terms of
volume per unit of time

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76
Q

Blood hydrostatic pressure

A

force blood exerts against the walls of a blood vessel or heart chamber

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77
Q

Blood pressure

A

force exerted by the blood against the wall of a vessel or heart chamber; can be described with
the more generic term hydrostatic pressure

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78
Q

brachiocephalic artery

A

brachiocephalic artery
single vessel located on the right side of the body; the first vessel branching from the aortic
arch; gives rise to the right subclavian artery and the right common carotid artery; supplies
blood to the head, neck, upper limb, and wall of the thoracic region

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79
Q

brachiocephalic vein

A

brachiocephalic vein
one of a pair of veins that form from a fusion of the external and internal jugular veins and the
subclavian vein; subclavian, external and internal jugulars, vertebral, and internal thoracic veins
lead to it; drains the upper thoracic region and flows into the superior vena cava

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80
Q

Capillary.

A

capillary
smallest of blood vessels where physical exchange occurs between the blood and tissue cells
surrounded by interstitial fluid

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81
Q

Capillary bed

A

capillary bed
network of 10–100 capillaries connecting arterioles to venules

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82
Q

Common carotid artery

A

right common carotid artery arises from the brachiocephalic artery, and the left common carotid
arises from the aortic arch; gives rise to the external and internal carotid arteries; supplies the
respective sides of the head and neck

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83
Q

Common iliac artery

A

branch of the aorta that leads to the internal and external iliac arteries

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84
Q

Common iliac vein

A

one of a pair of veins that flows into the inferior vena cava at the level of L5; the left common
iliac vein drains the sacral region; divides into external and internal iliac veins near the inferior
portion of the sacroiliac joint

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85
Q

Compliance

A

degree to which a blood vessel can stretch as opposed to being rigid

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86
Q

Continuous capillary

A

most common type of capillary, found in virtually all tissues except epithelia and cartilage;
contains very small gaps in the endothelial lining that permit exchange

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87
Q

Descending aorta

A

portion of the aorta that continues downward past the end of the aortic arch; subdivided into the
thoracic aorta and the abdominal aorta

88
Q

Diastolic pressure

A

diastolic pressure
lower number recorded when measuring arterial blood pressure; represents the minimal value
corresponding to the pressure that remains during ventricular relaxation

89
Q

Elastic artery

A

(also, conducting artery) artery with abundant elastic fibers located closer to the heart, which
maintains the pressure gradient and conducts blood to smaller branches

90
Q

Femoral artery

A

continuation of the external iliac artery after it passes through the body cavity; divides into
several smaller branches, the lateral deep femoral artery, and the genicular artery; becomes the
popliteal artery as it passes posterior to the knee

91
Q

Femoral vein

A

drains the upper leg; receives blood from the great saphenous vein, the deep femoral vein, and
the femoral circumflex vein; becomes the external iliac vein when it crosses the body wall

92
Q

Feneatrated capillary

A

fenestrated capillary
type of capillary with pores or fenestrations in the endothelium that allow for rapid passage of
certain small materials

93
Q

Filtration

A

In the cardiovascular system, the movement of material from a capillary into the interstitial fluid,
moving from an area of higher pressure to lower pressure

94
Q

Hepatic portal system

A

hepatic portal system
specialized circulatory pathway that carries blood from digestive organs to the liver for
processing before being sent to the systemic circulation

95
Q

Inferior vena cava

A

large systemic vein that drains blood from areas largely inferior to the diaphragm; empties into
the right atrium

96
Q

Lumen

A

lumen
interior of a tubular structure such as a blood vessel or a portion of the alimentary canal through
which blood, chyme, or other substances travel

97
Q

mean arterial pressure (MAP)

A

mean arterial pressure (MAP)
average driving force of blood to the tissues; approximated by taking diastolic pressure and
adding 1/3 of pulse pressure

98
Q

Muscular artery

A

muscular artery
(also, distributing artery) artery with abundant smooth muscle in the tunica media that branches
to distribute blood to the arteriole network

99
Q

Net filtration pressure

A

force driving fluid out of the capillary and into the tissue spaces; equal to the difference of the
capillary hydrostatic pressure and the blood colloidal osmotic pressure

100
Q

Pulmonary artery

A

one of two branches, left and right, that divides off from the pulmonary trunk and leads to
smaller arterioles and eventually to the pulmonary capillaries

101
Q

Pulmonary circuit

A

pulmonary circuit
system of blood vessels that provide gas exchange via a network of arteries, veins, and
capillaries that run from the heart, through the body, and back to the lungs

102
Q

Pulmonary trunk

A

pulmonary trunk
single large vessel exiting the right ventricle that divides to form the right and left pulmonary
arteries

103
Q

Pulmonary veins

A

two sets of paired vessels, one pair on each side, that are formed from the small venules
leading away from the pulmonary capillaries that flow into the left atrium

104
Q

Pulse

A

alternating expansion and recoil of an artery as blood moves through the vessel; an indicator of
heart rate

105
Q

Pulse pressure

A

difference between the systolic and diastolic pressures

106
Q

Reabsorption

A

reabsorption
in the cardiovascular system, the movement of material from the interstitial fluid into the
capillaries

107
Q

Resistance

A

any condition or parameter that slows or counteracts the flow of blood

108
Q

Subclavian artery

A

subclavian artery
right subclavian arises from the brachiocephalic artery, whereas the left subclavian artery arises
from the aortic arch; gives rise to the internal thoracic, vertebral, and thyrocervical arteries;
supplies blood to the arms, chest, shoulders, back, and central nervous system

109
Q

Subclavian vein

A

located deep in the thoracic cavity; becomes the axillary vein as it enters the axillary region;
drains the axillary and smaller local veins near the scapular region; leads to the brachiocephalic
vein

110
Q

Superior vena cava

A

superior vena cava
large systemic vein; drains blood from most areas superior to the diaphragm; empties into the
right atrium

111
Q

Systolic pressure

A

systolic pressure
larger number recorded when measuring arterial blood pressure; represents the maximum value
following ventricular contraction

112
Q

Tunica externa

A

tunica externa
(also, tunica adventitia) outermost layer or tunic of a vessel (except capillaries)

113
Q

Tunica intima

A

tunica intima
(also, tunica interna) innermost lining or tunic of a vessel

114
Q

Tunica media

A

tunica media
middle layer or tunic of a vessel (except capillaries)

115
Q

Vein

A

blood vessel that conducts blood toward the heart

116
Q

Venous reserve

A

volume of blood contained within systemic veins in the integument, bone marrow, and liver that
can be returned to the heart for circulation, if needed

117
Q

Venule

A

venule
small vessel leading from the capillaries

118
Q

atrioventricular (AV) node

A

atrioventricular (AV) node
clump of myocardial cells located in the inferior portion of the right atrium within the
atrioventricular septum; receives the impulse from the SA node, pauses, and then transmits it
into specialized conducting cells within the interventricular septum

119
Q

atrioventricular bundle

A

atrioventricular bundle
(also, bundle of His) group of specialized myocardial conductile cells that transmit the impulse
from the AV node through the interventricular septum; form the left and right atrioventricular
bundle branches

120
Q

atrioventricular bundle branches

A

atrioventricular bundle branches
(also, left or right bundle branches) specialized myocardial conductile cells that arise from the
bifurcation of the atrioventricular bundle and pass through the interventricular septum; lead to
the Purkinje fibers and also to the right papillary muscle via the moderator band

121
Q

atrioventricular septum

A

atrioventricular septum
cardiac septum located between the atria and ventricles; atrioventricular valves are located
here

122
Q

atrioventricular valves

A

atrioventricular valves
one-way valves located between the atria and ventricles; the valve on the right is called the
tricuspid valve, and the one on the left is the mitral or bicuspid valve

123
Q

Atrium

A

atrium
(plural = atria) upper or receiving chamber of the heart that pumps blood into the lower
chambers just prior to their contraction; the right atrium receives blood from the systemic
circuit that flows into the right ventricle; the left atrium receives blood from the pulmonary
circuit that flows into the left ventricle

124
Q

Auricle

A

extension of an atrium visible on the superior surface of the heart

125
Q

Bicuspid valve

A

(also, mitral valve or left atrioventricular valve) valve located between the left atrium and
ventricle; consists of two flaps of tissue

126
Q

Bundle of his

A

(also, atrioventricular bundle) group of specialized myocardial conductile cells that transmit the
impulse from the AV node through the interventricular septum; form the left and right
atrioventricular bundle branches

127
Q

Cardiac cycle

A

cardiac cycle
period of time between the onset of atrial contraction (atrial systole) and ventricular relaxation
(ventricular diastole)

128
Q

Cardiac notch

A

cardiac notch
depression in the medial surface of the inferior lobe of the left lung where the apex of the heart
is located

129
Q

Cardiac plexus

A

paired complex network of nerve fibers near the base of the heart that receive sympathetic and
parasympathetic stimulations to regulate HR

130
Q

Cardiac reflexes

A

series of autonomic reflexes that enable the cardiovascular centers to regulate heart function
based upon sensory information from a variety of visceral sensors

131
Q

chordae tendineae

A

chordae tendineae
string-like extensions of tough connective tissue that extend from the flaps of the
atrioventricular valves to the papillary muscles

132
Q

Coronary arteries

A

branches of the ascending aorta that supply blood to the heart; the left coronary artery feeds
the left side of the heart, the left atrium and ventricle, and the interventricular septum; the right
coronary artery feeds the right atrium, portions of both ventricles, and the heart conduction
system

133
Q

Coronary sinus

A

coronary sinus
large, thin-walled vein on the posterior surface of the heart that lies within the atrioventricular
sulcus and drains the heart myocardium directly into the right atrium

134
Q

Coronary veins

A

coronary veins
vessels that drain the heart and generally parallel the large surface arteries

135
Q

Diastole

A

period of time when the heart muscle is relaxed and the chambers fill with blood

136
Q

electrocardiogram ecg

A

electrocardiogram (ECG)
surface recording of the electrical activity of the heart that can be used for diagnosis of
irregular heart function; also abbreviated as EKG

137
Q

Endocardium

A

innermost layer of the heart lining the heart chambers and heart valves; composed of
endothelium reinforced with a thin layer of connective tissue that binds to the myocardium

138
Q

Epicardium

A

innermost layer of the serous pericardium and the outermost layer of the heart wall

139
Q

Filing time

A

duration of ventricular diastole during which filling occurs

140
Q

Heart sounds

A

sounds heard via auscultation with a stethoscope of the closing of the atrioventricular valves
(“lub”) and semilunar valves (“dub”)

141
Q

Inferior vena cava

A

inferior vena cava
large systemic vein that returns blood to the heart from the inferior portion of the body

142
Q

Intercalated disc

A

physical junction between adjacent cardiac muscle cells; consisting of desmosomes,
specialized linking proteoglycans, and gap junctions that allow passage of ions between the
two cells

143
Q

left atrioventricular valve
, m

A

left atrioventricular valve
(also, mitral valve or bicuspid valve) valve located between the left atrium and ventricle;
consists of two flaps of tissue

144
Q

Myocardium

A

myocardium
thickest layer of the heart composed of cardiac muscle cells built upon a framework of
primarily collagenous fibers and blood vessels that supply it and the nervous fibers that help to
regulate it

145
Q

P wave

A

component of the electrocardiogram that represents the depolarization of the atria

146
Q

Pacemaker

A

cluster of specialized myocardial cells known as the SA node that initiates the sinus rhythm

147
Q

Papillary muscle

A

extension of the myocardium in the ventricles to which the chordae tendineae attach

148
Q

Pericardial cavity

A

pericardial cavity
cavity surrounding the heart filled with a lubricating serous fluid that reduces friction as the
heart contracts

149
Q

Pericardial sac

A

also, pericardium) membrane that separates the heart from other mediastinal structures;
consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium

150
Q

Pericardium

A

also, pericardial sac) membrane that separates the heart from other mediastinal structures;
consists of two distinct, fused sublayers: the fibrous pericardium and the parietal pericardium

151
Q

prepotential depolarization
z

A

(also, spontaneous depolarization) mechanism that accounts for the autorhythmic property of
cardiac muscle; the membrane potential increases as sodium ions diffuse through the always-
open sodium ion channels and causes the electrical potential to rise

152
Q

Pulmonary artery

A

pulmonary arteries
left and right branches of the pulmonary trunk that carry deoxygenated blood from the heart to
each of the lungs

153
Q

pulmonary capillary

A

capillaries surrounding the alveoli of the lungs where gas exchange occurs: carbon dioxide
exits the blood and oxygen enters

154
Q

Pulmonary circuit

A

blood flow to and from the lungs

155
Q

pulmonary valve

A

also, pulmonary semilunar valve, the pulmonic valve, or the right semilunar valve) valve at the
base of the pulmonary trunk that prevents backflow of blood into the right ventricle; consists of
three flaps

156
Q

Pulmonary veins

A

pulmonary veins
veins that carry highly oxygenated blood into the left atrium, which pumps the blood into the
left ventricle, which in turn pumps oxygenated blood into the aorta and to the many branches
of the systemic circuit

157
Q

Purkinje fibers

A

specialized myocardial conduction fibers that arise from the bundle branches and spread the
impulse to the myocardial contraction fibers of the ventricles

158
Q

Qrs complex

A

component of the electrocardiogram that represents the depolarization of the ventricles and
includes, as a component, the repolarization of the atria

159
Q

right atrioventricular valve

A

right atrioventricular valve
(also, tricuspid valve) valve located between the right atrium and ventricle; consists of three
flaps of tissue

160
Q

Semilunar valve

A

semilunar valves
valves located at the base of the pulmonary trunk and at the base of the aorta

161
Q

Septum

A

plural = septa) walls or partitions that divide the heart into chambers

162
Q

sinoatrial (SA) node

A

sinoatrial (SA) node
known as the pacemaker, a specialized clump of myocardial conducting cells located in the
superior portion of the right atrium that has the highest inherent rate of depolarization that then
spreads throughout the heart

163
Q

Sinus rhythm

A

sinus rhythm
normal contractile pattern of the heart

164
Q

spontaneous depolarization

A

spontaneous depolarization
(also, prepotential depolarization) the mechanism that accounts for the autorhythmic property
of cardiac muscle; the membrane potential increases as sodium ions diffuse through the
always-open sodium ion channels and causes the electrical potential to rise

165
Q

Sulcus

A

(plural = sulci) fat-filled groove visible on the surface of the heart; coronary vessels are also
located in these areas

166
Q

Systemic circuit

A

blood flow to and from virtually all of the tissues of the body

167
Q

Systole

A

period of time when the heart muscle is contracting

168
Q

T wave

A

component of the electrocardiogram that represents the repolarization of the ventricles

169
Q

tricuspid valve

A

term used most often in clinical settings for the right atrioventricular valve

170
Q

valve

A

in the cardiovascular system, a specialized structure located within the heart or vessels that
ensures one-way flow of blood

171
Q

Ventricle

A

one of the primary pumping chambers of the heart located in the lower portion of the heart; the
left ventricle is the major pumping chamber on the lower left side of the heart that ejects blood
into the systemic circuit via the aorta and receives blood from the left atrium; the right ventricle
is the major pumping chamber on the lower right side of the heart that ejects blood into the
pulmonary circuit via the pulmonary trunk and receives blood from the right atrium

172
Q

Action potential

A

Action potential: change in voltage of a cell membrane in response to a stimulus that
results in transmission of electrical signal

173
Q

Blood vessels:

A

the tubes of the circulatory system that close blood within it

174
Q

Blood

A

substance in blood vessels that is used for transport of gasses, hormones,
pathogens, and antibodies. Components (most to least) are: plasma (water, proteins,
nutrients, hormones, etc…), hematocrit (RBC), and buffy coat (WBC and platelets)

175
Q

Calcitonin

A

hormone secreted by the thyroid gland to regulate calcium levels in the body
through bone and kidney

176
Q

Calcite I’ll

A

Vitamin D3, produced by the small intestines during calcium deficiency

177
Q

Erythrocytes

A

Erythrocytes: RBC, contains hemoglobin that carry gasses

178
Q

Hematocrit

A

Hematocrit: volume of the blood that consists of only RBC

179
Q

Hemoglobin

A

Hemoglobin: the protein on RBC’s that oxygen binds to for transportation. The oxygen bind
to its 4 heme sites that contain iron, the iron is what oxygen attaches to

180
Q

Hormones

A

chemical messenger/signal transported by the bloodstream for long distance
signaling and bind to receptors on target cells. Slow signalling

181
Q

Leukocytes

A

Leukocytes: WBC, mainly released during pathogen introduction

182
Q

Lymph nodes:

A

small, bean shaped organ of the lymphatic system secondary lymphatic
organ that works to remove debris and pathogens from the lymph. A site of adaptive
immune responses

183
Q

Lymph vessel

A

the tubes of the lymphatic system where interstitial fluid enters the
lymphatic system to become lymph. Include lymphatic trunks and lymphatic ducts

184
Q

Lymph

A

interstitial fluid after it enters the lymphatic system – the fluid of the lymphatic
system

185
Q

Lymphocytes

A

WBC’s (B-cells, T-cells, plasma cells, and natural killer cells) used in the
adaptive immune response to fight against pathogens

186
Q

Natural killer cells (NK):

A

body’s first line defence against viruses and some cancers.
Contain cytoxic granules in its cytoplasm

187
Q

Neurotransmitter

A

signaling chemical released by nerve terminals that bind to and activate
receptors on target cells

188
Q

Osteoblasts

A

Osteoblasts: bone builders, responsible for creating osseous tissue

189
Q

Osteoclasts

A

Osteoclasts: bone breakers, responsible for releasing calcium into the bloodstream

190
Q

Parathyroid gland

A

Parathyroid gland: 4 part small gland a part of the endocrine system that regular calcium
in our bodies

191
Q

Parathyroid hormone

A

Parathyroid hormone: hormone secreted by the parathyroid glands to regulate calcium
levels in the body through the bone, kidney, and intestine

192
Q

Plasma protein

A

synthesized in the liver, consist of (most to least) albumin, globulins, and
fibrinogen. Their main function is for transportation, maintaining osmotic concentration, and
blood clotting

193
Q

Plasm

A

Largest component of the blood, made of water, proteins, nutrients, hormones,
pathogens, and more. Everything in the blood other than blood cells

194
Q

Platelets

A

: tiny blood cells that bunch up together to form clots and stop bleeding. Signals
are sent to the platelets during injury to a blood vessel

195
Q

Signalling mechanism

A

Signalling mechanism: way in which a signal in the body is sent. Can be electrical (action
potential) or chemical (neurotransmitter or hormone

196
Q

Thyroid gland

A

Thyroid gland: butter-fly shaped organ that releases hormones to control metabolism

197
Q

Five variables influence blood flow and blood pressure:

A

Cardiac output Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels.
Compliance The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. Veins are more compliant than arteries and can expand to hold more blood.
Volume of the blood blood volume decreases, pressure and flow decreases
Viscosity of the blood viscosity to increase will also increase resistance and decrease flow.
Blood vessel length and diameter The length of a vessel is directly proportional to its resistance: the longer the vessel, the greater the resistance and the lower the flow. As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood. Likewise, if the vessel is shortened, the resistance will decrease and flow will increase.

Recall that blood moves from higher pressure to lower pressure. It is pumped from the heart into the arteries at high pressure. If you increase pressure in the arteries (afterload), and cardiac function does not compensate, blood flow will actually decrease. In the venous system, the opposite relationship is true. Increased pressure in the veins does not decrease flow as it does in arteries, but actually increases flow. Since pressure in the veins is normally relatively low, for blood to flow back into the heart, the pressure in the atria during atrial diastole must be even lower. It normally approaches zero, except when the atria contrac

Only one of these factors, the radius, can be changed rapidly by vasoconstriction and vasodilation, thus dramatically impacting resistance and flow. Further, small changes in the radius will greatly affect flow, since it is raised to the fourth power in the equation.

198
Q

The Roles of Vessel Diameter and Total Area in Blood Flow and Blood Pressure

A

arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries. In fact, arterioles are the site of greatest resistance in the entire vascular network.

the total cross-sectional area of the body’s capillary beds is far greater than any other type of vessel. Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels. Part (c) shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance. However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels.

199
Q

Arteries vs veins

A

Arteries

General appearance
Thick walls with small lumens
Generally appear rounded
Tunica intima
Endothelium usually appears wavy due to constriction of smooth muscle
Internal elastic membrane present in larger vessels
Tunica media
Normally the thickest layer in arteries
Smooth muscle cells and elastic fibers predominate the proportions of these vary with distance from the heart)
External elastic membrane present in larger vessels
Tunica
externa
Normally thinner than the tunica media in all but the largest arteries
Collagenous and elastic fibers
Nervi vasorum and vasa vasorum present

Arteries
Conducts blood away from the heart
Rounded
High
Thick
Higher in systemic arteries
Lower in pulmonary arteries
Not present

Veins
Thin walls with large lumens
Generally appear flattened

Endothelium appears smooth
Internal elastic membrane absent

Normally thinner than the tunica externa
Smooth muscle cells and collagenous fibers predominate
Nervi vasorum and vasa
vasorum present
External elastic membrane absent

Normally the thickest layer in veins
Collagenous and smooth fibers
predominate
Some smooth muscle fibers
Nervi vasorum and vasa vasorum present

Conducts blood toward the heart
Irregular, often collapsed
Low
Thin
Lower in systemic veins
Higher in pulmonary veins
Present most commonly in limbs and in veins inferior to the heart

200
Q

Cardiovascular Centers in the Brain

A

The cardioaccelerator centers stimulate cardiac function by regulating heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve.
The cardioinhibitor centers slow cardiac function by decreasing heart rate and stroke volume via parasympathetic stimulation from the vagus nerve.
The vasomotor centers control vessel tone or contraction of the smooth muscle in the tunica media. Changes in diameter affect peripheral resistance, pressure, and flow, which affect cardiac output. The majority of these neurons act via the release of the neurotransmitter norepinephrine from sympathetic neurons.

201
Q

Baroreceptor Reflexes

A

Baroreceptors are specialized stretch receptors located within thin areas of blood vessels and heart chambers that respond to the degree of stretch caused by the presence of blood. They send impulses to the cardiovascular center to regulate blood pressure.

When blood pressure rises too high, the baroreceptors fire at a higher rate and trigger parasympathetic stimulation of the heart. As a result, cardiac output falls. Sympathetic stimulation of the peripheral arterioles will also decrease, resulting in vasodilation. Combined, these activities cause blood pressure to fall.
When blood pressure drops too low, the rate of baroreceptor firing decreases. This will trigger an increase in sympathetic stimulation of the heart, causing cardiac output to increase. It will also trigger sympathetic stimulation of the peripheral vessels, resulting in vasoconstriction. Combined, these activities cause blood pressure to rise.

202
Q

Chemoreceptor Reflexes

A

In addition to the baroreceptors are chemoreceptors that monitor levels of oxygen, carbon dioxide, and hydrogen ions (pH), and thereby contribute to vascular homeostasis. Chemoreceptors monitoring the blood are located in close proximity to the baroreceptors in the aortic and carotid sinuses. They signal the cardiovascular center as well as the respiratory centers in the medulla oblongata.

The chemoreceptors respond to increasing carbon dioxide and hydrogen ion levels (falling pH) by stimulating the cardioaccelerator and vasomotor centers, increasing cardiac output and constricting peripheral vessels. The cardioinhibitor centers are suppressed. With falling carbon dioxide and hydrogen ion levels (increasing pH), the cardioinhibitor centers are stimulated, and the cardioaccelerator and vasomotor centers are suppressed, decreasing cardiac output and causing peripheral vasodilation. In order to maintain adequate supplies of oxygen to the cells and remove waste products such as carbon dioxide, it is essential that the respiratory system respond to changing metabolic demands. In turn, the cardiovascular system will transport these gases to the lungs for exchange, again in accordance with metabolic demands.

203
Q

Endocrine Regulation

A

The catecholamines epinephrine and norepinephrine are released by the adrenal medulla, and enhance and extend the body’s sympathetic or “fight-or-flight” response They increase heart rate and force of contraction, while temporarily constricting blood vessels to organs not essential for flight-or-fight responses and redirecting blood flow to the liver, muscles, and heart.

Antidiuretic hormone (ADH), also known as vasopressin, is secreted by the cells in the hypothalamus and transported via the hypothalamic-hypophyseal tracts to the posterior pituitary where it is stored until released upon nervous stimulation. The primary trigger prompting the hypothalamus to release ADH is increasing osmolarity of tissue fluid, usually in response to significant loss of blood volume. ADH signals its target cells in the kidneys to reabsorb more water, thus preventing the loss of additional fluid in the urine. This will increase overall fluid levels and help restore blood volume and pressure. In addition, ADH constricts peripheral vessels.

The renin-angiotensin-aldosterone mechanism has a major effect upon the cardiovascular system (Figure 20.19). Renin is an enzyme, although because of its importance in the renin-angiotensin-aldosterone pathway, some sources identify it as a hormone. Specialized cells in the kidneys , called juxtaglomerular (JG) cells, respond to decreased blood pressure by secreting renin into the blood. Renin converts the plasma protein angiotensinogen, which is produced by the liver, into its active form—angiotensin I. Angiotensin I circulates in the blood and is then converted into angiotensin II in the lungs. This reaction is catalyzed by the enzyme angiotensin-converting enzyme (ACE).
Angiotensin II is a powerful vasoconstrictor, greatly increasing blood pressure.

Erythropoietin (EPO) is released by the kidneys when blood flow and/or oxygen levels decrease. EPO stimulates the production of erythrocytes within the bone marrow. Erythrocytes are the major formed element of the blood and may contribute 40 percent or more to blood volume, a significant factor of viscosity, resistance, pressure, and flow. In addition, EPO is a vasoconstrictor. Overproduction of EPO or excessive intake of synthetic EPO, often to enhance athletic performance, will increase viscosity, resistance, and pressure, and decrease flow in addition to its contribution as a vasoconstrictor.

Secreted by cells in the atria of the heart, atrial natriuretic hormone (ANH) (also known as atrial natriuretic peptide) is secreted when blood volume is high enough to cause extreme stretching of the cardiac cells. Cells in the ventricle produce a hormone with similar effects, called B-type natriuretic hormone. Natriuretic hormones are antagonists to angiotensin II. They promote loss of sodium and water from the kidneys, and suppress renin, aldosterone, and ADH production and release. All of these actions promote loss of fluid from the body, so blood volume and blood pressure drop.

204
Q

Autoregulation of Perfusion

A

neither specialized nervous stimulation nor endocrine control. Rather, these are local, self-regulatory mechanisms that allow each region of tissue to adjust its blood flow—and thus its perfusion. These local mechanisms include chemical signals and myogenic controls.

Chemical signals work at the level of the precapillary sphincters to trigger either constriction or relaxation. As you know, opening a precapillary sphincter allows blood to flow into that particular capillary, whereas constricting a precapillary sphincter temporarily shuts off blood flow to that region. The factors involved in regulating the precapillary sphincters include the following:
Opening of the sphincter is triggered in response to decreased oxygen concentrations; increased carbon dioxide concentrations; increasing levels of lactic acid or other byproducts of cellular metabolism; increasing concentrations of potassium ions or hydrogen ions (falling pH); inflammatory chemicals such as histamines; and increased body temperature. These conditions in turn stimulate the release of NO, a powerful vasodilator, from endothelial cells (see Figure 20.17).
Contraction of the precapillary sphincter is triggered by the opposite levels of the regulators, which prompt the release of endothelins, powerful vasoconstricting peptides secreted by endothelial cells. Platelet secretions and certain prostaglandins may also trigger constriction.

205
Q

Effect of Exercise on Vascular Homeostasis

A

For a healthy young adult, cardiac output (heart rate × stroke volume) increases in the nonathlete from approximately 5.0 liters (5.25 quarts) per minute to a maximum of about 20 liters (21 quarts) per minute. Accompanying this will be an increase in blood pressure from about 120/80 to 185/75. However, well-trained aerobic athletes can increase these values substantially. For these individuals, cardiac output soars from approximately 5.3 liters (5.57 quarts) per minute resting to more than 30 liters (31.5 quarts) per minute during maximal exercise. Along with this increase in cardiac output, blood pressure increases from 120/80 at rest to 200/90 at maximum values.

In addition to improved cardiac function, exercise increases the size and mass of the heart. The average weight of the heart for the nonathlete is about 300 g, whereas in an athlete it will increase to 500 g. This increase in size generally makes the heart stronger and more efficient at pumping blood, increasing both stroke volume and cardiac output.
Tissue perfusion also increases as the body transitions from a resting state to light exercise and eventually to heavy exercise result in selective vasodilation in the skeletal muscles, heart, lungs, liver, and integument. Simultaneously, vasoconstriction occurs in the vessels leading to the kidneys and most of the digestive and reproductive organs. The flow of blood to the brain remains largely unchanged whether at rest or exercising, since the vessels in the brain largely do not respond to regulatory stimuli, in most cases, because they lack the appropriate receptors.

As vasodilation occurs in selected vessels, resistance drops and more blood rushes into the organs they supply. This blood eventually returns to the venous system. Venous return is further enhanced by both the skeletal muscle and respiratory pumps. As blood returns to the heart more quickly, preload rises and the Frank-Starling principle tells us that contraction of the cardiac muscle in the atria and ventricles will be more forceful. Eventually, even the best-trained athletes will fatigue and must undergo a period of rest following exercise. Cardiac output and distribution of blood then return to normal.

206
Q

Layers of the heart

A

The pericardium is made up of two serous membrane layers, each composed of an epithelial lining with an underlying connective tissue. The pericardium keeps the heart in place, limits its motion, prevents it from over expanding, whilst the pericardial fluid reduces the friction between it and its surrounding structures.

Pericardial sac

The heart wall is made up of three layers, the endocardium, myocardium, and epicardium:

Endocardium

A smooth, thin membrane that lines the inner surface of the heart chambers, the endocardium is composed of a thin layer of endothelial cells, which lies over a thin layer of connective tissue. This innermost layer also covers the valves of the heart, and helps to prevent resistance as blood passes through the vessels and chambers of the heart.

Myocardium

The myocardium - the heart muscle itself, varies in thickness depending on its location, being thin in the atria and thick in the ventricles. It is composed of cardiac muscle fibers, which exhibit striations diagonally across the heart.

Epicardium

The epicardium is the thin, outer serous membrane of the heart wall, which is also described as the inner-most layer of the serous pericardium, known as the visceral pericardium. It is composed mainly of connective tissue mesothelial cells, which gives a smooth texture on the outer surface of the heart.

207
Q

Correlation Between Heart Rates and Cardiac Output

A

Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV.

208
Q

cardiovascular centern

A

The cardiovascular center receives input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. Any such increase in physical activity would logically warrant increased blood flow. The cardiac centers monitor these increased rates of firing, and suppress parasympathetic stimulation and increase sympathetic stimulation as needed in order to increase blood flow.
Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation

Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs.

209
Q

Phases of the Cardiac Cycle

A

At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole). Blood is flowing into the right atrium from the superior and inferior venae cavae and the coronary sinus. Blood flows into the left atrium from the four pulmonary veins. The two atrioventricular valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria and into the ventricles. Approximately 70–80 percent of ventricular filling occurs by this method. The two semilunar valves, the pulmonary and aortic valves, are closed, preventing backflow of blood into the right and left ventricles from the pulmonary trunk on the right and the aorta on the left.
Atrial Systole and Diastole

Contraction of the atria follows depolarization, represented by the P wave of the ECG. As the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular (tricuspid, and mitral or bicuspid) valves. At the start of atrial systole, the ventricles are normally filled with approximately 70–80 percent of their capacity due to inflow during diastole Ventricular systole (see Figure 19.27) follows the depolarization of the ventricles and is represented by the QRS complex in the ECG. It may be conveniently divided into two phases, lasting a total of 270 ms. At the end of atrial systole and just prior to ventricular contraction, the ventricles contain approximately 130 mL blood in a resting adult in a standing position. This volume is known as the end diastolic volume (EDV) or preload.
Initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high enough to open the semilunar (pulmonary and aortic) valves and be ejected from the heart. However, blood pressure quickly rises above that of the atria that are now relaxed and in diastole. This increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves. Since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction (see Figure 19.27).
In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary trunk and the aorta. Blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. Pressure generated by the left ventricle will be appreciably greater than the pressure generated by the right ventricle, since the existing pressure in the aorta will be so much higher. Nevertheless, both ventricles pump the same amount of blood. This quantity is referred to as stroke volume. Stroke volume will normally be in the range of 70–80 mL. Since ventricular systole began with an EDV of approximately 130 mL of blood, this means that there is still 50–60 mL of blood remaining in the ventricle following contraction. This volume of blood is known as the end systolic volume (ESV).
Ventricular Diastole

Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms.
During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. The semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase (see Figure 19.27).
In the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the atria into the ventricles, pushing open the tricuspid and mitral valves. As pressure drops within the ventricles, blood flows from the major veins into the relaxed atria and from there into the ventricles. Both chambers are in diastole, the atrioventricular valves are open, and the semilunar valves remain closed (see Figure 19.27). The cardiac cycle is complete.

210
Q

What happens to preload when there is venous constriction in the veins

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When there is venous constriction in the veins, it typically leads to an increase in preload. Preload refers to the volume of blood in the ventricles at the end of diastole, just before the heart contracts. Venous constriction results in increased venous return to the heart, as it enhances the force driving blood from the veins back into the heart. This increased venous return leads to an increase in the volume of blood in the ventricles during diastole, thus increasing preload.

In summary, venous constriction increases venous return, which increases preload by increasing the volume of blood in the ventricles before contraction. This, in turn, can lead to an increase in stroke volume and cardiac output.

211
Q

Why does increasing EDV increase contractility?u

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Increasing EDV increases the sarcomeres’ lengths within the cardiac muscle cells, allowing more cross bridge formation between the myosin and actin and providing for a more powerful contraction.

212
Q

Resistance vessel

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Arterioles are also called resistance vessels due to their ability to increase vascular resistance, which is a significant determinant of blood pressure.

213
Q

True or false? The plasma proteins suspended in blood cross the capillary cell membrane and enter the tissue fluid via facilitated diffusion.

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False. The plasma proteins suspended in blood cannot cross the semipermeable capillary cell membrane, and so they remain in the plasma within the vessel, where they account for the blood colloid osmotic pressure.

214
Q

What arteries play the leading roles in supplying blood to the brain

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The brain receives blood from two sources: the internal carotid arteries, which arise at the point in the neck where the common carotid arteries bifurcate, and the vertebral arteries (Figure 1.20). The internal carotid arteries branch to form two major cerebral arteries, the anterior and middle cerebral arteries.

215
Q

Why is plateau phase important

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This plateau phase allows for a longer muscle contraction and gives time for the nearby cardiac muscle cells to depolarize. This is important in allowing the heart to contract in a steady, uniform and forceful manner. Following the plateau phase is phase 3, also known as the repolarization phase.

216
Q

Where do you place a 3-lead ECG?

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The recommended 3-wire ECG lead placement is as follows. Place RA (white) electrode under right clavicle, mid-clavicular line within the rib cage frame. Place LA (black) electrode under left clavicle, mid-clavicular line within the rib cage frame.

217
Q

Heart sounds abnormal

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both cases, as the valves close, the openings within the atrioventricular septum guarded by the valves will become reduced, and blood flow through the opening will become more turbulent until the valves are fully closed. There is a third heart sound, S3, but it is rarely heard in healthy individuals. It may be the sound of blood flowing into the atria, or blood sloshing back and forth in the ventricle, or even tensing of the chordae tendineae. S3 may be heard in youth, some athletes, and pregnant women. If the sound is heard later in life, it may indicate congestive heart failure, warranting further tests. Some cardiologists refer to the collective S1, S2, and S3 sounds as the “Kentucky gallop,” because they mimic those produced by a galloping horse. The fourth heart sound, S4, results from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle, indicating failure of the left ventricle. S4 occurs prior to S1 and the collective sounds S4, S1, and S2 are referred to by some cardiologists as the “Tennessee gallop,” because of their similarity to the sound produced by a galloping horse with a different gait. A few individuals may have both S3 and S4, and this combined sound is referred to as S7.