1.

Description: Effect of two respiratory abnormalities – constricted lungs and airway

obstruction – on the maximum expiratory flow-volume curve. TLC = Total Lung Capacity,
RV = Residual Volume

A. What is maximum expiratory flow?

It’s the rate at which the flow (L/min) of air out of your lungs is at its maximum speed.

B. Why do we measure TLC?

Total Lung Capacity is a measure of the maximum amount that the lung can be expanded with
the greatest possible force so this helps us know if the lung is working properly and being able
to inhale enough air.

C. Why is there a decrease in the flow/speed of expiratory air flow after 400 L/min (in
the normal curve)?
Because after you exhale a specific amount of air, like in this case when you reach 5 L, there is
not enough air to pull open the elastic bronchi and bronchioles so the resistance to air flow
increases as the bronchi are less open and thus the speed decreases.

D. What does the term “constricted lung” mean? Give examples of diseases

Constricted lungs usually occur in fibrotic diseases when the lungs aren’t as stretchable and
can’t accommodate that much air. That means there is reduction in the compliance of the lung.
Examples of diseases include tuberculosis and fibrotic pleurisy.

E. What happens to TLC, RV, and maximum expiratory flow rate in constricted lungs?
Why? Explain using the graph above.

TLC will decrease because the lung isn’t able to accommodate as much air since the walls of
alveoli aren’t stretchable anymore and can’t hold in air. In the graph above, the TLC decreases
from 5.6i-sh L in the normal lung to 3 L/min in the constricted lung due to decrease in air
accommodation

RV will decrease because the rigid alveoli don’t want to hold in anymore air than they have to
so the residual volume decreases from 3 L (normal) to 0.8-ish L in the constricted lungs

Maximum expiratory flow will decrease because as we said before, max expiratory flow is
determined by how much air you can inspire into the lungs so if you can’t inspire that much air,
like in constrictive diseases, then your max expiratory flow will decrease. In the graph, the max
expiratory flow rate decreases from 400 L/min to about 200 L/min.

In cars, you have to put lots of gas in it to get maximum speed. If you don’t have a lot of gas,
your speed will decrease. Likewise, if you can’t inspire enough air into your lungs, your flow rate
will decrease.

F. What does the term “obstructed lung” mean? Name some diseases.

Obstructed lung means that there is something blocking the bronchioles- this something could
be smooth muscle from bronchial irritation, or mucus like in asthma. Either way, the
passageway for air is smaller and more difficult therefore there is higher resistance to air flow.
You therefore need a lot of positive pressure to push air out of the restricted bronchi. Some
diseases include asthma and in severe obstruction, emphysema.

G. Why do we care about obstructive lung diseases for expiration and not inspiration?

One would think that if the bronchi and bronchioles are obstructed with stuff it should affect
inspiration too right? Not really. When you inspire in normal cases, your bronchi naturally
expand due to negative pressure. So regardless of the stuff blocking bronchi, the bronchi will
still dilate and allow air to come in, barely affecting inspiratory flow.
 H. What happens to TLC, RV, and maximum expiratory flow rate in obstructive lung
diseases? Why? Explain using the graph.

RV will increase because during expiration when the bronchi are constricting, total constriction
of the bronchi will occur much earlier than expected due to the stuff like mucus blocking the
airway and basically thickening the walls. This will trap the air in the alveoli and prevent it from
being expired. (That’s why people who have asthma are described to have big barrel chests,
because they have so much residual volume left in the lungs & alveoli which enlarges the
thoracic cage. The barrel chest becomes especially prominent during asthma attacks.) The
residual volume increases form about 1.2 L (normal) to about 3.4 L in obstructive lungs.

TLC will increase because whenever you inspire, you’re adding more air into the already high
residual volume so the TLC will increase from 5.8 L (normal) to about 7 L in obstructive lungs.

Maximum expiratory flow rate will decrease because of the high resistance in the bronchi
making it really difficult to get air out. So speed isn’t really the priority anymore, the body just
wants to get as much air out as it can. It decreases from 500L/min to about 200 L/min in
obstructed lungs.

Note that with asthmatic patients the graph for this obstructed lung only occurs during asthma
attacks, not like everyday when they’re breathing normally.
 2.

Spirometric patterns normal, obstructive, and restrictive lungs

A. What is the significance of the FEV1 to FVC ratio (in normal lungs)? What is the normal
value?

The FEV1 is the Forced Expiratory Volume in 1 second. FVC is the Functional Vital Capacity. This
test measures how much air you can expire forcefully out of your body in 1 second. It helps us
understand if our expiratory process of the lung is working properly. The normal value is 80%
which means that if we breathe out really hard and measure the total amount of air that came
out each second, 80% of the total air would have come out of our body in the first second.

B. What is the significance of a RV to TLC ratio? What is the normal value for this ratio?

The significance of measuring the RV to TLC ratio is to see how much air is left in the lung at the
end of expiration in relation to how much new air can be added. The normal value for this ratio
is 25% meaning that only 25% of the air we inspire becomes residual volume.

C. What happens to the FEV1 to FVC ratio in obstructed lungs? Why? Explain using the
graph.
The FEV1 to FVC ratio decreases in obstructed lungs because both FEV1 and FVC decrease.

FVC was a measure of how much total air we could expire. As discussed earlier for the previous
graph, in obstructive lungs, we have a lot of trapped air in the alveoli because we can’t expire
air that much. So the total volume of expired air decreases, FVC decreases. In this graph FVC
decreases from 5 L (normal) to 3.1 L in obstructed lungs

FEV1 was a measure of how much air we could expire in the first second. In obstructed lungs,
we have more resistance so it will be much more difficult to expire air out, even in the first
second, and it will take wayyyy longer to reach FVC. The FEV1 decreased from 4 L to 1.3 L in the
first second in this graph.

The difference in the FVC decrease (5 – 3.1 = 2) is much less than the difference in the FEV1
decrease (4 – 1.3 = 3). So the FEV1 decreased more than the FVC, so therefore, the ratio of
FEV1 to FVC is decreased.

D. What happens to RV to TLC ratio in obstructed lungs? Why?

The RV to TLC ratio increases due to an increase in residual volume, aka trapped air, left over in
the lungs at the end of expiration. The TLC stays the same (technically speaking TLC actually
increases bc if you’re adding air to an already high RV, but we’re calling that an insignificant
change – also zoghaibi says it doesn’t change for some reason so we have to follow him). The
increase in RV is more than the TLC increase.

E. What happens to the FEV1 to FVC ratio in constricted lungs? Why? Explain using the
graph.

The FEV1 to FVC ratio increases or stays the same in constricted lungs.

FEV1 won’t really significantly change that much because in constricted lungs, the issue isn’t
with getting the air out, the issue is with the low quantity of air in the lungs. So FEV1 will
decrease, but only because the FVC was really low to begin with

The difference in the FVC decrease (5 – 2.8 = 2) is much higher than the difference in the FEV1
decrease (4 – 3 = 1). Thus we can say that FVC decreased more than FEV1, so therefore the
ratio of FEV1 to FVC is higher or increased.

F. What happens to the RV to TLC ratio in constricted lungs? Why?

The RV to TLC ratio increases because there is a much lower TLC, aka less air inspired and filling
up the lungs and RV doesn’t change (technically RV decreases in constricted lungs but its less
than the decrease in TLC so we count it as insignificant).
https://www.youtube.com/watch?v=r-hbFafLhsQ
 3.
A. Name 3 examples of COPD (Chronic Obstructive Pulmonary Diseases).

Chronic pulmonary emphysema, chronic bronchitis, asthma

B. Name 3 examples of restrictive pulmonary diseases

Diseases where you have a reduction in vital capacity and and FRC yet normal resistance,
diffuse interstitial pulmonary fibrosis where there is thick collagen deposits, pneumothorax
which introduces positive pressure compressing the lungs (like in stab wounds)

C. Describe how pulmonary emphysema is caused

In pulmonary emphysema, there is a chronic infection which first attacks your macrophages to
prevent them from killing the infection and then it causes the bronchioles to secrete a lot of
mucus which can obstruct the bronchi and bronchioles and therefore trap air in alveoli during
expiration.

Another big thing that happens is that the alveolar walls become weak and start breaking down
their walls and combining to form one big alveoli instead a bunch of small ones. This reduces
the surface area of the lungs and leaves too much CO2 in the lungs and not enough space for
O2 to come in.

D. How does pulmonary emphysema affect the lung function?

The bronchi obstruction increases airways resistance which makes it difficult to expire out air.

Loss of alveolar walls decreases diffusion capacity

Because the obstruction can be very severe in some parts of the lung and mild in other parts,
you will have very abnormal ventilation perfusion ratios throughout the lung

The loss of alveolar walls will cause pulmonary hypertension because the capillaries where the
bad alveoli walls are will constrict to redirect capillary blood to the relatively better alveoli

E. What happens to ventilation perfusion ratios in pulmonary emphysema?

The portions which are ventilated will have very high ventilation-perfusion ratios creating
physiologic dead space due to wasted ventilation

The portions which aren’t very well ventilated will have very low ventilation-perfusion ratio
creating physiologic shunt due to poor aeration of blood

F. What happens to FEV1/FVC ratio in pulmonary emphysema?

FEV1/FVC ratio decreases in pulmonary emphysema due to larger decrease in FEV1

4.
A. Describe what happens in pneumonia

In pneumonia, a bacteria called pneumococci attacks the alveolar membrane so the alveolar
membrane starts leaking pus into its alveoli causing the alveoli to become consolidated aka
filled with fluid

B. Give 3 ways pneumonia affects the lung function?

Pneumonia causes a reduction in the total available surface area of the membrane

It causes a decrease in ventilation-perfusion ratio

Both these effects cause hypoxemia (low O2) and hypercapnia (high CO2)

There is aslo a significant decrease in arterial hemoglobin saturation

C. What happens to ventilation-perfusion ratio in pneumonia?

There is a decrease in the ventilation-perfusion ratio so there is a physiologic shunt

 5.

Description: Effect of increased arterial blood pCO2, and decreased arterial pH (increased
hydrogen ion concentration) on rate of alveolar ventilation

A. What does this graph show? Explain your reasoning.

This graph shows that an increase in arterial pCO2 has a greater effect on increasing alveolar
ventilation than increasing the amount of hydrogen ions in the blood.

This is because hydrogen ions can’t cross the blood-brain barrier, only CO2 can (as shown in this
picture below). Yes, only hydrogen can stimulate the chemosensitive area, but CO2 can
combine with the H2O in the CSF and then dissociate to form HCO3- and H+ and that H+
formed can stimulate the chemosensitive area.
 B. How does the chemosensitive area control respiration?

Whenever there is an increase in blood pCO2 and it reaches the blood-brain barrier, the CO2
crosses the barrier and forms H+ ions (after doing a bunch of things).

The H+ ions stimulate the chemosensitive which stimulates an increase in alveolar ventilation

The effects of the central CO2 stimulation lasts for 1-2 days, therefore it has only an acute
effect in controlling respiratory drive.

C. Why does the central CO2 effect only last for a few days?

Because the kidneys, in response to the high H+ concentration in the blood, starts creating
more HCO3- which binds to H+ and reduces the amount of H+ in the CSF. It takes a few days for
the HCO3- from the kidneys to travel to the brain which is why the effect of central CO2 is so
short.
D. How do peripheral chemoreceptors respond to increase in CO2 (compared to central
chemoreceptors)?

Chemoreceptors are found in the carotid bodies and aortic bodies. Their impulses travel
through Hering nerves + glossopharyngeal and vagi nerves, respectively, to go to the dorsal
medullary respiratory area.

Peripheral chemoreceptors response to high CO2 occurs much more rapidly than that of central
chemoreceptors to high CO2 levels

Central chemoreceptors have a much more powerful effect to high CO2 levels than peripheral
chemoreceptors.

Peripheral chemoreceptors do not adapt. However, that doesn’t really matter bc they have
such little effect anyways
 6.

Description: The lower curve demonstrates the effect of different levels of arterial pO2 on
alveolar ventilation, showing a sixfold increase in ventilation as the pO2 decreases from the
normal level of 100 mmHg to 20 mmHg. The upper line shows that the arterial pCO2 was kept at
a constant level during the measurements of this study. pH was also kept constant

A. What does this graph show? Explain your reasoning.

This graph shows that low pO2 levels increase the amount of alveolar ventilation. This is
because decreased arterial oxygen stimulates the peripheral chemoreceptors.

B. Why are chemoreceptors more responsive to changes in O2 than changes in CO2?

Because chemoreceptors are constantly exposed to arterial blood, not venous blood, since
they’re located at the aortic and carotid bodies. And arterial blood more commonly has O2 so
any decrease in that O2 will stimulate them.

C. At what point of pO2 concentration in the graph does ventilation start increasing
rapidly? Explain why.

When the pO2 reaches levels below 60-70 mmHg, the ventilation starts increasing rapidly. This
is because at a pO2 of more than 60 mmHg, hemoglobin is still like 90% saturated with oxygen
so there’s no oxygen deficiency, per se. However, below 60 mmHg of O2 signals to the body
that there is not enough O2 and the peripheral chemoreceptors stimulate the dorsal medullary
group to increase inspiration.
 D. Is CO2 or O2 the major controller for respiration? Why?

CO2 is the major controller for respiration, not O2. This is because O2 doesn’t have any
significant effect on the respiratory center until it reaches crucially low levels. On the other
hand, since even marginal increases in CO2 can be very toxic, and since the only way we can get
rid of CO2 is through respiration, CO2 is the major controller for respiration, not O2.

Because the effect of hypoxia on ventilation is modest for PO 2s greater than 60-80 mmHg, the
PCO2 and the H+ response are mainly responsible for regulating ventilation in healthy humans
at sea level.

E. What does this graph above say about pO2 levels affect on respiratory center?

This graph again shows that only below 60 mmHg of O2, the carotid chemoreceptors start firing
to stimulate the respiratory center. Even if the O2 is lower than 100 mmHg, if it isn’t lower than
60-70 mmHg, the respiratory center will be unaffected because the chemoreceptors wont be
sending that many signals.
Because the effect of hypoxia on ventilation is modest for PO2s greater than 60-80 mmHg, the
PCO2 and the H+ response are mainly responsible for regulating ventilation in healthy humans
at sea level.

7. Describe the changes that occur to your respiration during acclimatization (like when
you climb a mountain).
1. Low O2 below 60 mmHg stimulates high ventilatory rates (up 400% more)
2. High ventilation means more O2 coming into the body and less CO2 in the
body
3. The body’s natural response is to inhibit the increase in ventilation due to the
central chemoreceptors sensing a decrease in arterial CO2
4. However, the central chemoreceptors effects wear off after 1-2 days and the
body gets used to the low CO2 and continues inhaling at high ventilatory
rates

8.

A. What does this graph show? Explain your reasoning.

This graph shows that pCO2 doesn’t change during exercise because even though the increase
in skeletal muscle in metabolism should increase it, there’s an increased alveolar ventilation to
get rid of the CO2.
 9.

10.

Description: Carbon dioxide dissociation curve

A. What does the yellow strip named “normal operating range” demonstrate?

It demonstrates that in arterial blood, pCO2 is 40 mmHg and in venous blood, pCO2 is 45
mmHg, meaning there is a range of 40 – 45 mmHg of pCO2 between arterial and venous blood

B. How does the volumes percent of CO2 change as it passes through tissues?

CO2 is 52 volumes percent before it passes through tissues and is 48 volumes percent when it
leaves the tissues
 C. What is the most abundant form of transport of CO2 in the body?

The most common form of transport of CO2 is as HCO3- (bicarbonate)

D. Which enzyme is responsible for turning CO2 into bicarbonate? And where is it
located?

Carbonic anhydrase is an enzyme found inside the RBC that combines CO2 + H2O = H2CO3- and
H2CO3- dissociates to form HCO3- and H+. HCO3- then can transport CO2 out of the RBC.

E. When HCO3- is transported out of the cell, there is another process that also
happens at the same time that brings a substance in. What is this process called?

It is called a chloride shift and when HCO3- is transported out of the RBC, Cl- moves into the
RBC by way of the bicarbonate-chloride carrier protein.

F. What is the name of the process by which CO2 is displaced from blood?

Haldane effect

G. Where in the body does the Haldane effect primarily take place in?

It takes place in the pulmonary capillaries

H. Describe how the Haldane effect works

In the pulmonary capillaries, when O2 binds to hemoglobin, it turns the hemoglobin very acidic.
This very acidic hemoglobin displaces CO2 from the blood. Also, the highly acidic hemoglobin
releases H+ ions which combine with HCO3- (the most abundant form of CO2 in blood) and
form H2CO3 which then dissociates into CO2 and is released into the alveoli.
 11.

Description: Carbon monoxide-hemoglobin dissociation curve. Note the extremely low

carbon monoxide pressures at which carbon monoxide combines with hemoglobin.

A. What do the small values of carbon monoxide gas pressure represent?

It shows how the smallest values of carbon monoxide can strongly compete with O2 for
hemoglobin. CO can bind with hemoglobin 250 times stronger than O2 can with hemoglobin
 12.

Description: Shift of the oxygen-hemoglobin dissociation curve to the right caused by an

increase in hydrogen ion concentration (decrease in pH). BPG = 2,3-biphosphoglycerate

A. WITHOUT looking back at the graph above, name all the factors that shift oxygen
dissociation curve to the right

a. Increase in CO2
b. Increase in temperature
c. Increase in hydrogen ion concentration (decrease in pH)
d. Increase in BPG

B. Differentiate between the Bohr and Haldane effect and where each of these
processes usually occur in the body

The Haldane effect describes how oxygen concentrations determine hemoglobin’s affinity for
CO2. Like in the lungs, the high alveolar O2 concentration enhances the displacement of CO2
from hemoglobin. Likewise, low O2 concentrations promotoe binding of CO2 onto hemoglobin.

The Bohr effect describes how carbon dioxide and H+ affect the affinity of hemoglobin for
oxygen. High CO2 and H+ concentrations cause a decrease in affinity of hemoglobin for O2 and
therefore enhances the unloading of O2. The Bohr effect happens usually in exercising muscle
where high CO2 concentration enhances the displacement of O2 from hemoglobin.

C.
 Description:

13.
A. What does circulatory shock mean?

Circulatory shock means there is an inadequate blood flow through the body, to the extent that
the body tissues are damaged because of too little oxygen and nutrients delivered to tissue.
Even the cardiovascular system begins to deteriorate and the shock leads to more shock

14.
A. What does cardiac failure mean?

Cardiac failure means the inability of the heart to pump enough blood to meet the
requirements of the body

B. Name the 2 acute effects of myocardial infarction

Decreased cardiac output and damming of blood in the veins (increased venous pressure)
 C. What kind of cardiac failure does this graph show?

This graph shows compensated heart failure

D. Describe what happens from point A to B to C to D

A to B: Acute heart failure

B to C: Sympathetic activity kicks in

C to D: Kidney retention of fluid

E. Why does right atrial pressure increase dramatically?

Because of the increased venous return

F. How is the chronic stage of kidney fluid retention beneficial in compensated cardiac
failure?
Because it increases the mean systemic filling pressure and distends the veins which reduces
TPR and facilitates blood flow to heart

G. Give 4 reasons why long term fluid retention can be detrimental.

a. Increased workload on already damaged heart

b. Overstretch the cardiac muscle
c. Pulmonary edema
d. Peripheral edema

H. What happens to cardiac reserve in compensated heart failure?

It is significantly reduced so you cant exercise, you can only do normal non-stressful activities
because your cardiac output can’t increase more than 5 L/min

15.

A.

What is this graph showing?

This graph shows decompensated heart failure

B. Describe what happens from point A to B to C to D to E to F

A: Before any compensation happens

B: Sympathetic stimulation increases cardiac output to 4 L/min (but still not enough for kidney
excretion – kidney needs 5 L/min to do excretion)

C: After one day, 4.2 L/min

D: Cardiac output still hasn’t reached 5 L/min but right atrial pressure is rapidly increasing to 9
mmHg

E: More edema and fluid retention by the kidneys

F: Increased right atrial pressure with reduced cardiac performance. This is the point of
decompensated heart failure

C. Which drug do you give to treat decompensated heart failure? Describe the mechanism
of this drug.

You give Digitalis which is a drug that strengthens the work and contractility of the heart by
inhibiting the Sodium-Potassium pump which will build up calcium inside the cell and cause
more action potential

D. How does the vicious cycle of cardiac deterioration arise?

Low arterial pressure = low coronary artery pressure = more deterioration of heart contractility

Note: a fall in coronary pressure below 80 mmHg can intitate deterioration of myocardium

E. Does acute cardiac failure cause peripheral edema? Why or why not?

No, acute cardiac failure does not cause peripheral edema because there is an initital fall in
capillary pressure before a rise (before sympathetic and kidney retention kicks in)

F. What is the role of ANP (Atrial Natiuretic Peptide)?

ANP is activated by stretch of right atrial wall and stimulates excretion of fluid from body by
kidneys

G. What are instances where high cardiac output failure arises?

Atriovenous fistula and Beriberi

 16.

A. What does this chest X-ray show? What condition is it commonly associated with?

It shows rib notching which is characteristic for coarctation of aorta.

B. What symptoms do patients with this condition commonly present with?

Patients with this condition commonly present with high blood pressure in the upper
extremities, muscle weakness, leg cramps, nose bleeds, and chest pain

C. Explain what happens in this condition and why do these symptoms occur?

 Normally coarctation happens just distal to the ligamentum arteriosum which is an

embryological remnant that connects the left pulmonary artery to the arch of aorta
 The ligamentum arteriosum is located between the arch of aorta and descending
thoracic aorta
 So first, remember that blood coming from the left ventricle goes through the arch of
aorta which continues as the descending thoracic aorta
 So just before the coarctation, you will have very high pressure because a lot of blood is
damming up behind the coarctation
 So there’s very high pressure in the upper extremities
 Blood flow downstream of the constriction is decreased so there will be lower blood
pressure in the lower extremities and you will have muscle pain there due to the lack of
blood supply and nutrients
 So, remember that the internal thoracic artery arises from the subclavian artery which is
located before the constriction
 Remember that anterior intercostal arteries come from internal thoracic artery
 And remember that the posterior intercostal arteries come from descending thoracic
aorta
 And descending thoracic aorta comes after the constriction
 However, note that posterior intercostal arteries for spaces 1 & 2 are connected to the
costocervical trunk, not descending thoracic aorta, and the costocervical trunk arises
before the constriction
 So now, remember again that before the constriction we have high pressure and after
the constriction, we have low pressures
 Normally, anterior and posterior intercostal arteries anastomose at the ribs and both
push against each other with equal pressures
 And usually, blood flow is from the posterior intercostal arteries to anterior direction
 But when there is coarctation of aorta, the anterior intercostal arteries have high
pressure and this creates reverse flow in the posterior intercostal arteries
 So no instead of blood flow going from posterior to anterior, it is going the opposite,
anterior to posterior
 Posterior intercostal arteries then dilate to accommodate the increased pressure
 This causes them to rub up against the rib and cause rib notching
 Rib notching mainly affects ribs 3-9
 Spaces 10, 11, and 12 have no anterior intercostal arteries so they aren’t affected by
backflow
 And remember spaces 1 and 2 came from the costocervical trunk which arised before
the constriction
 Remember, notching of the ribs is not due to high blood pressure of anterior intercostal
arteries, but by the dilation of posterior intercostal arteries

17. A. What coronary artery is this arteriogram of?

It is of the right coronary artery

B. Which coronary artery is this an arteriogram of?

This is an arteriogram of the left coronary artery

C. Which structures does the right coronary artery usually supply (in most people)?

Right atrium, right ventricle, SA node, and AV node (in cases of right coronary dominance)

D. Which structures does the left coronary artery usually supply (in most people)?

Left atrium and left ventricle (and AV node in cases of left coronary dominance)

E. Describe the pathway of the right coronary artery. Make sure to talk about artery to
SA node, artery to AV node, marginal branch, PIA, and right coronary dominance

1. Originates from right coronoary orifice behind right aortic valve

2. Starts travelling down through right coronary sulcus (located anteriorly between right
atrium and ventricle)
3. As it’s running down the right coronary sulcus, it first gives off an artery to the SA node
(in 55% - 60% of people)
4. Keeps running down and gives off a few atrial branches
 5. Keeps running down and gives off the marginal branch which supplies the right ventricle
6. Keeps running down and gives off a few more branches to the ventricle
7. Now this right coronary artery curves around the inferior/posterior surface of the heart
(around the posterior right ventricle)
8. And in 80% of people, the right coronary artery gives of PIA (Posterior Interventricular
Artery)
9. PIA supplies the posterior 1/3 of the interventricular septum
10. This is called right coronary dominance
11. The artery to AV node can either come from the terminal portion of the right coronary
artery right before it gives off PIA or from PIA itself. Or in cases of left coronary
dominace, it can come from the left coronary artery

F. Describe the pathway of the left coronary artery. Make sure to talk about the left
circumflex artery, left marginal artery, PIA, left coronary dominance, and LAD

1. Originates from the left coronary orifice from behind the left aortic valve
2. It travels down a bit through the left auricle and pulmonary trunk
3. Then it immediately gives off the left circumflex artery and LAD (Left Anterior
Descending) artery
4. It can also give off an artery to SA node in 40% of people
5. The left circumflex artery follows the left coronary sulcus, turns around to the posterior
side of the heart, gives off a few branches to supply the left atrium and left ventricle,
including the left marginal artery
6. In 15% of people, the left circumflex artery gives off PIA
7. This is known as left coronary dominance
8. In cases of left coronary dominance, the left circumflex artery can supply the AV node
9. Now the LAD
10. The LAD runs through the anterior interventricular sulcus and terminates at the apex
11. LAD supplies the anterior 2/3 of the interventricular septum
12. LAD also supplies the moderator band

G. What does right coronary dominance mean? How prevalent is it?

It means PIA is given off by the right coronary artery. It is in 85% of people

H. What does left coronary dominance mean? How prevalent is it?

It means that PIA is given off by the left circumflex artery of the left coronary artery. It is in 10%
of people

I. What does co-dominance of the coronary arteries mean? How prevalent is it?

It means that PIA is created by the anastomosis of the left circumflex with the right coronary
artery. It is in about 5% of the population.
 J. Why is it risky to have left coronary dominance?

Because if, God forbid, you get an occlusion in the left coronary artery, it means that both the
anterior 2/3 and posterior 1/3 of the interventricular septum will have no blood supply which
means that the ventricles won’t be able to pump any blood at all

People with right coronary dominance can still supply the posterior 1/3 of the interventricular
septum in case the left coronary artery becomes occluded so it’s not that risky.

K. What does PIA supply?

The posterior 1/3 membranous of the interventricular septum

(Hint: Think PIA, a girl, is weak and can’t supply the muscular part of the septum so it has to
supply the weak, membranous part. Also PIA with P supplies Posterior)

L. What does LAD supply?

LAD supplies the anterior 2/3 of the interventricular septum

(Hint: LAD is a strong boy so he only supplies the muscular anterior 2/3 of the interventricular
septum)

M. Which coronary artery supplies the SA node?

The right coronary artery supplies the SA node in 60% of people

The left coronary artery supplies the SA node in 40% of people

N. Which artery supplies the AV node?

The right coronary artery supplies the AV node in right coronary dominance

The left coronary artery supplies the AV node in left coronary dominance
O. What is the coronary sinus?

The coronary sinus vein is a huge vein located on the posterior side of the coronary sulcus and
travels from the left to right and opens into the right atrium

P. Where does the coronary sinus open?

It opens into the right atrium

 Q. What are the 3 veins that contribute to the coronary sinus?

Great cardiac vein, middle cardiac vein, and small cardiac vein

R. Describe the pathway of the great cardiac vein.

Great cardiac vein travels through the left anterior interventricular sulcus with LAD and empties
into the coronary sinus

S. Describe the pathway of the middle cardiac vein

Middle cardiac vein comes from the apex and travels alongside PIA upwards through posterior
interventricular sulcus until it empties into coronary sinus

T. Describe the pathway of the small cardiac vein.

Small cardiac vein runs along with right marginal artery, goes to coronary sulcus, and joins
coronary sinus.

U. What’s the purpose of a stent?

Stent keeps the artery open and maintains patency of the vessel
 18. A.

What abnormalities does this chest X-Ray show?

Left ventricle enlargement and notching of ribs

B. What are some causes of left ventricle hypertrophy?

Aortic stenosis, aortic regurgitation, hypertension

C. Where can you auscultate the heart valves?

 1st heart sound caused by closure of AV valves (normal)

o Mitral valve: 5th IC space (left) far from sternum
 o Tricuspid valve: 5th IC space (left) close to sternum
 2nd heart sound by closure of semilunar valves (normal)
o Aortic valve: 2nd IC space right to sternum
o Pulmonary valve: 2nd IC space left to sternum
 rd
3 heart sound heart at beginning to middle third of ventricular diastole by passive
filling of ventricles (abnormal)
 4th heart sound heard at last third of ventricular diastole by atrial contraction
(abnormal)

D. Which conditions cause systolic murmur?

Aortic stenosis, pulmonary stenosis, mitral valve regurgitation, pulmonary valve regurgitation

E. Which conditions cause diastolic murmur?

Mitral valve stenosis, pulmonary valve stenosis, aortic regurgitation, pulmonary regurgitation

F. Why might a coarctation of aorta cause left ventricular hypertrophy?

Because the left side of the heart has to work harder to push blood through the constricted
aorta

G. What is this an angiogram of?

Coarctation of aorta
 H. Measure the cardiothoracic ratio in the chest X-ray.

Measure the heart, lets say it’s 20 cm

Measure the thoracic cavity, let’s say it is 30 cm

Find the heart to thoracic cavity ratio, if it’s more than 50%, then it means there is cardiomegaly

19.

A. What condition is this an angiogram of?

Patent ductus arteriosus

B. What kind of shunt is this?

Left to right shunt

C. What cardiac and respiratory problems can be caused by this condition?

Decreased cardiac and respiratoy reserve and pulmonary edema leading to heart failure and
lung congestion.

D. When are the heart sounds of patent ductus arteriosus heard?

In systole and diastole

20. Which autoimmune disease causes the most valvular lessions?

Rheumatic fever

21. Describe tetralogy of

 22. Why might mitral stenosis cause dysphagia?

Because mitral stenosis will cause hypertrophy of left atrium and the left atrium is located in
front of the esophagus