BIO 161 – Cardiovascular - Answers
T Dic Charge – Winter 2008
Review Worksheet
1) Name the 3 different classifications of blood vessels.
Arteries, capillaries, veins
2) Identify the 3 layers of tissues in the two larger classifications of blood vessels, identifying which
are innermost or outermost for each.
Innermost – Endothelium
- smooth muscle – thicker in arteries than in veins
Outermost - Connective tissue
3) What is the function of each of the 3 layers that you identified in #2 above? How does its structure
meet that function?
Endothelium – provide smooth low-friction surface to optimize blood flow – very smooth
layer of cells/no irregularities
Smooth Muscle layer – vasoconstriction/vasodilation – circular arrangement of muscle fibre
sheets allow for contraction to narrow the lumen and relaxation to effect an increase in the
size of the lumen
Connective tissue – collagen fibres are tough protein that provides both form and protection
for the other two layers
4) Please complete the following table
Arteries
Capillaries
Veins
______ pressure
______ pressure
almost no pressure
_____ muscular walls
_____ muscular walls
____ muscular walls
Found deep
Superficial
Both (circle one)
Pulse?
found everywhere
Found deep
Superficial
Both (circle one)
Pulse
Pulse?
Flow – fast
Flow – fast
Flow – fast
Slow
Slow
Slow
Very slow (circle one)
Very slow (circle one)
Very slow (circle one)
Answers to be found on slide #6 in the lecture notes
5) From inside a heart chamber, identify the layers of tissue that you would encounter as you moved
outwards.
Endocardium, myocardium, visceral pericardium, parietal pericardium
6) Define the term “cardiac tamponade” and explains how it might come about
If pressure in the pericardium rises sufficiently due to fluid accumulation, the heart might
stop beating altogether – this is cardiac tamponade. The fluid might accumulate because of
trauma to the pericardium, disease (MI, HIV, mumps, etc.), or infection of the pericardium
7) Describe the formation of an atherosclerotic plaque on an arterial wall.
a) LDLs deposit on wall
b) WBCs (leukocytes) attracted to wall invoke inflammation – devour fats and become
“foam” cells
c) a cap may form on the foam cells that is thick and stable (doesn’t easily break away) or it
may be thin and fragile and could break away, resulting in a heart attack of stroke – this
answer, though not discussed in lecture, is well worth understanding from slide #8
8) Explain what structural component of arteries makes them very elastic, and what function this
serves.
The presence of elastin in all 3 layers of these vessels means they can expand and absorb the
shock of the systolic pulse of blood, and then slowly collapse to maintain arterial pressure
during diastole – hence, they are recognized as a pressure reservoir.
9) Start in the right atrium and describe EVERY structure (chambers, valves, vessels) a blood cell
would travel through (don’t worry about what’s nearby for this answer) as it completed one
complete circuit of the circulatory system and returned to the right atrium.
Right atrium  tricuspid valve  right ventricle  pulmonary (semilunar) valve 
pulmonary trunk  pulmonary arteries  arterioles  capillaries (lungs & alveoli) 
venules  pulmonary veins  left atrium  bicuspid (mitral) valve  left ventricle  aortic
(semilunar) valve  aorta  arteries  arterioles  capillaries  venules  veins 
inferior or superior vena cava or coronary sinus  right atrium
10) In the fetal heart, two chambers are connected via a hole in the wall between them. Which
chambers are involved, what is the name of the hole, and once it closes prenataly, what is the
closed hole then called? Why is this arrangement functional in the fetal heart (what is the logic
behind this evolutionary difference in fetal versus post-natal heart)?
The foramen ovale connects (and therefore shunts blood from) the right atrium to the left
atrium. Closed by birth, the depression seen mostly from the right atrial side of the
interatrial septum is called the fossa (depression) ovalis. Because fetal lungs are not the
source for oxygenation of the blood, the foramen ovale serves to efficiently bypass the lungs
for most of the blood flow.
11) What is the tissue between the two atria called? Between the two ventricles?
Interatrial septum and interventricular septum
12) Structures that prevent the eversion of valves in the heart are found attached to some but not all of
the valves. Which valves do have these structures, what are they (the structures) called, and to
what muscles are they attached? Which chambers are the structures/muscles found in?
The chordae tendinae are found in the ventricles, supporting and preventing the tricuspid
(right) and bicuspid (left) valves from everting into their respective atria. The chordae
tendinae are attached to papillary muscles on the inferior surface inside the ventricular
chamber. Eversion means flipping outwards, much like an umbrella might evert in a
windstorm.
13) Following up on question 12, why don’t the other valves have these structures (and which valves
are they)?
The aortic and pulmonary valves (both semilunar valves) don’t need this kind of support
because pressures in the aorta and in the pulmonary trunk are not high enough to threaten
eversion of the valve.
14) Describe the circulation of the heart tissue itself (ie. the coronary circulation). Include a
description of how the vessels are interconnected, and don’t forget the venous return.
The right coronary artery arises from the aorta and crosses down the right side of the heart
below the right atrium and then wraps around the posterior of the heart where it connects
(anastomoses) to the circumflex artery. The left coronary artery arises from the aorta and
moves over the left atrium where it divides into the interventricular, which runs roughly over
the interventricular septum and wraps around a point slightly lateral to the apex of the heart
to meet up with the anastomosis of the right coronary artery and the circumflex artery. The
latter is the second branch of the left coronary artery – it wraps around the left side of the
heart below the left atrium and then anastomoses with the right cornary and interventricular
arteries on the posterior surface of the heart.
The veins of the heart (not studied in lecture) collect venous blood in the coronary sinus,
which empties into the right atrium, where the blood mixes with blood from the vena cavae.
15) Define the terms
a) Stenosis
Narrowing (of anything) – in the heart, a stenosed valve could lead to congestive heart
failure
b) Valvular incompetence
If a valve leaks or in any way fails to function, it is said to be incompetent.
c) Heart murmur
Any leaky valve or other cause of irregular flow in the heart results in a sound heard on
ausculatation called a heart murmur. While a systolic murmur may be benign, ALL
diastolic murmurs are considered pathologic.
d) Ischemia
Lack of blood flow to a tissue, which can result in tissue necrosis (death).
e) Myocardial infarction
Death of heart muscle (myocardium), usually due to ischemia.
16) Where are precapillary sphincters found and what is their purpose? Give two examples of this
function.
At the capillary end of arterioles, these sphincters are used by the body to regulate perfusion
(blood flow) into certain capillary beds. The capillaries of the gut can be highly perfused
after eating or have reduced perfusion during a fight/flight reaction. Capillaries of the
extremities (hands/feet) might be highly perfused to shed heat in warm environments, or have
reduced perfusion to conserve heat in cold environments.
17) Sketch a normal ECG and identify the 3 waveforms we have studied. On the same diagram,
identify when the following events occur: Ventricular Repolarization, Atrial Repolarization,
Ventricular Depolarization, and Atrial Depolarization.
QRS complex
Ventricular
depolarization
& Atrial
repolarization
Atrial
depolarization
Ventricular
repolarization
T
P
Time (s)
0
0.2
0.4
0.6
0.8
18) Describe the origin and spread of an electrical event in the myocardium of a normal, healthy heart.
Include all structures in sequence, and indicate when different chambers of the heart are
contracting.
Sinoatrial node in superior right atrium  spreads across both atria (and the atria contract)
 atrioventricular node (slows signal and creates pause between atrial and ventricular
contractions  left and right bundle branches (bundles of His)  Purkinje fibres 
myocardia of both ventricles (ventricular contraction)
19) How do you explain the pause between the two phases of the heart contraction? Why is there such
a pause?
The atrioventricular node slows conduction of the depolarization between the atria and
ventricles and this results in the delay between the contractions of the atria and the
ventricles. The delay allows completion of ventricular filling (and atrial emptying) before the
ventricles contract.
20) Identify the name of the cardiological phenomenon in each of the following three diagrams, and
explain what is happening in each case. Consider the effect on Cardiac Output and the immediacy
of the danger to the patient.
Atrial fibrillation – the atrial myocardium is contracting in an uncoordinated fashion – very little
additional blood is moving into the ventricles – reduced cardiac output is the result – not
immediately fatal
Ventricular fibrillation – the ventricular myocardium is contracting in an uncoordinated fashion
– very little blood is moving if any, meaning Cardiac Output is essentially zero – fatal within 2-3
minutes
21) Fever is known to be associated with an increased heart rate. Describe the amount by which the
HR rises per degree of increase in the fever, identify the temperature limit to this rise, and briefly
explain why it happens.
HR rises 10 bpm (beats per minute) for each 1 degree C rise in body temperature, but this
rise reverses if the temperature rises above 40.5 to 41 degrees C. The rise is explained by the
increased metabolism of the SA node at higher temperatures, and the fact that repolarization
would happen faster (and thus the node would depolarize more frequently).
22) Identify the location and pace of the places in the myocardium that will spontaneously depolarize.
What happens in each case if one node leads the heart in depolarization?
SA node – 70-80 bpm – will result in the normal spread of depolarization through the heart
AV Node – 45-60 bpm – would result in synchronous depolarization/contraction of the atria
and ventricles with the atria contracting in the cephalic (towards the head) direction.
Purkinje Fibres – 15-40 bpm – would result in the ventricles contracting before the atria, and
the atria would be contracting from the AV node upward, in the wrong direction.
23) What is the technical term for the tissues identified in the previous question that describes their
property of spontaneously depolarizing?
Automaticity
24) What is Bundle Branch Block and what does it cause?
One or the other or perhaps both of the bundle branches in the interventricular septum are
damaged and do not conduct signals. This means the atria may beat normally, but the
Purkinje fibres would be the only tissue distal to the blockage that would still be capable of
automaticity and so would drive the contraction of the ventricles. Because they depolarize
less frequently than the SA node, the ventricular contractions would be less frequent and
there would be a disconnect (asynchrony) between the atrial and ventricular contractions.
25) While the heart muscle is capable of driving its own rhythm, what two nerves are responsible for
raising and lowering the HR in response to demands from the body? How is this actually
accomplished at the level of the SA node?
The vagus nerve (Cranial X) influences the SA node to take longer to repolarize and
therefore lowers HR in response to a drop in demand for oxygen from the body.
The accelerator nerve works the opposite way, to reduce the time of repolarization of the SA
node and therefore elevated the HR in response to increased demand (exercise, fight/flight
response)
26) What effects do Atropine and Digitalis have on the heart?
Atropine in small doses will slow the heart, but in higher doses causes the HR to rise
Digitalis is administered to produce a slow and steady rhythm – too much can depress the
heart to the point of stopping.
27) Define the clinical interpretation of a slow and a fast HR (that is, give each a name and define the
actual HR threshold for each).
tachycardia – high HR (over 100 bpm)
bradycardia – low HR (below 60 bpm)
28) Define the terms stroke volume and cardiac output.
SV is the amount of blood ejected by either ventricle in each beat
CO (or Q) is the amount of blood ejected by either ventricle over an entire minute.
29) An individual who is 40 years of age is exercising maximally and is determined to have a cardiac
output of 18 L/min. Assuming a normal HR for that age at maximal exercise, please determine the
stroke volume at exercise.
HRmax = 220-age = 220 – 40 = 180 bpm
CO=HR x SV so SV = CO/HR = 18000/180 = 100 ml
30) Explain what congestive heart failure (CHF) is.
Due to incomplete ventricular ejection (blood remains in the ventricle after systole), filling of
the ventricle limits the blood flow from the side of the circulation that empties into that side
of the heart (systemic for the right ventricle, pulmonary [lungs] for the left side). As blood
backs up on that side, pressure builds and edema in the tissues is the result result. The heart
will work harder as a result of decreased perfusion.
31) Name four possible causes of CHF
a) Coronary atherosclerosis
b) Persistent high blood pressure
c) Multiple myocardial infarcts
d) Stenosed valves
32) What is hemoptysis and what side of the heart would be implicated if the cause was CHF?
Hemoptysis is the coughing up of blood – if due to CHF, this would imply a left side defect in
which the left ventricle incompletely empties, blood backs up in the pulmonary circulation,
and pressure has become high enough to cause the movement of erythrocytes out of the
pulmonary capillaries and into the alveoli.
33) If the pulmonary valve is stenosed, describe what would happen to the heart and suggest a
symptom that one might notice externally that might point to this problem.
The right ventricle would have to work harder to push blood out into the pulmonary trunk,
so it would hypertrophy. Because ejection would likely be incomplete, this would be right
side CHF, and would likely result in systemic edema, resulting in swollen limbs, particularly
the lower legs/feet, or hepatic edema.
34) Define what blood pressure is and identify the two main factors that contributed to it.
BP is the pressure exerted on arterial walls – it is a combination of the effect of the volume of
the blood ejected by the heart into the vessels (SV) and the compliance (elasticity) of the
vessels.
35) Please sketch a graph that illustrates the decline in blood pressure from the aorta through the
systemic circulation until blood returns by the vena cava. Identify in which vessels the pulse
declines to zero as well. Use appropriate units of blood pressure and list all sizes of blood vessels
on both the aterial and venous sides of the capillaries, as well as the capillaries.
Important points: pulse is 120/80 at aorta but is already declining in arteries and has been
reduced to less than 20 mm Hg (100/80) before leaving the arteries
Mean pressure is about 80 upon entering arterioles
Pulse declines to zero in the arterioles
Pressure drops starting in smaller arteries and declines below 40 before entering capillaries, and
further below 20 upon leaving the capillaries
Pressure declines gradually from there to zero.
36) What two reasons can you use to explain the decline in pressure as blood travels throughout the
systemic circulation in a healthy, normal individual?
Distance – as distance increases, frictional energy losses result in the decline in pressure
Cross-sectional area – although progressively smaller vessels are encountered, the number of
vessels multiplies rapidly. The cross-sectional area of the aorta is surpassed by the enormous
increase in cross-sectional area of the arterioles and even more so in the capillaries.
37) Explain the effect of atherosclerosis on Blood Pressure
Both frictional increases and narrowing of the lumen (ie. a decrease in the cross-sectional
area) are results of atherosclerosis – both contribute to an INCREASE in blood pressure,
which is known as hypertension. In addition, the vessels with atherosclerotic plaques are less
elastic and so that also contributes to higher blood pressure
38) Explain what the Frank-Starling Mechanism (or simply Starling’s Law) refers to with respect to the
heart, and suggest its effect on Blood Pressure.
As venous return increases (perhaps due to increased contraction of skeletal muscle during
exercise, stretching of the ventricle by the additional volumes of blood returning to the heart
causes and increased force of contraction. This results in more blood being ejected into the
vessels by the ventricles, and thus causes a rise in Blood Pressure (recall that BP is influenced
in the aorta and early arteries by two things – the SV and the elasticity of the vessels)
39) As a person exercises, more blood is pumped back to the heart. Explain how this is so.
Increased skeletal muscle contraction results in a pumping effect on the veins. Due to the
arrangement of the valves in the larger venules and the veins and vena cavae, the blood
moves within the veins compressed by the muscles in the direction of the heart. This results
in more blood returning to the heart, or an increased venous return. See Frank-Starling,
above.
40) Please be sure to know the meanings of these terms: (check your text, a medical dictionary, or your
notes for definitions)
a) Ischemia
b) Edema
c) Vasoconstriction
d) Vasodilation
e) Pericarditis
f) Chordae Tendinae
g) Trabeculae Carnae
h) Papillary Muscles
i) Anastomosis
j) Stenosis
k) Systole
l) Diastole
m) Infarct
n) Depolarize
o) Repolarize
p) Automaticity
q) Tachycardia
r) Bradycardia
s) Stroke Volume
t) Cardiac Output
u) Polycythemia
v) Hepatic
w) Hypertension
x) Hypotension
y) Perfusion
z) Hemoptysis