MBBS 240

YEAR 1
SESSION 2021/ 2022
CARDIOVASCULAR SYSTEM
PHYSIOLOGY SGS QUESTIONS
(Lectures 10-12)
2/6/2022 (Thursday),
0800-1000 hrs & 1100-1300 hrs

1. A 60-year-old woman presented to the emergency department of Sg Buloh Hospital with

chest pain. The presenting doctor took a very thorough history and the following were
discovered. She is hypertensive with a previous history of smoking. She had many
attacks of chest pain over the last ten years. However, the attacks have occurred
every day for the past two weeks, forcing her to stop doing any work. Exertion in the
form of gardening precipitates the attacks. The pain is relieved by resting. The doctor
arranged for her to undergo coronary angiography, which demonstrated narrowing in
her anterior interventricular artery.

1. What is the possible cause of chest pain in this woman?

- The possible cause of chest pain in this woman is atherosclerosis in her anterior interventricular
artery
- Plaque is developed due to hypertension and smoking behavior
- Less blood flow to the heart muscle will cause chest pain

2. Describe the patterns of normal coronary blood flow:

a) in the ventricles during systole and diastole
- Blood flow through the coronary arteries is phasic.
- The intramyocardial tissue pressure will compress the coronary blood vessels, consequently
reducing blood flow to the left ventricle myocardium substantially.
- Most of the blood flows to the left ventricle, therefore, it occurs during diastole.
- Overall, the left ventricle receives around 80% of its blood flow during the diastolic phase of
the cardiac cycle.

b) through different parts/depths of myocardium

- The decrease in blood flow is not the same throughout the left ventricular myocardium or
the myocardial thickness.
- The decrease in blood flow during ventricular systole is more in the subendocardium than
the sub-epicardium as the intramyocardial tissue pressure is greater in the subendocardium
than in the sub-epicardium
- Thus, the endocardium only truly receives flow during diastole and is therefore extremely
dependent on an adequate diastolic filling period to maintain sufficient coronary flow.
- By contrast, the lack of compressive forces at the epicardial layer allows for perfusion
throughout the entire cardiac cycle.
- Therefore, there is a linear decrease in dependence on diastolic time fraction for the
maintenance of coronary flow in the endocardial to epicardial direction.
 3. Describe the mechanisms that regulate coronary blood flow. (ms 254)
(i) Blood flow is tightly coupled to oxygen demand.
-This is necessary because the heart has a very high basal oxygen consumption (8-10 ml
O2/min/100g) and the highest A-VO2(arteriovenous oxygen) difference of a major organ. At rest, the
heart extracts nearly 80% of the oxygen from each unit of blood delivered to it.
Whenever cardiac activity and oxygen consumption increase, coronary blood flow increases to meet
the demand(active hyperaemia) that is nearly proportionate to the increase in oxygen consumption.

(ii)Local metabolic control.

-Blood flow through the coronary system is regulated mostly by local arteriolar vasodilation in
response to the nutritional needs of cardiac muscle. That is, whenever the cardiac contraction is
increased, the rate of coronary blood flow also increases. Conversely, decreased heart activity is
accompanied by decreased coronary flow. This local regulation of coronary blood flow is similar to
that which occurs in many other tissues of the body, especially in the skeletal muscles.

(iii) Stimulation of the autonomic nerves to the heart can affect coronary blood flow directly and
indirectly.

The direct effects result from action of acetylcholine from the vagus nerves and norepinephrine from the
sympathetic nerves on the coronary vessels. The indirect effects result from secondary changes in
coronary blood flow caused by increased or decreased activity of the heart. The indirect effects, which
are mostly opposite to the direct effects, play a far more important role in the normal control of coronary
blood flow. Thus, sympathetic stimulation, which releases norepinephrine from the sympathetic nerves
and epinephrine and norepinephrine from the adrenal medulla, increases both heart rate and heart
contractility and increases the rate of metabolism of the heart. In turn, the increased metabolism of the
heart sets off local blood flow regulatory mechanisms for dilating the coronary vessels and blood flow
increases approximately in proportion to the metabolic needs of the heart muscle. In contrast, vagal
stimulation, with its release of acetylcholine, slows the heart and has a slightly depressive effect on
heart contractility. These effects decrease cardiac oxygen consumption and, therefore, indirectly
constrict the coronary arteries.

(iv) Direct Effects of Nervous Stimuli on Coronary Vasculature.

Norepinephrine and epinephrine can have vascular constrictor or vascular dilator effects, depending on
the presence or absence of constrictor receptors, alpha receptors, and the dilator receptors, beta
receptors. Both alpha and beta receptors exist in the coronary vessels. In general, the epicardial
coronary vessels have high numbers of alpha receptors, whereas the intramuscular arteries may have
high quantities of beta receptors. Therefore, sympathetic stimulation can cause slight overall coronary
constriction. Metabolic factors are the major controllers of myocardial blood flow. Whenever the direct
effects of nervous stimulation reduce coronary blood flow, the metabolic control of coronary flow usually
overrides the direct coronary nervous effects within seconds.
4. State 2 main causes of arrhythmias.
- Abnormal impulse formation (i.e Increased automaticity)
- Abnormal impulse conduction (i.e Re-entry)

4(a) List some examples of arrhythmias due to disturbed impulse formation.

- Sinus bradycardia
- Sinus tachycardia
- Respiratory sinus arrhythmia

NT
4(b) List some examples of arrhythmias due to disturbed impulse conduction.
Atrial Re-entry
- Atrial tachycardia
- Atrial fibrillation
- Atrial flutter

Atrio-Ventricular Nodal Reentry

- Supraventricular tachycardia

Ventricular Re-entry
- Ventricular tachycardia
- Ventricular fibrillation

Atrio-Ventricular Reentry
- Wolff Parkinson White

5. Briefly describe the mechanism of ectopic rhythm

• Ectopic rhythm is a disturbance of the cardiac rhythm frequently related to the
electrical conduction system of the heart, also known as premature contraction and
can be further classified as either a premature atrial contraction, or a premature
ventricular contraction
• The mechanisms are:
1. Increased automaticity
- The impulse is initiated simultaneously, without need of prior stimulation *
Characterized by:
- a) SA node: inappropriate discharge of SA node
- b) Ectopic pacemaker (an excitable group of cells that causes a premature
heartbeat outside the normally functioning SA node of the heart.): control atrial or
ventricular rhythm

2. Re-entry
- Cause primarily by abnormality in Local Reentry conduction Impulse
recirculate in the heart
- It is a repetitive activation without the need for any new impulse to be
generated
- Causing the re-entering impulses
 1
6. Briefly describe the conditions that may lead to ‘reentry phenomenon’

This figure shows several small cardiac muscle strips cut in the form of circles.
- If such a strip is stimulated at the 12 o’clock position so that the impulse travels in only one
direction, the impulse spreads progressively around the circle until it returns to the 12 o’clock
position. If the originally stimulated muscle fibers are still in a refractory state, the impulse then dies
out because refractory muscle cannot transmit a second impulse.
- However, three different conditions can cause this impulse to continue to travel around the
circle that is, cause re-entry of the impulse into muscle that has already been excited (circus
movement):
• If the pathway around the circle is much longer than normal, by the time the impulse returns to
the 12 o’clock position, the originally stimulated muscle will no longer be refractory, and the impulse
will continue around the circle again and again.
• If the length of the pathway remains constant but the velocity of conduction becomes
decreased enough, an increased interval of time will elapse before the impulse returns to the 12
o’clock position. By this time, the originally stimulated muscle might be out of the refractory state, and
the impulse can continue around the circle again and again.
• The refractory period of the muscle might become greatly shortened. In this case, the impulse
could also continue around and around the circle.

7. List some haemodynamic consequences (effect on cardiac output and BP), of some of the
common arrhythmias like:
a)Atrial fibrillation
- Decreased ventricular filling by atria (becomes important at high heart rates)
- Stasis
- Thrombo-embolism.
- If associated with increased ventricular contraction, affect ventricular filling time decreased CO

b)Sinus bradycardia
- Severely decrease the CO and consequently blood pressure
- Dizziness and syncope
- Provide opportunity for ectopic beats

c)Ventricular tachycardia
- High rates of ventricular contraction will severely reduce ventricular filling time lead to
- decrease SV
- decrease CO
- decrease BP
- Causes or aggravates heart failure
d)Ventricular fibrillation
- Uncoordinated contraction of the ventricle muscle
- CO falls to virtually zero.

8. In a routine medical check-up for university students, Aminah was told by the doctor in the
clinic that she has a murmur.
Briefly discuss how murmurs are produced.
Murmur sound is an abnormal heart sound caused by valvular lesion. It is due to disturbance
in the laminar blood flow. Timing of murmur depends on the location of the valve and the
types of dysfunction either stenosis or regurgitation. There are two types of murmur which are
systolic murmur and diastolic murmur. Systolic murmur occurs between S1 and S2. For
example, stenosis of aortic valve and regurgitation of mitral valves. Diastolic murmur occurs
between S2 and S1. For example, regurgitation of aortic valves and stenosis of mitral valves.
For regurgitation of mitral valve, during systole, the blood flows backward through the mitral
valve from left ventricle into left atrium causes decreasing net flow of blood from left atrium to
left ventricle, thus producing systolic murmur. For aortic stenosis, during ventricular ejection,
the blood is ejected from the left ventricle through a small opening of the aortic valve. This
causes resistance of the valve to be reduced and left ventricle fails to empty adequately,
hence systolic murmur generated.
For stenosis of mitral valve, during diastole, the blood passes through a stenosed mitral valve
from left atrium into left ventricle. Left atrium fails to empty adequately causing net flow of
blood reduced from left atrium to left ventricle. Thus, diastolic murmur produced. Other than
that, regurgitation of aortic valves can produce diastolic murmur. It occurs during diastole, the
blood flow backward from the aorta into the left ventricle causing the left ventricle fails to
empty adequately, then generates diastolic murmur.

9. Upon further history, she claimed that she was hospitalized at the age of three due to
rheumatic fever. List other conditions that may affect cardiac valves.
-Endocarditis which is an infection of the inner lining of the heart caused by severe infection in the
blood.
-Congenital diseases affecting the valves such as congenital bicuspid aortic valves(most common).
-Other types of heart diseases such as hypertension and myocardial infarction.
-Autoimmune disease such as lupus.
-Connective tissue disease(Marfan syndrome)
-Aging may cause calcium deposits on the valves causing stiff and thickened valves.
 10. She was then sent for an echocardiogram in which the mitral valve was seen to be
stenosed. Describe the blood flow in this situation.
Mitral stenosis (sempit- valve tak buka habis- AV valve stenosis produce diastolic murmur)
1. The narrowing of the mitral valve opening leads to difficulty in blood flow from the LA to the
LV during diastole.
2. It will produce a high resistance across the stenotic mitral valve which will result in high
pressure in the LA.
3. The pressure of the LA is higher than the LV during the diastolic filling.
4. Due to narrowing of the mitral valve, the ventricular filling is reduced.
5. Hence, the EDV will be reduced.
6. As a result the CO is reduced as well.
7. The high pressure of LA causes the pulmonary capillary hydrostatic pressure to increase as
well.
8. Hence, it will lead to pulmonary congestion and oedema.
9. Over time, LA enlarges and hypertrophy because it has to generate a high pressure when it
contracts against the high resistance of the stenotic valve.

11. Describe the abnormalities in blood flow involving the dysfunctioning AV and semilunar
valves.
Aortic stenosis (sempit – tak buka luas)
1. Aortic valve opening is narrowed resulting in a high resistance.
2. Hence, the left ventricle pressure becomes more than the aortic pressure during ejaculation.
3. The high resistance together with the turbulence of the distal to the valve will result in high
pressure gradient across the stenotic valve.
4. As a result, it will increase the afterload and ESV which will lead to reduction in SV as well as
CO.
5. The high afterload causes the left ventricle to need a higher pressure to eject the blood.
6. Therefore, this will lead to left ventricle hypertrophy and eventually lead to diastolic
dysfunction.
7. This makes the left ventricle have less compliance and will have higher filling pressure at any
given EDV.
8. Overtime, high left ventricle end-diastolic pressure causes some of the blood to flow back to
the left atrium and pulmonary vein.
9. As a result, the pressure in the left atrium increases.
10. Hence, the left atrium will enlarge and hypertrophy because it has to generate higher pressure
when it contracts in order to complete ventricular filling.

Aortic regurgitation (cannot close- back flow)

1. The aortic valve fails to close completely, and this will result in the backflow of blood to the LV
after ejection.
2. LV filling will increase because at this point, the LV will receive the blood from the LA during
ventricular filling as well as from the backflow of the blood from the aorta.
3. As a result, the EDV will increase. Thus, the end- diastolic pressure increases as well.
4. As EDV increases, the SV will increase as well.
5. However, the CO will be reduced because the net amount of blood ejected into the aorta is
reduced because of the backflow of the blood into the LV.
6. The aortic diastolic pressure is lower than normal because blood more rapidly leaves the aorta
d/t backflow into the LV.
7. Hence the aortic pulse pressure increases.
8. The high LV end-diastolic pressure causes blood to flow back to the LF and pulmonary vein
causing the LA pressure to increase.
9. As a result, there will be pulmonary congestion and edema.

Mitral stenosis (sempit- valve tak buka habis- AV valve stenosis produce diastolic murmur)
1. The narrowing of the mitral valve opening leads to difficulty in blood flow from the LA to the LV
during diastole.
2. It will produce a high resistance across the stenotic mitral valve which will result in high
pressure in the LA.
3. The pressure of the LA is higher than the LV during the diastolic filling.
4. Due to narrowing of the mitral valve, the ventricular filling is reduced.
5. Hence, the EDV as well as the CO is reduced.
6. As a result the CO is reduced as well.
7. The high pressure of LA causes the pulmonary capillary hydrostatic pressure to increase as
well.
8. Hence, it will lead to pulmonary congestion and oedema.
9. Over time, LA enlarges and hypertrophy because it has to generate a high pressure when it
contracts against the high resistance of the stenotic valve.

Mitral regurgitation( tak boleh tutup – akan ada backflow – AV valve regurgitation produces a
systolic murmur)
1. Mitral valve fails to close completely during systole resulting in the back flow of the blood from
the LV to the LA.
2. The volume of blood filled in the LA increases because it obtains blood from the back flow as
well as the pulmonary vein.
3. As a result, LA’s pressure will increase.
4. During ventricular filling, the pressure of the LA will be transmitted to the LV.
5. LV pressure increases causing the EDV to increase as well as the SV.
6. However, the CO is reduced because the net amount of blood ejected to the aorta reduces d/t
back flow of the blood to the LA.
7. The high pressure of LA causes the pulmonary capillary hydrostatic pressure to increase and
this will lead to pulmonary congestion and oedema.
8. The LA will enlarge and hypertrophy d/t adaptation of the high volume of blood.