[Kufa Medical College – Cardiovascular Module Workbook – 2012-2013]

Semester 3

CONTENTS Page

Module staff……………………………..……………………………………………………………2

Timetable………………………………………………………………………………… 3

Introduction………………………………………………………………………………….……… 4

Summary of learning outcomes………………………………………………………… 4

Recommended Texts…………………………………………………………………… 5

Useful Web Sites………………………………………………………………………… 5

Assessment………………………………………………………………………………………… 6

Session 1
Introduction to the CVS, anatomy of the heart in situ and major 7
blood vessels

The cardiac cycle.

Session 2
Development of the cardiovascular system. 19

The anatomy and development of the heart.

Session 3 Congenital heart problems 31

Role of the autonomic nervous system 42

Session 4
Blood flow to tissues and its control 49

Session 5 Overall control of the cardiovascular system 64

Cellular and molecular events in the heart / drugs 769

Session 6

The electrocardiogram 93
Sessions 7
Special circulations 111
Session 8
Ischaemic heart disease 118
S ession 9

Heart failure 130

Session 10

Session 11 Shock 147

Session 12

Practice questions 155

Kufa Medical College – Cardiovascular Module Workbook

 CVS Module (S3)

Module staff
Module leader: Prof. Dr. Yesar M.H. Al-SHamma

Academic staff: Dr.Akeel A.Zwain

Dr.Ahmed N. Rajiab

Dr.shehab Ahmed

Dr.Maher Finjan

clinical staff: Dr.Muhammed Saeed

Dr.Hussain Serhan

Dr.Ihsan M.Ajeena

Dr.Muhammed Nurey

Dr.smeer hassan

Clinical educators: Dr.Fouad Shareef

Dr.Zehraa Abid Al-Alie

Dr.Bushra Abid Al-Ameer

Dr.Ali Ismaael

Dr.Falah Dinana

Dr.Muhannad Yahya

Dr.Asaad Nuaman

Dr.Asil Shaalan

Dr.Amina Abid Al-Bakee

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Cardiovascular System Timetable 2013

Session 1-introduction to the CVS/anatomy of the CVS

9:00-10:00 Lecture1.1 LT1&LT2 Introduction to the CVS Module leader Work
book page

10:00 10:30 Tutorial Seminar Introduction to anatomy Clinical 7-18

rooms educators

10:45 12:00 Anaomy Anatomy Pericardium&coronary Academic

Lab. circulation staff+clinical
educators

12:15 13:00 Lecture1.2 LT1&LT2 Histology-blood vessels & Academic staff

heart tissue

Session 2-The cardiac cycle Development of the heart

9:00-10:00 Lecture2.1 LT1&LT2 The heart as a pump Academic Work book
staff page

10:15 11:45 Group work Seminar Pressure/flows during Clinical 19-30

rooms cardiac cycle educators

Heart sounds

12:00 13:00 Lecture1.2 LT1&LT2 Development of the Academic

heart1 staff

Session 3-Anatomy of the heart & congenital heart defects

9:00-9:45 Lecture3.1 LT1&LT2 Development of the Academic staff Work
heart book page

9:45-10:30 Tutorial Seminar Surface& radiological Clinical 30-41

rooms anatomy of the heart & educators
introduction to anatomy

10:45-12:00 anatomy Anatomy Chambers of the heart Academic

Lab. staff+clinical
educators

12:15-13:00 Lecture3.2 LT1&LT2 Congenital heart Academic staff

defects
afternoon Formative Formative assessment Examination
assessment on the anatomy of the
heart

3-a
 9:00-10:00 Work book page

Session 4-the role of The autonomic nervous system

Lecture4.1 LT1&LT2 The autonomic nervous clinical staff
system

10:15 11:45 Group work Seminar The autonomic nervous Academic 42-48
rooms system staff+clinical
educators

12:00 13:00 Feedback LT1&LT2 Formative assessment Examination

feedback

Session 5-Blood flow to tissues and it's control

9:00-10:00 Lecture5. LT1&LT2 Factors affecting flow hrough Module leader Work book
1 tubes page

10:15-11:45 Group Seminar Pressure/flows and resistance Academic 49-63

work rooms staff+clinical
educators

12:00-13:00 Lecture5. LT1&LT2 Pressure and flow in he Module leader

2 systemic circulation

Session 6-Control of the cardiovascular system

9:00-10:00 Lecture6.1 LT1&LT2 Control of cardiac output Academic staff Work book
page

10:15 11:45 Group work Seminar Problems of the behavior Academic 64-78
rooms of the CVS under different staff+clinical
circumstances educators

12:00 13:00 Lecture6.2 LT1&LT2 Response of the whole Academic staff

system

Session 7-Cellular and molecular events ++Drugs of the heart

9:00-10:00 Lecture7.1 LT1&LT2 Cellular events in the Academic staff Work book
heart page

10:15 11:45 Group work Seminar Control of the heart beat Academic 79-92
rooms staff+clinical
educators

12:00 13:00 Lecture7.2 LT1&LT2 Action of drugs on the Clinical Staff

heart
 9:00-10:00 Work book page

3-b

Session 8-The electocardiogram

Lecture8.1 LT1&LT2 The electrical activity of Academic
the hear and ECG staff

10:15 Group work Seminar Analysis and Clinical 93-110

11:45 rooms interpretation of the ECG educators

12:00 Lecture8.2 LT1&LT2 Plenary lectures on Academic

13:00 ECG(review of group Staff
work)

Session 9-Special circulations

9:00-10:00 Lecture9.1 LT1&LT2 The Special circulations Academic Work book
staff page

10:15 11:45 Group work Seminar Special circulations Academic 111-117

rooms staff

12:00 13:00 Formative LT1&LT2 Written paper Examination

assessment
+feedback

Session 10-Ischemic hear disease

9:00-10:00 Lecture10.1 LT1&LT2 Causes of chest pain Clinical staff Work
+investigation and book page
management of angina
and MI

10:15-11:45 Group work Seminar Case studies on patients Clinical 118-129

rooms with chest pain educators

12:00-12:45 Lecture 10:2 LT1&LT2 Clinical skills clinical staff

After noon See notice ECG practical and Academic staff

demo
 9:00-10:00 Work book page

afternoon See notice ECG practical and Clinical staff

demo

3-c

Session 11-Heart failure

Lecture11.1 LT1&LT2 Hear failure Clinical staff

10:15-11:45 Group work Seminar Case studies on heart Clinical 130-146

rooms failure educators

12:00-13:00 tutorial Seminar Review of cases clinical

rooms educaors

After noon Lecture 11.2 See notice ECG practical and Clinical staff
demo

Session 12-shock&review of CVS

9:00-10:00 Lecture12.1 LT1&LT2 Review of CVS module Module leader Work book
shock page

10:15-12:00 Group work Seminar Shock &example Clinical 147-155

rooms summative style educators
questions
 9:00-10:00 Work book page

3-d
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Cardiovascular Module Workbook

Semeser3

Introduction

The broad aim of this module is that, by its end, you should understand the structure and
function of the human cardiovascular system, how its condition is assessed and how
cardiovascular function is altered in common diseases. You should also begin to understand
the broad principles of management of cardiovascular disorders.
The module will run on Wednesdays, beginning with a lecture at 9am. In some early
sessions this will be followed by time in the dissecting room, where you will learn about the
anatomy of the cardiovascular system. In other sessions you will complete group work
material with the help of a tutor. The final few sessions of the module are strongly clinical,
consisting of case-based discussions. In this way we hope that you will see the links between
the basic sciences and their clinical application, and lay a secure foundation for your
subsequent clinical work. You will also be expected to work in your own time either in the
dissecting room, by continuing study of workbooks, or in preparation for the next session. It is
important to take an integrated approach to your learning and to study the content of this
module in relation to a number of other modules.

Summary of intended learning outcomes

On completion of this module students should be able to:

1. describe the structure and relations of the heart and major blood vessels of
the body and relate their structure to function in the circulation
2. describe the operation of the heart as a pump, including the function of the
heart valves, and be able to use their understanding of the cardiac cycle as a basis
for physical examination of the heart
3. describe the development of the heart, some common congenital defects,
and the pathology of valvular problems.
4. describe the factors influencing blood flow to individual tissues, the
mechanisms of control of vascular resistance and the special features of the
pulmonary, cerebral, coronary, skin and skeletal muscle circulations
5. describe in general terms the role of the autonomic nervous system in the
control of cardiovascular function, including the concepts of local and central control
6. describe the mechanisms controlling cardiac output in the normal individual,
and how they operate in common situations such as exercise
7. describe the molecular and cellular events underlying the cardiac cycle, the
principles of altering heart rhythm and contractility by drugs, the categories of drugs
used for common cardiac conditions and the principles involved
8. describe the features of the normal electrocardiogram and their relationship
to electrical events in the heart, and be able to interpret changes in the ECG
produced by common clinical conditions
9. describe the structure and properties of the coronary circulation, and the
pathology and effects of ischaemic heart disease.
10. describe the assessment, diagnosis and management of a patient presenting
with acute chest pain
11. describe some common causes, major effects and treatment of heart failure

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12. describe the essential characteristics of shock

Cardiovascular Module Workbook

Dissecting room
In the dissecting room you will work in the same groups as in the Musculoskeletal module.
The organisation of dissecting room work will be explained to you, as will the appropriate
codes of behaviour and safety precautions necessary in the dissecting room. Please take
care to follow these rules.

Group work
Workbook material will be provided for all sessions. You should work together in your groups
to complete these. It is important that you bring along appropriate text books. You will have
a tutor who will quiz you on your understanding and help out when you are stuck. Answers to
group work will be posted on Blackboard the following week.

Self study
There are a number of self study exercises in the module handbook which you should work
through. To encourage active learning the answers to self-study questions will not be
provided. If you have any problems with these you can seek help via the discussion board on
Blackboard. You may work on CVS or musculoskeletal anatomy when the dissecting room is
open and not required for teaching. The histology laboratory will also be available to you.

Text books
The recommended books for the CVS module are:
Lilly LS Pathophysiology of Heart Disease 5th Edition, LW&W Hampton JR The ECG
made Easy 7 Edition, Churchill Livingstone
th

You may wish to consult a basic revision text such as:

Aaronson PI & Ward JPT The Cardiovascular System at a Glance 3rd Edition, Blackwell
Science

You will need a physiology text book such as:

Boron WF & Boulpaep EL Medical Physiology 2nd Edition, Saunders Elsevier
Berne RM & Levy MN Principles of Physiology 4th Edition, Mosby

You will also need to consult a variety of cross modular books such as:
Moore KL & Agur AMR Essential Clinical Anatomy 3rd Edition, LW&W
Moore KL & Dalley AF Clinically Orientated Anatomy 5th Edition, LW&W
Junquera, LC & Carneiro, J Basic Histology 11th Edition, Mosby
Sadler, TW Langman‟s Medical Embryology 11th Edition, LW&W
Rang HP, Dale MM, Ritter JM, Rang & Dale‟s Pharmacology 6th Edition, Churchill
& Flower R
Livingstone
Kumar P & Clarke M Clinical Medicine 7th Edition, Saunders
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Useful websites and resources

http://www.medicine.mcgill.ca/physio/vlab/cardio/vlabmenucardio.htm
Virtual laboratory web site from McGill University.

http://sprojects.mmi.mcgill.ca/heart/egcyhome.html
The EKG World Encyclopedia edited by Dr Michael Rosengarten of McGill University is a
useful resource with many examples and an EKG puzzler.

http://www.ecglibrary.com/ecghome.html

http://www.cvphysiology.com/index.html
This web-based resource by Dr R Klabunde, Associate Professor of Physiology at Ohio
University includes material from his book, „Cardiovascular Physiology Concepts‟.

Cardiovascular Module Workbook

Blackboard
Where possible slides used in the lectures will be posted on the Blackboard. There is also an
excellent histology self study site. I would encourage you to use the discussion board as a
forum between students and the module leader.

Assessment
This module will be assessed on the basis of satisfactory attendance and also in the End of
Semester Assessments (ESAs) from Semester 2 onwards.
In addition, material from the module will be included as part of the Integrated Medical
Sciences Assessment at the end of Phase 1.

To help you assess your own learning of the CVS module there will be 3 formative
assessments:

1. Week starting 14th February: formative quiz on early sessions

2. Starting on the 30th March: ECG quiz will be made available
3. 23rd March – written formative paper

Students who fail to complete these could be regarded as not having satisfactorily completed
the course.

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 [Kufa Medical College – Cardiovascular Module Workbook – 2012-2013]

Cardiovascular System

Session 1

Aims of this session

To provide an overview of the structure and function of the cardiovascular system

To emphasise the need for appropriate blood flow to different tissues of the body and
the functional elements in the cardiovascular system which are necessary to provide it
To study and appreciate the position of the heart in situ
To study and appreciate the structure and function of the pericardium and its
relationship to the phrenic nerves
1. To study the external features of the heart and major vessels, and to appreciate the
course of blood flow into and out of the heart
2. To study the structure of different types of blood vessels in relation to their function in
supplying blood to and from the tissues of the body

Structure of the session

Lecture 1.1 Introduction to the CVS Module (LT1& LT2)

Tutorial Introduction to Anatomy (Seminar Rooms)

Dissection Pericardium & Coronary Circulation (DR)

Lecture 1.2 Histology – Blood Vessels & Heart Tissues (LT1 & LT2)

Afternoon activities: Study of structure of blood vessels using textbooks, the le and the
histology laboratory.
Complete self study sections in workbook.
Continue work in the DR.

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Lecture 1.1

Learning outcomes

By the end of this lecture and with appropriate self study you should be able to:
describe the factors influencing the exchange of substances between the blood in
capillaries and the surrounding tissues
1. describe the critical importance of adequate blood flow for the maintenance of
capillary exchange
2. list typical blood flows in ml/min/g tissue and ml/min/organ for major organs of the
body,
including the brain, kidneys, heart muscle, gut, skeletal muscle and skin
describe the distribution of cardiac output over major organs of the body
describe the major functional components of the circulation
describe the distribution of blood volume over the major parts of the circulation

Lecture Synopsis

The cardiovascular system serves to supply cells in the body with their metabolic needs,
which requires a system of distribution of materials and exchange with the tissues. Exchange
with the tissues occurs at the capillaries, which are vessels lined with a single layer of
endothelial cells through which many substances may diffuse easily. 98% of exchange is by
diffusion.

Diffusion is affected by the

area available for exchange
the difficulty of movement through the barrier ('diffusion resistance')
the concentration difference ('gradient')

The area available for exchange in a tissue is determined by how many capillaries there are
per unit volume (the 'capillary density'). This varies from tissue to tissue and is highest in the
most metabolically active. Not all capillaries are always perfused, so it represents the
maximum area for exchange. Generally, however, area is not limiting.

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Diffusion resistance is determined by the nature of the barrier and the molecules which are
diffusing. A major component of diffusion resistance is the distance over which diffusion must
occur - the 'path length', itself dependent on capillary density. Lipid soluble molecules diffuse
easily through capillary cell membranes, hydrophilic molecules travel via pores which offer
little resistance to small molecules and ions, but prevent movement of molecules where
molecular weight exceeds 60,000. For small molecules, diffusion resistance, therefore, is not
limiting.

The supply of materials to the tissues therefore depends most critically on the concentration
gradients driving exchange. The relevant gradient is that between the capillary contents and
the nearby cells. This gradient does depend on the concentration of substances in the blood
entering the tissue, but the more important variable is the flow of blood through the capillary.
Unless blood is supplied at an appropriate rate, the gradients driving exchange will dissipate,
and nutrients will not be supplied at the right rate.

All other things being equal, then, the supply of nutrient to a tissue depends most critically on
maintaining the right flow of blood for the prevailing level of metabolic activity. The
cardiovascular system must maintain appropriate flows through all tissues. Consider the
following examples:
Blood Flow (ml/min)

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Min Max

750 750
Brain: The metabolic needs of the brain are
constant and can be met by a flow of 0.5
ml/min/g. The brain is extremely intolerant
of flow interruption.
Heart: At rest, the heart needs 0.9 ml/min/g but 300 1200
if the heart has to work hard this may increase
four fold. The heart is also extremely intolerant
of inadequate flow.
1200 1200
Kidney: Requires a high constant blood flow
to maintain its function, though most flow is not
nutritive.
Gut: (and liver): At rest the gut and liver,
which are connected in series via the hepatic
portal system, receives 1 ml/min/g. Digestion
of a meal generates a substantial increase in 1400 2400
flow. Short term flow reduction tolerable.
Skeletal muscle: The metabolic needs of
muscle vary enormously. At rest the blood flow
needs to be 0.03 ml/min/g, up to 6.0 ml/min/g
in exercise, but this may not meet metabolic
needs. Muscle can survive a degree of
anaerobic metabolism.
1000 16000
Skin: Skin is not metabolically very active and
may be supported by 0.01 ml/min/g, though
flow may increase to 1.5 -2 ml/min/g for
thermoregulation.
Rest of the body: A fairly constant demand of 200 2500
Total
200 200
The cardiovascular system as a whole must therefore: 5050 24250
deliver between 5 and 25 l.min-1 of blood to the body
maintain a blood flow of 750 ml.min-1 to the brain at all times
maintain blood flow to the heart muscle and kidneys at all
times

Meeting this specification

requires a pump - obviously
the heart distribution vessels -
the arteries
flow control - the output of the pump (the 'cardiac output') must be distributed
appropriately by restricting flow to those parts of the body which are easy to perfuse so as
to drive blood to those, often vulnerable, parts which are not so easy to get blood to. Flow
control is via resistance vessels - the arterioles and pre capillary sphincters
ability to cope with changes in the cardiac output. This requires capacitance in the
system - a 'store' of blood that can be called upon to cope with temporary imbalances
between the amount of blood returning to the heart and the amount that it is required to
pump out. This store is in the veins
Different vessels in the system perform these functions, and their structure, which you will be
examining in your self-study, reflects their function.

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At rest, the blood volume of about 5l is distributed as follows:

11% in the arteries and arterioles, 5% in the capillaries, 17% in the heart and lungs, 67%
in the veins.

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Cardiovascular Module Workbook

Dissection: Middle Mediastinum & Heart in situ (Pericardium, External

Features of the Heart, Major Vessels & Relations)

Introduction

The heart lies in the middle mediastinum; the mediastinum is the intervening region between
the right and left pleural cavities occupied by the lungs in the thoracic cavity.

The middle mediastinum consists of the pericardial sac containing the heart and its blood
vessels (coronary vessels) and the roots of the aorta, superior and inferior vena cava and
the pulmonary vessels.

Dissection: refer to pages 46-48 of: Anatomy – A Dissection Manual and Atlas by S. Jacob

Aims:

to study and appreciate the position of the heart in situ

to study and appreciate the structure and function of the pericardium and its relationship
with the phrenic nerves
to study the external features of the heart, major vessels (superior vena cava and its
tributaries, ascending aorta, arch of the aorta and its branches, pulmonary vessels and
inferior vena cava) and relations
to appreciate the course of blood flow into and out of the heart
to be able to indicate the surface anatomy of the heart on a subject

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Cardiovascular Module Workbook

Self Study: Major Arteries & Veins of the Body

Arteries

the head and neck Brachiocephalic the abdomen

trunk
Common Carotid, Abdominal Aorta & its paired branches:
External Carotid & its branches Suprarenal arteries
Facial artery Renal arteries
Maxillary artery Ovarian/Testicular arteries &
Superficial temporal artery/ its unpaired branches:
Internal Carotid Celiac artery
Superior Mesenteric artery
the thorax Inferior Mesenteric artery
Thoracic [Descending] Aorta & its
Intercostal branches and the pelvis Common
Iliac artery
External Iliac artery
Internal Iliac artery

Label the above named arteries on the diagram.

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You should also

know the major
arteries of the upper
limb (Subclavian,
Axillary, Brachial,
Radial and Ulnar
arteries) and the
lower limb (Femoral,
Popliteal, Anterior
and Posterior Tibial
arteries). These will
be
studied further in the
Musculoskeletal
System Module.

Copyright © 1998, Medical College of St Bartholomew‟s Hospital, London

Veins

the head and neck External the abdomen Inferior

Jugular vein Vena Cava
Internal Jugular vein Hepatic veins
Right and Left Brachiocephalic vein, Right & Left Renal veins &
Left & Right Testicular veins
the thorax
Superior Vena Cava and the pelvis Common
Iliac vein
External Iliac vein
Internal Iliac vein

Label the above named veins (except the hepatic portal vein) on the diagram.

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Copyright © 1998, Medical College of St Bartholomew‟s Hospital, London

The major veins of the upper limb (Subclavian, Cephalic, Basilic and Median
Cubital veins) and the lower limb (Femoral, Long Saphenous, Short Saphenous and
Popliteal veins) will be studied further in the Musculoskeletal System Module.

Cardiovascular Module Workbook

Self Study: Case Scenario to illustrate the importance of this region of anatomy

Malkit was duty Casualty Officer when the paramedics radioed to say they were blue lighting
in a 21-year old stabbing victim. They were puzzled because he was „sweaty, had a fast
heart rate and had a low BP‟ but was not in pain and had bled very little from a small stab

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wound in front of his chest. Malkit talked to the cardio-thoracic Registrar arranging for the
patient to be received in theatre.

After briefly examining the victim, the Registrar had the patient put onto a theatre table and
told the SHO to scrub up. As he was being anaesthetised, the Registrar cut his clothes off
and started painting the patient‟s chest. As soon as the patient was asleep the SHO draped
up and did a very rapid median sternotomy. He fixed the chest open with the rib spreader.
Blood shot everywhere as the SHO incised the pericardium from top to bottom. There was a
1cm stab wound in the anterior wall of the left ventricle, from which a jet of blood squirted into
the air at each systole until the SHO put his finger over the hole. The anaesthetist said,
“That‟s good, now his neck veins will go down and I can start to relax again!”

The Registrar put a few loose stitches over the SHO‟s finger covering the hole then pulled
them all tight together with no finger in the way. The Registrar said, “He has no other injuries
and thanks to a smart Casualty Officer he should do fine now. He will be in the 90% who
survive surgery from a stab wound to the heart.”

The SHO said, “I‟m surprised so many survive cardiac stab wounds. I thought it was much
more serious.”

“Aha” said the Registrar. “I am talking about survival in the 10% of patients who are still alive
when you get the chest open. I think you must be referring to the other 90% who are taken
straight to the mortuary.”

1. Why did the patient have a tachycardia, low BP and distended neck veins?

2. What else could cause a pericardial collection or effusion?

3. What would the patient‟s heart sounds have shown?

4. What is pericardiocentesis?

5. Why would it not help in this case?

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Self Study Exercises

On the diagram, label the following: On the diagram, colour the following:

Right & left brachiocephalic vein C (clavicle)

Superior vena cava 1st rib
Arch of the aorta Level of manubrio-sternal joint (-----)
Brachiocephalic artery 5th intercostal space
Left common carotid artery Left auricle & left ventricle
Left subclavian artery Right atrium & right ventricle
Left pulmonary artery
Pulmonary trunk On the diagram, mark the following:

Apex of the heart

Domes of the diaphragm (--------)

Copyright © 1998, Medical College of St Bartholomew‟s Hospital, London

On the diagram, mark (using different colour ink) the blood flow into and out of the heart.

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Copyright © 1998, Medical College of St Bartholomew‟s Hospital, London

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Self Study Directed Reading

1. The heart does not hang freely in the thorax; it hangs by great vessels inside the
pericardium. Write short notes about the pericardium and its components. How
does the heart move in the thoracic cavity? What constrains its movement?

2. What layers constitute the wall of the heart and how do they differ from the
pericardium? The pericardium is inextensible. When might this be important?

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Lecture 1.2 Histology of the Cardiovascular System

Structure of Blood Vessels (Types of Arteries, Veins & Capillaries)

Learning outcomes: By the end of this lecture and following completion of the self study you
should be able to:

1. describe how blood vessels (arteries, arterioles, capillaries, venules and veins) are
named.
2. describe the structure of different types of blood vessels in relation to their function in
supplying blood to and from the tissues of the body.
You should also revise the structure of cardiac muscle covered in the Tissues of the Body
module.

Introduction

You will need to know about the histology of various parts of the cardiovascular system.
Mostly, this will be achieved by self-study using the self learning session on the learning
environment and an atlas of histology and other supplementary resource materials. Light
microscopes and supplementary materials are also available in laboratory 321. In order to
make this self-study more effective there is a short lecture during session 1. The aim of this
exercise is to enable you to appreciate structure and function relationships when you study
the morphology and physiology of the cardiovascular system.

In this lecture only the structure function relationships of blood vessels will be studied. You
are expected to review the structure of heart muscle, its conducting tissue (Purkinje fibres)
and blood components on your own.

Types of Blood Vessels

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Arteries are blood vessels that carry blood away from the heart to supply the organs and
tissues of the body. Different arteries contain varying amounts of elastic fibres and smooth
muscle fibres in their walls; thus they are named elastic (conducting) and muscular
(distributing) arteries. The walls of the elastic arteries expand slightly with each heartbeat.
The muscular arteries branch into arterioles whose function is to regulate the amount of
blood reaching an organ or tissue and more generally in regulating blood pressure. The
diameter of the muscular arteries and arterioles is controlled by the autonomic nervous
system. The arterioles branch into smaller vessels (metarterioles), which carry blood into the
smallest vessels in the body, the capillaries.

A capillary wall is mostly one cell thick and allows exchange of substances between blood
and tissues. The capillary wall may be continuous or fenestrated. Both these types of the
capillaries may be surrounded partially by pericytes. In addition to these two types of
capillaries, there is a category of vessels found in the liver, spleen and the bone marrow,
called sinusoids, which are generally larger in diameter and may contain special lining cells
and an incomplete basal lamina. Under certain conditions, some blood cells leave the
circulatory system to enter the tissue spaces.

Capillaries merge into large vessels called the venules which merge to form even larger
vessels called the veins which carry blood towards the heart. The construction of a vein is
essentially similar to that of an artery, except that its wall is thinner and its lumen wider and
irregular. The veins usually contain semilunar paired valves that permit blood to flow in only
one direction; those veins are narrower than 1 mm in diameter and those in the thoracic and
abdominal cavities do not have valves. The veins collapse if blood pressure is not
maintained; the blood flow in arteries is the result of cardiac systolic pressure, whereas blood
flow in veins is, to a great extent, determined by the "muscle-pump" action in the leg and
pressure factors in the abdominal and the thoracic cavities.

Cardiovascular Module Workbook

It is important to realise that blood vessels reach almost every part of the body except
cartilage, epithelia, cornea and a few other structures.

Self learning - Histology of the CVS (learning environment)

Awareness and appreciation of the microstructure will enable enhance your understanding of the
function of the cardiovascular system. Dr Pallot has prepared an excellent self learning
histology session on the learning environment. You should undertake this in your own time.

There are also a number of slides available in the histology lab (321) for those who wish to
undertake the microscope study outlined below.

Microscopic Study

Before studying the microscopic structure of the blood vessels, familiarise yourself with the
general structure of a large blood vessel wall (3 layers - tunica intima, tunica media and tunica
adventitia) and its components (cellular and fibrous).

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Examine Slide 65 (large elastic artery - Aorta) and Slide 66 (large vein - Vena Cava) and
compare their structure. Elastic fibres in the vessel wall are best seen when the tissues are
stained with Weigert's Elastin stain (Examine Demonstration Slides of the Aorta and Vena
Cava.

Examine Slide 89 (Liver) and Slide 43 (Adrenal Gland); cords of cells are separated by
sinusoids (the lumen, which is lined by squamous endothelial cells, contains red blood cells).

Review the structure of cardiac muscle (Slide 27) and special cardiac muscle cells, the
Purkinje Fibres (Slide 47).

Self Study continued

1. What are arteriovenous shunts?

2. The larger blood vessels have their own blood supply. Why is it necessary to have a
separate blood supply and what are these vessels called?

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Cardiovascular Module Workbook

3. What are vena comitantes?

4. What structures in blood vessels help blood return to the heart?

Varicose veins (i.e. dilated, tortuous superficial veins) may occur following an
abnormality such as thrombosis in a deep vein. Can you explain this in view of your knowledge
of the venous drainage of the extremities?

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5. The coronary arteries are referred to as end arteries. What are end arteries? How does
this terminology apply to coronary arteries?

Cardiovascular System

Session 2

Aims of this session

to understand the basic structure of the heart to understand how the heart
develops in fetal life to understand the operation of the heart as a pump, and be
able to describe in detail the
cardiac cycle
to understand the principles of auscultation of the heart

Structure of the session

Lecture 2.1 The Heart as a Pump (LT1& LT2)

Group Work Problems on pressures/flows at various stages of cardiac cycle

Lecture 2.2 Development of the Cardiovascular System 1 (LT1 & LT2)

Afternoons: Continue self study work in the course book

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Lecture 2.1: The heart as a pump

Learning outcomes:

By the end of this lecture and appropriate self study you should be able to:

describe the basic structure of the heart, naming the chambers, valves, and main vessels
describe in general terms the properties of cardiac muscle which allow the heart to
operate as a pump

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define the terms Systole and Diastole describe how the organisation of the muscle
in ventricular walls facilitates the pumping of
blood
describe the main differences between the right and left heart
describe the sequence of pressure and volume changes in the left atrium and ventricle
over a complete cardiac cycle in the normal individual
describe when in the cardiac cycle each valve in the heart opens and closes, and the
pattern of flow through each valve
explain the origin of the 1st and 2nd heart sounds
given a diagram showing the pressure profile in the left atrium, left ventricle and
aorta for a
single cardiac cycle in a healthy adult, perform the following
tasks: label the pressure axes label the time base (assuming a
heart rate of 60 bpm) indicate the points at which the mitral and
aortic valves open and close indicate the position of the 1st and
2nd heart sounds
draw the profile of pressure changes in the internal jugular vein, labelling the 3 component
areas

Lecture synopsis

The heart as a pump

The heart is two pumps in series. Thin walled atria act as reservoirs to supply muscular
pumping chambers - the ventricles. In-flow and out-flow to the ventricles are separated by valves.
The right side of the heart pumps blood to the lungs (pulmonary circulation), the left side to the
body - or systemic circulation.

Cardiac muscle is a specialised form. The myocardium consists of individual cells joined by
low electrical resistance connections. The contraction of each cell is produced by a rise in
intracellular calcium concentration triggered by an all or none electrical event in the cell
membrane - the action potential. The cardiac action potential is very long, so over most of the
heart a single action potential will produce a sustained contraction of the cell lasting about 200
- 300 ms. Action potentials spread from cell to cell, so at each heart beat all the cells in the
heart normally contract.

Pumping action requires a regular, co-ordinated pattern of contraction. Action potentials are
generated spontaneously at regular intervals by specialised pacemaker cells. In the normal
heart the pacemaker is the sino-atrial node, in the right atrium. Excitation spreads over the
atria to the atrio-ventricular node, and thence down the muscular septum between the
ventricles to excite the ventricular muscle from the endocardial side, from where the
contraction spreads through the ventricular myocardium and up towards the AV junction where
the valves are located.

The period when the myocardium is contracting is known as SYSTOLE

The period of relaxation between contractions is DIASTOLE

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Contraction of the atria is not forceful, but the ventricular muscle is organised into figure of eight
bands which squeeze the ventricular chamber forcefully in a way most effective for ejection
through the out flow valve. The apex of the heart contracts first and relaxes last to prevent
back flow.

The cardiac cycle is the sequence of pressure flow changes and valve operations that occur with
each heartbeat.

As the ventricular muscle relaxes (i.e. early diastole), the intra-ventricular pressure falls, and
the atrio-ventricular valves (tricuspid and mitral) open as atrial pressure exceeds ventricular.
The atria have been distended by continuing venous return during the preceding systole, so
initially blood is forced rapidly from the atria into the ventricles - the 'rapid filling' phase. Filling of the
ventricles continue throughout diastole, at a steadily decreasing rate until the intra-
ventricular pressure rises to match atrial pressure. At low heart rates the ventricles are more
or less full before the next systole begins.

Atrial systole is the contraction of the atria, which forces a small extra amount of blood into the
ventricles. After a delay of about 100-150 ms the ventricles begin to contract (systole). As
intra ventricular pressure rises, so blood tends to flow the 'wrong way' through the A/V valves,
producing turbulence which closes the valves forcibly. The ventricles then contract
'isovolumetrically' and intra ventricular pressure rises rapidly until it exceeds the diastolic
pressure in the arteries, when the outflow (aortic and pulmonary) valves open. There is then
a period of rapid ejection of blood, and both intra ventricular and arterial pressure rise to a
maximum. Towards the end of systole intra ventricular pressure falls, and once it is below the
arterial pressure the outflow valves close, and when the atrial pressure is reached the A/V
valves open, and the whole process starts again.

These events are associated with sounds which are often used to assess the state of the heart.
Sound is produced by sudden acceleration and deceleration of structures or by turbulent flow.

In the normal heart there are always two sounds. Two others may be audible.

First heart sound: As the A-V valves close oscillations are induced in a variety of structures,
producing a mixed sound with crescendo-descendo quality - 'lup'.

Second heart sound: As the semi-lunar valves close oscillations are induced in other structures
including the column of blood in the arteries. This produces sound of shorter duration, higher
frequency and lower intensity than the first - 'dup'.

A third sound may be heard early in diastole, and a 4th sound is sometimes associated with atrial
contraction.

In exercise turbulent flow generates 'murmurs' in normal individuals, but at rest murmurs are
associated with disturbed flow, say through a narrowed valve, or back flow through an
incompetent valve.

Cardiac output: The volume pumped per minute by the left heart is known as the Cardiac
Output. As the pumping is intermittent, it is the product of the volume ejected per cardiac cycle
- stroke volume and the number of cycles per minute - the Heart rate. Both may vary.

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Group work

This group work consists of a series of short answer questions and multiple-choice questions
which you should attempt to answer. Each section of the preceding lecture has a few SAQs and
one MCQ associated with it.

The heart beat

Q2-1 From where does the blood flow into the right atrium?

Superior and inferior venae cavae and

the coronary sinus

Q2-2 What fraction of the blood flow into the right atrium comes a) from descending veins b)
ascending veins?

‫الجسم‬
20% from s.v.c. Upper limb ‫ & العلوي اما يجمع الدمالسفلي من يجمع منمنطقه البقيه‬head ‫نه‬5
80% from i.v.c.

Q2-3 What is the average pressure in the right atrium?

range 0 – 8 mmHg average

around 4mmHg

Q2-4 Which valve separates the right atrium and right ventricle? When in the cardiac cycle is
it a) open b) closed?

Tricuspid valve

Open in diastole
Closed in ventricular systole

Q2-5 How many action potentials are generated by the cardiac pacemaker at each heartbeat?

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One

Q2-6 What is a typical resting heart rate? How much blood is ejected from the left ventricle per
beat at rest? CO ‫اذا كال لكل دقيقه راح نحسب ال‬

Heart rate = 60 – 80 b/min

Stroke volume=EDV-ESV
Stroke volume = 80 mls

Q2-7 MCQ

Concerning the heart

T F

1. Blood flows from the right ventricle into the pulmonary Artery

2. In cardiac muscle cells are fused together forming multinucleate

fibres ‫كهربائيا‬

3. Once a heart beat is initiated all healthy cells in the myocardium

normally contract 5 ‫اما كلهن يتحفزن سوه او‬

4. In the ventricle a contraction, once begun, lasts for about 300 ms

5. The force of contraction of the ventricle can be increased by recruiting

previously quiescent muscle cells ! ‫اما كلهن يتحفزن سوه او‬
Heart rate

Q2-8 What will happen to the beating of the heart if the sino-atrial node is damaged?

There are other areas of the heart which can act as pacemakers.
The AV node is the next most rhythmic ‫وراح‬
‫يقل الرتم‬

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pacemakers ‫ ذني ال‬4‫ليش ميصير تنافس ب‬

Q2-9 Given the heart has more than one pacemaker, why don't different pacemakers compete
to drive the heartbeat in the normal heart?

Because they fire at a slower rate Rate ‫ اسرع‬AS ‫'ن ال‬

Q2-10 If nerves are to change heart rate where in the heart must they act?

Sino-atrial node (pacemaker)

Q2-11 If the heart rate is 60 bpm, what is the approximate duration of diastole?

700 ms
Sys ‫ زم تطلع الوقت لكل شربه وحده وتخلي وقت ال‬9
‫فنا‬ diastole ‫ ثابت والبقيه تنطيها لل‬300ms
1000ms ‫ ثانيه يعني لكل ضربه‬60 ‫ لكل‬60‫ال‬
700 ‫ والبقه‬for Sys 300‫و‬
Q2-12 What will happen to the duration of diastole if the heart rate increases to 120 bpm?

It will fall by approximately two thirds. Systole is relatively spared

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Q2-13 MCQ

T F

1. Regular beating of the heart requires pacemaker cells T

2. Electrical activity normally originates in the right ventricle

F

3. Electrical activity spreads down the septum via the T

bundle
of His

4. The first part of the ventricle to contract is the endocardial surface at T

the apex ‫من الداخل للخارج‬

F
5. The heart relaxes during systole

Filling of the heart in diastole

Q2-14 Draw a graph (volume against time) to show the rate of ventricular filling in diastole

‫هنا ال‬
3 ‫اقسام وهنه‬ ‫ يكون ع‬filling

1-Rapid 75%
2-minimal flow. 5% 3-
Atrium contraction 20%

Q2-15 What proportion of the ventricular filling occurs during the first 100 ms of diastole?

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‫ فهنا ممكن يكون اقل‬ms 300- 200 ‫ ياخذ وقت‬%70 ‫حاضره كايل انه اول فيز ابو‬7‫هوه با‬
75 – 80% 100ms ‫ ;نه فقط‬%70 ‫ال‬

‫عدل‬$‫ ليش ميصير بنفس ا‬0‫ للبط‬filling‫يعني ال‬

Q2-16 Why doesn't the ventricle go on filling at the same rate throughout diastole?

As intraventricular volume increases, intraventricular pressure inc reases so the

pressure gradient diminishes
The initial rapid filling phase is due to the abrupt release of blood from the atria.
The slow filling is due to further blood returning from the circulation

‫ورده‬%‫شيصير اذا ازداد ضغط ا‬

Q2-17 What will happen if the venous pressure supplying the atrium rises?

End-diastolic volume increases with a resultant increase in stroke volume

‫ بالتالي‬V ‫ والي حينزل لل‬R ‫حيزداد الذم الجاي لل‬

SV ‫ وايضا يزداد ال‬EDV ‫يزداد ال‬

Q2-18 MCQ

T F
٢٠٪ ‫هاي بس‬
1. The ventricles are filled by contraction of the atria F

2. When the atria contract, the mitral and tricuspid valves are T
open

3. The mitral and tricuspid valves open at the beginning of diastole ‫يبدي عند بدايه‬ F
‫ذين‬$‫ مل& ا‬diastole‫ن ال‬$ $ ‫ا‬7‫يزو فومتريك ري‬1‫كسيشن من ضمن ال دايستولك‬

4. Pressure in the ventricles rises towards the end of diastole T

5. The atrial pressure rises during systole T

Systole

Q2-19 What causes the mitral and tricuspid valves to close?

At the end of diastole the intraventricular pressure exceeds atrial pressure,

resulting in a brief backflow of blood which causes the atrioventricular valves to
close

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Q2-20 What happens to intraventricular volume just after the A/V

valves close? ‫كبنه انه الحجم يضل ثابت‬

It remains the same (the start of isovolumetric contraction)

Q2-21 What will happen if the valve becomes incompetent (leaks)?

‫ ن الصمام يكون مضطرب‬1 ‫صوت مرمر يصير‬

There will be turbulent backflow of blood giving rise to a systolic murmur on

auscultation

Q2-22 Why does the ventricle not empty completely into the arteries during systole?

Eventually the pressure gradient reverses so that arterial pressure is greater than
ventricular pressure
The residual volume in the ventricles serves as a small, adjustable blood
reservoir

Q2-23 What will happen if the heart muscle contracts harder?

The velocity of ejected blood flow will increase and the ejection fraction (the
ratio of stroke volume to end -diastolic volume) will increase
‫كلهن يزدادن‬
‫فروض ينسد الصمام ؟؟؟ هنا‬0‫كسيشن غير ا‬6‫يعني من يصير ري‬
‫بهر اللي‬I‫ زم ينتظر هل اجزاء القليله حتى الدم يرتد من ا‬I ‫نكول انه‬
‫يعتبر اشاره للصمام حتى ينغلق‬
Q2-24 Why doesn't the aortic valve close as soon as the heart muscle begins to relax?

Blood is still moving forward ! ‫الرجوع من ا(بهر للبطبوقت‬

The valve only closes when intraventricular pressure falls below arterial
pressure and a brief backflow of blood occurs

Q2-25 MCQ

T F

1. The aortic and pulmonary valves close at the onset of F

ventricular systole
‫ن يكون البط& مملوء‬/ T
2. During 'isovolumetric' contraction the
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pressure in the ventricles rises, but the intra-ventricular volume does

not change iso... contraction ‫هاي تعتبر نفسها مده ال‬
3. The aortic valve opens about 40 ms after the mitral valve
T closes

4. The mitral valve opens about 80 ms after the aortic valve

closes
T iso... relaxation ‫ال‬

5. The pressure in the aorta is at its lowest when the aortic T ‫يي صح قليل حتى يستقبل الدم‬

valve opens

Q2-26 Draw the normal profile of pressure changes in the jugular vein during the cardiac
cycle and label the a, c and v components. What produces these components?

Copy diagram supplied in group work or refer to Kumar & Clark

a wave - due to atrial contraction c wave - due to transmission of increasing
ventricular pressure, closing of tricuspid valve and possibly also transmission
from neighbouring carotid artery v wave – due to venous return to right
atrium while tricuspid valve is closed Heart sounds (this last section can
be done as self study)

Q2-27 Listen to your own heart with a stethoscope. How can you tell which is the first and
which is the second sound?

They have different qualities

The first heat sound is loudest and longest “lub”
The second sound has a higher pitch, shorter duration and lower intensity
“dup” The gap between the first and second sound is shorter than between the
second and first

Q2-28 Now step up and down onto a chair until your heart rate rises to about 120 (feel your
pulse). Listen to your heart again. Now, how can you tell which is the first and which is the
second heart sound?

It is more difficult. The gaps are shorter but the qualities of the two sound s are
still different

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Q2-29 Which sound is most affected in inspiration? Can you hear the change in yourself or
another subject?

There is physiological splitting of the second sound in inspiration. The first

sound is not affected

During inspiration blood is drawn into the thorax. This increase s right
ventricular pressure so closure of the pulmonary valve (P) is delayed.

Conversely, left ventricular stroke volume falls (as greater negative pressure
enlarges left atrial capacity, thus redu cing left atrial pressure and therefore
ventricular filling). So the aortic valve (A) closes early

Q2-30 How would narrowing of the aortic valve or first part of the aorta - aortic stenosis affect
the relationship between the pressure in the left ventricle and the pressure in the aorta?

It would increase the pressure gradient

The pressure in the aorta distal to the narrowing would be reduced

Q2-31 When in the cardiac cycle would you expect to hear a murmur if a patient has aortic
stenosis?

Systole

Q2-32 When in the cardiac cycle would you expect to hear a murmur if the mitral valve fails
to open properly? (mitral stenosis)

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Diastole
Turbulent blood flow from left atrium to ventricle through a narrowed valve

Q2-33 When in the cardiac cycle will you expect to hear a murmur if the mitral valve fails to
close properly? (mitral incompetence)

‫لذلك‬0‫ الصمام مينسد يفتح بشكل طبيعي كامالما با‬mitral ‫ ميصير شي لوالصمام <ن‬R‫ نقباض للشراي‬R‫البط‬0‫با‬
‫نبساط حيرجع فل < من ذين يضخ ويطلع الدم منصوت‬
Systole
Backflow of blood to the left atrium during ventricular systole

Q2-34 In the fetus a vessel - the Ductus Arteriosus connects the pulmonary artery to the
aorta, so that blood ejected from the right ventricle bypasses the lungs and goes directly to
the systemic circulation. The Ductus Arteriosus normally closes at birth, but occasionally
remains open. What would you hear through the stethoscope in an infant with such a 'Patent
Ductus Arteriosus'?

Continuous murmur through both systole and diastole (machinery murmur)

‫(نه دائما يجري الدم من ا(بهر للرئوي‬

Lecture 2.2: Early Development of the Cardiovascular System I

Background

Knowledge of the concepts discussed in the “Early Embryonic Development” lecture series,
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(TOB, Semester 1) is assumed. In particular you should know the consequences of the
processes of gastrulation and embryonic folding.

Objectives

By the end of this lecture and after appropriate self-learning you should be able
to:
Describe the formation and looping of the primitive
heart tube
Name the regions of the developing heart
Describe in brief the development of the great vessels

Reading

Chapter 12, Langman‟s Medical Embryology, SADLER, 11th edition

Synopsis

The cardiogenic field from which the heart, blood vessels and blood cells will develop is
created during gastrulation and at first lies at the cranial end of the embryo before folding
occurs.
As development of the cardiovascular system gets underway, a pair of tubes (endocardial
tubes) develops within the cardiogenic field in the 3rd week of development. The endocardial
tubes are brought together during embryonic folding and fuse in the mid-line to create the
primitive heart tube. The primitive heart tube is linear at first, receiving blood (inflow) at its
caudal pole and pumping blood (outflow) from its cranial pole. The primitive heart tube is
described as having four segments the (primitive) atrium, the (primitive) ventricle, bulbus
cordis and truncus arteriosus. Early in its development the cardiovascular system (heart and
vasculature) is highly symmetrical in marked contrast to the adult disposition.
The symmetrical arrangement of embryonic/fetal blood vessels is systematically remodelled
over the course of development. The process by which the adult disposition of the heart is
achieved begins with the process of looping of the primitive heart tube. Put simply, looping
places both the inflow and outflow cranially with the inflow dorsal to (behind) the outflow.
Evidence for the embryonic structures of the primitive heart tube persists in the adult (see
also 2nd lecture). With further growth and development the primitive atrium contributes a
(small) component to each atrium, the bulbus cordis give rise to (part of) the right ventricle
while the left ventricle is derived from the primitive ventricle. The truncus arteriosus ultimately
gives rise to the roots and proximal portions of the pulmonary trunk and aorta.

Self study

List the embryonic germ layer / layers that contribute to the cardiovascular system.

1. Explain fully how folding of the embryo contributes to the development of the
cardiovascular system.

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2. Flow of blood into the primitive heart tube is always at its caudal end true / false

Explanation:

3. The heart along with the developing gut is suspended in the true / false
intraembryonic coelom

Explanation:

4. Both the left and right atria develop entirely from structures present true/ false in
the primitive heart tube

Explanation:

What is the difference between the course of the left and right recurrent laryngeal
nerves in relation to the great vessels?

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Cardiovascular System

Session 3

Aims of this session to study the structure of the heart chambers and valves, and the
coronary circulation. to study the development of the cardiovascular system
to study how some common congenital abnormalities of the heart and great vessels
arise and, in general terms, what effects they may have.

Structure of the session

Lecture 3.1 Development of the Cardiovascular System II (LT1&2)

Tutorial Surface & Radiological Anatomy of Heart Introduction to Anatomy

(Seminar Rooms)
Dissection Chambers of the Heart (DR)

Lecture 3.2 Congenital Heart Defects (LT1&2)

Formative assessment: To be done in your own time, but before next Wednesday

A formative assessment will be placed on the Blackboard following this session. You must
download and complete this assessment before session 4. You should bring your completed
script to the group work in session 4 so that tutors can mark on the register that this
assignment has been completed. You will need knowledge of the material from sessions 1, 2
and 3 to complete the test. There will be a feedback lecture following the group work during
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which you will mark your papers. A random selection may be double marked. Students who
perform badly in this test can request to see a staff member to receive advice on their future
study habits, so that they can come to realise more what is meant by directed self learning.
This test is important for you, but is not a formal part of the module assessment, though
students who do not complete this could be regarded as not having satisfactorily completed the
morning sessions 1,2 and 3.

Lecture 3.1 : Early Development of the Cardiovascular System II

Background

The content of this lecture builds on the previous lecture (Early Development of the
Cardiovascular System I). Self-directed learning in this area is assumed.

Learning outcomes

By the end of this lecture and after appropriate self-learning you should be able to:

Relate the anatomy of the adult heart to embryonic structures

Describe the process of septation o
Formation of the inter-atrial septum o Formation of
the inter-ventricular septum
Understand the principles of the fetal circulation o
Fate of the fetal shunts

Synopsis

Once the primitive heart tube has looped, the most complex sequence of heart development
gets underway to create the “two pumps in series” configuration required. Therefore in the
process of septation the primitive heart tube becomes divided into chambers and the outflow
tract is subdivided into pulmonary trunk and aorta. Firstly, the junction between the atrium
and ventricle becomes constricted creating a narrow channel called the atrioventricular canal.

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Cardiovascular Module Workbook

This narrowing provides a framework by which the inter-atrial and inter-ventricular septa are
formed.
Central to the process of septation are the endocardial cushions that form both in the region of the
atrioventricular canal and truncus arteriosus. Endocardial cushions form in the region of the
atrioventricular canal and provide a platform toward which the septa grow inferiorly (inter –
atrial) or superiorly (inter – ventricular), dividing the heart into left and right sides. Endocardial
cushions forming in the truncus arteriosus contribute to the formation of a spiral septum
dividing the outflow into pulmonary trunk and aorta.
Atrial septation is complicated by the fact that the circulatory needs of the embryo/fetus are
different to those of the adult. Thus a right – to – left shunt (the foramen ovale) must be
maintained during life in utero, but this must be instantly sealable at birth.

Because of its complex developmental programme and the dramatic changes required for
the transition from pre- to post- natal life, a large proportion of congenital defects affect the
cardiovascular system. A deep understanding of the development of the heart and great
vessels will contribute to a better understanding of the clinical problems associated with their
malformation commonly seen in clinical practice.

Dissecting Room

Dissection: Chambers of the Heart (Anatomy – A Dissection Manual and Atlas by S. Jacob pp
49-51)
(Coronary arteries & veins of the Heart and internal appearance of the Heart)

Aims:

1. To study and appreciate the arrangement of the right and left coronary arteries & their
main branches supplying the heart.
2. To study and appreciate the arrangement of the main venous tributaries draining the
heart.
3. To study and appreciate the internal structure of the four chambers of the heart and
understand how this structure relates to their embryological development
4. To appreciate the structure of the valves of the heart and the great vessels in relation
to their function during blood flow to/from and within the heart.

Specific Objectives: By the end of the session and with appropriate self-learning, you should
be able:

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to identify and describe the distribution of the right and left coronary arteries.
to locate the main venous tributaries draining the heart tissue and describe the inflow
into the right chamber of the heart.
5. to describe the internal structure of the right and left atria of the heart in relation to
their development.
to explain the differences in the thickness of the walls of the ventricles of the heart.
to explain the structure and function of the valves of the heart and great vessels in
relation to the blood flow through them.
6. to describe the circulation of blood in the heart.

Cardiovascular Module Workbook

Introduction

The blood vessels of the heart muscle occupy grooves between different chambers of the
heart. Variations in the pattern of the blood supply to the heart muscle are common; study
some common variations illustrated in standard anatomy textbooks and atlases.

The internal structure of each of the four chambers reflects its embryological derivation and is
related to its function of the transport of blood from one chamber to the other. The structure of
the valves of the heart and great vessels reflect their function to ensure unidirectional blood
flow.

Examine the coronary arteriograms, aortogram and pulmonary arteriogram.

Self Study

Use your textbooks and the demonstration material in the Dissecting Room to answer the
following questions:

1. What are the adult derivatives of the septae primum and secundum?

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2. How is the primitive ventricle of the heart divided into right and left ventricles?

1. At birth, the three cardiovascular shunts necessary for fetal survival cease to function.
What are these shunts and what happens to them at birth?

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2. In what structure does the sinoatrial node arise and how and where is it incorporated
into the heart?

Cardiovascular Module Workbook

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Self Study – Coronary Circulation & Chambers of the Heart

Clinical Scenario highlighting underlying important regional anatomy

While swimming with his wife, Edward Jackson felt a tight pain over his precordium. Being a
consultant physician in his mid 50‟s with a family history of IHD, he made for the side and
beckoned his wife from the pool. On the car journey his pain worsened, became crushing
and spread down his left arm. He was feeling cold and clammy when they reached casualty.
He knew he felt too faint to walk into casualty and the next thing he knew he was on a trolley
in a bay, still in his swimming trunks. He had very excited junior doctors round him and
caught a whiff of burned flesh. Seeing paddle marks on his chest, he realised he must have
arrested and felt very relieved that junior doctors are so conscientious about knowing their
stuff.

He enjoyed uneventful progress in his own coronary care unit and made his juniors explain
things to him as with any other patient. However, he was anything but just another patient
and massacred them with questions about the relevance of his FH, the complications and
future risks of MI, why lifestyle changes are thought to help and the demography of IHD.

1. What events can interrupt the blood flow and what happens in the myocardium
when its local perfusion ceases?

2. Why is the pain felt in the front of the chest, felt down the left arm and what other
diagnoses can mimic it?

3. How would his juniors explain the cold clamminess and him feeling so faint?

4. Why did Dr Jackson have a cardiac arrest and why would electrical shocks help?

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5. Which vessels supply the front, back, right and left aspects of the heart?

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Medical

Self Study Exercises

On the diagram, label and colour the coronary vessels and mark the area of heart muscle
supplied by each of the main branches of the coronary arteries.

Copyright © 1998, Medical College of St Bar tholomew‟s Hospital, London

On the diagram, mark the approximate position of the bicuspid (mitral), tricuspid, aortic
and pulmonary valves.

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Copyright © 1998, Medical College of St Bartholomew‟s Hospital, London

What is the cardiac skeleton? What is its relationship with the valves of the heart and
those of the great vessels? What is its function during the transport of blood (a) from the
atria into the ventricles and (b) from the ventricles into the pulmonary trunk and the
aorta?

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The atrioventricular valves differ in structure but function in the same manner.
Describe what happens to the valvular components (e.g. cusps) during (a) blood flow from the
atria to the ventricles and (b) when the ventricles contract. What is the role of the
papillary muscles and the chordae tendineae during ventricular contraction?

The semilunar valves in the pulmonary trunk and aorta prevent blood flowing back into
the ventricles during ventricular relaxation. How is this achieved?

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What is the relationship of the cusps of the aortic semilunar valves to the openings of the
coronary arteries? During which phase of the cardiac cycle does most of the blood
supplying the heart muscle enter the coronary arteries?

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Lecture 3.1: Congenital Heart Disease

Learning outcomes: By the end of this lecture and with appropriate study you should be able
to:

describe the frequency and types of congenital malformation of the heart and great
vessels
appreciate the types and frequency of ventricular septae defects appreciate the
types and frequency of atrial septae defects understand the effects of a left to
right shunt understand the causes of congenital cyanotic heart defect describe
the functional importance of transposition of the great vessels describe the
functional importance of stenosis and atresia of the aorta and pulmonary
valve
understand the significance of a patent ductus arteriosus
describe the effects of coarctation of the aorta

Self Study

Use your text books and the demonstration material in the Dissecting Room to answer the
following questions:

1. What are the causes of coarctation of the aorta?

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2. Describe the group of cardiac defects known as the Tetralogy of Fallot.

1. What is transposition of the great arteries?

2. Several cardiovascular defects are associated with well-known syndromes.

Describe one syndrome and its associated anomalies.

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Cardiovascular System

Session 4

The Autonomic Nervous System

The aim of this session is to introduce the structure and function of the autonomic nervous
system and its role in the control of the cardiovascular system.

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Structure of the session

Lecture 4.1 The Autonomic Nervous System and the CVS (LT1 & LT2)

Group work: The ANS

Feedback session for the formative assessment (LT1 & LT2)

Lecture 4.1: The structure and function of the ANS

Learning outcomes:

By the end of the session and with appropriate self study you should be able to:

describe the critical anatomical features of the autonomic nervous system, such as the
existence of ganglia, and division into pre- and post-ganglionic neurones.
describe the key anatomical features of the sympathetic and parasympathetic branches
of the autonomic nervous system, including where pre-ganglionic fibres leave the CNS,
the location of ganglia and the relative length of the pre-and post-ganglionic fibres.
1. list the structures innovated by each of the sympathetic and parasympathetic
systems, and in broad terms, the effect of the sympathetic or parasympathetic
activity upon these structures.
2. name the usual chemical transmitters at the synapses between pre- and post-
ganglionic neurones in each of the sympathetic and parasympathetic branches, and
the type of receptors upon the post-ganglionic cell body.
1. name the usual chemical transmitter released from post-ganglionic neurones of the
parasympathetic system, and state the class of receptor upon which it normally acts.
2. name the usual chemical transmitters released from post-ganglionic neurones of the
sympathetic system and the types of receptor upon which it normally acts.
state in broad terms the distribution of different types of adrenoreceptor around the
body. state the action of the sympathetic nervous system on blood vessels in different
organs.
state the action of the sympathetic and parasympathetic system upon heart rate and
force of ventricular contraction.

Lecture Synopsis

The autonomic nervous system is an efferent system. Nervous activity flows out from the
central nervous system to the tissues. It is mostly involved in the control of involuntary
processes. The defining characteristic of the autonomic nervous system is that one nerve
cell in the pathway is located entirely outside of the central nervous system. The cell bodies
of these neurones are located in structures known as ganglia (sing. ganglion).
Pre-ganglionic fibres leave the CNS, and then synapse with post-ganglionic cell bodies in the
ganglia. The fibres of these cells run to the innervated structures and form neuro effector
junctions with effector cells. Transmission at both ganglionic synapses and neuro effector
junctions is by the release of chemical messengers - neurotransmitters.

The autonomic nervous system is divided into two branches, distinguished primarily by the
sites at which the pre-ganglionic fibres leave the central nervous system.

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Pre-ganglionic fibres of the parasympathetic system leave the CNS either in the cranial
nerves (i.e. directly from the brain) or from the sacral region - so called cranio-sacral outflow.
Generally speaking the ganglia of the parasympathetic system are located close to, or
sometimes within the structures controlled by the systems. Pre-ganglionic fibres therefore
tend to be long and post-ganglionic fibres short. There are however some ganglia in the
neck and abdomen, located further away from the target organs.

Pre-ganglionic fibres of the sympathetic branch leave the CNS from the thoracic and lumbar
regions - so called Thoraco-lumbar outflow. Synapses between pre - and post-ganglionic
neurones are mostly located in ganglia close to the spinal cord (the 'sympathetic chain'), so
pre-ganglionic fibres are short and post-ganglionic fibres long. Some ganglia are located in
the neck and abdomen, and these have longer pre-ganglionic fibres.

Most organs in the body are innervated by the sympathetic nervous system, rather fewer by
the parasympathetic. Some organs have both sympathetic and parasympathetic innervation
which generally, but not invariably, have opposing actions.

Construct a list of the actions of the parasympathetic and sympathetic systems:

Action of
Action of Sympathetic Transmitter & Parasympathetic Transmitter &
Organ
System receptor type System receptor type

dilatation (due to constriction (due to

contraction of radial contraction of
Pupil of the eye muscle of iris) sphincter muscle
NA (α1) of iris) ACh (M3)

Thick viscous NA (α1)

secretion (amylase Profuse watery
Salivary glands ACh (M3)
secretion) secretion
NA (β)

no SNS innervation
Airways of the circulating
action of circulating constriction ACh (M3)
lung A(β2)
A
Heart –SA node increase rate NA (β1) decrease rate
ACh (M2)

Heart – atrial increase force NA (β1) decrease force

muscle ACh (M2)

Heart –
ventricular increase force NA (β1) no effect
muscle
Blood vessels in
NA (α1) no effect

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most tissues constriction

Blood vessels in NA (β2) no effect

skeletal muscle dilation NA (α1) dilation ACh (?M3)

Blood vessels in
erectile tissue constriction inhibition
stimulation ACh (M3)
Gut -secretion

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Gut - motility NA (α1+2, β2) increased ACh (M3)

decreased

Gut -sphincters NA (α2, β2) dilatation

constriction Ach (M3)

NA (α1, β1, β3)

Adipose tissue lipolysis no effect

glycogenolysis and
Liver gluconeogenesis NA (α, β2) no effect
stimulate Na+

Kidney reabsorption / increase NA (β2) no effect

renin secretion

Sweat glands secretion ACh (M) no effect

(cholinergic)

Sweat glands circulating A

(palms of hands secretion (adrenergic) (α) no effect
etc)
Male sex organs ejaculation NA(α) erection ACh (?M3)

Chemical transmitters in the ANS

The pre-ganglionic fibres of both sympathetic and parasympathetic branches release the
neuro transmitter acetylcholine. Like all chemical transmitters it acts upon a receptor on the
ganglionic cell body. Receptors are categorised into types by their responses to different
agonists and antagonists. The acetylcholine receptor on the post-ganglionic cell bodies is of
the nicotinic type.

Most but not all post ganglionic parasympathetic fibres also release acetylcholine, which
usually acts on a different type of receptor on the effector cell - the muscarinic sub type.

Most but not all post-ganglionic sympathetic fibres release noradrenaline. Different effector
organs have difference receptor types for noradrenaline. There are two broad types -
receptors, and -receptors, but each is sub-divided according to responses to different drugs.
Much more information about the pharmacology of the autonomic nervous system will be
provided in the 'Membranes and Receptors' module.

-receptors are found in the

Broadly speaking -receptors are found on vascular smooth muscle.
heart, smooth muscle of the airways of the lung, adipose tissue and some blood vessels
particularly in skeletal muscle.
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The sympathetic system also includes the adrenal medulla. Pre-ganglionic fibres run to the
adrenal medulla which is made up of modified post-ganglionic cells, known as chromaffin
cells which secrete adrenaline into the blood stream. Circulating adrenaline will also act upon
receptors in the tissues, producing a more generalised effect.

The ANS and the CVS

The autonomic nervous system is intimately involved in the control of the cardiovascular
system via its action upon both blood vessels and the heart.

Blood Vessels
The smooth muscle in the walls of arteries, arterioles and veins is innervated by the
sympathetic branch of the autonomic nervous system. Except in specialised vessels,

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sympathetic activity causes constriction of arterioles - vasoconstriction. There is constant
activity in the sympathetic nervous system the sympathetic vasomotor tone tending to make
arteriolar smooth muscle contract. The tone varies from organ to organ, as does the
magnitude of its effect. In skin, for example, vasomotor tone is high, so arterioles, pre-
capillary sphincters and arterio-venous anastomosis are generally shut down. Variation in
sympathetic outflow produce large changes in skin blood flow, usually for purposes of
thermoregulation.

In skeletal muscles vasomotor tone is high at rest, but in exercise is antagonised both by
local release of vasodilator metabolites and by specialised vasodilator nervous activity.

In the gut vasomotor activity is high until a meal is consumed, when it is antagonised by
various vasodilator substances produced in gut tissue.

The circulation to the brain on the other hand is virtually unaffected by sympathetic activity.

The interplay between sympathetic vasoconstrictor tone and the action of vasodilator
substances is therefore the principal means by which the distribution of flow around the
cardiovascular system is controlled.

Sympathetic outflow to blood vessels is controlled from the hindbrain - via the 'vasomotor'
centres in the medulla oblongata.

Sympathetic activity also produces veno-constriction which is contraction of smooth muscle in

the walls of veins. This tends to increase venous pressure and force more blood back
towards the heart.

The parasympathetic branch of the ANS acts only on specialised blood vessels, though its
stimulating action on organs such as the gut is associated with the release of mediators which
may produce dramatic vasodilatation.

The heart

Heart rate is affected by both the parasympathetic and sympathetic branches of the ANS.
Parasympathetic activity tends to slow the heart rate. In the absence of any autonomic
activity the heart rate is about 100 bpm, so the normal resting heart rate of about 60 is

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produced by a constant parasympathetic 'tone'. Initially increases in heart rate are brought
about by reducing parasympathetic activity.

Sympathetic activity increases heart rate. Rises in heart rate beyond 100 bpm are brought
about by sympathetic stimulation. Both parasympathetic and sympathetic outflow to the heart
is controlled by centres in the medulla oblongata which themselves receive information from
sensory receptors detecting blood pressure ('baroreceptors') and higher centres in the CNS.

The force of contraction of heart muscle ('contractility' - see next session) is increased by
sympathetic activity.

The action of the parasympathetic system on heart rate is mediated via acetylcholine acting
on muscarinic receptors.

The action of the sympathetic system on heart rate and contractility is mediated via
Noradrenaline acting on β1 receptors. Adrenaline from the adrenal medulla also acts on the
heart. The autonomic nervous system therefore provides the central nervous centres
responsible for controlling the CVS with the means to affect the Total Peripheral Resistance
and distribution of blood flow, and the cardiac output.

Group Work: The autonomic nervous system

Address the following questions in your groups.

Q4-1 If you gave an individual an injection of adrenaline what would happen?

There would be an increase in heart rat e, stroke volume and therefore cardiac
output
The arterioles to the skin would vasoconstrict
The airways would dilate

Q4-2 What does an individual with a high circulating titre of adrenaline look like to an outside
observer?

Anxious
Sweaty (adrenergic sweating)
Pale
Dilated pupils

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Q4-3 Some individuals react to bee sting or nettle sting with a massive release of chemical
mediators tending to dilate blood vessels and constrict the airways of the lung. What
substance would you need to inject into some one suffering this 'anaphylaxsis' and why?

Adrenaline
Constriction of resistance arterioles caused by a high concentration of
adrenaline acting on α1 receptors increases blood pressure Relaxes
airways of the lung via action on β2 adrene rgic receptors

Q4-4 List the probable physiological effects of giving an individual a drug which antagonises
the action of noradrenaline at -adrenoreceptors.

Arteriolar vasodilation, reduces blood pressure and may cause postural

hypotension
Initial increase in heart rate mediated by baroreceptor reflex
Relaxes GI and urinary sphincters
Increases gut activity
Q4-5 List the probable physiological effects of giving an individual a drug which antagonises
the action of adrenaline and noradrenaline at -adrenoreceptors.

Decreased heart rate

Decreased cardiac contractility
Decreased systolic blood pressure

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Cardiovascular Module Workbook

Q4-6 Why does your mouth go dry when you are frightened?

Increased viscous secretions mediated by sympathetic nervous system

(as opposed to serous secretions enhanced by the parasympathetic system)

Q4-7 If sympathetic activity generally reduces gut motility why do many people get 'the runs'
if they are nervous?

Due to changes in the nature of gut secretion, mucous rather than serous,
causing an osmotic diarrhoea

Q4-8 Acetylcholine is removed from synapses by an enzyme - acetylcholinesterase. If this

enzyme is antagonised or inactivated, then excess acetylcholine will accumulate, particularly
at parasympathetic post-ganglionic neuro effector junctions. List the physiological effects of a
poison which inactivates acetylcholinesterase (such as a nerve gas or insecticide).

Effects on autonomic transmission: increased salivary, lacrimal, bronchial and

G.I. secretions, bronchoconstriction, reduced heart rate and blood p ressure,
constricted pupils
Effects on neuromuscular junction: initially muscular twitching then paralysis
due to NMJ blockade
Effects on the brain: initially excitation causing convulsions, later depression of
cerebral function, unconsciousness and resp iratory failure

Q4-9 What will an individual poisoned in this way look like?

Sweating. Serous secretions from nose and mouth, tears, muscular twitching, then
paralysis

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Q4-10 Which of the physiological changes above are most life threatening?

Respiratory muscle paralysis.

Q4-11 In principle, what sort of drug would you use to limit the autonomic effects of poisoning
with an acetylcholinesterase inhibitor?

Muscarinic receptor antagonists, e.g. atropine

Cardiovascular Module Workbook

Q4-12 Summary Self-Test

In session 6 we will examine how the cardiovascular system is controlled as a whole. A very
important part of those mechanisms is the action of the autonomic nervous system. Make
sure that you can complete the following simple statements from memory before session 6
begins.

1. An increase in sympathetic flow to the heart will .. increase... heart rate

2. An increase in parasympathetic flow to the heart will .. decrease. heart rate

3. Parasympathetic control of the heart is via the . vagus.. nerve

4. Sympathetic control of the heart is via the .. cardiac ... nerves

5. Increased sympathetic activity will ... increase.. the force of the heart beat

6. Sympathetic nerves release .. noradrenaline.. which acts on . β1 adreno-.. receptors to

. increase. heart rate and .. increase. force of contraction

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7. Parasympathetic nerves release .. acetylcholine. which acts on . muscarinic receptors

to . .slow. heart rate

8. The smooth muscle in the walls of most resistance vessels is innervated by the .
sympathetic..branch of the autonomic nervous system

9. sympathetic. nerves to blood vessels release . .noradrenaline. which acts upon α –

adreno-.. receptors to cause vasoconstriction

10. 'Vasoconstrictor tone' is due to the action of . noradrenaline.. on α – adreno- .receptors

11. Vasoconstrictor tone is antagonised by . local..metabolites

12. Total peripheral resistance is . blood pressure / cardiac output..

13. The cardiac output is the product of .. heart rate. and . stroke volume..

14. Sympathetic action on the heart will tend to .. increase. cardiac output

15. At rest the . parasympathetic..nerves to the heart are normally active, the sympathetic
are not

16. A reduction in parasympathetic activity will tend to . .increase. cardiac output

Cardiovascular System

Session 5

Blood Flow

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Aims of this session:

to understand the factors influencing the flow of fluids through tubes to

understand the concepts of flow, resistance and pressure to understand the
special factors affecting the flow of blood through blood vessels to understand
how resistance reveals control blood flow to individual tissue to appreciate the
range of factors affecting resistance vessels

Structure of the session

Lecture 5.1 Plenary session: Factors affecting flow through tubes (LT1 & 2)

Group work: Pressure, flow and resistance

Lecture 5.2 Pressures and flow in the systemic circulation (LT1 & LT2)

Directed Learning: Factors affecting tissue perfusion.

Properties of vascular smooth muscle.

Plenary session learning outcomes

By the end of this session and with appropriate self study you should be able to:

define the terms 'flow' and 'velocity' with respect to the movement of fluids through tubes
and state the relationship between them
describe what is meant by 'laminar' and 'turbulent' flow describe what is meant by
viscosity, and the effect of viscosity upon flow describe the effects of changes in tube
diameter on flow rate define the term 'resistance' to flow and state the factors which
affect flow resistance describe the relationship between pressure, resistance and
flow describe the effects of combining flow resistances in series and in parallel
describe the pattern of flow resistance and pressure over the systematic circulation
describe how the distensibility of blood vessels affects the relationship between flow
and
pressure describe how distensibility of blood vessels produces the property
of capacitance

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Lecture 5.1: Factors affecting flow through tubes

In order to understand how blood flows through blood vessels we must first consider the
physics of how fluids flow through rigid tubes.

First, definitions:

Flow:

Velocity:

If flow rate is constant then velocity varies inversely with the cross-sectional area of the tube.
This applies whether flow is through a single tube or a set of parallel tubes.

Example:

The flow through the systematic circulation is the same at each level - the arteries, arterioles,
capillaries and veins. Why is the velocity 500 mm.s-1 in the aorta, but only 0.1 mm.s-1 in the
capillaries, when 5 l.min-1 flows through both?

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Flow along tubes is driven by a difference of pressure between one end of the tube and the
other ('pressure gradient'). If all else remains the same what will happen to flow if the
pressure gradient increases?

There are two ways in which fluid flows through tubes - Laminar and Turbulent.

Laminar Flow Turbulent Flow

Draw diagrams of the two types of flow.

Mostly, flow in the circulation is laminar. Turbulent flow generates sound. In laminar flow
adjacent layers of fluid are moving along the tube at different velocities, and so must slide
over one another. The extent to which they can do this is determined by the viscosity. In
more viscous fluids the layers are harder to separate.

So for a given pressure gradient and a given tube what will happen to the average
velocity of flow if the viscosity of the fluid increases?

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As the velocity at the wall is zero, the wider the tube, the more velocity can increase towards
the middle of the tube as successive layers slide relative to one another. Average velocity, all
other things being equal, therefore increases as the surface area (proportional to radius 2) of
the tube.

If the average velocity (for a given pressure gradient) increases as the square of the radius,
and flow is velocity times surface area, which also increases as the square of the radius, then
for a given pressure gradient and viscosity, the flow increases by (surface area x surface
area), i.e. by radius4.

The effects of viscosity, tube radius and length of time is described by Poiseulle's law for
laminar flow.

Pressure gradient = Flow x 8 x h x l

r4 where h = viscosity l = length
r = radius

or, more simply

Pressure gradient = Flow x Resistance

where resistance = 8 x h x l

r4
For tubes in series, resistances add. Resistances in parallel may effectively be replaced by a
single equivalent resistance, which is always less than either of the single resistances.

In the systemic circulation:

The pressure in the aorta averages 100 mm Hg.

The pressure in the arteries of the arm averages 95 mm Hg

1. What is the resistance of arteries? High, medium or low?

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The pressure change from the beginning to the end of the arterioles is 60 mm Hg.

2. What is the resistance of arterioles? High, medium or low?

The pressure drop across the whole capillary bed is 25 mm Hg.

What is the resistance of all the capillaries together? High, medium or low?

Given that each capillary is very small, and individually will have a very high resistance, why
is their collective resistance relatively low?

Special properties of blood vessels

Blood vessels are not rigid pipes, their walls can stretch - they are 'distensible'. The force
tending to stretch the walls, and so increase the radius is the pressure difference between the
inside and outside of the tube - the transmural pressure. As pressure increases so the walls
stretch and resistance falls. Draw the relationship between pressure and flow in this case.

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Blood vessels close completely at supply pressures above zero. As pressure rises, so flow
increases dramatically, because the vessels distend.
If pressure changes suddenly, more blood will flow into than out of the tube as it distends.
Distensible tubes can therefore, in effect, 'store' blood - they have capacitance.

The walls of many blood vessels also contain smooth muscle. If this changes its state of
contraction, then the diameter of the vessel and will change as the relationship between
pressure and flow is altered.

Draw the change in the relationship between pressure and flow if the muscle contracts more.

What effect will such vasoconstriction have on resistance?

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What will happen to resistance if the muscle contracts less - vasodilatation?

Group work

This group work is intended to ensure that you have achieved the objectives specified for the
plenary session.

Flow and velocity

The heart is adapted to maintain a pressure gradient between the ventricles and the
atria which drives a flow of blood around the circulation. The volume of the flow, usually
measured in ml/sec or 1/min, must be sufficient to meet the metabolic needs of the body e.g. at
rest = 5 litre/min. to meet a body oxygen need of 250 ml/min (each litre of blood supplies
about 50 ml O2).

For a given pressure gradient the volume of the flow (Q) depends inversely upon resistive
forces in the circulation (R), namely the viscosity of the blood, the shear forces of the vessel walls
(vessel length) and vessel diameter.

In simple form Q = P/R

As flow through any component of the circulation (heart / arteries / capillaries / veins)
must equal the flow through any other (unless distension is to occur) and as the cross sectional

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area of the various vascular segments vary then, to keep flow rate constant, the velocity of flow
must vary inversely with cross sectional area.

So that Q = Velocity x Area and Velocity = Q/Area

As velocity increases – potential energy (pressure) is being converted into kinetic

energy (flow) so there will be a pressure drop (Bernoulli effect) as cross sectional area reduces.

Q5-1 If a tube has a cross-sectional area of 1 cm2, and the flow is 5 cm3.s-1, what is the
average velocity?

V = Q/A 5cm3sec- 1 / 1cm2 = 5cm/sec

Q5-2 If the flow remains constant, but the area of the tube increases to 10 cm2, what is the
new velocity?

V = Q/A 5cm3sec- 1 / 10cm2 = 0.5cm/sec

Q5-3 If a tube has a cross-sectional area of 1 cm2, and fluid is passing through it at an
average velocity of 5 cm.s-1, what is the flow?

Q=VxA 5cm sec- 1 x 1cm2 = 5cm3 sec- 1

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Q5-4 MCQ

Concerning flow through tubes T F

1. Flow is defined as the volume passing along the tube per T

unit time

2. Velocity is the rate at which a given particle in a fluid moves

T
along the tube

3. For a given size of tube velocity increases as flow increases T

4. For a given flow, velocity increases as the diameter of the tube F

increases

5. At a given velocity, flow is greater in a tube of greater T diameter

Viscosity
The effect of viscosity upon flow is complex and depends upon velocity of flow and the
dimensions of the tube. So that viscosity is low in vessels of small diameter, e.g. capillaries, but
high in the aorta (shear stresses low). At high velocity viscosity is lowered as RBCs form
rouleaux.

BUT IN GENERAL AN INCREASE IN VISCOSITY INCREASES RESISTANCE TO FLOW,

THEREFORE REDUCING FLOW FOR A GIVEN PRESSURE

Q5-5 Is blood more or less viscous than water?

Blood is about 3-5 times more viscous than water

Q5-6 Under what circumstances will blood become more viscous?

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Increase in cells, e.g. polycythaemia, an increase in red blood cells

Increase in plasma proteins, e.g. fibrinogen
Immunoglobulins e.g. myeloma

Q5-7 What will happen to the resistance of blood vessels to flow if blood becomes more
viscous?

It will increase

Q5-8 Blood contains cells and plasma, what effect will this have on the way it flows through
tubes?

The flow is laminar. The cells accumulate in the faster stream of blood flow in the
centre of the vessels whereas the plasma is mainly close to the vessel walls
flowing at a slower rate

Q5-9 MCQ
When a fluid flows along a tube in a laminar flow pattern T F

1. The velocity is greatest in the centre T

2. The average velocity for a given driving pressure is proportional to T the

cross-sectional area (and therefore to the square of the radius)

F
3. For a given driving pressure the velocity in the centre of the

tube is greater for a very viscous fluid than a less viscous T

4. The average velocity is inversely proportional to the viscosity of the T

fluid flowing

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5. The flow rate at a given pressure gradient is directly proportional to the fourth power
of the radius of the tube (true because this question takes in the r2 of question B and the
cross-sectional area of the tube r2l giving r4)

Flow resistance

Q5-10 If blood is supplied to the tissues of an organ via low resistance arteries feeding high
resistance arterioles which vessels will determine how much blood flows if it is supplied at a
constant pressure?

Arterioles

Q= /R

Q5-11 How will the situation change if the artery is partly occluded?

There would be reduced pressure beyond the occlusion so flow in the arterioles
would be reduced

Q5-12 MCQ Resistance = pressure gradient / flow

When fluid flows through tubes T F

1. The resistance of the tube is the ratio of pressure gradient to T

flow

2. If the resistance of a tube increases, but the supply pressure F

remains the same, flow will increase

3. If the flow through a tube is constant, and resistance

increases, the pressure gradient from one end of the tube to

the other will increase

4. If two tubes of equal resistance are connected together in series, the F

resistance of the combination is half that of each tube alone
twice

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5. If two tubes of equal resistance are connected together in parallel the F

resistance of the combination is twice that of
each tube alone half

Pressure in arteries

Q5-13 Where, in principle, do you think would be the best place to measure arterial
pressure? Why?

Aorta

Q5-14 How would your estimate of arterial pressure differ if you measured it in the arteries of
the lower leg of a person sitting or standing up?

Addition of hydrostatic pressure on standing

Q5-15 MCQ Pressure = flow x resistance

Over the circulation as a whole T F

1. There is a large pressure change over the length of the F

arteries

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2. The combined cross-sectional area of the capillaries is more than 45 T

times that of the large arteries

F

3. The velocity of blood flow is highest in the capillaries T

4. The low pressure gradient between the large veins and the right heart is associated
with a low velocity of blood flow in the veins

5. Pressure changes most over the arterioles T

Turbulent flow

Q5-16 Under what conditions will flow through a vessel become turbulent?

If the viscosity is low, the velocity high or if there is a change in diameter of the
vessel, e.g. an aneurysm causing widening or a stenosis causing narrowing

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Cardiovascular Module Workbook

Q5-17 What will you hear if you place a stethoscope over an artery when the flow through
that artery is laminar?

Nothing

Q5-18 What will you hear if you place a stethoscope over an artery when the flow through that
artery is turbulent?

A murmur or “bruit” (pronounced BROO'e - an unexpected audible swishing

sound or murmur heard over a vessel)

Q5-19 MCQ

In the blood vessels T F

1. Blood flow is laminar in most vessels

2. Blood flow becomes turbulent when the velocity exceeds a

critical value

3. The resistance to flow when it is turbulent is higher than when it is

laminar

4. Turbulent flow occurs only in very small blood vessels

5. Turbulence assists the closing of heart valves

Distensible vessels

Q5-20 Which vessels in the circulation are most distensible?

Veins

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Q5-21 What is it about their structure that makes them distensible?

Thin wall with relatively small amount of vascular smooth muscle cells compared
with the high resistance arterioles

Q5-22 Which vessels in the circulation are least distensible?

Arterioles

Q5-23 MCQ's Pressure = flow x resistance

Concerning the flow through distensible vessels T F

1. If the driving pressure increases, the flow resistance of a distensible

tube decreases T

2. If the driving pressure decreases, the flow resistance of the collapsible T

tube reaches infinity (i.e. flow stops) whilst the supply pressure is still above zero

3. If the driving pressure increases abruptly, the volume of blood F

contained in a distensible tube will fall

T
4. If the driving pressure suddenly increases, the flow through the tube in
the next few seconds will be greater in a more distensible tube

5. If the pressure in the fluid surrounding a distensible tube T

increases, the flow resistance through the tube will increase

Q5-24 Concerning the flow through distensible vessels

1. Contraction of the smooth muscle in the walls of a vessel T will reduce

the diameter of the lumen

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2. A reduction in lumen diameter produced by contraction of T smooth muscle

in the walls of a vessel may be reversed if the driving pressure increases

3. The curve relating flow to driving pressure in a distensible T tube is

shifted to the right (i.e. less flow at any given driving pressure) if the smooth
muscle in its walls contracts more

4. Contraction of smooth muscle in the wall of a distensible T tube will

lead to critical closure at an elevated driving pressure

5. Contraction of smooth muscle in the wall of a highly T

distensible vessel such as a vein will reduce its capacitance

Lecture 5.2: Pressures and flow in the systemic circulation

By the end of this lecture and with appropriate self study you should be able to:

define the terms 'Systolic' and 'Diastolic' arterial pressure and 'Pulse Pressure'
define the term 'Total Peripheral Resistance' describe how the elastic nature of
arteries acts to reduce arterial pressure fluctuation
between systole and diastole
draw the typical arterial pressure wave form describe the pulse wave describe
the role of arterioles as resistance vessels define the terms vasoconstriction and

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vasodilatation describe what is meant by 'vasomotor tone' and list the main factors
which affect it describe how 'vasodilator metabolites' modify vasomotor activity to permit
local control of
blood flow
describe reactive hyperaemia
describe autoregulation
define the terms 'central venous pressure' and 'venous return'

Lecture synopsis

The pumping action of the left heart drives blood around the systemic circulation.

The arteries serve as a high pressure distribution system. The pressure drop along the
arteries is low, as they have low resistance, but the blood leaves the arteries via the arterioles
which have a high resistance. A high pressure is therefore developed in the arteries to drive
the cardiac output out through the Total Peripheral Resistance - the collective resistance of
the arterioles.

The ventricle ejects blood intermittently. If the arteries were rigid, flow out through the
arterioles would occur only in systole, so pressure would have to rise very high, then fall to
zero in diastole. This does not happen because the walls of arteries stretch in systole,
allowing more blood to flow into the arteries than out, and limiting the pressure rise. The
'stored' blood then flows out through the arterioles during diastole as the pressure is
maintained by 'recoil' of the stretched arterial wall.

The peak pressure achieved in systole is the Systolic Pressure.

The minimum pressure reached in diastole is the Diastolic Pressure.

The difference between the two is the Pulse Pressure.

What are typical values for:

1. Systolic Pressure

2. Diastolic Pressure

3. Pulse Pressure

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Draw a typical pressure wave form in the arteries over two cardiac cycles:

What factors affect how far pressure rises in systole?

What factors affect how far pressure falls in diastole?

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The contraction of the ventricle also generates a 'pulse wave' which propagates along the
arteries faster than blood. This is felt at a variety of locations where arteries comes close to
the surface and can be pushed against a reasonably hard surface.

Resistance vessels

Arterioles control blood flow to tissues by variable flow restriction. Their walls contain much
smooth muscle whose state of contraction determines lumen diameter and therefore flow
resistance.

Decreases in flow are produced by reducing arterial diameter - VASOCONSTRICTION.

Increases in flow are produced by allowing arterial diameter to increase - VASODILATATION.

Muscles do not actively relax, so that it follows that, except under maximum flow conditions,
there must always be some vasoconstriction. Vasodilatation is therefore reduced vaso-
constriction. This continuous contraction of the muscle is known as vasomotor tone. Tone is
due to a number of factors. One of the main influences is the sympathetic branch of the
autonomic nervous system.

'Sympathetic vasoconstrictor tone' is modulated by substances produced in the tissues

supplied by individual arterioles. This can be seen if blood flow to an organ is temporarily
prevented. Local arterioles dilate maximally after a minute or two, so when perfusion is
restored blood flood is very high. This 'Reactive Hyperaemia' is due to metabolites
accumulating during the period when metabolism continues but no blood is flowing to remove
them. These metabolites are called 'vasodilator metabolites'.

What substances can act as vasodilator metabolites?

If the metabolites of a tissue change with no initial change in blood flow, then more
metabolites are produced, which are not carried away by the blood. These accumulate, dilate
the arterioles and, provided supply pressure remains constant, lead to increased blood flow.

Therefore:

At most levels of metabolic activity most organs can automatically take the blood flow
they need so long as the pressure in the arteries supplying them is kept within a certain
range.

1. What will happen if the metabolic activity of a tissue remains constant, but the
arterial pressure changes?

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2. Define the term 'autoregulation'.

Veins

The veins are low resistance, high capacitance vessels. The pressure in veins is much
affected by the volume of blood they contain. They contain most of the blood in the
circulation. Central venous pressure is the pressure in the great veins supplying the heart.
Gravity has a considerable effect on venous pressure.

Practical exercise in your own time.

Find a tape measure. Lie down for about ten minutes, then get a friend to measure the
circumference of each of your ankles. Stand as still as possible for 15 minutes, preferably in
a warm room, then, without moving, get a friend to measure the circumference of your ankles
again. Why are they different?

Now try wriggling your toes vigorously. Does this have any effect on the circumference of
your ankles? If so, why? (think about the structure of veins)

Cardiovascular System

Session 6

Control of the Cardiovascular System

The aim of this session is that you should understand how the various elements of the
cardiovascular system interact in the short term to maintain stable blood flow to vital organs in
the face of challenges such as exercise or alterations of blood volume. Specifically, you
should understand how the pumping activity of the heart is affected by changes in venous
return and total peripheral resistance.

Structure of the session

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Lecture 6.1 Control of the cardiac output (LT1 & LT2)

Group work: Problems on the behaviour of the cardiovascular

system under different circumstances

Lecture 6.2 Responses of the whole system (LT1 & LT2)

Afternoon work: Completion of workbook problems from morning session

Lecture 6.1: Control of cardiac output

Learning outcomes
By the end of this lecture and with appropriate self study you should be able
to:

1. describe the effects of changes in total peripheral resistance, at a given cardiac

output, on arterial and venous pressures
2. describe the effects of changes in cardiac output, at a given total peripheral
resistance, on arterial and venous pressures
3. explain how the cardiovascular system will be stable if the cardiac output is increased
by
rises in venous pressure and falls in arterial pressure, and vice versa
define the terms stroke volume, end diastolic volume and end systolic volume
describe the factors which determine how much the ventricles fill during diastole, and
draw
a graph of the relationship between end-diastolic volume in the left ventricle and venous
pressure
define the terms 'pre-load' and 'after-load' on the ventricular myocardium
describe how changes in end-diastolic volume affect the force of contraction of
the myocardium during the following systole.
1. draw a graph of the relationship between venous pressure and stroke volume at a
constant after-load (The 'Starling Curve')
2. define the term 'contractility' and describe, in principle, how the Starling curve is
changed
by factors which increase the contractility of the ventricular myocardium
3. state in words the effect of increases and decreases in venous return (and therefore
venous pressure) on cardiac output

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4. describe how changes in after load affect stroke volume and peak systolic pressure
at a
given pre-load
describe the way in which arterial receptors detect changes in arterial pressure
describe the effects of a fall in arterial pressure, detected by arterial baroreceptors,
upon
(i) heart rate (ii) ventricular contractility, and the autonomic mechanism which mediate
them
describe the effects of rises in venous pressure on heart rate describe in
very general terms the role of the medulla of the brain in cardiovascular
reflexes

Lecture Synopsis

The pumping action of the heart removes blood from the veins, and so tends to lower venous
pressure. The blood is pumped into the arteries, tending to elevate arterial pressure. All
other things being equal, the more the heart pumps the lower venous pressure will be, and
the higher arterial pressure will be.

Blood leaves the arteries via the resistance vessels and returns to the veins. If the Total
Peripheral Resistance falls, all other things being equal, then arterial pressure will fall and
venous pressure will rise.

Changes in cardiac output and Total Peripheral Resistance are therefore reciprocal in
effect upon both arterial and venous pressure.

Within individual tissues, the actions of vasodilator metabolites and other mechanisms will
modify flow resistance through arterioles to suit metabolic demand (see sessions 4 and 5).
Across the whole body the effect of those mechanisms is to make Total Peripheral Resistance
inversely proportioned to the body's need for blood flow.

If the system is to be demand-led and stable, then when TPR changes and tends to alter
arterial and venous pressure, the heart must change its pumping action to correct those
disturbances.

This will be achieved if the heart responds to rises in venous pressure and falls in arterial
pressure by increasing its output. In this lecture we will consider the mechanisms which
ensure that this occurs in the healthy individual.

Factors affecting Cardiac Output

The cardiac output is the product of stroke volume and heart rate. Stroke Volume is the
difference between end diastolic volume and end systolic volume.

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End diastolic volume is determined by the filling of the heart. During diastole the ventricles fill
as the venous pressure drives blood into them. As they fill so the passive stretch of the
ventricular wall causes intra ventricular pressure to rise, until it matches venous pressure,
when no more filling will occur. Within limits, the higher the venous pressure, the more the
ventricle will fill in diastole.

Draw the relationship between ventricular volume and intra ventricular pressure in diastole:

End systolic volume increases if venous pressure increases.

End systolic volume is determined by how much the ventricle contracts during systole. All
myocardial cells normally contract, so active tension is changed by factors which act directly
upon individual myocardial cells. These factors may be mechanical or chemical.

Mechanical factors

Because of the operation of the valves in the heart the mechanical forces acting on the
myocardium are different in diastole and systole. In diastole the ventricle is connected to the
veins, so venous pressure determines the end diastolic stretch or 'pre-load' on the
myocardium. Once systole begins the ventricles are isolated from the veins but connected to
the arteries, and the force necessary to expel blood into the arteries or the 'after-load'
determines what happens during systole. Pre-load and after-load may vary independently.

Like all muscles, if the myocardium is stretched before a contraction (i.e. the 'pre-load' is
increased) then, within limits, it will contract harder during the following systole. Therefore if
all other things are equal, increases in venous pressure (and therefore in end diastolic
volume) will lead to increases in stroke volume. This is 'Starlings law' of the heart and can be
summarised simply - More in: More out.

Draw the relationship between venous pressure and stroke volume:

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After-load determines the effect of a given force of contraction during systole. If it is easy to
eject blood (i.e. blood can leave the arteries easily via the total peripheral resistance), then
the volume in the ventricle will fall a lot in systole, but pressure will rise only a little.
Therefore, falls in TPR increase stroke volume by reducing after-load. If it is difficult to eject
blood, because blood will not readily leave the arteries (TPR high), then the stroke volume
will be less, but a much higher pressure will be generated.

For purely mechanical reasons therefore:

1. rises in venous pressure lead to increased stroke volume

2. falls in total peripheral resistance lead to increased stroke volume.

Chemical factors

The force of contraction of the ventricle always varies with pre-load, but the slope of this
relationship - the contractility can be affected by neuro-transmitters, hormones, or drugs
acting on the myocardium.
Noradrenaline and adrenaline increase contractility - a 'positive inotropic' effect. So increases
in sympathetic activity will increase stroke volume at a given pre-load and after-load (see
session 5).

Draw the effect of noradrenaline on the Starling curve:

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Many drugs are used to modify cardiac contractility. You will consider these in a later
session.

Factors affecting heart rate

The frequency of firing of the pacemaker cells in the sino-atrial node is affected by
neurotransmitters from both the sympathetic and parasympathetic branch of the autonomic
nervous system. Sympathetic activity increases heart rate, parasympathetic decreases it. At
rest parasympathetic activity predominates, so increases in heart rate up to about 100 bpm
are produced by turning off the parasympathetic control, rises about 100 bpm (up to a max.
around 200 bpm in the young) are produced by sympathetic stimulation.

The autonomic nervous system can therefore influence cardiac output by changing heart rate
(parasympathetic and sympathetic branch) and contractility (sympathetic branch).

The main factor influencing autonomic control of the heart is the activity of baroreceptors
which monitor arterial blood pressure. Stretch receptors in the walls of the aorta and the
carotid sinus at the bifurcation of the common carotid artery detect changes in arterial blood
pressure. This information is released to the medulla in the brain, where collections of
neurones - the 'cardiovascular centres' modify the behaviour of the heart and circulation via
the autonomic nervous system. Falls in arterial pressure lead to rises in heart rate and
contractility.

• baroreceptors ensure that if arterial pressure falls both heart rate and stroke volume tend to
rise

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There is also a minor effect of venous pressure (detected by stretch receptors in the atria and
great veins) on heart rate - if venous pressure rises, then heart rate rises (the 'Bainbridge
reflex').

Overall

Rises in venous pressure increase stroke volume

increase heart rate

and therefore increase cardiac output

Falls in arterial pressure increase stroke volume

increase heart rate

increase cardiac output

and therefore

If TPR falls, then arterial pressure will fall and venous pressure will rise. By all the
mechanisms described above, the heart will respond by pumping more, which will increase
arterial pressure and reduce venous pressure, so restoring the status quo - a stable system!

Group work and afternoon work

Consider the following questions and write your answers in the spaces provided. There are
also some multiple-choice questions for you to attempt. There are a large number of
questions which will take you some time to answer, but if you work through them you will gain
a good understanding of the operation of the CVS. You should therefore attempt as many as
you feel able, starting in the morning session, but continuing during the afternoons, and
possibly the Easter vacation.

Arterial and venous pressures

Q6-1 What will happen to (i) arterial pressure (ii) venous pressure if the heart stops?

Arterial pressure will fall

Venous pressure will rise

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Q6-2 Look in your text books to find out what is meant by the term 'mean filling pressure' of
the circulation

Pressure in the arteries and veins when the heart stops

Q6-3 What happens to mean filling pressure if the volume of blood in the circulation
increases?

It increases

Q6-4 MCQ

T F
1. A rise in cardiac output with no other changes in TPR will elevate
arterial pressure
2. A rise in TPR with no change in cardiac output will lead to a fall in
venous pressure
3. A rise in cardiac output with no change in TPR will lead to a fall in
venous pressure
4. A fall in TPR with no change in cardiac output will lead to a fall in

venous pressure

Starlings Law of the Heart

Q6-5 MCQ

T F
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arterial pressure
5. A fall in cardiac output at a constant TPR will lead to a rise in
1. The force of contraction of heart muscle depends upon the length of
the fibres at the end of diastole
2. If end diastolic volume is increased, the force of contraction will
increase
3. If total peripheral resistance falls, initially with no change elsewhere
in the circulation, then the force of contraction of the ventricles will
subsequently increase
4. If venous pressure falls initially with no other change in the
circulation, then stroke volume will fall
5. Starling's law of the heart relates stroke volume to arterial pressure

Q6-6 The Frank-Starling Law of the Heart

Q6-6a Draw the typical relationship between venous pressure (abscissa or x-axis) and stroke
volume (ordinate or y-axis) for a heart performing normally. Why, at the top end of this
'Starling Curve', does stroke volume fall with increasing venous pressure?

The muscle fibres reach a critical length beyond which they ar e unable to
contract efficiently. This may be due largely to the passive stiffness of cardiac
muscle fibres. You should compare this with the length – tension curve for
skeletal muscle and revise what you know about the contraction mechanism of
sarcomeres.
Note: The length – tension curve for cardiac muscle is much steeper than that
for skeletal muscle over normal sarcomere lengths. It falls off more steeply too.
The steeper rising phase reflects an increase in Ca2+ sensitivity with increased
sarcomere length. The steeper falling phase is due to the passive stiffness of
cardiac muscle fibres.

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Medical

Q6,6b DATA HANDLING EXERCISE

The data below are measurements from a patient undergoing volume resuscitation in the
intensive care unit. This data formed part of a study to provide an algorithm for managing
hemodynamics (McGee W.T. Journal of Intensive Care Medicine 2009; 24:352-360).

1. Plot the data to show how stroke volume (SV) varies as end diastolic volume
(EDV) increases. This is a Frank-Starling curve. Tips: You should put EDV on
the abscissa of your graph. There is no need to start the axes at zero.
You could start the EDV axis at 140ml and the SV axis at 50ml.
2. If the patient‟s BP is still low once the EDV has reached 250ml will there be any
benefit in giving further volume replacement to increase EDV more? Explain your
answer.

End diastolic volume (ml) stroke volume (ml)

160 60

170 65
180 70
190 75
200 85
215 92

225 98
240 100
250 100

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Q6-6c The Frank Starling curve is sometimes plotted as stroke volume versus venous pressure
or stroke volume versus end diastolic volume. What is the relationship between central
venous pressure(CVP) and EDV?

As the filling pressure (CVP) increases then the EDV increases.

Q6-6d
1. What is the physiological range for CVP?
2. What factors can increase or decrease CVP?
Physiological range 1-10mmHg
Factors increasing CVP: venoconstriction, transfusion
Factors reducing CVP: orthostasis, factors lowering blood volume eg
haemorrhage or dehydration
CVP depends on the total blood in the circulation and the distribution of the
blood.

Q6-7 How will the left ventricle respond if more blood is driven into it from the pulmonary
circulation? When might this occur?

The consequent increase in diastolic fibre length will result in a larger stroke
volume by the left ventricle and therefore increased out put

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Q6-8 What mechanism, therefore ensures that the right and left side of the heart pump the
same amount of blood per minute?

The Frank-Starling mechanism matches venous return to cardiac output

Increased cardiac output in one ventricle automatical ly increases the venous
return to the other ventricle. The consequent increase in myocardial fibre length
in this ventricle results in an increased output which would match the other side

Contractility

Q6-9 MCQ

T F F
1. Contractility is the force of contraction of the ventricle

2. Contractility of the myocardium is increased by adrenaline

3. Contractility of the myocardium is affected by the sympathetic

branch of the autonomic nervous system
4. If contractility increases the ventricle will eject less blood for a given
after load and pre-load
5. Increasing the end diastolic volume of the ventricle will lead to an
increase in contractility

Q6-9 b What will the effect of an increased sympathetic drive to the heart be on the shape of
the Frank-Starling curve?

Increase the steepness of the linear portion

Heart rate

Q6-10 MCQ

T F F
1. Heart rate is increased by substances with a negative
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chronotrophic effect
2. Noradrenaline has a positive chronotrophic effect
T
3. Acetylcholine is released by parasympathetic nerve fibres
T
4. Increased parasympathetic activity will slow the heart rate
T
5. Increased sympathetic activity will increase heart rate
T

Q6-11 What happens to the heart rate of a resting individual if he is given an antagonist of the
action of acetylcholine at muscarinic receptors (e.g. Atropine)?

It will increase (at rest the heart is under vagal influence)

Q6-12 Under what circumstances might a sudden increase in parasympathetic activity to the
heart occur? Why might this be dangerous?

Valsalva manoeuvre e.g. coughing, straining increases parasympathetic activity

and can slow heart rate.
Cold ice on the face or plunging into cold water could cause sudden slowing of
the heart rate and collapse

Carotid sinus massage also increases parasympathetic activity to the heart

Q6-13 What would happen to resting heart rate if an individual were given an antagonist of
noradrenaline acting at receptors? What effect would this drug have in exercise?

There would be not much effect at rest in under normal circumstances but it
would slow heart rate if there was excessive activation of the sympathetic nervous
system.

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A β- receptor antagonist would reduce the increase in heart rate response to

exercise and therefore there would be failure to increase cardiac output
appropriately

Note: At rest the heart is under vagal influence. If all nervous inputs to the heart
are removed, the heart would beat at about 80 -90 beats per minute

The baroreceptors

Q6-14 What would happen to the circulation if the discharge from the carotid sinus were
suddenly increased by the application of external pressure?

The heart rate would slow and stroke volume fall, due to increase in
parasympathetic activity

Q6-15 What happens to the output of the baroreceptors if there is a sustained rise in arterial
pressure - lasting hours or days?

They „reset‟ at a higher level

(Baroreceptors are good at controlling short -term changes in BP, but are not so
effective over longer timescales as they reset. You will learn about longer term control
of BP in your Urinary module)

Q6-16 MCQ

T
F A. Changes in arterial pressure are detected in the carotid sinus T

1. If arterial pressure falls then parasympathetic activity to the T

heart will fall and sympathetic activity increase
2. If arterial pressure rises than parasympathetic activity to the F
heart will fall
3. If right atrial pressure rises then parasympathetic activity to
the heart will fall T
4. If arterial pressure falls, stroke volume of the heart will tend to rise
T

Q6-17 What effect will sympathetic stimulation of vasomotor tissue in vascular beds such as
the skin and gut have (i) on Total Peripheral Resistance (ii) the circulation as a whole?

Total peripheral resistance will rise

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The circulation would be redirected but the mean circulatory pressure would not
alter
(Although there would be an initial rise in maBP, venous pressure would drop and
therefore cardiac output would drop)

Q6-18 What effect will sympathetic stimulation of smooth muscle in the walls of veins ('veno
constriction‟) have?

Increases venous return and cardiac output and will cause a rise in mean
circulatory pressure (as the fraction of the blood volume in the veins is very large)

Lecture 6.2: Responses of the whole system

Lecture synopsis and self study questions

We can now state a set of qualitative rules which will allow prediction of how the
cardiovascular system will change in the short term under different circumstances.

1. Total Peripheral Resistance is inversely related to the total metabolic need for
blood flow. More metabolic activity leads to lower TPR.

2. If cardiac output is unchanged, changes in Total Peripheral Resistance affect arterial

and venous pressure.

1. Falls in TPR increase venous pressure

2. Falls in TPR reduce arterial pressure

3. Changes in arterial and venous pressure affect the heart.

1. If venous pressure increases cardiac output will rise

2. If arterial pressure falls cardiac output will rise

4. At a constant TPR changes in cardiac output alter arterial and venous

pressure.

1. Increases in cardiac output decrease venous pressure

2. Increases in cardiac output increase arterial pressure

5. Arterial pressure changes reflexly affect TPR and venous capacitance.

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1. If arterial pressure falls the resistance to blood flow through certain

vascular beds such as the skin and gut will normally rise.

2. If arterial pressure falls venous capacitance will be reduced by veno-

constriction.

Rules 3 and 4 are the key. They are reciprocal in effect. The consequence of the heart
responding to changes in arterial and venous pressure is to correct those changes. In other words
at any given Total Peripheral Resistance there is only one cardiac output that the
system will sustain - that which matches the tissues' demands for blood flow.

Examples

1. Consider an individual with an artificial pacemaker driving an otherwise

normal heart. Whilst lying at rest his heart rate is suddenly increased
from 70 to 120 bpm with no other changes in the circulation initially.
What will happen?

Primary change: Heart Rate (HR) increased

Consequences: Initially, cardiac output tends to rise, but rises in cardiac output (CO)
lead to falls in venous pressure (rule 4). Falls in venous pressure will tend
to reduce diastolic filling of the ventricles which, by rule 4, will
reduce stroke volume.

So as the heart rate rises, stroke volume will tend to fall, keeping cardiac output the
same.

Cardiac output cannot normally be changed by action at the heart alone.

What will happen in this situation if venous pressure is very high at the outset (on the top part
of the 'Starling curve')?

2. An individual at rest consumes a meal.

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Primary change: Vasodilatation in the gut because of production of vasodilator

mediators and metabolites.

So: TPR falls

By rule 2, arterial pressure falls and venous pressure rises

But: by rule 3, rises in venous pressure lead to increased stroke volume.

Falls in arterial pressure are detected by baroreceptors, leading to
rises in heart rate and stroke volume.

cardiac output rises, tending by rule 4 to bring venous pressure back

Therefore: down to normal and arterial pressure back up to normal.

Total flow through the cardiovascular system rises and falls automatically with changes in
metabolic demand.

3. Exercise.

In principle, as exercise produces a large increase in metabolic demand for blood

flow the mechanism above could operate, but the speed and scale of the changes in venous
pressure in particular tend to overload the system.

As exercise begins there is a massive vasodilatation in muscle which tends to produce a

large fall in arterial pressure. The fall in TPR and 'muscle pumping' tends to produce a
large rise in venous pressure. In the absence of other mechanisms these changes would
be so great that the heart would be driven to the top of the Starling curve by the venous
pressure changes, limiting its capacity to control cardiac output.

This adverse effect is prevented in normal individuals by a rise in heart rate at the onset of
exercise, triggered by activation of the sympathetic system. This rise occurs before large
changes in arterial and venous pressure, so the rush of blood returning to the heart at the
onset of exercise is preceded by a rise in heart rate which prevents venous
pressure rising by pumping the extra blood immediately into the arteries.

This 'pre-emptive strike' on heart rate presents large changes in arterial and venous
pressure at the onset of exercise.

Sympathetic reflexes therefore maintain the system in the optimal state for other regulatory
mechanisms to operate.

4. An individual rises from lying to a standing position.

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Primary change: the effects of gravity increase transmural pressure of the superficial
veins in the lower extremities. Blood tends to 'pool' in the legs,
producing a transient fall in central venous pressure.

Consequences: as central venous pressure has fallen, cardiac output will tend to fall.

So, arterial pressure tends to fall

This fall is detected by baroreceptors, triggering rises in heart rate,

vasoconstriction in skin and gut to increase TPR and veno-
constriction to drive more blood back towards the heart.

Therefore: TPR rises, tending to stabilise arterial pressure and maintain

perfusion of vital organs such as the brain, but at the temporary
expense of reduced blood flow to some systems.

Changes in venomotor tone and flow through non-essential organs can

be used to stabilise the system.

How is this response modified if an individual has recently eaten or is in a hot

environment?

Why then do some people faint when they stand up?

5. Changes in blood volume.

(a) A subject loses 1l of blood after trauma.

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Primary change: Reduction in blood volume

Consequences: Less blood in the venous capacitance - venous pressure falls.

Fall in venous pressure leads to reduced diastolic filling.
Cardiac output falls.
Arterial blood pressure falls.

Fall in arterial blood pressure detected by baroreceptors.

Reactions: Reflex rise in heart rate.
Marked vasoconstriction.

Problem:
Low venous pressure exacerbated both by attempts to increase
cardiac output and the rise in TPR.
Heart rate rises more and more - very rapid feeble pulse.

Solution: The solution to this problem is to reverse the primary change

A reduction in blood volume leading to reduced central venous
pressure.
Venous pressure is increased physiologically by veno-constriction.
Fluid also tends to move from extra cellular space into the circulation -
auto-transfusion.
Water, electrolytes and red cells eventually replaced by homeostatic
mechanisms (see other modules).

1. What will happen in those tissues whose blood flow has been severely reduced by
vaso- constriction?

2. What effect might these changes have upon the tone of arterioles in those tissues?

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3. How might these changes affect the cardiovascular system and why might the effects
be very dangerous?

(b) Sustained increases in blood volume.

Occasionally because of changes in the kidney or diet, blood volume tends to increase. You
will hear more about the mechanisms in the "urinary tract" module next semester.

Primary change: Blood volume rises - producing a sustained increase in venous

pressure.

Consequences: Increased diastolic filling leads to increased cardiac output. Increased

cardiac output leads to increased arterial pressure as, at this stage,
TPR has not changed.

Increased cardiac output forces more blood through the tissues.

Those tissues that 'auto regulate' increase arteriolar tone to return flow
to normal, so TPR increases further, compounding the rise in arterial
blood pressure.

Cardiac output returns more or less to normal, but arterial pressure is

permanently raised - hypertension

The sustained increase in arteriolar tone in many vascular beds leads

to long term changes in resistance vessel walls, which render the TPR
rise more or less permanent, so arterial pressure is now persistently
elevated.

Partial solution: Reversal of the rise in blood volume will, particularly in the early stages
reduce blood pressure back towards normal - this is achieved with
diuretics, which are drugs which alter the body sodium balance by
interaction with the hormonal control of the kidney.

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Cardiovascular Module Workbook

Cardiovascular Module

Session 7

Cellular And Molecular Events In The Heart

The aim of this session is that you should understand the cellular basis of the heart beat, the
cellular mechanisms which determine heart rate and the cellular mechanisms determining the
force of contraction of the myocardium. This will provide the basis for understanding and
action of drugs on the heart.

Structure of the Session

Lecture 7.1 Cellular events in the heart (LT1 & LT2)

Group work: Control of the heart beat

Lecture 7.2 Drugs and the cardiovascular system (LT1 & LT2)

Lecture 7.1: Cellular and molecular events in the heart

Learning outcomes: By the end of this session and with appropriate self study you should be
able to:

describe the processes which generate the resting membrane potential of cardiac cells.
draw the changes in membrane potential of (i) ventricular cells (ii) pacemaker cells over
the cardiac cycle.
describe the membrane permeability changes and ionic currents underlying the
ventricular and pacemaker cell action potential.
describe in general terms, the processes of excitation - contraction coupling in ventricular
myocardial cells.
1. describe the factors influencing the changes in intra cellular free calcium concentration of
ventricular cells during the action potential.
2. describe the membrane potential changes in pacemaker cells associated with increases and
decreases in heart rate.
3. describe the cellular mechanisms controlling heart rate in the normal heart and the role of the
autonomic nervous system in this process.

Lecture synopsis

The behaviour of heart muscle depends critically upon the electrical properties of individual
cardiac muscle cells. Many drugs used to treat cardiovascular problems affect either the
electrical activity itself or the relationship between it and myocardial contraction.

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Pacemaker cells generate an electrical event at regular intervals - the cardiac action potential
which spreads over the myocardium, sometimes via cells specialised for rapid conduction to
produce a co-ordinated contraction in systole. The action potential is a characteristic
disturbance of the potential difference between the inside and outside of the cell, whose form
varies between ventricular cells, pacemaker cells and conducting cells.

The basis of electrical excitability in cardiac muscle cells is similar, but not identical to that in
nerve and striated muscle, which you are dealing with in the "Membranes and Receptors"
module.

The cardiac muscle cell in diastole

When the heart muscle is relaxed the potential difference between the inside and outside of
the cells is negative inside. Except for pacemaker cells (see below) this potential difference
is constant during diastole. The basis for this resting membrane potential is essentially the
same as in other cells. It arises by an interaction between differing concentrations of ions
inside and outside of the cell, and selective permeability of the cell membrane to those ions.

Ions cross membranes via ion channels. Ion channels are generally selective for one ion, and
rate at which ions can pass through is controlled by 'gating'. You will hear in the 'Membranes
and Receptors' module that ion channels oscillate between open and closed states and that
the proportion of time they spend open, which determines how many ions cross the
membrane, is affected by a variety of factors. 'Voltage gated' channels are affected by the
membrane potential, so that changes in membrane potential vary the number of ions which
pass the membrane in a given time. 'Ligand gated' channels are affected by the binding of
substances either directly to them or to their associated molecules.

Action potentials arise by the action of voltage-gated channels, though they may be triggered
by a variety of events.

This whole event is triggered in any one cell by a small starting depolarisation, taking the
membrane potential beyond the 'threshold' for opening the fast Na+ channels. For all cells
except the pacemaker, this small depolarisation comes about by spread of activity from
adjacent cells. That is to say a single action potential will propagate throughout the heart
muscle, aided by conducting fibres.

The Cardiac Action Potential

This action potential is very different to that you heard about in nerve and striated muscle. It
is much longer because of the plateau sustained mainly by calcium channels. The length of
the action potential is crucial. It ensures that once the action potential has begun in any part
of the heart it is long enough for the cell still to be depolarised when the last cell in the
myocardium starts its action potential. One action potential in the pacemaker therefore
generates just one action potential in every cell of the heart.

This action potential produces a single heart beat. You will hear from the 'Membranes and
Receptor' module that muscle cells contain a contractile apparatus made up of Actin and

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Myosin which is triggered to generate force by a rise in the concentration of Ca2+ ions in the
cell. In the heart the force generated in a cell, at a given degree of stretch, is proportional to
Ca2+ concentration. Intracellular Ca2+ concentration rises during the plateau phase, in small
part because of Ca2+ crossing into the cell via Ca2+ channels, and in large part because of
release of Ca2+ from intracellular stores. As Ca2+ concentration rises this triggers various
mechanisms tending to remove Ca2+ from the cytoplasm. These include re-uptake into
intracellular stores and the expulsion of Ca2+ from the cell in exchange for inward movement
of Na+ - 'sodium calcium exchange'.
The force of contraction therefore depends upon the balance between the rate of entry of Ca2+
to the cytoplasm and its rate of removal. Drugs which alter the force of contraction of the
heart affect one or both of these processes.
As the plateau phase is long, so the muscular contraction in systole is sustained for 200-300
ms - a duration which is essential for the normal pumping activity of the heart.

Pacemaker cells

The action potential of pacemaker cells is very different in form to that of ventricular
myocardial cells. It is also initiated by the cells themselves, rather than by conduction of
excitation from surrounding cells. In diastole the membrane potential of pacemaker cells is
not stable. It depolarises steadily. This change is known as the Pacemaker Potential. This is
thought to be due to a population of channels permeable to Na+ ions. These channels are
very different to the fast Na+ channels of the action potential.
Pacemaker cells do not have fast Na+ channels. As the membrane depolarises with the
pacemaker potential, however, voltage gated Ca2+ channels eventually open, producing a
faster rate of depolarisation to a positive membrane potential. The opening of these Ca2+
channels is not sustained. There is no 'plateau' and the action potential is triangular in shape.
As soon as the membrane is repolarised back to -80mV it begins to depolarise again slowly
i.e. the next pacemaker potential begins, until threshold is reached again and the next action
potential occurs.
Conducting fibres

Purkinje fibres conduct excitation through the ventricular myocardium. They have long action
potentials, but within the AV node the bundle of His there are cells capable of pacemaker
activity. Their natural rate however is much slower than the SA node, so they are normally
overridden. If however there is a conduction block they may become important.

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Group work: Electrical activity of the heart and the control of the heart beat.

Consider the following questions in your groups, with the help of your tutor. If you are not
able to complete them during the session, you should do so in your own time. You will
find information from your Membranes and Receptors module helpful.

Equilibrium potentials

Q7-1 The intracellular and extracellular concentrations of Na+ , K+, Ca2+ and Cl- (in mmol.l-1)
for cardiac muscle cells are give in the table below. Note: These values may be a little
different from those given in your Membranes & Receptors module as different types of cells

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have somewhat different intracellular ionic compositions depending on the relative

permeability of their membranes and the types and densities of ion transporters present.

The Equilibrium potentials for Na+ and Cl- ions are given in the table below. Using the Nernst
equation calculate the equilibrium potential for K+ and Ca2+.

ION Extracellular concentration Intracellular Equilibrium

(mmol.l-1) concentration potential (mV)
(mmol.l-1)
Na+ 140 10 70.5

K+ 4 140 -95.0

Ca2+ 1.2 0.0001* 125.4

Cl- 120 30 -37.0

(* value of [Ca2+] at rest)

Nernst Equation

Where R is the universal gas constant, T is temperature in oK, F is Faraday‟s number, z is

the valency of the ion and [Ion] is the concentration of the ion.

This can be simplified by working out the constants at 37oC and converting to log10.

NB: z = +1 for Na+ and K+. Remember to change it if the valency is different from +1

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Resting membrane potential

Consider the hypothetical situation of a cell whose membrane is only permeable to K+ ions.
K+ will tend to leave the cell down its concentration gradient. Since no negatively charged
particles can follow, the movement of K+ will charge up the membrane capacitance negative
inside and a membrane potential will develop. This will tend to oppose further outflow of K+
and eventually a stable equilibrium will be achieved with the membrane at the equilibrium
potential for K+.

Q7-2 What will be the membrane potential of a cell whose membrane was only permeable to
K+ ions?

-95.0 mV

Now, consider other hypothetical situations:

Q7-3 If the cell membrane were only permeable to Na+ ions what would the membrane
potential be?

70.5 mV

Q7-4 If the cell membrane were permeable only to Cl- - what would the membrane potential
be?

-37.0 mV

Q7-5 If the membrane was permeable only to Ca2+ - what would the membrane potential be?

125.4 mV

The actual membrane potential depends on the relative permeability to different ions, in
particular K+ and to a lesser extent Na+.

Q7-6 A membrane allowing only K+ to cross will have a potential of - 95mV, one allowing
only Na+ to cross a potential of +70 mV. What will the potential be (approx.) if it is 20 times
as easy for K+ to cross as Na+ to cross?

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Ignore Cl- ions and use the GHK equation from your Membranes & Receptors lectures (see
below).

Where PK= relative permeability of K+ and PNa = permeability of Na+ Using

concentrations of Na+ and K+ above and making PK = 20 and PNa = 1, you
should get:

Calculated out this will give a value of -67mV

The Cardiac Action Potential

Reminder a change to a less negative or positive potential is known as

depolarisation a change back to a negative potential is re-polarisation
a change to a more negative potential from the normal resting potential is known as hyper
polarisation

Q7-7 Draw the changes in membrane potential which occur with time during a ventricular
action potential and indicate the changes in conductance to Na+, K+ and Ca2+ occurring in
the different phases. Remember to label both time and voltage axes clearly.

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Q7-8 So long as the Ca2+ channels remain open the membrane will remain depolarised. In
the case of ventricular myocardial cells this 'plateau' phase lasts over 200 ms. What will
happen to the concentration of Ca2+ in the cell during this time?

The intracellular Ca2+ concentration will rise.

The Pacemaker Action Potential

Q7-9 Draw the changes in membrane potential which occur with time during a pacemaker
action potential (include a diastolic period). Label the axes and indicate on your diagram what
is happening to the ions channels at different points in the AP.

Q7-10 What ion channels are responsible for the upstroke of the pacemaker action
potential?

Ca2+ channels (nodal cells only have very few fast Na+ channels and these are largely
inactivated at the relatively depolarised potentials of these cells )

Q7-11 What will happen to the interval between action potentials if the membrane
depolarises more rapidly during diastole? How will this affect the heart rate?

The interval between APs will shorten and therefore the heart rate will increase.

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Q7-12 What will happen to the heart rate if the pacemaker potential depolarises less rapidly?

The heart rate will slow down.

Q7-13 You will remember for your lecture on the autonomic nervous system that the slope of
the pacemaker potential is affected by the binding of neurotransmitters to receptors on
the pacemaker cells.

Complete the following:

Noradrenaline acts on β1- adrenoreceptors to increase the slope of the pacemaker potential
and so increase heart rate. Acetylcholine acts on M2 muscarinic cholinergic

receptors to decrease the slope of the pacemaker potential and so slow down heart rate.

Blood Electrolytes and the Heart.

• The concentration of K+ in extracellular fluid varies in many diseases or through the use
of diuretics. The normal value is 3.5 - 5.5 mmol.l-1 . Increases are known as
hyperkalaemia, decreases as hypokalaemia.

You have used the Nernst equation above to calculate equilibrium potentials for various ions.

Q7-14 With intracellular [K+] of 140 mmol.l-1 and extracellular [K+] of 4 mmol.l-1 what did you
calculate EK to be?
-95mV

Q7-15 If extracellular [K+] rises to 10mmol.l-1 what will EK now be?

-70.5mV

The resting membrane potential is dominated by the permeability to K+ ions, although it is

never as negative as EK due to some permeability to Na+ ions.

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Q7-16 What effect will hyperkalaemia have on the membrane potential of ventricular
myocytes in diastole?

Cells are likely to depolarise (become less negative inside electrically) since
permeability to K+ dominates under resting conditions and the K+ concentration gradient
has decreased.

From your Membranes & Receptors Module you learned that fast Na+ channels are opened by
depolarisation but are also inactivated by continued depolarisation.

Q7-17 What effect might prolonged hyperkalaemia have on the steady state availability of
voltage-gated sodium channels?

Voltage gated sodium channels open only briefly under depolarisation and then
shut again. This shutting is to an inactivated state from which the channels
recover only at negative membrane potentials. Fewer Na+ channels are available
if the membrane potential is held depolarised by the increase in extracellular
[K+].
Q7-18 What may be the effect of this on the spread of excitation from cell to cell?

If fewer Na+ channels are available to make action potentials then the action
potentials will spread more slowly from cell to cell. The action potential depolarises
more slowly, and the threshold occurs at a more positive (or less negative)
membrane potential.

Q7-19 What will be the effect of the change of hyperkalaemia on the availability of the ion
channels that generate the pacemaker potentials?

A major class of ion channels that make pacemaker potentials are permeable to
both Na+ and K+. The current carried is called If in electrophysiological jargon
(If stands for funny current; see Berne & Levy Principles of Physiology p192).
Na+ entry through these channels depolarises the SA node cells. These channels
are peculiar in that they are activated at negative voltages, so fewer are
available if the pacemaker potential starts from a less negative value.

Q7-20 What effect will hyperkalaemia have on the pacemaker potential and the heart rate?

If fewer channels are activated to generate the pacemaker potenti al this potential
will be slowed and the heart rate will be reduced .

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Q7-21 What then is the risk to the heart of hyperkalaemia?

The heart may stop in diastole, owing to the lack of voltage gated sodium channels
to initiate the action potential.

Q7-22 What effect will hypokalaemia have upon the membrane potential of ventricular
myocytes in diastole?

The membrane potential is likely to become more negative owing to the increase
in the K+ concentration gradient across the cell membrane.

Note : the situation can be more complicated due to the unusual properties of some
K+ channels in cardiac myocytes, but a full explanation of this is beyond what can
be covered in this module.

Q7-23 What effect will hypokalaemia have on the spread of excitation from cell to cell?

The situation is the reverse of that found in hyperkalaemia. Since more voltage
gated sodium ion channels are available to make the action potential, it is likely to
spread more quickly from cell to cell.

Q7-24 What will the effect of hypokalaemia be on the pacemaker potential?

The increasingly negative membrane potential at the start of diastole results in the
activation of more of the ion channels that make the pac emaker potential. The
pacemaker potential is likely to be accelerated as a result

Q7-25 What then is the risk of hypokalaemia?

Since, paradoxically perhaps, the excitability of the myocardium is increased, ectopic

beats and arrhythmias are a likely re sult of hypokalaemia.

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Self Study Session: Drugs and the cardiovascular system

Force of Contraction of the Myocardium.

2+

Consider the changes in intracellular Ca concentration that occur during the plateau phase of
the cardiac action potential and the Ca2+ release from intracellular stores.

1. How does the binding of Noradrenaline to 1‫ك‬adrenoreceptors increase the force of contraction
of cardiac myocytes?

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2. What will happen to the concentration of Na+ inside the cells if the Na+/K+ pump in the
membrane is partially inhibited by a drug such as digoxin?

3. What effect will this have upon the process of expulsion of Ca2+ by 'sodium calcium
exchange'?

So, what effect would such a drug have upon the force of contraction of the heart? Why?

Autonomic nervous system and the heart.

1. Why do you give adrenaline intravenously to someone whose heart has stopped (i.e. in
'cardiac arrest')?

2. What would be the action of a ‫ ك‬adrenoreceptor antagonist on an individual with an abnormal

increase in heart rate arising above the level of the ventricles (i.e. a supra- ventricular
tachycardia SVT)

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3. What might be the effect of atropine upon an individual with an abnormally low heart rate
('bradycardia')?

4. Why are individuals whose coronary blood flow is compromised treated with ‫ ك‬adrenoreceptor
antagonists? What effect do these drugs have on the force of contraction of the heart, heart
rate and oxygen demand of the myocardium (i) at rest (ii) when the individual is excited or
stressed?

5. What effect would administration of an α1 adrenoreceptor antagonist have on the

cardiovascular system?

Antiarhythmic drugs

You will recall from the 'Membranes and Receptors' module that local anaesthetics block fast
Na+ channels. Generally, to do so the channel must be open or in the inactivated (refractory)
state.

1. What effect would you expect a local anaesthetic such as lignocaine have upon the ventricular
cardiac action potential?

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2. What therefore would you now expect the effect of lignocaine to be at a regular heart rate of
60 bpm?

3. What will be the effect of lignocaine upon a ventricular cell which has very recently (i.e. in the
last 400 milliseconds) fired an action potential, and then receives a further stimulus to depolarise it?

4. Can you now explain why local anaesthetics such as lignocaine have been used to treat
irregular heart rhythms - arrhythmias (or dysrhythmias)?

What mechanisms may be responsible for atrial fibrillation?

What complications might be associated with atrial fibrillation and how would you treat
this?

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1. Explain the mechanism of action of amiodarone and how it can help in the treatment of
arrhythmias.

Lecture 7.2: Action of drugs on the cardiovascular system.

The aim of this lecture is to introduce you to the classes of drugs which are used to treat
common cardiovascular conditions.

Learning outcomes: By the end of this session and with appropriate self study you should be
able to:

1. Describe the types of drugs used to treat patients with common cardiovascular
disorders.

2. Understand how some arrhythmias can arise.

3. Describe the classes of anti-arrhythmic drugs and the principles of their therapeutic
use.

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4. Describe the therapeutic uses of β-adrenoreceptor antagonists.

5. Define the term „inotropic‟ drug and the circumstances under which these drugs can
be used.

2. Describe how drugs can be used in the treatment of heart failure.

1. Understand the risk of thrombus formation with certain cardiovascular conditions and
how to treat this.

Lecture Synopsis
Drugs Acting on the Cardiovascular System

The aim of this lecture is to introduce you to the broad types of drugs used in the treatment of
cardiovascular disorders. It is not a comprehensive guide to pharmacological treatment in
this continually developing field, but rather an attempt to illustrate the ways in which drug
action is targeted to the cellular and molecular events in the heart and vasculature.

Drugs can be used to treat a variety of cardiovascular disorders, such as abnormal rhythm
(arrhythmias) heart failure, hypertension, angina as well as disorders blood clotting. Drugs
acting on the heart itself can alter heart rate or force of contraction. Such drugs can be useful
if it is necessary to reduce the workload of the heart following myocardial infarction (MI) or to
increase the heart‟s ability to pump in some cases of heart failure. Drugs acting on peripheral
resistance vessels are important in regulating blood pressure. Some drugs may act at more
than one site.

Disturbances of cardiac rhythm such as atrial fibrillation or tachychardia can be treated with
antiarrhythmic drugs of which several classes exist. Atrial fibrillation may occur as the result
of re-entrant loops or as the result of an ectopic focal point of excitation. These points of
excitation are frequently in the large veins entering the atria. Drugs used to treat arrhythmias
include Na+channel blockers such as local anaesthetics, β-adrenoreceptor antagonists, K+
channel blockers and Ca2+ channel blockers. The way in which these drugs act will be
discussed.
Drugs that affect the force of contraction will be considered. Cardiac glycosides such as
digoxin can, in some limited circumstances, be used to increase cardiac output in heart
failure. Cardiac glycosides act by inhibiting the Na+/K+ ATPase (Na pump) leading to an
increase in [Na+]in. The loss of the Na+ concentration gradient across the cell membrane
means that the Na+/Ca2+ exchanger cannot pump Ca2+ out of the cell so readily. The resultant
rise in [Ca2+]in causes an increased force of contraction. Adrenaline increases the force of
contraction by activating β1-adrenoreceptors but also increase heart rate. β- adrenoreceptors
blockers can be used to reduce the force and rate of contraction. β- adrenoreceptors
blockers are used in circumstances when you wish to decrease the work load of the heart
(eg following myocardial infarction).

Certain heart conditions such as atrial fibrillation and valve disease carry an increased risk of
thrombus formation. Anti-thrombotic drugs such as warfarin may be used in these cases. The

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antiplatlet drug aspirin is used following MI or in coronary artery disease where there is a risk
of MI to reduce the risk of platelet rich arterial clots forming.

Coronary artery disease can lead to angina or eventually MI. Nitrovasodilators are particularly
effective in the treatment of angina. These act primarily to dilate the veins, thereby reducing
central venous pressure (preload) and reducing the work of the heart. A secondary effect
may be due to dilatation of collateral coronary arteries improving blood supply to the heart.
They do not act by dilating arterioles.

Hypertension is an important cardiovascular condition since it carries a risk of developing

cardiovascular disease or stroke. Drugs used in the treatment of hypertension act to reduce
cardiac output and/or peripheral resistance. These include ACE-inhibitors (Angiotensin-
Converting Enzyme inhibitors), diuretics, adrenoreceptor blockers and calcium channel
blockers. Hypertension and its treatment will be covered further in the Urinary and Clinical
Pharmacology modules.

ACE-inhibitors and diuretics have an important role in the treatment of chronic heart failure.
ACE-inhibitors prevent the formation of the vasoconstrictor angiotensin II, thus promoting
vasodilation of arterioles and venous dilation. This decreases both afterload and preload to
the heart. ACE-inhibitors also have a diuretic action since angiotensin II promotes aldosterone
release from the adrenal cortex. You will find out later in the Urinary module that aldosterone
causes Na+ and water retention thereby increasing blood volume. Decreasing blood volume
decreases the preload to the heart.

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Session 8

The Electrocardiogram

The aim of this session is that you should understand the origin and characteristics of the
electrocardiogram, and start to learn about some common abnormalities of the ECG.
Structure of the session

Lecture 8.1: The electrical activity of the heart and the ECG (LT1 & LT2)

Group work: Analysis and interpretation of the ECG

Lecture 8.2: Plenary review of group work (LT1 & LT2)

You will find the book The ECG made Easy by John R Hampton a very valuable resource for
this session.

The ECG Quiz: An ECG Quiz will be available on Blackboard for those who wish to test their
understanding further

Intended learning outcomes:

By the end of this session and with appropriate self study you should be able to:

1. describe in general terms the pattern of spread of excitation over the normal heart from
the SA node to the AV node to the ventricles
2. describe and draw a diagram of the electrical conducting system of the heart and describe
how excitation normally spreads through the ventricular myocardium
3. describe the signal recorded by an extra cellular electrode placed near a myocardial cell
during systole
1. be able to state rules governing the sign of the signal recorded by a positive recording
electrode when depolarisation and repolarisation spreads towards and away from that
electrode
2. describe the form of signal recorded by a single electrode 'viewing' the heart from the
apex. Label the waves PQRST and identify the signals associated with atrial
depolarisation, ventricular depolarisation, and ventricular repolarisation

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1. describe how the QRS complex will change if the viewing electrode is moved around a circle
with the heart at its centre
2. be able to place positive and negative electrodes correctly to record from ECG leads I, II,
III, aVR, aVL, aVF and the chest leads V1-6 state the equivalent
single electrode view of leads I, II, III, aVR, aVL and aVF identify the
following abnormalities in ECG traces ventricular ectopic beats
atrial fibrillation ventricular fibrillation types of heart block
describe in outline the ECG changes associated
with the acute phase of myocardial infarction
myocardial ischaemia during exercise

The ECG traces in this session are the property of UHL trust and the
University of Kufa unless otherwise stated.

Lecture Synopsis

With each beat of the heart a large number of muscle cells undergo electrical changes in a
precisely defined sequence. The co-ordinated activity of such a large mass of muscle
generates a relatively large electrical signal which may be recorded by electrodes attached to
the body surface. The signal is known as the Electrocardiogram or ECG. The basic form of
the signal is determined by the pattern of electrical change in the heart, though what is
recorded is also affected by the position of the recording electrodes on the body.

Electrical changes in single cardiac cells

Contraction of each cell is triggered by an electrical event in its membrane - the Action
Potential. The potential difference across the cell membrane changes in a characteristic way.

Think back to the last session and draw the action potential recorded with an intra cellular
electrode from:

1. A ventricular myocardial cell

2. A sino-atrial node cell

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At the onset of the action potential the membrane potential changes from negative to positive
1. depolarisation. At the end of the action potential it changes back to negative
2. repolarisation. In the case of sino-atrial node cells the membrane drifts positive
between heart beats until it reaches the threshold for initiating another action potential. The rate of
this drift in potential therefore controls heart rate.

Action potentials spread over the heart in a precise pattern. First the atria depolarise, then
after a delay of about 120-200 ms at the Atrio-ventricular node activity spreads through the
inter ventricular septum to excite the ventricular myocardium from endocardial to epicardial
surface at the apex of the heart. Finally, excitation spreads up towards the base.

A wave of depolarisation therefore spreads in a broad direction defined as the 'electrical axis'
of the heart, which is somewhat to the left of the line of the inter-ventricular septum in the
normal heart.

All the ventricular myocardial cells depolarise before any start to repolarise. Repolarisation
does not follow the same sequence across the heart, as the cells at the outside of the
ventricle depolarise first, so the direction of spread of repolarisation is opposite to that of
depolarisation.

Electrodes placed outside of the heart will detect signals only when the membrane potential of
the myocardial cells is changing - i.e. during depolarisation and repolarisation, but not in
between. A ventricular action potential therefore generates two electrical signals at the body
surface, one at its beginning and one at its end.

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Draw the extra-cellularly recorded signals on the same time axis as an intra-cellularly
recorded ventricular action potential.

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Spread of excitation from cell to cell also generates a changing electrical field which will
induce an electrical signal in skin electrodes. In this case the nature of the signal depends
upon the direction of spread relative to the position of the recording electrode.

This may be predicted by rules:

1. depolarisation spreading towards a positive recording electrode yields an upward deflection

2. depolarisation spreading away from a positive recording electrode yields a downward deflection
3. repolarisation spreading towards a positive recording electrode yields a downward deflection
repolarisation spreading away from a positive recording electrode yields an upward deflection

In each case the amplitude (height) of the deflection depends on

1. how many cells are changing potential and how fast

2. how directly the wave of activity is travelling towards the
electrode directly towards /away yields a large signal obliquely
towards/away yields a smaller signal spread at right angles yields no
signal

Most properties of the ECG can be predicted from these rules.

1. The ECG recorded from an electrode 'viewing' the heart towards the apex

Draw the resulting ECG wave form, label the P, QRS, T waves.

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The P wave is associated with ......................... of the ........................

The QRS complex is associated with ................... of the ......................

The T wave is associated with ......................... of the ........................

The QRS complex has a complex shape because the effective 'direction' of spread of the
excitation changes as it conducts down the septum and then through the ventricular
myocardium (see group work later).

2. 'Viewing' the heart from different positions

If we concentrate just on the R wave (the biggest signal generally) the amplitude and polarity
will change as we move a positive recording electrode around the heart.

Draw the changes in the R wave as the electrode moves around the heart.

By 'viewing' the heart from several directions we can therefore work out the direction of the
major spread of excitation - the electrical axis of the heart - which may be altered in disease.

3. Using real electronics

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The amplifiers used to record the ECG have two inputs, not one, so at least two electrodes
have to be attached to the body surface. This complicates interpretation of the signals, but all
can be understood if you realise that the 'differential' amplifiers used to record the ECG take
the signal coming in on their negative input, invert it (i.e. turn it upside down) then add it to
the signal coming in on the positive input before multiplying the sum by a factor known as the
gain and then outputting it. If you know the 'views' of the positive and negative electrodes
you can therefore combine them to make an equivalent 'single electrode view'.

Example 1

Place the positive electrode on the lower left of the trunk, and the negative electrode on the
upper right. This electrode configuration is known as lead II. Draw the views of each
electrode. Then realise that a negative electrode's signal once inverted is the same as a
positive electrode's viewing the heart from the opposite direction. Draw the equivalent view of

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the negative electrode once inverted. Add the actual view of the positive electrode to the
equivalent view of the inverted negative electrode to get the final signal. In this case both
'look' the same way so the output is double that seen by a single positive electrode or in on
the lower left.

If the 'views' of the positive and equivalent negative are not identical - their combined view
lies midway between.

Example 2

The positive electrode on the upper left. The negative electrode on the upper right.

Construct the equivalent single electrode view.

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Group Work

The aim of this group work, and the time you spend on self-study and completing the ECG quiz
is to reinforce the concepts introduced in the lecture so that you can predict:

how the ECG wave form will change if conduction through the heart is altered
how the ECG wave form changes if you 'view' the heart from different directions
with
different electrode configurations
1. how the ECG wave form in different lead configuration will change if there is an unusually
large amount of muscle on the right or left of the heart
2. how the ECG changes in certain common situations - such as the acute phase of a myocardial
infarction (heart attack), when blood flow to the myocardium is compromised (myocardial ischaemia).

You should also be able to show the correct positioning or recording electrodes for performing
a 12 lead ECG.

These topics will then be followed up in later, clinical sessions.

The ECG wave form and events in the heart

Q8-1
Assume in these exercises that you are recording the ECG with an electrode configuration which
'views' the heart from the apex (e.g. Lead II). On the following diagram label the structures
involved in conduction of excitation over the ventricles.

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Images from Pathophysiology of Heart Disease ed. by L.S. Lil y © 2007 Lippincott Wil iams & Wilkins
Describe what is happening to electrical activity in the heart for each of the numbered points of
the ECG below.

1. sinoatrial node depolarisation(too small to be seen on ECG)

2. depolarisation of the atria (intranodal pathway) 3. delay at the
atrioventricular node

4. conduction down the right & left bundle branch leading to depolariation of
the ventricles

The following diagrams indicate the sequence of spread of excitation over the ventricles at each
phase of the QRS complex, and the average direction of spread.

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Images adapted from Pathophysiology of Heart Disease ed. by L.S. Lil y © 2007 Lippincott Wil iams & Wilkins

Q8-2 Looking at the diagrams above and the lead II ECG trace shown below explain in simple
terms why the QRS complex in lead II has the shape it does.

1. T

2. S
The QRS complex represents depolarisation through the ventricles. The deflection
shows the average direction through which the wave of depolarisation is
spreading (depolarisation spreads through the heart in many directio ns at once).
When the wave of depolarisation flows towards a unipolar lead or towards the
positive electrode of a bipolar lead the deflection will be upwards. Diagram 1
shows depolarisation of the septum from left to right. An electrode orientated to
the left ventricle will record a small initial downward deflection – the Q wave,
caused by spread of the stimulus away from the electrode.
Diagram 2 shows the spread of the stimulus down the right and left bundles and
through the ventricular muscle mass (the le ft ventricle has a larger muscle mass

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and hence a larger electrical force). The depolarisation is therefore towards the
electrode giving a large upward deflection – the R wave.

Diagram 3 shows the last region to be depolarised is the base of the ventricles close
to the annulus fibrosis. The spread is small and directed upwards and accounts for
the small negative deflection of the S wave.
In diagram 4 there is no further depolarisation and the recording returns to baseline.
Q8-3 remembering that ECG paper runs at a standard rate of 5 large squares per second (300
per minute) what are the heart rates of the
following ECGs, and are they normal or
abnormal?

II,III,aVf ‫اسفل‬

V1,V2 ‫ ال‬septal

V3,V4 ‫ال‬ Anterior

I,aVL,V5,V6 ‫ال‬ Lateral

The R – R interval is 4 large squares. Therefore the rate is 300/4 = 75 b / min

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The R – R interval is 1.8 large squares. Therefore the rate is 300/1.8 = 166 b / min

Q8-4 What causes the delay between the P wave (atrial depolarisation) and the QRS complex?

This is the time taken for excitation to spread from the SA node, through the atrial
muscle and the AV node, down the bundle of His and into the ventricular muscle.
Most of the time is taken up by delay in the AV node

Q8-5 What is the range of normal values of this P-R interval?

0.12 – 0.2 seconds (3 – 5 small squares)

Q8-6 This is a trace of first degree heart block. What has happened to the P-R interval?

From: The ECG Made Easy by John R. Hampton © 2003, Elsevier Science Limited

It is prolonged, indicating a delay somewhere between the SA node and the ventricles
(examples of conditions which can cause this are: i schaemic heart disease,
electrolyte imbalance, digoxin toxicity ).

Q8-7 Second degree heart block occurs when there is intermittent failure to conduct excitation
from atria to ventricles. What is happening in these two ECGs?

depolarisations are conducted to the ventricles. This is an example of second

degree heart block termed “2 to 1” ‫صار دروبد بيت‬

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One P wave is not followed by a QRS complex. Th is is second degree heart block
(for those interested, it is probably Mobitz type 2 since there does not appear to be
progressive lengthening of the PR interval ).

The causes of second degree heart block are similar to those of first degree heart
block.

Q8-8 In this ECG of complete heart block there is no relationship between the P wave and the
QRS complex.

8(i) Where is the block to conduction?

Between the atria and the ventricles. May be an acute phenomenon after M.I. or a
chronic state usually due to fibrosis around the Bundle of His

8(ii) What is the rate of atrial contraction?

P – P interval = 3.5 large squares. 300/ 3.5 = 85b/min

8(iii) What is the rate of ventricular contraction?

R – R interval = 8 large squares. 300/ 8 = 38 b/min

8(iv) Why is ventricular contraction rate so slow?

Because the automaticity of Purkinje fibres of the ventricles has a much slower rate
of firing than the SA node

8(v) Why are the QRS complexes a different shape to normal?

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Because of the abnormal spread of depolarisation from a ventricular focus

Q8-9 There are two main branches to the bundle of His - the right and left. If the left bundle
branch is damaged then the depolarisation of the left ventricle will be delayed relative to that of
the right ventricle. What has happened to the shape of the QRS complex in this ECG?

It has become wider because depolarisation is taking longer than normal. The normal
duration of the QRS complex is 0.12 seconds (3 small squares)

Q8-10
10(i) What is happening to give rise to the extra-systole in this ECG?

From: The ECG Made Easy by John R. Hampton © 2003, Elsevier Science Limited

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A wave of depolarisation has spontaneous ly arisen in the ventricle

10(ii) Why is the QRS complex of the extra-systole different to normal?

Because it has originated in an abnormal place, the spread of depolarisation is not via the normal route and
therefore takes longer.

Q8-11
11(i) What has happened to the rhythm in this ECG?

It is irregularly irregular

11(ii) Why are there no P waves?

Absence of atrial depolarisation

Individual atrial muscle fibres are contracting independently and there are only small
depolarisation waves of varying strength

11(iii) What is this called?

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Atrial fibrillation

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Cardiovascular Module Workbook

Remember the directions from which the standard leads look at the heart. Leads I, II and
aVL look at the left lateral surface of the heart; III and aVF at the inferior surface, and aVR at
the right atrium.

From: The ECG Made Easy by John R. Hampton © 2003, Elsevier Science Limited

Q8-12 The „full‟ ECG also includes 6 further leads - with the positive electrode connected to a
series of positions around the position of the heart in the chest. Label V1 to V6 on the
following diagram. How, in principle do the „single electrode views‟ of these leads relate to
the electrode position? (The answer is easy)

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From: The ECG Made Easy by John R. Hampton © 2003, Elsevier Science Limited

The leads are orientated in the horizontal or traverse plane as opposed to the standard and limb
leads which are orientated in the vertical or coronal plane

Q8-13 If the QRS complex is predominantly upwards the wave of depolarisation is moving
towards that lead. In the normal heart, the deflection is greatest in lead II. What has
happened to the cardiac axis in the following ECG‟s, and what may have caused the
changes?

The upward deflection is greatest in lead III, indicating that the axis has moved to
the right.
This occurs in right ventricular hypertrophy, e.g. from pulmonary conditions that put
a strain on the right side of the heart

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QRS complex is predominantly negative in lead III. This indicates left axis
deviation.

Q8-14
14(i) This ECG shows ventricular fibrillation. What do you see?

The appearance is disorganised with no QRS complexes

14(ii) How might you get the fibrillating ventricle back into near normal activity?

With a defibrillator; this discharges a high voltage field which depolarise the whole
heart allowing an organised rhythm to emerg e.
Cardiovascular Module Workbook

Q8-15 (i) This ECG was recorded during a myocardial infarction. What changes do you
see?

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Pathological Q waves (greater than 2mm in depth

ST elevation
Inverted T waves

15(ii) This is the same patient one month later. What has happened to the ECG now?

‫ موجوده‬Q ‫ال‬
‫بال‬
‫ طبيعي البقيه‬III,V1

‫غير طبيعي‬

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The ST segment and the T waves are now normal but there are persistent Q
waves.
You will cover the ECG changes with myocardial infarction again later in the module.

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Cardiovascular Module Workbook

Positioning of recording electrodes

Either during your group work session or in your own time you should familiarise yourselves
with the placement of electrodes for recording the 6 limb leads and six chest leads of the ECG.
You can practice as a group on volunteers.
On the diagram below indicate the placement of the electrodes required to record a 12 lead
ECG. You can refer to the diagram provided during group work. Describe the placement in the
box below. Do you know what colour these would be on a standard ECG machine?

Electrodes:

Left upper limb

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Right upper limb

Left lower limb

Right lower limb (neutral)

C1

C2

C3

C4

C5

C6

Cardiovascular Module Workbook

Cardiovascular System

Session 9

Special Circulations

The aim of this session is to examine the clinically relevant special features of the circulations
to the lungs, heart muscle, brain, skin and skeletal muscle.

Structure of the session

Lecture 9.1: The Special Circulations (LT1 & LT2)

Group work: Questions relating to special circulations

Formative Assessment Written Paper (plus feedback) (LT1 & LT2)

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Learning outcomes: By the end of this session and with appropriate self study you
should be able to:

1. state the major differences between the properties of the systemic and pulmonary
circulations.
2. state the normal pressures in the pulmonary artery, pulmonary capillaries and
pulmonary veins.
explain the concept of ventilation perfusion matching in the pulmonary
circulation.
describe the relationship between the mechanical work and oxygen demand of the
myocardium.
describe the particular features of the coronary circulation.
describe the consequences of partial or total occlusion of coronary
arteries. describe the factors which influence blood flow through the brain.
describe in broad outline the factors which influence blood flow through skin and
skeletal muscle.

Lecture Synopsis

This lecture will be concerned with the special properties of different parts of the circulation.
It will consider in some detail the pulmonary and coronary circulations and, in brief, the
cerebral circulation and circulation to the skin and muscle.

The Pulmonary Circulation

The entire output of the right heart is directed through the pulmonary circulation. Unlike the
systemic circulation, which is demand led, the pulmonary circulation is supply driven, it must
accommodate the entire cardiac output, whatever the systemic circulation determines it to be.

The metabolic needs of most parts of the lung are met by a separate part of the systemic
circulation - the bronchial circulation.

Medical

The pulmonary circulation therefore offers minimal flow resistance, and operates as a low
resistance, low pressure system.

Complete the following table:

Systemic

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circulation Pulmonary circulation

Mean arterial pressure

Mean capillary pressure

Mean Venous pressure

The pressure in the pulmonary capillaries is normally less than the colloid osmotic pressure,
so tissue fluid is not normally formed in the lungs. There is no overall control of the
pulmonary resistance, but the pulmonary arterioles can control the distribution of the cardiac
output over the lung. Blood is generally directed away from areas where oxygen uptake is
reduced.

Gravity also influences the distribution of blood flow through the lungs, as when standing, the
transmural pressure within blood vessels at the base of the lungs is elevated by gravity. This may lead
to some filtration of tissue fluid, but will also distend the vessels and increase flow to those
areas.

The lungs serve to exchange oxygen and carbon dioxide. In order for effective exchange to
occur blood flow ('perfusion') and air flow ('ventilation') to each part of the lungs must be
'matched'. Because of the way the gasses are carried in the blood, (see 'respiration' module
next semester) if there is a 'ventilation/perfusion mismatch' the blood leaving the lungs
will contain less oxygen and hypoxia will result.

Many cardiovascular and respiratory conditions lead to ventilation/perfusion mismatch, and

even in normal lungs there is a small mismatch because of the way in which gravity increases
blood flow to the base of the lungs when more air is delivered to the apices. This leads to, in
effect, some blood passing through the lungs without being properly oxygenated - the so-
called 'physiological shunt'.

The Coronary Circulation

The heart cannot stop for a rest, so blood flow through the coronary circulation must meet the
metabolic demands of the myocardium minute by minute.

The oxygen demand of the myocardium is determined by how much metabolic work is
done. This depends on the external work done and the efficiency with which metabolic
energy is converted to external work. The external work done by the heart per beat
depends upon the stroke volume and the arterial pressure.

The efficiency varies with different patterns of myocardial activity. If the ventricle is pumping
stroke volume against a low pressure then efficiency is high. Pumping the same stroke
volume against a higher pressure reduces efficiency. Pumping the same cardiac output into a
higher arterial pressure therefore requires much more blood flow.

During systole the tension in the walls of the ventricles compresses coronary vessels and
greatly reduces blood flow.

Coronary blood flow is therefore almost exclusively diastolic.

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In order to attain a mean blood flow appropriate to myocardial activity, therefore, the coronary
circulation must have a high blood flow in diastole to compensate for reduced blood flow in
systole.

At rest this problem is minimal. As heart rate increases diastole shortens much more than
systole. Consequently, the peak flow in diastole must increase very rapidly with rising heart
rate in order to maintain the necessary average flow.

Minor problems with the coronary circulation therefore become apparent only at higher
heart rates.

This makes the coronary circulation much more sensitive to arterial occlusion than other parts
of the circulation.

Control of the flow rate through the myocardium is almost entirely by the action of local
vasodilator metabolites upon coronary arterioles. The normal coronary circulation auto- regulates
very effectively.

The Cerebral Circulation

If the blood flow to the brain is reduced for even a few seconds then a subject will faint -
syncope - and significant reduction for more than three or four minutes can lead to permanent
brain damage or death.

The cerebral circulation therefore is paramount and in effect the rest of the circulation is
organised to ensure adequate cerebral perfusion. The normal cerebral circulation exhibits
very effective auto regulation via effects of local metabolites upon resistance vessels.
Carbon dioxide is a potent modulator of brain blood flow. Rises in the partial pressure of
carbon dioxide increase blood flow, falls reduce it.

Small alterations in cerebral blood flow have large effects, including headache and other
disturbances of cerebral function.

The Cutaneous Circulation

Most blood flow through skin is not nutritive, and much of the blood flows through arterio-
venous anastomoses rather than capillaries. This blood flow is heavily influenced by the
sympathetic nervous system and little affected by local metabolites, except that mediators
released from active sweat glands increase flow and circulating vasodilator mediators from
other sources sometimes increase skin blood flow. The main function of cutaneous
circulation is to maintain a constant body temperature.

Skeletal Muscle Blood Flow

The metabolic activity of skeletal muscle varies over an enormous range and so does the
blood flow. At rest most capillaries within a muscle are shut off by contraction of pre-capillary
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sphincters. Increases in blood flow are brought about mainly by opening up more capillaries
under the influence of vasodilator nervous activity and local metabolites which tend to reduce
tonic sympathetic vasoconstrictor tone.

Medical

Group Work

The pulmonary circulation.

Q9-1 Why is the pressure in the left atrium of a normal individual higher than the pressure
in the right atrium?

Because the resistance in the pulmonary circulation is low so there is less

pressure drop as blood enters the left atrium. The greatest resistance and
therefore the greatest pressure drop occurs in the systemic arterioles .

Q9-2 Describe the changes in pressure that will be recorded if a catheter with a pressure sensor
on its tip were advanced:

1. from the inferior vena cava into the right atrium

No change 0 –8mmHg

2. through the right ventricle into the pulmonary artery

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Systolic pressure unchanged 15 – 30 15 – 30 mmHg Diastolic pressure

increases 0– 8 4 – 12 mmHg

3. into a small branch of the pulmonary arterial tree, so that its tip 'wedges' or jams
into an artery and occludes it completely.

Same as left artrial pressure = 1 -10mmHg

Q9-3 Why might you be interested in measuring each of these pressures?

Provides information about the left side of the heart as well as the right heart
and will identify pulmonary hypertension

Q9-4 What will happen to the pressure in the left atrium as a subject breathes in and out?

The left atrial pressure goes down as a subject breathes in because blood stays
in the pulmonary circulation (right atrial pressure increases as the negative
intra-thoracic pressure draws blood in from the systemic veins) .

Q9-5 What will happen to the pressure in the pulmonary artery if the pumping action of
the left heart is compromised?

It will increase

Q9-6 What effects will this change have on the lungs in the short term

Would cause pulmonary oedema

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Q9-7 If pulmonary arterial pressure is increased over a long period (e.g. in the case of a
chronic left to right shunt as occurs with a ventricular or atrial septal defect) what effect
would you expect this to have upon the resistance vessels of the pulmonary circulation?

They become permanently narrowed (vascular re-modelling)

Q9-8 What will happen to ventilation/perfusion matching in the lung if some part of the
pulmonary arterial tree is occluded by, say thrombus? What is this condition called?

The area of lung concerned will no longer receive adequate blood flow despite
being normally ventilated, i.e. there will be ventilation / perfusion mismatch
Occlusion of part of the lung by a thrombus is referred to as a pulmonary
embolism.

Q9-9 Try to find out how, in principle, might you set about assessing the effectiveness of
ventilation/perfusion matching in a patient's lungs?

Arterial blood gases (pO2 and pCO2) will indicate the effectiveness of V/Q
matching but areas of mismatch may be d emonstrated by a lung scan
(radiological imaging after the injection of a radiopaque dye into the arteries
and Inhalation of a radioactive gas)
Medical

The Coronary Circulation

Q9-10 Look back at your 'Mechanisms of Disease' module. What might happen to
produce a partial occlusion of a coronary artery?

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Formation of an atheromatous plaque

Q9-11 Which parts of the myocardium will be affected if a patient has an occlusion in (i)
the right coronary artery (ii) the circumflex branch of the left coronary artery (iii) the left
anterior descending coronary artery?

1. posterior and inferior aspect (right atrium and right ventricle)

2. lateral aspect (left atrium)

3. anterior part of both ventricles and interventricular septum

Q9-12 Why will such an occlusion cause more problems in exercise than at rest?

Because the coronary vessels fill during diastole. During exercise, when the
heart rate rises, diastole becomes much shorter (systole is relatively spared)

Q9-13 What are the symptoms of mildly insufficient blood flow to part of the myocardium?

Angina – chest pain on exertion which goes away with rest

Q9-14 What will happen if blood flow to part of the myocardium is dramatically reduced?

The myocardium will become Ischaemic

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Q9-15 If these changes are not apparent at rest what would an individual have to do to
reveal them?

Exercise stress test – get patient to exercise (on a treadmill) with increasing
intensity
Look for ST depression on ECG or development of symptoms as an indica tor of
impaired blood flow to the heart.

The Cerebral Circulation

Q9-16 What will happen to the blood flow through the brain if a subject increases their
breathing ('hyperventilates') and so reduces the partial pressure of CO2 (pCO2) in arterial
blood?

Blood flow will reduce; decreased PCO2 causes vasoconstriction.

Q9-17 How should you deal with someone who faints because of a temporary reduction
in cerebral blood flow?

Lie them down to minimise the effects of gravity on the circulation and
maintain cerebral blood flow.

Q9-18 The brain is contained within a rigid cranial cavity. What special problems might this
pose for the cerebral circulation?

Space occupying lesions such as a tumour or haemorrhage will increase the

intracranial pressure and limit blood flow.

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Q9-19 What will happen to the ease of perfusing the brain if the pressure within the
cranial cavity (the 'intracranial pressure') rises? What effect do you think this may have on
arterial blood pressure and why?

Increased intracranial pressure will decrease perfusion of the brain within the
rigid cranial cavity. Ischaemia in the medullary centres activates a
sympathetically mediated response (Cushing‟s reflex) which raises mean
arterial pressure. This reflex help s to maintain perfusion of the brain.

Medical

Cardiovascular System

Session 10

Ischaemic Heart Disease

By the end of this session you should understand some of the common cardiovascular
causes of chest pain. You should be able to use common sense and knowledge of basic
medical sciences to begin to develop an insight into disease processes and to approach
clinical problems in a logical step-wise manner.

It will help your understanding of this session if you read up on ischaemic heart disease
before hand and make some attempt at answering the questions for cases 1 & 2. The ECGs
in figures 1&3 will be posted on the le and available at your group work sessions.

Structure of the session

Lecture: Causes of chest pain / Investigation and management of angina and

myocardial infarction (LT1 & LT2)

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Group work: Case studies on patients with chest pain

Lecture: Clinical Skills - Examination of the Cardiovascular System (LT1 &

LT2)

Lecture 11.1: Causes of chest pain / Investigation and management of angina and
myocardial infarction

Learning outcomes: By the end of this lecture and with appropriate self study you should be
able to:

appreciate the common causes of chest pain

describe the pathophysiology of angina and myocardial infarction
describe the risk factors for coronary atheroma describe the signs and
symptoms of angina describe the signs and symptoms of myocardial infarction
distinguish the characteristics of unstable angina and its underlying
pathophysiology describe the signs and symptoms of acute pericarditis
describe the investigations of the patient with angina describe the principles of
the exercise test to assess a patient with angina understand the drugs used in
the treatment of angina appreciate surgical treatments for angina understand
the management of unstable angina describe the investigation for myocardial
infarction describe the management of acute myocardial infarction

Lecture 11.2: Clinical Skills: Examination of the Cardiovascular System

Please refer to your Clinical Skills Module book for the learning outcomes of this lecture.

Case Studies

The following case studies each contain a number of questions which you should answer.
You will not be able to answer them without reference to texts. Long or complex answers are
not required - just the essentials. You can start work on cases 1 & 2 before coming to this
session. ECGs in figures 1 & 3 and the angiograms for case 2 will be posted on the le.

Case 1 John
Q11-1
John Smith is a 45-year-old Managing Director. On 23 June he had an 'executive health
screen' organised by his company. His electrocardiogram was normal (figure 1). His plasma

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cholesterol was 8mmol.l-1 (normal range 5.2 - 6.7 mmol.l-1). He was advised to stop smoking,
and to contact his GP to discuss a cholesterol lowering diet.

Q10-1(i) A conventional ECG records 12 'leads' (actually pairs of electrode positions) which
'look at' the heart from different directions. Look back to session 8 and draw diagrams to show
the effective single electrode views of leads 1 to 3, aVL, aVF, aVR, and the chest leads V1-V6.

Refer to figure 1.7 page 9 of ECG made Easy (6t h ed) or to figure 4.5 page 85 of
Lilly, Pathophysiology of Heart Disease (4t h ed.) for standard limb leads.
Refer to figure 1.9 page 10 of ECG made Easy (6t h ed) or to figure 4.7 page 86
of Lilly, Pathophysiology of Heart Disease (4t h ed) for precordial (chest) leads.

Q10-1(ii) What would you include in/omit from a cholesterol lowering diet?

Saturated fats, eg animal fat and dairy products, should be decreased to <10% of
dietary energy intake and replaced with monounsaturated fats eg.olive oil and
polyunsaturated fats eg fish oil, other oils

Q10-1(iii) Apart from cholesterol and smoking, list 3 other risk factors or markers for
coronary artery disease.

Hypertension Advancing age

Diabetes Male sex
Family history Obesity

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On 30 June John became ill in the locker room after a squash game. He complained of chest
pain which rapidly became very severe. The distribution of his pain is shown in figure 2. He
vomited, sweated profusely and looked very pale. His recent opponent, Dr G, dialled 999 and
called an ambulance, which arrived within 14 minutes and took John to the nearest Accident
and Emergency department. On arrival he was given a pain-relieving drug and another ECG
was recorded (figure 3).

Q10-1(iv) Compare the ECGs in figures 1 and 3. What differences can you spot?

The main difference is marked S -T elevation in leads V2, V3 and V4

Q10-1(v) How can you account for the distribution of pain in figure 2?

Figure 2

This is cardiac referred pain.

For explanation see section on cardiac referred pain on page 166 of Moore &
Dalley Clinically Orientated Anatomy 5t h Ed.

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Ischaemia in the heart stimulates pain endings. These afferent pain fibres enter
the spinal cord in segments T1 – T4 or 5 on the left side by travelling along with
sympathetic fibres and account for pain over the chest in these dermatomes.
Cardiac pain is also typically referred t o the left upper limb and neck region (T1
dermatome in arm; also medial cutaneous nerve of the arm often has branches
from 2n d and 3r d intercostal nerves).
Referred pain is also thought to result from a mixing of signals in the central
nervous system. Dermatomes of the neck region are C4 and C5
Q10-1(vi) How can you account for the pallor, sweating and vomiting?

Sweating and pallor are due to increased activity of the sympathetic nervous
system (adrenergic sweating and sympathetic mediated vasoconstrict ion)

The combination of sudden onset, severe chest pain in the distribution described, together
with ECG changes of acute heart muscle injury, strongly suggests acute coronary thrombosis
(blockage of a coronary artery with a blood clot or thrombus). John was transferred rapidly to
a coronary care unit and given a drug to cause the clot to dissolve. He made a good
recovery. Whilst he was in the coronary care unit, blood was taken and analysed for the
enzyme creatine kinase (CK) which is found in heart muscle.

Results were as follows:

CK (International Units/Litre)

30.06.01 evening 67
01.07.01 morning 2,500
01.07.01 evening 600
02.07.01 morning 150

Q10-1(vii) How do you account for the changes in blood CK activity?

Creatine kinase is released by infarcted myocardial cells.

It peaks within 12 - 24 hours and returns to normal by 48 hours. The
amount of enzyme released is a good guide to the extent of myocardial
necrosis.

Q10-1(viii) Which coronary artery do you think was blocked? (Hint: Look at the ECG before
and after, and think about the electrode views)

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Left anterior descending (interventricular) artery occluded. (septal leads

involved)

Q10-1(ix) Using conventional ECG terminology can you describe the changes in more
detail? Can you explain how injury could alter the ECG?

Initially ST segment elevation is seen in leads viewing the surface of the injured
tissue (infracted area). Note: the cellular basis for ST elevation is not fully
understood, but damaged cells will be electrically leaky and depolarisation may
spread from or to these damaged cells. The ST segment should be iso -electric
(no spread of depolarisation) since it corresponds to the time when all the
ventricular cells should be depolarised. When the ST segment normalises after a
few days there is usually T wave inversion.
In full thickness M.I. pathological Q waves develop later. This is because the
infarcted area, being electrically inert, creates an “electrica l window”, through
which depolarisation of distant healthy muscle is seen. As this depolarisation will
be in a direction away from the infarcted area a lead orientated towards this area
would show a negative deflection (the Q wave).

Q10-1(x) Can you think of any way in which the squash game could have precipitated the
thrombosis?

Exercise increases the heart rate and therefore the metabolic activity and oxygen
demand of the myocardium. However the increased heart rate results in
shortening of diastole (with relative sparing of systole) which compromises
coronary artery filling.

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Case 2: Satpal
Satpal Singh, aged 48, runs a knitwear factory. On 7 October, when in London on business,
he noticed he became breathless hurrying to catch the train. On his return to Kufa he had a
tight pain in the chest climbing the bridge to the station car park. The pain eased when he
rested for a few minutes. Over the next two weeks he noticed he got chest pain or become
short of breath whenever he exerted himself, and he consulted his GP. The GP found that
his blood pressure was normal, and there were no other abnormalities on examination. Mr
Singh has never smoked. There was a family history of diabetes but not of heart disease.
The distribution of pain was similar to that shown in figure 2. It was consistently related to

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exercise, particularly after meals or in cold weather. An electrocardiogram taken in the

surgery was normal.

Q10-2(i) List the similarities and differences (so far) between this case and case 1.

Similar character and distribution of pain - In both cases the pain was brought on
by exercise but in this case the pain resolved after a few minutes rest whereas in
the first case it rapidly became severe

Q10-2(ii) What is the name of the clinical syndrome of cardiac pain brought on by exertion
and relieved by rest?

Angina

Q10-2(iii) Does this man's normal electrocardiogram at rest rule out heart disease? If not,
why not.

Many people with ischaemic heart disease have normal ECGs at rest. T he ECG
needs to be repeated during exercise when the heart rate is increased and
coronary artery filling compromised

Satpal was given a prescription for aspirin and for the β adrenoreceptor antagonist
propranolol. He was referred to hospital for an exercise electrocardiogram. This involved
walking on a treadmill connected to an ECG machine. Whilst doing this he experienced his
typical chest pain, and the technician noticed ECG changes at the same time. His cholesterol
was normal, but he was found to be mildly diabetic. The diabetes was controlled with diet
alone, and on medication he became symptom-free.

Q10-2(iv) Can you explain why the ECG was normal at rest but became abnormal during
exercise?

Coronary artery filling is severely compromised in exercise due to shortening of

diastole by about two thirds

Q10-2(v) What abnormalities do you think the technician noticed in Satpal's ECG?

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S-T depression

Q10-2(vi) Beta blockers reduce heart rate increases on exercise, and tend to reduce blood
pressure: How would these help angina?

Reduces the oxygen demand of the myocardium

After a few weeks Satpal's symptoms returned, and despite increased medication, become
severe. He underwent coronary angiography (x-ray pictures of the coronary arteries). The
pictures of Satpal‟s coronary angiogram and a normal coronary angiogram will be provided to
your group in the work session.

Q10-2(vii) Can you see any abnormality in Satpal's coronary arteries? How would this
explain the symptoms?

Partial occlusion of the coronary arteries resulting in ischaemia to the

myocardium, particularly on exercise

Q10-2(viii) Think back to session 5, what is the relationship between the radius of a tube and
the resistance it offers to (laminar) blood flow?

The lower the radius of a tube the greater the resistance to flow

Q10-2(ix) 'The age adjusted relative risk for symptomatic coronary disease in Kufa Asians
compared to Whites is 1.46.‟ Explain.

U.K. Asians have a higher frequency of coronary hear t disease compared to

whites partly due to the higher rates of diabetes and hypercholesterolaemia

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Case 3: Karen

Karen Israel is a 37 year old marketing executive, married with two children aged 2 and 5.
She was admitted on 10 January with a history of increasingly severe episodes of chest pain
over the preceding 5 days. Initially the chest pain had only occurred on vigorous exertion,
then on climbing one flight of stairs, and on the day of admission it had occurred at rest. The
distribution of the pain was similar to cases 1 and 2, and she described it as a heaviness or
tightness in her chest. Physical examination on admission was normal.

Q10-3(i) Do you think her GP was wise to send her to hospital? If so, why?

Yes, increasing severity of pain over a few days

Q10-3(ii) Name two investigations you might do after admission to hospital.

ECG
Cardiac enzymes

The ECG was normal on admission. A few hours later, Karen suffered another episode of
chest pain at rest and during this episode it showed ST elevation in leads II, III and aVF,

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returning to normal in a few minutes. Cardiac enzymes were normal. Karen was treated with
aspirin, a beta blocker, and glyceryl trinitrate (a drug which dilates blood vessels by relaxing
smooth muscle). After a few days her symptoms settled and she was discharged.

Q10-3(iii) This clinical presentation is sometimes called 'unstable' or 'crescendo' angina.

Why?

Worsening angina with no predictable association of the pain to exercise

Q10-3(iv) See if you can find out the mechanism for unstable or crescendo angina. Why was
Karen given aspirin?

Thrombosis occurring on top of an atheromatous plaque which can cause

vasospasm
Aspirin reduces thrombotic risk and has been shown to reduce mortality.
Patients are also given heparin, an anticoagulant

Q10-3(v) What subsequent tests might be done as an outpatient?

Continuous ECG monitoring

Case 4: Mary

Mary Blore is a fiercely independent 78-year-old retired postmistress who lives on her own in
sheltered housing. Her daughter persuades her to come and see you because she became
very short of breath and had chest pain when they visited the Shires shopping centre
together. Mary has been taking an aspirin a day for the last three years, as she read in the
'Daily Telegraph' it was good for the heart.

Mary is slim and looks fit for her age, but seems very pale. On examination her blood
pressure is 160/90 (normal), but there is a loud systolic murmur radiating to the neck and the
cardiac apex beat is forceful and heaving. She admits to some indigestion, and says her
bowel motions are occasionally dark. You take some blood for a blood count and

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haemoglobin estimation, and find the haemoglobin is only 6 grams per dl of blood (normal
>12G).

Q10-4(i) What would you conclude from the loud systolic murmur and forceful apex beat?

The signs could merely be due to severe anaemia as the increased cardiac
output may give rise to a “flow” murmur and forceful apex beat.

Aortic stenosis with left ventricular hypertroph y would also produce a loud
systolic murmur and forceful apex beat

Q10-4(ii) Would Mary's symptoms fit the clinical diagnosis of angina?

Yes

Q10-4(iii) Given that a gram of haemoglobin can carry 1.34 ml of oxygen when fully
saturated, how much oxygen could be carried by (i) a litre of blood with haemoglobin
concentration of 12g per dl; (ii) a litre of Mary's blood?

(i) 1.34 x 120 = 160 ml (ii)

1.34 x 60 = 80 ml

Q10-4(iv) Assuming the body's resting oxygen consumption remains the same, in someone
who gradually becomes anaemic (haemoglobin falls from 12g to 6g per dl blood), would you
expect resting coronary blood flow (i) to remain normal, or (ii) to increase to twice normal, or
(iii) to increase to more than twice normal. Why?

You would expect it to increase to twice normal. In reality it is less than that due
to other compensatory mechanisms

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Q10-4(v) How could anaemia cause or worsen angina?

Lack of oxygen carrying capacity of the blood means the heart has to work
harder to meet the demands of the tissues. There is also less oxygen in the blood
to supply the heart muscle. With severe anaemia, angina can develop even in the
absence of significant atherosclerotic damage to coronary arteries. Symptoms
of coronary artery disease would be worsened by anaemia .

Q10-4(vi) How could aortic stenosis cause or worsen angina?

Increased oxygen demand by the left ventricle which has to pump harder to force
blood through stenosed aortic valve
Abnormal myocardial relaxation compromising coronary artery filling

Case 5: James

James Ndolovu, a fourth year medical student, thought he might be getting flu but
nevertheless turned out for rugby practice. That night he felt very unwell, with severe central
chest pain. The pain felt particularly bad whenever he took a deep breath, when it felt almost
as if he were being stabbed. He also felt sore at the tip of his left shoulder. His flatmate
drove him to the casualty department. The medical registrar on call took a long time to listen
carefully to the front of his chest, looked at the ECG, and then made a confident diagnosis of
acute pericarditis (an inflammation of the serous membranes around the heart).

Q10-5(i) What was the registrar listening for?

Pericardial rub

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Q10-5(ii) Why did James feel pain in his shoulder?

Pericardium is supplied by the phrenic nerve (C3,4,5). The dermatomes for

C3,4&5 are in the shoulder and neck region.
May also be diaphragmatic irritat ion (again phrenic nerve C3,4,5)

Q10-5(iii) What are the similarities and differences between the pains of acute myocardial
infarction (case 1) and pericarditis?

Both are severe and central

Pain of pericarditis often “pleuritic” ie exacerbated by deep inspiration Also
made worse by lying flat, sternal pressure or swallowing Q10-5(iv) Find
out some of the causes of pericarditis.

Infective – viral
bacterial
T.B

Inflammatory - eg connective tissue disorders

Malignant infiltration Post M.I.

Additional Reading
Cox & Roper eds. Clinical Skills, Oxford Core Texts (OUP)
Douglas, Nicol Roper, eds. Macleod’s Clinical Examination 11th edition (Churchill
Livingstone)
Hampton, The ECG Made Easy 7th edition (Churchill Livingstone)
Lilly ed. Pathophysiology of Heart Disease 4th edition (LWW) Chapters 5-7 Cardiovascular
System

Session 11

Heart Failure

The aim of this session is that you should understand the effects of, pathophysiology of and
management of acute and chronic heart failure. You should be able to use your knowledge
of basic and applied medical sciences to begin to adopt a logical and step-by-step approach
to clinical problems.

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Structure of the session

Lecture: Heart failure and its management (LT1 & LT2)

Group work: Case studies on heart failure (seminar rooms)

Tutorial: Review of case studies (seminar rooms)

Learning outcomes: By the end of this session and with appropriate self study you should be
able to:

explain the pathophysiology of heart failure describe the clinical

characteristics of the principal types of heart failure, and the
circumstances which lead to its development
identify targets for drug action for the manipulation of cardiac output
describe the principles involved in the general management of heart failure, and
the
categories of drugs used in its therapy.

Lecture synopsis

Heart failure is a state „in which the heart fails to maintain an adequate circulation for the needs
of the body despite an adequate filling pressure‟.
It is important to understand Starling‟s law of the heart to appreciate what happens in heart
failure. The force developed in the myocardium depends on the degree to which the fibres
are stretched (or the heart is filled). In heart failure the heart can no longer produce the same
amount of force (or cardiac output) for a given level of filling.
Heart failure can affect one or both sides of the heart. However right sided heart failure rarely
occurs on its own (but can in the case of chronic lung disease). The most common scenario
is one of left-sided heart failure which raises pulmonary arterial pressure leading to additional
right-sided heart failure. When both ventricles are affected we refer to this as congestive
heart failure.
The sympathetic nervous system and the Renin-Angiotensin-Aldosterone System (RAAS) are both
activated in heart failure in an attempt to maintain cardiac output. These have the effect of
making an already struggling heart work harder. In addition, angiotensin II can damage the
heart and other organs. You will do more on the RAAS in the Urinary module, but you should
know that a drop in blood pressure (as occurs in heart failure) stimulates renin release from
the kidneys. Renin is an enzyme which catalyses the conversion of angiotensinogen to
angiotensin I. Angiotensin I is converted to angiotensin II by the action of Angiotensin
Converting Enzyme (ACE). ACE inhibitors are used in the treatment of heart failure to prevent the
production of angiotensin II which is a powerful vasoconstrictor and promotes the release of

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aldosterone from the adrenal cortex. Aldosterone causes salt and water retention in the
kidneys, increasing blood volume. ACE inhibitors thus have an indirect vasodilatory and
diuretic effect, both of which are beneficial in the treatment of heart failure. Diuretics are also
important in the treatment of heart failure to reduce blood volume and thus oedema. In the
lecture other hormonal effects will also be considered.
The formation of peripheral oedema occurs due to right-sided heart failure. Failure of the
right side of the heart to pump effectively raises venous pressure and therefore capillary
pressure. An increased capillary hydrostatic pressure favours the movement of water out of
the capillaries. Pulmonary oedema occurs due to left sided heart failure which raises left atrial
pressure and thus the pressure of vessels in the pulmonary system. (Since these vessels
have a low resistance this also causes an increase in pulmonary artery pressure.) As well as
impaired ability of the heart to contract (systolic dysfunction), there can be impairment of the
filling of the heart (diastolic dysfunction). This triggers the same neurohumoral systems as
systolic dysfunction.

Additional Reading
Cox & Roper eds. Clinical Skills, Oxford Core Texts (OUP, 2005)
Douglas, Nicol Roper, eds. Macleod’s Clinical Examination 11th edition (Churchill Livingstone,
2005)
Lilly ed. Pathophysiology of Heart Disease 4th edition (LWW, 2007) Chapter 9

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Case 1 Edward

Edward is a 54-year-old bricklayer. He is married with 3 grown up children. He is 5' 10" tall,
and his weight has increased gradually over the last 10 years to 89 kg (14 stone). He tends
to use his car even for short trips as he feels he expends enough energy during his working
day up and down ladders carrying bricks. Over the last few months he has found himself
getting increasingly tired by the end of the day at work, and has found that he is 'puffing' a bit
when he tries to climb a ladder quickly.

Q11-1.1 What other things would you want to know about Edward's life style? Write down
your guesses as to the answers you would get.

Does he smoke? If so, how much How

much alcohol?

On questioning he admits to:

Swelling of his ankles towards the end of the day, which usually disappears by the
following morning, but has become increasingly more obvious over the last 3 weeks.
Getting up at night to pass urine 2 or 3 times when previously he could go through the
night without disturbance.

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Needing to use 4 pillows at night to be comfortable.

Occasional central chest discomfort which he says is due to 'indigestion'.

Think about your physiology.

Q11-1.2 What factors determine how much tissue fluid is formed in any part of the body? (a
diagram would be easiest)

Hydrostatic pressure forcing fluid out

Oncotic pressure drawing fluid back in

Q11-1.3 What, then has changed in Edward's ankles to cause swelling?

Increased hydrostatic pressure in the venous system

Heart „pump failure‟ increased end systolic volume decreased capacity for
venous return during diastole

Q11-1.4 Why is it only his ankles which are swelling up at this stage?

Heart failure only mild at thi s stage so only dependent areas involved
- effect of gravity

Q11-1.5 Why does the swelling go away at night?

Legs no longer below level of heart

Q11-1.6 What happens to the return of blood to the heart when we lie down?

Blood returning to the heart is increased(less pooling of blood in peripheral

veins)

Q11-1.7 Why might Edward be short of breath when lying flat?

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Pulmonary oedema due to increased hydrostatic pressure in the pulmonary

circulation
Worse when lying flat due to effects of gravity (increased hydrostatic pressure
in capillaries at the apex of the lungs – also more blood returning to the heart, less
stored in peripheral veins)

Q11-1.8 From what you know or can guess about Edward and his life style do you think he will
be prone to indigestion?

Smoking causes heartburn (relaxes the oesophagogastric sphincter)

Alcohol causes gastritis and heartburn

Your examination of Edward reveals:

An obese man with a plethoric (florid) complexion, slightly breathless at rest, and more so
when undressing.
A pulse rate of 80-90 beats per minute.
Arterial blood pressure of 170/95.
Jugular vein pulsation visible in the neck
Apex beat displaced to the left and forceful in character.
Scattered wheezing on auscultation of the chest.
Swelling of the ankles.
Urine analysis indicates presence of glucose (<2%) and a trace of protein.

Q11-1.9 What is suggested by visible jugular pulsation in the neck?

Raised central venous pressures

Q11-1.10 How might this relate to the swelling of Edward's ankles?

Increased pressure in the venous system oedema

(increased pressure at venous end of capillaries causes an increased capillary

hydrostatic pressure)

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Q11-1.11 Why might the apex beat be forceful and displaced to the left? What does this tell
you about the size of Edward's heart and which chamber is most affected?

Heart size enlarged

Left ventricle mainly affected

Q11-1.12 What investigations would you request in order to find out the size of Edward's
heart?

Measure cardiothoracic ratio on chest X-ray (however ventricular hypertrophy is

not always evident as 40-50% of patients with left ventricular failure hav e a
normal cardiothoracic ratio. You would also see signs of pulmonary oedema on a
chest X-ray)

A better investigation would actually be ec hocardiogram (cardiac ultrasound).

This gives information on how the heart is functioning as well as structural
information.

Q11-1.13 Wheezing is caused by narrowing of airways in the lung. What factors might
contribute to this narrowing in Edward's case? (Think about his lifestyle as well as your
developing ideas of his clinical condition).

1. Heart failure causes oedema of the airways (cardiac asthma)

2. Smoking causes airways disease

Q11-1.14 Try to suggest why Edward is breathless on exertion.

Poor oxygenation of the blood in the lungs

Plus poor delivery to tissues
This becomes more critical during exertion as the O2 demand of his body
increases
Therefore has to breathe faster

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By this stage you should have decided that Edward's heart is not able to pump blood as well
as it should - he has Congestive Heart Failure.

Q11-1.15 What is 'congestive' heart failure?

Affects both sides of the heart

Q11-1.16 What will happen to the pressures in Edward's pulmonary circulation?

Increased hydrostatic pressure

Q11-1.17 Why do you think Edward's heart is failing? What might have produced long-term
stress on the myocardium in his case?

Ischaemic myocardium due to coronary artery d isease

Major risk factor – smoking

Q11-1.18 What other factors have contributed to Edward's problem?

Alcohol can directly damage cardiac muscle

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Treating Edward

Q11-1.19 How, in general terms, might you expect to treat Edward? (Think about reducing
the workload on his heart).

Rest – to reduce demands of the heart

Drugs to reduce pre-load by venodilatation ( venous return)
And after-load by arteriolar dilatation ( total peripheral resistance (TPR))

Q11-1.20 Try to suggest the specific sorts of drugs you might use.

Diuretics
ACE inhibitors
Vasodilators – nitrates
Calcium channel blockers

Case 2

Sarah
=
6.3 )
=

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Sarah is 38 years old. She has 3 children between 8 and 15 years old. She works part xtne
-time
for 3 hours per week in a local college. She does not smoke and drinks a small sherry on
special occasions only. She is 5' 4" tall and weights 60 kg (9.5 stone). Sarah has noticed
over the past 3 weeks that she becomes increasingly short of breath. She has noticed that she
has to stop and catch her breath when walking up a hill to do her shopping when previously
this had been no problem for her. She has also found, over the last few months that simple
household chores (e.g. bed making) have become more exhausting. Her family have also
noticed that she always looks tired and falls asleep in front of the TV early in the evening.

You question Sarah further and discover:

She has noticed 'palpitations' occurring at irregular intervals, but with increasing frequency
recently.
She has an irritating cough particularly during the night, which wakes her from sleep.
She has had a single episode of coughing up a small amount of blood (haemoptysis).
She was hospitalised for the last 3 weeks of her pregnancy because of shortness of
breath and ankle swelling.
She suffered from 'growing pains' as a young child, and was scolded for being excessively
'fidgety' at college.

Q11-2.1 Can you think of one other question you would ask a woman of reproductive age
who is suffering from tiredness and lack of energy? potapans

Heavy periods ? iron deficiency anaemia stration

Your examination of Sarah reveals:

A woman of average build comfortable at rest.

She has a 'high colour' over her cheek bones (no make up!) but is otherwise pale.
Her pulse rate is about 100 per minute, and irregular in rhythm.
Jugular pulsation is not visible in her neck, and her ankles are not
swollen. ve,Mitral Mr Steness
On listening to the chest you hear a heart murmur, which occurs in mid diastole, and is
associated with a distinct sound just after the second heart sound.
On listening to the chest you hear fine 'crepitations' at the lung bases.

On the basis of your knowledge of physiology, have a go at the following questions:

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Q11-2.2 Given Sarah's pulse rate and rhythm at rest do you think it likely that her heart is
being driven by the sino atrial node pacemaker?

No

Q11-2.3 If not, where is her heart rhythm originating?

Multiple sites in the atria

Q11-2.4 So, what is causing Sarah's 'palpitations'?

Arrhythmias Tachscoldi
-Sig
polditation Symptom
->

Q11-2.5 Describe the characteristics of the ECG you would expect to record from Sarah.

Atrial fibrillation – loss of P waves

irregular R – R intervals

Q11-2.6 Through which valves is blood flowing at a high rate in diastole?

Atrioventricular

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Q11-2.7 Can you, therefore, suggest what might be happening in Sarah's heart to produce
the murmur you have heard?

Stenosed mitral valve

Q11-2.8 From session 9, can you suggest a technique which might be used to verify your
suspicions about Sarah's valve problem?

Cardiac catheterisation could be used to reveal a pressure gradient between the

left atrium and left ventricle.

Note: It would be usual to first investigate with echocardiography and where this is
inconclusive use cardiac catheterisation

Q11-2.9 What does the absence of ankle swelling and no visible jugular pulsation tell you
about the abnormality of Sarah's cardiovascular system?

That the right heart is not affected

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Q11-2.10 Fine crepitations sound something like bubbles of air moving around in water. X
- What therefore do you think might be happening in Sarah's lungs? Why is the change
most obvious at the base of the lungs rather than the apex?

Pulmonary oedema – fluid in alveolar spaces

MildorF
or
The lung bases are affected more than the apices due to the effects of gravity O

Q11-2.11 Why might Sarah have coughed up blood?

Venous congestion in lungs

Increased venous pressure can lead to rupture of c apillaries

Q11-2.12 Can you suggest why Sarah might be breathless?

Pulmonary oedema

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Q11-2.13 A full blood count shows that Sarah has a haemoglobin of 8.5 g.dl-1 (normal range
12-14). Why might she be anaemic? What effects will this have upon her?

Heavy periods or poor diet

This will exacerbate her breathlessness

Q11-2.14 Why do you think that Sarah has deteriorated recently?

The anaemia means her heart has had to work harder

Q11-2.15 What groups of drugs will be needed in her immediate treatment?

Diuretics to control pulmonary oedema

Digoxin, or β-blockers to slow down her ventricular rate
Treat anaemia – iron replacement
Also anticoagulation (warfarin) because of the risk of thrombus formation due to
atrial fibrillation

Q11-2.16 What might you do to prevent the problem recurring?

Mitral valve repair

Case 3 John

John is a 48-year-old University lecturer in physiology. He is a heavy smoker, but drinks no

alcohol. He is married and has 2 healthy children. He finds his job very stressful. John tries
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to keep fit by playing squash once a week. Recently he has noticed some chest discomfort
towards the end of a long rally. About 5 days ago this discomfort lasted for about 30 minutes,
continuing after he had stopped playing and throughout his shower.
Tonight he went to bed as usual, but awoke at 2.00 am intensely breathless. He felt as though
he was choking and had to sit on the edge of the bed, being unable to lie down flat. He
thought he was going to die. His wife dialled 999 and the ambulance service took him
immediately to the local hospital.
On admission it is obvious that he is very ill. He is sitting bolt upright on the trolley in the
casualty department.

You examine him, and discover:

He looks pale, frightened and slightly blue in colour.

He is generally cold to the touch, particularly his hands and feet.
He is sweating profusely.
His blood pressure is elevated at 210/110 mm Hg.
His breathing is very fast and noisy.
On auscultation of his chest, the heart sounds are very difficult to hear because of loud
respiratory noises (crepitations) which extend all over his chest, but are particularly
obvious at the lung bases posteriorly.

Q11-3.1 What physiological changes make him:

look pale?
feel cold to the touch?

Vasoconstriction of arterioles supply skin

(cutaneous vasculature)

Vital
SK.n is outlimp. So bled shifts to organs

Q11-3.2 Why is he sweating profusely but cold? What part of the nervous system is
responsible?

Sympathetic activity

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Q11-3.3 Why does he appear blue? Where will this cyanosis be most obvious?

Cyanosis – peripheries (fingers and toes)

poor O2 delivery to tissues

Q11-3.4 Which pacemaker will be driving John's heart?

SA node

Q11-3.5 Which branch of the autonomic nervous system will be affecting John's heart?

Sympathetic

Q11-3.6 What do you think John's cardiac output will be: normal, elevated or reduced?

Reduced

Q11-3.7 Why, then, is his arterial blood pressure so high?

Sympathetic stimulation to arterioles

Q10-3.8 What is making all of the noise in John's chest as he breathes? Why is the noise
loudest at the base of his lung?

Pulmonary oedema
The effect of gravity when standing means that the capillaries at the base of the
lungs have a higher hydrostatic pressure than those at the apices. The pulmonary
oedema is therefore greatest at the bases in the standing position.
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Q11-3.9 What do you think has happened in John's heart?

Myocardial infarction has lead to acute heart failure

Q11-3.10 Which side of the heart has been affected?

Left

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Q11-3.11 Why is John so breathless?

Pulmonary oedema

Q11-3.12 Why can't John lie down?

Pulmonary oedema is exacerbated by lying down (increased venous return to right

heart)

Q11-3.13 What do you think will be happening to:

1. the oxygen content

2. the CO2 content of John's blood?

PaO2 initially PaCO2 may fall due to increased respiratory rate or may be
normal, but eventually it can increase due to impaired gas exchange.

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Q11-3.14 What do you think might happen to John if you do nothing?

He would die

Investigations

Q11-3. 15 What would John's ECG appear like? (Draw it! - over several beats. If you are
feeling clever choose appropriate leads to make your point (see session 10))

Probably still some ST elevation (Coved S – T segment)

Inverted T wave
Pathological Q waves
Left ventricle affected - Probably anterior M.I. which wou ld be evident in the
precordial leads

Q11-3.16 From your 'Mechanisms of Disease' Module (and CVS session on IHD) - what
biochemical investigations should you perform on John's blood?

Cardiac enzymes (eg creatine kinase) or cardiac isoforms of troponins T & I

Cardiac troponins are the gold standard

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Q11-3.17 What other investigations would you perform?

chest X-ray (CXR) arterial

blood gasses (ABGs)

Treatment – immediate

Q11-3.18 How might you get more oxygen into John's blood?

O2 mask

Q11-3.19 What types of drugs would you use to treat John immediately?

Nitrates (venodilation will reduce preload (ie filling pressure) and therefore
reduce workload of heart)
Diuretics (reducing blood volume will reduce preload)
Diamorphine (Patients with acute heart failure are very anxious. Morphine will
help to reduce anxiety and also causes peripheral vasodilation; both reducing
the work of the heart)

Q11-3.20 What is the outlook for John likely to be, and how should he be treated in the
longer term?

Outlook is reasonable
Long term treatment: ACE inhibitors
Diuretics
Nitrates
(Could also include lifestyle changes and treatment with statins and aspirin in
answer)

Q11-3.21 When the immediate crisis is past, you ask John about his family history of disease
- what might he tell you?

Family history of Ischaemic heart disease

Possible diabetes
Hypercholesterolaemia

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Case 4 Arthur

Arthur is a 68-year-old retired coal miner. He has for many years suffered from chronic
bronchitis. He is quite severely incapacitated, and receives a disability pension from the Coal
Board as he was retired early because of 'dust disease' of the lungs. He lives on his own on
the 4th floor of a tower block, and relies on a neighbour to do most of his shopping for him, as
he finds it very difficult to get out, particularly in winter. He used to smoke heavily, up to 25
'roll ups' a day, but stopped 3 years ago after an admission to hospital for pneumonia. He
regularly takes medication for his lung problems, in the form of inhalers. He has a chronic
cough and produces about a cup full of creamy white sputum each day. His sputum turns
yellow if he has a chest infection, and he is prescribed antibiotics on these occasions.

Over the last month he has noticed:

1. His legs and ankles are swelling more and more - the swelling has now got up to his
mid thigh - and he can barely move his legs, which are very heavy.
His breathing problems are no worse than they have been for years.
He feels nauseous, and has lost his appetite. Despite this his weight is
increasingly rapidly.
2. Over the last few days his abdomen has begun to swell, and he now has a very
distinct pot belly.

You examine Arthur, and discover:

A weary looking, breathless man who looks older than his age.
He is slightly blue in colour, particularly his feet and hands - but warm to touch. His lips
are bluish in hue.
There is very obvious jugular venous pulsation, which is visibly pulsating up to the angle of
the jaw.
His pulse rate is fast (100 bpm) but his blood pressure is low, at 100/80.
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He has massive swelling of both his legs - extending right up into his groin, and up his back
to the mid lumbar spine.
His abdomen is swollen and distended.
His chest movements are laboured, and his chest expansion is poor, with obvious use
of all the muscles he can to breathe.
On auscultation of the chest there is evidence that air is not entering the lungs well, and
breathing sounds are very quiet.
The apex of the heart is difficult to feel, and the heart sounds are very quiet.

Think about Arthur's lungs:

Whilst you have not yet covered the respiratory system - try to work out the following from
common sense:

Q11-4.1 Do you think Arthur's lungs are easy or difficult to inflate with air?

Arthur may have extensive fibrosis due to advanced coal worker‟s pneumoconiosis
and therefore his lungs will be difficult to inflate Q11-4.2 What in principle
might change in the lungs to make it more difficult:

1. to stretch the lungs in inspiration?

2. to move air through the airways?
3. both of these?

1. Harder to stretch the lungs in inspiration due to fibrosis

2. Inflammation of airways
3. Loss of support of airways collapse

Q11-4.3 What makes Arthur's normal sputum creamy? Why does it turn yellow when he has
an infection (cf 'Mechanisms of Disease')?

Since he has suffered chronic inflammation in his lungs for a number of yea rs
inflammatory cells such as neutrophils will be present in his sputum giving it a
creamy appearance.

In addition when he suffers an infection the sputum becomes yellow reflecting the
additional presence of other white blood cells and bacterial debris

Q11-4.4 How well do you think Arthur's blood will be oxygenated as it passes through his
lungs?

Poorly

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Q11-4.5 How easy do you think it will be for Arthur's right heart to push blood through his
pulmonary circulation?

Difficult

Concerning Arthur's cardiovascular system

Q11-4.6 If Arthur is of normal size, and jugular pulsation is visible to the angle of his jaw - can
you work out what his central venous pressure will be in mm Hg? (note: Mercury is 13.6
times as dense as blood). (Hint - you will need to look at your own chest and neck and work
out roughly how far the angle of the jaw is above the right atrium when sitting at 45°).

Use sternal angle to approximate level of right atrium and measure vertical height to angle of
jaw (approx. 15cm above right atrium). You could try measuring the height of the angle of the jaw
from the sternal angle on one of your friends when they are sitting at 45o.

CVP x 13.6 = 15cm

CVP = 150mm/13.6
11mmHg

Q11-4.7 How does your estimate of Arthur's central venous pressure fit with what you know
of the normal cardiovascular system?

Much higher

Q11-4.8 Why, then, are Arthur's legs and abdomen swelling up?

Oedema secondary to hydrostatic pressure in venous system

Q11-4.9 Why does Arthur feel nauseous? (Think about swelling in the abdomen)

Hepatomegaly
Swelling of gastric mucosa

Q11-4.10 If Arthur is eating much less, why is he gaining weight?

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Oedema

Q11-4.11 Which organ in the body will be responsible for the weight gain?

Kidneys are producing less urine (salt and water retention). They are secreting
renin which activates the renin -angiotensin-aldosterone system.

Q11-4.12 Which side of Arthur's heart do you think is causing problems - the right or the left?

Right

Q11-4.13 If you were to perform a chest X-ray, what would you expect the size of Arthur's
heart to be?

May appear normal in early stages; later may be enlarged

Q11-4.14 When you perform a full blood count on Arthur - his haemoglobin level is 16 g.dl-1,
which is higher than normal. Why should Arthur's haemoglobin be elevated? What
advantage or disadvantage will it be to him? How long do you think it has been elevated?

Erythropoietin secondary to hypoxia

Advantage is O2 carrying capacity of bl ood
Disadvantage is viscosity

Your conclusions

Q11-4.15 What was the primary problem causing Arthur's condition?

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Chronic obstructive pulmonary disease (COPD) and lung fibrosis

Q11-4.16 Which side of the heart has failed - and why?

Right heart failure secondary to lung disease (cor -pulmonale)

Treatment

Q11-4.17 How, in principle, would you set about treating Arthur?

Diuretics Treat airways disease – O2, Steroids, agonists ‫كانما‬

‫ربو‬

Q11-4.18 How might you reduce his swelling?

Diuretics

Q11-4.19 How might you help his heart?

Treat the lungs

Q11-4.20 What is the long-term outlook for Arthur?

Poor

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Cardiovascular System

Session 12

Shock

The aim of this session is that you should pull together and revise a number of topics dealt
with in this module by examining the phenomenon of shock.

Structure of the session

Lecture Review of CVS module, applying what you know to shock (LT1 & LT2)

Group work Questions on shock + revision questions (seminar rooms)

Learning outcomes: By the end of this session and with appropriate self study you should be
able to:

describe the essential characteristics of shock describe the

characteristics of hypovolaemic shock describe the characteristics of
cardiogenic shock describe the characteristics of mechanical shock
describe the characteristics of anaphylactic shock describe the
characteristics of septic ('toxic') shock describe the general feature of
management of the various types of shock.

Shock
There is no unique definition of the term 'shock'. It is used to describe acute circulatory
failure with either inadequate or inappropriately distributed tissue perfusion, resulting in
generalised lack of oxygen supply to cells.
Inadequate tissue perfusion may come about in a number of ways:

1. Cardiogenic shock:
Inability of the heart to eject enough blood
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(e.g. in ischaemic cardiac damage)

2. Mechanical shock:
Due to a restriction on the filling of the heart
(e.g. Cardiac tamponade)
Obstruction to blood flow through the lungs
(e.g. Pulmonary embolism) (iii)
Hypovolaemic shock:
Due to loss of circulating fluid volume
(e.g. haemorrhage)
(iv) Normovolaemic (distributive) shock:
Due to uncontrolled falls in peripheral resistance
(e.g. in Sepsis or Anaphylaxis)

You will have considered cardiogenic shock in previous sessions. Group

work

The following questions are all designed for very brief answers (often one word). Rattle
through them as quick as you can to check your understanding.
Where you are asked a question 'What will pressure/flow/cardiac output etc., etc., be', the
answer required is one of raised, lowered, or normal, not actual numbers.

Mechanical Shock

Q12-1 What is meant by the term 'pulmonary embolism'?

Occlusion of a pulmonary artery caused by a fragment of thrombosis carried

through the blood stream must ofthe time from Peripheral deetrig

Q12-2 Where might the embolism come from (cf 'Mechanisms of Disease').

A venous thrombosis in the deep veins of the leg, occasionally the iliac veins or
i.v.c

Q12-3 What will happen to (i) the right heart (ii) the left heart if blood flow through the
pulmonary circulation is compromised?

Pressures in the right heart would increase

Blood flow to the left heart would be reduced, diastolic pressure would fall and
there would be a reduction in stroke volume and cardiac output

Q12-4 What will happen to the pressure in (i) the right atrium (ii) the left atrium?
would increase would decrease

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Q12-5 What will be the pressure in the pulmonary artery?

Increased

Q12-6 It is possible to insert a catheter into the venous side of the circulation, up into the right
atrium, through the right ventricle, and into the pulmonary artery. A pressure transducer attached to
this catheter will then read pulmonary arterial pressure. If the catheter is then pushed
forward so that it jams or 'wedges' into a branch of the pulmonary artery, the recorded
pressure will fall to match that in the left atrium. Why?

Because the catheter occludes further flow in the small vessels distal to it and
therefore communicates directly with the pulmonary veins and left atrium

Q12-7 What would this 'pulmonary arterial occlusion pressure' ('PAOP') be in the case of
pulmonary embolism?

Reduced

Q12-8 So, what will the jugular venous pressure be?

Increased

Q12-9 What will the cardiac output be?

Reduced

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Q12-10 Where will the changes in arterial blood pressure be detected physiologically?

Arterial baroreceptors in the carotid sinuses and aortic arch

‫النه تتحسس للتمدد‬

Q12-11 Which branch of the autonomic nervous system will be activated?

Sympathetic

Q12-12 What then will happen to (i) heart rate (ii) peripheral resistance?

1. heart rate would increase

2. peripheral resistance would increase

Q12-13 How might you detect poor perfusion of the periphery? What will happen to (i) the
colour (ii) the temperature of the skin?

1. bluish discolouration – cyanosis

2. feel cold

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Q12-14 Now consider a case where blood or some other fluid accumulates between the
epicardial surface of the heart and the pericardium - 'Cardiac Tamponade'.

'Cardiac Tamponade'

Q12-15 What will happen to the diastolic filling of the heart, and why?

There will be reduced filling of the ventricles in diastole as they are compressed
by the surrounding pericardial fluid

Q12-16 What, in this case, will be the (i) central venous pressure (ii) pulmonary artery
pressure (iii) left atrial pressure (iv) cardiac output?

1. raised
2. raised (iii) raised
(iv) reduced

Explanation
1. central venous pressure is raised because the heart cannot fill theref ore
blood build up in the venous system
2. pulmonary artery pressure is raised because blood cannot empty
properly from the pulmonary veins into the left atrium. This leads to
pulmonary congestion. The pulmonary vasculature has a low resistance
and normally operates at low pressure. The raised pulmonary venous
pressure can therefore be transmitted back to the pulmonary artery.
3. Left atrial pressure is raised due the compression of the heart
4. Cardiac output is reduced because the heart cannot pump adequately
because it cannot fill adequately

Q12-17 So, what will happen to the arterial pressure?

It will fall
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Q12-18 What do you need to do to help a patient with cardiac tamponade?

Remove some of the pericardial fluid (pericardiocentesis)

Q12-19 Where, precisely, will you insert your needle?

In the pericardial space, beneath the xiphisternum to avoid damaging the

coronary vessels

Hypovolaemic shock

Q12-20 What will happen to the volume of blood in the veins if a patient has suffered a
haemorrhage of, say, one litre of blood?

It will be reduced

Q12-21 What then will happen to central venous pressure?

Falls

Q12-22 So, what will happen to (i) the end diastolic volume of the heart (ii) the cardiac output
(iii) the arterial pressure?

1. falls
2. falls
3. falls

fall in venous return fall in

end diastolic volume fall
in stroke volume fall in

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cardiac output fall in

blood pressure Q12-23
Which structure will
detect the fall in arterial
blood pressure?

Baroreceptors in the carotid sinus

Q12-24 Which branch of the autonomic nervous system will be activated?

Sympathetic

Q12-25 What will happen to (i) total peripheral resistance (ii) heart rate (iii) stroke volume?

1. increases
2. increases
3. increases

Q12-26 How will the patient's hands feel?

Cold

Q12-27 What will the pulse feel like?

Rapid
Thready(weak)

Q12-28 You may wish to increase the pre-load on the patient's heart by infusing fluid. What
might you use to increase circulating fluid volume?

Blood is the fluid of choice after haemorrhage

While waiting for compatible blood, crystalloid solution (electrolytes), colloids
such as plasma, haemaccel or starches (HES) can be used

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Q12-29 What is the advantage of infusing solution containing colloid (high molecular weight
substances)? (Think about tissue fluid formation)

Increases oncotic pressure and retains fluid in the intravascular space

Q12-30 How would you know what volume to infuse?

Insert a catheter to measure central venous pressure.

Infuse fluid rapidly until the CVP rises into the upper half of the normal range

Anaphylactic Shock

Q12-31 List some chemical mediators released during anaphylaxis. (Look at your
Mechanisms of Disease module)

Histamine leukotrienes prostaglandins cytokines kinins

Q12-32 What effect do these mediators have upon vascular smooth muscle?

Vasoculation Relaxes If
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Falls

Q12-33 So what will happen to total peripheral resistance?

(*)

Q12-34 What will the patient's hands feel like? What will the patient look like?

Warm VosCilation

Q12-35 What will happen to the arterial pressure?

Falls EvE-
Q12-36 What will happen to (i) the heart rate (ii) the cardiac output?

1. heart rate increases

2. Increases (until hypovolaemia occurs due to capillary leak)

Q12-37 What will the pulse feel like?

Fast and bounding

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Q12-38 What will happen to the central venous pressure?

Falls

Q12-39 What sort of drug would you use to treat anaphylaxis?

Adrenaline is administered to overcome the hypotension caused by the extreme

vasodilation.

Septic or Toxic Shock

Q12-40 Suggest some mediators which are released during an overwhelming bacterial
infection (septicaemia)?

Bacterial derived endotoxins

Host derived inflammatory mediators – tumour necrosis factor; Interleukin - 1

Q12-41 What effect do these mediators have on vascular smooth muscle?

Relaxes vascular smooth muscle

Q12-42 What will happen to total peripheral resistance?

Falls

Q12-43 What will happen to arterial pressure?

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Falls
Q12-44 What will happen to (i) heart rate (ii) cardiac output?

1. increases
2. increases

Q12-45 What will the pulse feel like?

Fast and bounding

Q12-46 What sorts of drugs might you use to treat toxic shock?

Antibiotics
In severe toxic shock there is capillary leakage and hence colloids would have to
be given to maintain the circulating volume. The colloid increases the oncotic
pressure, drawing fluid into the capillaries.

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Practice Questions

The following questions are in a similar format to module specific questions in the ESAs. The
answers should be brief, never more than a sentence or two and often just a few words.

Q1
Brian, aged 45, is unused to exercise, but has a son aged 12 who is keen on rugby. In a
moment of foolishness Brian decided to play a short game with his son and some friends.
After a few minutes of charging around he became very breathless, and felt faint, with a tight
constricting pain in his chest. At one point his legs gave way and he stumbled and fell. After
lying down for an hour or two, however, he felt fine. After some days of deliberation he
presents himself to you, his GP.

You record Brian‟s ECG at rest and find it normal. Draw and label his lead II ECG.

Refer to text book

Max.
Mark Actual
Mark

Your ECG machine also records the augmented leads aVR, aVL, aVF. Draw Brian‟s
aVR lead ECG at rest.

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Refer to text book and note that this is an inverted image of the lead
II trace when the axis is normal

Max. Actual
Mark Mark

You decide to send Brian for an exercise stress test. In two sentences, what
does this involve?

Walking / running on a treadmill with continuous ECG monitoring whilst

increasing the level of exertion.

Max. Actual
Mark Mark

You discover evidence of poor myocardial perfusion. What changes have

you now seen in Brian‟s ECG? Why did you not see these at rest?

Depression of the ST segment in exercise. This is only evident during

exercise because, as the heart rate increases, diastole is
disproportionately shortened and therefore coronary artery filling
is compromised while the oxygen demand is increased.

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Max. Actual
Mark Mark

You arrange for Brian to have a catheter examination. A catheter inserted

into the groin is used to inject contrast medium into his coronary arteries.
List, in order, the blood vessels through which the catheter must pass to
reach the left coronary artery. List three possible „wrong turns‟ it might take
on the way.

femoral artery external

iliac artery common
iliac artery
aorta
left coronary artery

Wrong turns left

subclavian artery left
common carotid artery
brachiocephalic trunk

Actual
Max. Mark
Mark

You discover that Brian has a major occlusion in the left anterior descending
(anterior interventricular) coronary artery. Which parts of the heart might be
poorly perfused as a result?

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anterior aspect of AV septum

right and left ventricles apex

Max. Actual
Mark Mark

Q2
Rachel was born yesterday. During a routine examination with a stethoscope you detect
signs of a patent ductus arteriosus.

What abnormalities in the sounds associated with the heart beat are consistent
with a patent ductus arteriosus?
Continuous murmur throughout systole and diastole (machinery murmur)
Explanation: Since the pressure on the left side of the heart is higher
throughout the cardia c cycle blood is always moving from the aorta
to pulmonary artery.

Max. Actual
Mark Mark

After birth, in which direction will blood flow through a patent ductus? What
might be the consequences for the circulation of the baby?
left to right (aorta to pulmonary trunk) consequence:
right ventricular overload

Max. Actual
Mark Mark

Will the baby be cyanosed?

No
Explanation: Since the shunt is from left to right side blood is not bypassing
the lungs

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Actual
Max. Mark
Mark

What normally makes the ductus close at birth?

Increased oxygen levels
Explanation: The increase in oxygen level causes contraction of smooth
muscle cells

Max. Actual
Mark Mark

In the foetus, which has the highest vascular resistance – the pulmonary or
systemic vascular bed?
pulmonary

Max. Actual
Mark Mark

What is the foramen ovale?

passage between the atrial cavities in the fetus (arises after the development
of the septum secundum)

Max. Actual
Mark Mark

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What will be the consequence for the circulation if the foramen ovale does not
close at birth?

A patent foramen ovale usually has no clinical consequence.

Added information:
It can take on significance if the right atrial pressure increases
allowing a right to left shunt and mixing deoxygenated blood with
oxygenated blood in the left atrium. It can also be the route by which
a systemic venous embolism can reach the cerebral circulation and
cause a stroke.

Max. Actual
Mark Mark

What is the term for a persistent opening in the interatrial septum and where
does it most commonly occur?

atrial septal defect

Max. Actual
Mark Mark

Why might right ventricular hypertrophy develop?

The atrial septal defect allows a left to right shunt which causes right
ventricular overload

Actual
Max. Mark
Mark

Occasionally the shunt may reverse due to a rise in pulmonary vascular

resistance. What would be the consequences of this?

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hypoxia cyanosis

Max. Actual
Mark Mark

Q3
John, aged 52, considers himself fit for his age and plays badminton regularly. After his
normal Tuesday night game he becomes ill with a rapid onset of severe chest pain. He
vomited, sweated profusely and looked very pale. You suspect that John has a myocardial
infarction.

You take an ECG. Draw the ECG changes you will be looking for. Why might
these ECG changes be more prominent in some of the twelve ECG „leads‟
than others?

initial change ST elevation

later changes T-wave inversion, pathological Q -waves

The changes will be more prominent in those leads „looking at‟ the infracted
area.

Actual
Max. Mark
Mark

You note that the ECG disturbance is greatest in the ECG lead V4. Sketch the
electrode positions on the chest for leads V1-V6.

V1 4t h intercostal space (ICS) to right of sternum

V2 4t h ICS to left of sternum
V4 5t h ICS midclavicular line
V6 6t h ICS midaxillary line
(Sketch of above)

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Max. Actual
Mark Mark

You take a blood sample from John and assay it for an enzyme. Which
enzymes or enzymes did you specify? Why is its level elevated?

creatine kinase -MB

troponins (TnI and TnT; not actually enzymes, but regulatory proteins)

lactate dehydrogenase (but this is slower to peak and not so specific)

[1 mark each for any of the above]

Max. Actual
Mark Mark

You think that John has been stabilised, but a few hours later his problem becomes much worse
and he develops ventricular fibrillation.

What is VF?

ventricular fibrillation – abnormal rapid ventricular activity with loss

of co-ordinated contraction

Actual
Max. Mark
Mark

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What effect will it have on his cardiac output?

Loss of cardiac output

Actual
Max. Mark
Mark

Draw the pattern you would see on his ECG.

Max. Actual
Mark Mark

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Cardiovascular Module Workbook

What is the principle behind the use of a defibrillator? Where on John will you
place the paddles?

Depolarises the heart

Stops all electrical activity, allowing re -coordination of the cardiac impulse

Max. Actual
Mark Mark

You might also give John an injection of a local anaesthetic - lignocaine.

Describe the mechanism by which local anaesthetics prevent ventricular
fibrillation.

Lignocaine (lidocaine) blocks fast Na+ channels in the open or

refractory (inactivated) state. It associates and dissociates
rapidly, allowing the upstokes of the action potentials to take
place at a normal heart rate, but preventing premature beats. It
also binds to Na+ channels in ischaemic tissue which is
depolarised

Max. Actual
Mark Mark

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Q4
Clare, aged 37, is a dynamic public relations consultant who leads a hectic life. Over the past
few days she has experienced increasingly frequent episodes of chest pain, described as
heaviness or tightness in her chest. Initially the chest pain occurred on exertion, but now it is
occurring at rest. Clare is admitted to hospital and a blood sample is taken for assay of
cardiac enzyme(s). They are not elevated, but during her episode of chest pain there are
ECG changes suggestive of severely reduced coronary perfusion which disappears once the
pain recedes.

What is likely to be reducing coronary blood flow in Clare‟s case?

Unstable atheromatous plaque ruptures leading to thrombus

formation and vasoconstriction (unstable angina)

Max. Actual
Mark Mark

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You decide to treat Clare with glyceryl trinitrate. What does this drug do? By
what mechanism?

Reduces the workload of the heart by causing venodilation (this reduces

preload)
Also causes dilation of arteries (not arterioles) including collateral coronary
arteries and may improve blood supply to the heart

Mechanism of action – relaxation of vascular smooth muscle

Max. Actual
Mark Mark

You treat Clare with a ‫ ك‬Blocker. Name 3 organs in the body on which a non-
selective ‫ ك‬adrenoreceptor antagonist will act. List in each one the effects of
its action.

heart – slow heart rate and reduce contractility lungs

– bronchoconstriction
blood vessels in skeletal and cardiac muscle – vasoconstriction via
blocking β2receptors
(if it was very unselective and also acted at α1 receptors on
peripheral vessels it would cause vasodilation) liver –
decrease glycogenolysis

[1 mark each for tissue and correct action]

Max. Actual
Mark Mark

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Q5
Janet, aged 48, has been suffering from frequent headaches over the past few months. You
suspect she has hypertension.

List the critical steps in measuring Janet‟s blood pressure normally.

Select the correct cuff size and fit correctly

Inflate cuff around upper arm whilst palpating the radial pulse
Inflate to 30mmHg above the point where the pulse disappears
Release pulse slowly, listening with stethoscope over brachial artery
First Korotkoff sound = systolic pressure
Fifth Korotkoff sound (where sounds disappear) = diastolic pressure

Max. Actual
Mark Mark

What values would you consider as indicating hypertension?

systolic > 140 mmHg diastolic

> 90 mmHg

but there is wide inter-individual variation

Actual
Max. Mark
Mark

You decide to treat Janet with diuretics (drugs to increase urine production).
Why?

reduce circulating volume and thus reduce cardiac output

note: mean aBP = CO x TPR

Actual
Max. Mark
Mark

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Describe the changes which will have taken place in Janet‟s blood vessels if
she has been hypertensive for some time.

atheroma development
weakening of blood vessel walls

Max. Actual
Mark Mark

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Where in the body could you directly visualise these changes?

retina

Max. Actual
Mark Mark

Q6
Shane is 19 years old and feels himself to be very fit. He plays football regularly, but has
always been aware that on exercise his heartbeat is very obvious to him, though his exercise
tolerance is good. He presents to you for a routine medical as he is due to start work as a
British Telecom technician.

You detect that he has a forceful apex beat and a loud mid systolic murmur.
Explain why these signs are consistent with a diagnosis of aortic stenosis.

Forceful apex beat suggests left ventricular hypertrophy. (The left

ventricle will hypertrophy since it has to work harder to push blood out
of the stenosed aortic valve.)
Loud systolic murmur occurs due to turbulent blood flow through the
stenosed aortic valve as blood is ejected in syst ole.

Max. Actual
Mark Mark

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You send Shane to the catheter laboratory, where a catheter is inserted into
an artery in his groin and pushed towards the heart, into the left ventricle and
then withdrawn over the aortic valve. Describe and explain the pressure
recorded as the catheter moves from the ventricle through the aortic stenosis.
How might these pressure changes tell you how severe the stenosis is? (Hint:
think about pressure flow and resistance)

There would be a marked drop in systolic pressure between the left

ventricle and the aorta. The more severe the stenosis, the greater
the pressure drop would be.

Max. Actual
Mark Mark

Why would he have left ventricular hypertrophy?

The left ventricle will hypertrophy since it has to work harder to

push blood out of the stenosed aortic valve.

Max. Actual
Mark Mark

What will have happened to the electrical axis of Shane‟s heart?

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There may be left axis deviation (but not always)

Max. Actual
Mark Mark

Why might he later present with angina?

The increased workload of the heart increases oxygen demand. Also

oxygen supply is compromised because reduced aortic pressure and
elevated left ventricular diastolic pressure makes it harder to fill the
coronary arteries.

Max. Actual
Mark Mark

Q7
Bert, aged 76, is having trouble with his left leg. It often feels cold, and minor abrasions
take an inordinate time to heal. You suspect that he has an occlusion of one of the
arteries supplying the limb.

What is the most common cause of peripheral vascular disease?

atheroma development
Max. Actual
Mark Mark

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What are the risk factors? List 4.

smoking
diabetes
hypertension
hyperlipidaemia or hypercholesterolaemia
positive family history
Max. obesity Actual
Mark Mark

2
Why will you place your finger on the top of Bert‟s foot? What will you be
feeling for, and why might the changes you feel indicate an arterial occlusion?

To feel for the dorsalis pedis pulse

An absent pulse may indicate occlusion of arteries proximal to the pulse.

Max. Actual
Mark Mark

Name three arteries would you consider as potential sites for the occlusion?
How might you determine where the occlusion is?

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anterior tibial artery

popliteal artery femoral
artery

If the pulse is present in both the femoral and popliteal arteries,

but absent from the dorsalis pedis, then the occlusion is likely to be
in the anterior tibial artery
If the pulse is absent in the popliteal artery, but present in the
femoral artery, then the occlusion is likely to be in the femoral
artery distal to the point at which the pulse was measured. (note:
an arteriogram can be used to confirm the exact site)

Max. Actual
Mark Mark

You decide to replace the damaged section of artery with an artificial graft.
During the operation you cross clamp Bert‟s abdominal aorta in order to work
on the blood vessels. What will happen to the resistance vessels in Bert‟s
lower body during the period of cross clamp?

There will be an increase in the pressure in the resistance vessels proximal

to the clamp and a reduction distal to the clamp.

Max. Actual
Mark Mark

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