Clinical ECG (electrocardiography)

Clinical ECG (Electrocardiography)


Clinical ECG also known as electrocardiography is a non invasive diagnostic tool which measures the hearts electrical activity by the means of recording electrodes, these electrodes are applied to the outer extremities and chest region.

Electrocardiography has moved on a lot in the last 40 years the introduction of ECG exercise stress testing and advanced digital signal processing methods mean enhanced electrocardiography. Physicians can now investigate and treat cardiac related arrhythmias much sooner than before.

This dissertation will cover anatomy and physiology of the heart and display various diseases and conditions related within. An experiment will be conducted to show rate and rhythm change due to lifestyle and smoking habits, tobacco smoking increases the risk of cardiac death possibly by altering the substrate for propagation or introduce heart related disease such as pulmonary hypertension, arterial stenosis and other diseases which can cause ventricular tachyarrhythmias. To test this hypothesis, 3 subjects were tested one of which was a smoker. Various heart diseases which were obtained from participants ECG waveform are discussed in this report. Various factors were addressed where ethical issues were concerned.


I would like to express my gratitude to all those who gave me the possibility to complete this dissertation. I want to thank the Department of Medical Engineering for giving me permission to commence this dissertation in the first instance, to do the necessary research work and to use departmental laboratory.

I am deeply indebted to my supervisor Dr. M. Youseffi from the University of Bradford whose help, stimulating suggestions and encouragement helped me in writing of this dissertation.

I want to thank all the participants for their help and involvement in research, and finally a big thanks to my family for their support and suggestions for improvement.

1. Introduction

1.1 General

This project is about clinical ECG and how this diagnostic tool is used in everyday clinical applications. ECG has transformed how clinicians can view and diagnose the heart without invasive action. Although the method of ECG has never really changed dramatically, a few leads with electrodes attached to the patients outer skin is all that makes this vital diagnostic tool. We will discuss the hearts anatomy and physiology and how the ECG can diagnose and treat cardiac arrhythmias. We will discuss some common signs for early disease and how the waveform can illustrate vital information about a particular heart, and show how lifestyle can influence heart rate/rhythm.

1.2 Historical background

ECG has been around for many years it was first introduced in the late 80s and has transformed a lot in the last 40 years. Early ECG recordings were made by putting both the patients arms and leg in a bucket of salty water and putting a wire from an instrument for measuring changes in electrical current. Modern electrocardiographs are more sophisticated but work on the same principles, using electrodes (metal plates or plastic patches covered in a gel) and leads instead of wires and buckets of water. Nowadays a 12 lead ECG has involved in routine usage including new ECG testing such as exercise stress tests and the introduction of advanced digital signal processing methods mean enhanced electrocardiography.

1.3 The topic research

I will research many areas of ECG, these will include introduction to clinical ECG the usage of ECG, the heart in detail which will cover chambers of the heart, passageways, structure of the heart and overall heart function. We will further look into heart disease and what causes poor heart function and performance especially when smoking is introduced. An experiment will be conducted which will show the difference of heart performance and general overview of a normal heart, athletics heart and a smokers heart. The experiment will discuss how heart performance can be affected for each subject after external exercise is applied and how a smoking subjects heart copes with the above including the analysis of the results.

1.4 Discussions of aims & objectives

1.4.1 Aims

Understanding the hearts functions and how the heart does its jobs, to understand how the heart is performing and what causes the heart to detoriate and its consequences. To show how smoking can affect heat rate and rhythm.

1.4.2 Objectives

How waveforms correspond to heart functions, how ECG can detect heart arrhythmias. Including showing how heart function/performance can be affected due to lifestyle using basic lead II experiment.

1.5 Scope of dissertation


This whole report will focus on heart function and what happens if the heart does not perform normal. We will discuss common diseases and how waveforms can diagnose heart arrhythmia. we cannot include personal patient information all patients will be identified as subjects a, b, c etc. a monitoring ECG lead II will be used for the experiment. the results not to be 100% accurate, as 12 lead ECG is required for diagnosis.

1.5.2.Chapter summary

The first chapter will discuss the introduction of this project. Chapter two will be on clinical ECG and what the ECG waveform tells us. This will be followed by the anatomy and physiology of the heart which will talk about the hearts internal and external features and their functions. Chapter four will focus on heart diseases and their causes including treatments followed by ECG interpretation this chapter is vital in understanding what the waveform is telling us about the heart in question. Chapter six is on basic understanding of leads and what the leads mean and their position on the body. The final chapter will be the experiment; this will include the preparation/design of the experiment including the results/analysis.

Chapter 2 Introduction to ECG

Summary of chapter

In this chapter we are going to look at what ECG is and the usages of clinical ECG. We will also discuss what each part of the ECG waveform means in terms of information and how the waveform corresponds to the physiology of the heart.


  • Explain ECG and its role in medical care
  • Discuss the components of the ECG
  • What the letters of the ECG correspond to

2.1 Definition of ECG

The heart beats in an arithmetic manner whilst pumping blood around the body. In order to measure this electrical process, Electrocardiogram (ECG) is a form of test that can measure this.

Just as the electrical activity of the pacemaker is communicated to the cardiac muscle, echoes of the depolarization and repolarization of the heart are sent through the rest of the body. By placing a pair of very sensitive receivers (electrodes) on a patients body, echoes of the hearts electrical activity can be detected. The record of the electrical signal is called an electrocardiogram (ECG).

Whilst the heart beats, it produces electrical impulses. This is recorded by the ECG. The electrical impulses can show the hearts condition and any heart disorders that may exist.

In order to monitor a patients response to a treatment we can use ECGs. Moreover, this information is vital as it can reveal any heart arrhythmias in the patient.

The information gathered from ECG can be used to diagnose all types of illness. On the other hand ECG can also be used to monitor how patient is coping with treatment.

* It is important to take an electrocardiogram of patients whom suggest symptoms of angina, dyspnoea or palpitations or those who feel there heart is at an abnormal rate.

2.2 Usage of ECG

  • ECG can show abnormalities of the heart these can include diseases in the coronary arteries. But heart rate will be normal at rest so an exercise stress test is performed if narrowing is suspected.
  • If the patient has had a recent heart attack or earlier attack this can be picked up in a ECG recording.
  • An ECG can be used for seeing how the patient is responding to treatment
  • Can show bradycardia/slow heart rate or tachycardia/fast heart rate rhythm abnormalities.
  • Can show ventricular hypertrophy/increase in heart muscle can be due to high blood pressure
  • To detect a lack of minerals in the erythrocytes

The recordings of the ECG is usually a pattern of a baseline broken by a p wave, a QRS complex and a t wave. Because the ECG reflects the electrical activity of the heart. If there are interruptions of the electrical signal generation or transmission, the ECG changes. These changes can be useful in diagnosing changes within the heart.

Components of the ECG

  • The baseline (isoelectric line) is a straight line on the ECG. It is point of departure of the electrical activity of the cardiac cycle.
  • The p wave results from atrial depolarization
  • QRS complex is a result of ventricular depolarization and initiates ventricular contraction.
  • The t wave results from ventricular repolarization.
  • An interval is part of the ECG containing at least one wave and a straight line.
  • A segment is the period of time between two waves.

Chapter 3 Anatomy and Physiology of the heart

Summary of chapter

In this chapter we will examine the heart in detail. We will look at the anatomy and physiology of the heart. We will examine different sections of the heart and their roles. We will discuss the pathways and channels the heart uses to deliver blood to the cells.


  • Understanding the role of the heart
  • Examining the heart in sections
  • Circulatory system

3.1 Examining the heart

All cells need oxygen and nutrients to survive. They receive this from the surrounding fluid i.e. blood. Blood can only provide oxygen and nutrients and remove waste products only when in motion known as homeostasis. As soon as blood remains stationary, waste removal stops, ligands e.g. hormones or leukocytes e.g. white blood cells cannot reach destination. So ultimately the whole cardiovascular system relies on the heart.

Unlike most other muscles, the heart never rests. The heart has a pumping capacity of 8000 litres of blood per day around the body and also beats at a rate of 100,000 times on average each day. This shows that it is a very powerful organ working hard to keep us going. We will now examine the heart and its surroundings in further detail.

The main function of the heart is to deliver oxygen-rich blood to all the cells in the body.

Arteries are pathways to deliver blood and the veins are the passageways through which the blood is collected and returned to the heart. The adult heart weighs between 200 to 425 grams (7 to 15 ounces) and is about the size of your fist. Your heart is a muscle which, unlike other muscles of the body, has to work round the clock to keep your blood circulating.

3.2 The heart in detail

To understand the anatomy and function, we have divided the heart into two sections; the interior and exterior. In this chapter we are going to examine both sections in further detail.

3.2.1 Interior

Vena Cava the vena cava is a large vein that brings the deoxygenated (impure) blood back to the heart and empties it in the right atrium.

Aorta the aorta is the largest artery which collects blood pumped from left ventricle to branch and deliver the oxygen rich blood to various organs and tissues in the human body.

Pulmonary arteries as part of the pulmonary circulation, pulmonary arteries carry the de-oxygenated blood from the right ventricles to the lungs for oxygenation

Pulmonary veins blood, after oxygenation in the lungs, is brought back to the heart by pulmonary veins and delivered to the left atrium.

Atria there are two atria (right & left), which are two of the four muscular chambers of the heart.

The right Atrium fills the right ventricles with deoxygenated blood which was collected from the vena cava. This delivery is regulated by the tricuspid valve.

The left atrium collects the oxygenated blood and fills the left ventricle. This delivery is regulated by the mitral valve.

The right ventricle collects the impure blood from the right atrium and delivers it to the lungs for purification. This delivery is regulated by the pulmonary valve.

The left Ventricle collects the pure blood from left atrium and delivers to Aorta which pumps it around the body. This delivery is regulated by Aortic valve.

3.3 Chambers of the heart.

The heart (cardia) is a muscular pump with four (4) separate chambers into which enter the major blood vessels carrying blood to and from the rest of the body. The upper two chambers (atria) which receive blood are much smaller than the two lower chambers (ventricles) which pump it out. Two associated with each circuit. The right side of the heart receives blood from the systemic circuit i.e. the right atrium which then collects in the right ventricle ready to pump into the pulmonary circuit and empties it into the left ventricle, which then contracts, ejecting blood into the systemic circuit. When the heart beats, both the atrias and ventricles contract and eject the same amount of blood volume into the systemic/pulmonary circuits.

The right side of the heart deals with blood that has been used throughout the body and so is depleted i.e. starved of oxygen. This blood comes into the heart via the upper right chamber, passes immediately through a valve (in this case the Tricuspid Valve) into the lower right chamber where it is pumped out into the lungs where the poisonous carbon dioxide it has collected in the body is removed and the blood is replenished with oxygen. The oxygen-enriched blood is then dealt with by the left side of the heart. Blood enters the left atrium and is pumped out through the lower left ventricle to the complete body.

The four chambers of the heart are roughly similar in shape but the left side, which has to be strong enough to pump blood to the furthest parts of the body even fingers and toes are larger and more muscular. The two sides of the heart are completely sealed from one another. To get from one side of the heart to another, blood has to go through the lungs or the entire circulatory system.

When it leaves the heart, blood passes into major artery, the aorta, and from there travels along the network of arteries into smaller arterioles and finally into capillaries from where it is absorbed into the cells. From there it moves back through the veins to the heart again, completing the cycle. It takes about twenty seconds for one blood cell to complete the full cycle. In the major arteries blood travels at about two kilometres an hour. Each contraction moves about 80mLs of blood, that adds up to over 8000 litres a day.

3.3a electrical system of the heart

The heart rate is regulated by electrical impulses generated by the pacemaker within the heart. Without any assistance, the heart would beat about forty times a minute. This would not be enough for all the activities the body is required to perform so there is a sort of spark plug to push the rate up higher. This consists of a group of special nerves, forming what is commonly known as a pacemaker, which produces an electrical charge and raises the heart rate as demand requires. The pacemaker is located on the right atrium, and a large nerve (the bundle of his) connects it to the two ventricles.

The hearts pumping energy comes from a built-in electrical conduction system. The Sino atrial (SA) node is the natural pacemaker, which when electrical impulse is released causes the atria to contract. The signal is then passed on to the antrio ventricular (AV) node and then to the conduction pathways (bundle of His) to provide electrical stimulus to the ventricles. In normal circumstances, this heart continues to pump for our entire life. If the pumping system fails in any way the patient will become severely ill or die. This will be discussed in more detail later.

3.4 The heartbeat

The heart is a pump and each contraction of the heart represents one heartbeat. Pulse or Heart Rate is the amount of beats for every 60 seconds. The heart rate is controlled by the brain, which depends on age, stress, exercise, surrounding temperature, hormones etc. The heartbeat is a two part pumping action. Systole (contraction) and Diastole (relaxation).

Systole (ventricular contraction)

Activities in systole which happen are:

  • The tricuspid and mitral valve shut to stop regurgitation occuring into the respective atria;
  • Blood from the right ventricle is pumped into lungs through Pulmonary artery;
  • Left ventricle pumps blood to the rest of the body via the Aorta;

Ventricular contraction

  • The Vena cava empties the oxygen starved blood into the top right atrium;
  • The pulmonary veins empty the oxygen rich blood in to left atrium;

In a normal resting adult, the heat beats 60-80 times per minute, which means all the above happens in less than a second.

Diastole (ventricular relaxation)

Activities in diastole which happen are:

  • The tricuspid and the mitral valves open;
  • Deoxygenated blood travels from right atrium to right ventricle;
  • Oxygen rich blood flows from the left atrium to the left ventricle.

In a normal resting adult, the heat beats 60-80 times per minute, which means all the above happens in less than a second.

Although the heart generates its own beat, the heart rate (beats per minute or BPM) and strength of contraction of the heart are modified by the sympathetic and parasympathetic divisions of the autonomic nervous system.

The sympathetic system acts as an accelerator, speeding up and increasing the hearts contractile force. Whenever demand for oxygen rise, e.g. exercise, feeling scared or if blood pressure drops, the sympathetic input increases, this causing the contraction and HR to increase. Sympathetic influence increases during inhalation.

The parasympathetic input acts like a brake, slowing down the heart. When you relax, the heart rate reduces due to parasympathetic input kicking in. Parasympathetic influence increases during exhalation.

3.5 Heart valves

The main function of the valves is to regulate and prevent the backflow of the blood. There are four important valves in the heart.

Tricuspid Valve

This valve is located between the two right chambers, the right atrium and right ventricle. When the right atrium is filled with deoxygenated blood and when it contracts, it is pumped into the right ventricle through this valve. When the right ventricle contracts this causes the valve to shut to prevent any backflow into the right atrium. . The valve is made from three cusps of tough cartilage, and this is how its name is derived.

Mitral Valve

This valve is located between the left chambers of the heart, the left atrium and the left ventricle. When contraction occurs blood is pumped from the left atrium into the left ventricle via the mitral valve, when the left ventricle contracts and pumps the blood around the body it once again causes the mitral valve to shut to stop any regurgitation back into the left atrium.

Pulmonary Valve

The pulmonary valve coordinates the oxygen depleted blood from the right ventricles to the lungs for purification.

Aortic Valve

This valve delivers rich oxygenated blood to the rest of the body via the left ventricle.

3.6 Exterior

The Pericardium

The pericardium is the fluid filled sac that surrounds the heart. The heart literally floats in this pericardial fluid. To make this clear lets give the example of a fist pushing inside a balloon. The fist is the heart and the balloon is the pericardium. The air space between the balloon and fist is called the pericardium cavity.

The lining of the pericardium is a subtle serous membrane. This membrane is known as visceral pericardium, or epicardium. We will discuss the linings of the heart muscles later.

The pericardium cavity is filled with pericardial fluid, this is around 10 20 ml of fluid and is secreted from the lining membrane it acts as a lubricant which stops friction between the pericardial membranes.

The pericardium has several functions to keep the heart within the chest cavity. To prevent over expansion of the heart due to increase blood volume.

3.7 The Heart Wall

A section through the hearts wall shows three layers: an outer Epicardium, a middle Myocardium, and an inner Endocardium.


This is the outer layer of the heart and acts as the protective layer due to it having underlying connective tissue.


The middle layer or myocardium is the thickest and most important. It consists mostly of muscle and it is the contraction and relaxation of this muscle that results in the hearts pumping action.


The innermost layer is called the endocardium and is a thin smooth lining for the inner surfaces of the heart chambers and valves.

3.8 The Pulmonary and Systemic Circulation

The circulatory system provides oxygen, nutrients and other critical substances to all the cells in the body and at the same time removing waste products. Cardiovascular system is another name for this. It consists of the heart, blood and blood vessels. Whilst blood circulates it collects oxygen through gas exchange in the lungs, a ligand e.g. hormone in the blood stream and nutrients which are then given to all the cells in the body. Waste products such as cellular waste and poison gases such as carbon dioxide which are then excreted by the kidneys and lungs.

Arteries are passageways through which the blood is delivered and the veins are the passageways through which the blood is collected and returned to the heart. Blood travels through a sophisticated network of pathways, ultimately leading to the delivery of oxygen and nutrients and waste removal to the cells. This pathway can be divided into the pulmonary and systemic circuit. The pulmonary circuit deals with blood entering and exiting the gas exchange surfaces of the lungs and the systemic circuit which transports oxygenated blood around the body and back. Each circuit begins and ends at the heart, and blood travels through these circuits in sequence. For e.g. blood returning to the heart from the systemic circuit before re-entering the systemic circuit.

Blood first travels away from the heart by the arteries which interconnect with veins. This connection is done by the capillaries which join to both the smallest arteries and the smallest veins. These capillaries which are small, thin walled and are known as exchange vessels, because of these properties nutrients, oxygen and waste removal are done between the blood and surrounding tissues via the capillaries.

3.9 Blood vessels

The body has a number of vessels, Such as arteries, capillaries and veins. They deliver blood to all the body and back again by the heart in a fixed system of closed tubes. The oxygenated blood is carried by the arteries and deoxygenated blood from the veins.

An image of the main components of the human circulatory system. The heart (placed between the lungs) delivers blood to the lungs, where it picks up oxygen and circulates it throughout the body by means of a system of blood vessels. (Reproduced by permission of The Stock Market.)The arteries at first are big in diameter but branch out into small vessels known as arterioles which can be buried deep in tissues. Arterioles can further branch into small vessels such as capillaries. The blood can exchange oxygen and other nutrients through the walls of the capillaries. At the same time capillaries turn into small veins known as venules, these will increase and grow into veins which will take away blood back to the heart.

Exchange of nutrients is done only in the capillaries due to the fact it has a thin wall made of a single cell thick.

The walls of capillaries are only one cell thick. Of all the blood vessels, only capillaries have walls thin enough to allow the exchange of materials between cells and the blood

The structures are different in each of them. All have a small hollow centre but the walls of the arteries are much more thicker and stronger which gives it the capabilities of being elastic so it can expand as blood is travelling through them as the heart beats.

The veins are much more flexible and can return blood back to the heart by the skeletal muscle which contracts against them and pushes the blood along. Inside the veins are valves which prevent the blood flowing back.

Chapter 4 types of heart diseases

Summary of chapter

This whole chapter will look at the hearts mal function and its consequences. We will see what causes the heart to fail and its treatments. We will discuss common diseases that affect the heart and its performance. Many different types of disease can affect different parts of the heart and also the surrounding organs.


  • Explain what a failing heart is
  • Common conditions that affect the heart
  • Common diseases that affect the hearts performance
  • Treatments

4.1 Understanding of heart failures.

First off heart failure is a condition and not a disease. The heart cannot pump sufficient amounts of blood to meet the tissues needs. The heart starts to weaken this is normally over a period of time. As the filled chambers cannot pump all its contents, fluid build up occurs this can happen in the tissues and lungs also known as congestion.

The heart can fail in several ways either by the muscle wall becoming too thin and fragile to an extent that they dilate (stretch) so much that there is not enough force to deliver the blood all round the body. The muscles can increase in size or thicken. This can lead to less elasticity. The chambers cannot collect enough blood so in turn the tissues are deprived of their needs. Sometimes abnormal heart valves can fail leading to regurgitation or even stenosis. The valves (tricuspid, mitral) control the blood flow which enters or leaves the heart. They can narrow causing aortic stenosis, this leads to blood backing up. Sometimes the valves cannot shut properly causing blood to leak; this is a common problem with the mitral valve due to heart failures.

The shape of the heart can change over time due to the body compensating for abnormal pumping which is called remodelling. Heart failures can effect specific parts of the body this depends if the failure occurs right/left side of the heart. However the failure takes place, body organs lack the nutrients and oxygen they need and waste removal is reduced, over time breakdown of vital systems is introduced.

Left-ventricular heart failure. Failures of the right side of the heart tend to be less common then the left side of the heart. This can be due to contraction or relaxation abnormalities. Systolic/diastolic.

Systolic. Systolic heart failures are problems in contraction. The muscles are weak and find it hard to pump sufficient amounts of blood. The dilation of left ventricles causes blood to accumulate in the lungs; this is known as pulmonary edema. Usually occurring in people aged between 50+ who have had myocardial infarction previously.

Diastolic. Diastolic is problems with filling up. The left ventricles can become thick and stiff when this happens the muscle cannot relax as normal, so the chamber of the heart cannot fill up full, as this happens fluid which enters the heart is backed up. The affects of this is the swelling up of the veins and tissues which surrounds the heart (congested). Patients with high blood pressure obese are prone to diastolic failures typically.

Right-ventricular heart failure. RVHF is normally due to failure of the left side of the heart. Because the right hand side of the heart collects bloods, any failures here causes a back log of blood as a result swelling of ankles, feet and abdomen are common.

Ejection fraction (EF) calculation is used by doctors to calculate the severity of heart failure. This shows the % of blood which is being pumped out by the heart (left ventricle) at each beat. Ejection fractions are considered normal between 50 70 %.

Those classified with having LVHF tend to have a preserved (EF) of over 50% or a reduced (EF) less than 50%.


Causes of heart failure can come about in many ways. It can be from circulation abnormal condition, or end stage cardiac arrhythmia, it can even be direct. The heart tries to correct/compensate for abnormal behaviour caused by these conditions, which over time can lead to failure. This is known as remodelling. What ever the case may be, the weaker the pumping action of the heart will mean less blood travelling to the kidneys on turn this will cause the retention of h2o and n+ which causes edema, this can cause damage to other parts of the body.

4.2 High blood pressure

Also known as hypertension, this condition is one of the biggest contributors to heart failure in absence of (MI). The arteries become hardened, brittle and can rupture, causing a stroke, heart attack or other serious injury to vital organs. The muscle of the heart will thicken to compensate for the increased hypertension. The power of the contractions will get weak over time and cause problems in relaxing in reality the natural filling of the heart will be prevented.

The identifiable causes include smoking, obesity, kidney disease, even medicine such as the contraceptive pill and other diseases too. Hypertension can be prevented by keeping the weight low and not eating excessive amounts of salts and even not smoking. Doing exercise helps keep the blood pressure low.

4.3 Palpitations

Palpitations are strong rapid heart beats, which may be irregular. They can occur during exercise, anxiety and stress but settle quiet quickly. Almost everyone will experience some sort of palpitation. Attacks can last as short as a few seconds or even hours. Palpitations can indicate heart problems such as poor heart functions.

4.4 Cor pulmonale

Cor Pulmonale is also known as pulmonary hypertension or right heart failure. This is reflected by the right side of the heart being enlarged due to it working hard. The right side of the heart deals with the pulmonary circuit or blood being sent to the lungs for purification this can cause high blood pressure in the lungs. The reason for the high blood pressure is simply because due to lung damage the heart has to work a little harder than usual to pass blood through them. This can be due to emphysema i.e. smoking, in haled coal dust or asbestos, this contributes to lung damage. Because of persistent high blood pressure this causes more damage to the arteries further more inadequate oxygen enters the blood. Medication can be given to strengthen the heart and oxygen can be provided to help with shortness of breath.

4.5 Coronary arterial disease

Process called atherosclerosis commonly called "hardening of the arteries". Its the most common cause for (MI). Due to stenosis build up this can be plaque / cholesterol build-up in the arteries. The narrowed arteries affect the pumping mechanism of the left side of the heart. This causes angina. If it becomes totally blocked the patients will suffer a myocardial infarction.

3.5.1 Damage after a heart attack

Now a days more people survive a heart attack, but the physical damage done to the muscles can further develop heart failures.

4.6 Cardiomyopathy

Cardiomyopathy means enlarged heart muscle disease. Disease and weakness of the heart muscle such as this are very common in older people due to the aging process. Almost any disease from an infection to a heart attack can cause cardiomyopathy. This disease damages the hearts muscle, which can lead to failure of the heart. Failures such as dilation (thinning) out of the muscle or make it hypertrophic (thick). Hypertrophic cardiomyopathy makes the muscle thick and contraction can be a problem, this would be loss of power in the heart muscle cells. To compensate this, the muscle cells grow. Dilated cardiomyopathy is the enlarged ventricles, the muscle is thin and the delivery of blood is reduced. It is indicated that viruses such as Coxsackie virus or other infections may be involved, where the persons antibodies fight its own proteins in the heart mistaking them for foreign bacteria.

4.7 Heart murmur

A heart murmur is abnormal sounds from the heart which can be heard by a stethoscope or any other device. The heart rhythm associated with abnormalities. Conditions such as extrasystoles (extra heart beats), rapid or slow beats are not murmurs. Heart murmurs is are caused by a disturbance to the smooth flow of blood through the heart, due to an abnormality in one of the four valves in the heart (e.g. abnormal hole between two chambers) or an increased rate of flow through the heart. Many murmurs are of no consequence and may disappear (in case of infant) as they get older. The heart has two main sounds. Caused by the closing of different valves. Murmurs heard between the first and second heart sounds are called systolic murmurs, and may be caused by vigorous exercise, leakage of the mitral/tricuspid valves. Narrowing of the pulmonary and aortic valves, a high fever or even a heart disease. Murmurs heard after the second heart sounds are called diastolic murmurs. They may be caused by narrowing of the mitral or tricuspid valves, a hole in the heart or anaemia. Other less common murmurs may be due to high blood pressure in the lungs or even disturbances in the electrical conduction pathways.

4.8 Heart infections

Introduction to heart infections

4.8.1 Endocarditis.

Endocarditis is a bacterial/fungal infection inside the heart normally in heart valves causing malfunction of heart valves. The infection causes clumps of bacteria to grow inside the heart or even infection from external such as respiratory or intravenous drug users which enters the blood stream and rests at the heart valves, and pieces can break off and travel through the arteries to cause problems elsewhere such as blindness, kidney failure, joint damage and bowel problems. It is diagnosed by taking blood and culturing it in a laboratory in order to detect any bacteria and an ECG may also be diagnostic. Large doses of antibiotics, often penicillin are given by injection for weeks.

4.8.2 Myocarditis

Myocarditis is a serious bacterial, viral (most common), parasitis (rare) or fungal (most serious) infection of the muscle in the heart wall. Myocarditis may also be due to an inflammation of the heart muscle caused by poison, toxins, irradiation and drugs e.g. cytotoxics used in cancer treatments.

Heart failure may develop as damaged heart muscles cannot contract normally. An ECG, blood test and echocardiogram confirm the diagnosis. The treatment depends on the cause of the problem, bacterial infections can be cured by antibiotics, but there is no real treatment for viral myocarditis which can lead to heart damage.

4.8.3 Pericarditis

Pericarditis is the inflammation or infection of the pericardium. It can be caused by viral i.e. influenza or bacterial infection. My also occur if the pericardium is affected by the spread of cancer cells from the lungs, lymph nodes other causes include tuberculosis of kidney failure. All forms cause chest pains, shortness of breath and a fever. The secretion of fluid by the damaged pericardium in to the tiny space between the heart puts pressure on the heart. In this case the heart may not be able to expand fully between each beats and becomes restricted. Causing the heart to fail as a pump (constrictive pericarditis). A pericardial effusion (collection of fluid within the pericardial sac) can be treated by inserting a needle through the chest wall and draining the fluid out.

4.9 Pulmonary embolism

A pulmonary embolism is when a clot, can be either blood or any other substance i.e. fatty plaque from high cholesterol which lodges itself into a smaller artery in the lungs. This restricts blood flow into that particular are and eventually that segment of lung will die. Pulmonary embolism can occur commonly after major surgery. Symptoms can include fainting, increased heart rate, anxiety, sweating, chest pains and even passing out. Cor pulmonale can occur due to back up pressure on the heart.

4.10 Pulmonary valve stenosis

The narrowing of the valve which regulates blood flow from the right ventricle to the pulmonary artery is called stenosis. It is usually a birth defect. Severe stenosis may cause chest pain, fainting and shortness of breath and must be corrected surgically. It is diagnosed by echocardiography (ultrasound scan). If left untreated can lead to sudden death.

4.11 Sinus Bradycardia

A slow heart rate (below 60 beats per min at rest) is felt by the patients as a slow pulse in their wrist or neck. This can be seen in very fit athletes due to the fact each beat produces more then enough oxygen as the ventricles is big and strong, the very old, patients who are recovering from a serious illness. Provided there is no serious underlying disease, a slow pulse (bradycardia) is not dangerous. Conditions such as blood pressure drop and heart rate slows can occur in a faint. Other causes may include such as a heart attack, congestive cardiac failure (damaged heart is unable to beat effectively) sick sinus syndrome and damage to the heart pacemaker. Other diseases that effect the heart and its function, may also cause bradycardia, including an under active thyroid gland (hypothyroidism), tumours, cancers and an increase in the pressure of the fluid surrounding the brain (cerebrospinal fluid).

4.12 Sinus tachycardia

Tachycardia indicates a rapid heart rate above the normal resting rate around 100 to 150 beats per minute. One reason for this condition can be oxygen levels drop, so the beats are faster to get the nutrients around the body. Because the beats are faster, patients may become excessively tired. Causes include exertion, fear or emotions, drinking a lot of caffeine, smoking, diseases e.g. anaemia, over active thyroid gland, kidney or liver disease even heart disease such as ventricular tachycardia or paroxysmal atrial, and drugs e.g. thyroxine, appetite suppressants. An ECG will show tachycardia and sometimes its cause. Blood and other tests will be necessary to find the cause, and this will determine the treatment.

4.13 Rheumatic fever

Rheumatic fever is seen as damage to the heart valves by inflammation this is normally due to bacterial infection. This used to be very common before the invention of antibiotics.

When a patient is seen as having this condition they show signs of two or more of widely different symptoms. every patient show different signs. These symptoms can include irregular heartbeat, fast pulse, inflammation of both the valves and heart, jerky body movements (chorea), joint pains arthritis, irregular red patches on the skin and fever.

Rheumatic fever can also lead to heart damage over a period of time and is followed by a streptococcal throat infection; sometimes streptococcal throat infection symptoms are not present in all the cases, so patient doesnt know until rheumatic fever develops. Roughly 70% of patients who have rheumatic fever will have leaky heart valves and will need replacing and permanent heart damage too, antibiotics are given to these patients when ever they visit the dentist or have an operation due to them being susceptible to infection (endocarditis).

The diagnosis is an ecg which shows prolonged PR interval, even examining the joints and skin. Once diagnosed antibiotics such as penicillin are used to get rid of any remaining infection and plenty of bed rest is needed. Paracetamol can be used to help with fever and joint pains.

4.14 Congenital heart disease (CHD)

This disease is a defect with the hearts structure. This is also from birth; the most common sort of birth defect is the CHD. Approximately 8 out of every 1,000 newborns have congenital heart defects, ranging from mild to severe. During the development of the embryo, the structure of the heart can be compromised. This means the heart wall/valves/arteries/veins of the heart can become defect causing the normal flow of blood to the heart to be altered. This could be the following:

  • Slow down
  • Go in the wrong direction or to the wrong place
  • Be blocked completely

Treatments to fix this can include medicine, surgery and even heart transplant; this all depends of the severity of the defect and condition of the patient along with the age.

Chapter 5 ECG interpretation

Summary of chapter

This chapter will discuss how to interpret ECG, to understand what the waveform is telling us about the heart. How clinically the waveform changes indicating an abnormal heart. We will look at the significance of waveform duration. And from the changes in ECG waveform what diseases are present.


  • What are the components of the ECG tracing
  • What physiologic events corresponds to each of these components
  • How to assess heart rate and rhythm
  • What each trace component of the ECG tells us

5. 1 Fundamentals of ECG Interpretation

All of the areas below need to be looked at before a diagnosis can be made.

  • Rate
  • Rhythm and conduction
  • P wave morphology
  • PR interval
  • QRS width
  • QRS axis
  • QRS - Initial deflection in each lead - Up? Down?
  • QRS Voltage
  • QRS morphology
  • ST segment Up? Down? Isoelectric?

5.2 heart rate determination

Add six seconds of QRS complex and multiply by 10 to give the BPM.

E.g. 6 multiply by 10 = 60 BPM

If the rhythm is regular, measure the distance between two R waves and divide this by 300 to get the heart rate.

e.g. 5 squares between R-R on the trace paper = 300/5 = 60 BPM

5.2.1 Calculation of heart rate

4.2.2 What is the rhythm?

Is there a p wave in front of every QRS complex?

Is there a p wave followed by a QRS complex

Do the p waves all look the same?

Is the rhythm regular? Regularly irregular? Irregularly irregular?

Are the QRS complexes narrow, wide or a mix of the two?

Is there a p wave in front of every QRS?

5.3 Components of the ECG

What do the components of the ECG trace tell us in terms of conditions or disease that may exist.

5.3.1 The P wave represents atrial depolarization

Right atrial enlargements results in tall p waves,

Left atrial enlargement leads to a double hump or M shaped p wave.

5.3.2 The P-R interval

The P-R interval represents time taken for the impulse sent from the SA node to travel to the ventricles.

Normal intervals of 0.12 to 0.20 (seconds) allows time for the atrium to finish contracting and fill the left ventricle.

Prolongation of the PR interval beyond 0.20 seconds = first degree AV block.

Long P-R interval = delay of impulse going through AV node = 1st degree AV block.

Short P-R interval = lack of normal delay in AV node = bypass tract i.e. choosing a different route.

5.3.3 QRS complex

The QRS complex represents time taken for the left ventricle to depolarize.

The normal QRS is narrow and takes less than 0.12 seconds.

Wide QRS indicates a delay in conduction, either because of block in one of the bundle branches or because the impulse is not travelling through the correct conduct pathways.

Block at or near the AV node causes AV block or a long p-r interval leading to 1st degree AV block.

Block in the left or right bundle causes left bundle branch block or right bundle branch block.

Bundle blocks may be a sign of serious heart diseases such as cardiomyopathy, infarction or ischemia.

What does a wide QRS beat mean?

If preceded by a sinus p wave at the appropriate PR interval, this is a sinus beat which is wide due to a block in the left or right bundle

If no p wave, beat originates in the ventricle either prematurely (PVC) or because no other beat came along (ventricular escape beat).

5.3.4 T waves

T waves are normally upright in most leads. T waves should be symmetrical. Abnormal T waves can be caused by ischemia or infarction, hypertrophy, abnormal conduction patterns, drugs, metabolic changes, CNS events etc.

abnormal T waves

  • inverted or flat where they should be upright
  • often asymmetric
  • often associated with abnormal S-T segments

Causes of dramatic T wave changes can be left ventricular hypertrophy, hypertrophic cardiomyopathy and Athletes heart syndrome.

Long QT syndrome

A disorder of myocardial repolarization characterized by prolongation of the QT interval on the ECG. When the ECG shows a QT interval greater than 0.36 - 0.44 seconds this is worrying.

5.3.5 U wave

The U wave, named by Einthoven in 1903, the u wave is the last electrical event that takes place in the cardiac cycle and is also the smallest. They represent repolarization of the purkinje fibres. Prominent u waves can be due to electrolyte abnormality such as hypokalemia or even in hypercalcemia. An inverted u wave can be present due to myocardial ischemia.

Chapter 6 ECG leads

Summary of chapter

This chapter is about Understanding of how clinical ECG is taken i.e. leads. We will discuss in early history how ecg was taken and how ecg can be taken today. There are many leads we can use to take a clinical ECG but each different leads provides different information and it is important to know what information each lead provides and how it can be used to assess the heart.


  • What are ECG leads
  • how to use the leads to record/monitor heart rhythm
  • positioning of leads

6.1 Introduction to why we use ECG leads

Early ECG recordings were made by putting both the patients arms and leg in a bucket of salty water (conducts electricity), and putting a wire from an instrument for measuring changes in electrical current. Modern electrocardiographs are more sophisticated but work on the same principles, using electrodes (metal plates or plastic patches covered in a gel) and leads instead of wires and buckets of water. A present day ECG machine is relatively small about the same size of shoe box but still quite expensive. An electrocardiogram is the single most important test for coronary heart disease due to narrowing of the arteries.

ECG leads are divided into numbers of different coloured wires, i.e. for monitoring up to 5 leads and for recording 10 wires for 12 lead ECG. A lead shows a particular angle of the electrical activity of the heart. A lead corresponds to a number of wires and not just a single wire or electrode. For example a full 12 lead ECG setup is 4 attached to each limb and the remaining 6 leads across the heart region as shown in figure 12. Although 10 wires have been used we get 12 pictures or leads.

To monitor or measure the hearts activity we need at least two electrodes, one electrode is looking or seeking between itself and the other electrodes. If we change the position of these electrodes we can get different viewing angles. Remember the electrodes doing the looking will always be a single electrode but the other electrodes can be single or joined together to form a reference point.

V1 is at the 4th intercostals space on the right hand side of the sternum. V2 is also on the 4th intercostal space but is on the left side of the sternum. V3 is just below v2 towards the midclavicular line. V4 is at the 5th intercostal space midclavicular line. V5 is at the anterior axillary line 5th intercostal line. V6 is at the side of the heart or the midline again on the same horizontal line as v5.

To have an ECG the patient is asked to strip to the waist including removal of bra for women so electrodes can be attached to the chest, arms and legs. They are held in place by elastic straps, suction caps or sticky pads. There is no discomfort or pain of any kind. While lying, the doctor will twist dials and move levers on the machine to measure the electrical activity being picked up from the body by the different leads. If the patient moves to any significant degree, the electrical activity generated in the muscles may interfere with the reading.

The machine will produce a graph consisting of a continous wiggly line that represents the activity of the heart. The graph may appear on either a screen or on a long strip of paper. A normal healthy heart has a characteristic pattern. Any irregularity in the heart rhythm or damage to the heart muscle will show up as being different from the normal pattern.

The interpretation of an ecg reading is a very complex task, and may take considerable time. Doctors receive special training in this art during their course. The letters p,q,r,s and t used to identify the main waves of an ecg tracing were chosen arbitrarily by william einthooven, the dutch physician who invented the ecg in 1903.

Unfortunatey the cardiograph only shows what is happening to the heart at the moment the reading is taken. It cannot always predict what will happen to the heart in the future.

NOTE: bipolar leads: seeking point is on one limb and the reference point on another limb i.e. I, II and III lead ECG.

Unipolar leads: here the reference point is made by several leads joint together and the seeking lead on another limb.

Chapter 7 clinical ECG testing and results

Summary of chapter

In this chapter we are going to clinically investigate the normal rhythms of a person compared to a volatile heart i.e. a smoker. We will set up an experiment using three people. We will calculate from the ECG waveform the information and display these with any abnormalities. The test will take place in a laboratory. I will place the ECG leads on the subjects and get them to exercise and take their results over a set period of time.


  • To observe rate and rhythm changes in the ECG associated with exercise and smoking.
  • To correlate electrical events as displayed on the ECG with mechanical events that occur during the cardiac cycle.
  • To explain/understand why heart arrhythmias are present and what causes them.
  • To become familiar with the electrocardiograph as a primary tool for evaluating electrical events within the heart.


  1. BIOPAC electrode lead set (ss2l)
  2. BIOPAC disposable vinyl electrodes (el503), 3 electrodes per subject
  3. BIOPAC electrode gel (gel1) and abrasive pad (elpad) or skin cleanser or alcohol prep
  4. Computer system
  5. BIOPAC student lab 3.7 software
  6. BIOPAC data acquisition unit (MP35/30)
  7. BIOPAC wall transformer (ac100a)
  8. BIOPAC serial cable (cblsera)

7.1 subject testing

Due to ethical issues the identity and personal information will be kept secret of the subjects. The test acquiring the following:-

Subject A will be a healthy person with no real serious heart issues

Subject B will be a keen gymnasium individual

Subject C will be an aggressive smoker

Subject A will walk around the laboratory at a steady or normal gait and then be asked to take an ECG reading. This reading will describe how the heart has responded to the bodys needs and how much strain the heart has undertaken due to activity.

The second subject, B. will be asked to exercise on a bike or treadmill for a constant time and after the set period of time will be asked to record the hearts condition via an ECG. The subject chosen for this task has been specifically a healthy individual who is used to exercising.

The last subject who is a smoker, subject C will be told to exercise exactly as subject B, and after the set period of time an ECG trace of their heart will be produced.

The test will show the condition of the heart of each individual before the test and how exercise changes the condition, rhythm of the heart and how the patient overall is, due to this new activity not only that but will show us clinically how smoking changes the hearts condition and to what extent. The biggest changes will be shown against the healthy subject B and smoker subject C. we will notice major differences in both these subjects from a change in time (S) of trace and volts (MV) of heart. And even show how the heart deals with these new changes to accommodate the already needs of the entire body. This test will provide us with great results and how we can, from the waveform of each individual heart show what condition the heart is in and what needs to be addressed.

We will use lead ii ECG the reason for this is because lead ii ECG is very good for monitoring the heart. And provides enough detail for our study.

Subject b and c will perform the exercise for 10 minutes, this will give the heart a good work out and the results obtained will be significant. The type of exercise we will make our subjects undertake will be very basic. They will exercise on a mountain bike which is adapted so they are in motion whilst standing still in the same spot. As the subject rides away the heart will get a good exercise and an increase in BPM.

We placed one electrode on the medial surface of each leg, just above the ankle and placed the third electrode on the right anterior forearm at the wrist (palm side).

Once this was done the LEAD II electrode configuration was established. The subjects were told to remove any wrist or ankle bracelets and were not in contact with any nearby metal objects i.e. faucets, pipes etc.

7.2 Calibration

The calibration procedure establishes the hardwares internal parameters (such as gain, offset and scaling). This test took only 8 seconds to complete and the individuals had to remain relaxed and still as possible during the calibration period. This was because the electrocardiograph is very sensitive to small changes in voltage caused by contraction of skeletal muscles, we did not want muscle (EMG) signals to corrupt the ECG signals. Once the test has been carried out, an ECG waveform with no large baseline drifts should be present. This will be done as mentioned for 10 minutes. We will produce an ECG after the exercise.

Set up of calibration

  • Attach electrodes, make sure subject is relaxed
  • Click calibrate
  • Wait for calibration procedure to stop
  • Check the calibration data:
    1. If correct, proceed to data recording
    2. If incorrect, redo calibration


Once calibration has been completed we can just click on record and the waveform of the subject will be recorded. This waveform will continue to copy until 1 minute, when the minute is over the test is complete and the next subject will take his/her ECG waveform and redo the calibration setup. Following is the results and analysis of each subjects tested.

7.3 Subject A: testing

Below is a detailed 20 second trace strip. Which show the P, QRS and T waves clearly. The millivolts (MV) and seconds of each wave are consistent and regular. This information shows clearly the subject has a normal healthy heart rate with no real underlying damage or disease. The BPM of 74 fall in the safe zone.

7.3.1 Subject A findings

Subject A seems to have an average bpm of 74 of a person this age. The rhythm is regular. A P wave is followed by a QRS complex, the P waves all look the same and the duration is 0.08 seconds, this falls within the safe zone.

Normal sinus rhythm the QRS complex shows a duration of 0.11 seconds, the s-t segment, Q-T interval and T waves are all within the safe zone. This subjects has a normal heart and heart rate with no real underlying problems. Results of this subject can be seen in table 3.

7.4 Subject B testing

Subject b has a bpm of 109, this can be explained, as prior to the ecg recording the subject was undergoing exercise on the test equipment. This shows that the patients heart had to beat faster and harder to keep the body nurished with oxygen and removal of waste products and to reduce the lactic acid build up in the muscles due to lack of oxygen supply.

The duration of the P wave 0.08 seconds, p-r interval 0.14 seconds and QRS complex 0.12 seonds all fall within the safe zone.but his q-t interval duration of 0.32 seconds fell short of the normal zone which was 0.36 -0.44 seconds also the S-T segments of 0.06 were half of the acceptable level of 0.16 seconds, and lastly the t wave duration was 0.11 seconds which was short of the normal level of 0.16 seconds which again was the normal duration. One explanation can be the subject can have ventricular hypertrophy, this occurs naturally as a reaction to aerobic exercise and strength training and also because of the ST-T wave change, which can be a sign for ventricular hypertrophy. in this case we cannot fully explain this 100% due to the fact we only monitored the patient with lead II ecg, a full 12 lead ecg would be required. And to fully test for ventricular hypertrophy an echocardiography would be done, during which the thickness of the muscle of the heart can be measured to indicate left ventricular hypertrophy.

We have to also understand the subject keeps fit and visits the gym regularly, a condition such as athletics heart syndrome may be present?. This is a common condition with athletics and is considered normal.

7.5 Subject C testing

Close up of R-R wave

  • wave at first 5 seconds ECG recording
  • wave at 30 seconds of ECG recording
  • wave at 60 seconds of ECG recording

7.5.1 Subject C findings smoker

This subject is a smoker who was measured. his average BPM was 130, at times in the test especially at the beginning he peaked to approx 140, which calmed back to 125 at the end of the test. Showing that his heart is beating twice as fast then normal. This subjects heart had shown to be working the hardest compared to all three subjects and especially subject B who was also exercising. During the ECG trace recording, the patient showed signs of left atrial enlargement; this can be seen clearly by the m shaped P wave. Circled in red.

(P mitrale). This is also commonly seen with mitral valve disease. Left atrial enlargement can also occur in association with systemic hypertension, aortic stenosis, mitral incompetence, and hypertrophic cardiomyopathy. Further tests would be needed to clarify the exact cause.

The subject did also show signs of U wave this can be seen as regular irregularly. Right Precordial Lead v3 and v4 are needed to determine this U wave better, but unfortunately were not available for this test. U waves are not always shown in every patients ECG waveform and are normally associated with the repolarization of the pukinje fibres. Because the electrical impulse of these fibres are small they are not always picked up by the ECG. And if a distinct U wave is visible this could suggest ischemia.

Kishida et al (1982) reported the following;

A negative U wave, whatever its nature, was specific for the presence of heart (related) disease, such as systemic hypertension, aortic and mitral regurgitation, and (chronic) ischemia

H. Kishida, J.S. Cole and B. Surawicz, Negative U wave: a highly specific but poorly understood sign of heart disease, Am J Cardiol 49 (1982), pp. 20302036.

The subjects S-T segments and t waves were not in the normal acceptable levels again this could be due to the U wave showing signs of ischemia, Hypertrophic cardiomyopathy.

The ST-T waves show a jagged line appearance this can be seen in the picture below.

Abnormal T waves can be seen in a variety of conditions other than myocardial ischemia, including:

  • Cerebrovascular disease
  • Mitral valve prolapse
  • Right or left ventricular hypertrophy
  • Conduction abnormalities (right or left bundle branch block)
  • Ventricular preexcitation
  • Myocarditis
  • Electrolyte imbalance

7.6 Discussion of findings

The results which were attained justify and fulfil the objectives which were set out at the beginning. Which were To observe rate and rhythm changes in the ECG associated with exercise and smoking. To correlate electrical events as displayed on the ECG with mechanical events that occur during the cardiac cycle. To show and explain how heart disease affects ECG waveform and how this is illustrated on the waveform. To become familiar with the electrocardiograph as a primary tool for evaluating electrical events within the heart

The results i achieved after my testing showed clearly that rate and rhythm can change due to lifestyle and personal habits. We observed both rate and rhythm changes during exercise and were able to correlate the electrical events displayed on the ECG with mechanical events and were able to use an electrocardiograph as a diagnostic tool for evaluating events in the cardiac cycle. We related the abnormal rhythms of the ECG with suggested arrhythmias, the suggested diseases are not confirmed due to not enough information to make a full diagnosis i.e. full 12 lead ECG required, as other leads are used to verify a particular disease as it looks at the heart from many angles/deflections.

The experiment was done in the university medical laboratory with three volunteers. All volunteers were happy to take part and no personal identification information was kept, to keep individuals anonymous. All subjects performed the test accurately and fair. Subjects who required exercise performed this on the training bike for 10 minutes followed by an ECG recording straight after. Electrodes were placed on the subjects extremities 5 minutes before the testing began, so performance and conductivity are not compromised. It is also deemed as good practice.

When analysing ECG signal, these 3 parameters are important, although others are used and have been described in chapter 5 LEADS.

  • Consistency of wave
  • Shape of wave
  • Time intervals

The results are as follows;

Subject A is a male, non smoker aged 47 seen as a normal healthy individual with no medical history of heart disease. The subject had been advised to remain silent and rest patiently for 5 minutes so that we can record a heart at rest. I did not want the results to be corrupted due to subject walking to the laboratory which would show the heart rate to be a little faster than usual, subjects who have to be tested on any equipment have a tendency to get a little nervous as soon as they see medical equipment and this triggers a faster heart rate. So its good practise to let the subject rest to individual normal levels. Once subject was ready ECG electrodes were placed and his ECG waveform was recorded for duration of one minute. The data recorded was placed in table 3. Duration and amplitudes were all normal see appendix table 1 for normal values. P waves were regular with durations of 0.08 second and amplitude of 0.1 mV which is with the normal zone, subject ECG results show SA node is firing accordingly. The sino atrial node is controlled by the autonomic nervous system. There are no abnormal P waves; all waves look similar and regular with no change. All P waves are followed by a QRS complex which is regular and consistent with durations of 0.11 seconds and amplitude of 0.6 MV all QRS complex have the same morphology. Duration of QRS complex show that this individual has no disease or condition related to the performance of his ventricles, the conduction pathways are working correctly. If there were signs of poor or blocked bundle branch diseases, the duration of the QRS complex would be long suggested the electrical impulse is travelling down the wrong pathway. T waves are again all consistent and regular with same shape and duration of 0.16 seconds and 0.23 MV are within normal levels. Subject A is showing no inhibition and conduction is normal, this subject has a normal sinus rhythm and criteria for normal sinus rhythm is met.

Criteria for normal sinus rhythm is:

P wave before each QRS complex with a p r interval of 0.12 to 0.20 seconds in duration- subject p r values was 0.15 seconds.

A QRS complex width of 0.04 o.12 seconds subject had 0.11 seconds duration

Q t interval less than 0.44 seconds- subject duration was 0.34 seconds

Heart rate between 50 to 100 beats per minute- subject beats per minute was 74


Subject B was an athletic male aged 26 with no previous heart diseases. Testing for this patient was a little different to subject A in terms of prep. This subject had to exercise on the bike to get his heart rate racing and increased pulse. We wanted to compare the performance of this individual against the heart performance of subject C who was a smoker. Comparison would be made as to how the heart deals with changes, example if the size/shape of the heart has been altered to provide the extra help and whether this alteration is overall deemed dangerous for later life.

i expected the subject to have a heart rate of between 100 and 150 due to oxygen levels dropping, so beats are faster to get nutrients to the cells around the body, or the chance of lactic acid build-up will increase. This is the process where the production of lactate is higher than the rate of removal due to increase power exercise. Its roughly 1 -2 mmol/L at rest in blood and over 20mmol/L at exercise

The subject was exercising for 10 minutes. Once the exercise had finished the electrode leads, LEAD II ECG were placed ready for the recording to take place. The electrocardiography of subject B was done and the following results were recorded Table 4 shows results for subject B. The beats per minute for this subject was 109 average, well within our predicted BPM of between 100 to 150, known as sinus tachycardia or fast heart beat. This is as described above, oxygen level drops so beats are faster to get nutrients and oxygen to the body and to remove waste products. P wave was 0.08 seconds and P-R interval of 0.14 seconds were within normal values. This shows there is no disease or damage associated with the atrials. QRS complex was 0.12 seconds no problems here. S-T segment was 0.06 which fell short of the normal value of 0.12 seconds, the Q-T interval was 0.32 which again fell short of the normal value of 0.36- 0.44 seconds and finally T wave was 0.11 seconds which did not make the normal value of 0.16 seconds also. This suggests that there is a shortage of duration with the ventricle or in other words, the process of ventricular contraction/relaxation is quicker than normal.

Because sometimes it is difficult to examine where S-T segment starts and finishes it is useful to measure the RT segment and t wave together. Essentially ST should be on the baseline but interference from muscle contraction can play havoc with the waveform.

The S-T segment represents the end of ventricular depolarization and beginning of ventricular repolarization. Any defect in this part of the wave i.e. elevated/inverted or not within normal values can suggest myocardial infarction/ischemia/hyperkalemia. Hyperkalemia can occur due to high electrolyte levels of potassium and can cause abnormal arrhythmias. This high level can occur due to power exercises, in this case our subject did exercise on a bike for ten minutes. K+ or potassium is released from muscles when exercising causing levels of k+ serum to increase. Potassium causes faster repolarization activities, so this can be the reason why this subjects results show faster S-T segments. High levels of k+ is not seen normal and is dangerous for patients at rest causing dangerous arrhythmias to exists. Some treatments to lower k+ levels include calcium agents or insulin which may not reduce levels but reduce the risks of fatal arrhythmias.

Shortening of Q-T interval is still unclear at this time but can be due to increased potassium as described above increased outward potassium causes short action potentials which lead to short Q-T intervals. All of this can simply be due to exercise and is not the symptoms of heart disease.

T waves showed to be shorter than the normal values, our subjects T wave was 0.11 Ms short of 0.16 Ms. Short or quick T waves is ventricular tachyarrhythmias. Abnormal T waves and ST segments may also be seen in healthy individuals, including well trained athletes. One explanation can be the subject can have ventricular hypertrophy, this occurs naturally as a reaction to aerobic exercise and strength training. In this case we cannot fully explain this 100% due to the fact we only monitored the patient with lead II ecg, a full 12 lead ecg would be required. And to fully test for ventricular hypertrophy an echocardiography would be done, during which the thickness of the muscle of the heart can be measured to indicate left ventricular hypertrophy.

We have to also understand the subject keeps fit and visits the gym regularly, a condition such as athletics heart syndrome may be present? This is a common condition with athletics and is considered normal.

The last of the testers is subject C he is a male aged 24 unfit with no known heart disease or any other illness including high blood pressure. Subject was exercising on the bike for 10 minutes just the same as subject B with the same bike. After the test was over patient did reveal he felt a faster rate of beat, also known as tachycardia. Subject was placed on a seat for the electrode leads to be attached. Subjects ECG was recorded. Results can be seen on table 5 and a comparison of normal ECG values are in table 1 appendix.

Subject C had a heart rate of 130 beats per minute on average. This was clearly the highest bpm we noticed with all three subjects. Although subject B did exactly the same exercise with the same parameters, his beats per minute reached no more than 110 beats. This is because athletes have known to have left ventricular hypertrophy or enlarged left heart muscle. Because of this the strength of athletes heart contraction can provide enough nutrients and oxygen for the cells in the whole body that a lower bpm can be reached compared to other non fit individuals. A clear M shaped hump can be seen in the waveform/P Mitrale. If a taller P wave was seen then this can indicate right atrial enlargement or P Pulmonale. Subject c showed sign of left atrial enlargement. This can be due to many reasons such as high blood volume in heart, high blood pressure, increased heart stiffness, mitral valve disease or even hypertrophic disease. Treatment can be to replace the valve, or diuretics can be given if blood volume is high in the heart. There are connections with atrial fibrillation and increased atrial enlargement, but we can discredit this as the subjects ECG waveform did not show atrial fibrillation. Left atrial enlargement can also occur in association with systemic hypertension, aortic stenosis, mitral incompetence, and hypertrophic cardiomyopathy. Further tests would be needed to clarify the exact cause. Subjects P wave and P-R intervals were not abnormal but doesnt mean no disease is present. Conduction pathway is normal, no signs of bundle branch block. QRS complex and morphology was normal, suggesting conduction pathway is normal. Initial ventricle depolarisation looks acceptable. ST-T waves show jagged or jerky movement, this can be due to interference and probably not linked to any disease, ideally 12 lead ECG would clarify this, which can show deflection i.e. elevated/inverted in other leads indicating ventricular disease or ischemia. The duration of the ST segment was half the normal values at 0.06Ms and elevated with no signs of ST aligned on the isoelectric line, suggesting myocardial infarction/ischemia. This subject is a smoker so ischemia may be prominent. It is sometimes difficult to diagnose ischemia just on ST segment changes, it is better to have previous ECG for comparisons. The T wave of this subject fell short of the normal value which was 0.12Ms. the morphology of the ST-T wave seems slightly thin and tall and abnormal suggesting a variety of conditions ischemia, electrolyte imbalances, cerebrovascular disease, mitral valve prolapsed, ventricular pre-excitation ventricular hypertrophy or heart muscle disease i.e. myocarditis which need further investigation to reveal the exact disease such as 12 lead ecg and blood test for electrolytle imbalance, echocardiography to reveal hypertophic conditions etc..

Electrolytes maintain homeostasis in the body and are vital for muscle and neuro functions, they help with fluid balance, contraction/relaxation of muscle contractions, electrical impulses across membrane O2 delivery and much more. If disturbances or imbalanced can cause severe abnormalities and if left untreated such as hypokalemia can lead to severe arrhythmias. Electrolytes include sodium, potassium, calcium, magnesium, chloride, phosphate and bicarbonate. This subjects ECG also shows signs of U wave appearance and this is normally associated with myocardial infarction/hypokalemia. For the moment we will continue and explore this U wave further.

The subject did show signs of U wave this can be seen as regular irregularly. U waves are not really understood but there are few hypothesis that state a U wave can indicate afterdepolarizations or associated with the repolarization of the pukinje fibres or further indicate serious heart disease and can lead to ischemia/myocardial infarction if prominent and inverted. We could not fully investigate this by just using LEAD II ECG. So the following can cause U waves. Appear for number of reasons which include sinus bradycardia, centrel nervous system disease, hypokalemia, quinidine and type 1A antiarrhythmics. Myocardial infarction if inverted, acute ischemia (angina or exercise- induced ischemia). Lead v3 and v4 are needed to determine this U wave better, but unfortunately were not available for this test.

Subject C heart rhythm showed electrical alternans as the heart had a period of strong amplitude followed by reduced amplitude in a regular sequence. Electrical alternans relate to pericardial effusion, the heart swings more in the pericardial fluid then at other times, this causes different electrical fields at every other beat, can be seen in patients with tachycardia.



This dissertation set out to demonstrate to understand how the heart functions and how the heart does this, to understand how the heart is performing and what causes the heart to detoriate and its consequences. To show how smoking can affect heat rate and rhythm. How waveforms correspond to heart functions, how ECG can detect heart arrhythmias. Including showing how heart function/performance can be affected due to lifestyle using basic lead II experiment. I demonstrated and explained all my objectives with some good results with the following findings.

This dissertation has demonstrated how critical the condition of the heart is, and if this vital organ is healthy all other organs are safe, but if this organ fails all other organs will be directly affected. The heart beat is like the rhythm of life and we can listen to this rhythm by a diagnostic tool called electrocardiograph (ECG). ECG is a non invasive tool which has the ability to measure electrical activities of the heart and plot the findings on trace paper. There are many key factors which influence the behaviour of ECG recordings such as the positioning of electrodes, the type of lead used, conductivity of electrodes on skin and interpretation of waveform and even external environmental factors i.e interference from metal objects like pipes, faucets etc.

ECG are not just used for diagnosis of cardiac arrhythmias, they can be used for metabolic disorders i.e. electrolyte imbalances such as Hyponatremia or hyperkalemia which affects the nervous system and increases the chance of irregular heartbeats including dehydration.

In practise, one can learn how physicians observe, approach and interpret ECG. For example atrial enlargement causes M shaped P waves and how Q waves are not always seen with all ECG recordings and are not always considered dangerous i.e. ventricular hypertrophy affects Q waves but this condition can be seen in athletes with a healthy heart.

i conducted an experiment to show how heart rate and rhythm can be affected by lifestyle and smoking. All three subjects produced waveforms showing how the heart copes under stress. The biggest factors which influenced the waveform was smoking. Smoking caused many alterations in the waveform compared to a normal sinus rhythm. Smoking introduced ischemia and even early stenosis in arteries. These results clearly showed a massive difference between lifestyle and heart condition. a normal rhythm of 70bpm approx can be seen in subject A, a non smoker who was in his mid 40s compared to the heart rhythm of a smoker in his late 20s who showed signs of ischemia. at the same time a thickness in left ventricle heart muscle can also be known as athlete heart syndrome which is considered normal for athletes but is a serious condition for an elderly.

This experiment was done in a laboratory with relevant equipment but changes could have been made to make the experiment much more accurate. I would have made extra effort in ensuring that exercise subjects applied the same efforts, so that the effort required by both subject was the same and fair i.e. a controlled stance on the bike so subjects did not move to avoid strenuous moments as this could have affected the hearts workload which overall would have affected the results. One major problem we had was not being able to use a full 12 lead diagnostic ECG, primarily because a 12 lead ECG was not available, as with ECG recording/monitoring in the hospitals the norm is to conduct testing with a full 12 lead ECG, the reasoning for this is simply because other leads are required to make a diagnosis. If ischaemic changes were present you would be interested in a particular area thus involving others leads. Different leads obtain different views of the heart. I would have also used a spirometry a lung testing device to measure lung performance a simple mouthpiece which the patients breaths into is attached to a recording equipment (spirometer). This would allow me to further prove how smoking can not only affect heart rate and rhythm changes but the affect of oxygen consumption i.e. Cor Pulmonale or pulmonary hypertension due to lung damage by smoking. All three subjects if performed an ECG at rest i am confident that no real disease or condition would be shown in the waveform thats the reason why an exercise stress test was done to highlight changes in heart condition when load is applied as any underlying disease would be highlighted in the waveform and , I would have also taken ECG at rest from all three subjects before their testing to comparison of before and after.

Over all the experiment was successful and clearly showed how smoking affects rate and rhythm and how left ventricular hypertrophy is seen as a common condition to athletes and not to regular non exercising individuals. Exercise stress testing is used to confirm heart disease as ECG at rest will show no real difference between a healthy patient and a patient with expected arterial stenosis.



The results we obtained show smoking does cause a degree of damage and introduce other heart related diseases and can not only affect the heart but other organs i.e. lungs vice versa. The test showed that a condition known as athletes heart syndrome - ventricular hypertrophy may be present in fit athletes or those who indulge in strenuous exercises such as running, swimming, long distance marathons and skiing. An is not seen as a dangerous condition, but can be for non exercising individuals. A concern does exist when these type of individual stops competing and return a life of non strenuous exercise, this can cause myocardial infarction due to the fact the heart is not conditioned as before and coronary artery disease increases. Also young athletes who die young tend to have hypertrophic cardiomyopathy were the heart goes into an abnormal rhythm during exercise due to enlarge muscle obstructing blood flow. When evaluating athletes it is better to do an echocardiogram for accurate diagnosis. The last subject who was a smoker showed signs of left atrial enlargement and ventricular ischemia suggested left side heart failure to some degree, showing smoking causes interruption in blood flow and that the heart has to beat faster to nourish the cells of a normal healthy individual.

Overall this dissertation has thought me so much and has strengthened my skills in clinical electrocardiography, my knowledge in cardiac arrhythmias has increased immensely and i know how to perform a basic Electrocardiography test and interpret the clinical ECG and report any diseases with viable medical knowledge. After experiencing the researched areas, I am going to continue studying in cardiology and improve ways of diagnosing diseases earlier and applying early treatments to avoid complete damage of the heart.

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