Download Mr John who is an obese 47 years old businessman was admitted to

ITA Chest Pain 1 Sessions (semester one week 4)
Introduction
Below you will find the same four patient scenarios you have discussed in
your small groups and structured tutorial in week 3.
This week, you will find a range of supplementary learning material in the
ITA. The material should help you in your task. Tutors will also be
present throughout the ITA session to answer any questions.
During the first 50 minutes, please read and discuss questions at the
end of all four scenarios and visit the ITA support material.
After this time, your group will be allocated one of these scenarios to
present to all the other groups in the final period of this ITA session.
Please spend a further 25 minutes discussing your allocated scenarios
(revisit the relevant ITA material) and arranging for one of you to talk
for 10 minutes to the full ITA group - discussing the answers to the
questions at the end of the scenario.
Scenario 1:
John is 47 years old; he is 1.75 meter tall and he weighs 98 kg. He owns a printing company employing seven
people. John inherited the printing company from his father who died suddenly of a heart attack in 1995. John is
married to Mary. Mary is 42 years old and works as a part-time receptionist at a local dental clinic. The couple
have three teenage children, a boy and two girls. John works about 90 hours per week and rarely sees his wife
and children. His company ran into financial difficulties and he worries incessantly about balancing the books.
John smokes 40 cigarettes per day since his teens. He attends frequent business dinners during which he enjoys a
few drinks. In an average week he consumes about 3 bottles of wine, 14 pints of beer and another seven double
whisky. Mary and the kids are members of a local fitness club, but John doesn’t have time to join them.
Four years ago, during a routine visit to his doctor, John was told that his blood pressure was high at 175/110. His
doctor advised him to change his life style and reduce his weight. John’s blood pressure remained high at around
170/100 on several subsequent visits to his doctor. He was then prescribed some tablets to lower blood pressure;
nevertheless, he often forgets to take them.
John woke-up in the early hours of one morning complaining of severe crushing central chest pain. The pain
radiates to his left arm. He became sick, vomiting twice, and he was sweating profusely. The pain lasted for more
than 30 minutes during which time Mary became really worried and decided to call for an ambulance. John was
taken to Ninewells Hospital.
a)
Answer the questions below. When answering each question think about the basic
principles (about which you may be learning) which are relevant the question
QUESTIONS
1.
What simple steps would be taken by medical staff upon John’s arrival at hospital?
2.
What should happen next once John’s condition is stable?
3.
What are the likely underlying mechanisms that caused John’s chest pain?
4.
What types of medications could be used to treat John’s acute condition?
5.
Why was it important that John’s blood pressure should have been lowered? How this could be achieved?
b)
Can you think about curriculum outcomes required to deal with John’s condition?
2
Scenario 2:
Ann is 58 years old. She has been troubled with osteoarthritis and joint pain for the last 20 years. Seven years
ago, following the death of her husband from lung cancer, Ann took early retirement from her work as a secretary
in a local firm. Four years ago, her two grown-up sons moved to work in London, and Ann has been living alone
since then. Two years ago, Ann started to experience severe pain affecting her left knee. The medications
prescribed by her doctor were not helping much; and he decided to send her to Ninewells hospital to see the
orthopaedic surgeon. The orthopaedic surgeon offered Ann surgery to replace her left knee putting her name on
the waiting list. For the last nine months, Ann was unable to walk to the local shops. She has been receiving help
from a neighbour since then. At last, Ann had the knee-replacement surgery 6 weeks ago. Everything seemed to
have gone very well and Ann was recovering well at home.
Yesterday, Ann was brought by an ambulance to the Accident and Emergency Department at Ninewells
complaining of severe pain on the right side of her chest and shortness of breath. The pain was sharp and made
worse by taking a deep breath and by movement. Approximately one hour prior to her admission, Ann coughedup a small amount of blood. She denied any fever or chills. Two days prior to her admission, Ann developed mild
pain in the right leg associated with swelling & redness especially at the back of the leg below the knee. The leg
pain seemed to be made worse by bending the foot upward towards the knee. Ann thought the leg pain was
unimportant, attributing it to muscle strain. She denied any personal or family history of blood clots.
a)
Answer the questions below. When answering each question think about the basic
principles (about which you may be learning) which are relevant the question
QUESTIONS
1.
What simple steps would be taken by medical staff upon Ann’s arrival at hospital?
2.
What should happen next once Ann’s condition is stable?
3.
Do you think that Ann’s chest pain is related to her recent surgery? Explain?
4.
How this condition may be life-threatening?
5.
What types of medications could be used to treat Ann’s acute condition?
6.
What problems related to Ann’s home circumstances should have been addressed before discharge from
hospital?
b)
Can you think about curriculum outcomes required to deal with Ann’s condition?
3
Scenario 3:
Jane is 34 years old. She works as a nurse in the children wards at Ninewells hospital. Jane lives in a first floor
flat with her boy friend Andrew, who works in a local supermarket. For the last 6 months, Jane became
progressively short of breath particularly on climbing stairs at work. She always felt tired and she eventually
stopped playing tennis with Andrew on Sundays as she used to do. Jane at first attributed her symptoms to lack of
fitness, but the breathing problem seemed to be worsening. Eventually, she found it difficult even climbing stairs
to her first-floor flat. Jane also felt a racing and erratic heart beat, and chest pain. She was worried that she may
have something wrong with her heart especially after watching a TV programme about blocked coronary arteries
and heart attacks. Jane then went to see her doctor. During the consultation, she recalled that she had rheumatic
fever at the age of 9. Her doctor listened to her heart with a stethoscope and found a murmur. Following a series
of investigations at Ninewells Hospital Jane was told that her symptoms are caused by a leaking atrio-ventricular
valve on the left side of the heart; and that the chest pain was secondary to the racing erratic heart beat. She has
been prescribed some medications and now feels better.
a)
Answer the questions below. When answering each question think about the basic
principles (about which you may be learning) which are relevant the question
QUESTIONS
1.
What is a cardiac murmur
2.
What is the relevance of rheumatic fever to the murmur heard by the doctor?
3.
What is the link between Jane’s leaking heart valve and shortness of breath?
4.
What gives rise to the racing erratic heart beat?
5.
What causes Jane’s chest pain?
6.
What should the medications prescribed for Jane seek to accomplish?
b)
Can you think about curriculum outcomes required to deal with Jane’s condition?
4
Scenario 4: Chest Pain - Ruptured aortic aneurysm
Rob is 61 years old. Rob has known for more than 3 years that he has high blood pressure and an aneurysm of his thoracic
aorta. This was discovered incidentally when Rob was investigated for a medical problem. When first diagnosed, the aortic
aneurysm was not giving Rob any symptoms; nevertheless, Rob was advised to come to the hospital for regular follow-up
to check his blood pressure and assess the size of the aneurysm. At first Rob complied with advice, but then felt that the
follow-up may not be as important as the doctor has indicated. Rob was lost for follow-up for the last 18 months.
Last night while watching TV with his wife, Rob developed a sudden onset severe central chest and upper back pain. The
pain was tearing and ripping in character. His wife phoned for an ambulance and he was taken to Ninewells Hospital. Rob
had urgent surgery, but sadly died in the operating theatre.
a)
Answer the questions below. When answering each question think about the basic
principles (about which you may be learning) which are relevant the question
QUESTIONS
1.
What urgent steps have been taken by medical staff upon Rob arrival at hospital?
2.
What is an aneurysm? What causes an aortic aneurysm? How are aortic aneurysms diagnosed?
3.
Why was the doctor concerned by the aortic aneurysm? How is the size of aneurysm assessed?
4.
What is the likely cause of Rob’s acute chest pain?
5.
Why was it important to control Rob’s blood pressure?
6.
What was the likely status of Rob’s blood pressure on admission to the hospital? Why?
7.
A large thoracic aortic aneurysm may put pressure on surrounding structures in the chest. Can you think
of possible pressure symptoms caused by a large thoracic aortic aneurysm?
b)
Can you think about curriculum outcomes required to deal with Rob’s condition?
5
Sem 1, CP1 Area1/1
What causes chest pain
anatomical consideration?
please examine the anatomical model of the thorax
Causes of Chest Pain
Chest pain may be caused by one or more of the
following causes:
Cardiac causes e.g.
•Coronary heart disease
•Dissecting or Ruptured aortic aneurysm
•Pericarditis (inflammation of the lining of the heart)
Respiratory causes e.g.
•Pulmonary embolism
•Pneumonia (infection)
•Pleurisy (inflammation of the lining of the lungs) secondary
infection cancer
•Pneumothorax (air in the pleural space outside the lungs)
including Tension Pnemothorax
Musculoskeletal or chest wall causes e.g.
•Costochondritis (inflammation of the costochondral joint)
•Rib pain e.g. rib fracture or bonny deposits from malignancy
•Non-specific musculoskeletal
Neurogenic causes e.g.
•Herpes zoster infection
•Psychological pain
Gastrointestinal causes e.g.
•Oesophageal spasm
•Oesophageal rupture
•Gastroesophageal reflux / Gastritis (inflammation of the
stomach)
•Peptic ulcer (ulcer of the lining of stomach or duodenum)
•Cholecystitis (inflammation of the gall bladder)
•Pancreatitis (inflammation of the pancreas)
Other Causes e.g.
•Sickle cell chest syndrome
Sem 1, CP1 Area1/2
What is acute
and
What is chronic chest pain?
Acute chest pain
Acute chest pain comes on suddenly and unexpectedly
About 20-40% of all medical admissions in UK are for acute
chest pain
The causes of acute life-threatening chest pain are
highlighted in red in the above list
Chronic chest pain
Chronic chest pain usually comes on gradually and persist
(either continuously or intermittently) for a long time (e.g.
weeks, months, or years)
Outlines for Emergency Management
Of
Acute Chest Pain
ABC
•
Give Oxygen
•
Establish an intravenous access
•
Attach patient to a cardiac monitor
•
Pulse oximetry
•
Relief pain e.g. give diamorphine intravenously
•
•Establish the cause of chest pain (history & examination +
investigations)
Administer treatment for specific cause
•
Chest X-ray Normal Male
Sem1, CP1 Area 2/1
Sem1, CP1 Area 2/2
Coronary Heart Disease
Coronary heart disease is the principal cause of death in the UK.
Coronary heart disease is caused by narrowing or blockage of the arteries
(coronary arteries) which supply the heart muscle with blood
The reduction in blood (and oxygen) supply to the heart muscle results is
chest pain
Chest pain caused by coronary heart disease comes in two main forms:
angina and myocardial infarction (heart attack)
Please play the short video marked
Left coronary artery”
Please play the short video marked
Right coronary artery
What is the extent of the problem and who is at risk of
developing coronary heart disease?
The above diagram was compiled by the British Heart Foundation Health Promotion Research Group,Department of Public
Health, University of Oxford,www.dphpc.ox.ac.uk/bhfhprg.
Angina
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Causes
•Usually caused by narrowing of coronary arteries (i.e. coronary heart disease)
•Angina may also result from reduction of blood (and oxygen) supply to the heart muscle
not caused by narrowed coronary arteries (i.e. coronary heart disease). Example
causes of angina other than coronary heart disease include: faster or irregular heart
beat, anaemia
•The causes of angina may co-exist e.g. coronary heart disease and faster heart beat
OR coronary heart disease and anaemia
Mechanism
•Angina is usually caused by narrowing of one or more of coronary arteries resulting in
reduction of blood supply to parts of the heart muscle.
•The usual cause of narrowing of coronary arteries is atheroma
•Atheroma is a fatty plaque which develop within the inside lining of the coronary arteries
resulting in narrowing of the artery lumen.
•Atheroma plaques usually develop in sections of the coronary arteries over a number of
years
•The blood supply to the heart muscle may be enough during rest even though one or
more of the coronary arteries are narrowed.
•During exercise and intense emotions, the heart muscle must work harder to pump
extra blood to the body.
•To work harder the heart muscle need extra blood (and oxygen) supply. The narrowed
coronary arteries will impede the delivery of extra blood (and oxygen) supply to the heart
muscle. The result is angina chest pain
Symptoms
•The usual symptom of angina is pain or discomfort felt across the front of the chest
•The pain may radiate to the arms, jaw, neck, stomach (upper abdomen)
•The pain is usually brought in by exertion e.g. walking uphill, running, etc.
•The pain is usually relieved by rest within 10 minutes or by GTN spray
Sem1, CP1 Area 2/4
Drugs used in the treatment of angina
Please refer to the causes and mechanisms of angina to appreciate the rational use of the specific drug classes listed
below.
At the simplest, angina occurs when the blood (and oxygen) supply to heart muscle is insufficient to satisfy its
metabolic demands.
Rational drug therapy therefore attempts to reduce the metabolic demand of heart muscle by decreasing the amount of
work that the heart performs. The table below lists drug classes and specific drugs that are commonly used to treat
angina, together with an indication of their major mechanism of action at the systems level.
Drug class and specific example
How administered
Major mechanism of action and
comments
Organic nitrates
(e.g. Glyceryl trinitrate; GTN)
Tablet held under the tongue
(sublingual route of
administration), or as a spray
In clinical doses, cause relaxation of
veins and decrease the amount
of blood returning to the heart.
Decreased blood return reduces
the volume of blood in the
ventricles of the heart which in
turn decreases the work that the
heart performs and consequently
its oxygen demand. GTN can be
used to terminate, or prevent,
angina attacks. Other organic
nitrates that have a longer
duration of action are used to
prevent attacks.
β-Adrenoceptor blockers
(e.g. Atenolol)
By mouth and swallowed
(oral route of administration)
Reduce the rate and force of contraction
of the heart, (particularly in
response to exercise) and thus
decrease cardiac work and
oxygen requirement. Used to
prevent angina attacks, but
should be avoided in asthmatic
patients because of a risk of
constriction of the airways
(bronchospasm).
Calcium antagonists
(e.g. Diltiazem)
By mouth and swallowed
(oral route of administration)
In clinical doses, cause relaxation of
arterial blood vessels and
decrease the resistance to blood
being pumped out of the
ventricles, decreasing work and
oxygen demand. Some drugs in
this class also cause cardiac
slowing and decrease in force of
contraction of the heart, again
reducing oxygen demand. Used
to prevent angina attacks.
Myocardial infarction
(heart attack)
Sem1, CP1 Area 2/4
03
Causes
•Usually caused by sudden blockage of a coronary artery or one of its
branches
Mechanism
•Myocardial infarction (heart attack) usually result when a blood clot (thrombus)
suddenly block a coronary artery or one of its branches
•The blood clot usually forms on top of a cracked atheroma. In other words blood
clots causing myocardial infarction usually develop in diseased coronary arteries
•The blood clot blocks blood flow to parts of the heart muscle
•The heart muscle will be damaged unless the blockage is undone quickly e.g. by
blood busting medications (thrombolysis) or by other mechanical means
•The extent of the heart muscle affected by blockage depends on the coronary artery
blocked
Symptoms
•The usual symptom of myocardial infarction is severe sudden onset pain across the
front of the chest
•The pain is usually more severe than the angina pain
•The pain may radiate to the arms, jaw, neck, stomach (upper abdomen)
•The pain usually lasts for more than 15 minutes and is not relived by rest or GTN
•The patient may sweat, feel sick, vomit or feel unwell
•The patient may collapse or even die suddenly if a large area of heart muscle is
affected; or if complications developed
Cardiac Troponins in the diagnosis of
Myocardial Infarction
•
Troponins are specific proteins present in skeletal and cardiac muscles.
•
Troponins which are specific to the heart muscle are called
CardiacTroponins.
•
Cardiac troponins are mainly of two types; Troponin T and I.
•
Like CK-MB (a heart enzymes) Cardiac Troponins are released in the
blood stream during acute myocardial ischaemia. Their presence in the
blood stream indicates the occurrence of damage to cardiac muscle e.g.
following acute myocardial infraction.
Cardiac Troponins are superior to other cardiac markers because:
1.
They are specific to heart muscle
2.
Their blood levels are negligible in healthy people making it
easy to detect any increase.
3.
Cardiac Troponins levels can thus predict the extent of
cardiac muscle damage i.e. higher levels of
CardiacTroponins are associated with more damage to
cardiac muscle.
4.
Cardiac Troponins blood levels usually increase within 4-6
hours after acute myocardial infraction and remain elevated
for at least 7 days. This would allow detection of
myocardial infraction that occurred several days ago.
An example ECG of Myocardial Infarction
Drugs used in the management of myocardial infarction (MI)
Sem1, CP1 Area 2/5
Please refer to the causes, mechanisms and symptoms of MI to appreciate the rational use of the specific drug classes
listed below.
Drug treatments of myocardial infarction (MI) aim to manage the patient immediately (relieve pain, restore blood supply;
reduce mortality) and also to prevent complications of MI, such as further damage to heart muscle involving an
increase in the area affected (infarct expansion).
The table below lists drug classes and specific drugs that are commonly used to manage MI, together with an indication
of their major mechanism of action. Note that the combination of drugs used differs between patients according to the
extent and consequences of a myocardial infarction
Immediate management
Drug class and specific example
Purpose, major mechanism of action and comments
Opiates
(e.g. Dimorphine)
Analgesic drugs given by intravenous injection to reduce the pain (and anxiety)
associated with acute myocardial infarction (AMI). Act as agonists at specific opioid
receptors in the nervous system that when strongly activated produce profound
analgesia.
Organic nitrates
(e.g. Glyceryl trinitrate; GTN)
Administered sublingually (or intravenously) to reduce cardiac work and relieve pain
associated with the area of cardiac muscle deprived of blood supply.
Antiplatelet drugs
(e.g. Aspirin)
Administered orally to prevent further aggregation of platelets and thrombosis. Act by
irreversibly inhibiting an enzyme (cyclo-oxygenase) that is in the synthetic pathway for
the formation of thromboxane-A2, a powerful inducer of platelet aggregation.
β-Adrenoceptor blockers
(e.g. Atenolol)
Administered by intravenous injection to reduce the rate and force of contraction of the
heart and to help limit the size of the damaged area of the heart (infarct). Also protect
against the development of abnormal cardiac rhythms (arrhythmias) that can prove
fatal.
Thrombolytic drugs
(e.g. Alteplase)
Administered by intravenous injection followed by intravenous infusion. Act to break
down emboli (detached clots) and hence re-establish blood supply to the affected
region of the heart (reperfusion). Mechanism involves the production of the enzyme
plasmin (from plasminogen) that breaks down the fibrin strands that hold the clot
together. For maximum benefit, these drugs must be administered soon after diagnosis.
Particularly useful in patients with a characteristic abnormality of the electrocardiogram
(ECG) known as S-T elevation.
Long term management
Antiplatelet drugs
(e.g. Aspirin)
Administered orally to suppress platelet aggregation.
β-Adrenoceptor blockers
Administered orally to reduce risk of complications and subsequent acute cardiac
problems. Choice of drug influenced by function of the left ventricle.
ACE (angiotensin converting enzyme) enzyme inhibitors
(e.g. Captopril)
Administered orally to patients in which dysfunction of the left ventricle is present. ACE
inhibitors prevent the synthesis of a peptide (angiotensin II) that constricts blood
vessels and indirectly enhances salt and water reabsorption by the kidney. Angiotensin
II also has direct effects upon the growth of cardiac muscle.
Organic nitrates
(e.g. glyceryl trinitrate, GTN)
Administered sublingually or as an aerosol spray. Used in patients with continuing
angina following MI.
Statins
(e.g. Simvastatin)
Administered orally to prevent further coronary events. Inhibit an enzyme (HMG-CoA)
involved in cholesterol synthesis, especially in the liver.
Sem1, CP1 Area 2/6
Important Risk Factors
For
Coronary Heart Disease
BLOOD PRESSURE
Risk of CHD is directly related to both systolic and
diastolic blood pressure levels. In adults aged 40-69
years, each 20mmHg increase in usual systolic blood
pressure or 10mmHg increase in usual diastolic blood
pressure, doubles the risk of death from CHD.The
2004 British Hypertension Society guidelines
recommend that drug treatment should be considered
for individuals with blood pressures of 140/90mmHg or
over, and that optimal blood pressure treatment
targets are a systolic blood pressure of less than
140mmHg and a diastolic blood pressure of less than
85mmHg (and lower still in people with diabetes).
Blood pressure levels are high in the UK. In England
37% of men and 34% of women have raised blood
pressure (more than 140/90mmHg) or are being
treated for raised blood pressure.The prevalence of
high blood pressure increases with age in both men
and women. Around 80% of men and 70% of women
with raised blood pressure are not receiving
treatment.Of those that are treated, over 60% remain
hypertensive.
DIABETES
Diabetes substantially increases the risk of CVD and
CHD. Men with Type 2 diabetes have a two to fourfold
greater annual risk of CHD, with an even higher (three
to fivefold) risk in women with Type 2 diabetes.
Around 3% of adult men and women in the UK
(around 1.3 million people) have diagnosed diabetes.
Prevalence increases with age: those aged 65-74 are
around 10 times as likely as those aged 25-34 to have
the disease. In Pakistani and Bangladeshi men and
women the prevalence of diagnosed diabetes is at
least five times that found in the general population.
As in many countries worldwide, diabetes is
increasing in England. Since 1991, rates have
increased by around two-thirds in men and a quarter
in women.
BLOOD CHOLESTEROL
Risk of CHD is directly related to blood cholesterol
levels. Blood cholesterol levels can be reduced by
drugs, physical activity and by dietary changes, in
particular a reduction in the consumption of saturated
fat.The CHD National Service Framework suggests a
cholesterol target of less than 5.0mmol/l.
In England the average blood cholesterol level in men
is about 5.5 mmol/l and in women 5.6 mmol/l. About
twothirds of adults have blood cholesterol levels
above 5.0 mmol/l and the prevalence of high blood
cholesterol increases with age in both men and
women. Blood cholesterol levels in England are high
by international standards, especially in women.
SMOKING
It is estimated that smoking causes over 30,000
deaths a year from CVD in the UK. Second-hand
smoke is also harmful to cardiovascular health.
Regular exposure to second-hand smoke increases
the risk of CHD by around 25%.
Until recently the proportion of adult cigarette smokers
in the UK had been decreasing rapidly but the decline
has now levelled off with the rate remaining relatively
stable since the early 1990’s. About 27% of men and
25% of women in Britain still smoke.
Cigarette smoking is more prevalent among manual
social groups than non-manual groups (31%
compared to 20%).Smoking rates vary considerably
between ethnic groups in the UK and are particularly
high (42%) in Bangladeshi men.
Compiled by the British Heart Foundation Health Promotion Research Group,Department of Public
Health, University of Oxford,www.dphpc.ox.ac.uk/bhfhprg
Sem1, CP1 Area 2/7
OVERWEIGHT AND OBESITY
Overweight and obesity increase the risk of CHD.
About 43% of men and 34% of women are overweight
in England and a further 22% of men and 23% of
women are obese. Overweight and obesity are also
common in children.Over a fifth of boys and a quarter
of girls aged 2-15 years in England are overweight or
obese.
In adults overweight and obesity increase with age.
Obesity is also more common in adults employed in
manual occupations, particularly in women. The
adverse effect of excess weight is more pronounced
when fat is concentrated mainly in the abdomen
(known as central obesity). Around one in four men
and one in five women in England have central
obesity.This is more common in adults employed in
manual occupations, especially women, and in South
Asian men, and women from all minority ethnic
groups.
The percentage of adults who are overweight or
obese is increasing rapidly in the UK, with rates
doubling since the mid 1980’s.There has also been a
steady increase in the prevalence of obesity in
children, with rates in England doubling in boys and
increasing by 30% in girls between 1995 and 2002.
PHYSICAL ACTIVITY
Physical activity lowers the risk of CHD.The activity
needs to be regular, of moderate intensity and
rhythmic such as brisk walking, dancing or cycling.
It is recommended that adults should aim for at least
30 minutes of moderate activity on five or more days
of the week.Only 37% of men and 25% of women in
England are active at this level, with activity declining
rapidly with age. Over the last 25 years, levels of
physical activity have declined in the UK. In England
the average number of miles per capita travelled each
year by foot fell by around a quarter, and by cycle by
around a third since the mid 1970’s.
Children are recommended to participate in moderate
intensity activity for at least an hour a day. In England
70% of boys aged 2-15 and 61% of girls are active at
this level. Rates decline steeply in girls after the age of
10 years, with only 50% active at the recommended
level by the age of 15.
An ambitious target for physical activity in England
has been proposed by the Government’s Strategy
Unit: to more than double the current proportion of
adults participating in 30 minutes of moderate activity
on five or more days a week to 70% by 2020.
ALCOHOL
Moderate alcohol consumption (one or two drinks per
day) is associated with a reduced risk of CHD. At high
levels of intake – particularly in "binges"- the risk of
CHD is increased.The Government recommends daily
sensible drinking benchmarks of no more than 4 units
of alcohol in men and 3 units in women. In addition
men should not drink more than 21 units a week and
women no more than 14 units a week.Overall 38% of
men and 23% of women in Great Britain consume
more alcohol than the daily recommended limits.
Slightly lower proportions, 27% of men and 17% of
women, drink more than the weekly recommended
levels. In the last 10 years these proportions have
risen by over 50% in women but remained stable in
men.
Binge drinking is highest in the 16-24 year age group
with 35% of young men and 28% of young women
binge drinking at least once a week. Professional
women drink on average twice as much each week as
those in unskilled manual jobs. In both men and
women, the highest rates of binge drinking are found
in Scotland,Wales and the North of England.
Compiled by the British Heart Foundation Health Promotion Research Group,Department of Public
Health, University of Oxford,www.dphpc.ox.ac.uk/bhfhprg
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Normal BP versus Age
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Drugs used in the treatment
of hypertension
ACE Inhibitor or angiotensin receptor blocker ACE inhibitors block the enzyme Angiotensin
Converting Enzyme (ACE) that is responsible for the
synthesis of a small peptide (angiotensin II) that
powerfully constricts blood vessels and indirectly
enhances salt and water reabsorption by the kidney
(both of which increase blood pressure). By blocking
the synthesis of angiotensin II, ACE inhibitors cause a
relaxation of the vasculature which lowers resistance
in the peripheral circulation and as a consequence
reduces blood pressure. Angiotensin receptor
blockers competitively antagonise the agonist activity
of angiotensin II at angiotensin receptors on vascular
smooth muscle cells (and elsewhere) causing
relaxation of blood vessels.
β-blocker (or β-adrenoceptor antagonist) - βblockers are drugs that prevent the agonist actions of
a neurotransmitter (noradrenaline) and a hormone
(adrenaline) at receptors (β-adrenoceptors) that are
important in blood pressure regulation. The effects of
β-blockers on blood pressure are complex and not
well understood, but three actions have been
suggested to contribute to their ability to lower blood
pressure: (1) an action of the heart that results in
slowing of the rate and force of contraction (hence
less blood pumped into the circulation per unit time)
(2) an action on the kidney to reduce the release of an
enzyme (renin) that by promoting the formation of
angiotensin II (see above) increases blood pressure,
and (3) an action in the central nervous system that
ultimately lowers blood pressure. There are objections
to all of these proposed mechanisms!
Calcium channel blocker – Calcium channel
blockers are drugs that act upon a special type of
calcium channel found in the cell membrane of
vascular smooth muscle cells and cardiac cells. In
vascular smooth muscle these channels, when
opened, allow Ca2+ to enter the muscle cell and
initiate contraction. By blocking the entry of Ca2+,
calcium channel blockers cause relaxation of arterial
blood vessels and hence reduce blood pressure.
Diuretic (Thiazide) – Diuretic drugs cause an
increase in the excretion of Na+ and water by the
kidney. As a consequence blood volume is somewhat
reduced and the blood pressure falls. However, this
does not entirely explain how thiazide diuretics work.
An additional action to relax vascular smooth muscle
cells (and reduce blood pressure) seems important,
but the mechanism of this effect is poorly understood.
α-blocker (or α-adrenoceptor antagonist) - αblockers are drugs that prevent the agonist action of a
neurotransmitter (noradrenaline) that is released from
the endings of nerves that innervate vascular smooth
muscle. When stimulated, such nerves cause
contraction of vascular smooth muscle and increase
blood pressure. By antagonising the effect of
noradrenaline at α-adrenoceptors, α-blockers reduce
blood pressure.
Spironolactone – spironolactone is a drug that acts
in the kidney as a weak diuretic (see above).
Spironolactone, like thiazide diuretics, causes
enhanced excretion of Na+ and water, but by a
distinct mechanism that involves blocking the actions
of the hormone aldosterone which promotes Na+ and
water reabsorption by the kidney. Sprinolactone is
therefore useful in conditions where elevated blood
pressure is due to abnormally high circulating levels
of aldosterone (e.g. Conn’s syndrome).
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Deep Vein Thrombosis (DVT)
and
Pulmonary Embolism (PE)
Deep Vein Thrombosis (DVT)
Definition of DVT
Deep Vein Thrombosis (DVT) is the formation of
blood clots within any deep vein
The deep veins are those veins which go through
muscles, not the superficial veins which are
commonly seen under the skin.
Common sites for DVT
The commonest sites for DVT are leg veins and
pelvic veins
Mechanism of DVT
DVT is precipitated by venous stasis or by
increased tendency of the blood to form clots
within the circulation
Risk factors for DVT
Symptoms of DVT
Although it is possible for DVT to occur for
no reason, some factors increase the risk for
DVT. These factors include:
1.
Increasing age
2.
Obesity
Although there may be no symptoms of
DVT (i.e. DVT only diagnosed when
complications develop), the commonest
symptoms of DVT are:
1.
3.
Immobility e.g. due to illness, surgery, long
distance flight, etc
2.
3.
4.
5.
6.
7.
8.
Pregnancy
Contraceptive bills
Previous DVT: this is because of damage
to lining of the veins
Cancer or treatment for cancer
Inherited conditions causing faulty clotting
of the blood
Pain and tenderness of the back (calf) of
the leg
swelling of the calf of the leg
Redness and warmness of the calf of the
leg: this is because blood will be diverted
from blocked deep veins to unblocked
superficial veins
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Pulmonary Embolism (PE)
Definition and Mechanism of PE
Symptoms of PE
Sometimes a blood clot (formed in the deep veins
because of DVT) may break off and travel with the
blood stream until it got stuck.
Small pulmonary embolus may cause no
symptoms at all.
The breaking travelling clot is called an ‘embolus’
An embolus travelling with the blood stream from
the leg veins usually go through the big chambers
of the heart before getting stuck in one of the blood
vessels going to the lungs the so called
‘pulmonary arteries’. The process is therefore
referred to as ‘pulmonary embolism’
Possible symptoms caused by medium-sized
pulmonary embolus include
1.
2.
3.
Chest pain: usually sharp pleuritic pain
which made worse by taking a deep
breath and by movement
Shortness of breath
coughing-up blood: so called
‘haemoptysis’
A large pulmonary embolus may cause collapse
and/or sudden death
Drugs used in the treatment deep vein thrombosis (DVT) and pulmonary embolism (PE)
Please refer to the causes and mechanisms of DVT and PE to appreciate the rational use of the specific
drug classes listed below.
The management of PE by drugs is dependent upon the severity of the condition. In some instances
anticoagulant drugs may be sufficient, but in others both anticoagulants and thrombolytic drugs may be
necessary. The commonly used anticoagulants are listed in the table below with an indication of their
action. See the table concerning ‘Drugs used in myocardial infarction’ for notes on thrombolytic drugs.
Drug
class
example
and
specific
Purpose, major mechanism of action and comments
Anticoagulant
(Heparin)
Used in the initial treatment of DVT and PE to prevent recurrent, fatal,
pulmonary embolism. Heparin works indirectly to inactivate thrombin,
which is required to convert fibrinogen to fibrin, a major component of
the clot. Heparin is administered by injection (intravenous initially,
followed by infusion, or subcutaneous administration) and has a rapid
onset, but short duration, of action. The major adverse effect of heparin
is bleeding, but this can be controlled relatively quickly by stopping drug
administration. The use of heparin is being superseded by low
molecular weight (LMW) heparins that offer advantages in ease of
administration.
Anticoagulant
(Warfarin)
Used alongside heparin, or LMW-heparin, in DVT and PE. Warfarin acts
as a blocker of clotting reactions that require vitamin K. It is active when
administered orally, but requires up to 2-3 days for an effective
anticoagulant effect to develop. Warfarin has a long duration of action
(several days), but if serious bleeding develops, its action can be
reversed by the administration of a concentrate of clotting factors.
Heart Valves
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Four heart valves prevent blood from flowing backwards.
These are: Tricuspid, Pulmonary, Mitral and Aortic valves.
In the heart:
De-oxygenated blood
Returns to the right atrium
•
Passes through the tricuspid valve into the right ventricle
•
Pumped by the right ventricle through the pulmonary valve
into
the pulmonary artery & pulmonary arterial
circulation
•
Oxygenated Blood
Returns to the left atrium
•
Passes through the Mitral valve into the left ventricle
•
•Pumped by the left ventricle through the aortic valve into
the aorta & systemic arterial circulation
What makes the heart beat at a
steady rhythm in a normal person?
The heart has a tiny in-built automatic timer
called the sinoatrial (SA) node.
•
The SA node is located in the right atrium
•
The SA node fires off electrical impulses at
regular intervals at about 60-80 beats per
minute when the person is resting and at faster
rates when the person is exercising.
•
In a normal person, the SA node controls the
heart rate making it to beat at a steady rhythm
•
ECG abnormal
ECG normal
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LEFT VENTRICULAR FAILURE (PULMONARY OEDEMA)
The force against which the left or right ventricle works to eject blood into the
systemic or pulmonary circulation is known as the afterload. Increased total
peripheral resistance increases left ventricular afterload. Raised blood pressure
(systemic hypertension) means that there is increased systemic total peripheral
resistance, which therefore causes increased left ventricular afterload and can lead
to left ventricular strain and increased muscle mass (hypertrophy). Long standing
hypertension may result in left ventricular failure causing elevated left-sided (i.e.
left atrial and left ventricular) pressures. The increased left-sided pressures (i.e.
preload) back up into the lungs and cause a rise in pulmonary capillary hydrostatic
pressure resulting in accumulation of fluid in the interstitial and intraalveolar lung
spaces: - a condition known as pulmonary oedema. Pulmonary oedema is
manifested clinically by varying degrees of shortness of breath
The shortness of breath may worsen in the supine position, compelling the
patient to sit up, a condition known as orthopnoea. This is because lying
down would increase venous return to the heart resulting in further increase
in preload. This may wake the patient suddenly during the night gasping for
breath, a condition known as paroxysmal nocturnal dyspnoea. To
obtain relief the patient must sit or stand up
RA
RV
PA
PA
LV
AO
Right Atrium
Right Ventricle
Pulmnany Artery
Left Arium
Left Ventricle
Aorta
A3 LAM
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FUROSEMIDE (FRUSEMIDE) IN ACUTE PULMONARY
OEDEMA
Furosemide or frusemide is a loop diuretic. Diuretics increase
urine output – usually of salt and water – and furosemide is called
a loop diuretic because its site of action is at the loop of Henle in
the kidney.
Furosemide was discovered in the 1960’s and revolutionised the
treatment of acute pulmonary oedema because unlike previous
diuretics with less immediate diuretic efficacy, it produced a huge,
rapid outflow of urine and could relieve breathlessness of
pulmonary oedema in just a few minutes. Its original trade name
was Lasix but patent protection (20 years) has long gone, so many
different generic versions of furosemide exist now as well as the
original Lasix.
The renal medulla is an unusually hypertonic region of the body
because in the ascending limb of the loop of Henle there are ion
transporting mechanisms which push sodium and chloride into the
interstitial fluid in this part of the kidney. The distal tubules of the
nephron pass through the hypertonic medulla, so water can be
removed from the tubules at this point by osmosis – but only if
antidiuretic hormone (ADH) is present. The distal tubule is only
permeable to water when ADH is secreted into the blood (from the
posterior pituitary gland).
Furosemide works by inhibiting the transporting pump which
pushes sodium and chloride into the renal medulla in the thick
ascending limb of the loop of Henle. So on the one hand it
increases the excretion of these ions in urine – but at the same
time it has caused a reduction in the osmotic pressure of the renal
medulla, so even if ADH is present there will be increased
excretion of water. This diuretic effect decreases the volume of
circulating blood and extracellular space, relieving preload and
afterload.
Furosemide can start to relieve breathlessness before the results
of diuresis become obvious. This appears to be the result of
generalised venodilation – perhaps by increased production of
prostaglandin from the kidney – which also helps to relieve cardiac
preload.
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Aneurysm of the Aorta
An aneurysm is abnormal enlargement or ballooning
of a segment of a blood vessel
•
The aneurysm may occur in any blood vessel, but it
commonly affects the aorta. The condition is called
aortic aneurysm
•
The commonest cause of
atheroma
•
aortic aneurysm
is
The aorta is the biggest artery in the human body
•
The aorta carries oxygenated blood from the main
pumping chamber of the heart (the left ventricle).
•
The aorta descends through the chest and abdomen
with many arteries coming off it to supply oxygenated
blood to different body parts.
•
Aortic aneurysm may occur in the section of the aorta
that passes through the chest (the condition is then
called thoracic aortic aneurysm)
•
Aortic aneurysm may occur in the section of the aorta
that passes through the abdomen (the condition is
then called abdominal aortic aneurysm)
•
The aneurysm weakens the aorta making it liable to
rupture under pressure. If this occurs, the patient may
have severe internal bleeding and becomes at risk of
sudden death
•
•Unfortunately,
most aortic aneurysms cause no
symptoms at all until they rupture!
Aortic aneurysm is usually diagnosed and followedup by radiological investigations e.g. an ultrasound or
CT scan
•
The aortic aneurysm usually tends to increase in size
with time. The larger the diameter of the aneurysm
the more likely it may rupture
•
If discovered, doctors aim to operate to repair aortic
aneurysms before they rupture i.e. when they reach a
certain size
•
Ruptured Atheromatous Aortic Aneurysm
A ruptured thoracic aortic aneurysm may give rise to
sudden onset severe central chest and upper back
pain and may cause sudden death
•
Plain Abdominal x-ray showing
“calcified abdominal aortic aneurysm”
PSYCHOSOCIAL PRINCIPLES
The psychosocial principles fall into three categories: Patient-centred
medicine, Human Behaviour and Social Causation of disease. All of
these contribute to our understanding of the relationship between doctor and patient; how the patient feels about their illness, how the patient functions as a part of a social unit, and why the patient behaves
the way they do.
Understanding how people behave when confronted with a serious
health problem is of great importance to doctors in deciding how to
communicate with the patient, and also in deciding how best to provide
advice and support. Understanding why patients sometimes don’t do
what you might expect is equally important.
Patients don’t exist in a vacuum; they exist in a context which includes
their family, friends, neighbourhood, society and other groupings. In
many cases, the nature of these groups, and how they interact, can
help us to understand who is more at risk of developing certain illnesses, why some groups of society are more likely to be unhealthy,
and what we as a society might try to do about it.
We also need to appreciate how common or rare certain conditions
are, and what it is that makes some people more likely to contract
them than others. This helps us to anticipate the scale of any response we may have to make, as well as being able to answer the
questions patients ask, such as “So how common is this then? Why
did I get it and not my Uncle Joe?”
Scenario 1
The acute nature of MI, and necessity for swift action in treatment can often mask the fact
that many social and behavioural issues underlie the high incidence (large number of new
cases) of coronary heart disease (CHD) in Scotland.
How many deaths from CHD were there in Scotland in the year 2003?
How does this compare with other EU countries?
What factors placed John at greater risk of experiencing MI?
What aspects of his lifestyle would you advise John to change?
Use the data below to answer these questions
NB Age standardized mortality
rates are rates that are adjusted to take account of the
age range and make-up of the
population in question. For
example, if the average age of
the population of Scotland was
different from that of NOrway,
we could not directly compare
the mortality rates for the two
countries. Age-standardization
allows us to do so.
Also look at the attached leaflets from the Health Education Board for Scotland (HEBS)
Scenario 2
Ann survived her pulmonary embolism. However, as a consequence, she will probably have
to take medication for the rest of her life to make clot formation less likely, and she will have
to be aware of potential factors which might increase the risk of her suffering another embolism.
Which of these are modifiable risk factors?
What does this mean?
These are some of the potential risk factors for embolism:
! Old age, especially if people have to spend a
lot of time in bed.
! Cancer increases the risk even more. However, most people who have pulmonary emboli do not have cancer.
! Surgery, especially in the abdomen.
! Genetic pre-disposition
! Being overweight/obese
! After a long journey without moving around,
the blood can clot in the legs where it will form
a deep vein thrombosis (DVT). This is also
sometimes called ‘Economy class syndrome’.
! Fractures of the pelvis and the lower limb.
! Smoking
! Pregnancy and childbirth.
Stage 1
Precontemplation
Patient has no direct intention
of changing their behaviour
Stage 2
Contemplation
Patient may intend to change
their behaviour at some time
in the future
Stage 3
Preparation
Patient is getting ready to
change their behaviour
in the near future
Theoretical models of human behaviour can help us to understand why it
is that patients may find it hard to
adapt to a diagnosis of serious illness by following advice that we may
give them - for example giving up
smoking. The model illustrated below is sometimes called the Readiness to Change Model, or the
Stages of Change Model. The five
stages are linked in both directions,
which means that people can go
backwards as well as forwards between the stages.
Stage 4
Action
Patient is changing their
behaviour now
Stage 5
Maintenance
Patient has reached a
steady state of change
in their behaviour
How would you use the model to
help you explain to Ann the steps
she may have to take to change her
lifestyle and minimise the risks of
future events?
Scenario 3
Jane has been given a diagnosis which would be very frightening for most people. When
a patient is given news like this, it is natural for them to wonder why it has happened to
them; what did I do to make myself ill?
Read the following extract from The Doctor’s Communication Handbook. Put yourself in
Jane’s position, and imagine how you would feel if it were you who had been diagnosed
with atrial fibrillation.
“When people become ill they ask themselves several questions, such as ‘What has
happened?’, ‘Why has it happened?’, ‘Why has it happened to me?’, ‘Why now?’, ‘What
should I do about it?’, ‘Should I go to the doctor?’, ‘Is it serious?’ and ‘Can it be treated?’
Think of the last patient you saw. What questions do you think they had asked themselves? Imagine that that patient was you. What would you be asking yourself?
Let us suppose that the last patient you saw was in surgical outpatients and she was a
lady aged 35 years presenting to the clinic with a nodular goitre. You have taken her history and found out she is married with no children. She first noticed a swelling in her neck
about six months ago, went to her GP three months ago and has waited for the out-patient appointment since her second visit to the GP two and a half months ago. The GP
has stated in his letter that the thyroid function tests were borderline normal and that
there is no family history of thyroid disease. In your detailed and systematic history taking
you have not discovered any symptoms referable to the thyroid gland, but the patient
does seem to be rather anxious. Examination confirms a moderately enlarged gland with
multiple small nodules, everything else is normal, but the patient seems to be slightly
trembly and perhaps sweating more than you would expect. Now step aside from your
history and examination and ask yourself what she might be thinking and feeling. Now do
it again.
Let us just consider some of her possible thoughts and feelings. First, she is almost certainly frightened. Hospitals are terrifying places to most people - they are pain and death
boxes with a funny smell. She is also afraid of the staff, especially the doctors, including
you. Doctors are frightening for several reasons, not least their association with the mysteries of life and death. They also tend to be dominant, powerful figures who have control
over one’s immediate and even long-term future. This patient knows that many doctors do
not say very much, and what they do say can be difficult to understand. She also knows
that doctors usually do not tell the whole truth.
She is also very concerned about herself. She has a lumpy enlargement in her neck,
which to her is cancer until proved otherwise, and she will take a lot of convincing because her aunt died of cancer of the gullet and she had lumps in her neck. She remembers that her aunt’s doctors lied to her aunt, and that the treatment was horrible and ineffective. She has heard vaguely about the thyroid gland and knows from a friend that one
of the treatments is radioactive. This concerns her because she desperately wants children, she knows time is passing and she fears that a dose of radioactivity may put paid to
her chances forever. She is also afraid of an operation because she has never been in
hospital and hates the idea of being ‘put to sleep’. She does not wish to lose control. She
also knows from friends, television and everyday experiences that operations go wrong
and the neck seems to be a pretty dodgy place. Her husband produced a bundle of
sheets from three websites he had found on the Internet about the thyroid gland. She did
not understand much of this information and could not bring herself to read some of the
more alarming parts. She wishes that her husband was with her, but worries that he has
not really wanted to talk about her neck or her coming to the hospital. She wonders if she
is now ugly and unattractive. The bottom line is that she does not want to die.”
from Peter Tate, “The Doctor’s Communication Handbook”, 4th edition, 2003, Radcliffe, Abingdon, UK.
How do you think the sentiments expressed above might alter your approach to Jane,
and the nature of the information you might gather from her?
Scenario 4
Rob was unfortunate in dying from his aneurysm at a relatively early age. The outcome might
have been very different if he had attended for regular check-ups as he was advised.
The Health Belief Model (see the diagram below) proposes that people will be motivated to
carry out protective health behaviours in response to a perceived threat to health. The perceived benefits of a course of action are weighed against the perceived barriers. It also proposes that a trigger event is often necessary to make a person change their behaviour.
Use the diagram below to help you answer the questions.
Which aspects of the Health Belief Model do you think might apply to the diferent stages of
Rob’s illness?
Why do you think Rob did not keep up his attendance at the hospital?
How does this model help us to understand why a serious health scare can make people
change their behaviour. For example, how does it help explain why suffering a heart attack
might help a patient to stop smoking?
Perceived
susceptibility
Perceived
severity
Demographic
variables
Perceived
benefits
Perceived
barriers
Cues to
action
Behaviour