Lola

Smith Case 1 Wrap

LOLA SMITH CASE WRAP

Case 1 (Chest Pain)

DIAGNOSIS: STABLE ANGINA

University of Adelaide
MBBS I 2017
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 Lola Smith Case 1 Wrap

TABLE OF CONTENTS
ANATOMY & PHYSIOLOGY .............................................................................................................. 3
1. SURFACE ANATOMY OF THE THORAX ............................................................................................... 3
2. STRUCTURE AND FUNCTION OF THE HEART ....................................................................................... 5
3. GROSS ANATOMY OF LUNGS 
 ..................................................................................................... 10
4. PLEURA & PLEURAL CAVITY .......................................................................................................... 10
5. CIRCULATION ............................................................................................................................. 11
6. CORONARY CIRCULATION ............................................................................................................. 11
7. MECHANISMS OF FLUID MOVEMENTS ........................................................................................... 12
PATHOLOGY & PATHOPHYSIOLOGY .............................................................................................. 13
1. MYOCARDIAL CELLS UNDER ISCHAEMIA ......................................................................................... 13
2. ATHEROSCLEROSIS AND ATHEROGENESIS ........................................................................................ 13
3. PAIN PATHWAYS & MECHANISMS ................................................................................................. 13
4. STABLE VS UNSTABLE ANGINA ...................................................................................................... 14
5. RISK FACTORS OF CAD ................................................................................................................ 14
6. RISK FACTOR VS CAUSE OF DISEASE ............................................................................................... 14
CLINICAL REASONING & CLINICAL SCIENCE ................................................................................... 15
1. HISTORY-TAKING & PHYSICAL EXAMINATION .................................................................................. 15
2. SYMPTOMS OF ANGINA ............................................................................................................... 15
3. COMMON DIFFERENTIAL DIAGNOSES ............................................................................................. 16
4. BASIC INVESTIGATIONS ................................................................................................................ 17
POPULATION HEALTH, EPIDEMIOLOGY ......................................................................................... 19
1. INCIDENCE, PREVALENCE, RISK FACTORS WITH CAD ......................................................................... 19
SOCIAL, CULTURAL & BEHAVIOURAL SCIENCE ............................................................................... 19
1. PSYCHOLOGICAL/SOCIAL FACTORS ................................................................................................ 19
2. DISCUSSIONS ............................................................................................................................. 19
3. CHECK UNDERSTANDING .............................................................................................................. 19
ETHICS & MEDICO-LEGAL ISSUES .................................................................................................. 19
1. PATIENT’S RIGHTS ...................................................................................................................... 19
2. ETHICAL ASPECTS OF CONFIDENTIALITY .......................................................................................... 19

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ANATOMY & PHYSIOLOGY

1. SURFACE ANATOMY OF THE THORAX

Describe the basic surface anatomy of the thorax.
• Thoracic wall surrounded by:
o Muscles, fat, skin
o Thoracic spine
o Thoracic cage
o Manubrium and sternum
o Pleura
• Boundaries of the thorax
o Thoracic cage
o Superior thoracic aperture
§ Posterior boundary: T1 vertebral body
§ Lateral boundary: first ribs
§ Anterior boundary: manubrium
§ Major structures that pass through: thymus,
trachea, oesophagus, phrenic + vagus nerves
common carotid arteries, subclavian veins
o Inferior thoracic aperture
§ Posterior boundary: T12 vertebral body
th th
§ Posterolateral boundary: 11 + 12 ribs
th
§ Anterolateral boundary: costal cartilage of 7 -
th
10 rubs
§ Anterior boundary: xiphoid process
§ Covered by the diaphragm
• Thoracic Spine
o Consists of 12 thoracic vertebrae
o Has facets on body to allow for articulation with ribs
• Thoracic cage (rib cage)
o Consists of 12 rib pairs
o True ribs (1-7): attached directly to sternum by
costal cartilages
o False ribs (8-10): converge anteriorly via costal
cartilages and are attached indirectly to sternum
o Floating ribs (11-12): have no attachments to the
sternal
o Head of rib articulates with body of vertebrae
o Tubercle of rib articulates with transverse process
of vertebrae

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• Diaphragm
o Sheet of muscle separating thoracic and abdominal cavities
o Striated/skeletal muscle
o Attachment points: sternum, costal cartilages, ribs, thoracic
vertebra
o Right side is higher than left side as liver pushes up on left side
o Apertures
§ Inferior vena cava – through central tendon (no
movement so no interference) at T8
§ Oesophagus – through curve of muscle (lumen is closed
to prevent contents flowing back up) at T10
§ Descending aorta – through back of diaphragm in front of vertebra at T12
• 3 Areas in the Thoracic Cavity
o Right + Left Pleural Cavities
§ Contains the two lungs
o Mediastinum
§ Superior mediastinum
Ø Above sternal angle-T1 vertebra
Ø Arch of aorta
Ø Superior Vena Cava
Ø Vagus + phrenic nerves
Ø Thymus
Ø Thoracic duct
Ø Trachea
§ Posterior mediastinum
Ø Behind the pericardium
Ø Thoracic Aorta
Ø Oesophagus
§ Anterior mediastinum
Ø In front of the pericardium
§ Middle mediastimium
Ø Pericardium with the heart
Ø Tracheal bifurcation
• Surface markings for heart
nd
o LEFT: 2 costal cartilage, 2.5 cm from sternum
th
o LEFT: 5 intercostal space, midclavicular line
rd
o RIGHT: 3 costal cartilage, 1cm from sternum
th
o RIGHT: 7 sternocostal junction

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• Surface Anatomy of the Thorax

o Midsternal line: middle of sternum
o Right + left midclavicular lines: parallel with midsternal line, passing through midpoint of each
clavicle
o Anterior axillary line
o Posterior axillary line
o Midaxillary line
o Midvertebral line: down midpoint of spine
o Right + left scapular lines: parallel with midvertebral line but passes through inferior angles of
the scapulae

2. STRUCTURE AND FUNCTION OF THE HEART

The 4 layers of the heart wall.
• Endocardium
o Consists of epithelial tissue
• Subendocardium
o Joins endocardium and myocardium
o Consists of loose fibrous tissue
o Contains vessels and nerves of conducting
system of heart
• Myocardium
o Consists of cardiac muscle (cardiomyocytes)
o Thickest layer
• Epicardium
o External layer formed by visceral layer of serous pericardium
• Pericardium
o Sac containing thin layer of fluid
o Covers the heart and beginning of great vessels
o Functions:
§ Provides lubrication
§ Fixes heart to mediastinum
§ Gives protection against infection
§ Prevents rapid overfilling
o Made up of two layers
§ External fibrous pericardium
§ Internal serous pericardium (visceral and perietal)

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The arrangement of the myocardium (to make the pumping action efficient) and the variation in

 myocardial muscle thickness.
• Myocardium is made up of cardiomyocytes interconnected to form branching fibres (syncytium)
• Striation
o Formed by segments of thick and thin protein filament

• T-Tubules
o Invaginations that transverse length of cell
o Allows influx of calcium ions during action potentials to reach throughout cell rapidly (which
initiates release of calcium ions from sarcoplasmic reticulum)
• Cells are joined by intercalated discs (3 types)
o Desmosomes: mechanically holds cells together
o Gap junctions: areas of low electrical resistance allowing
action potentials to spread
o Fascia adherens: helps transmit contractile forces
• Interlacing bundles of cardiac muscle fibres are arranged spirally
around circumference of heart
o Allows for ‘wringing’ effect
o When ventricular muscles contract, diameter of ventricles
decreases while apex is pulled upwards in a rotating manner
o Contraction of muscles cells
§ At rest, tropomyosin lies across the binding sites of actin, not allowing myosin heads
to bind
2+
§ When activated, Ca binds to troponin, changing the shape of tropomyosin and
exposing active sites on actin
§ Myosin heads can now bind to actin, and myosin pulls thin filaments inward

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• Left ventricle is thicker than right ventricles

o Pulmonary circulation is low pressure/resistance
o Systemic circulation is high pressure/resistance
o Therefore, the left side must work harder

Basic structure and arrangement of the valves in maintaining unidirectional flow.

Atrioventricular valves
• Tricuspid valve (RAàRV)
• Bicuspid (mitral) valve (LAàLV)
• Consists of cusps (flaps of fibrous tissue covered with endothelium)
• Prevents regurgitation of blood back into the atrium from the ventricle
• Eversion is prevented by papillary muscles & chordae tendinae
Semi-lunar valves
• Pulmonary valve
• Aortic valve
• Consists of 3 cups in a concave shape (when viewed superiorly)
• Prevent backflow of blood going into the major arteries
• Opened by internal pressure forcing them outwards
• Closed by backflow filling pocketlike cusps, pushing them closed
Fibrous skeleton of heart
• Consists of 4 bands of dense connective tissue (fibrous rings) which surrounds the 4 valves of the heart
• Fibrous skeleton stops electrical current, ensuring currents only travel through AV node

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The events of the cardiac cycle.

Event Direction of flow Electrical Activity Pressure ECG

SA node reaches
Atrial contraction causes an
Ventricular

P
Diastole

Atrial Contraction From atria to threshold and fires

increase in atrial pressure (AV
(1) the ventricles causing Atrial
Valves open)
depolarisation

Impulse reaches Ventricular contraction causes

Isovolumetric AV node and the ventricular pressure to
ventricular No blood flow begins to cause exceed atrial but does not yet PR
Ventricular Systole

contraction (2) ventricular exceed aortic pressure.

depolarization (AV Valves/SL Valves closed)

Blood flows
from ventricles Ventricular pressure exceeds
Ventricular Ventricles are aortic pressure.
to the aorta and QRS
ejection (3+4) depolarized
pulmonary (SL Valves Open)
arteries.

Arterial pressure exceeds

Isovolumetric
From veins to Ventricular ventricular pressure which still
Ventricular T
atria repolarization exceeds atrial pressure (AV
Ventricular Diastole

Relaxation (5)
Valves/SL Valves closed)

Atrial pressure exceeds

ventricular pressure because of
Ventricular Filling From atria to No electrical
inflow of blood from the TP
(6+7) ventricles activity
venous system. Thus AV valves
open

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The regulation of electrical activity.

Two specialisations of cardiac muscle cells:

• Contractile cells (99%)

o Does the mechanical work of pumping, doesn’t initiates its own action potential
• Autorhythmic cells:
o Doesn’t contract, but initiates own action potential
o Displays pacemaker potential: membrane potential slowly depolarises until threshold is
reached à action potential is fired

Action potentials in autorhythmic cells:

• Phase 4 (pacemaker potential)
+
o Opening of funny channels (If) allowing influx of Na
+ +
o Gradual closing of K channels reducing efflux of K
2+ 2+
o Opening of T-type Ca channels (as If closes) allowing influx of Ca (occurs midway through)
Þ Gradual depolarisation towards threshold
• Phase 0 (depolarization)
2+
o Closing of T-type Ca channels
2+ 2+
o Opening of L-type Ca channels allowing large influx of Ca
Þ Rapid increase in membrane potential
• Phase 3 (repolarization)
2+
o Closing of L-type Ca channels
+ +
o Opening of voltage-gated K channels, allowing efflux of K
Þ Decrease in membrane potential to initial potential
• Various autorhythmic cells have different rates of pacemaker potential
and thus, different rates of action potential initiation
o Faster rate is at the SA node, and thus, this is the pacemaker of the heart

Action potentials in cardiomyocytes:

• Phase 4 (resting)
o Membrane potential remains steady until stimulated by SA node
+ +
o K channels open are leaky, allowing K to leak outwards
Þ Membrane potential maintained
• Phase 0 (depolarization)
+ +
o Opening of voltage-gated Na channels, allowing rapid influx of Na
Þ Rapid increase in membrane potential
• Phase 1 (early repolarisation)
+
o Opening of transient K channels, allowing brief efflux of
+
K
Þ Membrane potential slightly decreases
• Phase 2 (plateau)
2+ 2+
o Opening of L-Type Ca channels, allowing influx of Ca
+ +
o Closing of some K channels, decreasing efflux of K
Þ Repolarization is prevented and plateau is prolonged
• Phase 3 (repolarization)
2+
o Closing of Ca channels
+ +
o Opening of K channels, allowing efflux of K
+
Þ Decrease in membrane potential to initial potential (at which the K channels close, leaving
only the leaky channels open)

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3. GROSS ANATOMY OF LUNGS 


Describe the gross anatomy of the lungs (not microstructure).
• Lie on either side of the mediastinum within thoracic cavity
• Left lung slightly smaller than the right due to the liver
• Each lung consists of
o Apex
o Base (sits on the diaphragm)
o Lobes (2/3)
§ Right has 3 lobes (superior, middle and
inferior) which is separated by the
oblique and horizontal fissure
§ Left has 2 lobes (superior and inferior) which is separated by the oblique fissure
o Surfaces – areas of the thorax that they face
§ Mediastinal surface faces lateral aspect of middle mediastinum, has the lung hilum
(where structures enter and leave the lung)
§ Diaphragmatic surface
§ Costal surface
o Borders – edges of the lungs
• Vasculature
o 2 pulmonary arteries (1 for each lung)
o 4 pulmonary veins (2 for each lung)

4. PLEURA & PLEURAL CAVITY

Describe the visceral and parietal pleura, as well as the pleural cavity. 

• Serous membranes that line lungs and thoracic cavity
• Parietal
o Covers internal surface of thoracic cavity
• Visceral
o Covers the lungs
• Pleural cavity contains small volume of serous fluid
o Lubricates surfaces
o Provides surface tension, pulling parietal and visceral pleura together ensuring when the
thorax expands, the lung also expands (pneumothorax – surface tension is lost when air enters
the cavity)
• Pleural Recesses
o Costodiaphragmatic
o Costomediastinal
o Areas in which fluid can collect (pleural effusion)

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5. CIRCULATION
Describe the layout of the circulation, in particular the relationship of the systemic and pulmonary
circulations that allows the oxygenation of blood in the lungs followed by delivery of oxygenated
blood to the periphery (body tissues), and return of deoxygenated blood to the heart.
• Deoxygenated blood from tissues à IVC/SPC à RA à RV à R/L Pulmonary arteries à Lungs
• Oxygenated blood from lungs à R/L Pulmonary Veins à LA à LV à Aorta à Systemic tissues

6. CORONARY CIRCULATION
The basic arrangement of the main coronary arteries and the areas of the heart supplied by each
artery (ie left, anterior descending, left circumflex and right coronary arteries).
• When aortic valve closes, backflow goes into coronary arteries (ventricular diastole)
• CA arises from aortic root
o Right Coronary Artery (RCA): supplies SA/AV node, RA, RV
§ Right marginal branch: supplies RV, apex
§ Posterior interventricular artery: supplies interventricular septum
o Left Coronary Artery (LCA): supplies left side of the heart
§ Left circumflex artery: supplies LA, LV
§ Anterior interventricular artery (left anterior descending LAD): supplies RV, LV, interventricular
septum
§ Left marginal artery: supplies LV

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An understanding of coronary veins and drainage into the coronary sinus.

• 5 vessels that drain into the coronary sinus
o Great cardiac vein originates at the apex and moves superiorly around the pulmonary trunk.
Travels up the anterior interventricular groove to the sulcus then travels with the LCx.
o Small cardiac vein goes around the right ventricle (following the RMA)
o Middle cardiac vein is located posteriorly and follows the Posterior Descending Artery
o Left marginal vein is posterior and superior to the middle and posterior ventricular veins.
o Left posterior ventricular vein is posterior and runs along the posterior sulcus to join the sinus.

An understanding that the myocardium itself requires a constant supply of oxygenated blood.

7. MECHANISMS OF FLUID MOVEMENTS

Demonstrate understanding of the determinants/mechanisms of fluid movements between
capillaries and the peripheral tissues (Starling’s forces): 
 a. Oncotic pressure 
 b. Hydrostatic
pressure c. Vascular permeability
4 forces that influenced fluid movement across capillary wall:

1. Capillary blood pressure (𝑃" )

a. Pressure exerted on inside of capillary walls
b. Tends to force fluid out
2. Plasma-colloid osmotic pressure (𝜋$ )
a. Due to large size of proteins, they remain in the blood
b. Osmotic pressure established
c. Tends to pull fluid in
3. Interstitial fluid hydrostatic pressure (𝑃%& ) à usually insignificant
a. Pressure exerted on outside of capillary walls
b. Tends to pull fluid in
4. Interstitial fluid-colloid osmotic pressure (𝜋%& ) à usually insignificant
a. Leakage of plasma protein may establish an osmotic gradient
b. Tends to pull fluid out

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PATHOLOGY & PATHOPHYSIOLOGY

1. MYOCARDIAL CELLS UNDER ISCHAEMIA

Describe how the function of myocardial cells alters under conditions of ischaemia (insufficient
blood supply).
• Under ischaemia, myocardial cells have inadequate oxygen supply to meet their demand
• Cells begin undergoing anaerobic respiration, increasing production of lactic acid
• May result in cell necrosis and fibrosis of the damaged area

2. ATHEROSCLEROSIS AND ATHEROGENESIS

Describe the basic features of atherosclerosis and how it develops (atherogenesis).
• Atherosclerosis is the build up of plaque inside the arteries
• Causes thickening and stiffening of arterial wall

3. PAIN PATHWAYS & MECHANISMS

Demonstrate a basic understanding of pain pathways and mechanisms by which these messages are
transmitted to the brain. Specifically, 
 a. an understanding of the sensory receptors for pain
(nociceptors); 
 b. the difference between A-delta and C nerve fibres, with regards to their structure,
speed of 
 conduction and the nature of the pain (sharp, dull, well localised, diffuse); 
 c. a basic
understanding of the transmission of the pain signal upwards through the 
 spinothalamic tract to
the somatosensory cortex in the brain. d. a basic understanding of the mechanism for referred pain.
Nociceptors
• Receptor for pain or injurious stimuli
• Types of nociceptors:
o Mechanical Nociceptor: responds to mechanical damage such as cutting, crushing or pinching
o Thermal Nociceptor: responds to temperatures extremes
o Polymodal Nociceptor: responds to all kinds of damaging stimuli

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A-delta fibres vs C-fibres

A-delta fibres C-fibres
Fast pain Slow pain
Stimulation of mechanical and thermal nociceptors Stimulation of polymodal nociceptors
Myelinated Unmyelinated
Produces sharp, prickling sensation Produces dull, aching, burning sensation
Easily localized Poorly localized
Occurs first Occurs second; persists for longer time
Pain Pathway

Primary afferent
Somatosensory
fibres synapse with Transmitted to Thalumus interprets
Stimulation of Impulses travel along Transmitted to dorsal cortex
Painful Stimulus second-order brainvia the pain and
Noiceptor snesory nerve fibre horn of spinal chord localises/discriminate
excitatory spinothalamic tract produces sensation
s pain
interneurons

Referred Pain

• Pain perceived at location other than at the site of painful stimulus

• Structures that experience referred pain are often innervated by nerves that synapse at the same
vertebral region as the structures experiencing the stimulus

4. STABLE VS UNSTABLE ANGINA

Understand the difference between stable and unstable angina.
Stable Angina Unstable Angina
Comes on with exertion, but not at rest Can come on at rest
Occurs over time Occurs due to acute plaque event
<75% occlusion of coronary artery >90% occlusion of coronary artery
Alleviated by rest Not alleviated by rest
Follows a ‘regular’ pattern Does not follow a regular pattern

5. RISK FACTORS OF CAD

Demonstrate a basic understanding of "risk factors" (modifiable and non-modifiable) for coronary
artery disease, and their significance to clinical medicine.
Modifiable Non-modifiable
• Smoking • Ethnicity
• Diet (high cholesterol) • Age
• Weight o >45 male
• Exercise o <55 female
• Drugs • Gender
• Hormone therapy • Post-menopausal
• Hereditary
Both • Past personal history of IDH
• Diabetes • Peripheral/artery disease
• Hypertension
• Cholesterol

6. RISK FACTOR VS CAUSE OF DISEASE

Understand the difference between a “risk factor” for, and a “cause” of disease.
A risk factor is any attribute, characteristic or exposure of an individual that increases the likelihood of
developing a disease or injury.

A cause is a known attribute that gave rise to the development of a disease in an individual.

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CLINICAL REASONING & CLINICAL SCIENCE

1. HISTORY-TAKING & PHYSICAL EXAMINATION

Show an understanding of the general approach to history-taking and physical examination of a
patient with ischaemic heart disease.
SEE APPROPRIATE CLINICAL SKILLS GUIDELINES

2. SYMPTOMS OF ANGINA
Link, in very basic terms, the symptoms of angina (including characteristics of pain, pain radiation)
to the underlying pathological and pathophysiological processes.

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3. COMMON DIFFERENTIAL DIAGNOSES

Demonstrate a basic ability to generate a list of common differential diagnoses for presentations
with chest pain, and understand the key features differentiating the major conditions.
Demonstrate a basic ability to apply the knowledge gained in this case to other similar
presentations, which may be caused by different conditions.
System Differential Symptoms

Angina Chest pain (crushing/tightness/pressure – dull) (1-10

Ischemia of the myocardium mins)
typically due to partial occlusion o Radiating to upper arm/jaw
of a coronary artery (typically Onset of pain with exertion
caused by CAD) Dyspnoea

Myocardial Infarction Acute/Unremitting pain (30-60 mins)

CV Ischemia of the myocardium o Radiating to upper arm/jaw
due to full occlusion of a Nausea/Sweating
coronary artery (typically Dyspnoea
caused by CAD) Light-headedness
Pericarditis Low-grade fever
Inflammation of the pericardium Chest pain – Sharp/Burning/Rubbing
Worse during inspiration/lying/swallowing
Cough
Pneumonia Productive cough
Pneumonia is an inflammatory Fever
condition of the lungs typically Sharp/Stabbing Chest pain (onset with breathing)
caused by infection. Fatigue
RS
Pulmonary Embolism Chest pain (pleuritic)
Pulmonary embolism is the Dyspnoea
occlusion of an artery in the Cough
lungs by an embolism Tachycardia
GORD Chest pain (burning – heartburn)
A chronic disease caused by o (often worse after eating/laying
the frequent reflux of gastric down/bending over)
GI
contents into the oesophagus Dysphagia
due to poor closure of the Regurgitation
oesophageal sphincter
Chest wall pain Sharper chest pain
(inc. Costochondritis/general o Sometimes onset with inspiration/cough
MS injury) Reproducible tenderness
MS
Inflammation of the costal
cartilage or physical damage to
the chest wall region
*thanks to Teham Ahmed

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4. BASIC INVESTIGATIONS
Not a learning objective but useful nonetheless
Blood Tests

• Procedure
o Done through venepuncture (intravenous therapy) into test tube
• Full Blood Count
o Identify presence of injection, anaemia or other blood disorders
• Cardiac troponin
o Troponin is a biomarker for acute MI
o Compare the levels of troponin (rise/fall)
• Electrolytes, urea, creatinine
• Check levels of certain fats, cholesterol, sugar, proteins in blood (abnormal levels would be
concerning)

Electrocardiography (ECG)

• ST segment elevation/depression may represent

ischaemia/infarction
• Rhythm disturbances (atrial arrhythmias, heart
block, intraventricular septal conduction delays)
• Stress testing may also show abnormal changes in
heart rate/blood pressure, abnormal rhythms, SOB,
chest pain that may be characteristic of CAD/IHD

Chest X-Ray

• Assists in differentiating between respiratory and cardiac causes of dyspnoea

• Can help identify evidence of heart failure

Coronary Angiography/Cardiac Catheterization

• Thin, flexible tube (catheter) is placed in blood vessel the threaded into coronary arteries where
dye is released
• X-rays are then taken allowing blood flow through coronary arteries to be studied

Echocardiography

• Transthoracic echo (TTE), transoesophaeal echo (TOE)

• Provides information about chamber size/shape, blood flow velocities, systolic/diastolic function,
valve function…

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Electrocardiogram

Lead Placement

• 12 leads = 6 limb leads + 6 chest leads

• Lead is the specific arrangement of a pair of connections (electrodes)
• Bipolar leads – records difference in potential between two electrodes (only leads I, II, III)
• Unipolar leads – records potential under one exploring electrode (though two electrodes are still used,
other is used as a neutral reference point)
• Limb leads
o I – right arm to left arm
o II – right arm to left leg
o III – left arm to left leg
o aVR – right arm
o aVL – left arm
o aVF – left leg
• Chest leads
th
o V1 – 4 intercostal space, right of sternum
th
o V2 – 4 intercostal space, left of sternum
o V3 – midway between V2 and V4
th
o V4 – 5 intercostal space, midclavicular line
th
o V5 – 5 intercostal space, anterior axillary line
th
o V6 – 5 intercostal space, midaxillary line

ECG

• P wave = atrial depolarization

• QRS complex = ventricular depolarization
• T wave = ventricular repolarization

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POPULATION HEALTH, EPIDEMIOLOGY

1. INCIDENCE, PREVALENCE, RISK FACTORS WITH CAD

Demonstrate an early awareness of the incidence, prevalence, and risk factors associated with
coronary artery disease.
• ISH responsible for ~ 20,000 deaths in 2013 (of the ~43,000 death from CVD)
• Men are at higher risk of contracting and dying to ISH than woman for all age groups
• 75% of the total deaths by IHD were people older than 75 years
• Epidemic of IHD is slowly decreasing in Australia
• Aboriginal and Torres Strait Islander people are 2.5 times more likely to die to ISH than the rest of the
Australian population
• Low socioeconomic groups are at 2 times more risk of death by IHD than high socioeconomic
groups

SOCIAL, CULTURAL & BEHAVIOURAL SCIENCE

1. PSYCHOLOGICAL/SOCIAL FACTORS
Describe the psychological and social factors contributing to heart disease.

2. DISCUSSIONS
The diagnosis of coronary artery disease

The need for lifestyle change to reduce the risk of future problems arising from coronary artery

 disease with people of different social and cultural backgrounds.

3. CHECK UNDERSTANDING

Describe how you would check the patient’s understanding of the information you have provided.

ETHICS & MEDICO-LEGAL ISSUES

1. PATIENT’S RIGHTS
Demonstrate an understanding of the patient’s rights, particularly in regards to privacy,
confidentiality and informed consent.

2. ETHICAL ASPECTS OF CONFIDENTIALITY

Describe the ethical aspects of confidentiality in respect of divulging patient information to family
members.

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