Chest Pain
Cardiology in the ED
Ballarat Emergency Medicine Training Hub
Contributors – Dr Jaycen Cruickshank
Mark Hartnell & Ballarat ED physicians
Material from DR.MUHAMMAD FAROOQUE MB BS DTCD
Chest pain & syncope
Learning objectives
Note syncope covered in another presentation

This session will examine contrasting clinical cases of chest pain that may
be due to potentially lethal causes such as myocardial infarction or more
benign causes such as costochondritis. Important features in the history
that help discriminate different causes of chest pain and syncope will be
discussed along with appropriate initial investigations.
Learning objectives

To name the common and important medical conditions that cause chest
pain and their characteristic features on history.
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To rapidly diagnose and manage acute myocardial infarction
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To interpret ECGs in myocardial ischaemia and arrhythmias.
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To name the common and important medical conditions that cause syncope
and their characteristic features on history and exam.
Refer to ED lecture series and self directed
workbooks
Pre reading

Hughes T & Cruickshank J. Adult Emergency Medicine at a Glance.
Chichester, West Sussex, UK : John Wiley & Sons, 2011.
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Chapter 21 Slow heart rate. Chapter 32 Fast heart rate.
Chapter 34 Chest pain: cardiovascular.
Chapter 35 Chest pain: non cardiovasular
Other learning resources
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BHS guidelines
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Follow this link to the presentation on BHS intranet (http://dev-intranet/node/370)
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MJA consensus guidelines
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https://www.mja.com.au/sites/default/files/issues/184_08_170406/suppl_170406_fm.pdf
https://www.mja.com.au/sites/default/files/issues/191_06_210909/bri10275_fm.pdf
Cruickshank J. Initial management of cardiac arrhythmias. Vol 37, (7) 516520 2008 Australian Family Physician.
http://www.racgp.org.au/afp/200807/200807cruickshank.pdf
Learning objectives
Focus on cardiac ischaemia
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To rapidly diagnose and manage acute myocardial
infarction – BHS and national guidelines and
systems.
To interpret ECGs in myocardial ischaemia and
arrhythmias
Investigation and treatments in myocardial
ischaemia - what and when
Pitfalls and red flags
Including what to do with atypical presentations
Causes of Chest Pain
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Oesophageal
 Oesophagitis
 Oesophageal spasm
Musculoskeletal
 Muscle injury, spasm
 Costochondral joint
inflammation
Skin
 Herpes Zoster (Shingles)
Emergency Medicine
6 deadly causes of chest pain

Acute coronary syndromes
Aortic dissection
Pulmonary Embolus ** most commonly presents with dyspnea
Pericardial Tamponade / Myo- & Pericarditis
Oesophageal Rupture
Tension Pneumothorax
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(6 things on a list is too many, but…)
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….but luckily some diagnoses
predictable for clinicians…
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Myo/pericarditis – a diagnostic ECG
Oesophageal rupture – a classic historyHx
Tension pneumothorax – a classic
examination
Pleuritic pain has a differential diagnosis that
generally does not include cardiac ischaemia
Leaving three ‘problems’:

Acute Coronary Syndromes, Aortic dissection
Pulmonary Embolus
Assessment
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Pre- and post test probability
Pre test probability influenced by factors such as:
History of previous coronary disease
Angina, AMI, coronary angiogram or angioplasty,
coronary surgery
History of cardiac risk factors
Smoking, Hypertension, High Cholesterol, Diabetes
Mellitus
Diagnostic approach to Acute Coronary Syndromes is
often a ‘risk assessment’ rather than a ‘diagnosis’
History of the complaint
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By far the most predictive assessment
Do it well, saves time!
Know the classic story for the complaints but
beware of the pitfalls
If you can make a confident diagnosis DON’T
do tests “JUST IN CASE”
History – typical descriptions
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Pleuritic Pain = Pain
worse on inspiration
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Sharp, stabbing
Localised
Worse on inspiration,
coughing
May be worse on sitting
up or leaning forward
Not related to exertion
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Oesophageal pain
•
•
•
•
•
Usually “Burning” but
may be dull ache
Worse after meals
Worse on lying down
Relieved by antacid
Oesophageal spasm
may be relieved by GTN
History & ECG: pericarditis
•
•
•
•
•
Due to pericardial inflammation: pericarditis
Central or Left side
Sharp, stabbing
Worse on movement, on breathing, lying flat
Relief sitting forward
History typical of
Myocardial ischaemia
•
•
•
•
•
•
•
•
“Angina Pectoris” = Pain in the chest
Central chest pressure, tightness,
squeezing
Intensity increases over a few
minutes
Radiation to shoulders, arms, neck,
jaw
Worse with exertion
May be relieved by rest
May be relieved by Glyceryl Tri
Nitrate (GTN)
Associated sweating, nausea,
dyspnoea

Often not described as a
“pain” but as
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Pressure
Discomfort
Ache
Tightness
May be mistaken by patient
(and doctor) for indigestion
History pitfalls
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Response to analgesia
type does not make a
diagnosis
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cardiac pain can get
better with antacid
Oesophageal pain
improves with GTN
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“Atypical” pain
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Is common
Does not exclude
ischaemia
May be more common in
women, renal failure
Some patients have no pain
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“Silent” ischaemia or
infarction
More common in diabetics
due to neuropathy
ACS – history pitfalls
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Painless AMI common with age, women and
diabetics
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Prev stroke or heart failure also risks
By age 85 MAJORITY of AMI painless
Anginal ‘equivalents’ include:
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Dyspnoea (commonest)
With age: syncope, weakness, confusion
Elderly women also: cold sweats & dizziness
Which features of pain make myocardial
ischaemia more or less likely?
More likely
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Radiates to shoulders
Worse on exercise
Associated dyspnoea
Less likely
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Stabbing, sharp
Pleuritic
Worse on changing position
Very localised
Reproduced by palpation or
movement
Very brief (seconds)
Very prolonged (constant for
days)
Radiates to the legs
No past history of AMI or angina
Response to analgesia

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The “GI cocktail” has only been studied
poorly, mostly other drugs get given around
the same time
Not safe to make a discharge decision based
on the response
Chest wall tender & AMI
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7% of AMI or unstable angina have partially
or fully reproducible pain
Important to note if the pain produced is the
same one
Be suspicious if there is no proceeding
history of injury
Acute coronary syndromes
https://www.mja.com.au/sites/default/files/issues
/191_06_210909/bri10275_fm.pdf
ECG interpret in <5mins.
ECG – your opinion?
Basic investigations
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ECG, CXR and bloods
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In Emergency Department an ECG in most if not
all patients.
More useful as ‘rule in’ than ‘rule out’
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ECG in AMI 50% sensitivity, 90% specificity
ECG not useful in PE or aortic dissection
Acute Coronary Syndrome
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Difference between risk Ax & diagnosis
Blood tests are not diagnostic tests (unless
positive)
Ruling out AMI in a stable patient with a nondiagnostic ECG is the difficulty
prognosis v diagnosis #1
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The same coronary lesion in one patient
might be tolerated or a disaster
Increased rate of complications with:
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LV dysfunction
DM
HTN / LVH
Probably renal failure
prognosis v diagnosis #2
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Diagnostic probability determines approach
to diagnosis…
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?EST / ?angiography / ?inpatient or outpt.
Dif tests different risks & level of sensitivity
Risk profile defines Rx decisions…
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Risk v benefit of dif antiplatelet Rx
Admit to CCU or ward
Assessing risk
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Risk factors don’t help in the ED
ECG and biomarkers do
Many systems, none perfect, and following
the guideline of your hospital including getting
expert help is sensible and medico-legally
correct
ED role: determine disposition immed RX
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Risk Ax of complications = discharge
TIMI 7 rule (for an example)
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5 on Hx:
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Age>65, >2 IHD RF’s, known stenosis, >2
episodes angina in 24H, aspirin use
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2 tests: ECG changes / positive troponin
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HIGH risk = ECG / trop +ve / TIMI > 2
LOW risk = normal ECG & trop, TIMI <3
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30 day mortality 1.7%
ECG as rule out AMI test
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Not known how useful a normal ECG is:
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AMI rate ?<1%, up to 7%
It is known that an abnormal non-diagnostic
ECG = risk for missed AMI
Probably with passing time a normal ECG
begins to decrease likelihood of at risk ACS
but this has not been shown
Blood markers - troponin
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Troponin I or T rise within 3-6H and then
remain elevated for about one week
Serial testing, at least 6H after symptom
onset improves sensitivity
In ACS an increased troponin is a marker for
increased risk of AMI and death
Does NOT diagnose cardiac ischaemia
myoglobin
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One study showed excellent rule out figures
for 90 minute testing of troponin and
myoglobin levels
Rx in ACS
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Aspirin should be given immediately
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Rapid decisions on reperfusion
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alternative clopidogrel if truly contraindicated
Based on ECG only
All other decisions less time dependent
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Can involve further consultation
Need risk / benefit analysis
Adjunctive Rx in ACS
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Further antiplatelet options:
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Symptomatic / pain control
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Heparin (LMW v unfractionated)
clopidogrel
Glycoprotein IIb/IIIa inhibitors
GTN / morphine
Secondary prevention
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BBlockade / statins
Thrombolysis (fibrinolysis)
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50% flow return rate where indicated
But 15% re-occlude (and do badly)
1% patients have a major bleed
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Usually intra-cranial haemorrhage
Using LMW heparin as opposed to UFH:
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Some evidence more benefit
PCI v thrombolysis
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Guideline varies with:
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time from symptom onset
Time to get to catheter lab (balloon inflation)
Lesser factors inc localisation of AMI and relative
risk / benefit thrombolysis
All other things being equal esp in anterior
AMI PCI better option
Guideline for PCI v ‘lysis
CABG’s
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Routine after STEMI
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Considered if poor LVF
‘appropriate’ anatomy
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Emergency
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Means LAD or severe vessel disease
Considered in cardiogenic shock
Failed reperfusion and persistent pain
All above is level B recommendation
Role of PCI high risk ACS
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Still being defined:
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‘current problem versus the next one’
Different approaches tried:
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Risk stratify & PCI high risk
Maximise non-invasive Rx
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Then PCI ‘breakthrough’
PCI all patients
PCI high risk ACS
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PCI all approach reduces hospitalisations
But low risk patients potentially do worse
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Peri-procedural AMI
Current Cochrane recommendation is that
‘may be a benefit in early PCI if risk
stratification in high category’
AORTIC DISSECTION
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Challenging diagnosis,
lethal if missed (75% in
2/52), prob.s if Rx as ACS
Classic Hx:
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Sudden onset ripping /
tearing PIC, radiates to
back (interscapular,
migratory) & Hx HTN
Not sensitive enough
Best approach is risk factor
assessment
Be aware of atypical
presentations
Risk factors for Aortic
Dissection
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HTN
Aortic valve
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Abnormal Aorta – mainly congenital
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Bicuspid, previous surgery
Coarctation / Marfan’s / Ehlers-Danlos
Arteritis (Giant cell)
Aortic ‘stresses’
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PREGNANCY, COCAINE, TRAUMA
Atypical presentations AD
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Atypical history
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Non-classical pain, chest or back only, severe &
sharp pain, abdo pain
Syncope
Acute stroke (& peripheral neuro)
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Others just get too weird & make you paranoid
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Eg. Pulsatile stenoclavicular joint!!
AD - imaging
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Widened mediastinum (62%) and abnormal
aortic contour (50%) most sensitive CXR
findings
Normal CXR may decrease the likelihood but
if examination, Hx and RF’s raise suspicion
needs further imaging
Oesophageal rupture
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Ruptures due to developing a tear due to
raised intra-luminal pressure
Classical triad is forceful emesis, chest pain
and subcutaneous emphysema
Prefer to sit up and may have chest signs
CXR usually abnormal on left side
Oesophageal rupture problems
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Definitive diagnosis usu on CT,
can do oesophagogram (can
be false negatives)
Vomiting can be absent in 21%
Can occur in kids, can be right
sided
Patients are UNWELL, only
needs pursuing in atypical
case if SICK
Myo and pericarditis
Pulmonary Embolism
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Classic triad about 20%:
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Typically some combination of:
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Pleuritic PIC, dyspnoea & haemoptysis
SOB, PIC, tachypnoea, tachycardia
Dypnoea commonest (about 80%)
Pleuritic pain not sensitive or specific
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44% with, 30% without in one study
Needs infarction
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more likely in existing lung disease, implies smaller clot?
PE investigations
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No test is ideal
Can have normal tests & be very unlucky
Classic diagnosis for combining pre- and
post-test clinical probability
PE – more worrying facts
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Mortality hasn’t changed
Rate of asymptomatic PE not known
Not known what the actual incidence is
Most diagnosed at autopsy in US
10% deaths after diagnosis, 90% before
Up to a third of PE’s asymptomatic?
PE - ECG
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ECG has many reported associations
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S1Q3T3 about 12% of PE & normal pt.s
Sinus tachy not that common
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Range is 8-69% in 6 studies
Commonest is anterior T wave inversion
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All from study of pt. s AFTER diagnosis
68% pt.s with confirmed PE
ECG doesn’t ‘rule in’ or ‘rule out’
PE - ABG
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Tells you nothing about the cause of hypoxia
only the magnitude
If you know there is hypoxia already you don’t
need to do it
If you really need to you can calculate an A-a
gradient WITHOUT removing O2
PE – pre test probabilty
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Multiple systems for doing this
Most widespread and validated is Well’s
score
Note dif. Well’s score for PE & DVT
PE – Well’s criteria
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3 points for:
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PE ‘most likely diagnosis’
Signs and symptoms suggesting DVT
1.5 points for:
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PR>100, past Hx (PE/DVT), immobilisation
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1 point for:
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Haemoptysis or malignancy
<2 low (10%), 2-6 i/med (25%), >6 high (50%)
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Well’s – use in practice
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Need to not automatically apply
Eg. some pt.s will be moderate risk almost
everty time they come to ED
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(& DON’T need a scan everytime)
D-dimer
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Only use is in a low risk patient
A negative test makes PE very unlikely
A slightly positive test IS a positive test
Imaging – CTPA and VQ
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CTPA has high negative predictive value
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Alternative diagnosis up to 40%
Better if abnormal CXR (VQ less useful)
Inconclusive rates up to 10%
VQ scanning if normal perfusion scan
effectively excludes (but only in 14%)
PE – more on VQ scanning
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Normal perfusion excludes (14% of pt.s)
‘non-diagnostic’ (73%) covers:
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Low probability, 15-30% have PE
Intermediate, >30% have PE
High probability, >85% have PE
VQ – combining pre & post
test assessment
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Low clinical and low scan, <5% have PE
Low clinical and i/med scan, same % PE
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Also negative LL ultrasound, <3% PE
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High probability clinical & scan, >95% PE
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Main problem is high clinical and
low/intermediate scans, rate is 15-75%
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(often cardiopulmonary disease, past PE)
Imaging pregnant patients
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Most advice is to investigate as normal
D-dimer will be positive in pregnancy
No consistant agreement re VQ v CTPA
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VQ isotopes renal excreted, bladder near uterus
CTPA has contrast as well as radiation
Tempting to try leg ultrasound
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But only 80% PE have LL DVT
The ‘Gold Standard’

There isn’t one!
Pulmonary angiography was once but
mortality almost 1%, morbidity 2-5%
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Compared to warfarin:
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1-2% mortality
5-25% morbidity
Food for thought
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What is the mortality rate of a d-dimer?
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I didn’t think it was a PE, just thought I better
do one anyway….
The result is ‘not negative’…
Better order a CTPA…
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Anaphylactic contrast reaction? Cancer?
False positive, warfarin, car accident?
PERC rule – test free!
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A rule which is applied after ‘gestalt’
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Defined as <15% by physician after Ax
This was the case in 2/3 of patients
These patients had VTE rate of 3.3%
Rule aimed for false negative rate of <2%
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Approx rate PE/death after –ve imaging
Further tests inc. false +ve (not less miss)
PERC rule…
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The rule is:
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“PERC negative” AND gestalt = <1%
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Age<50, PR<100, no haemoptysis, no E2 Rx, no
surgery 4/52 (=ETT), no past VTE, no unilateral
leg swelling (from looking!)
Study centres inc NZ (more like us??)
Thought to reduce tests by 20%
Idea is not to do ANY tests
PE – less worrying facts
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A spectrum of disease ranging from a normal
physiological process to death?
Process of using a pre-test and post-test
probability seems to work
“PERC positive” and –ve gestalt = PE 5%
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Ie less than the suspected 15%
The PERC rule also determined that
immobilisation was 6H knees bent
Spot diagnoses
Spot diagnoses
Some final points
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Examine patients properly
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Beware chest wall tenderness in AMI

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Expose and look at the chest (eg. Zoster)
but back tenderness reproducing chest pain is
very useful
How you get rid of the patients pain does not
diagnose but HELPS THE PATIENT!!

Give them everything ASAP