Chest Pain Cardiology in the ED

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Chest PainCardiology 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

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Chest pain syncopeLearning objectivesNote
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.
• To rapidly diagnose and manage acute myocardial
  infarction
• To interpret ECGs in myocardial ischaemia and
  arrhythmias.
• To name the common and important medical
  conditions that cause syncope and their
  characteristic features on history and exam.

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Pre reading

• Hughes T Cruickshank J. Adult Emergency
  Medicine at a Glance. Chichester, West Sussex, UK
  John Wiley Sons, 2011. 
• Chapter 21 Slow heart rate. Chapter 32 Fast heart
  rate.
• Chapter 34 Chest pain cardiovascular.
• Chapter 35 Chest pain non cardiovasular

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Other learning resources

• BHS guidelines
• Follow this link to the presentation on BHS
  intranet (http//dev-intranet/node/370)
• MJA consensus guidelines
• 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) 516-520 2008 Australian
  Family Physician. http//www.racgp.org.au/afp/2008
  07/200807cruickshank.pdf
•  

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Learning objectivesFocus on cardiac ischaemia

• 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

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Causes of Chest Pain

• Oesophageal
• Oesophagitis
• Oesophageal spasm
• Musculoskeletal
• Muscle injury, spasm
• Costochondral joint inflammation
• Skin
• Herpes Zoster (Shingles)

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Emergency Medicine6 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
• (6 things on a list is too many, but)

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.but luckily some diagnoses predictable for
clinicians

• 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

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Assessment

• 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

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History of the complaint

• 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 DONT do
  tests JUST IN CASE

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History typical descriptions

• Pleuritic Pain Pain worse on inspiration
• Sharp, stabbing
• Localised
• Worse on inspiration, coughing
• May be worse on sitting up or leaning forward
• Not related to exertion

• 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

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History ECG pericarditis

• Due to pericardial inflammation pericarditis
• Central or Left side
• Sharp, stabbing
• Worse on movement, on breathing, lying flat
• Relief sitting forward

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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
• Pressure
• Discomfort
• Ache
• Tightness
• May be mistaken by patient (and doctor) for
  indigestion

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History pitfalls

• Response to analgesia type does not make a
  diagnosis
• cardiac pain can get better with antacid
• Oesophageal pain improves with GTN

• Atypical pain
• Is common
• Does not exclude ischaemia
• May be more common in women, renal failure
• Some patients have no pain
• Silent ischaemia or infarction
• More common in diabetics due to neuropathy

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ACS history pitfalls

• Painless AMI common with age, women and diabetics
• Prev stroke or heart failure also risks
• By age 85 MAJORITY of AMI painless
• Anginal equivalents include
• Dyspnoea (commonest)
• With age syncope, weakness, confusion
• Elderly women also cold sweats dizziness

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Which features of pain make myocardial ischaemia
more or less likely?

• More likely
• Radiates to shoulders
• Worse on exercise
• Associated dyspnoea

• Less likely
• 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

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Response to analgesia

• 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

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Chest wall tender AMI

• 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

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Acute coronary syndromes
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ECG interpret in lt5mins.
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ECG your opinion?
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Basic investigations

• ECG, CXR and bloods
• In Emergency Department an ECG in most if not all
  patients.
• More useful as rule in than rule out
• ECG in AMI 50 sensitivity, 90 specificity
• ECG not useful in PE or aortic dissection

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Acute Coronary Syndrome

• Difference between risk Ax diagnosis
• Blood tests are not diagnostic tests (unless
  positive)
• Ruling out AMI in a stable patient with a
  non-diagnostic ECG is the difficulty

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prognosis v diagnosis 1

• The same coronary lesion in one patient might be
  tolerated or a disaster
• Increased rate of complications with
• LV dysfunction
• DM
• HTN / LVH
• Probably renal failure

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prognosis v diagnosis 2

• Diagnostic probability determines approach to
  diagnosis
• ?EST / ?angiography / ?inpatient or outpt.
• Dif tests different risks level of sensitivity
• Risk profile defines Rx decisions
• Risk v benefit of dif antiplatelet Rx
• Admit to CCU or ward

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Assessing risk

• Risk factors dont 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
• Risk Ax of complications discharge

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TIMI 7 rule (for an example)

• 5 on Hx
• Agegt65, gt2 IHD RFs, known stenosis, gt2 episodes
  angina in 24H, aspirin use
• 2 tests ECG changes / positive troponin
• HIGH risk ECG / trop ve / TIMI gt 2
• LOW risk normal ECG trop, TIMI lt3
• 30 day mortality 1.7

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ECG as rule out AMI test

• Not known how useful a normal ECG is
• AMI rate ?lt1, 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

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Blood markers - troponin

• 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

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myoglobin

• One study showed excellent rule out figures for
  90 minute testing of troponin and myoglobin levels

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Rx in ACS

• Aspirin should be given immediately
• alternative clopidogrel if truly contraindicated
• Rapid decisions on reperfusion
• Based on ECG only
• All other decisions less time dependent
• Can involve further consultation
• Need risk / benefit analysis

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Adjunctive Rx in ACS

• Further antiplatelet options
• Heparin (LMW v unfractionated)
• clopidogrel
• Glycoprotein IIb/IIIa inhibitors
• Symptomatic / pain control
• GTN / morphine
• Secondary prevention
• BBlockade / statins

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Thrombolysis (fibrinolysis)

• 50 flow return rate where indicated
• But 15 re-occlude (and do badly)
• 1 patients have a major bleed
• Usually intra-cranial haemorrhage
• Using LMW heparin as opposed to UFH
• Some evidence more benefit

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PCI v thrombolysis

• Guideline varies with
• 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

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Guideline for PCI v lysis
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CABGs

• Routine after STEMI
• Considered if poor LVF
• appropriate anatomy
• Means LAD or severe vessel disease
• Emergency
• Considered in cardiogenic shock
• Failed reperfusion and persistent pain
• All above is level B recommendation

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Role of PCI high risk ACS

• Still being defined
• current problem versus the next one
• Different approaches tried
• Risk stratify PCI high risk
• Maximise non-invasive Rx
• Then PCI breakthrough
• PCI all patients

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PCI high risk ACS

• PCI all approach reduces hospitalisations
• But low risk patients potentially do worse
• Peri-procedural AMI
• Current Cochrane recommendation is that may be a
  benefit in early PCI if risk stratification in
  high category

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AORTIC DISSECTION

• Challenging diagnosis, lethal if missed (75 in
  2/52), prob.s if Rx as ACS
• Classic Hx
• 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

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Risk factors for Aortic Dissection

• HTN
• Aortic valve
• Bicuspid, previous surgery
• Abnormal Aorta mainly congenital
• Coarctation / Marfans / Ehlers-Danlos
• Arteritis (Giant cell)
• Aortic stresses
• PREGNANCY, COCAINE, TRAUMA

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Atypical presentations AD

• Atypical history
• Non-classical pain, chest or back only, severe
  sharp pain, abdo pain
• Syncope
• Acute stroke ( peripheral neuro)
• Others just get too weird make you paranoid
• Eg. Pulsatile stenoclavicular joint!!

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AD - imaging

• Widened mediastinum (62) and abnormal aortic
  contour (50) most sensitive CXR findings
• Normal CXR may decrease the likelihood but if
  examination, Hx and RFs raise suspicion needs
  further imaging

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Oesophageal rupture

• 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

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Oesophageal rupture - problems

• 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

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Myo and pericarditis
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Pulmonary Embolism

• Classic triad about 20
• Pleuritic PIC, dyspnoea haemoptysis
• Typically some combination of
• SOB, PIC, tachypnoea, tachycardia
• Dypnoea commonest (about 80)
• Pleuritic pain not sensitive or specific
• 44 with, 30 without in one study
• Needs infarction
• more likely in existing lung disease, implies
  smaller clot?

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PE investigations

• No test is ideal
• Can have normal tests be very unlucky
• Classic diagnosis for combining pre- and
  post-test clinical probability

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PE more worrying facts

• Mortality hasnt 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 PEs asymptomatic?

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PE - ECG

• ECG has many reported associations
• All from study of pt. s AFTER diagnosis
• S1Q3T3 about 12 of PE normal pt.s
• Sinus tachy not that common
• Range is 8-69 in 6 studies
• Commonest is anterior T wave inversion
• 68 pt.s with confirmed PE
• ECG doesnt rule in or rule out

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PE - ABG

• Tells you nothing about the cause of hypoxia only
  the magnitude
• If you know there is hypoxia already you dont
  need to do it
• If you really need to you can calculate an A-a
  gradient WITHOUT removing O2

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PE pre test probabilty

• Multiple systems for doing this
• Most widespread and validated is Wells score
• Note dif. Wells score for PE DVT

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PE Wells criteria

• 3 points for
• PE most likely diagnosis
• Signs and symptoms suggesting DVT
• 1.5 points for
• PRgt100, past Hx (PE/DVT), immobilisation
• 1 point for
• Haemoptysis or malignancy
• lt2 low (10), 2-6 i/med (25), gt6 high (50)

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Wells use in practice

• Need to not automatically apply
• Eg. some pt.s will be moderate risk almost everty
  time they come to ED
• ( DONT need a scan everytime)

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D-dimer

• Only use is in a low risk patient
• A negative test makes PE very unlikely
• A slightly positive test IS a positive test

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Imaging CTPA and VQ

• CTPA has high negative predictive value
• 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)

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PE more on VQ scanning

• Normal perfusion excludes (14 of pt.s)
• non-diagnostic (73) covers
• Low probability, 15-30 have PE
• Intermediate, gt30 have PE
• High probability, gt85 have PE

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VQ combining pre post test assessment

• Low clinical and low scan, lt5 have PE
• Low clinical and i/med scan, same PE
• Also negative LL ultrasound, lt3 PE
• High probability clinical scan, gt95 PE
• Main problem is high clinical and
  low/intermediate scans, rate is 15-75
• (often cardiopulmonary disease, past PE)

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Imaging pregnant patients

• Most advice is to investigate as normal
• D-dimer will be positive in pregnancy
• No consistant agreement re VQ v CTPA
• VQ isotopes renal excreted, bladder near uterus
• CTPA has contrast as well as radiation
• Tempting to try leg ultrasound
• But only 80 PE have LL DVT

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The Gold Standard

• There isnt one!
• Pulmonary angiography was once but mortality
  almost 1, morbidity 2-5
• Compared to warfarin
• 1-2 mortality
• 5-25 morbidity

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Food for thought

• What is the mortality rate of a d-dimer?
• I didnt think it was a PE, just thought I better
  do one anyway.
• The result is not negative
• Better order a CTPA
• Anaphylactic contrast reaction? Cancer?
• False positive, warfarin, car accident?

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PERC rule test free!

• A rule which is applied after gestalt
• Defined as lt15 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 lt2
• Approx rate PE/death after ve imaging
• Further tests inc. false ve (not less miss)

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PERC rule

• The rule is
• Agelt50, PRlt100, no haemoptysis, no E2 Rx, no
  surgery 4/52 (ETT), no past VTE, no unilateral
  leg swelling (from looking!)
• PERC negative AND gestalt lt1
• Study centres inc NZ (more like us??)
• Thought to reduce tests by 20
• Idea is not to do ANY tests

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PE less worrying facts

• 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
• Ie less than the suspected 15
• The PERC rule also determined that
  immobilisation was 6H knees bent

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Spot diagnoses
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Spot diagnoses
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Some final points

• Examine patients properly
• Expose and look at the chest (eg. Zoster)
• Beware chest wall tenderness in AMI
• 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