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.

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.

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.

   Chapter 21

Slow heart rate

. Chapter 32

Fast heart rate

. Chapter 34

Chest pain: cardiovascular

. Chapter 35

Chest pain: non cardiovasular

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/200807/200807cruickshank.pdf

Learning objectives Focus 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

Causes of Chest Pain

   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  (6 things on a list is too many, but…)

….

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

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’

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 DON’T do tests “JUST IN CASE”

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

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

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

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

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

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

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

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

 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

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

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

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

Assessing risk

 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  Risk Ax of complications = discharge

TIMI 7 rule (for an example)

 5 on Hx:  Age>65, >2 IHD RF’s, known stenosis, >2 episodes angina in 24H, aspirin use  2 tests: ECG changes / positive troponin  HIGH risk = ECG / trop +ve / TIMI > 2  LOW risk = normal ECG & trop, TIMI <3  30 day mortality 1.7%

ECG as rule out AMI test

 Not known how useful a normal ECG is:  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

 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

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

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

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

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

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

Guideline for PCI v ‘lysis

CABG’s

 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

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

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’

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

Risk factors for Aortic Dissection

 HTN  Aortic valve   Bicuspid, previous surgery Abnormal Aorta – mainly congenital  Coarctation / Marfan’s / Ehlers-Danlos   Arteritis (Giant cell) Aortic ‘stresses’  PREGNANCY, COCAINE, TRAUMA

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!!

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 RF’s raise suspicion needs further imaging

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

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

Myo and pericarditis

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?

PE investigations

 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

 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

 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 doesn’t ‘rule in’ or ‘rule out’

PE - ABG

  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

   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

 3 points for:  PE ‘most likely diagnosis’  Signs and symptoms suggesting DVT  1.5 points for:  PR>100, past Hx (PE/DVT), immobilisation  1 point for:   Haemoptysis or malignancy <2 low (10%), 2-6 i/med (25%), >6 high (50%)

Well’s – use in practice

 Need to not automatically apply  Eg. some pt.s will be moderate risk almost everty time they come to ED  (& DON’T need a scan everytime)

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

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%)

PE – more on VQ scanning

  Normal perfusion excludes (14% of pt.s) ‘non-diagnostic’ (73%) covers:   Low probability, 15-30% have PE Intermediate, >30% have PE  High probability, >85% have PE

VQ – combining pre & post test assessment

 Low clinical and low scan, <5% have PE  Low clinical and i/med scan, same % PE  Also negative LL ultrasound, <3% PE  High probability clinical & scan, >95% PE  Main problem is high clinical and low/intermediate scans, rate is 15-75%  (often cardiopulmonary disease, past PE)

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

The ‘Gold Standard’

 There isn’t one!

 Pulmonary angiography was once but mortality almost 1%, morbidity 2-5%  Compared to warfarin:   1-2% mortality 5-25% morbidity

Food for thought

 What is the mortality rate of a d-dimer?

   I didn’t 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?

PERC rule – test free!

 A rule which is applied after ‘gestalt’    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%  Approx rate PE/death after –ve imaging  Further tests inc. false +ve (not less miss)

PERC rule…

 The rule is:   Age<50, PR<100, no haemoptysis, no E2 Rx, no surgery 4/52 (=ETT), no past VTE, no unilateral leg swelling (from looking!) “PERC negative” AND gestalt = <1%  Study centres inc NZ (more like us??)  Thought to reduce tests by 20%  Idea is not to do ANY tests

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

Spot diagnoses

Spot diagnoses

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