User Tools

Site Tools


the adult patient with chest pain in the ED

see also:

  • strongly consider dissection and need for urgent CT angiogram in those aged over 30yrs (only 7% occur in those under 40yrs - mainly those with underlying Marfans or other CT disorder) AND:
    • “THUNDERCLAP” SUDDEN onset severe chest pain (maximal within seconds rather than minutes) even if this is slowly IMPROVING, especially if PH hypertension or pain radiates to jaw, back or abdomen even if there is a mild troponin rise suggesting a NSTEMI!
    • NEW severe chest pain PLUS new NEUROLOGY in the absence of trauma

initial Mx in ED:

if there is a possibility of acute ischaemic cardiac chest pain:

  • ECG machine analyses are OFTEN WRONG do NOT rely upon them
    • only 60-70% sens/spec for STEMI, often over diagnoses AF, may count a tall T wave as QRS, QTc calculation may be erroneous if wavy baseline, etc
    • they generally do not use Sgarbossa Criteria and do not identify subtle changes of evolving STEMI-equivalents
    • apparently they cause over 10,000 deaths worldwide each year
  • ECG interpretation can be complex and requires thousands of ECG interpretations to become expert - have a low threshold for asking senior colleagues for their interpretation and repeat ECGs within an hour if not clear - even cardiologists have sens/spec of only 60-70%
    • 4% of STEMI's are isolated posterior STEMIs and are amongst the most commonly missed STEMI
      • if ant ST depression, do posterior ECG leads and look for post STEMI!
      • flipping an ECG upside down will not distinguish post STEMI from ant ischaemia - do the posterior leads!
    • don't forget looking at the aVR lead, especially if patient looks sick and there are other leads with ST depression:
      • ST elevation in aVR without other DDx cause in this scenario suggests STEMI-equivalent or at least global cardiac dysfunction and high risk of cardiogenic shock and poor outcomes with left main disease, prox LAD or triple vessel disease - DON'T give clopidogrel type meds as this impacts options for bypass surgery for next 5 days
      • DDx of ST elevation in aVR includes:
        • LBBB
        • other causes of global cardiac ischaemia: post-arrest, dissection, SVTs (esp. AVRT), any cause of shock
        • submassive PE - ST elevation in V1-2, aVR with R axis is strongly suggestive of pulm hypertension and if acute this is most likely a large PE
        • severe LVH with strain with very high BP (Rx the BP and see if it resolves)
        • severe hypoK, tricyclic antidepressant overdose, hyperkalaemia, Brugada
    • if ECG looks bizarre - consider hyperkalaemia and if so, Rx ASAP
    • a “broad complex tachy” could be a STEMI - check for a lead with narrow QRS complexes and if present then the “broad complex” leads are probably ST elevations and it is really a narrow complex tachy with ST elevation!
  • triage 2 to a cardiac monitored cubicle
  • oxygen if SaO2 < 93% or if in shock (oxygen is no longer advised to be given routinely!)
  • cardiac monitor as risk of cardiac arrhythmias, basic set of observations
  • early 12 lead ECG
    • senior consult ASAP for consideration of urgent angioplasty (or perhaps thrombolysis) as may be an AMI or critical LAD stenosis if ANY of:
      • acute ST elevation and no LBBB:
        • does it fit STEMI criteria or could it be a sign of an evolving STEMI
      • Smith-Modified Sgarbossa Criteria if Left Bundle Branch Block (LBBB) - new LBBB of itself is NO LONGER an indication for cath lab as of 2013, but see Smith-Modified Sgarbossa Criteria for ischaemic features in LBBB
        • ST segments should be iso-electric or opposite to the QRS direction (ie. should be discordant), the following suggest STEMI-equivalent:
          • Sgarbossa A: concordant ST elevation >= 1mm - only need 1 lead to classify for cath lab activation
          • Sgarbossa B: concordant ST depression >= 1mm in V1-3 - only need 1 lead to classify for cath lab activation
          • original Sgarbossa C: no longer used as not accurate
          • revised Sgarbossa C: proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave
          • can be used in paced rhythms but as pacers in RV result in neg QRS in all V1-6, Sgarbossa B can apply to V1-6 if paced to improve sensitivity/spec
          • NB. concordant ST depression >= 1mm in leads other than V1-3 should be watched but not an indication for cath lab
      • posterior STEMI:
        • ant. ST depression with positive QRS and upright T in V1
        • ie. evolve ECG changes opposite direction to ant STEMI in V1-3 they develop ST depression, evolving R waves instead of Q waves
      • Wellen's syndrome (indicates critical LAD stenosis) - isolated new biphasic T waves in V2-3
      • de Winter syndrome - upsloping ST depression with symmetric tall narrow peaked T waves in V2-6
        • generally indicates acutely unstable prox. LAD occlusion and is an indication for urgent cath lab
      • features which suggest possible evolving STEMI (repeat ECG every 10-15 minutes if possible, but at least within 1hr):
        • possible new T inv aVL
        • hyperacute T waves (DDx hyperkalaemia):
          • broad, tall T waves which could fit the QRS inside, or,
          • straight or convex initial segments
        • Wellen's sign of terminal T inv of ST segment (ie. biphasic) in ant leads
        • any ST elevation in V1-2 with RBBB (should be ST depression)
        • ST depression - reciprocal ST depression often precedes STEMI esp. in RCA occlusions (reciprocal ST depression is absent in 30% of ant STEMIs though)
          • in ant leads, could be posterior STEMI (do posterior leads) or anterior ischaemia (could also be normal as in RBBB)
          • check aVR
      • features strongly suggestive of submassive PE:
        • T inv in inferior AND ant-septal leads - almost diagnostic of pulmonary hypertension and if acute this generally means PE
          • a 2014 study showed PE was strongly associated with the presence of inverted T in both leads III and V1-2 and maximum magnitude T inversion in leads V1-2. The combination of these 2 findings identified PE with 98% sensitivity and 92% specificity. 1)
        • ST elevation in aVR, V1-2 with R axis deviation
        • NB. SI QIII TIII only occurs in 4% of PEs and may be baseline so NOT helpful
  • IV access & send bloods for FBE, U&E, glucose, cardiac enzymes (usually CK, troponin), (plus clotting profile if thrombolysis likely)
  • specifically assess their risk of having aortic dissection using the ADD assessment tool
    • if ADD score 2 or 3 then urgent CT Angiogram, if ADD score 1, consider angio if no better explanation found
  • aspirin (acetylsalicylic acid) 300mg o crushed if:
    • not already had aspirin that day
    • unlikely to be aortic dissection
    • not allergic (in which case consider alternatives)
  • treat chest pain as appropriate eg GTN, morphine +/- proton pump inhibitors (PPIs) if suspect gastro-oesophageal reflux (BUT 15% of ACS improves with antacids - NOT diagnostic!)
  • CXR when available preferably whilst on cardiac monitor
  • if no acute ST elevation or new LBBB on ECG and no other obvious aetiology:
Diabetics and the elderly often present with painless ACS and may present with SOB, diaphoresis, or just malaise - have a low threshold for suspecting a cardiac cause
young patients under 30 yrs of age without significant co-morbidities or bariatric status are very unlikely to have an infarct HOWEVER, THC use within past 1hr confers a 5x risk and cocaine use a 24x risk of STEMI compared with non-users.2)

if PE is most likely:

  • triage 2 or 3, preferably to a cardiac monitored cubicle
  • oxygen if SaO2 < 93% or if in shock (oxygen is no longer advised to be given routinely!)
  • IV access and bloods for FBE, U&E, +/- clotting, +/- D-Dimer if no reason it should otherwise be elevated and PE risk is low enough that a -ve DDimer will be sufficient to exclude it.
  • 12 lead ECG
  • CXR to exclude other pathology
  • consider V/Q scan or CTPA

causes of chest pain:

potentially life threatening that need excluding in EVERY patient presenting to ED:



not usually life threatening:




proximate history:

is the patient pregnant?

where is the pain located?

  • NB. visceral pain is poorly localised and thus oesophageal pain may resemble cardiac
  • myocardial ischaemia, central PE, dissection and oesophageal pain classically is mid-sternal or left peristernal
  • lateral chest wall pain worse on inspiration is more likely to be pleural (eg. PE causing pulmonary infarct, pleurisy, pneumonia) or chest wall pain (eg. musculoskeletal, shingles), but may be biliary
  • aortic dissection pain depends upon location of dissection:
    • ascending aorta ⇒ ant. chest pain
    • arch aorta ⇒ pain in neck & jaw
    • descending aorta ⇒ interscapular pain (32% of Type A dissections present with posterior chest pain)
  • other causes of pain radiating to upper back:
    • biliary colic
    • pancreatitis
    • AAA
    • thoracic spine pain
    • posteriorly located PE / pulmonary conditions involving pleura
    • musculoskeletal
    • shingles (dermatomal and with rash)

does the pain move or radiate to any part of the chest, back, neck or arm?

  • when substernal pain radiates to neck, jaw, shoulder or arm the likelihood of AMI increases 3-4 fold, but differentials still include oesophageal pain or aortic dissection
  • although pain of aortic dissection is classically described as tearing, sudden onset pain radiating to the back, < 30% of pts actually experience it in the back - may be only if tear originates distal to subclavian artery. It most commonly resembles AMI on history.

what does it feel like?

  • although ischaemic cardiac pain classically is dull or pressure-like but ~20% may describe it as 'sharp'!
  • if pressure-like pain ⇒ 24% had AMI, 30% had unstable angina
  • if burning pain ⇒ 23% had AMI, 21% had unstable angina
  • if sharp or stabbing pain ⇒ 5% had AMI, 17% had unstable angina
  • severe, abrupt onset ripping or tearing pain is highly suggestive of aortic dissection
  • THUS, presence of burning or stabbing pain does NOT EXCLUDE acute myocardial infarction (AMI/STEMI/NSTEMI) !!

how long has the pain been there?

  • AMI is usually more severe than angina and longer lasting (>10min)

what was associated with the onset of the pain?

what, if anything relieved it?

  • relief by nitrates does not exclude oesophageal spasm, so is unhelpful
  • relief by antacid/topical anaesthetic combination does not exclude myocardial ischaemia
  • does the pain change with position, movement, exertion or breathing?
  • pain on exertion is typical of stable angina whereas unstable angina is at rest or of increasing frequency
  • pain on movement may suggest chest wall pain but does not exclude AMI
  • pericarditis is typically worse lying down
  • pericardial, pulmonary, pleural and chest wall pain tends to be respirophasic - worse on inspiration
    • 21% of pts with respirophasic pain had PE

are there any associated symptoms:

  • such as SOB, nausea, vomiting, diaphoresis, syncope, near-syncope, cough, fever, sputum production or haemoptysis?
  • SOB is most important of these symptoms:
    • 14% of pts with AMI have SOB as their sole complaint
    • 50% of pts with AMI have SOB
    • 84% of pts with PE have SOB and 88% have chest pain
  • nausea and diaphoresis may also be associated with AMI but with much lower predictive value
  • fever & cough tend to suggest pneumonia but this cannot be diagnosed on history alone
  • was any medication or drug, esp. cocaine or erythromycin, taken prior to onset of pain?

is there any recent history of trauma to the chest?

past history:

past episodes of similar pain, its evaluation & diagnosis

  • PH AMI:
    • ⇒ 5% annual mortality due to subsequent AMI, 50% are sudden deaths
    • ⇒ 10-15% experience a 2nd AMI but survive

risk factors:

  • NB. NOT helpful in diagnosis of a condition if PH of that condition or diagnostic evidence of it now
  • NB. relative risk factors derived from population studies may NOT apply to an individual pt in ED!
    • BUT remember, ~50% AMI pts do not have obvious risk factors, so absence does not mean no IHD!
    • absolute, independent risk factors:
      • FH coronary heart disease esp. if close male relative develops it before age 65yrs
      • hypertension - at least moderate for > 5 years but NOT if well controlled
      • diabetes mellitus - IDDM for > 5 years even if well controlled although risk declines with control. NIDDM has lower risk.
      • cigarette smoking - in proportion to amount and duration within past 10 years
      • hyperlipidaemia - raised total cholesterol with raised LDL but others less clear
    • relative risk factors:
      • male, age > 35 yrs, obesity, sedentary lifestyle
  • pulmonary embolism risk factors:
  • aortic dissection risk factors:
    • hypertension - 70-95% are hypertensive before the dissection, 70% have LVH
    • Marfan's syndrome
    • history of coarctation of aorta
    • bicuspid aortic valve
    • PH of iatrogenic manipulation of aorta - catheterisation of aorta/coronary arteries or surgery
    • BUT NOT: atherosclerosis, pregnancy (without HT), or PH syphilis
  • oesophageal pain risk factors:
    • PH sensitivity to gastric acid & gastro-oesophageal reflux
    • PH disorders of motility - spasm, achalasia or hypertonic lower oesophageal sphincter
    • BUT NOT hiatus hernia as this occurs in 50% people over 50yrs age and so is not helpful
  • cardiac tamponade non-traumatic risk factors:
    • “pleuritic” PIC in a pt with PH cancer should be evaluated for cardiac tamponade as carcinoma metastatic to the pericardium is the most common non-traumatic cause of cardiac tamponade!
    • pts with AIDS also have higher incidence of cardiac tamponade from either acute infectious pericarditis or Kaposi's sarcoma involving pericardium.


  • physical examination of the pt with chest pain is of limited usefulness as the findings are generally not specific to a disease process with a few exceptions.
  • apprehensive, anxious, diaphoretic pt with a sense of impending doom often has significant myocardial injury
  • a new murmur:
    • may be suggestive of papillary muscle dysfunction is only present in a minority of pts with AMI or unstable angina
    • a new aortic insufficiency murmur would suggest aortic dissection
  • extrasystolic sounds are non-specific although occur more often in AMI and a mid-systolic one occurs in 80% of pts with mitral valve prolapse who present with story of angina.
  • widely split S2 with loud pulmonic component may be heard if PE is large enough to cause pulm. HT & consequent delayed closing of pulmonary valve
  • muffled heart sounds with raised JVP and hypotension with tachycardia & narrowing pulse pressure with pulsus paradoxus > 10mmHg confirms cardiac tamponade
  • tension pneumothorax may also present with raised JVP, tachycardia, hypotension, narrowed pulse pressure but there is hyper-resonance, decreased breath sounds, and possibly midline shift and subcutaneous emphysema
  • tachypnoea occurs in 92% of pts with pulmonary embolism (PE)
  • tachycardia:
    • 44% of pts with PE
    • most pts with aortic dissection have systolic BP > 160mmHg BUT 20% may have hypotension, this is particularly more likely if dissection is of ascending aorta where it is due to haemopericardium rather than exsanguination.
  • radial-radial delay (>20mmHg in BP differenctial in each arm) or radio-femoral delay suggests aortic dissection but is present in a minority of pts
  • chest wall tenderness:
    • well localised tenderness over costochondral joints suggest costochondritis but does NOT exclude AMI as up to 15% of pts with AMI experience chest wall tenderness and does not exclude PE
  • pleural or pericardial friction rub
    • pericardial rub is usually 3 component, heard best with pt sitting forward & is present in most cases of pericarditis


12 lead ECG:

  • this is the single most important test, its predictive value is much better than that of history or examination

acute ST elevation :

  • initial ECG diagnostic for acute myocardial infarction (AMI/STEMI/NSTEMI) in only 25-50% pts
  • serial ECGs 91% specific & 40% sensitive for AMI ⇒ standard criteria for initiating thrombolytic therapy or PCI
  • indicates worse short term prognosis for the pt with AMI than without ST elevation
  • check:
    • morphology of ST:
      • ACS ST elevation generally is convex with ST rising above a line from J point to top of T BUT may be concave initially
    • reciprocal changes:
      • seen in 75% of inf. AMI pts & in 30% ant. AMI pts, thus if present strongly supports a ACS cause
    • dynamic changes:
      • in high risk patients with normal ST segments, consider serial ECGs every 20min for early diagnosis
    • exclude non-ACS causes of ST elevation:
      • benign early repolarisation
      • LVH
      • LBBB
      • PE, stroke, aortic dissection, pericarditis
  • if acute ST elevation suggestive of AMI then consider urgent angioplasty or thrombolysis:
    • see cardiology and
      • AMI angioplasty management / Management of STEMI
  • Tako-Tsubo cardiomyopathy (TTC):
    • acute chest pain with raised ST in chest leads, transient akinesis of apex and distal half ventricle with compensatory hyperkinesis of the basal walls which is frequently precipitated by psychological or physical stress, especially in post-menopausal women
    • accounts for 2% of chest pain with ST elevation - usually self-limiting with small rise in troponin, CK but requires angiography to show normal vessels.
      • Chestpain_tako-tsubo_NEJM2007.pdf

new ST depression:

  • on serial ECGs more sensitive (75%) but less specific (77%) for AMI as it is more often assoc. with angina
  • serial ECGs have sensitive of ~36% for unstable angina
  • initial prognosis may be better, long term prognosis may be worse as myocardium remains in jeopardy
  • BEWARE ST depression in V1-3 as this may represent posterior AMI esp. if large R wave &/or upright T wave in V1-3 ⇒ this is becoming an indication for PCI, do posterior leads & discuss with cardiology.
  • BEWARE ST depression in BBB - this could indicate AMI if terminal part of the QRS is negative
    • see Non-STEMI ACS criteria 

T inversion:

  • isolated new biphasic T waves in V2-3 suggests critical stenosis of LAD (Wellen's syndrome) - discuss with cardiology
  • T inv in inferior AND anterior leads is 99% specific for PE (usually a large saddle PE - ignore it and death is likely)
  • SI QIII (TIII) or new RBBB suggests PE

suggested indications for 15 lead ECG in pts with suspected AMI:

  • ST segment depression or suspicious isolectric ST segments in V1-3
  • borderline ST segment elevation in leads V5 and V6 or in leads II, III and aVF
  • all ST segment inferior AMIs (elevation in leads II, III and aVF)
  • isolated ST segment elevation in lead V1 or ST segment elevation in lead V1 > V2
  • symptoms suggestive of RV ischaemia:
    • epigastric pain
    • hypotension after nitroglycerin administration
  • NB. validity of 15 lead ECG not tested on general pop.n of pts presenting with PIC
  • NB. ECG changes other than ST elevation in V4R, V8, V9 are of little diagnostic value
  • NB. posterior leads frequently have low amplitudes (< 10mm), requiring careful interpretation for presence of ST elevation

cardiac markers


  • main use in chest pain is to exclude pathologies such as pneumothorax, pneumonia, cardiac failure
  • usually normal or non-specific in pts with PE but may show wedge-shaped pleural-based infiltrate, an elevated hemidiaphragm or prominent pulmonary vasculature.
  • findings in aortic dissection:
    • presence of a pleural cap, depressed left mainstem bronchus, deviation of the oesophagus, indistinct aortic knob, or widened mediastinum
    • normal CXR does not excl. dissection
    • ⇒ consider D-Dimer +/- aortography (NB. static & dynamic CT scan is as sensitive but does not show the surgeon the exact starting point in most instances).


  • of debatable value in diagnosis of PE, it may demonstrate a AA gradient which is not evident on SaO2 alone, as hyperventilation may maintain a normal SaO2 but there may actually be a substantial AA gradient.

D-Dimer, VQ scan or CT-PA for suspected pulmonary embolus:

  • also may help exclude acute aortic dissection
  • D-Dimer has high sensitivity for acute aortic dissection but low specificity thus a negative D-Dimer with normal CXR may be sufficient to exclude an acute dissection but not a chronic one.

CT aortography if features consistent with aortic dissection

  • NB. this is a different test to CT PA for PE and both use IV contrast thus avoid doing both as high contrast load.

further Mx of possible ischaemic chest pain

chestpain.txt · Last modified: 2023/09/08 05:44 by gary1

Donate Powered by PHP Valid HTML5 Valid CSS Driven by DokuWiki