the adult patient with chest pain in the ED
initial Mx in ED:
if there is a possibility of acute ischaemic cardiac chest pain:
triage 2 to a cardiac monitored cubicle
oxygen if SaO2 < 93% or if in shock (oxygen is no longer advised to be given routinely!)
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early 12 lead ECG
senior consult
ASAP for urgent angioplasty (or perhaps thrombolysis) as may be an
AMI or critical LAD stenosis if ANY of:
IV access & send bloods for FBE, U&E, glucose, cardiac enzymes (usually CK, troponin), (plus clotting profile if thrombolysis likely)
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if
ADD score 2 or 3 then urgent CT Angiogram, if ADD score 1, consider angio if no better explanation found
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not already had aspirin that day
unlikely to be aortic dissection
not allergic (in which case consider alternatives)
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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.
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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
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causes of chest pain:
potentially life threatening that need excluding in EVERY patient presenting to ED:
common:
uncommon:
not usually life threatening:
common:
musculoskeletal pain
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pleuritis
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uncommon:
history:
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:
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
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how long has the pain been there?
what was associated with the onset of the pain?
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acute SOB and respirophasic PIC that occur during positive pressure ventilation or after trauma suggest tension
pneumothorax.
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
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pericardial, pulmonary, pleural and chest wall pain tends to be respirophasic - worse on inspiration
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!
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BUT remember, ~50% AMI pts do not have obvious risk factors, so absence does not mean no IHD!
absolute, independent risk factors:
relative risk factors:
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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
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examination:
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:
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
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tachycardia:
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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:
pleural or pericardial friction rub
pericardial rub is usually 3 component, heard best with pt sitting forward & is present in most cases of
pericarditis
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investigations:
12 lead ECG:
acute ST elevation :
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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:
if acute ST elevation suggestive of AMI then consider urgent angioplasty or thrombolysis:
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.
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
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:
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
CXR:
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).
ABG's:
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:
CT aortography if features consistent with aortic dissection
further Mx of possible ischaemic chest pain