Approach to the Patient with

Chest Pain
 Acute Chest Pain is the most common reason for
seeking care in ED
 Approximately 8 million ED annual visit in US
 Only 15-25% patient actually have ACS
 Dx of ACS missed in 2% of patients
 Can lead to Substantial consequences
 Short term Mortality increases 2 fold as compare to those who
are admitted
Common Causes of Acute Chest
Pain
 Cardiac
 Vascular
 Pulmonary
 GIT
 Musculoskeletal
 Infectious
 Psychological
 Cardiac Causes
Angina Retrosternal chest pressure, burning, Duration 2-10min
or heaviness radiating occasionally to Precipitated by exercise,
the neck, jaw, epigastrium, shoulder or emotions, cold weather
left arm
Unstable Same as angina but may be more Typically <20min
Angina severe

Acute MI Same as angina but may be more Sudden onset, usually lasting
severe >30mins
Often associated with SOB

Pericarditis Sharp pleuritic pain, aggravated by Pericardial friction rub

changes in position
 Vascular Causes
Aortic Excruciating ripping pain of Usually occurs in the setting of
Dissection sudden onset in the anterior HTN of Connective tissue
aspect of the chest often disorder
radiating to the back.

Pulmonary Sudden onset of Dyspnea and Signs of Rt sided heart failure

Embolism pain Dyspnea, tachypnea, tachycardia

Pulmonary Substernal chest pressure Pain associated with dyspnea

Hypertension and sign of pulm HTN
 Pulmonary Causes
Pleuritis or Pleuritic pain over the Pain lateral to midline
Pneumonia involved area associated with dyspnea

Tracheobronchitis Burning discomfort in Associated with coughing

midline

Spontaneous Sudden onset of unilateral Abrupt onset of dyspnea and

Pneumothorax pleuritic pain with dyspnea pain
 GIT Causes
GERD Burning substernal and Aggravated by large meal,
epigastric discomfort, 10-60 postprandial recumbency, relieved
mins in duration by antacid

Peptic Ulcer Prolonged epigastric or Relieved by antacid or food

substernal burning

Gallbladder Prolonged epigastric or Rt Following a meal

disease upper quadrant pain

pancreatitis Prolonged intense epigastric Risk factors

and substernal pain Alcohol, hypertriglyceridemia,
medications
 Musculoskeletal Causes
Costochondritis Sudden onset of intense Local tenderness
fleeting pain Swelling and inflammation over
the affected joint

Cervical disc Sudden onset of fleeting pain May be reproduced with

disease movement of neck

Trauma or strain Constant pain Reproduced by palpation or

movement of affected part
 Infectious and psychological causes
Herpes Zoster Prolonged burning pain in a Vesicular rash, dermatological
dermatological distribution distribution

Panic disorder Chest tightness with SOB Patient may have other evidence
lasting >30mins, unrelated to of emotional disorder
exertion or movement
 Diagnostic Considerations
 History
 Physical examination
 ECG
 Chest X-ray
 Biomarkers
 Non Invasive Testing
 History
 Character of Pain
 Site, Onset, character, radiation, association, time,
exacerbating factors, severity
 Studies have suggested that response to nitroglycerine
may not reliably discriminate cardiac chest pain from
non-cardiac chest pain.
 Risk factors
 Advanced age, male sex, diabetes, HTN, atherosclerosis
 Physical examination
 Initial examination should focus on to identify
 Potential precipitating causes
 e.g HTN
 Important comorbid conditions
 e.g COPD
 Evidence of hemodynamic complications
 Congestive heart failure, New MR, Hypotension
 Vitals and examination of peripheral vessels
 Whose clinical findings do not suggest MI then search
for non-coronory causes
 ECG
 Should be obtained with in 10 mins of ER arrival
 ST segment abnormalities (>0.05mV) strongly
suggestive
 Non specific changes
 Minimal ST segment change or T wave inversion of
<0.2mV
 Completely normal ECG do not exclude possibility of
ACS
 Risk of MI with H/O of CAD is 4%
 With no H/O of CAD, risk of MI is 2%
 Patient with normal ECG have better prognosis as
compare to those with abnormal ECG
 Normal ECG has negative predictive value of 80%-90%
 Availability of previous ECG improves diagnostic
accuracy
 Serial ECG improves the clinician ability to diagnose
acute MI
CXR
 Should be obtained for all patients with chest pain
 Can show pulmonary edema
 More useful for diagnosing other disorders
 Widened mediastinum, Aortic knob
 Signs of PE
 Atelectasis, elevated hemi diaphragm, pleural effusion,
Hampton hump or western mark sign
 Pneumothorax
 pneumonia
 Biomarkers
 TROPONINS
 Preferred diagnostic biomarker
 Many conditions can lead in rise of Troponin other than
MI
 Myocarditis
 Myocardial contusion
 Cardioversion or Defibrillation
 Lt ventricular strain pattern from congestive heart failure
 Rt ventricular strain pattern from PE
 Extreme exercise
 Hypertensive crisis
 Renal disease
 Severe Sepsis
 With serial sampling upto 12 hr after arrival in hospital
offers a sensitivity of 95% and specificity of 90%
 Using only a single sample at initial evaluation has a
sensitivity of just 70% - 75%
 With availability of more sensitive assays, sensitivity for
detecting with single sample is 90%
 Patient seen with in 3 hrs of onset of chest pain
 High sensitive assay has sensitivity of 80% - 85%
 Older assay has sensitivity of 55%
 High sensitivity assays with even lower limits of
detection (0.001 ng/mL or <1 pg/mL) is in development
 When such assays were performed in patient with
NSTEMI
 72% patient has circulating troponin levels at baseline
 28% had levels above the limit of detection
 When such assays were used in patient arriving at the
ED with chest pain, approximately a quarter have
undetectable levels with 100% negative predictive value
 CKMB
 Until advent of troponin, CKMB was biomarker of choice in
diagnosing MI
 It can be found in
 Skeletal muscles
 Tongue
 Diaphragm
 Small intestine
 Uterus
 Prostate
 Advantage of CKMB is a shorter half life, useful in diagnosing
reinfartction
 Other markers
 Serum myoglobin
 Smaller molecule, diffuses through interstitial fluid more rapidly,
become abnormal as early as 30 mins after MI
 Its not specific
 Many patients with myocyte necrosis have elevated levels of
inflammatory biomarkers
 CRP, Serum Amyloid , Myeloperoxidase, Interlukin-6
 No study showed any benefit on Rx from these new markers
 FDA has approved IMA (Ischemia modified albumin) for
clinical use
 Clinical specificity of IMA for ACS remains an era of further
investigation
 D-Dimer test
 Helps to rule out PE
 B-type natriuretic peptide
 Arise in the setting of increased ventricular wall stress
 Commonly aid in diagnosis of heart failure
 Testing strategy
 2007 National academy of clinical biochemistry suggest
that patient with very low probability of ACS should not
undergo measurement of biomarkers because false
positive result can lead to unnecessary hospitalization
 ACC, AHA, and NACB guidelines recommend
TROPONIN as the preferred first line marker but CKMB
is an acceptable alternative.
 If the initial set of marker is negative, another sample
should be drawn 3-6hrs later.
NACB recommendations for use
of Biochemical markers for Risk
stratification in ACS
 Class I
 Pt with suspicion of ACS should undergo early risk
stratification based on (level of evidence C)
 History
 Physical examination
 ECG
 Biomarkers
 Cardiac troponin is preferred marker, should b
measured in all patients with suspected ACS (level of
evidence A)
 Blood should be obtained for testing on arrival at the
hospital and 6-9 hr later (level of evidence B)
 Class IIa
 Measurement of CRP may be useful in addition to a
cardiac troponin for assessment of patient with ACS.
(Level of Evidence A)
 Measurement of BNP may be useful in addition to
cardiac troponin for assessment of patient with ACS.
(Level of Evidence A)
 Class IIb
 Measurement of ischemic biomarkers in addition to
cardiac troponin and ECG may aid in excluding ACS in
patient with low clinical probability of MI (level of
Evidence C)
 A multimarker strategy that include measurement of 2
or more pathobiological diverse biomarkers, in addition
to Troponin may aid in enhancing risk stratification in
patient with ACS (Level of Evidence C)
 Early therapeutic sampling of cardiac Troponin, 2-4hrs
after arrival may be appropriate (Level of Evidence C)
 Class III
 Biomarkers of necrosis should not be used for routine
screening of patient with probability of ACS (Level of
Evidence C)
 Early non invasive testing
 Treadmill Electrocardiography
 Inexpensive and available easily
 Most studies have used BRUCE or MODIFIED BRUCE
treadmill protocol.
 Exercise testing is safe and has a negative predictive
value >99% and positive predictive value is <50%
 Patient with low clinical risk for complications can safely
undergo exercise testing after 6-8hr of an evaluation
which reveal no evidence of MI.
 For low risk patient with no evidence of MI after serial
ECG and biomarkers, outpatient stress testing ideally
with in 24 hrs and no later than 72 hrs has proved safe.
 Indications Contraindications

 2 sets of cardiac enzymes @ 4  New or evolving ECG

hrs intervals should b Normal abnormalities on the rest
tracing
 ECG @ time of arrival shows
no significant abnormality  Abnormal cardiac enzymes
levels
 Absence of resting ECG
abnormality  Inability to perform exercise

 Absence of Ischemic chest  Worsening or persistent

pain at the time of exercise ischemic chest pain
testing
 Imaging Test
 Stress echocardiography and radionuclide scans are the
preferred non invasive testing modalities for patient
who cannot undergo treadmill ECG
 Imaging studies are expensive but have increased sensitivity
 Imaging should be performed with in 2 hrs of the resolution
of the symptoms.
 Sensitivity of stress echo is 85% - 90% and its specificity is
80% - 95%
 In myocardial perfusion imaging the result are less
interpretable in patients with previous MI
 It becomes difficult to exclude weather the abnormalities are
preexisting unless a prior study is available.
 Echocardiography can be used to detect wall motion
abnormality.
 Base line WMA correlates with worse prognosis
 Cardiac Magnetic Resonance Imaging (MRI)
 A study has used cardiac MRI to quantify myocardial
perfusion, ventricular function in patient with chest pain, the
sensitivity for ACS was 84% and the specificity was 85%.
 The addition of T2-weighted imaging, which can detect
myocardial edema and thus help differentiate acute from
chronic perfusion defect.
 Coronary computed tomographic angiography (CTA)
 Coronary CTA has sensitivity of approx. 90% and specificity of
65% - 90% for coronary stenosis which is greater than 50%.
 Coronary CTA has been evaluated in a study of patients with
chest pain seen in ED.
 Of 368 patients with a non diagnostic ECG and negative initial
biomarker, ACS was ultimately diagnosed in 31 of them.
 Approx half of patients were free of CAD and remaining 50%
had evidence of atherosclerosis, with 32% having minor
plaque and 18% having stenosis greater than 50%
 So coronary CTA is best to study anatomic data rather than
functional data.
Diagnostic Approach to a
patient with Chest Pain
 Stabilize. Assess for
Assess vital
Unstable STEMI
signs
Massive PE
Aortic Dissection
St Pericardial Effusion
a
bl
STEMI
e
(Localized STE)

Obtain 12 ST Depression or Elevated and Hx

lead ECG TWI C/W ACS
NSTEMI
Check
Ischemic
Biomarkers
ECG Normal and Hx C/W
diagnostic Diffuse ST ACS
or Yes elevation Possible UA
suggestive Pericarditis

N
O
 CXR Area of Lucency
Diagnostic or between lungs Pneumothorax
suggestive Yes and parenchyma

N Infiltrates (and
O hx and labs c/w Pneumonia
infection)

Widened
Mediastinum and
hx C/W AoD

Dissection
Aortic dissection
Dedicated imaging
to assess for AoD
(CT, MRI, Echo)
No Dissection
Consider alternative
diagnosis
 N
O

Assess Risk for Assess Risk Assess Risk for

ACS and check for PE AoD
ischemic
L H H
Biomarkers
O ig i
Hx C/W ACS W h g
and NSTEMI h
Check CTPA L
^Biomarkers
D- or V/Q O
Hx C/W ACS Dimer scan W Imaging
and Norm UA CT, MRI,
Biomarkers TEE

Hx not C/W NSTEMI or

ACS and Alternative
^Biomarkers Dx Consider Consider
PE
Alternative Alternative AoD
Hx not C/W Consider Dx Dx
ACS and Norm Alternative
Biomarkers Dx
Evaluation and management of
patients suspected of having
ACS
 Symptoms suggestive of ACS

Non Chronic Stable Possible Definite

Cardiac Dx Angina ACS ACS

NSTE STE
Rx of
Rx as ECG changes, ongoing
Chronic
indicated by Non diagnostic pain, + biomarkers, Evaluation for
Stable
alternative Dx ECG and Norm hemodynamic reperfusion
Angina
initial Biomarkers abnormality therapy

No recurrent pain Follow up for 4-8hrs

Negative follow up studies ECG, Biomarkers

Stress study to provoke Recurrent ischemic

ischemia Pain or + follow up
Consider evaluation of LV studies
function if ischemia is present Dx of ACS confirmed

Negative Positive
Nonischemic, low risk ACS Dx of ACS confirmed

Outpatient follow-up Admit to Hospital and Rx as ACS

Thank You