Evaluation of Chest Pain

William Norcross, M.D.

Evaluation of Chest Pain

• Dictum: • With any chief complaint or symptom complex, first rule-

out (R/O) life threats. • The stopping point in the R/O should be at the point of

your conviction and personal satisfaction that the life threat does not exist.

• The R.O process may be very short and simple, e.g. a directed histroy, but if you're not convinced that the life threat is absent, pursue the R/O as far as necessary.

Chest Pain is very common.

• > 40 recognized entities in differential diagnosis• Life threat (practical)

• Acute coronary syndromes (ACS)• Aortic dissection• Pulmonary embolus (PE)• Pneumothorax• Pneumonia

• Obscure• Boerhave’s Syndrome• Usually are discovered in W/U of above.

Life-Threat Ruled Out

• Other entities• Musculoskeletal/serosal problems

• e.g. costochondritis, intercostal muscle spasms/strain, pericarditis, pleurisy

• Treat with NSAID, opiates, acetaminophen, local measures

• GI pathology • Dyspepsia, GE reflux esophageal spasm• Some bad abdominal pathology presents as chest pain

– e.g. perfodrated viscous, pancreatitis, cholecystitis– Usually apparent by H&P

• Treat with antacids, antispsmodics, etc.

Approach to Non-Life Threats

• Less urgent• Trial & error approach• Evaluation

• H&P, ancillary tests (CRX, EKG, perhaps dimers and cardiac markers)

Approach to Non-Life Threats

• Pneumonia, pneumothorax easy to diagnose• Note: the diagnostic modality for tension pneumothorax is an

intracostal needle, not a CXR.

• ACS, PE, aortic dissection: all easy to diagnose if you do the work-up

• Triggered by suspicions raised by initial evaluation and R/O life threat

Bad things to miss

• High mortality out-of-hospital (if undiagnosed)

Pulmonary Embolism

• Physical exam: tachycardia, tachypnea, sats, R heart findings, leg findings

• Ancillary - EKG, CXR, nonspecific d-dimer is usually (sensitivity > 85%)

• Assign likelihood of PE (low, high, intermediate) based on clinical gestalt or grading scales (e.g. Well’s Criteria)• If low probability and d-dimer is , quit (probably)• If intermediate or high, or if low with d-dimer, further study

(V/Q, CT angio, perhaps dopplers)

Aortic dissection

• History triggers; sudden,radiation, ripping/tearing• Risk factors: HTN, Marfan’s, coarctation, aortic valve

replacement, bicuspid aorta• PE:

• Severe pain, distress (usually), pulses, BP differential, AI murmur, neuro deficits

• All are insensitive markers, varied specificity• Ancillary data

• CXR: usually abn (90%) wide mediastinum, abn aorta; non-specific, 10% “normal”

• EKG: may show ST segment elevation

Acute Coronary Syndrome

• Most important due to commonality as well as lethality

• Top of differential, first inquiry• ‘ACS’ against the field of everything else

ACS

• History: Full historyOnly 4 things are truly predictive of ACS

1. Presence of chest pain2. Chest pain as chief complaint3. Radiation to shoulder(s)4. History of previous MI

• Risk factors (traditional) are not predictive in ED setting

ACS• PE: full physical

• Only 4 things predictive:1. Hypotension2. Diaphoresis3. Rales4. S3

• Markers• CKMB | troponin : sensitivity < 50% at 6 hrs• Neg markers with unstable angina and often initially neg

with MI• Neg first set mandates at lest on additional set

ACS: EKG

• Diagnostic of MI (1 mm elevation ST segments in anatomically contiguous leads) about 50% of the time.

• Non-diagnostic (usually non-specific ST/T waves) in around 50% MI.

• Normal 5 - 10% MI• If ST as above there is 80% likelihood of AMI• If new ST 1 mm with inverted T in anatomically

contiguouse leads, 20% chance of AMI, 20 -- 50% change unstable angina (UA).

• If old ST changes as above and acute chest pain, 5% chance AMI and 20 - 50% UA.

Acute Coronary Syndrome

• If ACS is Ruled In (with EKG or markers) treat and admit.

• If not, then:• If strong suspicion, teat, admit, further R/O• If convinced not ACS (or other potentially serious

problem) -• treat symptoms, outpatient manage

• If unsure - • treat, admit, further R/O

ACS

• Approached with clinical gestalt. • More objective decision aids available (ACI - TIPI).• Clinical sensitivity of either approach, > 95%.• Not good enough: the 5% (approximate) do badly.

• If in doubt, assume the worst, treat and admit for further evaluation.

References

1. Evaluation of the Patient with Acute Chest Pain. Lee. N Engl J Med 2000; 342: 1187-1195.2. Missed Diagnosis of Acute Cardiac Ischemia in the Emergency Department. Pope and others. N

Engl J Med 2000; 342: 1163-70. Editorial N Engl J Med 2000; 342: 1207-1209.3. Is this Patient Having a Myocardial Infarction? Panju and others. JAMA 1998;280:1256-63.4. Prediction of the need for intensive care inpatients who came to Emergency Departments with

acute chest pain Goldman and others. N Engl J Med 1996; 334:1498-1504.5. ST-segment Elevation in Conditions other than Acute Myocardial Infarction. Wang and others. N

Engl J Med 2003; 349:2128-2135.6. Triage of patients with Acute Chest Pain and Possible Cardiac Ischemia: The Elusive Search for

Diagnostic Perfection. Goldman and others. Ann Int Med 2003; 139: 987-995.7. Comprehensive strategy for the evaluation and triage of the chest pain patient. Tatum. Ann Emerg

Med 1997;29:116-125.8. A computer protocol to predict myocardial infarction in emergency department patients with chest

pain. N Engl J Med 1988; 318:797-803.9. Prognostic Importance of the Physical Examination for heart failure in non ST elevation Acute

Coronary Syndromes: The Enduring value of Killilp Classification. JAMA 2003; 290: 2174.10. Use of the Acute Cardian Ischemia Time Insensitive Predictive Instrument (ACI-TIPT) to assist with

Triage of Patients with Chest Pain. Selker. Ann Int Med 1998; 129:845-855.11. Impact of a Clinical Decision Role on Hospital Triage of Patients with suspected Cardiac Ischemia in

the Emergency Department. Reilly and others. JAMA 2002; 288:342-350.