CHEST PAIN WORKUP

Pt is a 41 year-old white female who presents for chest pain and SOB.

c/c: “My side is killing me and I feel like I can’t breathe.”

HPI: Pt returned yesterday from a cross-country trip and she awoke to experience sudden onset chest pain and diffi culty breathing. Pain was rated 7/10, does not radiate, and per Pt, has been worsening. Pt has had no prior similar episodes of chest pain or SOB.

HISTORY

PMH: None.PSH: None.OB/Gyn: P0G0, normal menstrual cycles with no

irregularities.All: NKDA.Meds: Daily multivitamin.Fam: Father (DM2), Mother (HTN)Soc: No Tob, no EtOH, no illicit drug usage.ROS: +Chest pain, +SOB; no cough, no abdominal

pain, no nausea, no vomiting, no diarrhea, no constipation, no blood in stool, no pain on urination.

HISTORY, CONTINUED

VS (abn only): Temp 100.4 deg F, HR 116, RR 22HEENT: WNL.Neck: Moderate JVD, no carotid bruits.Chest: No tenderness, breath sounds reduced on left

side.Heart: Tachycardia, normal rhythm, normal S1/S2, no

murmurs, gallops, or rubs.Abd: Soft, non-distended, non-tender, BS+.Extr: No edema, peripheral pulses UE/LE 2+ and

symmetric.

PHYSICAL

ANY INITIAL DIFFERENTIALS SO

FAR?

Casting a relatively wide net initially, common causes of chest pain include: Myocardial infarction Myocardial ischemia (e.g. stable, unstable, Prinzmetal’s

angina) Aortic dissection GERD (a much more common cause of ch/pain than you

might think) Pneumothorax Pulmonary embolism Pneumonia Costochondritis Drug-induced (e.g. cocaine) myocardial ischemia

DIFFERENTIAL DIAGNOSES

SO, WHICH INITIAL IMAGING/LABS SHOULD WE

GET?

The most important imaging/labs in this work-up (in no particular order) are: ECG Serial cardiac enzymes (CK-MB, Troponin-I; now and at every 8 hours until

3 samples have been drawn) Echocardiography CXR ABG CBC/electrolytes, Ca2+ Continue monitoring VS

This is not to say you couldn’t order additional tests/labs; however, these imaging/labs will: Cover the diff erentials in our chest pain work-up Focus on the most serious (i.e. life-threatening) targets in our chest pain

work-up (the ones which clinically you cannot aff ord to miss) Help to conserve costs (typically, both our Pt and our attending will not be

happy if we order every test under the sun)

INITIAL IMAGING/LABS

IMAGING/LAB RESULTS

Take a quick precursory glance to see if there’s anything abnormal:

Are the lungs full (i.e. not collapsed) and clear of blood/fluid?

Is there any mediastinal shift or widening?

How about the size of the heart? (Normal is <1/2 chest width)

What we’re looking for generally is to be able to rule out some of our differentials

CXR RESULT

This CXR looks pretty normal:

Lungs are full (i.e. no pneumothorax) and clear (i.e. likely no pneumonia).

There is no mediastinal shift (i.e. no tension pneumothorax) or widening (no aortic dissection).

Size of the heart is normal (no CHF).

CXR RESULT, CONTINUED

Echo shows no cardiac wall abnormalities

ECHO RESULTS

So what does our Pt’s ECG indicate?First look at leads II and V5

Does this look like a normal ECG tracing?

ECG RESULTS

Looks like we are dealing with sinus tachycardia Normal QRS width No ST segment elevations/depressions or T-wave

changes

ECG RESULTS, CONTINUED

CK-MB Increases within 4 to 8 hours Returns to NL in 48-72 hours

Troponin-I Increases within 3 to 5 hours Peaks at 24-48 hours Returns to NL in 5 to 14 days

For our Pt, initial draws showed normal CK-MB and Troponin-I Subsequent draws demonstrate no increase in CK-MB or

Troponin-I levels. What does this indicate to us?

CARDIAC ENZYME RESULTS

Notably, the lack of an elevation in CK-MB and Troponin-I distinguishes this from a myocardial infarction (which would demonstrate an elevation in cardiac enzymes over time)

CARDIAC ENZYME RESULTS, CONT’D

ABGs demonstrate hypoxemia (low blood O2) and hypocapnia (low blood CO2) with a pH >7.4

Because the pH is >7.4 and CO2 is low, what might this indicate to you?

ABG RESULTS

A pH of >7.4 means the Pt is in alkalosis

Low CO2 means we’re blowing off CO2, in this case due to hyperventilation

As such, the problem must be related to respiratory alkalosis, which is an acid-base disorder commonly associated with the problem we’re dealing with.

Have you figured out what it is yet?

ABG RESULTS, CONTINUED

So, whittling down our diff erentials, we have: Myocardial infarction/ischemia

No cardiac enzyme elevation, no ST elevation/depression or T-wave changes on ECG Aortic dissection

No mediastinal widening, no ripping/tearing chest pain radiating to back, no hx trauma (e.g. seatbelt injury)

GERD No vomiting, cough, etc. on ROS; no PMH indicative of acid refl ux (see history)

Pneumothorax No collapsed lungs, no mediastinal shift

Pulmonary embolism SOB with a clear CXR (doesn’t always have to be clear, but if you see a clear

CXR w/ fever, tachycardia, and tachypnea, think PE), fever, tachycardia, tachypnea, ABG demonstrating respiratory alkalosis, DVT risk(s) with 2/3 on Virchow’s Triad (no endothelial damage, but hypercoagulable state and stasis present [long cross-country trip in hx])

Pneumonia Fever; but WBC WNL, clear CXR

Costochondritis No persistent chest wall tenderness to palpation (see physical exam)

Drug-induced (e.g. cocaine) myocardial ischemia Unlikely, no hx drug usage (see history)

DIFFERENTIAL DIAGNOSES, REVISITED

SO WHAT’S OURDIAGNOSIS?

What we’re deal ing with here is l ikely a pulmonary embolism (PE).

How do we know this? Primari ly due to the fol lowing: Sudden onset chest pain in the presence of:

Tachycardia Tachypnea, and Fever

With hypoxia and hypocarbia (respiratory alkalosis) on ABG In the presence of a clear CXR (note: can be abnormal, but CXR’s are typically

normal with PE) With DVT risks (look for aspects of Virchow’s Triad)

In addition there is: No elevation in cardiac enzymes, and No ST/T-wave changes (although sometimes there can be nonspecifi c ST changes with

a PE)

I f our suspicion is high based on the above, we would not wait for further exams to give heparin; however, there are subsequent tests we’l l discuss to confi rm a PE in a cl inical setting.

DIAGNOSIS

A PE represents an embolism which has become lodged within the pulmonary arteries, which obstructs blood fl ow through the lungs, causing: Increased pulmonary arterial pressure, Increased right ventricular pressure, and V/Q perfusion ratio abnormalities (as some areas, while still

ventilated, have had their blood flow cut off by the embolus, so no gas exchange occurs)

Most commonly, a PE is the result of a deep vein thrombosis (DVT) in the lower extremities; however, it can also be due to: Air emboli Amniotic fluid emboli Fatty emboli Septic emboli, etc.

PE

To confi rm a PE, we follow this rubric: If there is a low clinical suspicion of a PE, acquire a D-dimer to

rule out. If there is a clinical suspicion of PE (or an abnormal D-dimer),

then do the following: Acquire a spiral CT scan (highly sensitive for PE and the test of choice

with an abnormal CXR). If inconclusive or unable to be performed, then conduct a Doppler ultrasound of the legs.

If a DVT is present, treat for PE. If no DVT is present, acquire a V/Q scan (requires a normal CXR to be accurate).

An angiogram is the gold standard in PE; however, it’s rarely performed because of its high mortality risk of 0.5% (and we typically can figure out a PE without it)

So, how do we treat an instance of PE?

PE, CONTINUED

PE TREATMENT

Hospital admission

Pt management: Start Pt on heparin

Bridge to warfarin (INR 2-3) Place IVC fi lter if contraindications exist to anticoagulation Have Pt wear compression stockings Encourage early ambulation

Thrombolysis only in the presence of a massive PE/DVT

So, to recap remember a few key things: Think PE if you see new-onset chest pain in the presence of fever,

tachycardia, tachypnea, DVT risks, and a clear CXR. Furthermore, look for respiratory alkalosis with hypoxemia and hypocapnia on

the ABG, which is a classic fi nding with PE. Also, remember Virchow’s Triad as it applies to DVT risks:

Hypercoagulability Endothelial damage, and Stasis

PEs can be confirmed by: Spiral CT (especially in the presence of an abnormal CXR)

If a spiral CT in inconclusive/unavailable, get a Doppler U/S of the lower extremities If no DVT on U/S, acquire a V/Q scan (only accurate in the presence of a normal CXR)

Note: if your clinical suspicion of PE is low (e.g. low DVT risks, etc.), acquire a D-dimer to rule out PE.

If your clinical suspicion of PE is high, don’t wait on confi rmation to start heparin

Lastly, PEs are managed with: Heparin, warfarin (once bridged to INR 2-3), and DVT ppx

(stockings/ambulation).

IN SUMMATION

Emergency Medicine Education Online Available at: http://www.emedu.org

FlickRiver, Medical Imaging Gallery Available at: http

://www.flickriver.com/groups/medimg/pool/interesting/

BIBLIOGRAPHY