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 difficulty 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 deg F, HR 116, RR 22  HEENT: 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 differentials 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 afford 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 hours  Troponin-I  Increases within 3 to 5 hours  Peaks at 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 differentials, 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 reflux (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 OUR DIAGNOSIS?

 What we’re dealing with here is likely a pulmonary embolism (PE).  How do we know this? Primarily due to the following:  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 nonspecific ST changes with a PE)  If our suspicion is high based on the above, we would not wait for further exams to give heparin; however, there are subsequent tests we’ll discuss to confirm a PE in a clinical setting. DIAGNOSIS

 A PE represents an embolism which has become lodged within the pulmonary arteries, which obstructs blood flow 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 confirm 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 filter 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 finding 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 confirmation 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:  FlickRiver, Medical Imaging Gallery  Available at: BIBLIOGRAPHY