Your shift is running smoothly. You’ve been applying all the fantastic FOAMed (what’s FOAM/FOAMed?
) you learned this week and life couldn’t be better. You pick up the next chart: a 50yF sent by her family doc to the ED – she presented to his office a few hours after a 10 minute syncopal episode at home preceded by chest pain. The note says: Please rule out cardiac ischemia.
She’s obese and has a history of diet-controlled DM. She’s never syncopized before and doesn’t recall previous episodes of chest pain. The event happened in the morning – 15-20 minutes of squeezing epigastric pain/pressure, followed by presyncope, followed by syncope. She hit her head and has a small lac over the eyebrow. Since the episode she’s felt generally unwell and so proceeded to see her FD.
On exam, vitals are a temp of 36, pulse 104 and regular, BP 140/90 at triage and then approximately 170/110 (all 4 limbs), RR 20, sat 94-96%. Normal glucose. She’s obese. She’s a bit anxious but otherwise in no distress, looks well. Breathing is not laboured. Her CVS exam is unremarkable, lungs clear and no edema.
The ECG, already done, is on her chart and this is what you see.
What do you see?
Breakdown: HR ~110, regular. Sinus tachycardia. Axis normal (well, borderline RAD). QT a bit long. She also has inverted T’s in V1-V4 plus III, AVF.
Bloodwork is back. Troponin comes back at 0.6 (normal <0.12). Chest X-ray is unremarkable.
Slam dunk for cardiac ischemia/ACS, right? ASA, clopidogrel, fonda/LMWH of your choice, admit to medicine/cardiology. Next patient, please.
… Hmmm, those inverted T’s look suspicious. Could this be something else? And yes, yes it could. How about a pulmonary embolism? In fact, T inversion in inferior and anterior leads is very specific for PE. Check this article here
. Need confirmation? Check out Dr Mattu and Dr Smith reinforce it here
You ask a few more Q’s on history. Previous PE/DVT? No. Hemoptysis, cancer, leg swelling/pain? No. Recent surgery/immobilization? No. Exogenous hormones? No. Recent travel – yes, arrived from Pakistan 1 week ago. Weak risk factor but let’s go with it.
You add a D-dimer. Your gut tells you that you know it’ll be positive. It’s back at >4000.
CTPA is ordered and here it is below:
Saddle PE, extensive. Though not officially reported by radiology, the RV is big. Bigger than LV.
A bit about PE’s regarding ECG and troponin…
- Sinus tachycardia is common on ECG.
- S1Q3T3 (“cor pulmonale”) indicates RV strain, is a commonly cited ECG finding, but it is only present in <25% of cases. Its presence probably indicates a larger clot burden.
- Looking back at the above ECG in this case, you could argue there is an S1Q3T3 type pattern here, although the Q in lead III is pretty small.
- A study by Kosuge et al showed that, regarding T wave inversions in III and V1-V3, “the sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of APE were 88%, 99%, 97%, and 95%, respectively”
The patient presented here had a sub
massive PE. This article (http://circ.ahajournals.org/content/122/11/1124.full
) by Piazza and Goldhaber discusses the pathophysiology, classification and management of submassive PE. This table (http://circ.ahajournals.org/content/122/11/1124/T1.expansion.html
) is a handy breakdown of risk-stratifying submassive PE’s, according to patient appearance, cardiac biomarkers, and RV function. A positive/elevated troponin, elevated BNP or dilated RV on echo/CT are indicators of submassive PE. A massive PE
, on the other hand, is a PE with arterial hypotension (SBP >40 mmHg drop from previous) or signs of shock.
A bit about cognitive errors and bias…
Biases in this particular case include the following:
- Anchoring: the tendency to perceptually lock onto certain features in a presentation too early, thus “anchoring” onto a Dx; in this case it could have easily been labelled as ACS
- Diagnosis momentum: patients get labelled with a Dx and this gets “stickier and stickier” along the process; family doc thinks ACS, triage thinks ACS, etc, etc
- Premature closure: committing to a Dx before it is fully confirmed; in this case, “ischemic changes” on ECG and positive troponin could have easily led to prematue closure on Dx of ACS
Learning points from this case:
- not all “ischemic changes” (ie, T-wave inversions) are acute coronary syndrome
- not all elevated troponins are acute coronary syndrome
- it would have been very easy to get locked into the cognitive bias of settling on ACS as the diagnosis, treat with ASA, clopidogrel and an anticoagulant; this would have been detrimental to the patient
- always think about your biases whenever you are assessing a patient, especially if the puzzle pieces don’t really fit the way they should
While you’re at The Chart Review
, you may as well check out my earlier post on CXR findings in PE
. Just do it, you know you want to.
As always, I would love to hear/read your feedback/comments/questions. Feel free to post below or find me on Twitter @ETtube.
Amal Mattu’s EKG of the week website with cases of PE:
Dr Steve Smith’s ECG site with cases of PE:
Articles on PE ECG’s and submassive PE:
Kosuge et al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. Am J Cardiol
. 2007 Mar 15;99(6):817-21 http://www.ncbi.nlm.nih.gov/pubmed/17350373
Piazza and Goldhaber. Management of Submassive Pulmonary Embolism. Circulation. 2010; 122: 1124-1129
Resources on cognitive errors:
Croskerry. The Importance of Cognitive Errors in Diagnosis and Strategies to Minimize Them. Academic Medicine. 2003; 78(8):775-780
Emergency Medicine Cases podcast, Episode 11.