I came across this 65/M who was brought to the ED with Shortness of breath on exertion and recurrent episodes of syncope over 2 weeks. Otherwise his history was limited. He came in with stable Vital Signs (RR- 20/min) and a normal systemic examination.
What next? Yes, We got the 12 lead ECG for him:
Interestingly, this was read as:
Computer: Anterior Wall Ischemia
EM Resident: R/O ACS
Cardiology Fellow: Anterior Wall Ischemia
Cardiology and Neurology Consult was asked for, and he got a head CT (though his CNS exam was normal) and got a set of biomarkers from Cardiology (including d-dimer!). And guess what, his troponin was reported normal but d-dimer was elevated! So we ended up getting a CT Pulmonary Angiogram for him.
This guy had bilateral PTE and showed up with HR in 90s, BP 120/70 SpO2 >95% RR 20/min on ambient air. He was taken up for thrombolysis in view of recurrent syncope and possible cerebral hypo perfusion.
This case raised a few questions:
1. Was his presentation concerning enough for this deadly disease?
2. Did we miss anything on the ECG?
3. Why did we do a head CT?
4. Why was he thrombolysed when the teaching is thrombolysis is reserved for massive PE?
Lets go through each one of them:
1. Syncopy and PE
About 10-15% of the patients with pulmonary embolism present with syncope. The textbook history of PE with acute chest pain/SOB and hemoptysis is seen rarely. We need to do a good history asking all the possible risk factors + complete physical exam and then risk stratify them based on clinical decision rules. A common finding which is not documented on the charts is the "calf exam".
Even after all this, it is not possible to pick every patient with PE!
In addition to all this we need to watch for other deadly cause of syncope!
Acute Coronary Syndrome
Arrythmias (Heart Blocks/Brugada/HOCM/WPW/QTc Syndromes/ARVD)
Intra abdominal bleed (Ruptures Spleen/Ovarian Cyst)
So, classic presentation of PE is rare. Apart from ACS/Arrythmias we need to think of other deadly differentials of syncope and in the ED - PE should always be in the lost of differentials of syncope!
2. ECG and PE
His ECG was read as Anterior wall Ischemia but then how do we explain the inferior TWI?
ECG is not a great tool to pick up PTE but should be used as only an adjunct to history and physical. Again classic S1Q3T3 is rare.
In fact his ECG showed something more important. There were "Simultaneous TWI in inferior and Precordial Leads" which suggested RV strain. Other ECG changes that may be seen PE are:
Non Specific changes
NORMAL ECG (ECG in PE can be normal!)
The most important ECG finding for PE, which we should know is probably "Simultaneous TWI in inferior and precordial leads". Pattern of TWI between Acute Pulmonary Embolism (APE) and ACS can be differentiated.
3. Role of head CT while evaluating syncope?
4. When do we thrombolyse PE?
PE can be classified as :
- Massive: with SBP < 90mm Hg
- Subamssive: with SBP > 90 but with RV dysfunction/Positive troponin
- Non Massive: No Hypotension/No RV Dysfunction/Negative Troponin
Lets summarise the take home points:
- Keep PTE always in your list of differentials for syncope.
- Simultaneous TWI in inferior and precordial leads is PE until proven otherwise.
- Avoid doing a routine head CT for syncope with unremarkable CNS exam.
- Thrombolyse massive PE, and for submissive PE go for shared decision making.
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