Syncope that Kills!

This week we have a case for review,
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:

(ACEPs clinical policy on syncope strongly recommends that an ECG be obtained in 
the initial evaluation of patients with syncope)

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
Subarachanoid Hmg
AAA
Aortic Dissection
Ectopic Pregnancy
Arrythmias (Heart Blocks/Brugada/HOCM/WPW/QTc Syndromes/ARVD)
Intra abdominal bleed (Ruptures Spleen/Ovarian Cyst)
Vertebrobasilar TIA
GI Bleed

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:
Sinus Tachy
RBBB
RAD
P Pulmonale
Atrial Arrythmias
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?

This guy showed up with a normal CNS exam. Is head CT justifiable for such patients with syncope and a normal CNS exam. Well, Strokes generally do not lead to syncope but a rare exception may occur in the setting of global bilateral cerebral ischemia or basilar artery disease affecting the reticular activating system, leading to ischemia that may present as a stroke. However, in the evaluation of a patient with TIA, MRI/MRA (not a CT scan) is a much better choice.

In patients with sudden onset of a severe headache in the setting of a possible syncopal event (with concern for a subarachnoid hemorrhage), doing an emergent head CT on arrival is very reasonable. Patients who present to the ED after a brief syncopal event, without focal neurologic symptoms, headache, altered mental status, or associated trauma, and who are not taking anticoagulants, are unlikely to benefit from a routine head CT.

In 2006, AHA/ACC stated that a neurologic cause of syncope should be considered only if suggested by history or physical examination.

4. When do we thrombolyse PE?

PE can be classified as :

1. Massive: with SBP < 90mm Hg
2. Subamssive: with SBP > 90 but with RV dysfunction/Positive troponin
3. Non Massive: No Hypotension/No RV Dysfunction/Negative Troponin

Thrombolysis is traditionally recommended for PE with hemodynamic compromise, with which most of us would agree. But in the above mentioned case, lytics were administered. Well, this may be justified based on his history of recurrent syncope and elevated Pulmonary artery pressures on ECHO which suggested RV Dysfunction. Thrombolysis always come with risk of bleeding and we need to do shared decision making in such scenarios. There might be a case where patients looks really sick with PTE but holding the blood pressure!

Lets summarise the take home points:

1. Keep PTE always in your list of differentials for syncope.
2. Simultaneous TWI in inferior and precordial leads is PE until proven otherwise.
3. Avoid doing a routine head CT for syncope with unremarkable CNS exam.
4. Thrombolyse massive PE, and for submissive PE go for shared decision making.

For Further Reading:

1. http://www.aapsus.org/articles/42.pdf
2. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347:878-885.
3. Kapoor WN, Karpf M, Maher Y, Miller RA, Levey GS. Syncope of unknown origin. JAMA. 1982;247:2687-2691.
4. Grossman S. Testing in syncope. Intern Emerg Med. 2006;1:135-136.
5. Castelli R, Tarsia P, Tantardini C, et al. Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope. Vasc Med 2003;8:257–61.
6. Courtney DM, Kline JA: Identification of prearrest clinical factors associated with outpatient fatal pulmonary embolism. Acad Emerg Med 8: 1136, 2001.[PMID: 11733290]
7. Ferrari E, et al. The ECG in pulmonary embolism. Chest. 1997;111:537-43
8. Differences in negative T waves among ACS,APE-  Kosuge M, Ebina T, et al – Eur Heart Journal cardiovasc care – 2012
9. Kosuge M, Kimura K, Ishikawa T, et al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. Am J Cardiol 2007;99(6):817-21.
10. Jankowski K, Kostrubiec M,et al. Electrocardiographic differentiation between acute pulmonary embolism and non-ST elevation acute coronary syndromes at the bedside. Ann Noninvasive Electrocardiol 2010;15:145–50
11. Moderate pulmonary embolism treated with thrombolysis (from the "MOPETT" Trial). Mohsen Sharifi, Curt Bay, Laura Skrocki, Farnoosh Rahimi, Mahshid Mehdipour, “MOPETT” Investigators Am J Cardiol. 2013 January 15; 111(2): 273–277.  Published online 2012 October 24. doi: 10.1016/j.amjcard.2012.09.027
12. Fibrinolysis for patients with intermediate-risk pulmonary embolism. Guy Meyer, Eric Vicaut, Thierry Danays, Giancarlo Agnelli, Cecilia Becattini, Jan Beyer-Westendorf, Erich Bluhmki, Helene Bouvaist, Benjamin Brenner, Francis Couturaud, et al. N Engl J Med. 2014 April 10; 370(15): 1402–1411.  doi: 10.1056/NEJMoa1302097