Pulmonary Embolus: See the echo, and believe the ECG!

Too many people are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. In particular, two beliefs stick in my craw:

“The most common sign of PE on the ECG is tachycardia”

This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%). Likewise, the average heart rate in Kosuge’s 2007 study was only 94!

“PE = S1Q3T3”

S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge has found that only 20-22% of PE patients had an S1Q3T3, while the TWI in leads III and V1 was far more sensitive.

The Case

An 80-something year old male was brought to the ED by EMS, feeling weak. 

He said that this had been going on for about a week, and was getting worse. Only when directly queried did he admit to orthostasis, and in fact had syncoped while shopping the day prior. He denied any chest pain, but endorsed some mild dyspnea.

He had a history of CAD, PCI, and a remote history of a PE. His memory and the records were vague on this last point, and he was not on anticoagulation.

His vitals and exam were unremarkable. Since this could have been ACS, or even mild CHF, a troponin and BNP were ordered.

The ECGs

An ECG was immediately obtained:

The baseline wanders, but there is a clear S1Q3T3. Furthermore, there is T wave
inversion (TWI) in the anterior leads, from V1 to V5,. These findings suggest RV strain

Kosuge showed in 2007 that, in patients with anterior TWI and symptoms suggestive of either ACS or PE, TWI in both leads III and V1 strongly favored PE over ACS.¹ 

A recent update from Kosuge confirms and extends those results, demonstrating that TWI in both leads III and V1 and/or peak TWI in leads V1 or V2 was extremely sensitive and specific for PE (versus ACS due to LAD occlusion).²

So, the ECG proves it, right? Unfortunately, when the emergencu physician reviewed the ECG from 5 months prior...

An arguable S1Q3T3, and TWI in III and V1-V4.

… and from 7 years prior...

'Bout the same.

... it seemed like the ECG findings were, perhaps, simply chronic. Well, when in doubt, break out the ultrasound!

The Echos

Parasternal long-axis

There is a dilated and hypokinetic RV, while the anterior wall contracts nicely.

Parasternal short axis

Septal bowing, or D-shaped septum (“Movahed’s sign?”)

Apical 4-chamber

Markedly dilated, hypokinetic RV free wall, with preserved apical contractility
(a.k.a. McConnell’s sign)

Triscuspid valve – color Doppler

Moderate regurgitation,  max velocity 5 m/s by CW Doppler, indicating very high pulmonary artery pressure

Clinical course

Given the patient’s CKD, and the stable hemodynamic status, unfractionated heparin was started, and the patient was admitted. A V/Q scan the following day confirmed an acute PE, apparently with significant chronic emboli as well! Anticoagulation was bridged to oral therapy, and the patient was discharged back home.

Bottom line:

The ECG can be very helpful is suggesting PE. Many physicians are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. 

In particular, two elements of the conventional wisdom are often uttered without considering the evidence:

“The most common sign of PE on the ECG is tachycardia”

This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%).³ Likewise, the average heart rate in Kosuge’s study was only 94!

“No S1Q3T3 = no signs of PE”

S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge found that only 20-22% of PE patients had a PE,¹,² while the TWI in leads III and V1 was far more sensitive.

Perhaps the ECG isn’t completely sensitive for picking up every tiny sub-segmental embol-ette.  Remember, though, that the ECG isn’t that sensitive for picking up every little troponin leak either! But the ECG is darn good for picking up the STEMI patient that needs emergent therapy, and the analogy with PE is likely true as well – the ECG will suggest the diagnosis in patients who are at high risk from large PEs.

1.         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):817-821. doi:10.1016/j.amjcard.2006.10.043.

2.         Kosuge M, Ebina T, Hibi K, et al. Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circ J Off J Jpn Circ Soc. 2014;78(2):483-489.

3.         Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M. The ecg in pulmonary embolism : Predictive value of negative t waves in precordial leads—80 case reports. Chest. 1997;111(3):537-543. doi:10.1378/chest.111.3.537.