Friday, December 5, 2014

EKG Challenge #5 Case Conclusion: Impostor!

You are working in the emergency department when an otherwise healthy middle-aged woman presents following a syncopal episode.  She complains predominantly of shortness of breath and chest pain that radiates to her shoulder and jaw.  She has no other pertinent history besides being a smoker and her father having a myocardial infarction at an early age.  Her vitals are initially stable, but she soon becomes tachycardic and hypotensive.  Her labs are drawn and her ECG is below:


Because of concern for possible ST elevation in V1-V3,  the patient was emergently taken to the cath lab.  Findings?   Clean coronaries.


The EKG is re-examined and the differential diagnosis of deadly chest pain is considered.  An S1Q3T3 pattern is noted. A PE-protocol CT is performed which finds a large saddle PE.


S1Q3T3


PE protocol CT for this patient

The patient has an echocardiogram demonstrating flattening of the septum and RV dilation consistent with right ventricular strain. The patient is anticoagulated with heparin, stabilizes, and does not require thrombolysis.  She is later found to have an underlying gynecologic malignancy.

Contrary to what we set out believing when we begin in medicine, most pathology does not fit neatly into a diagnostic box.  While we memorize as medical students that ST elevation = MI and S1Q3T3 = PE, the waters are much muddier and the diagnosis often less clear in real life.

While the electrocardiogram (ECG) is not the most sensitive test for acute pulmonary embolism (PE), there are abnormalities that may help physicians make the diagnosis in the right clinical context.  Often taught abnormalities more specific for PE are S1Q3T3 (20-25% of acute PE patients), right ventricular strain (anterior and inferior T wave inversion, 4-11% of acute PE patients), and new incomplete right bundle branch block [1,2,3,4].  Although these findings may be uncommon in acute PE, they are more frequent in patients with massive acute PE with hemodynamic compromise.  Sinus tachycardia is also found in many patients with PE, however it is common in many other conditions.

 ECG with the classic S1Q3T3 pattern in a patient with a massive PE resulting in cardiovascular collapse.

One study of patients with acute massive PE found that S1Q3T3, qR morphology in V1, RBBB, ST elevation in lead V1, ST elevation in aVR, and ST depression in leads V4 to V6 were associated with cardiogenic shock [5].

While ST elevation is more commonly associated with acute coronary syndrome (ACS), it can also be associated with massive pulmonary embolism.  These patients may be mistakenly sent to the cath lab for percutaneous intervention, only to be found to have minimal coronary artery disease, further delaying the diagnosis of PE.  Since these findings are more commonly found in patients with hemodynamic instability from their PE, many of them can suffer increased morbidity and mortality from the delay in diagnosis.  Many of these case reports have noted that these ST elevations are commonly in the anterior leads with many having ST elevations in lead aVR along with the other classic ECG findings of acute PE described above [6,7,8,9,10].

An example ECG [10] demonstrating ST elevation in a patient with massive PE.  Note there again appears to be a S1 as well as ST depression in lead I.  There is a definite Q3 in lead III.  Also note a similar abnormality in aVR as in our presented patient, although not a full ST elevation.

ST elevation in the often ignored lead aVR has often been associated with left main coronary artery (LMCA) occlusion or wide-spread coronary artery disease.  Many times these patients will have widespread ST-segment depression in leads V4 to V6.  The finding of ST elevation in aVR in patients with massive acute PE is often found in patients with cardiogenic shock associated with ST elevations in leads III and V1.  This mimic of ischemic disease most likely results from the ischemia caused by a massive PE.  The large clot burden decreases RV output and LV preload, subsequently leading to decreased myocardial perfusion.  The RV strain against the large PE likely exacerbates the ischemic picture.  The leads aVR (RV outflow [11]), III (inferior RV), and V1 (anterior RV) all reflect the ischemia found in the RV [12].  The associated V4-V6 ST depression found in some patients with massive acute PE likely reflects the subendocardial ischemia from the decreased LV output. 

In a case series by Zhong-Qun and colleagues [12], they found similar ECG findings (below) on three patients with massive PE who were hemodynamically unstable.  All the patients had elevations in aVR as well as ST depressions in I, V4-V6.  There also appears to be an S wave in each lead I in all three patients as well as Q waves in lead III in at least two patients.  There is also evidence of ST elevation in V1 in two patients.


There is another great similar case over in Life in the Fastlane, where the patient also presented after a syncopal episode and ultimately suffered PEA arrest from a massive PE.  Again ST elevations are seen in anterior leads as well as aVR.  The ECG also demonstrates new RBBB with right ventricular strain (deep T wave inversions in leads V1-V3), other common findings in acute PE. 

Take home points:
-Specific acute PE ECG abnormalities are not common, but are more likely to be present with increasing severity of pulmonary embolism
-ST elevations may occur in massive acute PE, usually associated with ST elevations in leads aVR and V1, look for other classic PE ECG abnormalities and keep PE on the differential
-although not discussed above, consider bedside echo to help you make the correct diagnosis.


References:
1. Panos RJ, Barish RA, Whye DW Jr, Groleau G. The electrocardiographic manifestations of pulmonary embolism. J Emerg Med. 1988;6(4):301.
2. Kosuge M1, Kimura K, Ishikawa T, Ebina T, Hibi K, Kusama I, Nakachi T, Endo M, Komura N, Umemura S. 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.
3. Ullman E, Brady WJ, Perron AD, Chan T, Mattu A. Electrocardiographic manifestations of pulmonary embolism. Am J Emerg Med. 2001 Oct;19(6):514-9.
4. Witting MD, Mattu A, Rogers R, Halvorson C. Simultaneous T-wave inversions in anterior and inferior leads: an uncommon sign of pulmonary embolism. J Emerg Med. 2012 Aug;43(2):228-35.
5. Kukla P, McIntyre WF, Fijorek K, Mirek-Bryniarska E, Bryniarski L, Krupa E, Jastrzebski M, Bryniarski KL, Zhong-qun Z, Baranchuk A. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med. 2014;32(6):507-10.
6. Ciliberti P, Rapezzi C, Villani C, Boriani G. Massive pulmonary embolism with acute coronary syndrome-like electrocardiogram mimicking acute left main coronary artery obstruction. J Emerg Med. 2012 Oct;43(4):e255-8.
7. Yamagami F, Mizuno A, Shirai T, Niwa K. A savage sequence: ST-segment elevations with pulmonary embolism. Am J Med. 2014 Sep;127(9):820-2.
8. Zhan ZQ, Wang CQ, Nikus KC, He CR, Wang J, Mao S, Dong XJ. Electrocardiogram Patterns during Hemodynamic Instability in Patients with Acute Pulmonary Embolism. Ann Noninvasive Electrocardiol. 2014 Nov;19(6):543-51.
9. Yeh KH, Chang HC. Massive pulmonary embolism with anterolateral ST-segment elevation: electrocardiogram limitations and the role of echocardiogram. Am J Emerg Med. 2008 Jun;26(5):632.e1-3.
10. Falterman TJ, Martinez JA, Daberkow D, Weiss LD. Pulmonary embolism with ST segment elevation in leads V1 to V4: case report and review of the literature regarding electrocardiographic changes in acute pulmonary embolism. J Emerg Med. 2001 Oct;21(3):255-61.
11. George A, Arumugham PS, Figueredo VM. aVR - the forgotten lead. Exp Clin Cardiol. 2010 Summer;15(2):e36-44.
12. Zhong-Qun Z, Chong-Quan W, Nikus KC, Sclarovsky S, Chao-Rong H. A new electrocardiogram finding for massive pulmonary embolism: ST elevation in lead aVR with ST depression in leads I and V(4) to V(6). Am J Emerg Med. 2013 Feb;31(2):456.e5-8.

Submitted by Steven Hung (@DocHungER), PGY-2
Faculty Reviewed by Doug Char
Special thanks to Heather Webb (@webbmd) for yet another great case.

1 comment:

  1. Suppose you've got an equivocal bedside ultrasound for R heart strain and the EKG did not clearly show the classic S1Q3T3 pattern (so your suspicion or PE and MI are roughly equal), should this patient go to the cath lab or the CT scanner first? I suppose if we were at a community center without rapid access to PCI or thrombectomy it may not matter and we could just thrombolyse with TPA (correct me if I'm mistaken here), but I'm curious as to what others at a tertiary center capable of either intervention would do first.

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