Introduction with a case
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A 45-year old man presented to the hospital with chest pain and dyspnea. His troponin was positive, and EKG showed T-wave inversions in the inferior leads and V1-V4. He was pale, diaphoretic, tachycardic, and borderline hypotensive with a systolic blood pressure ranging from 85-110mm. He was taken urgently for cardiac catheterization, which demonstrated no significant coronary artery disease. When he was taken off bedrest, he got up to use the commode and had a PEA arrest. Autopsy revealed pulmonary embolism.
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This post describes two EKG patterns of PE which mimic MI. Patients presenting with chest pain, these EKG patterns, and troponin elevation are often misdiagnosed with MI. In one multi-center study, 3% of all PE patients were admitted with an incorrect diagnosis of MI (Kukla 2011). These EKG patterns are associated with submassive or massive PE, so immediate recognition and appropriate therapy is essential.
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Pattern #1: RV strain pattern
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PE causing RV strain (Panduranga 2013).
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RV strain pattern
- T-wave inversion in V1 and V2
- At least one of the following:
- T-wave inversion in lead III
- The precordial lead with deepest T-wave inversion is V1 or V2
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The most common MI-mimic is caused by RV strain with T-wave inversion (TWI) in leads V1-V4. TWI in these leads typically raises concern regarding the possibility of ischemia involving the left anterior descending coronary artery (i.e., Wellen's pattern). However, this is also reported in up to 40% of patients with PE (Kukula 2014)(1).
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Differentiation from MI
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Kosuge 2014 compared 107 PE patients and 248 MI patients who presented with TWI in at least two leads between V1-V4. The distribution of TWI is different among these two groups: PE patients are more likely to have TWI in the inferior leads and V1-V2, whereas MI patients are more likely to have TWI in V5-V6 (figure below). Among these patients, the combination of TWI in V1 and lead III was 87% sensitive and 96% specific for PE. A similar finding was reported by Witting 2012, who found the combination of TWI in V1 and lead III to be 11% sensitive and 95% specific among all patients presenting with PE.
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Kosuge 2014 also noticed that the precordial lead with the maximal amount of TWI differed between patients with PE versus MI (figure below). By combining the criteria of (maximal TWI in V1-V2) and/or (TWI in V1 and III), this increased the sensitivity for PE to 98% while maintaining a specificity of 92% compared to MI.
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For additional detail and examples, please see several great videos by Amal Mattu discussing this EKG pattern here, here, and here.
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Differentiation from chronic RV strain
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RV strain pattern may be seen in chronic pulmonary hypertension (for example due to severe COPD or obesity hypoventilation syndrome). Clinical history as well as prior EKG, echocardiographic, or CT angiography data can help sort out whether this is acute or chronic.
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Pattern #2: RV injury pattern
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Less commonly, PE presents with widespread ST elevations and depressions. For example, the EKG below is from a PE patient with RV dilation, repeated syncope, and elevated troponin at Genius General Hospital.
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This pattern has been discussed occasionally in the literature, and was recently re-introduced in a case series by Zhong-qun 2013. These authors proposed that ST elevation in aVR with ST depression in leads I and V4-V6 is associated with massive PE.
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RV injury pattern (2)
- ST elevation in aVR and ST depression in lead I (3)
- ST elevation in V1-V3 and/or ST depression in V4-V6
Comparing EKGs of patients with PE who presented with widespread ST changes reveals the RV injury pattern. In the limb leads, the current of injury consistently projects towards the right leading to ST elevation in aVR and ST depression in lead I (see below), as described by Zhong-qun. In the precordial plane, some patients have a current of injury which projects anteriorly causing ST elevation in V1-V3 (red arrow below), whereas other patients have a current of injury which points more laterally causing isoelectric ST segments in V1-V3 (orange arrow below). Depending on the direction of these currents, there may or may not be ST depression in V4-V6. All patients have some ST deviation present in the precordial leads (ST elevation in V1-V3 and/or ST depression in V4-V6).
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Direction of the current of injury varies between the red arrow and the orange arrow (4).
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STE in aVR is common in PE but generally ignored. Among a series of 500 patients with PE, Kukula 2014 found STE in aVR in 36% of patients, and in 65% of patients with cardiogenic shock from PE. STE in aVR was the most sensitive EKG finding among patients with cardiogenic shock due to PE. Janata 2012 found STE in aVR among 34% of patients with PE, and similarly found this more often among patients with severe PE.
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Differentiation from MI
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RV injury pattern is easily mistaken for MI. Some PE patients have a combination of Q-waves and STE in the anterioseptal and/or inferior leads, closely simulating ST-elevation MI. It is increasingly recognized that ST elevation in aVR may be seen in MI as a marker of severe coronary artery disease, so this feature may also lead clinicians towards a diagnosis of MI.
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One feature which may be helpful to distinguish PE from MI is rightward deviation of the terminal component of the QRS vector. In patients with RV injury pattern, RV conduction is delayed and the terminal portion of the QRS complex reflects the right ventricle contracting. Thus the final portion of the QRS complex usually has an axis between +90 degrees and -150 degrees, which produces a terminal S-wave in lead I and a terminal R-wave in lead III. This is not usually seen in myocardial infarction unless there is underlying complete right bundle branch block. It's easy to remember this pattern because the terminal forces in leads I and III point towards each other:
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Another feature which may help distinguish PE from MI is TWI if present. PE patients may simultaneously have both RV injury and RV strain patterns. As discussed above, the distribution of TWI may help differentiate PE from MI.
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Clinical Correlation Required
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Relationship to PE severity
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Both RV strain and RV injury patterns tend to occur in more severe PE. Echocardiographic RV dysfunction occurs in 75-80% of patients with either pattern (Kosuge 2014, Janata 2012). There are many case reports of PE patients who are stable at admission, but then suddenly crash with new-onset hypotension and a repeat EKG revealing an RV injury pattern.
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Synergy of EKG with echocardiography
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These EKG patterns are usually associated with echocardiographic features of pulmonary embolism including right ventricular dilation. MI is also often associated with abnormalities visible on echocardiography. Therefore for patients who present with these EKG patterns, bedside echocardiography is often helpful in differentiating between PE and MI.
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The Bottom Line
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RV strain pattern
- T-wave inversion in V1 and V2
- At least one of the following:
- T-wave inversion in lead III
- The precordial lead with deepest T-wave inversion is V1 or V2
RV injury pattern
- ST elevation in aVR and ST depression in lead I
- ST elevation in V1-V3 and/or ST depression in V4-V6
Conclusions
- Acute PE often mimics MI by causing two patterns, which may occur together or separately. Both patterns are usually associated with submassive or massive PE, requiring immediate recognition and treatment.
- RV injury pattern must be included in the differential diagnosis of ST elevation in aVR.
- RV injury pattern is not specific for PE. In the presence of this pattern, a terminal S-wave in lead I and a terminal R-wave in lead III may point towards PE.
- When there is uncertainty regarding whether the patient has PE or MI, there should be a low threshold to obtain immediate bedside echocardiography.
Notes
(1) The frequency of EKG findings among case series depend on factors including the intensity of CT scanning to detect small pulmonary emboli and the study location (i.e., Kukla 2014 was performed a tertiary care centers, which tend to receive patients with submassive or massive PE in transfer). Therefore, the sensitivity may not translate from one center to another.
(2) These findings have been reported in the literature previously. This combination of features is based on my review of the above cardiograms, and has not been previously reported to my knowledge. This should be considered a preliminary finding at best. These findings are clearly not specific for PE, but rather are intended to suggest the possibilityof PE.
(3) Since aVR and lead I point in nearly opposite directions, ST elevation in aVR and ST depression in lead I are really measuring the same electrical current. If there is equivocal ST elevation in aVR then lead I may be used as a tie-breaker: significant ST depression in lead I would suggest that there is indeed some real ST elevation in aVR.
(4) Appreciate permission of Mike Cadogan to use this image, with modifications (original image at LITFL site).
References
Ciliberti 2012 Massive pulmonary embolism with acute coronary syndrome-like electrocardiogram mimicking acute left main coronary artery obstruction. Journal of Emergency Medicine.
George 2010 aVR – the forgotten lead. Experimental and Clinical Cardiology.
Janata 2012 The role of ST-segment elevation in lead aVR in the risk assessment of patients with acute pulmonary embolism. Clinical Research in Cardiology.
Lee 2013 Critical ostial left main and right coronary artery stenosis secondary to takayasu arteritis in a young female simulating pulmonary embolism at presentation. Journal of Invasive Cardiology.
Kosuge 2014 Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circulation Journal.
Kukla 2014 Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. American Journal of Emergency Medicine.
Levis 2011 EKG Diagnosis: Pulmonary Embolism. The Permanente Journal.
Livaditis 2004 Massive pulmonary embolism with ST elevation in leads V1-V3 and successful thrombolysis with tenecteplase. Heart.
Mohsen 2013 Variable ECG findings associated with pulmonary embolism. BMJ Case Reports.
Petrov 2013 Submassive pulmonary embolism – a watch-and-wait strategy with anticoagulation alone or advanced therapy with thrombolysis. American Journal of Medicine Studies.
Spodick 1972 Electrocardiographic responses to pulmonary embolism: Mechanisms and sources of variability. American Journal of Cardiology.
Toprak 2014 Pulmonary embolism with ST-segment elevation in V1-3 and AVR treated successfully by catheter directed high-dose bolus thrombolytic therapy under cardiopulmonary resuscitation. American Journal of Emergency Medicine.
Ullman 2001 Electrocardiographic manifestations of pulmonary embolism. American Journal of Emergency Medicine.
Zhong-qun 2013 A new electrocardiogram finding for massive pulmonary embolism: ST elevation in lead aVR with ST depression in leads I and V4-V6. American Journal of Emergency Medicine.
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