A 59-year old-male with a past medical history of uncontrolled hypertension and polysubstance use disorder presents with exertional dyspnea that started 2 weeks ago. He reports associated bilateral lower extremity swelling, right greater than left, that started 2 days ago. An ECG is obtained on arrival (Figure 1).
Interpretation:
Rate: 76 bpm; Rhythm: normal sinus rhythm; Axis: normal axis (I: pos, II: pos., aVF: pos) Intervals: PR: 147, normal; QRS: 90, normal; QT: 441, normal; P-Waves: present and associated with every QRS; QRS Complex: abnormal Q wave in lead III, good R wave progression; ST Segment/T-waves: T wave flattening in lead II, T wave inversions in leads III, aVF, and V1-3, & biphasic T wave in V4
The patient was subsequently admitted for further cardiac work-up and ultimately diagnosed with a right renal mass complicated by renal vein thrombosis, IVC thrombus, and extensive bilateral pulmonary emboli. The patient was started on rivaroxaban during his admission and discharged to home on 2 liters of oxygen 11 days later when deemed clinically improved and stable.
One week later, the patient re-presented with 2 days of worsening shortness of breath and increasing oxygen requirement from 2 liters to 4 liters. A ECG was obtained in triage (Figure 2).
Figure 2. Second ECG.
Interpretation:
Rate: 113 bpm; Rhythm: sinus tachycardia; Axis: right axis deviation (I: neg, II: pos., aVF: pos) Intervals: PR: 161, normal; QRS: 89, normal; QT: 400, normal; P-Waves: present and associated with every QRS; QRS Complex: good R wave progression; ST Segment/T-waves: T wave inversions in leads III, aVF, and V1-V4
The emergency physician immediately performed a point-of-care echocardiogram and found evidence of right heart strain (D-sign, poor IVC variability) and visible IVC thrombus, no pericardial effusion, and preserved ejection fraction. The Pulmonary Embolism Response Team (PERT) was activated. CT pulmonary angiography demonstrated worsening PE clot burden with evidence of right heart strain and pulmonary infarcts. Thrombectomy was deemed to not be feasible due to the extent of tumor burden, hypoxia, and right heart strain. The patient was admitted to the MICU for medical management of submassive pulmonary embolism.
Discussion:
When examining an ECG for signs of acute pulmonary embolism (APE), traditionally taught and suggested patterns include:
P pulmonale: P waves with >2.5mm in leads I, II, III, aVF, aVR, aVL, or >1.5mm in V1
Right axis deviation: Negative QRS lead I, positive QRS lead III/aVF
Left axis deviation: Positive QRS lead I, negative QRS lead III/aVF
S1S2S3 pattern: S waves >1.5mm in leads I, II, III
S1Q3T3 pattern: S waves in lead I >1.5mm, Q wave in lead III >1.5mm, and negative T wave in lead III
Low voltage QRS: Amplitude of <5mm in all limb leads
Clockwise rotation: R wave amplitude=S wave amplitude in precordial leads at V5 or beyond
Unfortunately, these findings have repeatedly been shown to be highly variable (1-3).
Therefore, what ECG findings are most suggestive of APE? A retrospective study conducted by Kosuge et al. identified the pattern of negative T waves in lead III and V1 and/or peak negative T wave in V1-V2 to have a sensitivity of 98% and specificity of 92% for identification of APE (1). Notably, the findings of negative T wave in lead III and V1 or peak negative T wave in V1-V2 alone both had a sensitivity of 87% and specificity of 96% for APE. When compared to acute coronary syndrome (ACS), negative T waves were distributed around aVL and V2-4 with peak negative T wave most frequently identified in leads V3-V4 (Figure 3).
Figure 3. Adapted from Kosuge et al. (1).
This case demonstrates:
Suggested criteria with high sensitivity and specificity for APE
Electrocardiographic changes when known APE begins to cause right heart strain, and
Lack of suggested T wave findings consistent with ACS.
The ECG in Figure 1 demonstrates a negative T wave in lead III, negative T wave in V1, and peak negative T wave in V2. The patient was diagnosed with APE during this visit without signs of right heart strain. The patient later returned to the ED with worsening symptoms and signs of right heart strain on point-of-care ultrasound. The ECG in Figure 2 also demonstrates a negative T wave in lead III, negative T wave in V1 but with a shifted peak negative T wave in V2-V3. With increasing right heart strain, peak negative T often moves from V1 toward V6 which explains the peak negative T beginning to move from V1 in Figure 1 to V2-V3 in Figure 2. The second ECG with APE and right heart strain can still further be differentiated from ACS by noting that there is a lack of negative T waves in aVL, peak negative T wave beyond V3, or ST elevations/depressions.
Take Away Points:
When there is high clinical suspicion for APE, pay close attention on ECG to leads III and V1-V2 for negative T wave inversions.
Get in the habit of looking not just for T wave inversions, but also where the peak negative T wave is located in the precordial leads to help differentiate between possible ACS versus APE.
Maintain a high clinical suspicion for APE when the combination of T wave inversions in lead III, T wave inversions in lead V1, and peak negative T wave in leads V1-2 is identified (sensitivity 98%, specificity 92%).
Authored by Michael Hohl, MD.
Resources:
Kosuge M, Ebina T, Hibi K, et al. Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circ J. 2014;78(2):483-489. doi:10.1253/circj.cj-13-1064
Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW 3rd. The electrocardiogram in acute pulmonary embolism. Prog Cardiovasc Dis. 1975;17(4):247-257. doi:10.1016/s0033-0620(75)80016-8
Qaddoura A, Digby GC, Kabali C, Kukla P, Zhan ZQ, Baranchuk AM. The value of electrocardiography in prognosticating clinical deterioration and mortality in acute pulmonary embolism: A systematic review and meta-analysis. Clin Cardiol. 2017;40(10):814-824. doi:10.1002/clc.22742