ECG Cases 14: Q-waves and Occlusion MI | EM Cases (2024)

Nine patients presented with potentially ischemic symptoms and Q-waves. Which patients had Occlusion MI?

Case 1: 70yo with past medical history of hypertension, an hour of shoulder pain. Borderline tachycardia, other vitals normal. Old then new ECG:

Case 2: 90yo with past medical history of hypertension, 9 hours of dyspnea. HR 110 bpm, BP 110, RR 40, O2sat 88%, afebrile. Old then new ECG:

Case 3: 30yo previously well, with exertional syncope

Case 4: 70yo history of prior MI/cardiomyopathy, three hours of epigastric pain. HR 50 bpm, other vitals normal.

Case 5: 30yo previously healthy, with 11 hours of constant chest pain. AVSS.

Case 6: 75yo with past medical history of hypertension and dyslipidemia, 2 hours of chest pain, dyspnea and lightheadedness. Borderline tachycardia, BP 120, O2sat 92%. Old then new ECG:

Case 7: 65yo previously healthy and well with 8 hours of constant chest pain. AVSS.

Case 8: 60yo previously healthy and well with 12 hours of constant chest pain. AVSS.

Case 9: 60yo with history of hypertension and dyslipidemia, one day on/off chest pain, now constant. HR 50 bpm, other vitals normal. Old then new ECG:

Q-waves and Occlusion MI

With normal conduction, ventricular depolarization travels left to right in the septum and then through both ventricles, with net forces towards the larger left ventricle. So, in the normal ECG, right sided leads have small positive R waves and larger negative S waves, and left sided leads can have tiny negative “septal Q” waves and positive R waves. Q-waves can be physiological (normal vector heading away from aVR, V1 or III), secondary to abnormal depolarization (eg reversed septal depolarization in LBBB, abnormal conduction in LVH, accessory pathway in WPW), or pathological (eg from MI or cardiomyopathy). Posterior MI doesn’t produce Q-waves on the 12 lead (unless associated with inferior or lateral MI), but instead produces tall R waves in the anterior leads.

Differential diagnosis of Q-waves

1. Physiological (normal vector heading away from aVR, V1 or III)
2. Secondary to abnormal depolarization (reversed septal depolarization in LBBB, abnormal conduction in LVH, accessory pathway in WPW)
3. Pathological (MI, cardiomyopathy)

As the Fourth Universal Definition of MI summarizes: “A QS complex in lead V₁ is normal. A Q-wave <0.03 s and <0.25 of the R wave amplitude in lead III is normal if the frontal QRS axis is between −30^o and 0^o. A Q-wave may also be normal in aVL if the frontal QRS axis is between 60^o and 90^o. Septal Q-waves are small, nonpathological Q-waves <0.03 s and <0.25 of the R-wave amplitude in leads I, aVL, aVF, and V₄–V₆. Pre-excitation, cardiomyopathy, TTS, cardiac amyloidosis, LBBB, left anterior hemiblock, LVH, right ventricular hypertrophy, myocarditis, acute cor pulmonale, or hyperkalemia may be associated with Q-waves or QS complexes in the absence of MI.” [1] It lists the following ECG changes as associated with prior MI (in the absence of LVH or LBBB):

1. Any Q-wave in leads V2-V3>0.02s or QS complex in leads V2-V3
2. Q-wave >0.03s and >1mm deep or QS complex in leads I, II, aVL, aVF, or V4-V6 in any two leads of a contiguous lead grouping
3. R wave >0.04s in V1-V2 and R/S>1 with a concordant positive T wave in absence of conduction defect

Myocardial infarctions used to be retrospectively dichotomized into Q-wave vs non-Q-wave MI, with the former considered to have had irreversible transmural necrosis. The STEMI paradigm shifted the dichotomy from observing the evolution of Q-waves to reperfusing those with ST elevation, but maintained the view that Q-waves represented late and irreversible infarction. The AHA’s 2013 STEMI guideline states that “the majority of patients will evolve ECG evidence of Q-wave infarction,” and the 2014 NSTEMI guidelines state that “significant Q-waves are less helpful…suggesting prior MI.”[2-3]

As a consequence, a “completed Q-wave infarct” is associated with withholding reperfusion from patients diagnosed with STEMI within 12 hours of first medical contact [4]. But new Q-waves can develop after as little as one hour of ischemic symptoms, and are associated with larger infarcts, lower EF and higher mortality [5-6]. As another study of STEMI patients treated within 12 hours of symptom onset found, “myocardial salvage was still substantial in patients with early QW, indicating that patients with STEMI and early QW frequently have favorable outcome after reperfusion despite presumed transmural and irreversible myocardial damage. The presence of early QW in patients presenting with significant ST-segment elevations within 12 hours after onset of clinical relevant symptoms should therefore not exclude patients from treatment with primary PCI.” [7]. As further proof that Q-waves can be acute and reversible, a follow-up study of STEMI patients with new Q-waves treated within six hours of symptom onset found that 39% eventually regressed—associated with greater spontaneous or collateral circulation, less peak enzyme levels, and a greater EF [8]. The 2017 ESC guideline now states that “the presence of Q-wave on the ECG should not necessarily change the reperfusion strategy [9], and the 2018 Fourth Universal Definition of MI explains that “in general, the development of Q-waves indicates myocardial necrosis, which starts minutes/hours after the myocardial insult. Transient Q-waves may be observed during an episode of acute ischemia.”

On the other hand, old anterior QS waves with persisting ST elevation (LV aneurysm morphology) are the most frequently misdiagnosed form of ST elevation in ED patients presenting with chest pain, and can lead to unnecessary cath lab activation [10]. ECG machines and STEMI criteria can not tell the difference, but past medical history, symptom duration, prior ECG and other ECG criteria can help with this distinction. Acute ischemia produces hyperacute T waves (relative to the preceding QRS complex) that can help differentiate new STE from old STE. If the differential is LV aneurysm vs anterior STE (i.e. not STE from LBBB or LVH), then a single lead in V1-4 with a T wave amplitude to QRS amplitude ratio > 0.36 identifies STEMI with a sensitivity of 92% and specificity of 81%. False negatives arise when the symptoms have been present for more than 6 hours, because hyperacute T waves diminish and can become inverted [11-12].

Back to the cases

Case 1: Anterior Q-wave secondary to LBBB, no sign of Occlusion MI, unnecessary cath lab activation.

• Heart rate/rhythm: borderline sinus tach
• Electrical conduction: LBBB
• Axis: left from LBBB
• R-waves/Q-waves: anterior R waves replaced by QS waves, and loss of tiny “septal Q” waves in I/aVL, from LBBB
• Tension: no hypertrophy
• ST/T: appropriately discordant ST/T wave changes, no Smith-modified Sgarbossa criteria

Impression: “new LBBB” which led to cath lab activation. But no ECG features of Occlusion MI in patient with atypical symptoms. Trops and cath negative.

Case 2: RBBB with acute Q-wave from LAD occlusion, delayed diagnosis.

• H: sinus tach
• E: old RBBB, new first degree AV block
• Axis: left
• R-wave/Q-wave: old tall anterior R waves from RBBB, new Q-waves V2-5 and inferiorly
• Tension: no hypertrophy
• ST/T: new inappropriately concordant ST elevation V2-6

Impression: In contrast to LBBB that reverses septal depolarization and produces anterior Q-waves and discordant ST elevation, RBBB does not disturb septal depolarization, so there should be no Q-waves and discordant ST depression. But here there are new Q-waves and concordant ST elevation, a sign of RBBB with occlusion MI (a high risk infarct). Initially missed by computer and physician and treated with puffers for presumed COPD. First Troponin I = 15,000, cath lab activated: 100% LAD occlusion. Peak troponin 42,000 and cardiac arrest.

Case 3: Q-waves from LVH, appropriate diagnosis.

• H: NSR
• E: normal conduction
• A: normal axis
• R: large voltage and inferolateral QR waves from LVH
• T: LVH
• ST/T: mild secondary ST/T waves changes

Impression: LVH with secondary changes. Trops negative. HOCM on echo.

Case 4: LV aneurysm, unecessary cath lab activation

• H: sinus brady
• E: normal conduction
• A: right axis from lateral Q
• R: R waves replaced by anterolateral QS waves
• T: no hypertrophy
• ST/T: V2-3 mild ST elevation and terminal T wave inversion, T/QRS <0.36 (eg in V2: 4/25 = 0.16)

Impression: LV aneurysm morphology with acute symptoms but without hyperacute T waves. Cath lab was activated based on anterior ST elevation but this was the patient’s baseline ECG. Trops and cath negative.

Case 5: acute Q-wave from LAD occlusion, delayed diagnosis

• H: NSR
• E: normal conduction
• A: borderline right axis deviation
• R: anterior R waves replaced by QS waves in V2-4
• T: no hypertrophy
• ST/T: anterior ST elevation that doesn’t meet STEMI criteria, but in V3 the T/QRS ratio = 5/9= 0.55

Impression: Anterior QS wave with hyperacute T waves despite prolonged symptoms. Concave ST elevation was presumed from early repolarization due to patient’s age, but Q-waves anteriorly are an exclusion criteria for early repolarization. First Trop I was 3,000 and referred to cardiology as NSTEMI, then cath lab activated: 95% mid LAD occlusion. Peak trop 38,000. On discharge ECG, T/QRS in V3 diminished to 5/16=0.31.

Case 6: Acute Q-wave after only 2 hours of chest pain from LAD occlusion, rapid diagnosis.

• H: sinus tach
• E: normal conduction
• A: normal axis
• R: anterior R waves replaced by QS waves, fragmented QRS in V3
• T: no hypertrophy
• ST/T: V1-2 mild STE, V1-3 hyperacute T wave (massive in V3: T/QRS = 5/3=1.7), deWinter T wave in V4, inferolateral reciprocal STD

Impression: Multiple signs of proximal LAD occlusion. Cath lab activated: 95% proximal LAD occlusion, first Trop I of 2,000, peak at 50,000. Next day ECG had persisting anterior QS waves but reduction of hyperacute T waves.

Case 7: Acute (and transient) Q-wave from LAD occlusion, delayed diagnosis.

• H: NSR
• E: normal conduction
• A: normal axis
• R: QS waves in V1-3
• T: no hypertrophy
• ST/S: mild ST elevation V1-2 with inferior reciprocal STD; V2 has T/QRS: 4/10=0.40

Impression: Subacute LAD occlusion with diminishing hyperacute T waves. ECG repeated 2 hours later after first Trop I of 6,000: loss of hyperacute T wave and beginning of T wave inversion. Referred to cardiology as NSTEMI but cath lab activated: 95% LAD occlusion, peak Trop 18,000, EF 40%.

Follow up ECG: Regression of anterior Q-waves, recovery of EF to 60%.

Case 8: Subacute LAD occlusion, rapid diagnosis.

• H: NSR
• E: normal conduction
• A: normal axis
• R: anterior QS waves, fragmented QRS
• T: no hypertrophy
• ST/S: mild anterior STE, anterolateral TWI

Impression: LAD QS waves and deep TWI but ongoing chest pain. Cath lab activated: 99% LAD occlusion. First Trop I of 50,000, with EF 37% and apical aneurysm.

Case 9: Acute Q/tall R from infero-posterior occlusion MI, delayed diagnosis.

• H: sinus brady
• E: normal conduction, small u waves
• A: normal axis
• R: new tall R in V2 and new QR waves inferiorly
• T: no hypertrophy
• S: inferior straightening STE with hyperacute T waves and reciprocal STD in I/aVL, and ST depression in V2

Impression: Inferior and posterior occlusion MI, missed by computer and first physician because of Q-waves. Inferior Q and anterior tall R waves can be from old inferior/posterior MI. However, these are new compared to the old ECG, in a patient without a cardiac history and with new onset ischemia symptoms, and with hyperacute T waves. Cath lab activated by second physician: 100% RCA occlusion. First Trop I of 2,300, peak of 46,000. Discharge ECG: QR waves in III/aVF have evolved into QS waves, hyperacute T waves from acute coronary occlusion have evolved into T wave inversion after reperfusion, I/aVL reciprocal changes have resolved, and tall R wave in V2 has persisted.

Take home points for Q-wave and Occlusion MI

1. Q-waves can be physiological (in aVR, V1 and III, and tiny Q’s laterally), secondary to depolarization abnormalities (LBBB, LVH, WPW), or pathological (acute or chronic). Acute ischemic Q-waves are associated with high risk infarcts and delayed reperfusion, while old infarct QS waves with persisting ST elevation (LV aneurysm morphology) are associated with unnecessary cath lab activation.
2. New ischemic symptoms with new Q-waves can indicate Occlusion MI, especially if accompanied by hyperacute T waves and reciprocal changes.
3. STEMI criteria and automated interpretation can not distinguish between acute MI and LV aneurysm, but patient’s history, symptoms and other ECG criteria can. One lead in V1-4 with QS waves and T/QRS> 0.36 differentiates acute MI from LV aneurysm, but hyperacute T waves diminish and invert with subacute presentations.

References for ECG Cases 14: Q-waves and Occlusion MI

1. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol 2018 Oct 30;72(18): 2231-2264
2. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 AACF/AHA guideline for the mangement of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circ 2013 Jan 29;127(4):e362-425
3. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelins. J Am Coll Cardiol 2014 Dec 23;64(24):3139-3228
4. Welsh RC, Deckert-Sookram J, Sookfram S, et al. Evaluating clinical reason and rationale for not delivering reperfusion therapy in ST elevation myocardial infarction patients: insights from a comprehensive cohort. Int J Cardiol 2016;216:99-103
5. Raitt MH, Maynard C, Wagner G, et al. Appearance of abnormal Q-waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J of Am Coll Cardiol 1995 Apr;25(5): 1084-1088
6. Andrews J, French JK, Manda SOM, et al. New Q-waves on the presenting electrocardiogram independently predict increased cardiac mortality following a first ST-elevation myocardial infarction. Eur Heart J 2000 Apr;21(8): 647-653
7. Topal DG, Lonbord J, Ahtarovski KA, et al. Association between early Q-waves and reperfusion success in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention: a cardiac magnetic resonance imaging study. Circ Cardiovasc Interv 2017 Mar;10(3):e004467
8. Nagase K, Tamura A, Mikuriya Y, et al.Significance of Q-wave regression after anterior wall acute myocardial infarction. Eur Heart J 1998 May;19(5):742-6
9. Ibanez B, James S, Agewall S. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: the Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018 Jan 7;39(2):119-177
10. Brady W, Perron A, Ullman E. Errors in emergency physician interpretation of ST-segment elevation in emergency department chest pain patients. Acad Emerg Med Nov 2000;7(11): 1256-1260
11. Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J of Emerg Med 2005;23:279-287
12. Klein LR, Shroff GR, Beeman W, et al. Electrocardiographic criteria to differentiate acute anterior ST-elevation myocardial infarction from left ventricular aneurysm. Am J of Emerg Med 2015;33:786-790

Share your interesting ECG cases with us!

Send to Jesse@emergencymedicinecases.com