Learn how Q/QS complexes in V1–V2 point to prior septal infarct (age indeterminate) and how to avoid traps like digoxin effect and PE strain.
ECG evidence of pathologic septal Q waves/QS in V1–V2 supports a prior septal infarct (age indeterminate) rather than acute STEMI, digoxin effect, or PE strain.
An 82-year-old man living in a nursing home presents to you with extreme shortness of breath. He denies having chest pain and has no history of coronary artery disease. His history includes gastroesophageal reflux disease (patient is taking omeprazole), type 2 diabetes mellitus (patient is taking glargine and metformin), hypertension (patient is taking lisinopril and hydrochlorothiazide), congestive heart failure (patient is taking digitalis), and Alzheimer dementia (patient is taking donepezil and memantine).
On examination, he has some rales at both lung bases, 3+ pitting edema of both feet and ankles, with some tenderness in both calves. There is a small diabetic ulcer on his right heel with a black eschar and some surrounding erythema. There appears to be right-upper quadrant tenderness and hepatomegaly. As part of his workup, you obtain electrocardiography (ECG; see Figure).
Figure.
What is your diagnosis?
Answer Options:
In this item, the keyed answer (C) is reasonable and consistent with modern ECG interpretation, but the database remediation is incomplete because it does not anchor the interpretation to contemporary definitions of infarction patterns (and it over-emphasizes “dating” an infarct from ECG alone).
Boards commonly test that pathologic Q waves (or QS complexes) in V1–V2 indicate septal infarction (often prior), whereas acute STEMI requires *acute ischemic ST-segment changes in a consistent lead distribution* plus clinical context. The Fourth Universal Definition of MI (ESC/ACC/AHA/WHF, 2018) supports using pathologic Q waves as evidence of myocardial infarction (often prior), but ECG alone cannot reliably establish timing—hence “indeterminate age.”
- The stem’s dyspnea + calf tenderness + edema pushes test-takers toward PE, even though classic PE ECG findings are neither sensitive nor specific.
- “Digitalis” in the med list triggers anchoring on digoxin effect, but digoxin effect is primarily ST-segment “scooping” and related repolarization changes—not isolated septal Q waves.
- Learners confuse Q waves (prior infarct marker) with acute STEMI criteria (ST elevation in a coronary territory).
| Option | What It Tests / Implies | Why It’s Wrong Here |
|---|---|---|
| A. acute anterior STEMI | Looks for ST elevation in V1–V4 (± reciprocal changes) | Pathologic Q/QS in V1–V2 without convincing acute STE pattern is more consistent with prior septal infarct than acute anterior STEMI. |
| B. acute posterior STEMI | Expects ST depression + tall R waves in V1–V3; confirm with posterior leads V7–V9 | Septal Q/QS pattern is not the classic posterior MI pattern (posterior MI gives **tall R** in V1–V2, not deep Q). |
| C. septal infarct of indeterminate age | Recognizes Q waves/QS in V1–V2 as prior septal infarct | Best match to the described ECG interpretation target. |
| D. digitalis effect | “Scooped” downsloping ST depression, shortened QT (often), toxic rhythms if overdose | Digoxin effect does not present as isolated septal Q waves; also QT prolongation is **not** a typical digoxin effect (digoxin more often shortens QT via shortened ventricular AP). |
| E. acute PE with right heart strain | Sinus tachy, RBBB, right axis deviation, T inversions V1–V4, S1Q3T3 | These are nonspecific and not described as the key ECG abnormality; PE cannot be diagnosed from ECG alone. |
Pathologic Q waves/QS in V1–V2 = think septal infarct (often old); acute STEMI requires acute ST-segment criteria in a vascular territory.
1. Recognize ECG patterns consistent with prior septal infarction (pathologic Q waves/QS in V1–V2) versus acute STEMI patterns.
2. Distinguish digoxin effect and PE right-heart strain ECG clues from infarction patterns, and understand their diagnostic limitations.
The stem provides multiple “clinical lures” (dyspnea, calf tenderness, digoxin use) to bait you into diagnosing PE strain or digoxin effect. The board-style move is to answer the question that was asked—“What is your diagnosis?” based on the ECG pattern—and not to over-weight the clinical narrative when the prompt is explicitly testing ECG recognition.
A 64-year-old man is asymptomatic at a pre-op visit. ECG shows QS complexes in V1–V2 with normal ST segments and T waves. Most likely interpretation?
ECG shows horizontal ST depression in V1–V3 with tall R waves in V2. Best next step to confirm suspected posterior MI?
A patient on digoxin has ECG with “scooped” downsloping ST depression in lateral leads and a shortened QT interval. Best interpretation?
Which ECG finding is most associated with acute PE with right ventricular strain (though not diagnostic)?
A 58-year-old has crushing chest pain. ECG shows ST elevation in V2–V4 with reciprocal ST depression in II, III, aVF. Best diagnosis?
How would your differential and immediate workup change if this patient’s ECG instead showed sinus tachycardia with new RBBB and T-wave inversions V1–V4, and bedside ultrasound demonstrated RV dilation?
Q1: Can you determine “age” of an infarct from ECG Q waves?
A: The ABFM/ABIM generally expects recognition that Q waves suggest prior infarction, but timing is often indeterminate without prior ECGs/biomarkers (Fourth Universal Definition of MI, 2018).
Q2: What’s the fastest way to separate posterior MI from septal Q waves on exam day?
A: Posterior MI typically shows ST depression + tall R in V1–V3; septal infarct shows Q/QS in V1–V2.
Q3: What are the classic “digoxin effect” ECG changes?
A: “Scooped” ST depression, T-wave changes, and sometimes shortened QT; toxicity more often causes arrhythmias (e.g., atrial tachycardia with block) than isolated Q waves.
Q4: Does an ECG diagnose pulmonary embolism?
A: No—ECG findings are supportive at best. The boards test that PE is a clinical/imaging diagnosis, with ECG used to assess strain and exclude mimics.
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