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Myocardial Infarction: ECG Presentations, Clinical Suspicion, and Management Protocols

ACS Diagnostic Framework

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PART 1: ECG PRESENTATIONS OF MI

The Classic Temporal Evolution (Mnemonic: "HATE Q")

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1A. STEMI - Anatomic Lead Localization (Mnemonic: "All Indians Lie Poste Right")

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1B. STEMI Equivalents (Mnemonic: "WDAP" - these do NOT look like classic STEMI but require emergent cath)

1. Wellens Syndrome

• Type A (25%): Biphasic T waves in V2-V3 (negative then positive)
• Type B (75%): Deep symmetric T inversions in V2-V3
• ECG features: isoelectric or minimally elevated ST (<1mm), no Q waves, no significant R-wave loss
• Represents LAD stenosis - natural history is progression to massive anterior STEMI
• Key point: patient may be pain-free when this is seen; do NOT stress test these patients - Rosen's EM, p. 1001

2. De Winter Pattern

• Upsloping ST depression at the J point with tall, symmetric (hyperacute) T waves in precordial leads V1-V6
• ST elevation in aVR
• Represents proximal LAD occlusion - functionally equivalent to anterior STEMI
• Present in ~2% of LAD occlusions; does NOT evolve to classic ST elevation
• 2026 systematic review: thrombolysis is considered when PCI is delayed (PMID: 41663344)

3. aVR Elevation Pattern

• ST elevation in aVR (≥1mm) with diffuse ST depression in ≥8 leads
• Indicates left main or proximal LAD occlusion (severe multivessel disease / ischemia)
• High mortality; treated as emergent - newly reclassified from "STEMI equivalent" to "High-Risk NOMI" in 2026 literature (PMID: 41798790)

4. Posterior MI

• Classic 12-lead shows: ST depression in V1-V3, tall/broad R wave in V1-V2, R/S ratio ≥1, upright T in V1
• These are reciprocal of posterior ST elevations
• Confirm with posterior leads (V7-V9): ST elevation ≥0.5mm
• Always associated with inferior or lateral MI

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1C. NSTEMI and Non-Diagnostic ECG Changes

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1D. Confounding Patterns - When ECG Interpretation Is Difficult

Left Bundle Branch Block (LBBB) - Modified Sgarbossa Criteria

• Concordant ST elevation ≥1mm in leads with positive QRS = 5 points
• Concordant ST depression ≥1mm in V1-V3 = 3 points
• Discordant ST elevation ≥5mm = 2 points
• Score ≥3 = highly specific for AMI

• Concordant ST elevation ≥1mm = positive
• Concordant ST depression ≥1mm in V1-V3 = positive
• Proportionally excessive discordant ST elevation: ST/S ratio ≤ -0.25 (ST:S ratio <-0.25)

Ventricular Paced Rhythm (VPR)

• Mimics LBBB pattern; apply same Sgarbossa criteria
• Pacemaker spikes precede QRS; leads V5-V6 often predominantly negative (unlike true LBBB)

Right Bundle Branch Block (RBBB) in ACS

• RBBB does NOT obscure inferior or anterior ST elevations as much as LBBB
• New RBBB with ACS presentation carries independent adverse prognosis (PMID: 39546998)
• ST elevation in V1-V3 behind RBBB can still indicate STEMI

Left Ventricular Aneurysm

• Persistent ST elevation after old MI (weeks to months)
• Well-formed Q waves in V2-V5 with absent reciprocal changes - key differentiator from acute STEMI

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PART 2: WHEN TO SUSPECT MI EVEN WITH A NORMAL ECG

The 3 Groups Where ECG Fails Most Often

Group 1: Posterior MI

• Standard ECG shows only mirror-image changes (tall R, upright T, ST depression V1-V3)
• If suspected: perform posterior leads (V7, V8, V9)
• Mnemonic: "POSTERIOR = MIRROR" - everything is flipped

Group 2: Right Ventricular MI

• Inferior STEMI is the giveaway - then look for RV involvement
• ST elevation in V4R is diagnostic; often isoelectric on standard ECG
• Clinical triad: hypotension + clear lungs + elevated JVP in setting of inferior STEMI = RV infarct
• AVOID nitrates (preload-dependent); give IV fluids first

Group 3: Very Early Presentation (<2 hours)

• May show only nonspecific changes or be completely normal
• Serial ECGs every 15-30 minutes mandatory
• High-sensitivity troponin is the key adjunct

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Clinical Suspicion When ECG Is Normal - Patient-Specific Red Flags

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Risk Stratification Scores for Suspected ACS

• Age ≥65 years (+1)
• ≥3 CAD risk factors (+1)
• Known coronary stenosis ≥50% (+1)
• Aspirin use in past 7 days (+1)
• ≥2 anginal events in past 24h (+1)
• ST deviation ≥0.5mm (+1)
• Elevated cardiac markers (+1)

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PART 3: ACUTE MI PROTOCOL - WHEN AND WHAT TO GIVE

Immediate "MONA BASH" Protocol (first 10-30 minutes)

• RV infarction (causes fatal hypotension - preload dependent)
• Recent phosphodiesterase-5 inhibitor use (sildenafil/tadalafil within 24-48h)
• Systolic BP <90 mmHg

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STEMI-Specific: Reperfusion Strategy

• Door-to-balloon time <90 minutes (or <120 min if transfer needed)
• Available 24/7 at a capable center

• Give within 30 minutes of ED arrival (door-to-needle time)
• Agents: tPA, tenecteplase (TNK), reteplase
• Window: symptoms <12 hours (can extend to 24h if ongoing symptoms/ECG changes)

• Prior intracranial hemorrhage (absolute)
• Active bleeding (absolute)
• BP >180/110 unresponsive to treatment (relative)
• Recent surgery within 3 weeks (relative)
• NOT for NSTEMI or ST depression (UNLESS posterior MI suspected)
• NOT for patients presenting >24 hours after symptom onset who are now asymptomatic - Washington Manual of Medical Therapeutics

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NSTEMI/Unstable Angina Protocol (2025 ACC/AHA & 2023 ESC Guidelines)

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Prophylactic/Secondary Prevention Protocol (Post-MI)

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Quick Visual Summary

MI ECG SPECTRUM
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
STEMI    → ST elevation in anatomic leads + reciprocals
Equivalents:
  Wellens → Deep T inversions V2-V3 (LAD critical stenosis)
  De Winter → Upsloping STD + hyperacute T (proximal LAD occlusion)
  Posterior → Tall R + STD V1-V3 (check V7-V9)
  aVR elev → ST ↑ aVR + diffuse STD (LM/proximal LAD)
NSTEMI   → STD ± T inversions ± normal ECG
─ Key: Serial ECGs + hs-Troponin in ALL suspected ACS ─
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

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• Harrison's Principles of Internal Medicine 22E (2025), Chapter 247 - ECG Myocardial Ischemia
• Rosen's Emergency Medicine, 10th Ed - Chapter 64: Acute Coronary Syndromes
• Tintinalli's Emergency Medicine, Table 49-4 - ECG ST-Segment Criteria for AMI
• Goldman-Cecil Medicine, Chapter 57 - ACS Figure 57-1
• Washington Manual of Medical Therapeutics - ACS Reperfusion
• 2023 ESC Guidelines for Management of ACS
• 2025 ACC/AHA Guidelines for Acute Coronary Syndromes
• PMID 41663344 (De Winter + thrombolysis, 2026 systematic review)
• PMID 41798790 (aVR as high-risk NOMI, 2026 review)
• PMID 39546998 (RBBB in ACS, 2024 review)

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Shock in an 80-Year-Old Female: Full Clinical Analysis

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Step 1: Clinical Reasoning - What Type of Shock?

• BP 50 mmHg (profound hypotension) / altered consciousness for 1 day
• Decreased oral intake 2-3 days (dehydration)
• Unremarkable ECG (argues against cardiogenic, or acute STEMI as primary cause)
• No peripheral edema
• No raised JVP
• Chest clear on auscultation
• 80-year-old female

Most Likely Diagnoses in Order of Priority

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Step 2: Why the Elderly Are Different - Critical Clinical Points

"Sepsis in older adults may present atypically - without fever, without leukocytosis, with altered sensorium as the only sign." - Sepsis in Aging Populations review (PMID: 39744263)

Mnemonic: "FAIL SAFE" for Atypical Presentations in the Elderly

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Step 3: The Adrenal Insufficiency Problem - This Is the Pivot Point

1. She is already receiving steroids + norepinephrine + dobutamine - if adrenal crisis is the cause, steroids would be life-saving and this patient may be on the right treatment inadvertently
2. Adrenal crisis presents identically to septic shock: hypotension (90%), fever (66%), confusion (42%), vomiting (47%)
3. 8% of patients with adrenal insufficiency have a crisis per year; 6% of episodes are fatal
4. Adrenal crisis is often precipitated by intercurrent illness - the "poor oral intake for 2-3 days" is exactly this trigger
5. An elderly female with a prior history of prolonged corticosteroid use (e.g., for asthma, COPD, arthritis, skin disease) has HPA axis suppression and is extremely vulnerable

• Hyponatremia (dilutional + mineralocorticoid loss)
• Hyperkalemia (aldosterone deficiency)
• Hypoglycemia
• Eosinophilia (unexpected finding in "sepsis" - think Addison's)
• Low cortisol

"Adrenal crisis may occur despite increase in glucocorticoids with stress. It may be the initial manifestation of adrenal insufficiency." - Symptom to Diagnosis, 4th Ed.

• Hyperpigmentation (gums, palmar creases, knuckles, areolae) - only in primary AI
• Salt craving history
• History of vitiligo or other autoimmune disease
• Prior or current steroid use (any route)
• Hyponatremia + hyperkalemia combination

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Step 4: What to Do - Systematic Diagnostic Workup

Immediate Bedside Assessment (First 10 Minutes)

Investigations to Order Simultaneously

• Urine dipstick + culture (most common source in elderly women)
• Chest X-ray (occult pneumonia)
• TSH (myxedema crisis if hypothermic)
• Procalcitonin (more reliable than WBC in elderly)
• ACTH level (if time allows, alongside cortisol - before any steroids if possible, but do NOT delay treatment)

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Step 5: Bedside POCUS - The Game Changer

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Step 6: Management Protocol - What Has Been Given, What's Still Needed

Already Given (Assessment)

What Still Needs to Be Done

• SSC 2021: 30 mL/kg IV crystalloid in the first hour for sepsis-induced hypoperfusion
• BUT in elderly patients - give cautiously and reassess frequently (risk of fluid overload, diastolic dysfunction)
• Use passive leg raise test to assess fluid responsiveness before each bolus
• Target: MAP ≥65 mmHg (not necessarily a normal BP - aggressive BP targets in elderly cause harm)

Step 1: Norepinephrine (first-line, strong recommendation)
        ↓ if MAP inadequate
Step 2: Add Vasopressin 0.03 U/min 
        (when NE dose ≥0.25 mcg/kg/min for ≥4 hours)
        ↓ if still inadequate
Step 3: Add Epinephrine
        ↓ if cardiac dysfunction present
Step 4: Dobutamine added to norepinephrine

• SSC 2021: Give IV hydrocortisone 200 mg/day (50 mg q6h or continuous infusion) when:
  • NE or epinephrine dose ≥0.25 mcg/kg/min for at least 4 hours AND
  • Still hemodynamically unstable
• Do NOT use ACTH stimulation test to guide steroid use in shock
• If adrenal crisis suspected independently: give hydrocortisone 100 mg IV stat immediately

• Aggressive BP targets (MAP 65 is appropriate; pushing to 80+ increases arrhythmia and ischemia risk)
• Fluid overload - use stroke volume variation or IVC assessment
• Aminoglycoside dosing - adjust for renal function
• Drug interactions - check for ACE inhibitors, ARBs, beta-blockers that lower BP

• Most common sepsis sources in elderly women: UTI/urosepsis, pneumonia, biliary sepsis, skin/soft tissue
• Obtain urine culture, CXR, consider CT abdomen if no source found

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Step 7: The Myxedema Crisis Consideration

• Hypothermia (low temperature is often the clue)
• Altered consciousness disproportionate to vital signs
• Bradycardia (but ECG said unremarkable - may be slow rate)
• Constipation history, dry skin, macroglossia, delayed relaxation of reflexes
• Hyponatremia
• Hypoglycemia

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Summary Decision Tree for This Patient

80F, BP 50, ASOC, 2-3d poor intake, clear chest, no edema, no raised JVP
                           ↓
           DISTRIBUTIVE or MIXED (Hypovolemic + Distributive) SHOCK
                           ↓
     ┌─────────────────────┼──────────────────────┐
     ▼                     ▼                      ▼
  SEPTIC                ADRENAL                MIXED
  SHOCK                 CRISIS              (both above)
  (most likely)    (must not miss)
     ↓                     ↓
  Source?           Hyponatremia?
  Blood cx           Hyperkalemia?
  Urine cx          Hypoglycemia?
  Procalcitonin     Hyperpigmentation?
  CXR               Steroid history?
  CT abdomen         ↓              
                  Cortisol + ACTH
                  (send before more steroids)
                  
Also check: Troponin/echo (silent MI), TSH (myxedema), lactate

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Key Points Summary

1. Most likely: septic shock from an occult source - UTI is most common in elderly women, often without dysuria or fever
2. Adrenal crisis must be excluded actively - it mimics septic shock, is common in elderly, and the steroids already given may be masking the diagnosis
3. ECG normal does NOT rule out MI - send troponin; silent MI in elderly women is well-documented
4. Dobutamine is not automatically indicated - only if POCUS confirms cardiac dysfunction with preserved filling pressures
5. POCUS is the fastest diagnostic tool - distinguishes all shock types at bedside
6. Fluid resuscitation first - 30 mL/kg crystalloid (with caution in elderly); reassess with PLR after each 500 mL
7. Vasopressin is the logical next vasopressor before escalating norepinephrine further
8. Steroid dosing: hydrocortisone 200 mg/day IV when NE dose ≥0.25 mcg/kg/min for ≥4h (SSC 2021)
9. Glucose monitoring - hypoglycemia is common in adrenal crisis and sepsis in elderly
10. Check TSH - myxedema crisis is a great mimicker in elderly females

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• Harrison's Principles of Internal Medicine 22E (2025), Chapter on Shock - vasopressor management
• Rosen's Emergency Medicine 10th Ed - Chapters 64, 106, Vasoactive Drug Therapy
• Symptom to Diagnosis 4th Ed, Chapter 24 - Adrenal Insufficiency, p. 7379-7445
• Frameworks for Internal Medicine - Distributive Shock, p. 299
• Surviving Sepsis Campaign International Guidelines 2021 (SCCM/ESICM)
• NICE Guideline NG243: Adrenal Insufficiency (2024)
• PMID: 39744263 - Sepsis in Aging Populations, Cureus 2024
• PMID: 38200360 - The critically ill older patient with sepsis, Ann Intensive Care 2024
• Cleveland Clinic Journal of Medicine 2024 - Primary Adrenal Insufficiency: When to Suspect