EKG Interpretation for CET: How to Identify Lethal Arhythmias and Myocardial Infarction Patterns Instantly

When you work as a CET, seconds matter. Your job is not to make the final diagnosis; it’s to recognize dangerous patterns fast and alert the team. This guide shows you how to spot lethal arrhythmias and myocardial infarction (MI) patterns instantly, and why each clue matters. You’ll learn a reliable 60‑second scan, the must‑know red flags, and the common traps that cost time.

A 60‑Second EKG Scan That Works Under Pressure

Think “patient first, then pattern.” You’re not just reading paper—you’re matching the strip to the person in front of you.

• Confirm the patient and symptoms. Chest pain, shortness of breath, syncope, or hypotension changes how urgently you act.
• Check the rate. Use the 300‑150‑100‑75‑60‑50 rule for regular rhythms. For irregular rhythms, count QRS in a 6‑second strip and multiply by 10. Rate matters because extreme brady/tachy can be life‑threatening on their own.
• Regular or irregular? This steers your rhythm differential (e.g., irregularly irregular suggests atrial fibrillation).
• Narrow or wide QRS? Narrow (<120 ms) usually means supraventricular. Wide (≥120 ms) could mean ventricular origin or aberrancy. Wide + fast = dangerous until proven otherwise.
• Are P waves present and related? AV dissociation points toward ventricular rhythms or complete heart block.
• Scan ST segments and T waves. Identify contiguous leads with elevation or depression and look for reciprocals. This helps separate true STEMI from mimics.
• Compare with any prior EKG. Stable old changes lower suspicion. New changes raise it.
• Rule out artifact and lead misplacement. Don’t call a code on a shaky line.

Why this order? It mirrors clinical risk. Rate and QRS width triage most lethal rhythms quickly. ST‑T changes, when grouped by leads, uncover MIs that need immediate action.

Lethal Arrhythmias You Must Call Immediately

These kill by stopping effective cardiac output. Your job: identify fast, check for a pulse, and trigger the emergency response.

Ventricular fibrillation (VF)

• What you see: Chaotic, disorganized baseline. No P waves, no QRS, no pattern.
• Why lethal: No organized contraction means no pulse and no perfusion.
• Pitfalls: Coarse artifact can mimic VF—always check the patient and another lead. If the patient is talking, it’s not VF.
• Action: No pulse = call code, start compressions, prepare defibrillation.

Pulseless ventricular tachycardia (VT)

• What you see: Wide, fast, usually 150–220 bpm, monomorphic or polymorphic. Often regular.
• Why lethal: Without a pulse, it is functionally the same as VF.
• With a pulse: Still a true emergency; patients can rapidly deteriorate.
• Clues favoring VT over SVT with aberrancy: Very wide QRS (≥140–160 ms), AV dissociation, capture beats, fusion beats, extreme axis, concordance across V1–V6.
• Action: No pulse = defibrillate. Pulse but unstable = urgent synchronized cardioversion (notify team immediately).

Torsades de pointes (polymorphic VT)

• What you see: Polymorphic VT with QRS amplitude that “twists” around the baseline. Often preceded by prolonged QT.
• Why lethal: Degenerates to VF or causes sudden syncope.
• Clues: Long QT on the baseline strip; drugs/electrolytes commonly involved (e.g., low K/Mg, certain antiarrhythmics).
• Action: Treat as unstable VT. Flag prolonged QT so the team can correct magnesium and electrolytes.

Asystole

• What you see: Flatline or nearly flat baseline in two leads. No P, no QRS.
• Why lethal: No electrical activity, no output.
• Pitfalls: Loose leads and low gain can mimic asystole. Always confirm in two leads and check the patient.
• Action: Start compressions, call code. Defibrillation is not useful for asystole.

Pulseless electrical activity (PEA)

• What you see: Any organized rhythm on EKG, but no pulse on exam.
• Why lethal: Electrical activity without mechanical output.
• Action: Check central pulse. If absent, start compressions and alert the team to hunt for reversible causes (e.g., hypovolemia, hypoxia, tamponade).

Complete heart block (3rd‑degree AV block)

• What you see: P waves and QRS complexes march independently. Often a slow escape rhythm (junctional with narrow QRS or ventricular with wide QRS).
• Why dangerous: Profound bradycardia and sudden asystole risk.
• Clues: Regular P‑P, regular R‑R, but PR intervals vary randomly because there’s no relationship.
• Action: If symptomatic (hypotension, syncope), escalate immediately for pacing readiness.

Irregular wide tachycardia (think AF with WPW)

• What you see: Very fast, irregular, wide complexes without consistent P waves.
• Why dangerous: Can deteriorate to VF; some common AV nodal drugs worsen it.
• Clues: Rate can vary from 180–250+; bizarre wide beats; preexcitation may be visible in sinus rhythm as a delta wave and short PR.
• Action: Treat as high risk; notify immediately.

VT vs SVT With Aberrancy: Don’t Guess—Weigh the Evidence

Wide tachycardia demands a decision. If you’re unsure, default to VT—it’s safer and more often correct in adults, especially with heart disease.

• Favors VT: Age >35, history of MI or structural disease, QRS ≥160 ms, AV dissociation, capture or fusion beats, concordant precordial QRS (all positive or all negative V1–V6), extreme axis (northwest), negative QRS in aVR begins with an initial R in aVR (Brugada sign), notching on downstroke of S in V1–V2 (Josephson sign).
• Favors SVT with aberrancy: Prior EKG shows same bundle branch block pattern; clear P waves with fixed PR; response to vagal maneuvers.

Why this matters: Mislabeling VT as SVT delays shock and increases mortality.

Myocardial Infarction Patterns You Must Know

Your goal: spot patterns that signal acute coronary occlusion. EKG changes cluster in “contiguous leads”—neighbors that view the same heart region.

Lead group map

• Inferior: II, III, aVF (right coronary or left circumflex)
• Lateral: I, aVL, V5–V6 (left circumflex or diagonal)
• Anterior: V3–V4 (LAD)
• Septal: V1–V2 (proximal LAD)
• Posterior (mirror image): seen as ST depression in V1–V3 with tall R waves

STEMI criteria (at the J‑point) in ≥2 contiguous leads

• Limb leads (I, II, III, aVL, aVF): ≥1 mm
• Other precordial leads (V1, V2, V3, V4, V5, V6): ≥2 mm
• V2–V3 sex/age thresholds: men ≥2 mm if ≥40 years; ≥2.5 mm if <40 years; women ≥1.5 mm

Why these numbers: They reduce false positives from normal variants, especially in V2–V3.

Reciprocal changes

• ST elevation in one wall often causes ST depression in the opposite wall (e.g., inferior elevation with aVL depression). Reciprocal changes increase specificity for MI.

Early occlusion patterns (before classic ST elevation)

• Hyperacute T waves: Broad, tall, and fat at the base, localized to a vascular territory. They precede ST elevation.
• de Winter pattern (LAD occlusion): Up‑sloping ST depression 1–3 mm in V1–V6 with tall, symmetric T waves; often slight ST elevation in aVR. Treat like STEMI.
• Wellens syndrome (critical proximal LAD): After pain resolves, deep symmetric T‑wave inversions or biphasic T waves in V2–V3, with little or no ST elevation. High risk of large anterior MI.

Localizing STEMI by leads

• Inferior (II, III, aVF): Look for reciprocal depression in aVL. If ST elevation is greater in III than II, suspect right coronary artery and consider right ventricular involvement.
• Lateral (I, aVL, V5–V6): Often with inferior or anterior involvement depending on the culprit vessel.
• Anterior/septal (V1–V4): Large territory, often more unstable. Look for loss of R‑wave progression and new pathologic Q waves.
• Posterior: ST depression in V1–V3 with tall R waves and upright T waves (mirror of ST elevation). Confirm with posterior leads V7–V9.

Q waves

• Pathologic Q waves are ≥40 ms wide or ≥25–30% the height of the following R wave in ≥2 contiguous leads (except aVR). They suggest transmural injury or prior infarct.

Posterior and Right Ventricular MI: The Silent Traps

Posterior MI

• Clues on standard EKG: Horizontal ST depression in V1–V3, tall broad R waves in V1–V2, upright T waves. It’s the mirror image of ST elevation you can’t see on the back of the heart.
• Confirm: Place posterior leads V7–V9 (left posterior axillary to scapular line). ≥0.5 mm ST elevation is significant (≥1 mm improves specificity).
• Why it matters: Posterior MI is often missed and carries high risk if untreated.

Right ventricular MI (RVMI)

• Suspect when: You see inferior STEMI and the patient is hypotensive or preload sensitive.
• EKG tip: Obtain right‑sided V4R; ≥1 mm ST elevation supports RV involvement.
• Why it matters: Nitrates can drop preload and worsen hypotension; identifying RVMI changes immediate management.

ST Elevation Mimics You Should Rule Out Fast

Pericarditis

• Pattern: Diffuse concave ST elevation in many leads with PR depression; reciprocal PR elevation and ST depression in aVR.
• Why distinct: Unlike STEMI, it’s widespread and not limited to a single coronary territory, and usually lacks reciprocal ST depression (except in aVR/V1).

Early repolarization

• Pattern: Stable concave ST elevation, prominent J‑point notching (“fishhook”), mostly in V2–V5, unchanged over time and without symptoms.
• Why distinct: No reciprocal changes and no evolving pattern.

LBBB or paced rhythm

• Challenge: Baseline ST‑T discordance makes STEMI hard to see.
• Use Sgarbossa criteria: Concordant ST elevation ≥1 mm in any lead; concordant ST depression ≥1 mm in V1–V3; excessively discordant elevation ≥5 mm. Modified (Smith) version uses proportional discordance (ST/S ratio ≤ −0.25) to improve accuracy.

Left ventricular aneurysm

• Pattern: Persistent ST elevation with deep Q waves weeks after a prior MI. Stable appearance over time.

Brugada pattern

• Pattern: Coved ST elevation with T‑wave inversion in V1–V3 (type 1). Can mimic anterior STEMI.
• Why important: Risk of malignant ventricular arrhythmias; requires expert review.

Artifacts, Lead Misplacement, and Pacemakers

Artifacts

• Muscle tremor: Baseline quiver, often worse in limb leads; ask the patient to relax or warm them.
• 60‑cycle interference: Regular, high‑frequency noise; check grounding and electrical devices.
• Loose leads: Wandering baseline, sudden flatline in one lead only; re‑prep skin and reattach.

Lead misplacement

• Limb lead reversal (RA/LA): Lead I becomes negative; aVR becomes positive; axis flips. It can simulate inferior MI. Always suspect if P in lead I is negative.
• V1–V2 too high: Can mimic anterior ischemia or cause false ST changes. Feel the sternal angle and place at the 4th intercostal space.
• V4–V6 too medial or too high: Alters R‑wave progression; double‑check landmarks.

Pacemakers

• Identify: Small vertical spikes before P (atrial pacing), before QRS (ventricular pacing), or both (dual‑chamber).
• Failures: Failure to capture (spike with no response), failure to pace (no spikes when expected), undersensing/oversensing (inappropriate pacing behavior). Any new instability requires rapid escalation.

Calculations and Measurements That Save Seconds

• Rate (regular): 300‑150‑100‑75‑60‑50 across large boxes between R waves.
• Rate (irregular): Count QRS in 6 seconds and multiply by 10.
• PR interval: 120–200 ms normal (3–5 small boxes). Longer suggests first‑degree block; short PR with delta wave suggests WPW.
• QRS width: <120 ms narrow; ≥120 ms wide (ventricular or bundle branch block).
• QT: If QT looks > half the R‑R interval, suspect prolonged QT. This sets the stage for torsades.
• Axis quick look: Positive in I and aVF = normal; positive I, negative aVF = left; negative I, positive aVF = right; both negative = extreme.
• Pathologic Q waves: ≥40 ms wide or ≥25–30% of the ensuing R in contiguous leads.

Rapid Review Checklists

Instant rhythm red flags

• No P, no QRS, chaotic = VF → defibrillate (if pulseless)
• Wide, fast, regular = VT until proven otherwise
• Twisting polymorphic VT + long QT = torsades
• Flatline in two leads = asystole (check leads, then act)
• Organized rhythm but no pulse = PEA
• P and QRS march independently = complete heart block
• Irregular, very fast, wide = consider AF with WPW

STEMI pattern triggers

• Elevation in ≥2 contiguous leads + reciprocal depression elsewhere
• Inferior ST elevation with aVL depression; check V4R for RVMI
• ST depression V1–V3 with tall R = posterior MI; place V7–V9
• de Winter (upsloping depression V1–V6 with tall T) = LAD occlusion
• Wellens (deep symmetric T inversion V2–V3 after pain) = critical LAD

STEMI mimics to exclude

• Pericarditis: diffuse concave ST elevation + PR depression
• Early repol: stable J‑point notching, no reciprocal changes
• LBBB/paced: apply Sgarbossa/modified Sgarbossa
• LV aneurysm: persistent elevation with Q waves, unchanged
• Brugada: coved ST in V1–V3

Practice Cases (Mental Drills)

Case 1: A 66‑year‑old with chest pain. EKG shows 3 mm ST elevation in II, III, aVF; 1 mm ST depression in aVL; blood pressure soft. What else do you do?

• Answer: Inferior STEMI with reciprocal changes. Obtain V4R to assess RVMI (affects immediate management). Alert team now.

Case 2: A 58‑year‑old feels lightheaded. EKG: wide, regular tachycardia at 180 bpm. No clear P waves. Occasional normal‑looking beat amid wide beats.

• Answer: VT until proven otherwise. The normal‑looking beat is likely a capture beat. Treat as high risk and escalate immediately.

Case 3: A 52‑year‑old had chest pain that resolved. EKG shows deep, symmetric T‑wave inversions in V2–V3, no ST elevation, normal troponin pending.

• Answer: Wellens pattern (critical proximal LAD). High risk for large anterior MI; requires urgent evaluation despite pain relief.

Putting It All Together

Start every read with the patient, then apply your 60‑second scan: rate, regularity, width, P‑QRS relationship, ST‑T changes, and artifacts. Call lethal rhythms by their defining features. Localize MI using contiguous leads and reciprocals, and remember the hidden zones—posterior and right ventricle. When something doesn’t fit, think mimics and misplacement. With repetition, these patterns become automatic, and your speed and accuracy can save lives.

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com