Common ECG abnormalities and what the patterns often indicate

On a rainy commute, I stared at the tiny zigzags on a printout and felt oddly protective of them—like they were a diary my heart kept without telling me. I’m not a cardiologist, and I don’t pretend to be one; I’m a curious person who keeps meeting friends and relatives coming home with an ECG result and a worried expression. So I started collecting the patterns that show up a lot, what they often mean, and how I try to think about them without spiraling. What follows is my journal-style guide, shaped by reputable sources and a healthy respect for uncertainty.

The moment the waves stopped looking like noise

The first real shift happened when I realized an ECG is just a time-stamped picture of electrical direction and timing. Each beat marches through three checkpoints: the atria (P wave), the delay at the AV node (PR interval), and the ventricles (QRS and then the reset or ST–T). My early high-value takeaway was this: if I can name the rate, the rhythm regularity, and the intervals, everything else feels less mysterious. Even simple anchors help—like spotting a regular rhythm versus one that’s “irregularly irregular.” I also liked knowing that many “abnormalities” are contextual, not emergencies by default.

• Rate: roughly count boxes or use devices; note if it’s slow (<60), normal (60–100), or fast (>100).
• Rhythm: regular or irregular; is there a P wave before each QRS and a QRS after each P?
• Intervals: PR, QRS width, and QT/QTc; a prolonged interval can hint at conduction delay or medication/electrolyte effects.

When I need a simple, trustworthy overview to ground me, I skim patient-friendly explainers from major organizations. A few that I keep bookmarked are here:

• MedlinePlus Electrocardiogram
• NHLBI Electrocardiogram
• American Heart Association ECG overview
• Mayo Clinic What is an ECG

Patterns I see again and again

I started keeping a short notebook of frequent ECG patterns and what they often suggest. These are not diagnoses, just common associations that help me interpret a report with calmer eyes.

• Sinus bradycardia (slow but regular, normal P before each QRS): often shows up during sleep, in athletes, or with certain medications like beta-blockers. It can be perfectly normal if you feel fine. If there’s dizziness, fatigue, or fainting, that’s a reason to check in.
• Sinus tachycardia (fast and regular with P before each QRS): frequently due to fever, stress, pain, dehydration, anemia, or over-caffeination. It’s the body’s “more output now” setting rather than a rhythm disorder on its own.
• Atrial fibrillation (irregularly irregular, no consistent P waves): the atria are quivering, and the ventricles are responding in a choppy way. This pattern raises stroke risk over time, so discussions about rate/rhythm control and anticoagulation often follow.
• Atrial flutter (sawtooth flutter waves, often with regular conduction ratios): can be episodic and may feel like palpitations or fatigue; sometimes treated similarly to AFib but has its own rhythm quirks.
• Premature beats—PACs (atrial) and PVCs (ventricular): extra early beats that can feel like a “skip” or thump. In healthy hearts, occasional PVCs/PACs are common. Frequent PVCs can reduce pumping efficiency and may warrant evaluation.
• First-degree AV block (PR prolonged but every P conducts): usually benign. The signal strolls through the AV node a bit slowly.
• Mobitz I (Wenckebach) (PR lengthens until a beat drops): often well-tolerated, especially at rest or sleep; pattern matters over panic.
• Mobitz II (sudden dropped QRS without prior PR lengthening): more concerning because it can progress; context and symptoms guide urgency.
• Third-degree AV block (complete dissociation of P and QRS): atria and ventricles beat independently; usually requires prompt attention.
• Right bundle branch block (RBBB) (RSR′ in V1, wide QRS): can be incidental; sometimes appears with pulmonary issues. Compare to prior ECGs.
• Left bundle branch block (LBBB) (wide, notched QRS with discordant ST–T changes): often implies underlying structural disease. It can make ischemia harder to read and requires special criteria in chest-pain settings.
• ST elevation (J-point upsloping above baseline in contiguous leads): can signal acute injury/occlusion in the right context, but also occurs in pericarditis or early repolarization. Reciprocal ST depression increases concern for a coronary blockage.
• ST depression and T-wave inversion: can reflect ischemia (supply-demand mismatch), electrolyte shifts, or recovery (“memory”) after abnormal conduction or pacing.
• Pericarditis signatures (diffuse concave ST elevation, PR depression): often accompanied by chest pain that eases when leaning forward; clinical story matters.
• QT prolongation (best judged as QTc): associated with certain medications, low potassium or magnesium, and some genetic syndromes. It increases risk of torsades de pointes, especially when multiple risk factors stack up.
• Hyperkalemia (peaked T waves, wider QRS as it worsens): a lab problem that can turn into an electrical emergency; medications and kidney function often intersect here.
• Hypokalemia (flattened T, prominent U waves): palpitations and ectopy may flare; repletion and finding the cause matter.
• Left ventricular hypertrophy (high voltages with “strain” ST–T patterns): commonly linked to long-standing high blood pressure or valve disease.
• Early repolarization (J-point notching/slurring, often in young healthy people): usually benign, though context still rules.
• Paced rhythms (wide QRS with pacing spikes): interpretation shifts; the device dictates the pattern.

How I walk through a strip without getting overwhelmed

I made a little mental flow to avoid rabbit holes and keep my notes tidy.

• Step 1 Notice the basics: rate, rhythm regularity, are P waves present, is PR prolonged, is QRS wide, and does the ST segment look elevated or depressed in groups of leads (contiguous territories).
• Step 2 Compare with old ECGs if available; a “new” block or fresh T-wave inversions can mean more than a single odd wave in isolation. Ask what changed, not just what’s “abnormal.”
• Step 3 Confirm with the clinical story: chest pain, fever, medications, electrolytes, thyroid, caffeine, stress, sleep, and device/lead placement. I jot questions for a clinician instead of assuming the ECG alone is the verdict.

When my curiosity outpaces my confidence, I return to evidence-based primers and patient education pages (see the sources above and below). They’re refreshingly practical and keep me honest about what an ECG can—and cannot—say by itself.

Little habits that helped my future self

I started treating each ECG like a snapshot in a photo album, not a personality test. That mindset made me calmer and more precise.

• Keep copies of prior ECGs in a phone folder or patient portal. It’s incredible how often “unchanged from baseline” turns worry into relief.
• Track symptoms with timestamps and context: caffeine intake, sleep, exercise, illness. Patterns pop out when I review them next to the ECG date.
• Review medications for QT-prolonging potential and interactions, especially when starting something new. Pharmacists are wonderful allies for this.
• Sanity-check lead placement if a reading looks bizarre. Misplaced precordial leads can fake anterior infarct patterns or alter axis.
• Respect the lab values: potassium, magnesium, calcium, and thyroid panels often explain rhythm changes better than any magnifying glass.

What the territories whisper

ECG leads are like neighborhoods. If multiple neighbors complain together, it’s newsworthy. Grouping leads helps me interpret better:

• Inferior leads (II, III, aVF): right coronary artery territory; bradycardia and AV block may tag along.
• Lateral leads (I, aVL, V5–V6): circumflex or diagonal branches.
• Anterior/septal leads (V1–V4): left anterior descending artery; watch for big anterior changes with reciprocal shifts.
• Right-sided or posterior views (V4R, V7–V9): helpful when inferior MI or posterior ischemia is suspected.

Learning to think in contiguous groups made ST changes less abstract. For example, diffuse ST elevation across many territories nudges me to consider pericarditis, whereas elevation in a tight cluster with reciprocal depression elsewhere rings the ischemia bell louder.

When my inner alarm says slow down

Most ECG quirks aren’t emergencies, but some patterns and stories make me pause and seek professional input sooner.

• Chest pain with new ST changes, especially with sweating, nausea, or shortness of breath.
• Syncope or near-syncope, or palpitations paired with dizziness or low blood pressure.
• Very wide QRS or newly prolonged QTc, particularly if starting or combining medications known to affect conduction.
• High potassium on labs or kidney issues with concerning ECG changes.
• Rapid heart rates that don’t settle with rest, hydration, or addressing a clear trigger like fever.

Even then, I remind myself that an ECG is a clue, not the entire case file. Troponins, echocardiography, stress testing, and the clinical exam round out the picture when needed.

Tricky look-alikes I keep on my radar

Some patterns masquerade as others. Having a short “don’t get fooled” list saved me time.

• Early repolarization vs pericarditis vs STEMI: early repol often in young, healthy people with J-point notching; pericarditis tends to have PR depression and widespread concave ST elevation; STEMI hangs together by territory with reciprocal changes.
• Hyperventilation or anxiety can shift ST–T subtly; context, repeat tracing, and symptom story help.
• Lead misplacement can flip axis or mimic infarcts; check limb lead reversal and V1–V2 position if things don’t add up.
• Bundle branch block can produce “secondary” ST–T changes—don’t overcall ischemia without clinical correlation.

Why the report language feels so heavy

Automated interpretations are cautious by design. Words like “possible,” “nonspecific,” or “cannot rule out” try to avoid missing something important. I’ve learned to treat the algorithm as a helpful—but fallible—colleague. My notes now include: what the computer said, what I see, what changed from prior ECGs, and what symptoms match (or don’t). This little structure keeps me grounded when a report looks scarier than the clinical story.

What this changed for me

After a few months of reading and asking better questions, my mindset shifted. I stopped looking for a single “right answer” and started looking for direction. Does this tracing suggest a conduction delay, an atrial rhythm issue, or a supply-demand problem? Should we check electrolytes, review meds, compare to prior? Those questions turned out to be more useful than hunting for exotic diagnoses on day one.

Short list of things I now do on repeat

• Compare with old ECGs before reacting.
• Check the story (chest pain timeline, fever, meds, caffeine, sleep, stress).
• Look for patterns across contiguous leads rather than isolated beats.
• Respect intervals (PR, QRS, QTc) and electrolytes.
• Write down questions for the clinician instead of guessing.

FAQs I keep hearing from friends

1) Does an ECG alone diagnose a heart attack?
Answer: Not by itself. It’s an important clue, especially if there are ST-segment changes, but clinicians also consider symptoms, timing, physical exam, and blood tests (like troponin). The combination tells the story more reliably than any one piece.

2) Are PVCs dangerous or just annoying?
Answer: Many people have occasional PVCs and feel fine. Frequency, symptoms, and underlying heart health matter. If PVCs are frequent, new, or paired with dizziness, shortness of breath, or chest discomfort, it’s worth a check-in to look for triggers (electrolytes, sleep, caffeine) and assess the heart muscle.

3) What is a “normal” QTc?
Answer: QTc is a heart-rate–adjusted measure of the reset time. Instead of chasing a single number, I look for changes from prior readings and consider medications and electrolytes. Clinicians use thresholds to flag risk, but interpretation is personalized and context-dependent.

4) Can smartwatches replace a clinic ECG?
Answer: Single-lead wearables are amazing for capturing episodes (especially irregular rhythms like AFib), but they don’t replace a 12-lead ECG. They’re complementary—great for trend-spotting and bringing real-time data to your clinician.

5) If my ECG says “nonspecific ST-T changes,” should I worry?
Answer: “Nonspecific” means the pattern isn’t clearly pointing to a single cause. Hydration, electrolytes, medications, or normal variants may play a role. Pairing the ECG with symptoms, labs, and prior tracings usually clarifies whether it’s meaningful.

Sources & References

• MedlinePlus Electrocardiogram
• NHLBI Electrocardiogram
• American Heart Association ECG overview
• Mayo Clinic ECG test

This blog is a personal journal and for general information only. It is not a substitute for professional medical advice, diagnosis, or treatment, and it does not create a doctor–patient relationship. Always seek the advice of a licensed clinician for questions about your health. If you may be experiencing an emergency, call your local emergency number immediately (e.g., 911 [US], 119).