The QRS Complex

The QRS complex is ventricular depolarization. Follow the impulse. It leaves the SA node, crosses the atria, pauses at the AV node, then drops down the His bundle, both bundle branches and the Purkinje network into the ventricular muscle. The septum lights up first. The free walls follow. Width tells you how fast the impulse spreads through the ventricles.

A narrow complex means the normal conduction system is carrying the impulse. Both ventricles activate within about 110 ms. A bundle branch block delays one ventricle, and that side activates late, by slow cell-to-cell conduction. Ventricular origin is the other route to a wide complex. Pacing or ventricular ectopy skips the system altogether.

• Q wave: first negative (downward) deflection. R wave: first positive deflection. S wave: negative deflection after an R wave.
• Capital vs lowercase: Capital letters mean big deflections. Lowercase letters mean small ones. R′: a second positive deflection (rSR′). QS: entirely negative, with no R wave.

1. Pick the widest lead: scan the 12 leads and measure the widest QRS (often lead II, V1 or V5–V6).
2. Mark the onset: where the QRS leaves the baseline after the PR segment.
3. Mark the J point: where the QRS meets the ST segment.
4. Count: 1 small box = 40 ms (0.04 s); 5 small boxes = 200 ms (0.20 s). Measure 3 or more beats; in an irregular rhythm, average several beats.
5. Classify: ≤110 ms normal; 110–119 ms incomplete block; ≥120 ms wide.
6. Check V1 and V6: name the bundle branch pattern only after the width is confirmed.

R-wave progression: normally the R wave grows from V1 toward V4, and the transition (R = S) sits at V3–V4. Poor progression and the voltage criteria for hypertrophy are on the R Wave page. Pathologic Q waves get their own page, Q Wave. Axis and fascicular blocks sit on the Cardiac Axis page.

A QRS of 120 ms or more means ventricular activation took longer than it should. Start with the mechanism. The table groups the causes that way, and the rhythm types live on the Ventricular Rhythms page.

ECG Criteria

• Duration: ≥120 ms (≥0.12 s; 3 or more small boxes)
• Morphology: bundle branch-like, notched, or bizarre. Compare the complex with the sinus beats, and with an old ECG if one exists.

Causes

Clinical Significance

• Wide with tachycardia in an adult? That is ventricular tachycardia until proven otherwise.
• A new wide QRS with hypotension, syncope, shock or chest pain needs treatment now. See Bedside Management.
• A change from the patient's baseline matters more than the width alone. A new bundle branch block or a new wide QRS is that change.

A bundle branch block delays one ventricle, and that ventricle activates late through slow cell-to-cell conduction. The QRS widens to 120 ms or more. Expect the ST segments and T waves to run opposite (discordant) to the terminal QRS. Figures 2 to 5 show the patterns.

ECG Criteria

Incomplete block, at 110–119 ms, looks the same with a narrower QRS.

Causes

• RBBB: normal variant in healthy and young people; right ventricular strain (pulmonary embolism, pulmonary hypertension); structural or ischemic heart disease.
• LBBB: ischemic heart disease; hypertensive heart disease with LVH; cardiomyopathy; aortic valve disease; degenerative conduction disease.

Clinical Significance

• Isolated RBBB in a patient without heart disease? Often benign.
• LBBB is usually structural. It hides the usual ST-segment clues. That is why you need a prior tracing to compare against.

Expect a wide QRS when one ventricular site does the pacing. The ventricles activate in a fixed order from that site. Its shape depends on where the lead sits. Seeing a paced complex is no sign of infarction or block. It is what pacing looks like.

ECG Criteria

• Pacing spike before each paced complex (look in leads II and V1)
• Wide QRS with a morphology set by the pacing site
• Discordant ST-T change is expected. Compare with the previous 12-lead

Clinical Significance

• Standard ST-segment criteria do not work on a paced beat. Compare with a prior paced 12-lead, or use the Smith-modified Sgarbossa approach.
• When pacing is needed, a spike alone does not prove capture. Confirm it with the pulse and the SpO₂ waveform.
• Missing spikes, or an escape rhythm in a paced patient, mean a device check is needed.

Sodium-channel blockers slow phase 0 of the cardiac action potential. The QRS widens. Hyperkalemia does it another way. It partly depolarizes the resting membrane and slows conduction. Both are reversible. Both can progress to ventricular arrhythmia or asystole if you do not treat them.

Sodium-Channel Blockade

• QRS ≥100 ms (maximal limb-lead width): in the landmark tricyclic overdose series, seizures showed up at this width. Ventricular arrhythmias showed up only at 160 ms or more.
• Terminal R wave in aVR ≥3 mm: it catches seizures and arrhythmia well, but its positive predictive value was about 43%. Treat it as a supporting sign, not a verdict.
• Serum drug level: it did not predict seizures or arrhythmia in that same series. Treat the ECG and the patient.
• Treatment: sodium bicarbonate is COR 1 (LOE B-NR) for adult tricyclic or tetracyclic cardiotoxicity, COR 2a (C-LD) for children with the same, and COR 2a (C-EO) for other sodium-channel blockers (2025 AHA Part 10, recommendations 1, 2 and 5). Whether the endpoint is pH about 7.50 or resolved hypotension and QRS widening is debated (AHA 2025 Part 10, supportive text). The ceilings (serum pH 7.55, serum sodium 155 mEq/L) are E3 house position, which cites AHA 2025 Part 10 Table 4; that table could not be checked, so they are not verified against AHA text.

Hyperkalemic QRS Widening

Expect this order: peaked T waves, then flattened P waves, then PR prolongation, then QRS widening, and finally a sine-wave pattern. QRS widening is a late sign. The T Wave page covers that progression. Serum potassium guides the treatment. Calcium stabilizes the myocardium while potassium-shifting therapy starts. In cardiac arrest, though, the 2025 AHA rates IV calcium, sodium bicarbonate and insulin with glucose COR 2b. That means effectiveness is not well established (Part 10, Hyperkalemia recommendations 1 to 3).

Low QRS voltage means small QRS deflections across the limb or precordial leads. It is nonspecific, so it will not name the cause for you. With tachycardia, hypotension or shock, think of pericardial effusion and tamponade.

ECG Criteria

• Low voltage: small QRS deflections across the limb or precordial leads. Compare with the prior ECG. Amplitude changes with body habitus and the lead set.
• Electrical alternans: beat-to-beat change in QRS amplitude (and sometimes axis) in an otherwise regular rhythm.

Causes

• Pericardial effusion, especially with tamponade physiology.
• Other causes exist. The pattern alone cannot name them.

Clinical Significance

• Electrical alternans with tachycardia and hypotension: treat as possible tamponade and call for physician evaluation and point-of-care ultrasound.
• Repeat the 12-lead ECG as the patient changes, and compare each tracing with the last.

A wide QRS can have several causes. Separate the common mimics with the table before you act on a label.

Artifact and Lead Misplacement

• Precordial placement: leads placed high or low shift the R and S waves. They can mimic a bundle branch or a hypertrophy pattern.
• Motion and shivering: tremor in transport can look like wide, bizarre complexes. Confirm on a second lead or a repeat 12-lead.
• Limb lead reversal: swapped limb electrodes flip the polarity of leads I and aVR, and that can mimic an abnormal pattern. Compare with the baseline.

In adults, a wide-complex tachycardia of uncertain origin gets managed as ventricular tachycardia. That is the E3 working rule. AHA 2025 Part 9 makes no recommendation for an uncertain rhythm. The table sorts the approach by stability. The medication table has the doses.

Stability and Actions

Medications and Energy

Doses vary by protocol; follow local protocols and medical direction. Adult amiodarone, procainamide and cardioversion doses come from the 2025 AHA ACLS and Part 9 recommendations. Pediatric procainamide and stable pediatric amiodarone come from the PALS 2020 algorithm. Pediatric calcium comes from NASEMSO v3.0. Calcium chloride and insulin-dextrose rates come from UKKA 2026, and they differ from the FDA label. The sodium bicarbonate doses are the E3 house position. They cite AHA 2025 Part 10 Table 4, which was not independently checked.

Pediatrics

• Age-dependent width: the QRS runs shorter in infants and children, and it changes with age. Judge width against age-specific percentile charts, not the adult ≥120 ms cutoff alone.
• Wide complex with tachycardia: in children, SVT with aberrant conduction is the most common cause, but the rhythm can still be ventricular. With cardiopulmonary compromise, cardiovert urgently: 0.5–1 J/kg, then 2 J/kg if that fails (2025 AHA Part 8, COR 2a, C-EO). Without compromise, get expert consultation before any antiarrhythmic (2025 AHA Part 8, COR 1, C-LD). For a regular monomorphic WCT without compromise, adenosine can be useful, alongside expert consultation (2025 AHA Part 8, COR 2a, C-EO).
• Weight-based drugs: use Weight-Based Dosing and the Pediatric Vital Signs ranges.

Other Populations

• Pacemaker or ICD: a paced QRS is the finding to expect. Confirm capture, and compare with the previous paced 12-lead.
• Athletes and young adults: incomplete or complete RBBB is often a normal variant. Compare with an old ECG.
• Pregnancy: an unstable wide-complex tachycardia gets synchronized cardioversion, the same as in non-pregnant patients. For a stable one, the same agents apply: amiodarone or procainamide (AHA 2025 Part 9 WCT rec 3, COR 2b), after obstetric input.
• Kidney failure or potassium-raising drugs: check potassium early when the QRS widens.

1. Measure the QRS in the widest lead, from onset to J point, and classify it as ≤110, 110–119, or ≥120 ms.
2. Establish the rhythm: a narrow complex, a wide and regular complex, or a wide and irregular complex.
3. Assess the patient. If unstable, go straight to the stability table.
4. Look for a cause before any antiarrhythmic: a prior ECG, a pacing spike, pre-excitation (short PR, delta wave), drugs or toxins (sodium-channel toxicity), and potassium (hyperkalemia). Treat those causes first; see Bedside Management.
5. Check V1 and V6 to classify a bundle branch block, only after the width is confirmed.
6. For a new LBBB with chest pain, apply the Smith-modified Sgarbossa criteria and follow the local STEMI pathway.

Common Pitfalls

• Calling a wide complex a bundle branch block before you confirm the width and the rhythm.
• In adults, the habit of calling a wide, regular tachycardia SVT with aberrancy.
• Calling a new LBBB a STEMI, or waving it off as chronic with no prior ECG to check.
• Reaching for an AV-nodal blocker on a wide-complex tachycardia whose rhythm you do not know.
• Judging voltage or morphology from one lead or one beat in an irregular rhythm.