Introduction
The QRS complex a window into ventricular depolarization, shaped by the direction and magnitude of electrical forces within the heart. Rather than memorizing waveforms, a vector-based understanding explains why QRS complexes differ between leads and how disease alters their appearance. This framework provides a reliable foundation for interpreting abnormal ECGs in the emergency department.
Ventricular Depolarization
The QRS complex is not a single electrical event. It is a record of millions of myocardial depolarization vectors summing together in real time. What we see on paper is simply the net direction and magnitude of these forces as viewed from different angles.
Ventricular depolarization occurs in three main phases:
- Septal depolarization
- Main ventricular depolarization
- Late basal depolarization
Depolarization begins in the interventricular septum and travels anteriorly and rightward. This initial vector explains small septal Q waves in lateral leads and early R waves in right-sided leads.
The bulk of the left ventricle then depolarizes, generating a large, dominant vector directed leftward, posteriorly, and inferiorly. This vector is responsible for most of the QRS amplitude and largely determines the frontal axis.
Finally, the high basal regions depolarize in a posterior–superior direction, subtly shaping the terminal portion of the QRS.
Sequential ventricular depolarization vectors: septal (A) → dominant LV (BC) → basal (D). From Cardiovascular Physiology Concepts 🔗 Link
QRS Morphologies
Each ECG lead is simply a different “camera angle” of the same electrical event. Because the vectors are the same but the viewing angle changes, the QRS of the same beat can look dramatically different from lead to lead
- Limb leads view the heart in the frontal (coronal) plane
- Precordial leads view the heart in the horizontal plane
Although we label the QRS as having three components (Q, R, and S waves), many leads will not display all three waves. If a vector runs perpendicular to a lead, it produces little or no deflection and may appear isoelectric. Some different nomenclatures appear below:
A Practical Framework for Reading the QRS
Every QRS interpretation should systematically assess six core features:
- Amplitude / height
- Duration / width
- Morphology
- Pathologic Q waves
- Frontal axis
- Precordial transition zone (Z-axis)
How Pathology Changes the QRS Complex
Hypertrophy
A larger ventricle produces more electrical force, resulting in larger voltage.
ECG Example: Left ventricular hypertrophy with large R waves in the lateral (left sided) leads (I, V5-V6) and deep S waves in V1-V2
ECG Example: Right ventricular hypertrophy with R axis and tall R waves in the anterior leads (V1-V4)
Infarction or Scar
Infarcted myocardium is electrically silent. When one region stops contributing, opposing vectors become unopposed, exaggerating remaining forces and shifting vector direction.
ECG Finding | Vector Explanation |
Pathologic Q waves | Unopposed vectors pulling away from infarct |
Poor R-wave progression | Loss of anterior depolarization forces in an anterior MI |
Tall R waves opposite infarct | Loss of opposing counterbalance |
Axis deviation | Net vector shifts away from silent myocardium |
Pseudo-LVH | Remaining vectors exaggerated which can mimic LVH |
ECG Example: Anterior MI with Q waves and loss of R wave progression
Pericardial Effusion or Insulation
Fluid, fat, or infiltrative material around the heart does not change vector direction, but it dampens signal transmission, producing globally low voltage. Think of it like listening to a speaker under a blanket: the sound is the same, just quieter. Low voltage is defined as ≤ 5mm qrs amplitude in all limb leads or ≤ 10mm in all precordial leads.
ECG Example: Pericardial effusion demonstrating low qrs amplitude in all leads.
Common causes of low voltage include:
• Pericardial effusion
• Obesity
• Hypothyroidism (myxedema)
• Amyloidosis
• Large pleural effusions (sometimes regionally, e.g., V5–V6)
Bundle Branch Blocks
In bundle branch block, one ventricle depolarizes late, so early electrical forces from the normally conducting ventricle are temporarily unopposed. This is followed by delayed activation of the blocked ventricle, producing out-of-sequence vectors that distort QRS morphology and widen the complex. The QRS is prolonged because depolarization of the blocked ventricle occurs via slow cell-to-cell conduction through ventricular myocardium, which is far less efficient than rapid conduction through the His-Purkinje system.
ECG Example: Left Bundle Branch Block
ECG Example: Right Bundle Branch Block
Putting it all together
The QRS complex provides information about ventricular depolarization, conduction, and myocardial integrity. Systematic assessment of QRS amplitude, duration, morphology, axis, and precordial transition helps identify hypertrophy, infarction, conduction disease, and conditions that alter electrical signal transmission. These findings should always be interpreted across the entire ECG and in clinical context.
Resources
- Brady WJ, Harrigan RA. Critical Decisions in Emergency and Acute Care Electrocardiography. Philadelphia, PA: Elsevier; 2015.
- Cardiovascular Physiology Concepts. Ventricular depolarization and the QRS complex. https://cvphysiology.com/arrhythmias/a016
- Chou TC. Electrocardiography in Clinical Practice. 6th ed. Philadelphia, PA: Elsevier; 2008.
- Davila C. The ECG. Self-published; 2024
- ECGwaves.com. QRS complex nomenclature and morphology. https://ecgwaves.com
- Garcia TB. 12-Lead ECG: The Art of Interpretation. 2nd ed. Burlington, MA: Jones & Bartlett Learning; 2015.
- Garcia TB, Garcia DB. Arrhythmia Recognition: The Art of Interpretation. 2nd ed. Burlington, MA: Jones & Bartlett Learning; 2017.
- Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th ed. Philadelphia, PA: Elsevier; 2008.
This post is for education and not medical advice.