Skip to main content

PVC Localization on ECG: A Quick Guide for Clinicians

PVC Localization on ECG: Lets start with this ECG Case:

Premature ventricular contractions (PVCs) are common arrhythmias often seen on routine ECGs or Holter monitors. While isolated PVCs are frequently benign, identifying their site of origin can be clinically important—especially in patients with symptoms, frequent ectopy, or underlying structural heart disease. ECG morphology offers valuable clues to help localize the origin of these ectopic beats within the ventricles.


Basic Principles:

PVCs originate from a single focus in the ventricular myocardium. Because of this, the activation spreads outside the normal conduction system, creating wide and bizarre QRS complexes. The QRS morphology and axis during a PVC provide hints about where in the ventricles the beat originates.


Key Clues to Localization:


1. Outflow Tract PVCs (RVOT/LVOT)




Most common type in structurally normal hearts.


LBBB pattern in V1 (dominant S wave).


Inferior axis (positive QRS in II, III, aVF) — indicating superior origin.


RVOT PVCs show early R-wave transition (V3 or later), whereas LVOT PVCs tend to transition earlier (V1–V2).



2. Fascicular PVCs (Left Ventricular Septum)




Seen in young patients; often idiopathic.


Relatively narrow QRS with RSR' or RBBB pattern.


Right axis deviation or superior axis in posterior fascicular origin.



3. Mitral/Tricuspid Annulus PVCs




Variable morphology, often with sharp notching and slightly wider QRS.


May mimic outflow tract PVCs but with different axis and transition patterns.


Often require detailed mapping for exact localization.



4. Epicardial Origin




Broader QRS, initial slurring (pseudo-delta wave), and delayed intrinsicoid deflection.


Precordial QRS transition is delayed (after V4).


Often found near coronary venous system or outflow tract region.



Clinical Pearls:


Always compare PVC morphology across multiple leads.


Look for axis, bundle branch pattern in V1, and precordial transition.


Outflow tract PVCs are most common—and usually benign.


Epicardial or multiple morphologies may suggest structural heart disease.



Understanding PVC localization can guide further testing (like cardiac MRI or electrophysiology study) and help determine suitability for catheter ablation.


Author’s Note:

ECG remains a powerful, low-cost tool. With practice, PVC localization can be quickly assessed at the bedside, giving deeper insights into patient management.



Comments

Popular posts from this blog

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB)

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB) Why this differentiation matters Brugada pattern is a malignant channelopathy associated with sudden cardiac death, while incomplete RBBB is usually a benign conduction variant. Mislabeling Brugada as iRBBB can be fatal; overcalling iRBBB as Brugada can lead to unnecessary anxiety and ICD implantation. --- 1. Basic Definitions Brugada ECG Pattern Primary repolarization abnormality Genetic sodium-channel disorder Characteristic ST-segment elevation in V1–V3 Risk of ventricular fibrillation and sudden death Incomplete RBBB (iRBBB) Depolarization abnormality Delay in right ventricular conduction Common in healthy individuals Usually asymptomatic and benign --- 2. ECG Morphology: Side-by-Side Comparison QRS Duration Brugada: QRS usually <120 ms iRBBB: QRS <120 ms, but with RBBB morphology --- V1–V2 Pattern (Key Differentiator) Brugada Pseudo-RBBB appearance ST elevation ≥2 mm ST segment is coved or saddleback Terminal QRS bl...

π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š

 π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š in  Patient with AF and acute IS/TIA European Heart Association Guideline recommends: • 1 days after TIA • 3 days after mild stroke • 6 days after moderate stroke • 12 days after severe stroke Early anticoagulation can decrease a risk of recurrent stroke and embolic events but may increase a risk of secondary hemorrhagic transformation of brain infarcts.  The 1-3-6-12-day rule is a known consensus with graded increase in delay of anticoagulation between 1 and 12 days after onset of ischemic stroke or transient ischemic attack(TIA), according to neurological severity based on European expert opinions. However, this rule might be somewhat later than currently used in a real-world practical setting.

Acute Treatment of Hyperkalemia

Acute Treatment of Hyperkalemia – A Practical, Bedside-Oriented Guide Hyperkalemia is a potentially life-threatening electrolyte abnormality that demands prompt recognition and decisive management. The danger lies not only in the absolute potassium value but in its effects on cardiac conduction, which can rapidly progress to fatal arrhythmias. Acute treatment focuses on three parallel goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing excess potassium from the body. Understanding this stepwise approach helps clinicians act quickly and rationally in emergency settings. Why Hyperkalemia Is Dangerous Potassium plays a key role in maintaining the resting membrane potential of cardiac myocytes. Elevated serum potassium reduces the transmembrane gradient, leading to slowed conduction, ECG changes, ventricular arrhythmias, and asystole. Importantly, ECG changes do not always correlate with potassium levels, so treatment decisions should be based on clinical c...