ECG rhythms Premature beats
Sinus rhythm with premature ventricular complexes ECG
Sinus rhythm with premature ventricular complexes. Sinus beats are interrupted by early, wide, differently shaped QRS complexes with no P wave before them.
A 30-second recording of the heart model, played in real time. Run live starts the engine itself with this rhythm.
Computed by the TracingsMD heart model (Junkers engine): simulated for education, not a patient recording and not for diagnosis.
Measured on this recording
| Ventricular rate | 75/min |
|---|---|
| PR | 158 ms |
| QRS | 84 ms; wide beats 153 ms |
| QT | 354 ms |
| QTc (Bazett) | 394 ms |
| QTc (Fridericia) | 380 ms |
What it is
An early beat that starts in the ventricles instead of the sinus node. It spreads slowly through ventricular muscle, so the QRS is usually wide (120 ms or more) and differently shaped, usually with an ST segment and T wave pointing opposite to the QRS, and no P wave before it. The sinus rhythm continues underneath: the next sinus P wave usually falls inside the PVC and is not conducted, leaving a full compensatory pause. PVCs are common, even in healthy people.
How to read this strip
| Rate | 60–100/min (sinus beats). |
|---|---|
| Rhythm | Regular, broken by early beats. |
| P waves | Sinus P waves; one hidden in each PVC. |
| PR | Normal in sinus beats. |
| QRS | Narrow sinus beats; early beats wide (≥120 ms). |
| QT | Normal in sinus beats. |
Causes
- Often no cause is found, especially in a structurally normal heart; stress, lack of sleep, alcohol and stimulants can increase them.
- Structural heart disease: previous myocardial infarction, cardiomyopathy, heart failure, valve disease.
- Acute myocardial ischemia.
- Low potassium or magnesium.
- Drugs and toxins: sympathomimetics (for example beta-agonists), digoxin toxicity, cocaine and other stimulants.
- Hypoxia, hyperthyroidism.
- A catheter or pacing wire tip irritating the right ventricle.
What to consider
- Treat the patient, not the beat: occasional PVCs in a person without symptoms or heart disease usually need no treatment.
- Check potassium, magnesium, ischemia, drugs and stimulants; in hospital, check whether a central line is too deep or a pulmonary artery catheter has slipped back into the right ventricle.
- Frequent, symptomatic or complex PVCs (couplets, runs) call for a search for structural heart disease: 12-lead ECG, echocardiogram and ambulatory monitoring to measure the PVC burden.
- A very high PVC burden (often quoted as more than 10–15% of all beats) can weaken the left ventricle (PVC-induced cardiomyopathy), which may recover when the PVCs are suppressed with drugs or catheter ablation.
- After a myocardial infarction, suppressing PVCs with class I antiarrhythmic drugs increases mortality: treat the cause, and use a beta-blocker when indicated.
- Three or more ventricular beats in a row at a rate above 100/min are ventricular tachycardia. PVCs with syncope, or that increase with exertion, need prompt evaluation.
Key point
A wide early beat without a preceding P wave, followed by a full compensatory pause, is a PVC.
Not to be confused with
- Sinus rhythm with premature atrial complexes — A PAC has an early P wave and usually a narrow QRS. These early beats are wide with no P wave before them.
- Ventricular tachycardia — VT is three or more ventricular beats in a row at a rate above 100/min. Here single early beats sit between sinus beats.
- Second-degree AV block, Mobitz II — In Mobitz II a P wave fails to conduct with no early beat. Here the pause follows an early wide beat.