Ventricular trigeminy
These are caused by the premature discharge of a ventricular ectopic focus which produces an early and broad QRS complex.
Extrasystoles are usually normal, being common in middle age. The patient may feel an occasional missed beat.
Patients with no ischaemic heart disease or cardiomyopathy have an excellent prognosis.
Ventricular extrasystoles after myocardial infarction are associated with increased mortality.
They may be the presenting feature of viral myocarditis.
Ventricular ectopics are common and usually of no clinical significance (1):
- often arise from specific sites such as the right ventricular outflow tract and can affect people of all ages
- may be completely asymptomatic and discovered incidentally on a routine ECG or they are experienced as 'missed beats'
- in structurally normal hearts, they are not dangerous and can be difficult to suppress with medication which is thus best avoided
- in the presence of significant structural heart disease, frequent ectopy marks an increased risk of sudden cardiac death and specialist advice should be sought (1)
- rarely they have the potential to induce ventricular fibrillation particularly if they coincide with the T wave of a preceding beat - this is described as the 'R on T phenomenon'
- ventricular bigeminy
- this occurs when a ventricular premature beat follows each normal beat
- ventricular trigeminy
- occurs when there is a ventricular premature beat following two normal beats
Ventricular Premature Contraction (VPC) (2)
Diagnostic criteria
Depolarization of the ventricles occurs by an impulse originating from an ectopic ventricular focus.
There is no causally related preceding P wave since the impulse originates from the ventricles.
Since the impulse originates from an ectopic ventricular focus, depolarization wave does not propagate over fast Purkinje fibers but by cardiac myocytes which results in slow conduction and hence a wide QRS complex (>120ms).
Compensatory Pause
Definition: The sum of the pre-VPC and the post-VPC intervals equals to 2 times of the interval between two sinus beats.
For a full compensatory pause to occur, there are 2 necessities:
1. There must be a stable sinus rhythm. Sinus arrhythmia must not be seen.
2. There must be ventriculoatrial block (the VPC must not interrupt the sinus rhythmicity) or ventriculoatrial conduction occurs but fails to reset the sinus node.
Rarely a VPC may not have a compensatory pause.
During sinus rhythm, compensatory pause after a VPC is NOT seen
1. IF there is sinus arrhythmia.
2. IF there is ventriculoatrial conduction resetting the sinus node.
Compensatory pause is not possible in irregularly irregular rhythms such as atrial fibrillation or multifocal atrial tachycardia.
By definition, interpolated VPCs also do not have compensatory pauses.
After a VPC, a compensatory pause is usually observed. Usually, compensatory pause is not observed after an atrial premature beat (APB). Compensatory pause after an APB is very rare. Compensatory pause after an APB suggests that the APB failed to reset the sinus node.
When a VPC occurs during aberration due to increased heart rate (acceleration-dependent aberration), its compensatory pause may result in temporary disappearance of the aberration.
Clinical significance
Observation of VPS in a subject without organic heart disease is not significant.
VPS is the most common type of arrhythmia.
VPS is not specific for a certain disease.
Not all wide QRS complexes are due to VPC:
- Ventricular pacemaker stimulation results in wide QRS (His bundle pacing is an exception).
- Aberrant conduction of a supraventricular impulse to the ventricles (aberrancy) causes wide QRS.
- WPW syndrome causes wide QRS complexes.
Sometimes, artifacts may look like VPCs.
Reference:
- BHF Factfile (March 2005). Ventricular Arrhythmias.
- Alpaslan M. Ventricular premature contraction. doctorecg.com (accessed 3/6/2020)
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