Ventricular Extrasystole

A ventricular extrasystole is the expression of an impulse that arises prematurely in an ectopic ventricular focus and is, in some way, related to the preceding sinus beat. Each unifocal ventricular extrasystole, in any particular tracing, has a constant or fixed coupling interval to its preceding conducted sinus beat.

Original Editor - Elyssa Abou Jamra

Top Contributors - Elyssa Abou Jamra, Kim Jackson and Lucinda hampton  

Introduction

It s a type of cardiac arrhythmia with premature contractions of the heart ventricules. It is characterized by the premature QRS complex on ECG that is of abnormal shape and great duration (generally >129 msec). It is the most common form of all cardiac arrhythmias. Premature ventricular complexes have no clinical significance except in concurrence with heart diseases.

The most common forms of premature ectopic ventricular impulse formation are ventricular extrasystoles and ventricular tachycardia. The manifestation of the ectopic rhythm may be an expression of underlying disease.

Epidemiology

The prevalence of PVCs is directly related to the study population, the detection method, and the duration of observation. PVCs are more likely to be detected in older patients, patients with more comorbidities, and patients who are monitored for longer durations of time

In patients with no known heart disease, PVCs have been seen in approximately 1 percent of routine 12-lead electrocardiograms (ECG) of 30 to 60 seconds duration and up to 6 percent of ECGs of two minutes duration ,. By comparison, when 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs ., ,The occurrence of frequent PVCs accounting for more than 20 percent of overall heart beats is rare, seen in less than 2 percent of patients.

There is an age-related increase in the prevalence of PVCs in normal individuals and those with underlying heart disease ,,,. The prevalence of PVCs increase with age and in the presence of other factors, such as faster sinus rate, hypokalemia, hypomagnesemia, and hypertension .

Etiology

The mechanism is still debatable, there are two current theories.

The reentry theory is based on the assumption of a localized area of refractoriness within the immediate vicinity of the ectopic focus. The sinus impulse is, therefore, unable to penetrate the ectopic focus, but after activating the surrounding myocardium, approaches it from another direction. The focus will by now have regained its excitability and is, therefore, able to respond to and propagate the reentering impulse, thereby initiating a further activation.process-the extrasystole.

The theory of ectopic enhancement assumes that an extrasystole is generated within the ectopic focus itself and that it is precipitated as a result of some enhancing effect or influence by the preceding sinus beat. ,Cogent experimental support has recently been presented in support of the theory of ectopic enhancement.

Pathophysiology

(A) Automaticity is the ability of cardiac cells to depolarize spontaneously and initiate an action potential in the absence of external electrical stimulation. It is the result of diastolic depolarization caused by a net inward current during phase 4 of the action potential, which progressively brings the membrane potential towards threshold.

(B) Triggered activity corresponds to impulse initiation resulting from oscillations in membrane potential that are dependent on the preceding action potential (afterdepolarizations). If the afterdepolarizations are of sufficient amplitude, a new action potential is triggered. Afterdepolarizations may occur during phase 2 or 3 of the cardiac action potential (early afterdepolarizations) or during phase 4, after full repolarization (delayed afterdepolarizations).

(C) Reentry occurs when an action potential fails to extinguish itself and reactivates a region that has recovered excitability. It requires the presence of 2 pathways with different electrophysiological properties separated by an area of unexcitable tissue. When a premature excitation wavefront encounters the obstacle, unidirectional block occurs in one pathway and the wavefront travels down the other pathway, propagating in a circus movement to the site of block. If this pathway has recovered its excitability, the depolarization wavefront will complete the circuit and cause another depolarization to be propagated. Interruption of the reentrant circuit at any point along its path should terminate the circus movement. Modified with permission from reference

Assessment

History:

• Detailed history of the presenting symptom - including onset, duration, associated symptoms and recovery.
• Check for other cardiac symptoms including chest pain, breathlessness, syncope or near syncope (eg, dizziness), and arrhythmia symptoms (eg, sustained fast palpitations).
• If there is history of syncope, note that:
  1. Exertional syncope should always raise alarm of a sinister cause.
  2. Rapid recovery after the syncopal event, without confusion or drowsiness, is characteristic of cardiac syncope.
• Family history - for early cardiac disease or sudden death.
• Previous cardiac disease or coronary heart disease (CHD) risk factors.

Examination

• Blood pressure
• Pulse
• Pulse oximetry
• Cardiac findings
• Cardiopulmonary findings
• Neurologic findings

Investigations

• Resting 12-lead ECG.
• FBC and TFTs.
• Electrolytes.

Other investigations:

• Serum calcium and magnesium.
• If symptoms have a long duration (many hours), advise the patient to attend their GP surgery or A&E for a 12-lead ECG during the next episode.
• Ambulatory ECG monitoring:
  1. If symptoms are short-lived but frequent (>2-3 times per week), use a 24-hour Holter monitor.
  2. If symptoms are short-lived and infrequent (<1 per week), use an event monitor or transtelephonic recorder.
• Echocardiography - to assess LV function and heart structure.
• Exercise stress testing - the relation of extrasystoles to exercise may have prognostic importance.
• Further non-invasive cardiac imaging may be required.

Symptoms

Many patients are entirely asymptomatic, whereas other describe symptoms of:

• palpitations (heart pounding, irregular, skipped, or paused heartbeat)

or they may convey more generalized symptoms such as

• dizziness
• near-syncope
• dyspnea
• chest pain
• fatigue.

Symptoms can be due to the ventricular extrasystole itself, to the compensatory pause followed by a hypercontractile beat (Starling effect), or to a reduction in effective cardiac output .

Triggering Factors

1. Stress
2. dehydration,
3. poor sleep,
4. caffeine,
5. alcohol,
6. medication
7. health changes,
8. stimulant or recreational drug use,
9. temporal relationship between phases of hormonal cycles and *PVC burden in women

Treatment

Patients with no symptoms/minor symptoms only - no heart disease, ventricular extrasystoles which reduce in frequency on exercise testing, and no documented ventricular tachycardia:

• These patients can be reassured.
• Reducing caffeine intake (if high) can be tried to see if this reduces symptoms.
• If treatment is desired, consider beta-blockers.

Patients with no heart disease, but with frequent ventricular extrasystoles (>1,000 per 24 hours):

• No treatment is required, but these patients may merit long-term follow-up, with periodic reassessment of LV function, particularly for those with very high-frequency extrasystoles.

Patients with no heart disease, with frequent unifocal ventricular extrasystoles and particularly if ventricular tachycardia or salvos are induced on exercise:

• Consider catheter ablation - this may be curative and results are often good.

Patients with cardiac disease:

• Ventricular extrasystoles may indicate either an arrhythmia risk or the severity of the underlying disease; therefore, consider the level of risk for sudden cardiac death.
• Beta-blockers may be indicated either for the underlying cardiac disease, or because they may reduce the frequency or symptoms of ventricular extrasystoles.
• Consider implantable cardiac defibrillators if at high risk of serious ventricular arrhythmia.
• Consider catheter ablation as adjunctive treatment.

Also treat any underlying cardiac disease and contributing factors - eg, hypertension, electrolyte abnormalities, ischaemia or cardiac failure.

Summary

1. Ventricular ectopic beats (PVCs) are frequently seen in daily clinical practice and are usually benign.
2. Presence of heart disease should be sought and, if absent, indicates good prognosis in patients with PVCs.
3. Unifocal PVCs arising from the right ventricular outflow tract are common and may increase with exercise and cause non-sustained or sustained ventricular tachycardia. Catheter ablation is effective and safe treatment for these patients.
4. B-blockers may be used for symptom control in patients where PVCs arise from multiple sites. It should also be considered in patients with impaired ventricular systolic function and/or heart failure.
5. Risk of sudden cardiac death from malignant ventricular arrhythmia should be considered in patients with heart disease who have frequent PVCs. An implantable cardioverter defibrillator may be indicated if risk stratification criteria are met.
6. PVCs have also been shown to trigger malignant ventricular arrhythmias in certain patients with idiopathic ventricular fibrillation and other syndromes. Catheter ablation may be considered in some patients as adjunctive treatment.