Ventricular Extrasystole: Difference between revisions

No edit summary
No edit summary
Line 1: Line 1:
<div class="editorbox">
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.<div class="editorbox">
'''Original Editor '''- [[User:Elyssa Abou Jamra|Elyssa Abou Jamra]]
'''Original Editor '''- [[User:Elyssa Abou Jamra|Elyssa Abou Jamra]]


Line 5: Line 5:
</div>  
</div>  
== Introduction ==
== Introduction ==
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. This is evident from the fact that each unifocal ventricular extrasystole, in any particular tracing, has a constant or fixed coupling interval to its preceding conducted sinus beat.
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. <ref>[https://www.ncbi.nlm.nih.gov/medgen/56236 Ventricular extrasystoles]</ref>
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. <ref>[https://www.ncbi.nlm.nih.gov/medgen/56236 Ventricular extrasystoles]</ref>



Revision as of 12:57, 22 November 2021

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[edit | edit source]

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. [1]

The most common forms of premature ectopic ventricular impulse formation are ventricular extrasystoles and ventricular tachycardia. [2] The manifestation of the ectopic rhythm may be an expression of underlying disease. [3]

Prevalence[edit | edit source]

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 [4]

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 [5],[6]. By comparison, when 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs .[7], [8],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[9].

There is an age-related increase in the prevalence of PVCs in normal individuals and those with underlying heart disease[5] ,[6],[8],[10]. The prevalence of PVCs increase with age and in the presence of other factors, such as faster sinus rate, hypokalemia, hypomagnesemia, and hypertension .[6]

Mechanism[edit | edit source]

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.[3] ,[11]Cogent experimental support has recently been presented in support of the theory of ectopic enhancement.[12]

Assessment[edit | edit source]

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:
    • Exertional syncope should always raise alarm of a sinister cause.
    • 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

Cardiovascular system including blood pressure, heart murmurs and any signs of cardiac failure.

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:
    • If symptoms are short-lived but frequent (>2-3 times per week), use a 24-hour Holter monitor.
    • 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.[13]


ECG findings

The diagnostic and clinical significance of ventricular extrasystoles must be assessed in the context of the following parameters:

  • Analysis of the extrasystolic configuration as a diagnostic expression of the myocardial state;
  • The duration of the coupling interval relative to the refractory period;
  • The associated electrocardiographic manifestations;
  • The associated clinical state.

Treatment[edit | edit source]

Patients with no symptoms/minor symptoms only - no heart disease (including normal LV function), infrequent ventricular extrasystoles, 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.[14]

Summary[edit | edit source]

  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.[15]

References[edit | edit source]

  1. Ventricular extrasystoles
  2. Mackenzie J: Diseases of the Heart. London, Oxford University Press, 19 13
  3. 3.0 3.1 Scherf D, Schott A: Extrasystoles and Allied Arrhythmias. London, William Heinemann, 1953
  4. Marcus GM. Evaluation and Management of Premature Ventricular Complexes. Circulation 2020; 141:1404.
  5. 5.0 5.1 HISS RG, LAMB LE. Electrocardiographic findings in 122,043 individuals. Circulation 1962; 25:947.
  6. 6.0 6.1 6.2 Simpson RJ Jr, Cascio WE, Schreiner PJ, et al. Prevalence of premature ventricular contractions in a population of African American and white men and women: the Atherosclerosis Risk in Communities (ARIC) study. Am Heart J 2002; 143:535.
  7. Sobotka PA, Mayer JH, Bauernfeind RA, et al. Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease. Am Heart J 1981; 101:753.
  8. 8.0 8.1 Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977; 39:390.
  9. Yang J, Dudum R, Mandyam MC, Marcus GM. Characteristics of unselected high-burden premature ventricular contraction patients. Pacing Clin Electrophysiol 2014; 37:1671.
  10. Glasser SP, Clark PI, Applebaum HJ. Occurrence of frequent complex arrhythmias detected by ambulatory monitoring: findings in an apparently healthy asymptomatic elderly population. Chest 1979; 75:565.
  11. Schamroth L: The physiological basis of ectopic ventricular rhythm.. A unifying concept, in Sandoe E, Julian DG, Bell JW (eds): Management of Ventricular Tachycardia. Role of Mexilitene. Amsterdam, Excerpta Medica, 1978, p 83
  12. Moe GK, Jalife J, Mueller WJ: Reciprocation between pacemaker sites: Re-entrant parasystole? in Kulbertus HE, (ed): Reentrant Arrhythmias. Mechanisms and Treatment. Lancaster, M.T.P. Press, 1977, p 271
  13. Robinson KJ, Sanchack KE; Palpitations. StatPearls Publishing 2019.
  14. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death; European Society of Cardiology (August 2015)
  15. G André Ng. Treating patients with ventricular ectopic beats. Heart 2006;92:1707–12.