Ventricular Arrhythmia

Ventricular Arrhythmia

History & Epidemiology

Ventricular arrhythmia is a condition where the pumping of the heart ventricles is abnormal. Ventricular arrhythmias produce a broad range of conditions, from premature ventricular complex to ventricular fibrillation. The clinical presentations can vary, from lack of symptoms to cardiac arrest.1

The term “arrhythmia” was introduced in 1872 by the German physiologist Rudolph Heidenhain2 and has been used since.

The development of ventricular arrhythmias depends on factors such as familial history, genetic variants, heart conditions, and even certain medications.1 People with advanced heart disease are at risk for ventricular arrhythmias, especially in the elderly population.3

Ventricular arrhythmias cause about 300,000 deaths per year in the US, accounting for almost half of deaths from cardiac causes.4 Cases of ventricular arrhythmias can be lethal, as when presenting with ventricular fibrillation or when caused by myocardial infarction.5

Ventricular arrhythmias are unusual in children but can show in patients with congenital heart disease. The incidence of ventricular arrhythmia increases with age, peaking in the middle decades of life, the same age for incidence of structural heart diseases. However, idiopathic ventricular arrhythmias can occur at any age. Men suffer more frequently from ventricular arrhythmias than women since ischemic heart disease is more prevalent in men, and ischemia predisposes for ventricular arrhythmias.6

Presentation & Diagnosis of Ventricular Arrhythmia

The most common, easily detectable symptoms of ventricular arrhythmias are palpitations, light-headedness, syncope, and chest pain. Based on clinical presentation, however, ventricular arrhythmias be categorized as hemodynamically stable or unstable.7

  • Hemodynamically stable arrhythmias show no symptoms or minimal ones, such as palpitation.
  • Hemodynamically unstable ventricular arrhythmias can present with a presyncope, syncope, or sudden cardiac death or cardiac arrest.

There are specific etiologies of ventricular arrhythmias8:

  • Idiopathic ventricular arrhythmia without structural heart disease can present with right ventricular outflow tract tachycardia, left ventricular outflow tract tachycardia, or left posterior fascicular ventricular tachycardia.
  • Ischemic cardiomyopathy mainly shows monomorphic ventricular tachycardia but can also be seen with polymorphic ventricular tachycardia, and a ventricular tachycardia storm may occur.
  • Nonischemic cardiomyopathy, where polymorphic ventricular tachycardia is more common than monomorphic ventricular tachycardia, and the myocardial scar is more commonly localized to the epicardium or mid-myocardium than the endocardium.
  • Arrhythmogenic right ventricular dysplasia, in which an electrocardiogram may show right ventricular dilation with systolic dysfunction, and an electrophysiologic study typically demonstrates reduced endocardial voltage indicative of scar.
  • Hypertrophic cardiomyopathy, which mainly presents with nonsustained or polymorphic ventricular tachycardia or ventricular fibrillation. Murmur caused by outflow tract obstruction and bisferiens pulse are common signs.
  • Genetic arrhythmia syndromes are diagnosed with a long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, early repolarization syndrome, or (rarely) with a short QT syndrome.

Ventricular Arrhythmia Diagnostic Workup

For a diagnosis, the health provider should start with a physical examination looking for hypotension, tachypnea, signs of diminished perfusion (including a reduced level of consciousness, pallor, and diaphoresis), high jugular venous pressure, Cannon A waves when the atria are in sinus rhythm, and variation in the intensity of first heart sound (S1) produced by loss of atrioventricular synchrony. The patient may also be affected by a particular mental status involving signs of anxiety, agitation, and/or lethargy.6

If signs of ventricular arrhythmia appear during physical examination, an electrocardiogram (ECG) is required for confirmation. Laboratory studies to measure electrolyte levels, including calcium, magnesium, and phosphates, may also be necessary, in combination with cardiac troponin I enzymes, concentration levels of which would determine myocardial ischemia. A toxicology screen is recommended if there is a suspicion that recreational or therapeutic drug consumption, such as cocaine or methadone, could be causing ventricular arrhythmia.6

Differential Diagnosis

Common symptoms that can be confused with other pathologies include exercise intolerance, chest pain, dyspnea, presyncope, and syncope.

When performing an ECG, it is difficult to differentiate a ventricular arrhythmia presenting a complex tachycardia from supraventricular tachycardia. Some criteria on the 12-lead ECG that define ventricular arrhythmia include the absence of an RS complex in the precordial leads, an RS interval of greater than 0.1 seconds in any precordial lead, and atrioventricular dissociation with or without fusion, with or without capture beats. If the differentiation from supraventricular tachycardia is still uncertain after the 12-lead ECG, it is preferable to assume ventricular arrhythmia.8

Management of Ventricular Arrhythmias

The management of ventricular arrhythmia principally depends on the patient’s hemodynamic status and clinical condition.

Nonpharmacotherapy for Ventricular Arrhythmia Treatment

When sustained ventricular tachycardia is present, the patient requires urgent conversion to sinus rhythm. If hemodynamically unstable with monomorphic ventricular tachycardia, the patient should be immediately treated with synchronized direct-current cardioversion. Unstable polymorphic ventricular tachycardia should be treated with immediate defibrillation.6

Pharmacotherapy for Ventricular Arrhythmia Treatment

In hemodynamically stable patients with monomorphic ventricular tachycardia and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous procainamide or beta-blockers such as amiodarone or sotalol. If the left ventricular function is impaired, amiodarone (or lidocaine) is preferred. When pharmacological therapy is unsuccessful, sedation and synchronized cardioversion should be applied.8

If the patient shows runs of polymorphic ventricular tachycardia punctuated by sinus rhythm with QT prolongation, magnesium sulfate, isoproterenol, pacing, or a combination should be used. Also, the administration of phenytoin and lidocaine may help.6

Ventricular Arrhythmia Treatment: Side Effects, Adverse Events, Drug-Drug Interactions

Amiodarone is particularly associated with long-term adverse effects such as pulmonary, thyroid, cardiac, skin, and ocular toxicities.10 Moreover, its chronic administration has been associated with complex medication interactions,1 including with fingolimod and certain drugs to treat hepatitis C, such as ledipasvir and sofosbuvir.

If untreated, malignant ventricular arrhythmia can result in serious adverse events, such as syncope, sudden cardiac arrest, and death.

References

1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018. 138:e272–e391. doi: 10.1161/CIR.0000000000000549

2. Anderson ME, Antzelevitch C, Balser JR, et al. Basis and Treatment of Cardiac Arrhythmias. Springer; 2006. doi: 10.1007/3-540-29715-4

3. Tan NY, Roger VL, Killian JM, et al. Ventricular arrhythmias among patients with advanced heart failure: A population-based study. J Am Heart Assoc. 2022; 11:e023377. doi: 10.1161/JAHA.121.023377

4. Foth C, Gangwani MK, Alvey H. Ventricular tachycardia. In:StatPearls: NCBI Bookshelf version. StatPearls Publishing; 2022. Updated 2021 Aug 11.

5. Sattler SM, Skibsbye L, Linz D, et al. Ventricular arrhythmias in first acute myocardial infarction: Epidemiology, mechanisms, and interventions in large animal models. Front Cardiovasc Med. 2019; 6:158. doi: 10.3389/fcvm.2019.00158. eCollection 2019.

6. Compton SJ. Ventricular tachycardia. Medscape. Updated Dec 2017. Accessed Sept 28, 2022.

7. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol.2016; 48(5); e247-e346. doi: 10.1016/j.jacc.2006.07.010

8. Dresen WF, Ferguson JD. Ventricular arrhythmias. Cardiol Clinics. 2018 Feb;36(1):129-139. doi: 10.1016/j.ccl.2017.08.007.

9. Jons C, Sogaard P, Behrens S, et al. The clinical effect of arrhythmia monitoring after myocardial infarction (BIO-GUARD|MI):study protocol for a randomized controlled trial. Trials. 2019; 20:563. doi: 10.1186/s13063-019-3644-5

10. Doyle JF, Ho KM. Benefits and risks of long-term amiodarone therapy for persistent atrial fibrillation: A meta-analysis. Mayo Clin Proc. 2009;84(3):234-242. DOI: 10.1016/S0025-6196(11)61140-3

Author Bio

Francina Agosti is a freelance science and medical writer based in Canada. She holds a PhD in neuroscience, and she worked in academia for 10 years. Now she writes scientific and medical articles for digital magazines, and she also works as a scientific consultant for biotech and biopharma companies.