I. Ventricular Arrhythmias: What every physician needs to know.

Ventricular arrhythmias include:

  • Premature ventricular contractions (PVCs)

  • Nonsustained ventricular tachycardia

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  • Sustained ventricular tachycardia (VT) (>30 seconds, heart >100 bpm )

  • Accelerated idioventricular rhythm (AIVR with VT rate <100 bpm)

  • Ventricular fibrillation (VF)

  • Torsades de pointes

II. Diagnostic Confirmation: Are you sure your patient has a Ventricular Arrhythmia?

A PVC is recognized as a premature ventricular beat and must not be preceded by a P wave that may have been conducted with aberrancy (distortion of the QRS). PVCs can be uniform or multiform. They can occur singly or in short runs. The origin of the PVC could be identified by the morphology (RBBB or LBBB) in lead V1. The axis (leads 1, AVF) will determine the site such as the apex or outflow tract. If there is a need to quantify the PVC count, a Holter recording is justified.

NSVT is defined as 3 consecutive PVCs, but <30 seconds.

Sustained ventricular tachycardia is recognized as follows: The QRS is wide, the rate is fast (>100 bpm). It interrupts sinus rhythm, with the first beat of VT occurring before the next sinus P wave or after the P wave but with a shorter P–R than when in sinus. There could be fusion of the first VT beat if it occurs at a reasonable P–R interval, allowing sinus conduction through the atrioventricular (AV) node to the ventricle.

If AV dissociation is present, then the diagnosis is VT (Figure 1). Concordance of the QRSs, all negative (especially) or all positive, in the precordial leads is highly suggestive of VT. The onset of the R to the nadir of S >100 ms in any precordial lead is also suggestive of VT.

Figure 1.

Ventricular tachycardia. Note the dissociation of the P waves (top strip).

Other forms of sustained monomorphic VT include:

  • Verapamil sensitive VT. This VT originates from the lower left ventricular septum with the electrocardiogram (ECG) showing a right bundle block and superior axis. The QRS is narrower than other forms of VT.

  • Right ventricular (RV) dysplasia VT (ARVC) is characterized by fatty infiltration of the RV free wall. The VT shows a left bundle branch block (LBBB) pattern and the resting ECG in sinus may show T inversion in V1-V3. Notching of the QRS, called epsilon waves, may be present (Figure 2). A variant of this condition is RV outflow tract (RVOT) (Figure 3)/ LV outflow tract (LVOT). This type of tachycardia has an inferior axis. It may be difficult at times to distinguish between ARVC and RVOT. However, QRS >120 ms in lead 1, earliest onset of QRS in V1, notching of the QRS in several leads, and transition V5, V6 favors ARVC (see reference by Hohhmayer et al.)

  • Bundle branch reentrant VT is usually seen in nonischemic dilated cardiomyopathy (see below).

  • Brugada syndrome characterized with RBBB and ST elevation in leads V1-3 (Figure 4).

  • AIVR is “slow VT” and is seen in the periinfarction period and is defined as a VT rate <100 bpm. At times it may compete with the sinus beats, and fusion (conducted sinus beat and VT beat capturing the ventricle) will occur (Figure 5).

  • Ventricular fibrillation is an extremely fast and chaotic rhythm and should not be mistaken. Death is imminent. Make sure that there is no artifact in the trace. In this case, close observation will show the QRSs marching through the trace and the patient feels fine (Figure 6). Early repolarization in the inferior and lateral ECG leads can lead to ventricular fibrillation and sudden cardiac death.

  • Torsades de pointes is a polymorphic VT (Figure 7) and is often seen in the congenital or acquired long Q–T syndromes. Other forms of polymorphic VT with normal Q–T include catecholaminergic polymorphic ventricular tachycardia (CPVT) (genetic defect in the ryanodine receptor of the sarcoplasmic reticulum), ischemia, or digitalis intoxication.

  • Short Q–T (Figure 8) syndrome is a genetic condition and has been associated with sudden cardiac death.

Figure 2.

Red showing epsilon wave in ARVD.

Figure 3.

Right ventricular outflow track.

Figure 4.

Brugada pattern.

Figure 5.

AVIR: fourth QRS is fused; fifth and tenth QRSs are pure sinus beats.

Figure 6.

Note the QRSs are marching through (red arrows)the artifacts simulating VT?VF

Figure 7.

Torsades de Pointes.

Figure 8.

Short QT.

A. History Part I: Pattern Recognition:

Symptoms of ventricular arrhythmias may vary, depending on the frequency, rate, duration, and therapies. The patient may complain of palpitations, dizziness, or syncope.

At times, the post-PVC beat will be felt (e.g., fullness in throat) due to the enhanced contraction. With respect to therapies, for example, beta-blockers are not very good for suppressing PVCs, but the patient may feel less of a burden. Ventricular arrhythmias may or may not be associated with heart disease.

However, sustained monomorphic VT offers a clue to the presence of coronary heart disease. It is reasonable to think, therefore, that most ventricular arrhythmias are often associated with structural heart disease.

B. History Part 2: Prevalence:

All types of ventricular arrhythmias may occur in normal and abnormal hearts. It is imperative to “work-up” the patient for the presence or absence of structural heart disease.

The following clues may help:

  • Frequent PVCs in the young may be associated with mitral valve prolapse, but can also be seen in normal hearts. Its density will increase with age.

  • Environmental factors such as use of “hard” drugs and alcohol may provoke these arrhythmias. Of note, cardiotonic agents (oral and IV) may aggravate ventricular arrhythmias.

  • Nonsustained and sustained VT could be an expression of coronary artery disease or a nonischemic cardiomyopathy. A special type of VT in nonischemic cardiomyopathy is bundle branch reentry (see below).

  • Verapamil-sensitive VT may be brought on by exercise.

  • ARVC is genetic and inherited as an autosomal dominant trait with variable penetrance.

  • Torsades de pointes is associated with long Q–T and maybe acquired (e.g., drugs) or inherited. In acquired long Q–T syndrome, women are at a higher risk of developing torsades.

  • Short Q–T syndrome is genetic.

C. History Part 3: Competing diagnoses that can mimic Ventricular Arrhythmia.

The most important differential from ventricular arrhythmias is a supraventricular rhythm with aberrancy. At times it becomes very difficult to distinguish VT from SVT with aberrancy.

The following clues will help:

Supraventricular rhythmias with aberrancy are identified with P waves before each QRS. However, the Ps must be positive in leads 2, 3, and AVF suggesting a sinus origin. If the Ps are negative, then all bets are off, since VT can cause retrograde 1:1 conduction or even retrograde Wenckebach.

The clues to VT are applied as above. Atypical atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), and ectopic atrial tachycardia (EAT) with aberrancy are preceded by negative P waves. In typical AVNRT, the P wave is usually buried in the QRS and cannot be seen.

In AF, aberrancy is not uncommon, especially when the ventricular rate is fast. The early wide QRS beats are usually seen after a long cycle. This is called the Ashman’s phenomenon. This occurs because the long cycle sets up slower conduction in the bundles, with the right being lazier than the left. The next early beat will be distorted (aberrancy), and usually with a right bundle pattern.

In hyperkalemia, the QRS is wide, the Ts are peaked and the P waves are absent. This is still sinus, but you cannot see the Ps. Class 1 drugs, such as flecainide and propafenone, may widen the QRS.

Look for P waves (sinus, atrial flutter) that could be the driver of the QRS. At times these drugs can cause proarrhythmia and VT is very possible. Antidromic Wolff Parkinson White (WPW) tachycardia will present with a wide QRS. Again, look for P waves. Look for delta waves on the baseline ECG.

D. Physical Examination Findings.

Check the pulse. Classify as fast or slow. Is it regular with a regular irregularity. Is it irregular irregular? In AF, there might be a discrepancy between the apical and radial pulses.

Check blood pressure. If low, it does not help to distinguish VT from SVT. In VT, with sinus rhythm, you may see occasionally cannon waves in the neck. If there is AV dissociation, fusion beats, or capture beats, S1 may vary.

E. What diagnostic tests should be performed?

The ECG is a classic test, and most often the arrhythmia can be easily diagnosed. If a ventricular arrhythmia is diagnosed, the presence of heart disease must be excluded.

The ECG can approximate the site of the PVCs. Those originating from the LV will show a right bundle branch block pattern, and those from the right ventricle will show a left bundle branch block pattern.

The axis will determine from which site of the ventricle-inferior axis comes from the base of the heart, while a superior axis will originate from the apex (see above). Histories and physicals are essential. A Holter recording will quantify the density of the arrhythmia over a 24-hour period.

Keep in mind that high-density ventricular arrhythmias may occasionally lead to a cardiomyopathy. An echocardiogram is often helpful. If VT is present, try to identify the origin—RVOT, LVOT, RV, LV, LV septum. The age of the patient, history of coronary artery disease (CAD), and family history will help. At times, there will be a need for coronary angiography and/or EP studies.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

  • Electrolytes are often very helpful. Check the potassium and magnesium. Hypokalemia and hypomagnesemia can be risks for torsades.

  • Check the patient to rule in or out heart failure—distended neck veins, rales, edema, etc.

  • Troponins will diagnose injury. Keep in mind that with periinfarction VT or VF, while in-hospital mortality is higher, the long-term prognosis is good, and there is no need to implant the implantable cardioverter-defibrillator (ICD) (see Section III).

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

  • A simple radiograph can be helpful. Look for cardiomegaly, heart failure, left ventricular hypertrophy (LVH), and calcification of the valves.

  • An echocardiogram can be very helpful to determine: chamber size, valve pathology, segmental wall abnormalities, LVH, septal hypertrophy, and function (ejection fraction).

  • Magnetic resonance imaging (MRI) at times can better define structure and function, including indications of the presence of infiltrative diseases such as arrhythmogenic right ventricular dysplasia (ARVD).

  • Coronary angiography or perfusion imaging is appropriate to include/exclude the presence of CAD.

  • Electrophysiology (EP) studies are necessary for diagnostic and therapeutic reasons, especially in hypertrophic cardiomyopathy (HCM) or even Brugada syndrome. At times, patients with CAD, NSVT episodes, and syncope may need to be studied (see below). In the event of an EP-induced sustained ventricular arrhythmia, an ICD may be considered, especially in HCM.

III. Management.

Benign PVCs (absence of heart disease), if symptomatic may be treated with a beta-blocker. However, if the patient continues to complain, even after reassurance, there might be a need for flecainide or propafenone.

If the PVCs are originating from the RVOT/LVOT and there is related cardiomyopathy, ablation might be considered, since this might be curative. The data on defining PVC burden in this condition is lacking. The thought here is that very “frequent” PVCs (burden of 10% to 20%) might compromise ventricular function over time and that suppression either by drug or ablation could be protective.

This is especially true for RVOT/LVOT PVCs. Recently, with respect to the PVCs, the wider the QRS or originating form of the epicardium, the more likely the LV function will recover. This is independent of PVC density.

While NSVT is not predictive over ejection fraction (EF) or high-density PVCs, it may be predictive of future events in HCM, and implantation of an ICD might be warranted especially in the presence of syncope and positive family history for sudden death.

Presence of sustained VT (depending on etiology), comorbidities, and patients’ input, will all be important in making good decisions. Here are some ideas:

Sustained hemodynamically compromised monomorphic VT due to CAD is best treated with an ICD, assuming that revascularization is not an option. Make sure that there are no correctible conditions, such as electrolyte imbalances, ischemia, periinfarction (24-48 hours), or catheter induced.

The ICD will not prevent recurrent arrhythmia episodes, thus amiodarone plus a beta-blocker will prevent ICD shocks. At times, ablation of the VT might be necessary.

  • RVOT/LVOT—ablation offers good protection and without the need for antiarrhythmic drugs

  • ARVC-ICD if symptomatic bundle branch reentry VT in nonischemic cardiomyopathy—ablation of the right bundle (Figure 9).

  • VF or aborted cardiac arrest in the absence of an acute MI is an indication for an ICD.

Figure 9.

A PVC is blocked retrogradely in the RBB, goes transseptally to the LBB,going up retrogradely and then antegradely down the RBB creating a continuous loop and a sustained bundle branch reentrant ventricular tachycardia.

Class I indications for an ICD include: Primary prevention for patients at risk of sudden cardiac death (VT/VF) on optimal medical therapy (BBs, angiotensin-converting enzyme inhibitors [ACEIs]) with prior MI (greater than 40 days) and LVEF <35%, and patients with a cardiomyopathy and functional Class II and III. Certain patients with HCM, Brugada, and Long Q–T syndromes will also qualify for this therapy. Secondary prevention-aborted cardiac arrest, and hemodynamically compromising sustained VT.

A. Immediate management.

Sustained VT with hemodynamic embarrassment requires immediate attention. Electrical cardioversion (EC) is required. If the patient is awake, alert with “good” blood pressure, IV drugs (e.g., lidocaine), or even synchronized EC after sedation are options.

Torsades is often self-limiting, the reason being that the tachycardia itself will lead to termination.

We see this response by increasing the heart rate with either Isuprel or pacing. Magnesium supplement is often used and can be helpful in terminating or preventing torsades episodes. The cause of the torsades must be determined-acquired, long Q–T drugs (the list is quite long and includes sotalol, dofetilide, methadone, or a congenital condition), long Q–T 1-3 being most common. The offending drug must be discontinued.

In the congenital variety, history and ECGs might offer clues. Beta-blockers can offer some protection in long Q–T 1 and 2, and mexiletine in long Q–T 3. In the presence of syncope, the ICD is preferred (Table 1).

Table I.n

B. Physical Examination Tips to Guide Management.

Bradycardia, if tolerated, is a good measure of beta-blocker activity and is considered a good prognostic sign in heart failure and/or in patients with prior MIs. Other physical findings may not be helpful to measure a therapeutic response.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Electrolyte imbalances are arrhythmogenic and should be checked for periodically. Genetic testing may be necessary at times to distinguish the types of arrhythmogenic cardiomyopathies (e.g., Brugada, inherited long and short Q–T, ARVC, CPVT).

D. Long-term management.

Drugs that have been associated with reduction of sudden cardiac death include ASA, beta-blocker, ACEI, spironolactone, and PUFA (polyunsaturated fatty acids). While it is assumed that sudden death is arrhythmic death, there may not be a correlation.

Amiodarone and sotalol can prevent ICD inappropriate and appropriate shocks.

Nonpharmacologic therapies to reduce ventricular arrhythmia include Bi-V pacing, ICD, left ventricular assist device (LVAD), coronary artery bypass graft (CABG), and transplantation.

E. Common Pitfalls and Side-Effects of Management

Drugs are very difficult to take on a regular basis. Antiarrhythmic agents, if successful, must not be missed. Keep in mind that antiarrhythmic agents can be proarrhythmic in that they can worsen the arrhythmia.

For example, flecainide and propafenone may provoke sustained VT, and sotalol may cause torsades. Beta-blockers are very useful, but not without side effects such as symptomatic bradycardia, heart block, and fatigue.

Every effort should be made to make sure that the patient is compliant with such medicines. Amiodarone has numerous side effects, such as liver, thyroid, and lung toxicities, but it can suppress ICD shocks that may impair quality of life.

At all cost, every effort should be made to reach doses achieved in large clinical trials with positive outcomes (see Table 1).

IV. Management with Co-Morbidities

Diabetes—statins, ACEIs, and angiotensin receptor blockers (ARBs) are very useful and may affect outcomes in this condition.

Hypertension—ACEIs, ARBs, beta-blockers are preferred especially in those with renal disease, and post MI and/or heart failure

There are certain limitations of mandatory drugs:

  • Nonselective beta-blockers should be avoided in patients with bronchospasm

  • ASA in the bleeding patient

  • Spironolatone in renal failure ACEIs and ARBs in acute renal failure

  • Calcium channel blockers in systolic heart failure

  • Stop smoking if applicable.

  • Alcohol in moderation. Excess alcohol can be toxic to the myocardium and may provoke cardiac arrhythmias (especially AF).

  • Hard drugs such as cocaine may provoke acute coronary syndrome with vasospasm of the coronaries.

  • Excessive caffeine, in some susceptible patients, may initiate AF.

  • Calorie restriction

  • Keep calm—anxiety is detrimental. Data on yoga and meditation might suggest beneficial effects.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Check for symptoms of dizziness, palpitation, shortness of breath, chest pain, and ICD shocks if applicable. ICD shocks may worsen the patient’s quality of life. Thus check for depression.

A rare shock may not warrant additional therapies, but frequent multiple shocks is an indication for antiarrhythmic therapy, such as amiodarone, sotalol, and beta-blockers. Check pulse, blood pressure, weight gain, leg swelling, and for excessive sweating.

B. What's the Evidence for specific management and treatment recommendations?

  • PVCs, if symptomatic, can be successfully treated with beta-blockers or with flecainide or propafenone in the absence of structural heart disease.

  • NSVT may not be predictive over high PVC counts (>10/hr). However, in the MUSTT trial, EP induced sustained VT in the presence of low EF, the ICD therapy will be beneficial.

  • Sustained VT often requires ICD therapy and /or revascularization. Ablation is an option in RVOT/LVOT, bundle branch reentry VT.

  • Amiodarone is perhaps the most potent antiarrhythmic in suppressing all types ventricular arrhythmia episodes.

  • IV verapamil can be useful in verapamil sensitive VT. In long-term therapy, short acting verapamil (tid dosing) is preferred, since the l-enantiomer (antiarrhythmic property) may escape the liver metabolism. With sustained release preparations, the l-enantiomer is removed with first pass metabolism. Ablation is preferred.

  • Torsades, if acquired, is mandatory to omit the offending drug that might have prolonged the Q–T interval. If congenital, beta-blocker (types 1 and 2) and mexiletine (type 3), in addition to ICD if applicable, can offer protection. VF or aborted cardiac arrest is an indication for an ICD barring comorbidities.


Ruskin, J. “Ventricular extrasystoles in healthy subjects”. N Eng J Med. vol. 312. 1985. pp. 238(PVCs can occur in structurally normal hearts and are often benign.)

Chugh, SS. “First evidence of premature ventricular contraction complex-induced cardiomyopathy: a potentially reversible cause of heart failure”. JCE. vol. 11. 2000. pp. 328-9. (Since ventricular dyssynchrony can lead to LV dysfunction, high-density PVCs may be easily ablated without the need for drugs.)

Ryden, L. “A double blind trial of metoprolol in acute myocardial infarction: effects on ventricular arrhythmia”. N Eng J Med. vol. 308. 1983. pp. 614-8. (While PVCs may carry a risk of sudden cardiac death in the post-MI model or heart failure, beta-blockers without suppressing PVCs can prevent sudden death.)

Singh, SN. “Prevelance of NSVT in patients with PVCs and heart failure treated with vasodilator therapy”. JACC. vol. 32. 1998. pp. 942-7. (With high-density PVCs, NSVT does not seem to be an independent risk for sudden cardiac death.)

Singh, SN. “Survival trial of antiarrhythmic therapy in congestive heart failure”. NEJM. vol. 333. 1995. pp. 77-82. (Amiodarone in heart failure patients is very effective in suppressing PVCs and episodes of NSVT, but without a change in total mortality.)

Buxton, AE. “Randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigation”. NEJM. vol. 341. 1999. pp. 1882-90. (In patients with NSVT,CAD, and with EP-induced sustained VT will benefit from an ICD. However, it will be helpful to stratify by EF and bypass the EP testing.)

Haissaguerre, M. “Sudden cardiac death associated with early repolarization”. NEJM. vol. 358. 2008. pp. 2016-23. (It is very difficult to determine who will have sudden death as early repolarization is common and often ignored. A history of syncope; family history of sudden cardiac death, especially in the young; and early repolarization changes in the inferolateral leads may offer clues to high-risk patients.)

Roden, D. “Long Q–T syndrome”. NEJM. vol. 358. 2008. pp. 169-76. (This paper offers clues on how to recognize and treat patients with long Q–T syndromes.)

Gussak, I. “Idiopathic short QT interval: a new clinical syndrome”. Cardiology. vol. 94. 2000. pp. 99-102. (This is a rare genetic condition. Quinidine is perhaps the best drug to prolong the Q–T and may offer clinical benefit.)

Brugada, P. “Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report”. JACC. vol. 20. 1992. pp. 1391(This is a genetic condition with channelopathies and should be treated aggressively. The patients at times need to be challenged with antiarrhythmic drugs to show the Brugada pattern of ST and RBBB in V1.)

DiBase, L. “Antiarrhythmic effect of reverse remodeling induced by resynchronization therapy”. JACC. vol. 52. 2008. pp. 1442-9. (There is now evidence that reverse remodeling of the LV, may decrease ventricular arrhythmia density.)

Stevenson, WG. “Multicenter thermacool VT ablation trial investigators”. Circulation. vol. 118. 2008. pp. 2773-82. (VT therapy at times may require ablation especially in those who have failed drug therapy.)

Hohhmayer, KS. “Electrocardiographic comparison of ventricular arrhythmias in patients with arrhythmogenic right ventricular cardiomyopathy and right ventricular outflow tract tachycardia”. JACC. vol. 58. 2011. pp. 831-838. (This paper includes the EKG patterns of both conditions and is quite helpful in distinguishing one from the other.)

C. DRG Codes and Expected Length of Stay.