Ventricular Tachycardia – Classification

Ventricular Tachycardia – Classification

Ventricular tachycardia is a common arrhythmia. The manifestations include mild symptoms of palpitation to sudden death. In next few blog posts, we will try to understand the basics of ventricular tachycardia/fibrillation and we will discuss management of these arrhythmias.


Ventricular arrhythmias are defined as arrhythmias that originate below the bifurcation of His bundle, in the specialized conduction system, the ventricular muscle, or in combination of both tissues.


Ventricular Tachycardia ECG

(Image created by Karthik Sheka, M.D. [CC BY-SA 2.5 (], via Wikimedia Commons)

There are different classifications of ventricular arrhythmias, according to their duration, morphology of QRS complexes, and clinical characteristics.

Classification According to Duration

(1) Premature ventricular complexes (PVC): isolated complexes originating from the His-Purkinje system or ventricular myocardium.
(2) VT: 3 or more consecutive QRS complexes at a rate greater than 100 beats per minute.
(3) Nonsustained VT: VT that terminates spontaneously within 30 seconds.
(4) Sustained VT: continuous VT lasting for ≥30 seconds or that requires an intervention for termination (such as cardioversion).

Classification According to Morphology of QRS Complexes

(1) Monomorphic VT: VT that has a similar QRS configuration from beat to beat. Some variability in QRS morphology at initiation is not uncommon.
(2) Multiple monomorphic VT: more than one morphologically distinct monomorphic VT, occurring as different episodes or induced at different times.
(3) Polymorphic VT: VT that has a continuously changing QRS configuration indicating a changing ventricular activation sequence.
(4) Pleomorphic VT: VT that has more than one morphologically distinct QRS complex occurring during the same episode of VT, but the QRS is not continuously changing.
(5) Ventricular flutter: rapid VT that has a sinusoidal QRS configuration that prevents identification of the QRS morphology.
(6) VF: ventricular tachyarrhythmia that has a totally chaotic

Classification According to Clinical Characteristics

(1) Clinical VT: VT that has occurred spontaneously based on analysis of 12-lead ECG QRS morphology and rate.
(2) Hemodynamically unstable VT: VT that causes hemodynamic compromise requiring prompt termination.
(3) Incessant VT: continuous sustained VT that recurs immediately despite repeated spontaneous or therapeutic termination.
(4) Repetitive monomorphic VT: continuously repeating episodes of self-terminating nonsustained VT.
(5) VT storm: 3 or more separate episodes of sustained VT within 24 hours, each requiring termination by an intervention.
(6) Unmappable VT: VT that does not allow interrogation of multiple sites to define the activation sequence or perform entrainment mapping. It may be due to hemodynamic
intolerance that necessitates immediate VT termination, spontaneous, or pacing-induced transition to other morphologies of VT, or repeated termination during mapping.

In the next post, we will discuss clinical features and ECG features.


Primary prevention ICD in Nonischemic cardiomyopathy

There is a recent online first article in NEJM  ( Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure – DANISH Study). The study is summarized below:


The benefit of an implantable cardioverter–defibrillator (ICD) in patients with symptomatic systolic heart failure caused by coronary artery disease has been well documented. However, the evidence for a benefit of prophylactic ICDs in patients with systolic heart failure that is not due to coronary artery disease has been based primarily on subgroup analyses. The management of heart failure has improved since the landmark ICD trials, and many patients now receive cardiac resynchronization therapy (CRT).


In a randomized, controlled trial, 556 patients with symptomatic systolic heart failure (left ventricular ejection fraction, ≤35%) not caused by coronary artery disease were assigned to receive an ICD, and 560 patients were assigned to receive usual clinical care (control group). In both groups, 58% of the patients received CRT. The primary outcome of the trial was death from any cause. The secondary outcomes were sudden cardiac death and cardiovascular death.


After a median follow-up period of 67.6 months, the primary outcome had occurred in 120 patients (21.6%) in the ICD group and in 131 patients (23.4%) in the control group (hazard ratio, 0.87; 95% confidence interval [CI], 0.68 to 1.12; P=0.28). Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005). Device infection occurred in 27 patients (4.9%) in the ICD group and in 20 patients (3.6%) in the control group (P=0.29).


In this trial, prophylactic ICD implantation in patients with symptomatic systolic heart failure not caused by coronary artery disease was not associated with a significantly lower long-term rate of death from any cause than was usual clinical care.

This is the summary of the study. This study proves the point that primary prevention ICD doesn’t reduce the all cause mortality. But there are few points to consider in this very well designed study:

  1. SCD was the cause of death in 24 out of 120 (20%) total deaths in the ICD group. SCD was the cause of death in 46 out of 131 (35%) total deaths in the non-ICD (usual care group). So that means majority of mortality even in the non-ICD usual care group are due to non arrhythmic causes.
  2. The number of non-arrhythmic mortality in the ICD group is 96 out of total of 120 (80%) and in the non-ICD group is 65%.
  3. The question still remains that – How is a device (i.e. ICD) which prevents arrhythmic deaths, is expected to reduce the All Cause Mortality (the primary end point of this study) when the majority of deaths are due to non-arrhythmic causes.
  4. When considering the sudden cardiac deaths, ICD definitely reduced the mortality [Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005)].

This study is a landmark study. It shows that the present indications for primary prevention ICD in non-ischemic cardiomyopathy are likely  include patients who may not after all benefit from a primary prevention ICD. It further shows that ICD is effective in preventing SCD in non-ischemic cardiomyopathy.

So to conclude this important study shows that we need to find markers of SCD in non-ischemic cardiomyopathy so that ICD implantation can be more effectively done in patients who are at high risk of SCD.

(Disclaimer: The views expressed are entirely personal of the author of this blog and are aimed towards an educational discussion on the study. These opinions are not meant for application in medical practice and are for the purpose of discussion only)

Keywords: Electrophysiology, Cardiomyopathy, Implantable cardioverter defibrillator, Sudden cardiac death

Arrhythmia or Disorders of Heart Rhythm

Arrhythmias or disorders of heart rhythm are a group of diseases characterized by abnormality of heart beat. Our heart is expected to beat in a certain way. In an adult individual the heart normally beats 60 t0 100 times per minute, in a regular manner (that means a nearly constant interval between two beats ). There are some normal variations, like in children the heart beat is faster, in some healthy persons and trained athelets the heart beat can be slower, during sleep the heart beat is normally slower.

Definition of Arrhythmia:

Arrhythmia is defined as any deviation from this normal pattern of heart beat.

What are the types of Arrhythmia?

Heart rhythm disorders are basically of two types. When the Heart rate is abnormally high it is called TACHYCARDIA. When the heart rate is abnormally slow it is called BRADYCARDIA. There can be irregular heart beats even if the heart rate is between 60-100, those cases are also Arrhythmic.

What is the relation of arrhythmias to other heart diseases?

Arrhythmias can be divided into two types based on heart diseases

  1. Arrhythmias occurring in persons having no underlying structural heart disease are called- IDIOPATHIC ARRHYTHIMAS
  2. Arrhythmia also arise in persons who have underlying structural heart diseases.

What are the symptoms of Arrhythmia?

Arrhythmias due to slow heart rate (Bradycardia) commonly cause

  1. Lethargy
  2. Fatigue
  3. Palpitation
  4. Light headedness
  5. Syncope (Transient loss of consciousness followed by full recovery)
  6. Sudden death

Arrhythmias due to fast heart rate (Tachycardia) commonly produce symptoms of

  1. Palpitation
  2. Faintness and light headedness
  3. Syncope (Transient loss of consciousness followed by full recovery)
  4. Sudden death
  5. Reduced pumping capacity of heart and related symptoms
  6. Some arrhythmias like atrial fibrillation can produce abnormal clotting of blood inside heart which can migrate to brain to cause stroke and paralysis.

How serious are Arrhythmias?

Some arrhythmias are benign and non life threatening, but they cause troublesome symptoms of palpitation and skipped beats.

Some arrhythmias are life threatening and can cause even sudden death. It all depends on the origin and type of arrhythmias and any other underlying heart disease.

How to diagnose arrhythmia?

Arrhythmias are commonly diagnosed by

  • ECG
  • Holter monitoring
  • Sometimes long term monitoring like – event recorders, loop recorders etc.
  • In some case Cardiac Electrophysiological study is required to diagnose a rhythm disorder.

What are the treatments available?

  1. Some transient arrhythmias terminate on their own and don’t need any specific therapy
  2. Underlying cause needs to be treated like- drugs, electrolyte disturbances, etc
  3. Medicines are usually the first line treatment
  4. Catheter Ablation: It is a procedure done in cardiac cathlab where an arrhythmia is ablated commonly by application of radiofrequency energy inside the heart. It is a safe procedure with prospect for complete cure of the arrhythmia.








Cardiology MCQ – 14.05.2016

What is the most probable site of origin of the tachycardia in a patient with structurally normal heart ?

MA VT epicardial1. Right ventricular outflow tract

2. Mitral annular VT

3. Tricuspid annulus

4. Idiopathic left fascicular VT

Atrial septal defect and Pregnancy – Patient Information

What is atrial septal defect (ASD)

Atrial Septal defect is an abnormal communication between the upper two chambers of the heart namely left atrium and right atrium. Normally the left and right atrium are separated by the interatrial septum. So in atrial septal defect (ASD)  a part of the interatrial septum is missing. See the image below

Atrial Septal Defect

(Source :

In patients with ASD there is mixing of oxygenated blood of left side with venous blood on the right side.

Pregnancy Issues:

Patients with even a large unrepaired secundum atrial septal defect usually tolerate pregnancy without complications. In cases where the ASD has been closed either by surgery or by device, the course of pregnancy is similar to a normal female without heart disease, except when there are preexisting problems with heart rhythm or pulmonary hypertension.


The complications include

1- Disorders of heart rhythm – e.g. Atrial fibrillation

2. Pulmonary hypertension – where there is increased pressure in the blood vessels of the lung.

3. Paradoxical embolism – Sometimes blood clots formed in the leg veins (increased chances in pregnant females) can pass through the defect in the heart and get lodged in the brain and can cause stroke .

  1. Elective closure of ASD before contemplating pregnancy is advisable
  2. Meticulous attention should be paid to the maternal leg veins, particularly during peridelivery, because deep venous thrombosis could precipitate a paradoxical embolus and stroke.
  3. In case of any complication like atrial fibrillation, pulmonary hypertension, close follow-up with a cardiologist is recommended.
Keywords: Congenital heart disease, pregnancy and heart disease, Patient information, atrial septal defect.

Xray chest showing thickened and calcified pericardium

Eggshell calcification of the heart in constrictive pericarditis

 Eggshell calcification of the heart in constrictive pericarditis

Rajesh Vijayvergiya, Ramalingam Vadivelu, Sachin Mahajan, Sandeep S Rana, Manphool Singhal

World J Cardiol 2015 September 26; 7(9): 579-582

43/M presented with dyspnoea on exertion NYHA class III since 6 months. No other positive history.

On Examination:

HR-100/min  BP- 100/64   JVP- elevated, 18 cm; prominent X and Y descent

CVS: S1 S2 normal, Pericardial knock +

CXR : Calcified pericardium seen. See image

Echo: Thick, calcified pericardium.   > 25%  respiratory variation of mitral inflow velocities . Significant LV diastolic dysfunction









post bt shunt seroma

Interesting image- Post BT shunt seroma- a rare complication

Indian Heart J. 2014 Mar-Apr;66(2):227-30.

Post Blalock-Taussig shunt mediastinal mass – a single shadow with two different destinies

Rohit MK1, Vadivelu R2, Khandelwal N3, Krishna S3.

One of the rare complications following BT shunt surgery is seroma formation. It usually is benign and  x ray chest will reveal a mediatinal mass (left upper). CT scan usually confirms the diagnosis. Usually managed conservatively.

Image description:

Axial contrast chest CT obtained in a helical mode. The sagittal oblique maximal intensity projection image shows a small hypodense lesion of fluid attenuation seen adjacent to the BT shunt. No calcification, enhancement, septae, air foci or solid component was seen. Features are consistent with a post operative seroma. Thin long arrow points BT shunt. Broader, short arrow points seroma


dilated aortic root

When to intervene in patients with bicuspid aortic valve and dilated aortic root or ascending aorta

Circulation – December 4, 2015

Surgery for Aortic Dilatation in Patients with Bicuspid Aortic Valves:

 A Statement of Clarification from the American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines

Intervention in Patients with BAV and Dilatation of the Aortic Root (Sinuses) or Ascending Aorta:

  1. Operative intervention to repair or replace the aortic root (sinuses) or replace the ascending aorta is indicated in asymptomatic patients with BAV if the diameter of the aortic root or ascending aorta is 5 cm or greater


  1. Operative intervention to repair or replace the aortic root (sinuses) or replace the ascending aorta is reasonable in asymptomatic patients with BAV if the diameter of the aortic root or ascending aorta is 0 cm or greater and an additional risk factor for dissection is present (eg, family history of aortic dissection or aortic growth rate ≥0.5 cm per year) or if the patient is at low surgical risk and the surgery is performed by an experienced aortic surgical team in a center with established expertise in these procedures


  1. Replacement of the ascending aorta is reasonable in patients with BAV undergoing AVR because of severe aortic stenosis or aortic regurgitation when the diameter of the ascending aorta is greater than 4.5 cm
Reversal of factor X a inhibition

New Drug : Andexanet Alfa- Reversal agent for Factor X a inhibitors

NEJM- Nov 2015 – ANNEXA-A and ANNEXA-R ClinicalTrials

As of now the major limiting factor with the use of novel anticoagulants is the absence of  reversal agents in case of bleeding complications.

To find a solution to this problem, a new drug has been recently tested in ANNEXA-A and ANNEXA-R trials. Andexanet alfa, a new drug designed to reverse factor X a inhibition.

In the trial, Andexanet alfa was given to apixaban and rivoraxaban administrated healthy volunteers. Within minutes of administration anti factor Xa activity was reduced by more than 90% without any toxic or serious thrombotic effects.

Approach to the management of Venous thromboembolism

Step 1 :Confirm PTE or DVT diagnosis

Step 2: Look for contraindications for full dose anticoagulation. If contraindications exist then insert IVC filter.

Step 3 : If no contraindication then look for impending venous gangrene (in case of DVT) or cardiopulmonary collapse (cardiogenic shock/ RV dysfunction in case of PTE). If yes then start thrombolysis

Thrombolysis for DVT:

Indications : Impending venous gangrene, symptom duration < 14 days and low risk of bleeding

Mode : a)Catheter directed thrombolysis (CDT) : Fluroscopy guided placement of multiside holed catheter (pigtail) into the thrombus segment and infusing alteplase for 1-3 days at a rate of 0.5 mg to 3 mg/hour (50 mg diluted in 50 ml of NS). CDT is superior to systemic anticoagulation alone because of reduced post thrombotic syndrome and reduced bleeding complications

b)Pharmacomechanical Catheter directed thrombolysis (PCDT)

PCDT uses either the “Power Pulse” or “isolated thrombolysis” techniques. Power Pulse employs the AngioJet rheolytic thrombectomy system (Bayer, Warrendale, PA) to deliver and disperse the thrombolytic agent by a powerful pulse-spray injection. After bathing the clot in the thrombolytic agent, the AngioJet catheter aspirates the softened thrombus fragments. Isolated thrombolysis uses the Trellis peripheral infusion system (Covidien, Mansfield, MA) to deliver the thrombolytic agent directly into the clot. The agent is then circulated within the clot by an oscillating wire.

Advantage of PCDT over CDT : Reduced dose and infusion duration of alteplase thereby reducing bleeding complications and better efficacy

Thrombolysis for PTE :

For PTE there is insufficient evidence to recommend thrombolysis via a pulmonary artery catheter rather than systemic thrombolysis

Systemic thrombolysis dose: Alteplase 100 mg (10 mg as iv bolus over 10 min f/b 90 mg in 100 ml of NS infused over 2 hours)

Step 4

If there is no evidence of impending gangrene or cardiopulmonary collapse then initiate systemic anticoagulation

Phases of anticoagulation treatment:

Initial phase0 to 10 days:

IV or SC unfractionated heparin/LMWH/Fondaparinux/Rivaroxaban/Apixaban

Long term phase- 10 days to 3 months

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)


Extended phase-3 months to indefinite 

Indictions for extended therapy- 1.unprovoked/recurrent VTE    2. Malignancy related VTE

Drugs :

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)


Newer agents : Rivaroxaban(15 mg bd)/Apixaban(10 mg bd)/Edoxaban/Dabigatran(110 or 150 mg bd)

Pros- No need for INR monitoring, non-inferior or slightly efficacious then warfarin/acitrom, lesser major bleeding rates

cons- costlier, lesser availability especially in developing countries and no specific reversal agents