Michael cvbf Naushad

This chapter deals with ventricular tachycardia from a clinical perspective, with emphasis on ECG diagnosis, definitions, management and clinical characteristics. Ventricular tachycardia is a highly nuanced arrhythmia which originates in the ventricles. A wide range of conditions may cause ventricular tachycardia and the ECG is as nuanced as are those conditions. Regardless of etiology and ECG, ventricular tachycardia is always a potentially life-threatening arrhythmia which requires immediate attention. The ventricular rate is typically very high (100–250 beats per minute) and cardiac output is affected (i.e reduced) in virtually all cases. Ventricular tachycardia cause immense strain on the ventricular myocardium, simultaneously as the cause of the arrhythmia already affects cellular function. This results in electrical instability which explains why ventricular tachycardia may progress to ventricular fibrillation. Left untreated, ventricular fibrillation leads to asystole and cardiac arrest. All health care providers, regardless of profession, must be able to diagnose ventricular tachycardia.

Patients with ventricular tachycardia almost invariably have significant underlying heart disease. The most common causes are coronary heart disease (acute coronary syndromes or ischemic heart disease), heart failure, cardiomyopathy (dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy), valvular disease. Less common causes are arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), Brugada syndrome, long QT syndrome, sarcoidosis, Prinzmetal’s angina (coronary vasospasm), electrolyte disorders, congenital heart disease and catecholamine induced ventricular tachycardia.

The vast majority of patients with ventricular tachycardia either have coronary artery disease (ischemic heart disease), heart failure, cardiomyopathy or valvular heart disease. In these populations one of the strongest predictors of sudden cardiac death is left ventricular function. Individuals with reduced left ventricular function (e.g defined as ejection fraction <40 %) are at high risk of sudden cardiac arrest.

Ventricular tachycardia may be classified as idiopathic if no cause can be identified. Idiopathic ventricular tachycardia has a more favorable prognosis, as compared with other forms of ventricular tachycardia.

Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. As mentioned above VT causes hemodynamic compromise. The rapid ventricular rate, which may be accompanied by already impaired ventricular function, does not allow for adequate filling of the ventricles, which results in reduced stroke volume and reduced cardiac output.

Most patients experience presyncope or syncope if the arrhythmia is sustained. In its fulminant course, VT degenerates to ventricular fibrillation, which then degenerates into asystole and cardiac arrest. Importantly, the progress from VT to cardiac arrest may be aborted either spontaneously or by means of treatment. Interestingly, treatment of VT is considered one of the greatest advances in cardiology. Until 1961, patients with acute myocardial infarction were placed in beds located far away from physicians’ and nurses’ stations in order to not disturb the patients’ rest. It was believed that the mere presence of physicians and nurses caused harmful stress. Approximately 30% of patients died in the hospital and fatal tachyarrhythmias was presumably the leading cause. Animal studies conducted in the late 1950s, 1960 and 1961 showed that VT could be terminated by delivering an electrical shock. This prompted physicians to construct coronary care units, in which all patients with acute myocardial infarction were monitored with continuous ECG and ventricular tachyarrhythmias were handled by means of immediate resuscitation and defibrillation.

Acute coronary syndromes are subdivided into unstable angina (UA), ST elevation myocardial infarction (STEMI) and non ST elevation myocardial infarction (NSTEMI). The risk of VT is high in these conditions. Moreover, the risk is highly time-dependent, being highest in the hyperacute phase (the first minutes to hours after symptom onset). The vast majority of individuals who die in the acute phase of myocardial infarction actually die from ventricular tachyarrhythmias. Death due to pumping failure (i.e cardiogenic shock) is less common. Because the risk is highest in the first minutes to hours, most deaths occur outside of the hospital. The risk of VT (and thus ventricular fibrillation) diminishes gradually as time elapses. In addition to time, the major determinant of VT is the extent of the ischemia/infarction. The larger the ischemic are the greater the risk of arrhythmias.

The ECG allows for subclassification of ventricular tachycardia. The discussion below may be perceived as advanced, but the reader should know that it is not required that all clinicians be able to classify ventricular tachycardias; merely being able to recognize it is sufficient. Therefore, the purpose of the discussion below is to present the reader with several types of ventricular tachycardia just for reference.

Ventricular tachycardia with duration <30 seconds is classified as non-sustained ventricular tachycardia. Sustained ventricular tachycardia has duration >30 seconds.

In monomorphic ventricular tachycardia all QRS complexes display the same morphology (minor differences are allowed). This indicates that the impulses originate in the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease etc) monomorphic ventricular tachycardia is typically caused by re-entry. Refer to Figure 1.

The Purkinje fibers in the interventricular septum appear to have an important role in ventricular tachycardia among patients with coronary heart disease. These Purkinje fibers appear to be highly arrhythmogenic in the setting of myocardial ischemia, particularly re-ischemia. Because any impulse arising in the interventricular septum will enter the Purkinje network (to some degree) the QRS complexes tend to be shorter than arrhythmias originating in the free ventricular walls. QRS duration is generally 120 to 145 ms in ventricular tachycardias arising in the septum.

Fascicular ventricular tachycardia is an idiopathic form of VT. It is caused by re-entry in the fascicles of the left bundle branch (i.e in the Purkinje fibers). Fascicular ventricular tachycardia occurs in people aged less than 50 years of age, and predominantly in males. The QRS complexes display morphology similar to right bundle branch block and there is left axis deviation.

Right ventricular outflow tract (RVOT) ventricular tachycardia is a monomorphic VT originating in the outflow tract of the right ventricle. The arrhythmia is mostly idiopathic but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Because the impulses originate in the right ventricle, the QRS complexes have left bundle branch appearance and the electrical axis is around 90°. Refer to Figure 2.

A ventricular tachycardia with varying QRS morphology or varying electrical axis is classified as polymorphic. The rhythm may be irregular. Polymorphic ventricular tachycardia is typically very fast (100–320 beats per minute) and unstable. There are several types of polymorphic ventricular tachycardia. The most common cause is myocardial ischemia. The second most common cause is prolonged QTc interval (Long QT syndrome).

Familial catecholaminergic polymorphic ventricular tachycardia (CPVT) is an hereditary ventricular tachycardia in which emotional or physical stress induce the arrhythmia, which may lead to circulatory colapse and cardiac arrest. This type of ventricular tachycardia may be bidirectional (see below). The diagnosis is established by means of exercise stress testing since the sympathetic activity induces the tachycardia.

Brugada syndrome causes polymorphic VT (mostly during sleep or fever).

Early repolarization and hypertrophic obstructive cardiomyopathy also causes polymorphic VT.

Bidirectional ventricular tachycardia means that the QRS morphology alternates from one ebat to another. In most cases it alternates between two variants of the QRS complex.  Bidirectional ventricular tachycardia is seen in familial CPVT, digoxin overdoes and long QT syndrome. Refer to Figure 3.

Coronary artery disease (ischemic heart disease) is by far the most common cause of ventricular tachycardia and the mechanism is mostly re-entry. As mentioned earlier in this chapter, re-entry occurs when there is a central block ahead of the depolarizing impulse and the cells surrounding the block has varying conductivity. In ischemic heart disease, the central block is typically ischemic/necrotic myocardium (which do not conduct any impulses) while the surrounding cells have dysfunctional conduction due to ischemia. Ventricular tachycardia due to ischemia poses a high risk of degenerating into ventricular fibrillation and cardiac arrest.

Hence, ventricular tachycardia in coronary artery disease is mostly monomorphic. It may be polymorphic, if there are several ectopic foci or if the impulse from one foci spreads varyingly.

The ECG provides valuable information regarding the location of the ectopic foci causing the tachycardia. This is done by classifying ventricular tachycardias broadly as either “left bundle branch appearance” or “right bundle branch appearance”. Ventricular tachycardias with ECG waveforms reminding of a left bundle branch block (dominant S-wave in V1) originate in the right ventricle. The opposite is also true, namely that ventricular tachycardias reminding of right bundle branch block (dominant R-wave in V1) originates in the left ventricle. This might be useful in trying to decipher what the cause of the ventricular tachycardia may be. Figure 4 and Figure 5 below shows examples.

Occasionally supraventricular tachycardias (which mostly have normal QRS complexes, i.e QRS duration <0.12 seconds) may display wide QRS complexes. This might be due to concomitant bundle branch block, aberration, hyperkalemia, pre-excitation or side effect of drugs (tricyclic antidepressants, antiarrhythmic drugs class I). It is fundamental to be able to differentiate supraventricular tachycardias with wide QRS from VT and the reason for this is simple: VT is potentially life-threatening, whereas supraventricular arrhythmias rarely are. Hence, wide QRS complexes do not guarantee that the rhythm is ventricular in origin.

Fortunately, there are several characteristics that separate ventricular tachycardia from supraventricular tachycardias (SVT). These characteristics can be used separately or in algorithms (which are easy to use) to determine whether a tachycardia with wide QRS complexes (often called wide complex tachycardia) is a ventricular tachycardia or an SVT. Before dwelling into these characteristics and algorithm it should be noted that 90% of all wide complex tachycardias are ventricular tachycardias! If the patient suffers from any of the conditions stated above as risk factors for ventricular tachycardia, one should be very prone to assume that it is ventricular tachycardia.

Characteristics of ventricular tachycardia are now discussed.

AV dissociation means that atria and ventricles function independently of each other. On the ECG this manifests as P-waves having no relation to QRS complexes (P-P intervals are different from R-R intervals, PR intervals vary and there is no relation between P and QRS). Note that it is often difficult to discern P-waves during VT (esophagus ECG may be very helpful). If AV dissociation can be verified, VT is very likely to be the cause of the arrhythmia. However, occasionally the ventricular impulses may be conducted retrogradely through the His bundle and AV node to the atria and depolarize the atria synchronously with the ventricles; thus VT may actually display synchronized P-waves.  The following ECG shows VT with AV dissociation (the arrows point at P-waves).

If the start of the tachycardia is recorded it is valuable to assess the initial beats. If the R-R intervals during the start of the tachycardia were irregular, it suggests ventricular tachycardia. This is called warm-up phenomenon and is characteristic of ventricular tachycardia. Supraventricular tachycardias do not display warm-up phenomenon (with the exception of atrial tachycardia).

Ventricular tachycardia is not induced by premature atrial beats, but supraventricular tachycardias typically do. If the start of the tachycardia is recorded, one must examine whether it was preceded by a premature atrial beat.

If a ventricular impulse is discharged simultaneously as the atrial impulse enters the His-Purkinje system, the ventricles will be depolarized by both. The resulting QRS complex will have an appearance resembling both a normal QRS and a wide QRS. Such beats are called fusion beats, and such beats are diagnostic of ventricular tachycardia. Figure 6 shows an example.

Occasionally during a ventricular tachycardia, the atrial impulse will break through and manage to depolarize the ventricles. This is seen as the occurrence of a normal beat in the midst of the tachycardia. Such beats are called capture beats and they are also diagnostic of ventricular tachycardia.

Ventricular tachycardia is mostly regular, although the R-R intervals may vary somewhat. Discrete variability in R-R intervals actually suggest ventricular tachycardia. However, polymorphic ventricular tachycardia may be irregular. Supraventricular tachycardias may also be irregular; the most common being atrial fibrillation. Note that pre-excitation during atrial fibrillation causes an irregular wide complex tachcyardia, with heart rate >190 beats per minute in most cases.

Individuals with previously existing conduction defects (right or left bundle branch block) or other causes of wide QRS complexes (pre-excitation, drugs, hyperkalemia) should have their ECGs during tachyarrhythmia compared with the ECG during sinus rhythm (or any earlier ECG). If the QRS morphology during the tachyarrhythmia is similar to the QRS complex in sinus rhythm, it is likely to be an SVT. Moreover, if the patient has recently had premature ventricular complexes, and the QRS during tachyarrhythmia resembles that of the premature ventricular complexes, then it is likely to be ventricular tachycardia.

Electrical axis between –90° and –180° strongly suggests ventricular tachycardia (although antidromic AVRT is a differential diagnosis). If the electrical axis during tachycardia differs >40° from the electrical axis during sinus rhythm, it also suggests ventricular tachycardia. If the tachyarrhythmia has a right bundle branch block pattern but the electrical axis is more negative than –30° it suggests ventricular tachycardia. If the tachyarrhythmia has a left bundle branch block pattern but the electrical axis is more positive than 90° it suggests ventricular tachycardia. In general, left axis deviation suggests ventricular tachycardia.

QRS duration >0.14 s suggest ventricular tachycardia. QRS duration >0.16 s strongly suggest ventricular tachycardia. Note that ventricular tachycardia originating in the interventricular septum may have a relatively narrow QRS complex (0.120–0.145 s). Antidromic AVRT may also have >0.16 s. Class I antiarrhythmic drugs, tricyclic antidepressants and hyperkalemia may also cause very wide QRS complexes.

Concordance means that all QRS complexes from lead V1 to lead V6 head in the same direction; all are either positive or negative. If any lead displays biphasic QRS complexes (e.g qR complex or RS complex) there cannot be concordance. Negative concordance (all QRS complexes being negative) strongly suggest ventricular tachycardia). Positive concordance (all QRS complexes being positive) are mostly due to ventricular tachycardia but may be caused by antidromic AVRT. The following figure presents concordance. To conclude, concordance is strongly suggestive of ventricular tachycardia.

If there is no QRS complex from lead V1 to lead V6 which is an RS complex (i.e consists of an R wave and an S wave), then ventricular tachycardia is very likely.

It is not recommended that adenosine be administered when ventricular tachycardia is suspected, because adenosine may accelerate the frequency and aggravate the arrhythmia. Occasionally adenosine is still administered (when suspecting that the arrhythmia is actually a SVT with wide QRS complexes). If adenosine do not have any effect or if it accelerates the tachycardia, it is likely to be ventricular tachycardia.

In addition to these characteristics, researchers have developed several algorithms to differentiate ventricular tachycardia from SVTs. These algorithms are briefly outlined below (refer to Management and Diagnosis of Tachyarrhythmias for details)

This is the most used algorithm. If any of the five criteria below are fulfilled, a diagnosis of ventricular tachycardia can be made.

All in all, Brugada’s criteria have very high sensitivity (90%) and specificity (60–90%) for diagnosing ventricular tachycardia.

The algorithm above frequently fails to differentiate ventricular tachycardia from antidromic AVRT. Although antidromic AVRT is an uncommon cause of ventricular tachycardia, it is important to be able to differentiate these entities. The older the patient and the more significant the heart disease, the more likely is ventricular tachycardia. The Brugada group has also developed an algorithm to differentiate antidromic AVRT from ventricular tachycardia. The algorithm follows:

Polymorphic ventricular tachycardia and fibrillation in structural heart disease with normal QT interval

Polymorphic ventricular tachycardia occurring during QT prolongation, with the characteristic twisting of the points, is referred to as torsade de pointes (TdP). The risk of degeneration into ventricular fibrillation and cardiac arrest is high. Torsade de pointes is treated as follows:

Ventricular arrhythmias in arrhythmogenic cardiomyopathies and channelopathies are mostly treated with antiarrhythmic agents.

Management

Schleifer JW, Sorajja D, Shen W. Advances in the pharmacologic treatment of ventricular arrhythmias. Expert Opin Pharmacother 2015;16:2637–51.

Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer 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 Com. Europace 2006;8:746–837.

Priori SG, Blomstro ̈ m-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Europace 2015;17:1601–87.

Tung R, Vaseghi M, Frankel DS, Vergara P, Di Biase L, Nagashima K et al. Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: an International VT Ablation Center Collaborative Group Study. Heart Rhythm 2015;12:1997–2007.

Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA 2006;295:165–71.

Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-ofhospital ventricular fibrillation cardiac arrest. Resuscitation 2013;84:1512–8.

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