Continuing Education Activity

Ventricular tachycardia (VT) is a wide complex arrhythmia of ventricular origin, defined as three or more consecutive beats at a rate of more than 100 beats per minute. Sustained ventricular tachycardia is defined as tachycardia that continues for more than 30 seconds or leads to hemodynamic compromise within 30 seconds and requires intervention. On the other hand, non-sustained ventricular tachycardia lasts less than 30 seconds and does not cause hemodynamic instability. Ischemic heart disease is the most common cause of ventricular tachycardia, and VT has a wide range of clinical presentations, including palpitations, chest pain, shortness of breath, syncope, and cardiac arrest. This activity reviews the evaluation and management of ventricular tachycardia and highlights the importance of an interprofessional team in managing patients with ventricular tachycardia.

Objectives:

• Explain the pathophysiologic basis of ventricular tachycardia.
• Summarize the differential diagnoses of ventricular tachycardia.
• Describe the evaluation and management of patients presenting with ventricular tachycardia.
• Explain the importance of a comprehensive healthcare system with particular emphasis on communication between interprofessional teams to facilitate prompt and thorough delivery of care to patients with ventricular tachycardia.

Introduction

Ventricular tachycardia (VT) is a wide complex tachycardia, defined as three or more consecutive beats at a rate of more than 100 per minute, arising from the ventricle.[1]  Ventricular tachycardia is a potentially life-threatening arrhythmia, and it is responsible for the majority of sudden cardiac deaths in the United States.[2] It is classified by duration as non-sustained or sustained ventricular tachycardia. Non-sustained ventricular tachycardia is defined as ventricular tachycardia of fewer than 30 seconds duration that does not lead to hemodynamic instability, while sustained VT lasts more than 30 seconds or requires intervention within 30 seconds due to hemodynamic compromise.[3] 

On the basis of QRS morphology, VT is divided into monomorphic and polymorphic ventricular tachycardia. Monomorphic VT is characterized by a single, stable QRS morphology with no beat-to-beat variation, while polymorphic VT has beat-to-beat variation in QRS shape and multiple QRS morphologies.[4] Torsades de Pointes is a form of polymorphic ventricular tachycardia (occurs in the setting of the long QT interval), characterized by waxing and waning of QRS amplitude, giving it the name "twisting of the points."[5] Bidirectional ventricular tachycardia is another form of polymorphic ventricular tachycardia and has a characteristic beat-to-beat change in the QRS axis. It is commonly seen in the setting of digitalis toxicity and patients with catecholaminergic polymorphic ventricular tachycardia (CPVT).[6] 

Ischemic heart disease is the most common cause of ventricular tachycardia, and 5 to 10% of patients with acute coronary syndrome are found to have ventricular arrhythmias. Ventricular tachycardia in acute coronary syndrome is usually polymorphic, while monomorphic ventricular tachycardia is a sign of a myocardial scar.[7] Accelerated atrioventricular rhythm (AIVR) is a monomorphic ventricular tachycardia, referred to as a sign of successful reperfusion, and it has a strong association with infarct size.[8][9] 

Ventricular tachycardia is a major contributor to sudden cardiac death in patients with ischemic and non-ischemic cardiomyopathy. Ventricular tachycardia in cardiomyopathy is usually monomorphic due to scar-related reentry, and its degeneration into ventricular fibrillation may result in cardiac arrest or even sudden cardiac death.[10][11] The clinical presentation of ventricular tachycardia varies from palpitation to sudden cardiac death. For appropriate management of VT and prevention of sudden cardiac death, it is essential to understand the pathophysiology of ventricular tachycardia and underlying structural heart disease. In this chapter, we summarize the etiology and epidemiology of ventricular tachycardia and discuss the evaluation and management of patients present with ventricular tachycardia.

Etiology

Ventricular tachycardia accounts for approximately 8% of cases of wide-complex tachycardia.[12] The most common cause of ventricular tachycardia is underlying ischemic heart disease. Ventricular tachycardia in the presence of acute coronary syndrome is usually polymorphic, while the monomorphic VT is a characteristic feature of myocardial scar-related reentry. Ventricular tachycardia predicts a higher risk of death after acute myocardial infarction. [13] 

The other causes of ventricular tachycardia include ischemic or non-ischemic dilated cardiomyopathy, adult and congenital structural heart disease, inherited cardiac channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity.[14] Infiltrative cardiomyopathy can result from systemic lupus erythematosus, sarcoidosis, amyloidosis, rheumatoid arthritis, and hemochromatosis.[15] In the presence of a substrate, ventricular tachycardia is triggered by multiple factors; the most common triggers include myocardial ischemia, hypokalemia, hypomagnesemia, hypocalcemia, sepsis, and metabolic acidosis. 

Inherited cardiac channelopathies are more common in young individuals. The long-QT syndrome is the most common inherited cardiac channelopathy, and Torsades de Pointes is the characteristic feature of the long-QT syndrome.[16] The other inherited channelopathies responsible for ventricular tachycardia include Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, and malignant early repolarization syndrome.[17] Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and myocarditis are responsible for ventricular tachycardia and cardiac arrest/sudden cardiac death.

Idiopathic ventricular tachycardia is an uncommon class of ventricular tachycardia. It is usually found in younger people, with no evidence of structural heart disease. The most common idiopathic ventricular tachycardia arises from outflow tracts, mitral/tricuspid annulus, and fascicles of the left bundle branch.[18] Idiopathic VT is benign, responds really well to calcium channel blockers, and has an excellent outcome after catheter ablation.[19] 

Epidemiology

Ventricular tachycardia and ventricular fibrillation cause most cases of sudden cardiac death, with an estimated rate of 300,000 deaths each year in the United States.[2][20] Sudden cardiac deaths caused by ventricular tachyarrhythmias account for approximately half of the deaths related to cardiac causes.[20]  Ventricular tachycardia is strongly associated with coronary artery disease; around 15% of the patients with coronary artery disease are found to have ventricular tachycardia.[21] The incidence of ventricular tachycardia is relatively higher in men due to a higher incidence of coronary artery disease; however, the incidence in women is expected to increase with the rising incidence of coronary artery disease.

Ventricular tachycardia is much more common in the setting of acute coronary syndrome, and around 5 to 10% of the patients presenting with acute myocardial infarction are found to have ventricular arrhythmias within the first few days of the presentation.[22][23]  Patients with myocardial infarction, who develop ventricular tachyarrhythmias after the first two days of myocardial infarction, have an increased risk of death as compared to those having VT within the first two days.[24] Ventricular tachycardia is rare in children but can occur in the presence of inherited channelopathies or structural heart disease.

Idiopathic ventricular tachycardia is less common, and it is estimated to have an incidence of around 15 per 100,100 individuals in the general population. Its incidence increases with age, and there is no difference between men and women. The incidence of idiopathic VT has increased over the last two decades, mainly because of early diagnosis and increased awareness. The age at the diagnosis of idiopathy VT varies from 2nd decade to the 70th decade, but the mean age at the time of diagnosis is reported as 52 years in one study.[25]

Pathophysiology

Mechanism of Ventricular Tachycardia

Ventricular tachycardia is a diverse group of tachyarrhythmias, and its cellular mechanism depends on the underlying structural heart disease and channelopathy. Understanding the mechanism of ventricular tachycardia helps in the risk stratification of patients and guides appropriate management strategies. Reentry is the most common mechanism of ventricular tachycardia, followed by triggered activity and enhanced automaticity.[26] Reentry is the mechanism of scar-related ventricular tachycardia and bundle branch reentry VT.[27] Sustained reentrant ventricular tachycardia may degenerate into ventricular fibrillation, resulting in cardiac arrest or sudden cardiac death in patients with structural heart disease.[28]

The basic mechanism of ventricular tachycardia in long QT syndromes is triggered activity due to early after-depolarization. While delayed after-depolarization is the main mechanism of ventricular tachycardia in catecholaminergic polymorphic VT, verapamil-sensitive VT,  and digoxin toxicity.[6] Enhanced automaticity may also play a role in catecholaminergic VT. Although the mechanism of idiopathic ventricular tachycardia (outflow tract VT) is unclear, delayed after-depolarization is proposed as the possible mechanism. Most outflow tract VTs terminate in response to adenosine, suggesting cyclic AMP-mediated delayed after-depolarization is the main mechanism of these ventricular tachycardias.[29][30] 

Hemodynamic Consequences of Ventricular Tachycardia

The hemodynamic effects of ventricular tachycardia depend on coronary artery disease,  left ventricular systolic function, valvular heart disease, and other co-morbid conditions. The rapid ventricular rate in VT leads to low cardiac output due to a significant reduction in preload as well as stroke volume.[31] In the presence of structural heart disease, coronary artery disease, and left ventricular systolic dysfunction, the hemodynamic changes may lead to systemic hypotension, coronary and cerebral hypoperfusion, syncope, and even cardiac arrest. Coronary hypoperfusion further impairs hemodynamics, leading to ventricular fibrillation and even sudden cardiac death.[32] 

Ventricular tachycardia is relatively well tolerated in patients with a structurally normal heart, but incessant VT may lead to tachycardia-induced cardiomyopathy, hemodynamic instability, heart failure, and syncope. [33] In patients with inherited ventricular arrhythmias, including long QT syndrome, arrhythmogenic cardiomyopathy, catecholaminergic polymorphic VT, and Brugada syndrome, VT may degenerate in ventricular fibrillation and result in hemodynamic collapse, even in the presence of normal left ventricular systolic function.[34][35]

History and Physical

Clinical presentation of ventricular tachycardia varies, depending on the patients` age, co-morbid conditions, underlying structural heart diseases, and mechanism of ventricular tachycardia. Although the common symptoms of ventricular tachycardia include palpitations, shortness of breath, chest pain, and syncope, the patients may present with cardiac arrest or even sudden cardiac death.[36][37] Patients with idiopathic ventricular tachycardia usually present with palpitation during exercise or emotional stress, but shortness can be the first presentation due to heart failure and tachycardia-induced cardiomyopathy. Syncope and cardiac arrest are rare clinical presentations of idiopathic ventricular tachycardia in patients with no evidence of structural heart disease.[38]

Ventricular tachycardia in the presence of coronary artery disease may present with chest pain, syncope, shortness, and cardiac arrest. Ventricular tachycardia in the presence of left ventricular systolic dysfunction is not tolerated well and results in significant hemodynamic compromise patients usually present with syncope, shortness of breath (due to pulmonary edema), cardiac arrest, and even sudden cardiac death. While those with implantable cardioverter-defibrillator (ICD) may present with ICD shocks.[36] Patients with ventricular tachycardia due to channelopathies may have syncope, cardiac arrest, and sudden cardiac death as the first presentation; that is why it is essential to have a three-generation detailed family history while evaluating a young patient with ventricular tachycardia.[39]

The clinical examination of ventricular tachycardia may include hypotension and signs of heart failure. Elevated jugular venous pressure and cannon waves can be found even in hemodynamically stable patients. The detailed precordial examination may reveal the signs of underlying structural heart disease and signs of adverse effects of antiarrhythmic drugs, e.g., amiodarone.[40]

Evaluation

History and Physical Examination

Detailed history and clinical examination are pivotal in evaluating a patient with ventricular tachycardia. All patients undergoing evaluation for ventricular tachycardia should be asked about the risk factors for atherosclerotic cardiovascular diseases, prior history of palpitations, syncope, or ventricular tachycardia, and history of inherited cardiac conditions in the first-degree relatives.[41] Clinical practice guidelines recommended a three-generation, detailed family history in patients with suspected cardiac channelopathies.[42] Although a physical examination may help identify underlying structural heart disease, it is essential for managing patients presenting with ventricular tachycardia.[43]

Electrocardiographic Evaluation

The first step in evaluating presumed ventricular tachycardia is a 12-lead electrocardiogram (ECG).[44][45] A 12-lead ECG should be done during VT (if possible) and during sinus rhythm. A 12-lead ECG in sinus rhythm helps diagnose the underlying cause of ventricular tachycardia, e.g., myocardial ischemia/infarction, long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy. Patients with ventricular tachycardia having symptoms associated with exertion, ischemic heart disease, or suspected to have catecholaminergic polymorphic ventricular tachycardia should undergo further testing with a treadmill stress test.[46] Patients having syncope, presyncope, or palpitations with no arrhythmia detected on a single 12-lead ECG should undergo further evaluation with ambulatory ECG monitoring.[47] In patients with infrequent symptoms suspected to be due to ventricular tachycardia, an implantable loop recorder can be considered.

Echocardiogram and Other Non-invasive Imaging

In patients with ventricular tachycardia and possible structural heart disease, an echocardiogram is recommended to evaluate the cardiac structure and function.[48][49] An echocardiogram is an essential tool for diagnosing hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy (ARVC). Cardiac computed tomography (CT) and cardiac magnetic resonance (CMR) imaging can be considered in selected patients. Cardiac MRI not only defines the myocardial scar but also helps diagnose infiltrative heart diseases, ARVC, and myocarditis.[50]In younger patients with an episode of unexplained cardiac arrest secondary to ventricular tachyarrhythmia, CT coronary angiography can be used to confirm the presence or absence of coronary artery anomalies.[51] It is also helpful for the diagnosis of coronary artery disease. [42][52]

Invasive Evaluation

 For patients presenting with cardiac arrest due to ventricular tachycardia due to presumed myocardial ischemia, an invasive coronary angiogram is recommended to evaluate coronary artery disease and guide the revascularization strategy.[53] Although an invasive electrophysiology study is no longer recommended for diagnosing ventricular tachycardia, it can be used in selected patients to assess the risk of sudden cardiac death who do not meet the criteria of ICD implantation.[52] An endomyocardial biopsy is indicated, in selected patients, for the diagnosis of myocarditis and infiltrative cardiomyopathies when non-invasive imaging is non-diagnostic.[54]

Genetic Testing

Genetic testing is not recommended as a routine test in patients presenting with ventricular tachycardia. However, in selected patients with suspected inherited cardiac channelopathies, genetic testing can be done to confirm the diagnosis.[55]Genetic testing should also be offered to asymptomatic family members of patients with congenital long QT syndrome, hypertrophic cardiomyopathy, catecholaminergic polymorphic VT, and right ventricular dysplasia.[3]

Other Investigations

Serum levels of potassium, magnesium, and calcium are essential investigations for diagnosing and managing patients with ventricular tachycardia. High-sensitivity cardiac troponin is required for the diagnosis of myocardial infarction. While natriuretic peptide is an excellent prognostic marker in patients with structural heart disease who present with ventricular tachycardia and have the risk of sudden cardiac death.[56]

Treatment / Management

Acute Management

Cardiac arrest is the life-threatening presentation of ventricular tachycardia. Patients presenting with cardiac arrest secondary to ventricular tachycardia should be resuscitated and managed according to the advanced life support (ACLS) algorithm.[57] In the absence of a cardiac arrest, patients with hemodynamically unstable ventricular tachycardia are managed with direct current cardioversion.[58] In hemodynamically unstable patients, intravenous amiodarone should be used to maintain the sinus rhythm if ventricular tachycardia does not respond to direct current cardioversion or VT recurs after successful cardioversion.[59] All hemodynamically unstable patients with myocardial infarction/ischemia-induced ventricular tachycardia should undergo coronary angiogram followed by revascularization. 

Ventricular tachycardia (VT) storm is one of the presentations of VT in patients with structural heart diseases. It is defined as three or more episodes of sustained ventricular tachycardia within 24 hours, which requires intervention in the form of antiarrhythmic drugs, anti-tachycardia pacing, or direct current cardioversion.[60] VT storm not only causes significant morbidity in the form of hospitalization and decompensated heart failure but also increases mortality. The initial management of VT storm includes intravenous antiarrhythmic drugs, intravenous beta-blockers, and direct current cardioversion along with sedation. In refractory conditions, patients may require intubation, mechanical circulatory support, and catheter ablation of ventricular tachycardia.[61]

In patients with structural heart disease and hemodynamically stable ventricular tachycardia, intravenous procainamide, amiodarone, and sotalol (depending on availability) are recommended for the acute treatment of ventricular tachycardia.[62]  Intravenous lidocaine can be used as an alternative antiarrhythmic drug if the drugs mentioned above are not available. Intravenous beta-blockers can be considered in patients with ventricular tachycardia secondary to ischemia.[63]

Intravenous beta-blockade and non-dihydropyridine calcium channel blockers are the first choice drugs for treating hemodynamically stable patients with idiopathic ventricular tachycardia.[64] Intravenous verapamil should be given as a bolus by using a large bore cannula. Direct current cardioversion may be considered if VT does not respond to antiarrhythmic drugs. Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying structural heart disease may not require any additional therapy.

Intravenous beta-blockade is the mainstay of treatment in hemodynamically stable patients with VT secondary to underlying cardiac channelopathies.[65] Intravenous magnesium and mexiletine can be considered in patients with long QT-induced stable VT.[66] Some patients with long QT syndrome may have incessant VT due to short-long sequence and R on T phenomenon; temporary pacing at a higher rate is effective in preventing Torsades de Pointes in these patients.[67] Serum potassium, magnesium, and calcium levels should be optimized in all patients presenting with ventricular tachycardia.

Long-Term Management

All patients with structural heart disease and left ventricular systolic dysfunction should be offered guidelines-directed medical therapy for heart failure.[68] Patients with ischemic cardiomyopathy who survive sudden cardiac arrest due to ventricular tachycardia, or experience hemodynamically unstable or stable sustained ventricular tachycardia, should have an implantable cardiac defibrillator (ICD) placed if their estimated meaningful survival is greater than one year.[69][70][71] Patients with unexplained syncope who have ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who do not meet the criteria for an ICD can undergo an electrophysiological study to assess the risk of sustained ventricular tachycardia, however, performing the study solely for risk stratification is not indicated.[72][73][52] If a sustained VT is induced during an electrophysiology study, implantation of an ICD should be recommended for the prevention of sudden cardiac death. 

In patients with ischemic cardiomyopathy who present with ventricular tachycardia, the long-term beta-blockade is recommended to prevent the recurrence of VT and reduce the risk of sudden cardiac death. If the patients present with recurrent episodes of ventricular tachycardia or ICD shocks despite being on the optimal doses of beta-blocking drugs, amiodarone, and sotalol are recommended to suppress the recurrent ventricular tachycardia.[74] Amiodarone is more effective than sotalol, and it has lower proarrhythmic properties; however, it has systemic adverse effects, which may result in the early discontinuation of therapy.

Catheter ablation has been proven as an effective treatment option for patients with drug-refractory ventricular tachycardia. It is recommended in a select group of patients with ischemic cardiomyopathy who continue to have sustained VT on antiarrhythmic drugs or are intolerant of amiodarone or other antiarrhythmic medications.[75][76][77] In VANISH trial, catheter ablation reduced the recurrence of VT, ventricular storm, and ICD shock as compared to antiarrhythmic drugs; however, it did not improve survival.[78]  The International VT Ablation Center Collaborative (IVTCC) study reveals that 70% of patients with structural heart diseases achieve freedom from VT after catheter ablation, and freedom from VT improves survival in this particular group of patients.[79] Ventricular tachycardia ablation is a relatively safe procedure in experienced centers with a procedure-related mortality of less than 1%. Vascular access-related complications are similar to other electrophysiology procedures, while stroke, tamponade, and atrioventricular blocks are rare.[78][79]

Patients with non-ischemic cardiomyopathy who survive sudden cardiac death due to VT or develop sustained VT with no reversible cause should have an ICD implanted for secondary prevention of SCD if they have an expected survival of more than a year with good quality of life. While amiodarone can be considered for preventing sudden cardiac death and recurrence of VT if the expected meaningful survival is less than a year.[42] In patients with recurrent VT, despite being on optimal heart failure therapy and beta blockade, contemporary guidelines recommend amiodarone and sotalol to prevent recurrent VT episodes. Catheter ablation can be considered in selected patients with drug-refractory VT, resulting in recurrent ICD shocks.[80]

In patients with ventricular tachycardia due to arrhythmogenic right ventricular cardiomyopathy (ARVC), the beta-blockade is helpful in reducing recurrent arrhythmia. All patients with ARVC who survive sudden cardiac death are recommended to have an ICD implanted for secondary prevention of sudden cardiac death.[81] While ICD can be considered in certain high-risk patients presenting with syncope and ventricular tachycardia but do not have a history of cardiac arrest.[58] In ARVC patients with recurrent VT and appropriate ICD shocks on beta blockers and antiarrhythmic drugs, catheter ablation can be considered in experienced centers where both endocardia and epicardial ablation facilities are available.[82]

Beta blockade is the mainstay of treatment for patients with congenital long QT syndrome and catecholaminergic polymorphic ventricular tachycardia (CPVT).[83] For patients with cardiac channelopathies, who survived cardiac arrest, an implantable cardioverter-defibrillator is indicated for secondary prevention of sudden cardiac death. In highly symptomatic patients on the optimal dose of beta blockers, left cardiac sympathetic denervation can be considered in experienced centers.[84] Implantation of an ICD for secondary prevention of sudden cardiac death is recommended in patients with Brugada syndrome, short QT syndrome, hypertrophic cardiomyopathy, and those with idiopathic polymorphic ventricular tachycardia, who survive sudden cardiac death due to ventricular tachycardia.[3]

Non-dihydropyridine calcium channel blockers and beta-blockade are effective treatment options for patients with idiopathic ventricular tachycardia. Most patients respond very well to beta-blockers and verapamil and do not require further treatment options.[85] Other antiarrhythmic drugs can be considered in patients with idiopathic VT who do not respond to beta blockers and calcium channel-blocking drugs. Catheter ablation is an effective therapy that can be considered in patients with idiopathic VT that does not respond to beta-blockers, calcium channel blockers, and other antiarrhythmic drugs.[86] 

Differential Diagnosis

Ventricular tachycardia is the most common cause of broad complex tachycardia. However, there are multiple other causes of broad complex tachycardia. The common differentials of VT include supraventricular tachycardia with bundle branch aberrancy, supraventricular tachycardia with preexcitation, antidromic atrioventricular tachycardia (AVRT), pacemaker-mediated tachycardia, and metabolic derangements.[87] 

A meticulous history, clinical examination, and electrocardiogram (ECG) help differentiate ventricular tachycardia from the other causes of broad complex tachycardia.[88] Electrocardiographic algorithms can be used to differentiate ventricular tachycardia from supraventricular tachycardia with aberrancy.[89][90] Careful interpretation of ECG may help identify the origin of VT and differentiate idiopathic VT from the other forms of ventricular tachycardia.[91][92] 

Prognosis

The prognosis of VT depends on the underlying etiology and the presence of structural heart disease. As coronary artery disease is the main cause of VT, patients with ischemic cardiomyopathy-related VT have the worst prognosis. The two-year mortality in these patients has been reported to be as high as 30% if they remain untreated.[93] However, the implantation of a defibrillator significantly reduces the incidence of sudden cardiac death and improves survival in these patients.[94] 

Patients with idiopathic ventricular tachycardia have excellent prognoses in the absence of other co-morbid conditions, and they are estimated to have longevity almost equal to the general population.[95]  Patients with hypertrophic cardiomyopathy, long QT syndrome, and arrhythmogenic right ventricular cardiomyopathy have a higher risk of sudden cardiac death, even in normal left ventricular systolic function. Beta-blockers reduce the burden of ventricular tachycardia in these patients, and implantable cardioverter defibrillators prevent sudden cardiac death.[96][97]

Complications

Complications of ventricular tachycardia depend on the underlying mechanism of ventricular tachycardia. The common complications of idiopathic ventricular tachycardia include tachycardia-induced cardiomyopathy and heart failure. Tachycardia-induced cardiomyopathy is much more common in patients with incessant episodes of VT and those with a genetic predisposition and other risk factors of cardiomyopathy, e.g., alcohol intake.[98] 

Cardiac arrest and sudden cardiac death are the major complications of inherited ventricular tachycardia as well as scar-related ventricular tachycardia. However, these complications can be minimized with early recognition and implantation of implantable cardioverter-defibrillator.[42] The beta-blockade has also been reported to reduce the incidence of sudden cardiac death in patients with cardiac channelopathies and ischemic cardiomyopathy.[99][3]

Deterrence and Patient Education

Ventricular tachycardia is a potentially life-threatening condition. Although palpitation is the most common presentation of ventricular tachycardia, patients may present with syncope, cardiac arrest, and even sudden cardiac death. All patients with broad complex tachycardia should undergo detailed evaluation, including three-generation family history, transthoracic echocardiogram, and cardiac magnetic resonance imaging (if required). Patients with a family history of sudden cardiac death at a young age are recommended to consult a cardiologist to evaluate cardiac channelopathies and other inherited cardiac conditions. Asymptomatic relatives of patients with inherited channelopathies and other inherited causes of ventricular tachycardia should consult a cardiac electrophysiologic and/or a geneticist for screening and genetic counseling.[55]

Enhancing Healthcare Team Outcomes

Cardiac arrest is a fatal presentation of ventricular tachycardia. Early recognition, bystander cardiopulmonary resuscitation (CPR), and public access to defibrillation have helped improve the rate of survival for patients who have an out-of-hospital cardiac arrest due to ventricular arrhythmias. However, survival after out-of-hospital still remains low.[100][101][102] [Level 1] Patient care after the return of spontaneous circulation (ROSC), with special emphasis on targeted temperature management (TTM) and cardio-cerebral resuscitation, has further improved survival.[103] [Level 2] A dedicated resuscitation team, with no clinical responsibilities that interfere with their participation in CPR, is the basic requirement for managing cardiac arrest. Effective communication among team members has also been identified as a positive factor in improving outcomes.[104]

In-hospital cardiac arrest shares a similarity with out-of-hospital cardiac arrest in that early cardiopulmonary resuscitation (CPR), and defibrillation are important factors in survival. [Level 1] Every minute treatment is delayed reduces survival by approximately 10%.[105] This makes the resuscitation team an essential part of ventricular tachycardia management. Resuscitation teams universally consist of physicians, nurses, anesthesiologists, and respiratory therapists coordinating their efforts. Hospitals that are high performing include more support staff (pharmacy, clerical, security, spiritual staff).[104] 

Management of a patient with ventricular tachycardia requires an interprofessional team. A cardiac electrophysiologic and a cardiac critical care nurse are essential to the team. Diabetic patients with ischemic heart disease should be seen by an endocrinologist to manage it properly. Strenuous exercise should be avoided as it may precipitate VT in some patients. All patients should be strongly encouraged to discontinue smoking. Patients presenting with VT secondary to (suspected) inherited cardiac conditions require a geneticist for genetic counseling and testing. The pharmacist should educate the patient on medication compliance and the need to follow up with the cardiologist, as well as perform medication reconciliation and contact the prescriber if they have any concerns about the patient's medication regimen. They can assist the clinical team in managing drug-drug interactions and making appropriate drug treatment selections. Nurses often coordinate activities between various providers, counsel patients, and assist in assessments and procedures. This interprofessional model will help drive optimal patient results in VT cases. [Level 5]

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Disclosure: Christopher Foth declares no relevant financial relationships with ineligible companies.

Disclosure: Manesh Kumar Gangwani declares no relevant financial relationships with ineligible companies.

Disclosure: Intisar Ahmed declares no relevant financial relationships with ineligible companies.

Disclosure: Heidi Alvey declares no relevant financial relationships with ineligible companies.