Rhythm, Ventricular Tachycardia (VT, V Tach)


Article Author:
Christopher Foth


Article Editor:
Heidi Alvey


Editors In Chief:
Jason Nagle


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes
Kavin Sugumar


Updated:
12/16/2018 4:27:04 PM

Introduction

Ventricular tachycardia is characterized as a wide complex (QRS duration greater than 120 milliseconds) tachyarrhythmia at a heart rate greater than 100 beats per minute. It is classified by duration as non-sustained or sustained. Non-sustained ventricular tachycardia is defined as more than 3 beats of ventricular origin at a rate greater than 100 beats per minute that lasts less than 30 seconds in duration.[1] When the rhythm lasts longer than 30 seconds or hemodynamic instability occurs in less than 30 seconds, it is considered sustained ventricular tachycardia.[1]

Further classification is made into monomorphic and polymorphic on the basis QRS morphology. Monomorphic ventricular tachycardia demonstrates a stable QRS morphology from beat to beat while polymorphic ventricular tachycardia has changing or multiform QRS variance from beat to beat.[1] Torsades de pointes is a polymorphic ventricular tachycardia that occurs in the setting of a long QT interval and appears as a waxing and waxing QRS amplitude on ECG.[1]

The final form of ventricular tachycardia is bidirectional ventricular tachycardia which has a beat-to-beat alternation in the QRS frontal plane axis.[1] It is associated with digitalis toxicity or catecholaminergic polymorphic VT.

Etiology

Ventricular tachycardia accounts for approximately 8% of cases of wide complex tachycardia.[2] The most common cause of ventricular tachycardia is underlying ischemic heart disease. Other causes include adult and congenital structural heart disease, acquired and inherited channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity.[3] Infiltrative cardiomyopathy can result from: systemic lupus erythematosus, sarcoidosis, amyloidosis, rheumatoid arthritis and hemochromatosis.[4]

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.[5][6] This accounts for approximately half of the deaths related to cardiac causes.[6] Risk factors for ventricular tachycardia are hypertension, previous myocardial infarction, chronic obstructive pulmonary disease (COPD), and ST-segment changes at presentation.[7] Patients presenting with acute myocardial infarction have ventricular fibrillation or ventricular tachycardia at a rate of 5% to 10%.[1][8] Ventricular tachycardia 48 hours after hospital presentation is associated with an increased risk of death compared to ventricular tachycardia occurring within the first 48 hours of hospital presentation.[9]

Pathophysiology

The mechanism for ventricular tachyarrhythmias includes enhancement of normal automaticity or abnormal automaticity, activity triggered by early or late afterdepolarizations, and reentry.[10] In acute myocardial infarction, the transient ischemia results in an increased concentration of extracellular potassium, which causes partial depolarization of the resting membrane potential.[10] This creates injury currents between the infarcted tissue and healthy myocardium that may trigger spontaneous activity.

History and Physical

A good history and physical can help you differentiate ventricular tachycardia from supraventricular tachycardia. Patients presenting with ventricular tachycardia are more likely to be older with a history of heart disease. A past medical history of heart failure, recent angina, and prior myocardial infarction all have a greater than 9% positive predictive value for ventricular tachycardia.[11] The physical examination findings of cannon A waves and variable intensity of the S1 heart sound suggest AV dissociation, a criterion favoring the diagnosis of ventricular tachycardia.[11]

Evaluation

The first step in the evaluation of presumed ventricular tachycardia is a 12-lead electrocardiogram (ECG).[12][13] Patients with ventricular tachycardia symptoms associated with exertion, ischemic heart disease, or catecholaminergic polymorphic ventricular tachycardia should undergo further testing with a treadmill stress test.[14] Patients having syncope, presyncope or palpitations with no arrhythmia detected on a single 12-lead ECG should undergo further evaluation with ambulatory ECG monitoring.[15] In patients with ventricular tachycardia and possible structural heart disease, .an echocardiogram is recommended.[16][17] Patients who undergo an episode of unexplained sudden cardiac arrest secondary to a ventricular tachyarrhythmia, CT, or coronary angiography can be used to confirm the presence or absence of ischemic heart disease.[18][19]

Treatment / Management

Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying cardiac comorbidities require no additional therapy.  Patients that are symptomatic and without cardiac comorbidities should be started on a beta-blocker due to favorable efficacy and safety profile.[20][21] If these patients continue to have episodes of non-sustained VT despite beta-blocker therapy, or cannot tolerate beta-blocker therapy, a calcium channel with atrioventricular nodal action such as verapamil or diltiazem can be used. The previously mentioned nondihydropyridine calcium channel blockers are contraindicated in the setting of structural heart disease or heart failure with reduced ejection fraction.[22]

Patients with sustained monomorphic ventricular tachycardia (SMVT) that are unstable should be managed following advanced cardiac life support (ACLS) guidelines. Hemodynamically stable patients should be pharmacologically cardioverted using an anti-arrhythmic medication. Intravenous amiodarone or procainamide can be used for this purpose. Procainamide will terminate between 50% and 80% of ventricular tachycardias, and it will slow the conduction of those that it does not terminate.[23][24][23] Amiodarone will convert about 30% of patients to sinus rhythm but is very effective in reducing the reversion rate of refractory SMVT.[25][26][27]

The first-line therapy for chronic treatment of patients with ischemic heart disease and VT is a beta-blocker therapy which is associated with a reduced risk of sudden cardiac death.[20][18][21] In patients with ischemic heart disease who have recurrent VT despite beta-blocker therapy, amiodarone or sotalol can be initiated however neither therapy has been associated with a decrease in mortality.[28][29][30] Amiodarone plus a beta-blocker has been associated with a greater decrease in the number of ICD shocks compared to sotalol monotherapy.[31][30][29]

Patients with ischemic heart disease that 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 1 year.[32][33][34][34] Patients with syncope who have ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who do not meet 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.[35][36][19]

Catheter ablation has a class 1 recommendation for patients with a history of myocardial infarction who continue to suffer from symptomatic sustained VT, or have failed or are intolerant of amiodarone or other antiarrhythmic medications.[37][38][39]

Differential Diagnosis

If possible, ventricular tachycardia should be differentiated from supraventricular tachycardia with aberrant conduction as the treatment strategies are different. Factors favoring the diagnosis of ventricular tachycardia include: QRS width greater than 0.14 seconds with right bundle branch block pattern or greater than 0.16 seconds with left bundle branch block pattern, AV dissociation, RS interval longer than 100 milliseconds in a precordial lead (Brugada's sign), QRS with negative concordance in the precordial leads, and ventricular fusion beats.[37]

Enhancing Healthcare Team Outcomes

Early recognition, bystander CPR, and public access defibrillation have all helped to increase the rate of survival for patients who have an out-of-hospital cardiac arrest however survival remains low at under 10%.[40][41][42] (Level I) After arrival at the hospital, post-arrest care order sets that pay significant attention to temperature control and cardio-cerebral resuscitation, have further improved survival.[43] (Level 2)

In-hospital cardiac arrest shares the similarity with out-of-hospital cardiac arrest in that early cardiopulmonary resuscitation (CPR), and defibrillation are important factors in survival. (Level I) Every minute that treatment is delayed reduces survival by approximately 10%.[44] This makes the resuscitation team an important part in improving outcomes of in-hospital cardiac arrest. However, there is significant variation amongst different hospitals in efficacy. Resuscitation teams universally consist of physicians, nurses, anesthesia, and respiratory therapists. Hospitals that were high performing included more support staff (pharmacy, clerical, security, spiritual staff).[45] Top-performing hospitals were also more likely to have a dedicated resuscitation team that had no clinical responsibilities that interfered with their participation in the team. Effective communication among team members was also identified as a positive factor in improving outcomes.[45]


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    Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN
Attributed To: Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN

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Rhythm, Ventricular Tachycardia (VT, V Tach) - Questions

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During a lobectomy, a patient suddenly develops ventricular tachycardia and hypotension. What is the first step in treatment?



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A 56-year-old male with no cardiac history complains of palpitations and lightheadedness for 1 hour. His blood pressure is 90/50 mmHg, and his heart rate is 160 beats/min. A cardiac monitor reveals tachycardia, regular rhythm, and wide QRS complexes (QRS of 0.14). At this point, which action would be appropriate?



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A 28-year-old is about to undergo surgery after being stabbed in the groin. As soon as he is induced, the patient develops rapid ventricular tachycardia. What is the appropriate next step in his management?



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Which of the following about ventricular tachycardia is false?



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Which of the following is the initial step in caring for a patient with the rhythm shown on the cardiac monitor in this image?

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A 45-year-old male has a monomorphic ventricular tachycardia and is hemodynamically stable. What is the best management for this patient?



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What should be the first intervention if an observed patient loses consciousness and is diagnosed with pulseless ventricular tachycardia?



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Which of the following drugs is best used to treat ventricular tachycardia in a patient with impaired left ventricular function?



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A 68-year-old female with a history of a myocardial infarction and chronic atrial fibrillation presents with palpitations of sudden onset one hour before the presentation. She does not report chest pain or lightheadedness. Medications include warfarin, metoprolol, and enalapril. The ECG shows a rate of 175 with wide complexes. What finding would support the diagnosis of ventricular tachycardia?

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Select the condition not associated with syncope caused by ventricular tachycardia.



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In addition to wide complex tachycardia, what is a characteristic of ventricular tachycardia?

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A patient with ventricular tachycardia on ECG loses consciousness. What is the next step in treatment?



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Which of the following antiarrhythmic drugs is not used to treat clinically stable ventricular tachycardia?



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Which of the following is preferred for treatment of ventricular tachycardia?



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Which of the following is most increased with ventricular tachycardia?



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In a patient with structural heart disease and a history of nonsustained ventricular tachycardia (VT), what is the next best step in management?



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Among patients with a history of non-sustained ventricular tachycardia which of the following co-morbidities is associated with the highest risk of sudden cardiac death?



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In a patient with ventricular tachycardia, which step should be taken first in the assessment and treatment of the patient?



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A healthcare provider notes this rhythm on a cardiac monitor after responding to a call for assistance. Which of the following tasks listed below would be the initial priority?

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A 17-year old is about to undergo surgery after being stabbed in the groin. As soon as he is induced, the patient develops rapid ventricular tachycardia but his blood pressure is stable. What is the next step in his management?



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A 65-year-old female with past medical history of atrial fibrillation, hypertension, chronic old left bundle branch block and diabetes mellitus is admitted to the hospital with community-acquired pneumonia. She is on dofetilide for atrial fibrillation and apixaban for anticoagulation. She is started on levofloxacin 750 mg IV for pneumonia. Twelve hours after the admission, the patient becomes unconscious, and the telemetry shows she has polymorphic ventricular tachycardia. Immediate defibrillatory shock was delivered, and patient reverted to sinus rhythm. The patient was transferred to the cardiac intensive care unit. It is noted that she is on levofloxacin which prolongs QTc and dofetilide also has QTc prolonging effect. Both medications are discontinued immediately. Which of the following should be recommended?



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While in the intensive care unit, a patient develops the rhythm shown in the image below. Which of the following is true of this condition? Select all that apply.

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An intensive care unit nurse is on an overtime shift and is floated to a telemetry unit. Slightly familiar with their surroundings, the nurse proceeds to receive bedside report on six patients. As fate would have it, 30 minutes into their shift an alarm sounds from the centralized telemetry monitoring station. The nurse grabs the nearby crash cart after a code blue is announced overhead and races to the room. The patient is unconscious, unresponsive, and without a pulse. The cardiac monitor displays the rhythm shown in the image below. How should the nurse proceed? Select all that apply.

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Rhythm, Ventricular Tachycardia (VT, V Tach) - References

References

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