Pulseless ventricular tachycardia
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]
Synonyms and keywords:
Overview
Pulseless ventricular tachycardia is an often fatal cardiac dysrhythmia where the regular rhythmic contraction of the heart is replaced by non-rhythmic, faster, yet inadequate contractions. These ineffective contractions do not appropriately perfuse the organ, leading to ischemia as well as heart failure. This condition requires immediate medical attention as it is an emergency and can lead to ventricular fibrillation and sudden death.[1]
Historical Perspective
Classification
Pulseless ventricular tachycardia as a ventricular tachycardia, may be classified based on the morphology of the QRS complexes into two subtypes/groups: monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia.
Pathophysiology
Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity.[2] Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.[3]
In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.[1]
Causes
Structural heart disease is the most common cause of pulseless ventricular tachycardia. Other causes include but are not limited to, drugs/medications, congenital heart diseases, not to mention congenital and inherited channelopathies. It is important to note that QT interval lengthening medications, as well as electrolyte disturbances, can also result in pulseless ventricular tachycardia.[4]
Differentiating Pulseless ventricular tachycardia from other Diseases
Pulseless ventricular tachycardia must be differentiated from other diseases that cause wide complex tachycardia, such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia.[5]
Epidemiology and Demographics
Ventricular tachycardia and ventricular fibrillation[6] are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn't account for deaths due to unwitnessed dysrhythmias.[7]
Risk Factors
Screening
According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms such as QT syndrome, hypertrophic or dilated cardiomyopathy and right ventricular dysplasia.[8][9]
Natural History, Complications, and Prognosis
On initial presentation, patients with impending pulseless ventricular tachycardia may present with signs of inadequate cardiac perfusion such as chest pain, shortness of breath, diaphoresis, palpitations, and syncope. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1. Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse. If defibrillation is not begun as soon as possible patients may progress to cardiac arrest and death. Common complications include but are not limited to anoxic brain injury, ischemic-reperfusion injury, infections, cardiac arrest and death. Prognosis is best if the tachycardia is treated almost immediately after onset. [1][10][11]
Diagnosis
Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Related Chapters
- Tachycardia
- Ventricular Tachycardia
- Wide complex tachycardia
- Ventricular fibrillation
- Supraventricular tachycardia
- ↑ 1.0 1.1 1.2 Foglesong A, Mathew D. PMID 32119354 Check
|pmid=value (help). Missing or empty|title=(help) - ↑ Armendares S, Pérez Treviño C (1968). "[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)]". Arch Inst Cardiol Mex (in Spanish; Castilian). 38 (6): 779–91. PMID 4237287.
- ↑ Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A (August 1991). "Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7". Cancer Res. 51 (15): 4097–101. PMID 1855225.
- ↑ Baldzizhar A, Manuylova E, Marchenko R, Kryvalap Y, Carey MG (September 2016). "Ventricular Tachycardias: Characteristics and Management". Crit Care Nurs Clin North Am. 28 (3): 317–29. doi:10.1016/j.cnc.2016.04.004. PMID 27484660.
- ↑ "Correction". Heart Rhythm. 15 (11): e282. November 2018. doi:10.1016/j.hrthm.2018.09.024. PMID 30267690.
- ↑ Tang PT, Shenasa M, Boyle NG (December 2017). "Ventricular Arrhythmias and Sudden Cardiac Death". Card Electrophysiol Clin. 9 (4): 693–708. doi:10.1016/j.ccep.2017.08.004. PMID 29173411.
- ↑ McNally B, Robb R, Mehta M, Vellano K, Valderrama AL, Yoon PW, Sasson C, Crouch A, Perez AB, Merritt R, Kellermann A (July 2011). "Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010". MMWR Surveill Summ. 60 (8): 1–19. PMID 21796098.
- ↑ Shoubkhova TS (July 1968). "[Determination of the particle size of suspensions of dried bacteria by the method of turbidimetric analysis]". Zh. Mikrobiol. Epidemiol. Immunobiol. (in Russian). 45 (7): 108–10. PMID 5731530.
- ↑ Flannery MD, La Gerche A (January 2019). "Sudden Death and Ventricular Arrhythmias in Athletes: Screening, De-Training and the Role of Catheter Ablation". Heart Lung Circ. 28 (1): 155–163. doi:10.1016/j.hlc.2018.10.004. PMID 30554599.
- ↑ Kang Y (August 2019). "Management of post-cardiac arrest syndrome". Acute Crit Care. 34 (3): 173–178. doi:10.4266/acc.2019.00654. PMC 6849015 Check
|pmc=value (help). PMID 31723926. - ↑ Kang JY, Kim YJ, Shin YJ, Huh JW, Hong SB, Kim WY (August 2019). "Association Between Time to Defibrillation and Neurologic Outcome in Patients With In-Hospital Cardiac Arrest". Am. J. Med. Sci. 358 (2): 143–148. doi:10.1016/j.amjms.2019.05.003. PMID 31200920.