Pulseless ventricular tachycardia overview
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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]
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. In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation, pulselessness and sudden death. In 1909,Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia. It was also first implied in 1921 that coronary occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia 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] As a result of markedly rapid ventricular contractions, diastole is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in cardiac output, and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, wide QRS complexes above 120 milliseconds, the dissociation between the atria and ventricles, presence of fusion beats, and an electrical axis between -90 to -180.[1] Because majority of wide complex tachycardia cases will be ventricular tachycardia, any wide complex tachycardia should always be assumed to be due to ventricular tachycardia until proven otherwise.
Historical Perspective
- There is limited information about the historical perspective of Pulseless ventricular tachycardia.
- Gallavardin in 1906 was responsible for the discovery of the rationale behind cardiac instability leading to ventricular tachycardia. He further put forth the idea that ventricular tachycardia could convert to ventricular fibrillation and lead to cardiac arrest and death.
- The first electrographic description of ventricular tachycardia was given by Thomas Lewis in 1909.
- Coronary occlusion was suggested to be the main cause of ventricular tachycardia in 1921.
- Several advancements have since been made in the diagnosis and management protocols on Ventricular tachycardia.
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.[3] 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.[4]
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.[5]
Life-threatening Causes
- Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. They are mainly due to acute conditions that promote rapid dysfunction of automaticity and include. but are not limited to;[6][7][8][9]
Common Causes
- Acid-base disturbances
- Antiarrhythmics
- Azithromycin
- Cardioversion
- Clarithromycin
- Claritin
- Cocaine
- Congestive heart failure
- Dilated cardiomyopathy
- Erythromycin
- Hypokalemia
- Hypomagnesemia
- Myocarditis
- Obstructive sleep apnea
- Pulmonary artery catheter
- STEMI
- Tricyclic antidepressants
Differentiating Xyz from Other Diseases
Epidemiology and Demographics
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.[10][11]
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][12][13]
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Interventions
Surgery
Primary Prevention
Secondary Prevention
References
- ↑ 1.0 1.1 1.2 1.3 Foglesong A, Mathew D. PMID 32119354 Check
|pmid=value (help). Missing or empty|title=(help) - ↑ "Ventricular tachycardia historical perspective - wikidoc".
- ↑ 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.
- ↑ Ajijola, Olujimi A.; Tung, Roderick; Shivkumar, Kalyanam (2014). "Ventricular tachycardia in ischemic heart disease substrates". Indian Heart Journal. 66: S24–S34. doi:10.1016/j.ihj.2013.12.039. ISSN 0019-4832.
- ↑ Meja Lopez, Eliany; Malhotra, Rohit (2019). "Ventricular Tachycardia in Structural Heart Disease". Journal of Innovations in Cardiac Rhythm Management. 10 (8): 3762–3773. doi:10.19102/icrm.2019.100801. ISSN 2156-3977.
- ↑ Coughtrie, Abigail L; Behr, Elijah R; Layton, Deborah; Marshall, Vanessa; Camm, A John; Shakir, Saad A W (2017). "Drugs and life-threatening ventricular arrhythmia risk: results from the DARE study cohort". BMJ Open. 7 (10): e016627. doi:10.1136/bmjopen-2017-016627. ISSN 2044-6055.
- ↑ El-Sherif, Nabil (2001). "Mechanism of Ventricular Arrhythmias in the Long QT Syndrome: On Hermeneutics". Journal of Cardiovascular Electrophysiology. 12 (8): 973–976. doi:10.1046/j.1540-8167.2001.00973.x. ISSN 1045-3873.
- ↑ 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.