Pulseless ventricular tachycardia overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]]. | Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]]. | ||
==Causes== | ==Causes== | ||
Revision as of 15:45, 14 June 2020
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Pulseless ventricular tachycardia Microchapters |
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Differentiating Pulseless ventricular tachycardia from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Pulseless ventricular tachycardia overview On the Web |
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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.
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.
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.
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
Epidemiology and Demographics
- Ventricular tachycardia and ventricular fibrillation[2] 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.[3]
- The majority of deaths due to ventricular arrhythmias occur In adults over 35 years of age.
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.[4][5]
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][6][7]
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 Foglesong A, Mathew D. PMID 32119354 Check
|pmid=value (help). Missing or empty|title=(help) - ↑ 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.