Please purchase the course before starting the lesson. Tachycardia is defined as a heart rate greater than what is considered normal for a child’s age. Like bradycardia, tachycardia can be life-threatening if it compromises the heart’s ability to perfuse effectively. When the heart beats too quickly, there is a shortened relaxation
phase. This causes two main problems: the ventricles are unable to fill completely, so cardiac output is lowered; and the coronary arteries receive less blood, so supply to the heart is decreased. There are several kinds of tachycardia, and they can be difficult to differentiate in children on ECG due to the elevated heart rate. Pediatric tachyarrhythmias are first divided into narrow complex or wide complex tachycardia. Measure the QRS complex on a standard ECG to assess its width.
Table 16 Narrow QRS ComplexAtrial flutter is an uncommon rhythm distinguished on an ECG as a sawtooth pattern. It is caused by an abnormal pathway that causes the atria to beat very quickly and ineffectively. Atrial contractions may exceed 300 bpm but not all of these will reach the AV node and cause a ventricular contraction. Most often, PALS providers will have to distinguish between two similar narrow QRS complex tachyarrhythmias: sinus tachycardia and supraventricular tachycardia (SVT). SVT is more commonly caused by accessory pathway reentry, AV node reentry, and ectopic atrial focus.
Table 17  Wide QRS ComplexVentricular tachycardia (VT) is uncommon in children but can be rapidly fatal. Unless the person has a documented wide complex tachyarrhythmia, an ECG with a QRS complex greater than 0.09 seconds is VT until proven otherwise. Polymorphic VT, Torsades de Pointes, and unusual SVT (SVT with wide complexes due to aberrant conduction) may be reversible, e.g. magnesium for Torsades, but do not delay treatment for VT. Any of these rhythms can devolve into ventricular fibrillation (VF). VT may not be particularly rapid (simply greater than 120 bpm) but is regular. Generally, P waves are lost during VT or become dissociated from the QRS complex. Fusion beats are a sign of VT and are produced when both a supraventricular and ventricular impulse combine to produce a hybrid appearing QRS (fusion beat) (Figure 14). Last reviewed: 30 Sep 2022 Last updated: 18 Oct 2019 SummaryA ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination due to hemodynamic instability. ECG findings include wide QRS complex (duration >120 milliseconds) at a rate greater than 100 bpm. Patients may have a normal cardiac output or may be hemodynamically compromised during episodes of ventricular tachycardia (VT). Presence or absence of symptoms does not differentiate VT from supraventricular tachycardia. Torsades de pointes: polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation. Sustained VT is usually observed in ischemic and nonischemic cardiomyopathy, but idiopathic VT may also be observed in patients without structural heart disease. Among patients with prior myocardial infarction or nonischemic cardiomyopathy, VT is usually due to reentry involving regions of slowed conduction adjacent to scar. Owing to the unpredictable and life-threatening nature of most etiologies of sustained VT, prophylactic implantable cardioverter defibrillator implantation is recommended in high-risk patients. DefinitionSustained ventricular tachycardia (VT) is a ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination earlier due to hemodynamic instability. VT is defined as a wide complex tachycardia (QRS 120 milliseconds or greater) that originates from one of the ventricles, and is not due to aberrant conduction (e.g., from
bundle branch block), at a rate of 100 bpm or greater. "Idiopathic" VT occurs in the absence of apparent structural heart disease (e.g., prior myocardial infarction, active ischemia, cardiomyopathy, valvular disease, arrhythmogenic right ventricular cardiomyopathy, left ventricular noncompaction, or other disorders of the myocardium), known channelopathy (e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, short QT syndrome), drug toxicity, or electrolyte imbalance. VT
can be described as monomorphic or polymorphic. Torsades de pointes is a polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation. Sustained VT usually results in hypotension and symptoms of weakness, syncope, or palpitations; however, the arrhythmia may be present in patients who are asymptomatic and normotensive.[Figure caption and citation for the preceding image
starts]: Sustained (monomorphic) ventricular tachycardiaFrom the collection of Prof Sei Iwai; used with permission [Citation ends]. History and examKey diagnostic factors
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Other diagnostic factors Risk factors
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More investigations to consider Treatment algorithmhemodynamically unstable ventricular tachycardia with a pulsetorsades de pointescatecholaminergic polymorphic ventricular tachycardiahemodynamically stable nonidiopathic sustained ventricular tachycardiahemodynamically stable idiopathic sustained ventricular tachycardianonidiopathic: at high risk for ventricular tachycardia or history of sustained ventricular tachycardia/cardiac arrest without identifiable reversible causeidiopathic ventricular tachycardiaContributorsAuthorsSei Iwai, MD, FACC, FHRSProfessor of Clinical Medicine New York Medical College Director, Cardiac Electrophysiology Westchester Medical Center Health Network Valhalla NY DisclosuresSI is on the Biosense-Webster speakers' bureau. He receives honoraria from Biotronik, Boston Scientific, and Medtronic for lectures, and research grant support from Boston Scientific. AcknowledgementsProf Sei Iwai would like to gratefully acknowledge Dr Kenneth Stein and Dr Richard Keating, previous contributors to this topic. DisclosuresKS declares he is an employee of and shareholder in Boston Scientific, a manufacturer of implantable cardioverter defibrillators and ablation catheters. RK declares that he has no competing interests. Peer reviewersSuneet Mittal, MDDirector Electrophysiology Laboratory The St. Luke's-Roosevelt Hospital Center New York NY DisclosuresSM declares that he has no competing interests. Kenneth A. Ellenbogen, MDKontos Professor of Cardiology Medical College of Virginia Richmond VA DisclosuresKAE declares that he has no competing interests. Kim Rajappan, MA, MD, MRCPConsultant Cardiologist and Electrophysiologist Cardiac Department John Radcliffe Hospital Oxford UK DisclosuresKR declares that she has no competing interests.
What is VT in ECG?Ventricular tachycardia is a heart rhythm problem (arrhythmia) caused by irregular electrical signals in the lower chambers of the heart (ventricles). This condition may also be called V-tach or VT. A healthy heart typically beats about 60 to 100 times a minute at rest.
Is there a QRS in VVentricular tachycardia refers to a wide QRS complex heart rhythm — that is, a QRS duration beyond 120 milliseconds — originating in the ventricles at a rate of greater than 100 beats per minute. This can be hemodynamically unstable, causing severe hypotension, and can thus be life-threatening.
Does ventricular tachycardia show up on EKG?Most cases of ventricular tachycardia are diagnosed through an electrocardiogram (ECG/EKG), which measures the electrical activity of the heart.
Does VT have P waves?VT is recognized by abnormally wide and bizarre QRS complex morphology. P waves are present but may be hiding in the QRS-T complexes. AV dissociation occurs due to the accelerated ventricular rate as compared to the sinus rate.
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Which electrocardiogram ECG characteristic is consistent with ventricular tachycardia VT )?
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