When it lasts only a few seconds, ventricular tachycardia may cause no problems. But when sustained, ventricular tachycardia can lower the blood pressure, resulting in syncope (fainting) or lightheadedness. Ventricular tachycardia can also lead to ventricular fibrillation (a life-threatening arrhythmia) and cardiac arrest.
Ventricular tachycardia may last for only a few seconds, or it can last for much longer. You may feel dizzy or short of breath, or have chest pain. Sometimes, ventricular tachycardia can cause your heart to stop (sudden cardiac arrest), which is a life-threatening medical emergency.
427.1The appropriate ICD‐9 code for ventricular tachycardia is 427.1 (HCC 96), Paroxysmal ventricular tachycardia, (with or without documentation of “paroxysmal”).
ICD-10 code I47. 2 for Ventricular tachycardia is a medical classification as listed by WHO under the range - Diseases of the circulatory system .
In ICD-10-CM the codes would be I47. 2, ventricular tachycardia, and code I46. 9, Cardiac arrest, unspecified.
I47. 2 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes.
Other specified cardiac arrhythmias I49. 8 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2022 edition of ICD-10-CM I49. 8 became effective on October 1, 2021.
Recurrent sustained ventricular tachycardia is one of the late complications following recovery from myocardial infarction. Our definition of “sustained” ventricular tachycardia relates to episodes which necessitate either cardioversion or parenteral medication for termination.
Another difference is the number of codes: ICD-10-CM has 68,000 codes, while ICD-10-PCS has 87,000 codes.
Non-sustained ventricular tachycardia (NSVT, or nonsustained V-tach) is an abnormal heart rhythm that starts in the ventricles, which are the lower chambers of the heart. It occurs as three or more consecutive heartbeats at a rate of more than 100 beats per minute and lasts for less than 30 seconds.
In ICD-10-CM the codes would be I47.2, ventricular tachycardia, and code I46.9, Cardiac arrest, unspecified.
If the cardiac arrest is due to “other” underlying condition (I46.8), the code first note is for the underlying condition, and we still have a code (I46.9) cardiac arrest, cause unspecified. There is also an Excludes 1 note for ventricular tachycardia, which states that if the documentation provides specificity regarding the type of tachycardia, ...
If cardiac arrest is the principal diagnosis with the ventricular tachycardia as a secondary diagnosis, the codes map to DRG 298 with a relative weight of 0.4395. If the ventricular tachycardia is the principal diagnosis and the cardiac arrest is a secondary diagnosis, it maps to DRG 310 with a relative weight of 0.5627.
The only time coders can use information in an EMT note without having the provider state it in the medical record is for recording of the complete Glasgow coma scale. Usually, if the patient is transported via ambulance, the EMT note is scanned into the record, but not always.
Ventricular tachycardia (VT) electrical storm (ES) is a severe clinical condition characterized by clustering episodes of ventricular arrhythmia in a short amount of time. The current definition of ES implies at least 3 distinct episodes of sustained VT or ventricular fibrillation (VF) within the last 24-h or the occurrence of incessant VT for at least 12-h. In patients with ICD, ES is defined by ≥ 3 appropriate device interventions in the last 24-h (separated by at least 5-min one from the other) either with antitachycardia pacing (ATP) or direct-current shock[1]. Although ES mainly occurs in patients with structural heart disease and low left ventricular ejection fraction (LVEF), it may affect also patients with inherited arrhythmic syndromes and structurally normal heart (i.e., Brugada syndrome and catecholaminergic polymorphic VT) representing a life-threatening condition requiring urgent medical care[2]. Several strategies have been proposed to manage ES with most of the data coming from small retrospective series, lacking large randomized-controlled trials. There are several substantial differences in the approach and treatment of ES in the setting of structural heart disease compared to primitive arrhythmic syndromes. In this review, we will focus on the management of ES in the setting of structural heart disease by summarizing the current therapeutic strategies in a stepwise approach based on available evidence (Figure (Figure11).
Electrical storm (ES) is a medical emergency characterized by repetitive episodes of sustained ventricular arrhythmias (VAs) in a limited amount of time (at least 3 within a 24-h period) leading to repeated appropriate implantable cardioverter defibrillator therapies. The occurrence of ES represents a major turning point in the natural history of patients with structural heart disease being associated with poor short- and long-term survival particularly in those with compromised left ventricular ejection fraction (LVEF) that can develop hemodynamic decompensation and multi-organ failure. Management of ES is challenging with limited available evidence coming from small retrospective series and a substantial lack of randomized-controlled trials. In general, a multidisciplinary approach including medical therapies such as anti-arrhythmic drugs, sedation, as well as interventional approaches like catheter ablation, may be required. Accurate patient risk stratification at admission for ES is pivotal and should take into account hemodynamic tolerability of VAs as well as comorbidities like low LVEF, advanced NYHA class and chronic pulmonary disease. In high risk patients, prophylactic mechanical circulatory support with left ventricular assistance devices or extracorporeal membrane oxygenation should be considered as bridge to ablation and recovery. In the present manuscript we review the available strategies for management of ES and the evidence supporting them.
Procainamide is a class IC agent no longer widely used (unavailable in most countries) that may be helpful to acutely terminate VAs and prevent recurrences. It acts as fast sodium channel blocker, while its active metabolite N-acetylprocainamide blocks potassium channels and accounts for much of the antiarrhythmic effect in vivoas well as side effects like QT interval prolongation. Up to date there are only two small randomized controlled trials analyzing its role in the acute treatment of tolerated VT. In the study by Gorgels et al[28], procainamide demonstrated its superiority to lidocaine in acute VT termination in 29 patients while in the more recent PROCAMIO trial, intravenous administration of procainamide was shown to be safe and more effective compared to amiodarone in the treatment of tolerated monomorphic VT[29,30]. The most important acute adverse reaction is hypotension (up to 30% patients) which requires drug discontinuation in 11% of cases[28-30]. Data regarding the long-term efficacy of procainamide in preventing VT are lacking, moreover chronic therapy is limited by a number of systemic side effects including lupus-like syndrome, gastrointestinal disturbances, and autoimmune blood impairments. Plasma procainamide concentrations can be useful in initial dose titration; however, monitoring of QRS and QT interval is a valid alternative to prevent drug toxicity.
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the bundle of his, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide qrs complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (av dissociation).
A cardiac rhythm characterized by 3 or more consecutive complexes in duration emanating from the ventricles at a rate of >100 bpm (cycle length: <600 ms).