Overview Show
BackgroundVentricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. Assessment and treatment of VPCs is challenging and complex, and is highly dependent on the clinical context. The prognostic significance of VPCs is variable and, again, best interpreted in the context of the underlying cardiac condition. The approach to the evaluation and management of VPCs has undergone dramatic changes in the last decade. Observational studies and inferences from typical electrophysiology studies were initially focused on ventricular ectopy triggering ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, as a mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). The Cardiac Arrhythmia Suppression Trial (CAST) and other arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit. [1] 
PathophysiologyVery few studies have evaluated the pathophysiology of VPCs in human subjects. Most of the information is derived from animal studies. Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity, as follows:
EtiologyCardiac causes of VPCs include the following:
Noncardiac causes of VPCs include the following:
EpidemiologyUnited States dataThe reported prevalence of VPCs varies between studies, depending on the population studied, duration of observation, and method of detection. In asymptomatic patients, VPCs are infrequently noted when only a single 12-lead ECG is used for ascertainment. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more VPCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. VPCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse. International dataData from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 VPCs per hour when 24-h Holter monitoring was used. [3, 4] In a study evaluating the features of frequent idiopathic VPCs in the Korean, investigators reported a mean patient age of 54.7 ± 16.8 years and a slight female preponderance (54.8%). [5] The most common typical VPC-related symptoms/signs were palpitation and a dropped beat (59.2%), whereas the most common ECG features were left bundle branch block, an inferior axis, and late precordial R-wave transition. Sex- and age-related demographicsThe Framingham heart study demonstrated increased prevalence of VPCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD. VPCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age. PrognosisThe prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. Overall, VPCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between VPC frequency and mortality, even in this group, is not robust. Importantly, no survival benefit in in any population has been convincingly demonstrated as a consequence of suppressing VPCs . In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting over 10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death. [6] Less frequent VPCs did not increase the risk. In general, multimorphic VPCs connote a poorer prognosis than uniform morphologic VPCs. In patients post-MI, frequent VPCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak. In 2 studies, frequent or complex ventricular ectopy (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during exercise was an independent predictor of death. [6, 7] However, in another study, frequent VPCs only during exercise did not independently predict an increased risk; instead frequent VPCs during recovery was a stronger predictor of death. [8] Frequent VPCs, especially when they occur in a bigeminal pattern, can cause or contribute to tachycardia-induced cardiomyopathy, which reversed by elimination of the PVCs through catheter ablation. [6, 9, 10, 11] However, the extent to which this can be generalized to larger populations remains uncertain. Caution is in order, primarily because prior attempts at pharmacologic suppression were associated with unexpected and deleterious outcomes. [12]
Author Jatin Dave, MD, MPH Part-Time Clinical Instructor, Department of Medicine, Harvard Medical School; Attending Physician, Division of Aging, Department of Medicine, Brigham and Women's Hospital; Medical Director of Geriatrics, Tufts Health Plan Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Tufts Health Plan, a not for profit organization. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Brian Olshansky, MD, FESC, FAHA, FACC, FHRS Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine Brian Olshansky, MD, FESC, FAHA, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, European Society of Cardiology, Heart Rhythm Society Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Astra Zeneca, Artivion<br/>DSMB. Chief Editor Jose M Dizon, MD Professor of Clinical Medicine, Clinical Electrophysiology Laboratory, Division of Cardiology, Columbia University College of Physicians and Surgeons; Attending Physician, Department of Medicine, New York-Presbyterian/Columbia University Medical Center Jose M Dizon, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society Disclosure: Nothing to disclose. Acknowledgements The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors John Michael Gaziano, MD, MPH; Revat Lakhia, MD; and Shivkumar H Jha, MD, to the development and writing of this article. In which part of the cardiac cycle is an ectopic impulse the greatest risk to the patient quizlet?Identify the area of the cardiac cycle in which an ectopic impulse causes the greatest risk to the patient? The patient is at greatest risk if the ectopic impulse falls on the T wave. This is called the R-on-T phenomenon.
What is the most vulnerable period of the EKG where an arrhythmia can be stimulated from an ectopic impulse?The vulnerable period (VP in Fig. 11-7 is actually phase 3 and represented in the ECG as the T-wave) is dangerous, because an electrical shock, when given during this period, will cause in itself ventricular fibrillation. Here is shown sinus rhythm and one ectopic beat followed by ventricular fibrillation.
What is a single ectopic beat that occurs as a result of an irritable focus in the atria?Supraventricular Tachycardia. Tachycardias arising from an ectopic focus in the atria or AV junction are called supraventricular tachycardias (SVT). Heart rate is faster than 150 per minute and commonly around 180 per minute.
Which term is used for the property of cardiac cell responding mechanically to an impulse?Properties of Cardiac Cells
The heart has pacemaker cells that can generate an electrical impulse without being stimulated by a nerve. The ability of cardiac pacemaker cells to create an electrical impulse without being stimulated by another source is called automaticity.
|
In which part of the cardiac cycle is an ectopic impulse the greatest risk to the patient
zusammenhängende Posts
Urheberrechte © © 2024 WIKIFI Inc.
