Ebook Clinical arrhythmology: Part 2

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Ebook Clinical arrhythmology: Part 2

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(BQ) Part 2 book Clinical arrhythmology presents the following contents: Diagnosis, prognosis and treatment of arrhythmias; the ECG and risk of arrhythmias and sudden death in different heart diseases and situations.

CH APTER Active Ventricular Arrhythmias In this chapter we will discuss premature ventricular complexes (PVC) both isolated and in runs, and the different types of ventricular tachycardia (VT), as well as ventricular fibrillation and ventricular flutter (Chapter 1, Table 1.1) Premature ventricular complexes Concept Premature ventricular complexes (PVC) are premature impulses (complexes) that originate in the ventricles Therefore, they present a different morphology from that of the baseline rhythm ● If the PVC are repetitive, they form pairs (two consecutive PVC) or VT runs (≥3) (Figures 5.1B and 5.3) Conventionally, a VT is considered to be sustained when it lasts for more than 30 s Infrequent short runs of non-sustained monomorphic VT are included in this section They correspond to Type 4B in Lown’s classification (Lown and Wolf 1971) (Figure 5.3 and Table 5.1) ● In this section we have not included runs of VT when they occur very frequently (repeated monomorphic non-sustained VT) (Figure 5.4), as they present clinical, hemodynamic, and therapeutic features that are more similar to sustained VT than to isolated PVC (Figure 5.3) (see Other monomorphic ventricular tachycardias) Torsades de Pointes-type VTs (Dessertene 1966) will not be included either Although they occur in runs, they are considered polymorphic VT and have quite different prognostic and therapeutic implications compared to isolated PVC or the short runs of classical monomorphic VT (Figure 5.5) ● Clinical Arrhythmology, First Edition Antoni Bayés de Luna © 2011 John Wiley & Sons Ltd Published 2011 by John Wiley & Sons Ltd ISBN: 978-0-470-65636-5 Mechanisms The PVC may be caused by extrasystolic or parasystolic mechanisms (Figures 5.1 and 5.2): 1) Extrasystoles, which are much more frequent, are induced by a mechanism related to the preceding QRS complex For this reason, they feature a fixed or nearly fixed coupling interval (Figure 5.1) This is generally a reentrant mechanism (usually micro-reentry, but also branch–to-branch, or around a necrotic or fibrotic area) (see Figure 3.6) They may also be induced by post-potentials (triggered activity) (see Figure 3.5), or, in some exceptions, may be due to supernormal excitability and conduction In the latter case, there should be some factor at a particular point of the cycle that turns the subthreshold stimulus into a suprathreshold stimulus, which triggers the premature impulse This may happen when the stimulus falls in the supernormal excitability zone (see Figure 3.15) 2) Parasystoles are much less frequent They are impulses that are independent of the baseline rhythm The electrophysiologic mechanism is an ectopic focus protected from depolarization by the impulses of the baseline rhythm In general, this is due to the presence of a unidirectional entrance block in the parasystolic focus (see Figure 3.17) A Table 5.1 Lown classification of premature ventricular complexes (PVC) (Lown and Wolf 1971), according to prognostic significance (Holter electrocardiogram) Grade 0: No PVC Grade 1: 80 ms), and interectopic intervals, which are multiples of the parasystolic cycle length Certain differences are permitted, as the discharge rate of the parasystolic focus may show fluctuations of up to 200 ms), and, contrary to this, as we have already explained, the coupling interval in some infrequent circumstances may be fixed (see Mechanisms) Furthermore, the lack of a mathematical relationship between interectopic intervals can be due to either incomplete protection of the parasystolic pacemaker (Cohen et al 1973), or to electronic modulation of the parasystolic rhythm (Oreto et al 1988) The hypothesis postulated by Kinoshita (1977) that parasystole may be explained by a reentry mechanism lacks any electrophysiologic and experimental demonstration (Oreto 2010) Bayes_c05.indd 184 1/22/2011 7:09:51 PM Active Ventricular Arrhythmias II A B C D 185 E Figure 5.6 Late trigeminal premature ventricular complexes (PVC) occurring in the interval PR, and showing progressive fusion degrees from C to E (see Figure 3.30) Electrocardiographic forms of presentation ● Premature ventricular complexes usually show a complete compensatory pause (the distance between the QRS complex preceding the PVC and the following QRS complex double the sinus cadence) (Figure 5.7A) This happens because the PVC usually fails to discharge the sinus node In consequence, the distance BC is doubles the distance AB, represented as two sinus cycles ● If the PVC discharges the sinus node, a noncomplete compensatory pause may be observed (BC

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  • Cover Page

  • Companion website

  • Title: CLINICAL ARRHYTHMOLOGY

  • ISBN 9780470656365

  • Contents

  • Foreword by Dr. Valentin Fuster

  • Foreword by Dr. Pere Brugada i Terradellas

  • Preface

  • Recommended General Bibliography

  • PART I Anatomical and Electrophysiological Considerations, Clinical Aspects, and Mechanisms of Cardiac Arrhythmias

    • CHAPTER 1 Clinical Aspects of Arrhythmias

      • Definition of arrhythmia

      • Classification

      • Clinical significance and symptoms

      • The importance of clinical history and physical examination in diagnosis and assessment of arrhythmias

      • The importance of surface ECG and other techniques

      • Electrocardiographic diagnosis of arrhythmias: preliminary considerations

      • References

      • CHAPTER 2 Anatomic and Electrophysiologic Basis

        • Anatomic basis

        • Electrophysiologic characteristics

        • References

        • CHAPTER 3 Electrophysiologic Mechanisms

          • Mechanisms responsible for active cardiac arrhythmias

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