TY - CHAP M1 - Book, Section TI - Reentrant Arrhythmias A1 - Ferry, David R. PY - 2007 T2 - ECG in 10 Days, 2e AB - Reentry—a disorder of impulse transmissionMechanisms of reentryReentry requires:At least two conduction pathwaysVariable block in one of the pathwaysIf two pathways have similar conduction velocities, the electrical impulses will merge distally and no arrhythmia will occur (see figure).If an event (e.g., a premature ventricular contraction [PVC]) occurs at the right time and place to make one of the two pathways refractory, the impulse will be blocked in that limb. If the impulse from the other limb travels back up the blocked limb, it may find the previously refractory area able to conduct.If the impulse reaches the initial branch point of the two pathways before the next normal impulse arrives from above, the arrhythmia can perpetuate itself.Properties of reentrant arrhythmiasReentrant arrhythmias start and stop abruptly (paroxysmally).They are usually initiated by a premature beat.The reentrant arrhythmias that have a discreet reentrant pathway [atrial flutter, AV nodal reentrant tachycardia [AVNRT], most ventricular tachycardia (VT)] are very regular.Reentrant arrhythmias can be terminated by any mechanism, which makes some part of the reentrant pathway refractory, including vagal maneuvers (AVNRT), chest thump (VT), medications which slow conduction (most reentrant arrhythmias) or electrocardioversion (all reentrant arrhythmias).The major reentrant arrhythmiasAtrial fibrillationMechanisms and causes (Day 5-01) (Day 5-02) (Day 5-03) (Day 5-04) DAY 5-01 DAY 5-02 DAY 5-03 DAY 5-04 The most likely cause of atrial fibrillation is microreentry between islands of atrial muscle in the vicinity of the insertion of the pulmonary veins into the left atrium.Atrial fibrillation requires a certain amount of atrial tissue to be present to sustain the arrhythmia (an important concept in therapeutic approaches).Atrial pressure overload (e.g., from heart failure, hypertensive heart disease, ventricular failure, or valvular heart disease) is the clinical situation responsible for the vast majority of cases.Heart rateThe multiple reentrant wave fronts combine to have an atrial rate of 400–600.The ventricular response is irregular.ECG morphologyThe baseline varies from coarse, irregular fibrillatory waves to virtually flat.The QRS complexes are narrow unless there is an intraventricular conduction defect (IVCD).Response to vagal maneuvers or AV nodal blocking medications (i.e., IV adenosine).These maneuvers do not affect the atrial fibrillation itself.The ventricular response is irregularly slowed.Atrial flutterMechanisms and causes (Day 5-05) (Day 5-06)Most examples are likely due to reentry.The common reentry pathway is counterclockwise around the tricuspid annulus and involving the interatrial septum.Atypical forms exist, which presumably have other reentrant pathways and are often faster than typical flutter. (Day 5-07)Atrial pressure overload (from similar causes as for atrial fibrillation) is responsible for the majority of cases. DAY 5-05 DAY 5-06 DAY 5-07 Heart rateThe atrial rate is 220–320, more commonly 280–320, with a median of 300.Patients receiving antiarrhythmic therapy (e.g., with quinidine, sotalol, or amiodarone) may have slower (as low as 200) flutter rates.The ventricular response is usually a whole even number division of the atrial rate (2:1, 4:1, 8:1), although alternating 2:1/4:1 or variable ventricular responses are encountered. (Day 5-08) (Day 5-09)One of Marriott’s laws—every absolutely regular supraventricular tachycardia with a rate of 150 is atrial flutter with 2:1 block until proven otherwise.Rarely, atrial flutter can present with ... SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accesscardiology.mhmedical.com/content.aspx?aid=1128943428 ER -