This particular arrhythmia can occur in various types of chronic heart disease. In this condition, the atria do not contract and relax sequentially during each cardiac cycle, resulting in a lack of contribution to ventricular filling. Instead, the atria display a continuous, uncoordinated rippling motion. On the ECG, there are no P waves, but instead, there are continuous irregular fluctuations in potential referred to as f waves. The activation of the AV node varies significantly from cycle to cycle, leading to an absence of a constant interval between successive QRS complexes or ventricular contractions. This irregularity affects the strength, volume, and rhythm of the pulse. In some cases, the atrial reentry loop and AV conduction pattern may be more regular than in atrial fibrillation, leading to the term atrial flutter.

Atrial fibrillation and flutter are generally not life-threatening, and individuals with these disturbances can usually function normally. However, because the atria do not contract and relax rhythmically, blood clots have a tendency to form in the atria. If these clots become dislodged, they may travel to the pulmonary or systemic vascular beds. To prevent the formation of such clots, patients with atrial fibrillation or flutter are typically treated with anticoagulant drugs like dicumarol. On the other hand, ventricular fibrillation, which is characterized by irregular, continuous, and uncoordinated twitching of the ventricular muscle fibers, can lead to loss of consciousness within seconds. This condition pumps no blood, and immediate resuscitation or spontaneous reversion to normal rhythm (which rarely occurs) is required to avoid death. Ventricular fibrillation may occur when the entire ventricle or a portion of it is deprived of its normal blood supply. It can also be triggered by electrocution or certain drugs and anesthetics. On the ECG, the fluctuations in potential during ventricular fibrillation are highly irregular.

Ventricular fibrillation often begins when a premature impulse arrives during the vulnerable period of the cardiac cycle, which corresponds to the downslope of the T wave on the ECG. During this period, the excitability of cardiac cells varies spatially, with some fibers still in their effective refractory periods, others having almost fully recovered their excitability, and some able to conduct impulses but at very slow conduction velocities. As a result, the action potentials are propagated over the chambers in irregular wavelets that travel along circuitous paths and at various conduction velocities. When a region of cardiac cells becomes excitable again, it is ultimately activated by one of the wave fronts circulating around the chamber, perpetuating the self-sustaining process.

In a normal subject, the electrocardiogram (ECG) recording (A) appears as Q SQ S P P T R R over a 1-second interval. However, in a patient with long QT syndrome, the ECG recording (B) shows an abnormal pattern with a prolonged QT interval.
Fig. 16.34A . This arrhythmia occurs in various types of chronic heart disease. The atria do not contract and relax sequentially during each cardiac cycle, and thus they do not contribute to ventricular filling. Instead, the atria undergo a continuous, uncoordinated rippling motion. P waves do not appear on the ECG; instead, the tracing shows continuous irregular fluctuations in potential called f waves. The AV node is activated at intervals that may vary considerably from cycle to cycle. Hence, no constant interval occurs between successive QRS complexes or between successive ventricular contractions. Because the strength of ventricular contraction depends on the interval between beats (see ), the volume and rhythm of the pulse are irregular. In many affected patients, the atrial reentry loop and the pattern of AV conduction are more regular than they are in atrial fibrillation. The rhythm is then referred to as atrial flutter.
•Fig. 16.34 Atrial(A)andventricular(B)fibrillation.
Atrialfibrillationandflutterarenotusuallylife-threatening;somepeoplewiththesedisturbancescanfunctionnormally.However,becausetheatriadonotcontractandrelaxrhythmically,bloodclotstendtoformintheatria.Suchclots,ifdislodged,maythentraveltothepulmonaryorsystemicvascularbeds.Patientswithatrialfibrillationorflutteraregenerallytreatedwithanticoagulantdrugssuchasdicumaroltopreventtheformationofsuchclots.Ventricularfibrillation,incontrast,leadstolossofconsciousnesswithinafewseconds.Theirregular,continuous,uncoordinatedtwitchingoftheventricularmusclefiberspumpsnoblood.Deathensuesunlessimmediateresuscitationisachievedortherhythmspontaneouslyrevertstonormal,whichrarelyoccurs.Ventricularfibrillationmaysupervenewhentheentireventricle,orsomeportionofit,isdeprivedofitsnormalbloodsupply.Itmayalsooccurasaresultofelectrocutionorinresponsetocertaindrugsandanesthetics.OntheECG(see
Fig.16.34B ),thefluctuationsinpotentialarehighlyirregular.
Ventricular fibrillation is often initiated when a premature impulse arrives during the vulnerable period of the cardiac cycle. This period coincides with the downslope of the T wave on the ECG. During this period, the excitability of cardiac cells varies spatially. Some fibers are still in their effective refractory periods, others have almost fully recovered their excitability, and still others are able to conduct impulses, but only at very slow conduction velocities. As a consequence, the action potentials are propagated over the chambers in many irregular wavelets that travel along circuitous paths and at various conduction velocities. As a region of cardiac cells becomes excitable again, it is ultimately activated by one of the wave fronts traveling around the chamber. Hence, the process is self-sustaining.
•Fig. 16.35 Electrocardiogramsrecordedfromanormalsubject(A) andfromapatientwithlongQTsyndrome(B). Q SQ S P PT T R R 1 sec. Normal Q SQ S P P T R R Long QT A B