Some types of SVT’s include: Sinus Tachycardia Atrial Tachycardia Atrial Flutter Atrial Fibrillation AVNRT (Atrioventricular Nodal Reentry Tachycardia), and AVRT (Atrioventricular Reentry Tachycardia) Tachyarrhythmias that originate within the ventricles are classified as either Ventricular Tachycardias or Ventricular Fibrillation. Ventricular tachycardias can be further classified as being monomorphic or polymorphic, as previously discussed.
In Sinus Tachycardia, the EKG deflection will show a normal P and R-wave depolarization, with a rapid tachycardic rate Sinus Tachycardia rates range between 100-180 BPM The underlying Mechanism for Sinus Tachycardia is Abnormal Automaticity (Hyper-Automaticity)
Atrial flutter produces an atrial rate between 250 and 400 BPM . The ventricular rate may increase, but it is always slower than the atrial rate. During atrial flutter, atrial impulses are conducted to the ventricles in various ratios. Even conduction ratios (2:1, 4:1) are more common than odd ratios (3:1, 5:1). In a 2:1 ratio, there are two flutter waves for every QRS complex. A constant conduction ratio (e.g., 2:1) results in a regular ventricular rhythm (most common). A variable ratio (e.g., 4:1 to 2:1 to 5:1) results in an irregular ventricular rhythm.
Atrial Fibrillation (AF) is characterized by random, chaotic contractions of the atrial myocardium. Patients have an atrial rate of 400 BPM or more , often too fast to measure on an EKG. A surface EKG shows atrial fibrillation as irregular, wavy deflections (fibrillatory waves) between narrow QRS complexes. The fibrillatory waves vary in shape, amplitude, and direction. The chaotic nature of atrial fibrillation results in a grossly irregular ventricular rhythm . The rhythm is considered controlled if the ventricular rate is less than 100 BPM; uncontrolled if the ventricular rate conducts to greater than 100 BPM. Mechanism: In AF, the multiple wavelets of reentry do not allow the atria to organize. The ectopic focus or foci are said to be located around or within the pulmonary veins. Drugs such as flecainide, sotalol and amiodarone can terminate and prevent atrial fibrillation. Drug therapy can be used before or after DC cardioversion to maintain sinus rhythm after cardioversion.
The primary mechanism of atrial fibrillation is thought to be multiple wavelet reentry . It occurs when adjacent cells in the atrial myocardium have different refractory periods (uneven recovery times). During multiple wavelet reentry: An electrical impulse passing through the atrial myocardium depolarizes excitable cells and moves around refractory cells The rerouted electrical impulse then stimulates any adjacent cells that have recovered their excitability By this time, the cells first stimulated are again excitable. The electrical impulse re-excites the cells and continues to move through the atria, exciting and re-exciting the cells it encounters Unlike a normal depolarization wave that travels from cell to cell in one direction, reentry waves wander across the myocardium, randomly splitting off and following different reentrant pathways (see illustration). This random movement causes the chaotic, uncoordinated contractions of atrial fibrillation.
Atrial fibrillation can also result from the rapid discharge of impulses from one or many ectopic (non-sinus) sites in the atria. The ectopic cells (called foci) depolarize independently of the sinus node and disrupt the normal sinus rhythm. Multifocal firing takes place at multiple atrial ectopic sites. The cells produce many depolarization waves that activate different areas of the atrial myocardium at different times. AF occurs because the myocardial cells do not contract and relax rhythmically, in normal synchronization with the sinus node. *Note: Because a mechanism of AF may be Mulifocal Firing, some would argue that AF is a disorder of Impulse Formation (abnormal automaticity), rather than Impulse Conduction (multiple wavelets of reentry). Some argue still that while ectopic or mulifocal firing may begin AF, it is reentry that sustains it. For purposes of laying out rhythm disorders in this presentation, AF has been identified as a disorder of Impulse Conduction due to how it is sustained. May it be understood, however, that it could arguably be classified under both disorder descriptions.
This summary table allows you to review and compare the disease characteristics of atrial flutter and atrial fibrillation. Keep in mind that: Atrial flutter and atrial fibrillation are closely associated and may occur alternately in the same patient Long episodes (a day or more) of atrial flutter can degenerate into atria fibrillation Once atrial fibrillation develops, it is likely to persist and increase in frequency and duration Early identification and treatment of atrial arrhythmias is critical for preventing disease progression.
Ectopic Atrial Tachycardia and Rhythm <ul><li>Ectopic, discrete looking, unifocal P' waves with atrial rate <250/min (not to be confused with slow atrial flutter). </li></ul><ul><li>Ectopic P' waves usually precede QRS complexes with P'R interval < RP' interval (i.e., not to be confused with paroxysmal supraventricular tachycardia with retrograde P waves shortly after the QRS complexes). </li></ul><ul><li>The above ECG shows sinus rhythm, a PVC, and the onset of ectopic atrial tachycardia (note different P wave morphology) </li></ul><ul><li>Ventricular response may be 1:1 (as above ECG) or with varying degrees of AV block (especially in the setting of digitalis toxicity. </li></ul><ul><li>Ectopic atrial rhythm is similar to ectopic atrial tachycardia, but with HR < 100 bpm </li></ul>
Atrial Flutter <ul><li>Origin: Right & Left Atrium </li></ul><ul><li>Mechanism: Reentry </li></ul><ul><li>Characteristics: Rapid, regular p-waves </li></ul>* Animation
Atrial Fibrillation (AF) <ul><li>Origin: Right and/or left atrium </li></ul><ul><li>Mechanism: Multiple wavelets of reentry </li></ul><ul><li>Rate 400 BPM </li></ul><ul><li>Characteristics: Random, chaotic rhythm; </li></ul><ul><li>atria quiver; associated with </li></ul><ul><li>irregular ventricular rhythm </li></ul>* Animation
Other AF Mechanisms Multifocal Firing <ul><li>Mechanism: Abnormal Automaticity (multi-sites) </li></ul><ul><li>Characteristics: Many depolarization waves; </li></ul><ul><li>activation occurs asynchronously; </li></ul><ul><li>not in rhythm with sinus node </li></ul>
Wide QRS Complex Tachycardia <ul><li>· QRS morphology in lead V1 for single premature funny looking beats is often the best clue to the origin, </li></ul><ul><li>Also consider a few additional morphology clues: </li></ul><ul><li>· Bizarre frontal-plane QRS axis (i.e. from +150 degrees to -90 degrees or NW quadrant) suggests ventricular tachycardia </li></ul><ul><li>· QRS morphology similar to previously seen PVCs suggests ventricular tachycardia </li></ul><ul><li>· If all the QRS complexes from V1 to V6 are in the same direction (positive or negative), ventricular tachycardia is likely </li></ul><ul><li>· Mostly or all negative QRS in V6 suggests ventricular tachycardia </li></ul><ul><li>· Especially wide QRS complexes (>0.16s) suggests ventricular tachycardia </li></ul><ul><li>· Also consider the following Four-step Algorithm reported by Brugada et al, Circulation 1991;83:1649: </li></ul>
<ul><li>The classic Brugada pattern ( type 1 ) consists of ST - segment elevations that descend and have an upward T - wave inversion (" coved type ") in leads V 1 through V 3 </li></ul><ul><li>Types 2 and 3 have " saddleback " ST - T waves, with descending ST segments and an upright T wave; in type 2, the T wave is also upright or biphasic </li></ul><ul><li>A slight prolongation of the QT interval in Brugada - type ECG may be observed in the right precordial leads, secondary to the prolongation of the action potential duration in the right ventricular epicardium The Brugada ECG patterns can be differentiated from typical right bundle - branch block patterns by the absence of widened S waves . </li></ul>
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