PACs originate in parts of the atrium other than the sinus node. These impulses occur before the sinus node depolarizes. They are conducted through the atrium and slow down, just like a normal sinus beat, when they reach the A-V node. They are conducted through the ventricle in the same fashion as a normal sinus beat. PACs are very common, and can be completely unknown to the person. Sometimes they are perceived as a &quot;skip&quot; or a &quot;pause.&quot;
A premature junctional contraction is a beat occurring earlier than expected that originates in the AV node or AV junction area. It is generally followed by a compensatory pause.
Premature ventricular contractions (PVCs) are also extremely common. These originate in the ventricle, and are sometimes perceived by patients as palpitations. Multiple, consecutive PVCs can trigger ventricular tachycardia. However, the vast majority are benign, and do not require treatment. PVCs are recognized by a broad, wide complex occurring earlier than a sinus beat would have been expected and is followed by a full compensatory pause (when the distance between the beats before and after the PVC equals twice the normal cycle length).
Not every premature beat is alike. This is an example of a variety of PVCs you may see.
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.
Premature Beats Premature Atrial Contraction (PAC) <ul><li>Origin: Atrium (outside the Sinus Node) </li></ul><ul><li>Mechanism: Abnormal Automaticity </li></ul><ul><li>Characteristics: An abnormal P-wave occurring </li></ul><ul><li>earlier than expected, followed </li></ul><ul><li>by compensatory pause </li></ul>
Premature Beats Premature Junctional Contraction <ul><li>Origin: AV Node Junction </li></ul><ul><li>Mechanism: Abnormal Automaticity </li></ul><ul><li>Characteristics: A normally conducted complex with </li></ul><ul><li>an absent p-wave, followed by a </li></ul><ul><li>compensatory pause </li></ul>
Premature Beats Premature Ventricular Contractions (PVCs) <ul><li>Origin: Ventricles </li></ul><ul><li>Mechanism: Abnormal Automaticity </li></ul><ul><li>Characteristics: A broad complex occurring earlier </li></ul><ul><li>than expected, followed by a </li></ul><ul><li>compensatory pause </li></ul>
Multifocal PVC <ul><li>Origin: Varies within the Ventricle </li></ul><ul><li>Mechanism: Abnormal Automaticity </li></ul><ul><li>Characteristics: Each premature beat changes axis; </li></ul><ul><li>implies a different focus origin for </li></ul><ul><li>each beat </li></ul>
ABERRANT VENTRICULAR CONDUCTION <ul><li>A term that describes temporary alteration of QRS morphology under conditions where a normal QRS might be expected. The common types are: </li></ul><ul><li>1. Through normal conduction pathways: </li></ul><ul><ul><li>Cycle-length dependent (Ashman phenomenon) </li></ul></ul><ul><ul><li>Rate-dependent tachycardia or bradycardia </li></ul></ul><ul><li>2. Through accessory pathways (e.g., Kent bundle) </li></ul>
“ Las Vegas” type betting odds of making the right diagnosis <ul><li>1) fat little initial r-wave, </li></ul><ul><li>2) notch or slur in the downstroke of the S wave, </li></ul><ul><li>3) a 0.06 sec or more delay from the beginning of the QRS to the nadir of the S-wave. </li></ul><ul><li>1&2-90% Aberrant Conduction </li></ul><ul><li>3- 50-50%- not helpful </li></ul><ul><li>4 -100:1 - Ventricular Ectopy </li></ul><ul><li>5 - m/p Vntricular with two exceptions : </li></ul><ul><ul><li>Some people with normal ECG’s do not have an initial little r-wave in the QRS of lead V1. If RBBB occurs in such a person the QRS morphology in V1 will be a qR instead of an rsR’. </li></ul></ul><ul><ul><li>In a person with a previous anterior or anteroseptal infarction the V1 QRS often has a QS morphology, and RBBB in such a person will also have a qR pattern. </li></ul></ul>
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>