22. Sinus Tachycardia >100b/min 1. Normal P waves 2. Normal or shortened PR interval 3. QRS and T vectors are normal 4. ST segments are normal 5. RR interval short <15mm 1500/100 = 15 Fig 3 Normal sinus rhythm Sinus tachycardia Sinus bradycardia
23. Sinus Bradycardia <60b/min 1. P waves are present and all are followed by a QRS 2. Normal and constant PR interval 3. QRS and T vectors are normal 4. ST segments are normal 5. RR interval long >25mm 1500/60 = 25 Fig 3 Normal sinus rhythm Sinus tachycardia Sinus bradycardia
24. Premature atrial contraction (PAC) 1. Arises from an ectopic focus in the atria. 2. Will have an identifiable P wave but the shape of the P wave may be altered 3. May have a normal QRS 4. May have a compensatory pause
25. The QRS may be altered if some of the ventricle is still in its refractory period. The compensatory pause is lacking because the SA node was reset. The rhythm has been shifted.
41. Mechanism is activation of multiple wavelets within the right and left atrium Recent studies have shown pulmonary vein foci trigger some episodes Atrial Fibrillation
78. Types of conduction over accessory pathway Orthodromic conduction: A premature impulse (APC, VPC) conducts antegradely through AV node, retrogradely through accessory pathway Antidromic conduction : Impulse conducts antegradely over accessory pathway and retrogradely over AV node
80. WPW: Initiation of SVT Supraventricular tachycardia • initiated by a closely coupled premature atrial complex (PAC) • blocks in the accessory pathway • but conducts through the AV node • retrograde conduction via accessory pathway • inverted P wave produced by retrograde conduction visible in the inferior ECG leads
81.
82. AVRT- note short RP interval, well seen P waves, an example of orthodromic conduction
89. 3.Mnomorphic VT 4. Polymorphic VT C. Ventricular flutter D. Ventricular fibrillation
90. actually a "retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat Ventricular Escape Beat there is no p wave, indicating that the beat did not originate anywhere in the atria Ventricular Beats & Rhythms
91.
92.
93. Premature Ventricular Complex (PVC) - Summary ECG Patterns Rate: can occur at any rate and with any rhythm Rhythm: normally irregular due to pause after PVC P wave: normally none associated with PVC; may be retrograde P-R: none evident QRS: usually wide (>.11s) and bizarre with T directed opposite QRS deflection; BBB configuration; different from flanking beats Comment: usually followed by fully compensatory pause; usually don't generate a peripheral pulse
Predictions about V:A time for DDX Circuits require two pathways with different conduction vel and different refractory periods
Tutorial of AF from PV
Anatomic barriers within the right atrium sustain the macro-reentry circuit. The AV node plays no part in the flutter circuit, so drugs aimed at altering the conduction of the AV node have no effect on the atrial rate.
Atrial flutter is distinguished from atrial tachycardia by the faster rate.
ECG characteristics of clockwise flutter are similar to those discussed in identifying counterclockwise flutter. A distinguishing difference is the pattern of the flutter waves. A “notched” upright pattern is often seen on the surface ECG inferior leads.
This slide shows a 12 lead ECG depicting clockwise flutter.
Wolff-Parkinson-White syndrome: Initiation of SVT We’ve all seen how sinus rhythm fuses in the ventricle. An appropriately timed premature atrial beat may block in the AP and conduct to the ventricle solely over the normal AV conduction system. That takes some time b/c of AV nodal delay, and if that is a sufficient amount of time for the AP to recover, then it may conduct the impulse back to the atrium and begin an endless loop reentrant tachycardia. Conduction occurs over the AV conduction system to the ventricle, via ventricular myocardium to the AP, back to the atrium over the AP and back to the AV conduction system via atrial myocardium. When you consider the physiology that is operative, you discover that it is really a misnomer to call this a supraventricular tachycardia, because its mechanism is just as dependent on atrial myocardium to complete the circuit as it is on ventricular myocardium. Nonetheless, because the ventricle is activated over the normal AV conduction system, and hence, the QRS complex is narrow, it is considered a form of SVT. This type of SVT, the most common type of SVT that occurs in the WPW syndrome, is called AVRT. When the circuit travels to the ventricle over the normal AV conduction system, the circuit is traversed in an orthodromic direction. Of course, the reverse circuit can also occur, though it is much much less common. Antidromic tachycardia activates the ventricles solely over the AP and travels to the atrium retrogradely over the normal AV conduction system. For the remainder of the round, I will not consider antidromic AVRT any further b/c it is rare.
Welcome to VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW . This module contains a discussion of the various characteristics and classifications of ventricular tachycardia (VT). ECG recognition and treatment of the various tachycardias will be explored. Focus is given to the use of RF ablation as a treatment for certain VTs.
VTs are generally classified as being either monomorphic or polymorphic. Detailed discussions of monomorphic VTs, (idiopathic, bundle branch, ventricular flutter,and ventricular fibrillation) will include a description of the rhythm, ECG characteristics, and treatment options.
Another characteristic, used to describe VT, is whether it is sustained or non-sustained.
PVC’s can lead to ventricular tachycardia or fibrillation in individuals with ischemic or damaged hearts. PVCs can occur in many combinations (e.g., bigeminal, trigeminal, couplets) or from many ectopic foci, (e.g., multifocal PVCs).
Ventricular tachycardia can be classified as being either monomorphic or polymorphic. The following slides present a discussion for each rhythm listed, along with EGC identification and treatment options. Ventricular flutter is rarely seen, and may be seen just prior to the onset of ventricular fibrillation. Torsades de pointes is associated with a long QT interval.
Monomorphic VT is regular, with uniform beat-to-beat morphology. It can be sustained, nonsustained, idiopathic or caused by bundle branch reentry.
ECG characteristics that help define VTs are: The QRS complexes are rapid, wide, and distorted. The T waves are large with deflections opposite the QRS complexes. The ventricular rhythm is usually regular. P waves are usually not visible. The PR interval is not measurable. A-V dissociation may be present. V-A conduction may or may not be present. It may be difficult to distinguish VT from SVT with aberrancy from a surface ECG. Many texts offer tips for distinguishing these rhythms. The presence of capture and fusion beats generally occur in VT.
This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.
This slide is a recording of RVOT VT.
Bundle branch reentry tachycardia is another VT that is treatable with RF ablation. With this type of tachycardia, the HV interval is increased. Ablation of the right bundle does cure this form of reentry. However, given the underlying LBBB, ablation of the RBBB results in either very impaired His/Purkinje function or in complete heart block. A pacer is usually required.
The most helpful criteria to consider when diagnosing VT due to bundle branch reentry is the comparison of this LBBB morphology to the LBBB seen in sinus. The morphology does not have to be exactly the same (if there is some conduction down the left bundle) but it should be really similar.
Rarely seen, ventricular flutter may occur just prior to the onset of ventricular fibrillation. It degenerates into ventricular fibrillation in a matter of seconds.
Ventricular fibrillation (VF) will convert to fine VF and then no electrical activity will be seen. Patients resuscitated from VF are deemed sudden cardiac death survivors.
The following ECG findings help electrophysiologists to diagnose VF: P waves and QRS complexes are not present. Heart rhythm is highly irregular. The heart rate is not defined (without QRS complexes).
A second classification of VT is polymorphic VT.
TdP is a rapid and distinct VT with a twisting configuration of the QRS morphology, associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT.
The early afterdepolarizations initiate the tachycardia; reentry sustains it.
Torsades de pointes (twists of points) is a unique VT in which the QRS complexes change from positive to negative and appear to twist around the isoelectric line.
Possible causes of TdP can include drugs that lengthen the QT interval. Causes can also be physical in nature.
The treatment for TdP can be with drugs, overdrive pacing, or cardioversion. Of note, isoproterenol is contraindicated in patients with hypertension or ischemic heart disease. Treatment with potassium is dependent on the potassium blood level and is only given if the patient is hypokalemic. The treatment for congenital TdP is beta blockade and/or an ICD. The treatment for acquired TdP is avoiding pauses (acutely) and reversing the underlying cause.
![[object Object],[object Object],[object Object],[object Object],Terminology and Basics ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)