Arrhythmias and Devices Module 1

Arrhythmias and Devices Module 1
Student Notes This module will give you the foundation information necessary for working toward more advanced knowledge in pacemaker operation. It is possible that you may require additional supplemental materials to enhance your knowledge or provide more practice. If you feel this is necessary for you, ask your instructor for suggestions on books or other tools. Instructor Notes This module should take approximately 2 hours to cover. To deliver this module the following materials are recommended: Printed participant guides for each participant Overhead projector and screen Optional: Whiteboard or flip chart While delivering the module engage the learners by asking questions and getting them to talk based on their previous knowledge. Evaluate the learners by delivering the knowledge check at the end of this module. An acceptable score is 90%. World Headquarters Medtronic, Inc. 710 Medtronic Parkway Minneapolis, MN USA Internet: Tel: (763) Europe Medtronic International Trading Sàrl Route du Molliau Ch Tolochenaz Switzerland Tel: (41 21) Asia-Pacific Medtronic International, Ltd. 16/F Manulife Plaza The Lee Gardens, 33 Hysan Avenue Causeway Bay Hong Kong Tel: (852) Canada Medtronic of Canada Ltd. 6733 Kitimat Road Mississauga, Ontario L5N 1W3 Tel: (905) Toll-free: 1 (800) Medtronic USA, Inc. Toll-free: 1 (800) (24-hour technical support for physicians and medical professionals) Latin America Medtronic USA, Inc. Doral Corporate Center II 3750 NW 87th Avenue Suite 700 Miami, FL 33178 USA Tel: (305)

Objectives Recognize typical rhythms and rhythm disorders
Student Notes Instructor Notes

Arrhythmias and Devices Overview
The Conduction System Normal Conduction Automaticity & Action Potential Causes of Rhythm Disorders Rhythm Disorders Categories Disorders of Impulse Formation Disorders of Impulse Conduction Mechanisms Arrhythmia Recognition and Classification Bradycardias Tachycardias Student Notes We will begin this series with a brief review of cardiac anatomy and the conduction system, we will then discuss the two categories of arrhythmia, and finally, we will discuss classification. Status check questions are provided. Instructor Notes

Cardiac Conduction Sinus Node
The Heart’s ‘Natural Pacemaker’ Rate of bpm at rest Sinus Node (SA Node) Student Notes The conduction system in a normal heart is comprised of and operates in the following way: The sinus node, located in the upper right atrium (known as the heart’s ‘Natural Pacemaker’), has ‘automaticity’, which will be discussed later. The sinus node’s rate of automaticity is normally faster than all other parts of the heart, and therefore, dictates the rate at which the entire heart beats. This is known as “Sinus Rate.” Its resting rate is usually between bpm in an adult, but it responds to metabolic demands, changing its rate as the need for oxygenated blood changes, for example,` in response to exercise, stress, hormones, etc. Instructor Notes Auto-animated slide

Cardiac Conduction AV Node
Receives impulses from SA node Delivers impulses to the His-Purkinje System Delivers rates between bpm if SA node fails to deliver impulses Atrioventricular Node (AV Node) Student Notes The atrioventricular node (aka: AV node, AV junction) is located between the atrium and the ventricles, in the inter-atrial septum, close to the tricuspid valve. It receives the impulse from the SA node and delivers it through the Bundle of His (the forefront of the His-Purkinje network). Conduction through the AV node is slow, allowing appropriate time for the atria to complete mechanical contraction prior to ventricular contraction. If the SA node fails to deliver an impulse to the AV node, the AV node itself will deliver an impulse to the Bundle of His at rates between bpm. Instructor Notes Auto-animated slide

Cardiac Conduction HIS Bundle
Begins conduction to the ventricles AV Junctional Tissue: Rates between bpm Bundle of His Student Notes Bundle of His with the AV node make up the AV junctional tissue. Junctional tissue also produces rates between bpm. Instructor Notes Auto-animated slide

Cardiac Conduction Purkinje Fibers
Bundle Branches and Purkinje Fibers Moves the impulse through the ventricles for contraction Provides ‘Escape Rhythm’: Rates between bpm Purkinje Network Student Notes Bundle branches & Purkinje fibers make up the Purkinje network (aka ventricular conduction system), and serve to distribute the electrical impulse to the cardiac muscle, allowing for depolarization (contraction) of the ventricles. In the absence of SA or junctional impulses, the ventricular conduction system can deliver impulses at rates between bpm, known as an ‘escape’ rhythm. Instructor Notes Auto-animated slide

Normal Sinus Rhythm Student Notes
We will begin by discussing the normal sinus rhythm. Instructor Notes Transition slide.

Impulse Formation in SA Node
Student Notes Initiation of the cardiac cycle normally begins with initiation of the impulse at the SA (sinoatrial) node. Instructor Notes

Atrial Depolarization
Student Notes After the SA node fires, the resulting depolarization wave passes through the right and left atria, stimulating atrial contraction and producing the P-wave on the surface ECG. Instructor Notes

Delay at AV Node Student Notes
Following activation of the atria, the impulse proceeds to the atrioventricular (AV) node, which is the only normal conduction pathway between the atria and the ventricles. The AV node slows impulse conduction, allowing time for the atria to contract and blood to be pumped from the atria to the ventricles prior to ventricular contraction. Conduction time through the AV node accounts for most of the duration of the PR interval. Just below the AV node, the impulse passes through the bundle of His. Instructor Notes

Conduction through Bundle Branches
Student Notes After the impulse passes through the bundle of His, it proceeds through the left and right bundle branches. Instructor Notes

Conduction through Purkinje Fibers
Student Notes Next the impulse passes through the Purkinje fibers (interlacing fibers of modified cardiac muscle). Instructor Notes

Ventricular Depolarization
Student Notes The impulse passes quickly through the bundle of His, the left and right bundle branches, and the Purkinje fibers, leading to depolarization and contraction of the ventricles. The QRS complex on the ECG represents the depolarization of the ventricular muscle mass. Instructor Notes

Plateau Phase of Repolarization
Student Notes The Plateau Phase lasts up to several hundred milliseconds. Instructor Notes

Final Rapid (Phase 3) Repolarization
Student Notes Repolarization of the ventricles generates a current in the body and produces the T-wave on the surface electrogram. This takes place slowly, thus generating a wide wave. Instructor Notes

Normal ECG Activation Student Notes Putting it together: An animated view of cardiac conduction and the associated ECG. Instructor Notes Auto-animated slide This pattern of depolarization results in efficient mechanical contraction – which is the purpose – to pump blood.

Reading ECG Squares Intervals and Timing
Horizontal axis – time: Each small square = 40 ms Each block = 200 ms (5 ea. 40 ms squares) Converting this to a rate in bpm: 1 min = 60,000 ms, so: 60,000/ms = bpm 60,000/600ms = 100 bpm Pacemakers and ICDs calculate intervals (ms), not in rates (bpm) Student Notes An ECG records the rate, rhythm, and size of each of the components. The rate of the waves is measured by the small squares on the horizontal axis of the ECG. Assuming a paper speed of 25 mm/second: Each small square represents 40 milliseconds. To make these measurements easier, the small squares are grouped into intervals of 5 that make up a large, bold square measuring 200 milliseconds. 1 minute = 60,000 ms To measure heart rate, count the boxes from the peak of one R-wave to the peak of the next R-wave, and then convert to beats per minute. For example, if the measurement between two R-wave peaks equals 1,000 milliseconds, the heart rate converts to 60 beats per minute (60,000/1000 = 60). The size in millivolts is measured on the Y or vertical axis. 1 Small box on this axis represents 1 mV, one large bold square = 5 mV. Instructor Notes Say: Several of the concepts discussed in this module require you to know how to determine heart rate from an ECG. This slide walks you through how to convert a measured interval to beats per minute. Hand out the “Pacemaker Code and Rate and Interval Conversion” pocket reference card (UC m EN). Explain that this tool can assist the student in determining rate from an interval measurement.

ECGs Annotation Normal Ranges in Milliseconds:
PR Interval 120 – 200 ms QRS Complex 60 – 100 ms QT Interval 360 – 440 ms Student Notes Time-to-wave intervals are commonly referred to by their respective place in the sequence. For example, the period of time that elapses between the P- and R-wave is called the P-R Interval, which has a normal range between 120 and 200 milliseconds. A measurement outside this range suggests a rhythm or conduction disorder. Instructor Notes

Status Check Inefficient contraction
This ECG shows a QRS duration of about 100 ms – a normal duration. If this represents efficient ventricular contraction… …then what effect could a QRS duration of 200 ms have on mechanical efficiency and cardiac output? Student Notes A wide QRS pattern suggests inefficient mechanical contraction from a loss of synchrony between the Right and Left Ventricles Instructor Notes Auto-animated slide, click for the answer to appear. Use this slide to begin discussion of what a wide QRS represents mechanically – inter- and intra-ventricular dyssynchrony. Ask what it might mean to a patient clinically to suffer from dyssynchrony, and what it might mean if it could be restored. Avoid in-depth discussion of CRT therapy, rather just introduce it here. Click for Answer Inefficient contraction

Status Check Match the term on the left with the description on the right P-R Interval AV Node Purkinje Network Bundle Branches Click for Answer Escape rate is bpm Connect His bundle to Purkinje network Student Notes Note: The answers on the left are out of order until the slide moves. Instructor Notes Auto-animated slide, click anywhere for answer to appear. Normally ms Depolarizes the Ventricles

We’ve Seen How the Normal Pattern of Conduction Occurs But:
What triggers the depolarization – what causes that first cell to depolarize? If a cell depolarizes, why does it result in depolarization in other cells? Student Notes Normal conduction is one thing, but what triggers conduction? What is the initiating event, and why does it occur? Transition slide Instructor Notes

Automaticity Cardiac Cells are unique because they spontaneously depolarize Upper (SA Node) 60-80 bpm Middle (AV Junction) 40-60 bpm Lower (Purkinje Network) 20-40 bpm Student Notes Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest and therefore, acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between bpm. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV Node generally takes the lead, beating at a rate of beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of bpm. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network. Instructor Notes Auto-animated slide

Automaticity Once a pacemaker cell initiates an impulse, its neighboring cells follow suit – like dominos. Student Notes Cardiac Cells are intimately connected to one another. Therefore, when one cardiac cell depolarizes, its current imposes on neighboring cells, causing them to depolarize, and so on. Areas of the heart have ‘pacemaker cells’ with their own ability to initiate a depolarization, at a rate that is fast enough to sustain life Other cells follow suit with depolarization The fastest pacemaker cells take over the heart rate – in a normal heart, the SA node drives the rate (60-80 bpm), and responds to changing metabolic demand If the SA node fails to fire, the AV node takes the lead (40-60 bpm), followed by the ventricular escape rhythm if all else fails to fire (20-40 bpm) Note: All cardiac tissue has the ability for automaticity. Instructor Notes

Action Potential of a Cardiac Cell
5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes Automaticity occurs as a result of an influx of Na+ and Ca++, and an outflow of K+ across the cardiac cell membrane. This action occurs in 5 Phases. Instructor Notes

5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes At rest, the trans membrane potential sits at approximately –90 mV. As the potential reaches a threshold of –70 to –60 mV, the upstoke of action potential is triggered. This is known as Phase 0. In Phase 0, there is a large influx of Na+ into the cell: The cell membrane changes from a resting value of near -90 mV to a value of about +15 to +30 mV (overshoot potential) Ca++ is unbound from the cell membrane and enters the cell, which increases contractility (Ellenbogen, Kenneth A. & Wood, Mark A. Basic Concepts of Pacing. Cardiac Pacing & ICDs, 3rd Edition. Malden, MA: Blackwell Science, Inc., 2002: ) Instructor Notes

5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes Following Phase 0 there is a rapid repolarization of the cell membrane, (Phase 1), to approximately 0mV. (Ellenbogen, Kenneth A. & Wood, Mark A. Basic Concepts of Pacing. Cardiac Pacing & ICDs, 3rd Edition. Malden, MA: Blackwell Science, Inc., 2002: ) Instructor Notes Auto-animated slide

5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes Phase 2 is known as the ‘Plateau Phase,’ used to describe the constant flow of calcium and sodium into the cell as potassium flows out, preparing the cell for re-polarization. (Ellenbogen, Kenneth A. & Wood, Mark A. Basic Concepts of Pacing. Cardiac Pacing & ICDs, 3rd Edition. Malden, MA: Blackwell Science, Inc., 2002: ) Instructor Notes Auto-animated slide

5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes Rapid repolarization occurs in Phase 3. This may be due to the continued outward flow of K+, and lessening of inward currents. This results in loss of the positive charge. It is during Phase 3 that a cell regains the polarity needed to respond to another polarizing electrical stimulus. (Ellenbogen, Kenneth A. & Wood, Mark A. Basic Concepts of Pacing. Cardiac Pacing & ICDs, 3rd Edition. Malden, MA: Blackwell Science, Inc., 2002: ) Instructor Notes Auto-animated slide

5 Phases Phase 0 Rapid or upstroke depolarization with an influx of sodium ions into the cell Phase 1 Early rapid repolarization with transient onward movement of potassium ions Phase 2 Plateau Phase: Continued Influx of Sodium and slow Influx of Calcium Phase 3 Repolarization: Potassium outflow Phase 4 Resting Phase Student Notes Once the membrane reaches -40 to -45 mV the charge falls quickly to the resting level. The cell membrane once again becomes polarized and the cycle begins again. (Ellenbogen, Kenneth A. & Wood, Mark A. Basic Concepts of Pacing. Cardiac Pacing & ICDs, 3rd Edition. Malden, MA: Blackwell Science, Inc., 2002: ) Instructor Notes Auto-animated slide

Refractory Periods ERP - Effective Refractory Period AKA: Absolute Refractory Period Phases 0, 1, 2, and early Phase 3 A depolarization cannot be initiated by an impulse of any strength RRP - Relative Refractory Period Late Phase 2 and early Phase 3 A strong impulse can cause depolarization, possibly with aberrancy “R on T” phenomena Student Notes ERP- Effective (or Absolute) Refractory Period Occurs during Phases 0 and 1, and early Phase 2 (may persist into early Phase 3). A second depolarization cannot be initiated during the ERP. RRP - Relative Refractory Period Occurs during late Phase 2 and early Phase 3. A strong impulse can cause depolarization, however, this may be conducted aberrantly (not normally) through the cardiac muscle. Instructor Notes Auto-animated slide

Causes of Rhythm Disorders
Congenital Present at birth due to genetics, or conditions during the peri-natal environment Cardiac and other diseases Myocardial Infarction, high blood pressure, cardiomyopathy, valvular heart disease Acquired Medications (even anti-arrhythmic Rx), diet pills, cold remedies, illegal drugs, caffeine and/or alcohol abuse, tobacco use... Student Notes Before discussing categories and types of disorders, keep in mind that these disorders arise from the peri-natal environment and/or genetics; frequently they can be a result of heart disease, but may be a side effect of another medical condition, or can be acquired via medications, tobacco, drug and or alcohol abuse, etc. Far too often a patient’s rhythm disorder arises from multiple causes. Instructor Notes

Causes of Rhythm Disorders
Secondary to other conditions Hyper-Thyroid Neurocardiogenic Syncope - Hypersensitive Carotid Sinus Syndrome (CSS) - Vasovagal Syncope (VS) Student Notes Some less common causes include: Hyper-Thyroid can cause a rapid or irregular heart rhythm Hypersensitive Carotid Sinus Syndrome (CSS) is a disease of the carotid sinus, a dilated portion of the carotid artery that has pressure-sensitive receptors that regulate heart rate and blood pressure. CSS is an extreme reflex response to carotid sinus stimulation, and usually results in bradycardia and/or vasodilation. It can be induced by, among other things, a tight collar, shaving, head turning, exercise, and, of course, carotid sinus massage. Vasovagal syncope is a neurally mediated transient loss of consciousness and can be triggered by prolonged standing, fear, mental anguish, physical pain, or anticipation of trauma or pain. The most common symptoms are dizziness, blurred vision, weakness, nausea, sweating, and abdominal discomfort. Instructor Notes

Rhythm Disorders 2 Categories
Impulse Formation Abnormal Automaticity Triggered Activity Disorders of Impulse Conduction Student Notes All rhythm disorders will fall into 1 of 2 categories depending on the underlying cause of the disorder. They are either caused by disorders of impulse formation or disorders of impulse conduction. Arrhythmic impulses may form because of increased automaticity or trigger(s). Instructor Notes Transition slide Auto-animated slide

Impulse Formation Abnormal Automaticity Triggered Activity Bradycardia: Abnormally slow rates usually due to disease Tachycardia: Excessively rapid rates due to ANS Student Notes For example, a bradycardia can be the result of slow or delayed impulse formation in the atria. A tachycardia, just the opposite – increased automaticity. Instructor Notes Auto-animated slide

Impulse Formation Abnormal Automaticity Triggered Activity Depolarization occurring in Phase 3 or 4 of the action potential can trigger arrhythmias Student Notes A stimulus occurring in the RRP may also trigger a tachycardia. Instructor Notes Auto-animated slide

Mechanisms of Rhythm Disorders Triggered Activity
Early Afterdepolarization Potential Causes: - Low potassium blood levels - Slow heart rate - Drug toxicity (ex. Quinidine causing Torsades de Pointes type of VT) Late Afterdepolarization Potential Causes: - Premature beats - Increased calcium blood levels - Increased adrenaline levels - Digitalis toxicity Student Notes Like automaticity, triggered activity involves the leakage of positive ions into a cell, resulting in new action potentials. However, unlike automaticity, Triggered Activity is not consistently spontaneous. Triggered Activity may be either a single or repetitive firing of a myocardial cell, or group of cells caused by re-excitation Ion leakages that occur late in Phase 3 or early in Phase 4 (after cell recovery has begun) are called afterdepolarizations, or late potentials. Afterdepolarizations can be the ‘trigger’ that causes ventricular tachyarrhythmias. Instructor Notes Auto-animated slide

Rhythm Disorders Two Categories
Impulse Formation Abnormal Automaticity Triggered Activity Impulse Conduction Student Notes Disorders of conduction may occur because conduction may be blocked or delayed, or extra conduction circuits may exist within the heart. Some examples of ECG diagnosis because of delayed or “aberrant” conduction may be familiar to you as Right or Left Bundle Branch Block. Absent conduction examples include “Complete Heart Block.” We’ll discuss reentry in more detail later. Instructor Notes Transition/Auto-animated slide Slow or Blocked Conduction Reentry

Mechanisms of Rhythm Disorders Slowed or Blocked Conduction
Impulse generated normally Impulse slowed or blocked as it makes its way through the conduction system Student Notes Slowed, or blocked conduction occurs when the impulse is generated normally, but is slowed or blocked as it tries to move through the conduction system. This may occur in various areas of the conduction system. The location of the slowing or block determines the type of conduction disorder. We will detail and describe more on conduction disorders later in this session. Instructor Notes Auto-animated slide

Rhythm Disorders Two Categories
Impulse Formation Abnormal Automaticity Triggered Activity Impulse Conduction Student Notes Instructor Notes Transition/Auto-animated slide Slow or Blocked Conduction Reentry

Mechanisms of Rhythm Disorders Reentry Model
Conduction paths are “mirrored” Pathway A: Slow conduction but short (fast) refractory Pathway B: Fast conduction but long (slow) refractory period Student Notes Reentry refers to an electrical impulse continuously traveling an electrical loop within the myocardium. The depolarization wavefront re-enters areas that have just been repolarized, creating a circular, continuous series of depolarizations and repolarizations. The following anatomic and physiologic properties create a re-entrant loop: Two parallel conduction pathways around a central obstacle (A and B in above figure). Conducting tissue connects the pathways at both ends. One of the pathways (A) conducts more slowly than the other. The other pathway, (B), exhibits unidirectional block, usually in the form of a substantially longer refractory period than the other pathway. Instructor Notes Auto-animated slide

A premature event occurs, which is conducted down the slow pathway. During this “antegrade” conduction, the fast or “retrograde” pathway is still refractory. A premature event occurs, which is conducted down the slow pathway. During this “antegrade” conduction, the fast or “retrograde” pathway is still refractory By the time the slow antegrade conduction is complete, the fast pathway is no longer refractory, allowing retrograde conduction to occur. Student Notes For reentry to occur, the following events must take place: A premature impulse occurs in the re-entrant circuit at a time when pathway A (with the short refractory period) is ready to accept the impulse, and pathway B (with the long refractory period) is still repolarizing from the previous depolarization. The impulse slowly travels through pathway A and reaches pathway B, just as pathway B completes its repolarization and is no longer refractory, which means it is ready to accept a stimulus. The impulse travels through pathway B in a retrograde direction and re-enters pathway A. The impulse is conducted antegrade through pathway A, and the circuit continues. Reentry does not display a “warm up” or “cool down” period. Instructor Notes Auto-animated slide This “circus” mechanism is maintained as long as the relationship between fast and slow conduction, and fast/slow refractoriness persists.

These are sometimes referred to as “circus tachycardias.” This mechanism explains one common arrhythmia seen in the EP lab: AV node re-entrant tachycardia. V-V Intervals ms A-V Intervals ms Student Notes This slide gives an ECG example of AV node reentry. Note the almost simultaneous depolarization of the atria and ventricles. A good resource on arrhythmia, especially reentry see: Fogoros, Richard N. Electrophysiologic Testing, 3rd Edition. Blackwell Science, Inc. 1999 Instructor Notes Auto-animated slide Note the almost simultaneous depolarization of the atria and ventricles.

Terminating Reentry Spontaneous termination
Another premature beat that disturbs the underlying conduction/refractoriness relationships Pace the heart at a rate above the tachycardia rate Abruptly stop pacing This is how implantable cardioverter-defibrillators can stop VT without a shock (ATP) Student Notes A way to differentiate between reentry and disorders of automaticity, or a triggered tachycardia, is via transient entrainment. With transient entrainment, pacing is used. The pacemaker paces at a rate faster than intrinsic tachycardia. When pacing is terminated, if the tachycardia stops, it was likely reentry. Unfortunately, it may return just as abruptly. Many re-entrant tachycardias are treated with ablation, however, not all. The earlier example of AV node reentry is one example that is often successfully treated with ablation. Instructor Notes

Bradycardia Classifications
Impulse Formation Impulse Conduction Disorders of Student Notes Instructor Notes Transition/Auto-animated slide

Sinus Arrest Impulse Formation Impulse Conduction Sinus Bradycardia Brady/Tachy Syndrome Student Notes Instructor Notes Transition/Auto-animated slide

Sinus Arrest Failure of sinus node discharge
Absence of atrial depolarization Periods of ventricular asystole May be episodic as in vaso-vagal syncope, or carotid sinus hypersensitivity May require a pacemaker Student Notes Sinus arrest occurs when there is a pause in the rate at which the SA node fires. With sinus arrest there is no relationship between the pause and the basic cycle length. Instructor Notes

Sinus Bradycardia Sinus Node depolarizes very slowly
If the patient is symptomatic and the rhythm is persistent and irreversible, may require a pacemaker Student Notes Sinus bradycardia occurs when the SA node fires at an abnormally slow rate (< 60 bpm). Instructor Notes

Brady/Tachy Syndrome Intermittent episodes of slow and fast rates from the SA node or atria Brady < 60 bpm Tachy > 100 bpm AKA: Sinus Node Disease Patient may also have periods of AF and chronotropic incompetence 75-80% of pacemakers implanted for this diagnosis Student Notes Brady-tachy syndrome occurs when the SA node has alternating periods of firing too slowly (< 60 bpm), and too fast (> 100 bpm). Brady-tachy syndrome often manifests itself in periods of atrial tachycardia, flutter, or fibrillation. Cessation of the tachycardia is often followed by long pauses from the SA node. Chronotropic incompetence—condition where the sinus node does not meet metabolic needs by increasing heart rate. Instructor Notes

Sinus Arrest Brady/Tachy Syndrome Sinus Bradycardia Impulse Formation Impulse Conduction Exit Block Student Notes Instructor Notes Transition/Auto-animated slide 1st Degree AV Block 2nd Degree AV Block 3rd Degree AV Block Bi/Trifascicular Block

Exit Block Transient block of impulses from the SA node
Sinus Wenckebach is possible, but rare Pacing is rare unless symptomatic, irreversible, and persistent Student Notes SA exit block occurs when the SA node fires, but the impulse does not conduct to the pathways that cause the atrium to contract. In SA exit block, there is a relationship between the pattern and the basic cycle length (because the sinus node continues to fire regularly), of approximately two, but less commonly three or four times the normal P-P interval. Instructor Notes

First-Degree AV Block PR interval > 200 ms
Delayed conduction through the AV Node Example shows PR Interval = 320 ms Not an indication for pacing Some consider this a normal variant (not an arrhythmia) Student Notes AV block can be described as a prolongation of the PR interval, the interval from the onset of the P-wave to the onset of the QRS complex. First-degree AV block is defined by a PR interval greater than 0.20 seconds (200 msec). First-degree AV block can be thought of as a delay in AV conduction, but each atrial signal is conducted to the ventricles (1:1 ratio). There are some who feel First-degree AV block is not an arrhythmia but a normal variant. In any case, it is not an indication for a pacemaker. Instructor Notes

Second-Degree AV Block – Mobitz I
Progressive prolongation of the PR interval until there is failure to conduct and a ventricular beat is dropped AKA: Wenckebach block Usually not an indication for pacing Student Notes Second-degree AV block is characterized by intermittent failure of atrial depolarizations to reach the ventricle. There are two patterns of second-degree AV block. Type I is marked by progressive prolongation of the PR interval in cycles preceding a dropped beat. This is also referred to as Wenckebach or Mobitz Type I block. The AV node is most commonly the site of Mobitz I block. The QRS duration is usually normal. Instructor Notes Auto-animated slide

Second-Degree AV Block – Mobitz II
Regularly dropped ventricular beats 2:1 block (2 P-waves for every 1 QRS complex) Atrial rate = 75 bpm, Ventricular rate = 42 bpm A “high grade” block, usually an indication for pacing May progress to third-degree, or Complete Heart block (CHB) Student Notes Mobitz Type II second-degree AV block refers to intermittent dropped beats preceded by constant PR intervals. To differentiate Mobitz I from Mobitz II, note the PR interval in the beats preceding and following the dropped beat If a difference between these two PR intervals is more than 0.02 seconds (20 msec), then it is Mobitz I. If the difference is less than 0.02 seconds, then it is Mobitz II. The infranodal (His bundle) tissue is most commonly the site of Mobitz II block. Unlike the graphic, Mobitz II is often accompanied by a wide QRS complex. Note: Advanced second-degree block refers to the block of two or more consecutive P-waves (i.e., 3:1 block). Instructor Notes Auto-animated slide

Third-Degree AV Block No impulse conduction from the atria to the ventricles Atrial rate = 130 bpm, Ventricular rate = 37 bpm Complete A – V disassociation Usually a wide QRS as ventricular rate is idioventricular Student Notes Third-degree AV block is also referred to as complete heart block. Characterized by a complete dissociation between P-waves and QRS complexes. The QRS complexes are not caused by conduction of the P-waves through the AV node to the ventricles. The QRS is initiated at a site below the AV node (such as in the His bundle or the Purkinje fibers). This “escape rhythm” is normally 40–60 bpm if initiated by the His bundle (a junctional rhythm) and <40 bpm if initiated by the Purkinje fibers. Instructor Notes Auto-animated slide

Fascicular Block Student Notes Bifascicular block is when 2 (with the exception of complete left BBB) of the conduction system pathways below the AV Node are blocked. They are defined as one of the following: Right bundle branch block and left posterior hemiblock Right bundle branch block and left anterior hemiblock - marked by prolonged QRS (> 120 ms or .12 seconds or longer) Complete left bundle branch block Instructor Notes Auto-animated slide Right bundle branch block and left posterior hemiblock Right bundle branch block and left anterior hemiblock Complete left bundle branch block

Trifascicular Block Complete block in the right bundle branch, and
Complete or incomplete block in both divisions of the left bundle branch Identified by EP Study Student Notes Trifascicular block occurs when 3 of the conduction system pathways are blocked below the AV Node. Trifascicular block can have the appearance of AV nodal block. Combinations that constitute trifascicular block are: Right bundle branch block, complete left anterior fascicular block, and complete left posterior fascicular block Combination of complete block in one or two subdivisions of the common bundle, and incomplete block in one or two subdivisions Instructor Notes

Bradycardia Classifications Summary
Sinus Arrest Impulse Formation Impulse Conduction Sinus Bradycardia Brady/Tachy Syndrome Exit Block Student Notes Instructor Notes Transition/Auto-animated slide 1st Degree AV Block 2nd Degree AV Block 3rd Degree AV Block Bi/Trifascicular Block

Status Check Click for Answer What is the most likely rhythm disorder that might result in a patient getting a pacemaker? Sinus node disease Sinus node disease is otherwise known as? Brady-tachy syndrome What are some symptoms a patient might complain of? Fatigue, shortness of breath, palpitations, inability to perform activities of daily living, vertigo, syncope, racing heart at rest, slow pulse rate Student Notes GXT—Graded Exercise Testing or Graded Exercise Stress Test Instructor Notes Auto-animated slide Click for answer

Status Check What are some simple diagnostic tests used to make this diagnosis? 12-lead ECG, GXT, Ambulatory ECG (Holter) Click for Answer Student Notes GXT—Graded Exercise Testing or Graded Exercise Stress Test Instructor Notes Auto-animated slide Click for answer

Terms Describing Ventricular Tachycardias
Paroxysmal (may be used with VT or SVT) Ectopic focus, sudden onset, abrupt cessation Sustained (usually used with VT) Duration of > 30 seconds Requires intervention to terminate Non-Sustained (usually used with VT) At least 6 beats or < 30 seconds Spontaneously terminates Recurrent (usually used with VT) Occurs periodically Periods of no tachycardia are longer than periods of tachycardia Student Notes Before we begin this session, let’s review some terms describing Tachycardias: Paroxysmal tachycardias originate from an ectopic focus and exhibit a sudden onset and an abrupt cessation, usually with a rate significantly faster than NSR Sustained tachycardias are those that last 30 seconds or more, or require intervention for termination Non-sustained tachycardias last at least 6 beats or less than 30 seconds. The tachycardia spontaneously terminates and requires no intervention. Recurrent tachycardias are characterized by occurring periodically, but occurrences are separated by periods of no tachycardia longer than the periods of tachycardia. Instructor Notes Say: There are different types of Ventricular Tachycardias. The next two slides define several of the terms associated with the different types.

Terms Describing Ventricular Tachycardias
Monomorphic Single focus Complexes are similar with equal intervals Polymorphic Multiple foci Complexes appear different with varied intervals Incessant Long periods of tachy, short periods of NSR Student Notes Polymorphic tachycardias originate from multiple foci. The complexes appear different from one another, and the coupling intervals are unequal. Incessant tachycardias have long periods of tachycardia interrupted by short periods of NSR. Instructor Notes More tachycardia terminology

Terms Describing SVT SVTs (Supraventricular Tachycardia)—originating from above the ventricles Paroxysmal: Sudden onset and spontaneous cessation Persistent: Requires intervention to terminate, usually >24-48 hour duration Permanent or Chronic: Unable to terminate Student Notes SVT, Supraventricular Tachycardias are tachycardia rhythms that originate above the ventricles (such as A fib/flutter & AVNRT) Instructor Notes Last term

Tachycardia Classifications
Impulse Formation Impulse Conduction Disorders of Student Notes All rhythm Disorders will fall into 1 of 2 categories depending on the underlying cause of the disorder. Disorders are either caused by disorders of impulse formation or disorders of impulse conduction. Instructor Notes Transition/Auto-animated slide

Tachycardia Classifications
Sinus Tachycardia Atrial Tachycardia Impulse Formation Impulse Conduction Premature Contractions Accelerated Junctional Rhythm Accelerated Idioventricular Rhythm (AIVR) Student Notes All rhythm Disorders will fall into 1 of 2 categories depending on the underlying cause of the disorder. Disorders are either caused by disorders of impulse formation or disorders of impulse conduction. Instructor Notes Transition/Auto-animated slide

Sinus Tachycardia Origin: Sinus Node Rate: 100-180 bpm
Mechanism: Abnormal or Hyper Automaticity (for example, exercise) Student Notes In Sinus Tachycardia, the ECG deflection will show a normal P- and R- wave depolarization, with a rapid tachycardic rate. Sinus Tachycardia rates range between bpm. The underlying Mechanism for Sinus Tachycardia is Abnormal Automaticity (Hyper-Automaticity). Instructor Notes

Atrial Tachycardia Origin: Atrium - Ectopic Focus Rate: >100 bpm
Mechanism: Abnormal Automaticity Student Notes Atrial tachycardia is defined as a series of 3 more consecutive atrial premature beats occurring at rate of > 100 bpm. Atrial tachycardia is usually paroxysmal (PAT – Paroxysmal atrial tachycardia)—it starts and ends abruptly. It can occur in healthy as well as diseased hearts, and may result from emotional stress or excessive use of alcohol, tobacco, or caffeine. Origin: Ectopic focus located in the atrium Mechanism: Abnormal Automaticity Instructor Notes

Premature Beats Premature Atrial Contraction (PAC)
Student Notes PACs originate in parts of the atrium other than the sinus node. These impulses occur before the sinus node depolarizes. PACs 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 "skip" or a "pause." Instructor Notes Origin: Atrium (outside the Sinus Node) Mechanism: Abnormal Automaticity Characteristics: An abnormal P-wave occurring earlier than expected, followed by compensatory pause

Premature Beats Premature Junctional Contraction (PJC)
Student Notes A junctional beat is a complex occurring earlier than expected that originates in the AV node or AV junction area. It is followed by a compensatory pause. Instructor Notes Origin: AV Node Junction Mechanism: Abnormal Automaticity Characteristics: A normally conducted complex with an absent P-wave, followed by a compensatory pause

Premature Beats Premature Ventricular Contraction (PVC)
Student Notes 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). Instructor Notes Origin: Ventricles Mechanism: Abnormal Automaticity Characteristics: A broad complex occurring earlier than expected, followed by a compensatory pause

PVC Patterns Bigeminy Trigeminy Quadrigeminy Every other beat
Every third beat Quadrigeminy Every fourth beat Student Notes Ventricular Premature beats that form patterns are classified according to the number of normal ventricular beats that occur between premature beats. Bigeminy – PVC every other beat; Trigeminy – PVC every third beat; or Quadrigeminy - PVC every fourth beat. Instructor Notes

Multifocal PVC Origin: Varies within the Ventricle
Mechanism: Abnormal Automaticity Characteristics: Each premature beat changes axis; implies a different focus of origin for each beat Note: PVCs by themselves are not a predictor of VT/VF, nor do they imply the need for a defibrillator Student Notes Not every premature beat is alike. This slide is an example of a variety of PVCs you may see. Instructor Notes

Accelerated Junctional Rhythm
Origin: AV Node or Junctional Tissue Mechanism: Abnormal Automaticity Characteristics: Occurs when AV nodal cells depolarize at a rate faster than the sinus node Student Notes Accelerated idiojunctional rhythm (or idionodal rhythm) occurs when the AV nodal rate accelerates to a rate faster than that of the sinus node, and takes over the rhythm. Junctional, or nodal rhythm, is also seen to take over a rhythm when the SA node fails to fire. However, in that instance, it is not accelerated. Origin: AV Node or Junctional Tissue Mechanism: Abnormal Automaticity Instructor Notes

Accelerated Idioventricular Rhythm
Origin: Ventricle Mechanism: Abnormal Automaticity Rate: Ventricular rate >sinus rate, but <VT Characteristic: May dominate and take over the underlying rhythm Student Notes Accelerated idioventricular rhythm (AIVR) is a form of ectopic or automatic ventricular arrhythmia. AIVR is characterized by a ventricular rate that is faster than the underlying sinus rate, yet slower than traditional VT. Because the rate is faster than the sinus rate, it dominates and takes over the rhythm. Origin: Ventricle Mechanism: Abnormal Automaticity (Hyper-Automaticity) Instructor Notes

Accelerated Idioventricular Rhythm
Sinus Rhythm being taken over by an Idioventricular Rhythm Student Notes Here we see how an AIVR eventually takes over from the slower sinus rhythm. Instructor Notes

Tachycardia Classifications Based on disorder
Sinus Tachycardia Premature Contractions Atrial Tachycardia Accelerated Junctional Rhythm Accelerated Idioventricular Rhythm (AIVR) Impulse Formation Impulse Conduction Atrial Flutter Student Notes Instructor Notes Transition/Auto-animated slide Atrial Fibrillation AVRT/AVNRT Ventricular Tachycardia Ventricular Fibrillation

Atrial Flutter Origin: Right and Left Atrium
Mechanism: Reentry, circus tachycardia, may be “clockwise” or “counter-clockwise” Rate: 250 – 400 bpm Characteristics: Rapid, regular P-waves, regular R-waves Student Notes 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. Instructor Notes

Atrial Fibrillation (AF)
Student Notes 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 ECG. A surface ECG 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. Instructor Notes Origin: Right and/or left atrium, pulmonary veins Mechanism: Multiple wavelets of reentry Atrial Rate: > 400 bpm Characteristics: Random, chaotic rhythm; associated with irregular ventricular rhythm

Atrial Fibrillation (AF)
Student Notes 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. Instructor Notes

AF Mechanism Paroxysmal: Sudden onset and spontaneous cessation
Persistent: Requires intervention to terminate, usually > hour duration Permanent or Chronic: Unable to terminate “AF begets AF” The more frequent the AF the more frequently it will re-occur and episodes tend to last longer Student Notes Electrical Remodeling is thought to be responsible for the progression of atrial fibrillation. It shortens the wavelength of an atrial impulse, and allows more reentry wavelets to coexist in the atria at a given time. The electrical remodeling effect is often called AF begets AF. It works like this: • When AF episodes are frequent or long, the refractory periods of myocardial cells become progressively shorter. This increases the excitable periods of myocardial cells and gives reentry waves more opportunities to self-propagate (spread). • The more wavelets present in the atria, the less likely they will self-extinguish. This increases the duration of an AF episode and decreases the likelihood AF will self-terminate or respond to cardioversion. Note: Increased atrial size due to underlying cardiovascular disease may contribute to an increased number of wavelets that can coexist in the atria. Instructor Notes

Other AF Mechanisms Mutifocal Atrial Tachycardia Single Foci
Mechanism: Abnormal Automaticity (multi-sites) Characteristics: Many depolarization waves; activation occurs asynchronously Not commonly used terms anymore, usually just called “AF” Single Foci Mechanism: Abnormal Automaticity (single-focus, usually in the Posterior Left Atrium) Characteristics: Rapid discharge; single ectopic site Parasystole – rare Student Notes 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. Instructor Notes

Atrial Flutter vs. Atrial Fibrillation
Summary of Disease Characteristics Atrial Flutter Atrial Fibrillation Atrial Rate 250 to 400 bpm 400 bpm Ventricular Rate/Rhythm Usually regular Varies with conduction Grossly irregular Pattern Saw tooth baseline Irregular or almost flat baseline “Irregularly irregular” Underlying Mechanism Reentry via macro re-entrant circuit Typically multiple wavelet reentry Student Notes 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 Instructor Notes

AVRT AV Re-entrant Tachycardia
An SVT caused by the existence of an extra pathway from the atria to the ventricles Extra pathway + AV Node = reentry Two Types Orthodromic Antidromic Student Notes AVRTs are caused by extra pathways that exist between the atria and the ventricles. The extra pathways are located outside, and in addition to, the AV Node. This re-entrant supraventricular rhythm’s circuit includes both the atrium and the ventricle, and uses an accessory atrioventricular pathway for at least one limb of the circuit. "Orthodromic" AVRT, which is the most common form, proceeds antegrade (from atrium to ventricle) over the AV node, and retrograde over an accessory pathway. "Antidromic" AVRT proceeds in the reverse direction, and has is a wide QRS tachycardia except when the accessory pathway is located in the right anteroseptal location very close to the His bundle. When multiple pathways are present, it is also possible for the circuit to use two pathways as a circuit. P-waves may or may not be seen, but they usually do not follow closely after the QRS if they are seen. The most common form of AVRT is Wolf-Parkinson-White (WPW) Syndrome, which we will consider in a moment. Instructor Notes Auto-animated slide

AVRT Orthodromic Accessory Pathway Mechanism: Reentry
Rate: bpm+ Characteristics: Extra electrical pathway to ventricles Accessory Pathway Conduction to the ventricles via the AV node (normal conduction) - then from Ventricles to the Atria via the accessory pathway. Produces narrow complex SVT. Student Notes Here is an example of the mechanism of reentry with patients having an A to V accessory pathway. The extra pathway serves as one limb of the reentry circuit Fast conduction properties A relatively slower refractory period The second limb of the circuit is the normal AV conduction pathway Conducts slowly, recovers quickly A tachycardia can be started by an appropriately timed premature atrial or ventricular beat. Should it occur when the pathway is in refractory, it will be conducted to the ventricles via normal AV conduction. If the impulse travels in the retrograde direction, the extra pathway may have recovered, conducting the impulse back to the atrium. This tachycardia is referred to as orthodromic (seen on the next slide), as the conduction travels antegrade through the AV node. The retrograde path is via the accessory pathway. Instructor Notes Auto-animated slide

AVRT Antidromic Accessory Pathway Mechanism: Reentry
Rate: bpm+ Characteristics: Extra electrical pathway to ventricles. Wide-complex QRS. Accessory Pathway Conduction to ventricles via the accessory pathway. The impulse is then conducted retrograde to atrial via the AV node. Produces a wide-complex SVT. Student Notes Here is an example of the mechanism of reentry with patients having an A to V accessory pathway. The extra pathway serves as one limb of the reentry circuit Fast conduction properties A relatively slower refractory period The second limb of the circuit is the normal AV conduction pathway Conducts slowly, recovers quickly A tachycardia can be started by an appropriately timed premature atrial or ventricular beat. Should it occur when the pathway is in refractory, it will be conducted to the ventricles via normal AV conduction. If the impulse travels in the retrograde direction, the extra pathway may have recovered, conducting the impulse back to the atrium. This tachycardia is referred to as orthodromic (seen on the next slide), as the conduction travels antegrade through the AV node. The retrograde path is via the accessory pathway. Instructor Notes Auto-animated slide

Wolff-Parkinson-White
Origin: A - V conduction outside the AV node. The Wolff pathway conducts faster than the AV node Mechanism: Reentry Rate: bpm – can be faster Characteristics: Short PR Interval (< 120 ms), wide QRS (> 110 ms), obvious delta wave Student Notes WPW is characterized by: 1) Short PR interval (120 ms or less) indicating that the impulse did not travel the path through the AV node 2) QRS is wide (110 ms or greater), again implying the impulse did not travel through the normal conduction system; and, 3) An obvious delta wave as a result of early conduction. A delta wave looks like a gradual onset of the QRS complex (above graphic) and the QRS is > 110 msec. The PR interval is typically less than 120 msec. As mentioned, the most common SVT in WPW is orthodromic, which creates a narrow complex QRS Approximately 7%-10% of WPW is antidromic, which creates a wide complex QRS (exaggeration of delta wave) Instructor Notes Auto-animated slide

AVNRT AV Node Re-entrant Tachycardia
Origin: AV Node Mechanism: Reentry Rate: bpm, faster in teenagers Characteristics: Normal QRS with absent P-waves Student Notes This is a reentrant supraventricular rhythm whose reentry circuit is located in the region of the atrioventricular node. It is characterized by a QRS morphology that is normal for the patient. The rate of AVNRT is commonly between bpm, and can exceed 250 bpm in teenagers. Note that on the ECG, P-waves are unseen, and are usually buried in the QRS. Approximately 60% of narrow-complex tachycardias are found to be caused by AVNRT A paroxysmal onset and termination is seen with AVNRT There is both a typical and atypical form of AVNRT Typical AVNRT is a result of a shift in conduction from the fast to the slow pathway, and is seen in 90% of the patients with AVNRT Atypical AVNRT is a result of a conduction shift from the slow to fast, or slow to the slow pathway. The atypical form is less common, occurring in 10% of the patients with AVNRT. AVNRT is not associated with underlying heart disease. It may present at any age, but usually occurs in the mid 40s. It may be more frequent in females, may occur at rest or with exercise, and appears to be catecholamine sensitive, as there are increased episodes with exercise, emotional stress, and caffeine. The frequency of AVNRT episodes can be from once every 2 or 3 years, to several times a day Instructor Notes

AVRT vs. AVNRT AVRT AVNRT Treatment: Ablation
180 – 260 bpm Narrow QRS if orthodromic Wide QRS if antidromic Delta wave + in SR PR < 120 msec 1:1 Conduction AVNRT 150 – 230 bpm Narrow QRS Short RP No delta waves Initiating PR long P-waves buried in QRS Conduction 1:1, or 2:1 when distal block present Treatment: Ablation Rarely is a pacemaker implanted Perhaps if AV node is injured during ablation Student Notes It is often difficult to differentiate between atrioventricular nodal reentry tachycardia and atrioventricular reentry tachycardia. Both are paroxysmal, narrow complex tachycardias AVRT is usually faster than AVNRT Instructor Notes Auto-animated slide

Tachycardia Classifications Based on disorder
Sinus Tachycardia Premature Contractions Atrial Tachycardia Accelerated Junctional Rhythm Accelerated Idioventricular Rhythm (AIVR) Impulse Formation Impulse Conduction Atrial Flutter Atrial Fibrillation AVRT/AVNRT Student Notes Instructor Notes Transition/Auto-animated slide Ventricular Tachycardia Ventricular Fibrillation

Monomorphic VT Classification Based on ECG Morphology
Origin: Ventricles (Single Focus) Mechanism: Reentry initiated by abnormal automaticity or triggered activity Characteristics: Rapid, wide and regular QRS. A-V disassociation Student Notes Monomorphic morphology indicates that electrical activity has a single point of origin or focus. Monomorphic VT is usually initiated by a PVC and sustained by reentry of a single loop. On this slide, we can see the ECG characteristics that help define VTs: Rapid, wide, and regular QRS complexes Rate of 120 bpm or greater Uniform beat-to-beat appearance The T-waves are large with deflections opposite the QRS complexes P-waves are usually not visible, therefore, the PR interval is not measurable Instructor Notes

Polymorphic VT Origin: Ventricles (Wandering Single Focus)
Mechanism: Reentry with movement in the circuit initiated by abnormal automaticity or triggered activity Characteristics: Wide and irregular QRS Complex that changes in axis Student Notes The QT, or repolarization syndrome, are typically associated with polymorphic VT are often called “torsades de pointes” due to the original French description of the QRS complexes as “twisting” about its axis. Polymorphic VT morphology has a single focus that nonetheless wanders through a number of different points of origin. ECG characteristics are: Broad (wide) QRSs Usually at rates of 120 bpm or greater (500 ms or less) Highly irregular QRS wave Variable beat-to-beat appearance Instructor Notes

Torsades de Pointes “Twisting of the points”
Origin: Ventricle Mechanism: Reentry (movement in focus) Rate: 200 – 250 bpm Characteristics: Associated with Long QT interval; QRS changes axis and morphology with alternating positive/negative complexes Student Notes Torsades de pointes (TdP – twists of points) is a distinctive VT in which the QRS complexes change in morphology from positive to negative and appear to twist around an imaginary base line. The changing patterns are due to a movement in the reentrant mechanism. TdP is associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT. Events leading to TdP are: Hypokalemia Prolongation of the action potential duration Early afterdepolarizations Critically slow conduction that contributes to reentry Instructor Notes

Ventricular Fibrillation (VF)
Student Notes 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) While multiple wavelets of reentry maintain VF, there is some belief that focal activation initiates it. Instructor Notes Origin: Ventricle Mechanism: Multiple wavelets of reentry Characteristics: Irregular with no discrete QRS

Tachycardia Classifications Summary
Sinus Tachycardia Premature Contractions Atrial Tachycardia Accelerated Junctional Rhythm Accelerated Idioventricular Rhythm (AIVR) Impulse Formation Impulse Conduction Atrial Flutter Student Notes This slide gives us a summary of the two categories of tachyarrhythmia, depending on the underlying cause of the disorder. Instructor Notes Atrial Fibrillation AVRT/AVNRT Ventricular Tachycardia Ventricular Fibrillation

Status Check Identify the Rhythm
Ventricular Tachycardia Sinus Bradycardia Complete Heart Block Atrial Fibrillation Ventricular Fibrillation Click for Answer Student Notes Instructor Notes Auto-animated slide Click for answer

Status Check Ventricular Tachycardia Sinus Bradycardia
Complete Heart Block Atrial Fibrillation Ventricular Fibrillation Click for Answer Student Notes Instructor Notes Auto-animated slide Click for answer

Upcoming Modules The Fundamentals of Cardiac Devices
Basic Concepts—Electricity and Pacemakers Applying Electrical Concepts to Pacemakers Pacemaker Basics Single and Dual Chamber Pacemaker Timing Advanced Pacemaker Operations Pacemaker Patient Follow-up Pacemaker Troubleshooting Pacemaker Automatic Features Student Notes Instructor Notes

Disclosure NOTE: This presentation is provided for general educational purposes only and should not be considered the exclusive source for this type of information. At all times, it is the professional responsibility of the practitioner to exercise independent clinical judgment in a particular situation.

Brief Statements Indications
Implantable Pulse Generators (IPGs) are indicated for rate adaptive pacing in patients who ay benefit from increased pacing rates concurrent with increases in activity and increases in activity and/or minute ventilation. Pacemakers are also indicated for dual chamber and atrial tracking modes in patients who may benefit from maintenance of AV synchrony. Dual chamber modes are specifically indicated for treatment of conduction disorders that require restoration of both rate and AV synchrony, which include various degrees of AV block to maintain the atrial contribution to cardiac output and VVI intolerance (e.g. pacemaker syndrome) in the presence of persistent sinus rhythm. Implantable cardioverter defibrillators (ICDs) are indicated for ventricular antitachycardia pacing and ventricular defibrillation for automated treatment of life-threatening ventricular arrhythmias. Cardiac Resynchronization Therapy (CRT) ICDs are indicated for ventricular antitachycardia pacing and ventricular defibrillation for automated treatment of life-threatening ventricular arrhythmias and for the reduction of the symptoms of moderate to severe heart failure (NYHA Functional Class III or IV) in those patients who remain symptomatic despite stable, optimal medical therapy and have a left ventricular ejection fraction less than or equal to 35% and a QRS duration of ≥130 ms. CRT IPGs are indicated for the reduction of the symptoms of moderate to severe heart failure (NYHA Functional Class III or IV) in those patients who remain symptomatic despite stable, optimal medical therapy, and have a left ventricular ejection fraction less than or equal to 35% and a QRS duration of ≥130 ms. Contraindications IPGs and CRT IPGs are contraindicated for dual chamber atrial pacing in patients with chronic refractory atrial tachyarrhythmias; asynchronous pacing in the presence (or likelihood) of competitive paced and intrinsic rhythms; unipolar pacing for patients with an implanted cardioverter defibrillator because it may cause unwanted delivery or inhibition of ICD therapy; and certain IPGs are contraindicated for use with epicardial leads and with abdominal implantation. ICDs and CRT ICDs are contraindicated in patients whose ventricular tachyarrhythmias may have transient or reversible causes, patients with incessant VT or VF, and for patients who have a unipolar pacemaker. ICDs are also contraindicated for patients whose primary disorder is bradyarrhythmia.

Brief Statements (continued)
Warnings/Precautions Changes in a patient’s disease and/or medications may alter the efficacy of the device’s programmed parameters. Patients should avoid sources of magnetic and electromagnetic radiation to avoid possible underdetection, inappropriate sensing and/or therapy delivery, tissue damage, induction of an arrhythmia, device electrical reset or device damage. Do not place transthoracic defibrillation paddles directly over the device. Additionally, for CRT ICDs and CRT IPGs, certain programming and device operations may not provide cardiac resynchronization. Also for CRT IPGs, Elective Replacement Indicator (ERI) results in the device switching to VVI pacing at 65 ppm. In this mode, patients may experience loss of cardiac resynchronization therapy and / or loss of AV synchrony. For this reason, the device should be replaced prior to ERI being set. Potential complications Potential complications include, but are not limited to, rejection phenomena, erosion through the skin, muscle or nerve stimulation, oversensing, failure to detect and/or terminate arrhythmia episodes, and surgical complications such as hematoma, infection, inflammation, and thrombosis. An additional complication for ICDs and CRT ICDs is the acceleration of ventricular tachycardia. See the device manual for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential complications/adverse events. For further information, please call Medtronic at and/or consult Medtronic’s website at Caution: Federal law (USA) restricts these devices to sale by or on the order of a physician.

Brief Statement: Medtronic Leads
Indications Medtronic leads are used as part of a cardiac rhythm disease management system. Leads are intended for pacing and sensing and/or defibrillation. Defibrillation leads have application for patients for whom implantable cardioverter defibrillation is indicated Contraindications Medtronic leads are contraindicated for the following: ventricular use in patients with tricuspid valvular disease or a tricuspid mechanical heart valve. patients for whom a single dose of 1.0 mg of dexamethasone sodium phosphate or dexamethasone acetate may be contraindicated. (includes all leads which contain these steroids) Epicardial leads should not be used on patients with a heavily infracted or fibrotic myocardium. The SelectSecure Model 3830 Lead is also contraindicated for the following: patients for whom a single dose of 40.µg of beclomethasone dipropionate may be contraindicated. patients with obstructed or inadequate vasculature for intravenous catheterization.

Brief Statement: Medtronic Leads (continued)
Warnings/Precautions People with metal implants such as pacemakers, implantable cardioverter defibrillators (ICDs), and accompanying leads should not receive diathermy treatment. The interaction between the implant and diathermy can cause tissue damage, fibrillation, or damage to the device components, which could result in serious injury, loss of therapy, or the need to reprogram or replace the device. For the SelectSecure Model 3830 lead, total patient exposure to beclomethasone 17,21-dipropionate should be considered when implanting multiple leads. No drug interactions with inhaled beclomethasone 17,21-dipropionate have been described. Drug interactions of beclomethasone 17,21-dipropionate with the Model 3830 lead have not been studied. Potential Complications Potential complications include, but are not limited to, valve damage, fibrillation and other arrhythmias, thrombosis, thrombotic and air embolism, cardiac perforation, heart wall rupture, cardiac tamponade, muscle or nerve stimulation, pericardial rub, infection, myocardial irritability, and pneumothorax. Other potential complications related to the lead may include lead dislodgement, lead conductor fracture, insulation failure, threshold elevation or exit block. See specific device manual for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential complications/adverse events. For further information, please call Medtronic at and/or consult Medtronic’s website at Caution: Federal law (USA) restricts this device to sale by or on the order of a physician.

Arrhythmias and Devices Module 1

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Arrhythmias and Devices Module 1

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