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  2. 2. Introduction A cardiac arrhythmia is an abnormality of initiation, timing, or sequence of cardiac depolarization. It can result in either tachycardia or bradycardia. What is Tachyarrhythmia? Tachyarrhythmia's are cardiac rhythms associated with an elevated heart rate, greater than 100 beats/min.
  3. 3. What Causes Tachyarrhythmia? Tachyarrhythmia results from one of the three mechanisms discussed below: I. Abnormal Automaticity:  Automaticity is the ability of cardiac cells to initiate spontaneous action potentials. In normal conditions, the sinus node has the fastest spontaneous firing and it acts as a predominant pacemaker.  AV node, His bundle, and Purkinje fibers fire an impulse at a progressively slower rate and are usually suppressed by the activity of the sinus node. When any of these cardiac cells start firing spontaneously, they cause abnormal automaticity and result in premature heartbeats.  Abnormal automaticity or spontaneous impulse generation can develop when pathologic conditions depolarize myocardial cells. For example, an injury current can develop between a depolarized ischemic cell and normal cells, leading to repetitive activity in the normal cells. Cellular depolarization can result from medications, ischemia, metabolic disturbance, or local trauma.
  4. 4. II. Triggered Activity: Usually, the heart cells have to contract once for each impulse but during a triggered activity the heart cells contract twice for each impulse. This is often caused by after-depolarizations because of electrical instability in the myocardial cell membrane. After-depolarizations can be either early or delayed. a. Early after-depolarizations (EADs):  They are related to increased calcium ion and sodium ion currents that maintain the plateau phase of the action potential.  They are important in the genesis of Torsades de Pointes.  They are facilitated by increased early repolarization. b. Delayed after-depolarization (DADs):  They arise from the repolarized membrane (phase 4).  They occur in states of increased intracellular calcium ions. Excessive intracellular calcium ions and generation of inward current by Na+/Ca+2 exchanger causes DAD.
  5. 5. III. Re-entry:  It is the most common mechanism for the formation of arrhythmia. It consists of an electrical pathway which causes an impulse to travel back into the atrium immediately after it has been depolarized, thus, depolarizing it again. This process will continue as long as the impulse encounters the cells that are receptive to it.  It occurs due to abnormal impulse conditions that result from anomalous anatomic pathway or poor impulse propagation.  Fibrotic changes in the heart associated with hypertrophy or injury can lead to areas of slow conduction and provide micro and macro pathways for re-entry. The three conditions required for re-entry to occur are:  Presence of two electrical pathways  Presence of unidirectional block in one pathway  Presence of slow conduction, which allows recovery of the excitability in the previously blocked area
  6. 6. Classification of Tachyarrhythmia's Tachyarrhythmia are classified based on their anatomic location of origin or width of the QRS complex. a. Based on Anatomical location:
  7. 7. b. Based on the width of the QRS complex: Tachyarrhythmia is broadly classified into either narrow complex tachycardia (NCT) or wide complex tachycardia (WCT) based on the width of the QRS complexes.
  8. 8. Steps to Diagnose Tachyarrhythmia from ECG Pattern Step 1 - Analyze the heart rate:  Tachyarrhythmia are associated with a heart rate greater than 100 bpm. Therefore, you should first check the heart rate by using the 10-second rule or by 300 rule, which was discussed in lesson 1 of the module.  In a 10-second rule, you need to count the number of QRS complexes present in a 10 second period and then multiply the number by 6. Step 2 - Analyze the rhythm: Tachyarrhythmia usually have an abnormal rhythm. Therefore, you should check the RR interval in the given ECG strip to determine whether the patient has a regular or irregular rhythm.
  9. 9. Step 3 - Check the width of the QRS complex: The width of the normal QRS complex is 60 to 120 millisecond (ms). Tachyarrhythmia is characterized by narrow or wide QRS complex. A narrow QRS complex has a duration of 120 ms (three small boxes). It indicates that the ventricles are depolarized through the His-Purkinje system. A narrow complex tachyarrhythmia does not compromise the circulation of blood and so they are easier to manage than a wide complex tachyarrhythmia. On the other hand, a wide QRS complex has an interval of greater than 120ms. It indicates that the ventricles are not depolarized normally. Any impulse generated in the ventricles will result in wide QRS completely as the impulse spreads completely or partially outside the conduction system.
  10. 10. Step 4 - Check the morphology of P wave: While examining the P waves, you should check the following aspects:  Are P waves present?  Do P-waves precede each QRS complex?  Do all the P waves have a uniform shape or have a varying shape?  Does P wave have normal configuration? The absence of P waves before a QRS complex indicates that the rhythm is either atrial fibrillation or the impulse originates in AV node. P waves that are present but not clearly associated with QRS complex are indicative of heart block. Step 5 - Determine PR interval and PR ratio: The duration of the normal PR interval is 120 to 200 millisecond (or 3 to 5 small squares). You can measure the PR interval by counting the number of small squares between the onset of the P wave and the beginning of the QRS complex. Then multiply the number of squares by 0.04 second. Check if the PR interval is within the normal range and if the PR interval constant throughout the ECG strip. A long PR interval can be observed in patients with atrial tachycardia and atypical AV nodal re-entry tachycardia.
  11. 11. The normal P: R ratio is 1:1. If the P: R ratio is 2:1,3:1, or greater, it indicates that the patient has focal or macro reentrant atrial tachycardia with AV nodal block. Step 6 - Check if the onset of palpitations is gradual or abrupt: A gradual onset suggests sinus tachycardia, whereas an abrupt onset suggests an arrhythmia. Let us learn in detail about the ECG changes associated with each type of tachyarrhythmia. Ectopic Beats Ectopic beats are the extra heartbeats that arise from the impulses generated at points in the myocardium other than sinoatrial node (the physiological pacemaker). Ectopic beats are the most common cause of irregular pulse. They are also referred to as premature contractions or extra systoles. They occur early in the cardiac cycle before the next sinus beat and are followed by a gap in the pulse known as a compensatory pause. The compensatory pause prevents the propagation of the next sinus beat.
  12. 12. Depending on the actual location, they are classified into two types: I. Supraventricular ectopic beats II. Ventricular ectopic beats Supraventricular Ectopic Beats (SVEBs) A supraventricular ectopic beat is an early atrial depolarization, which originates either in one of the atria or outside the sinoatrial node. It is characterized by a premature QRS complex in the ECG. SVEBs occur singly or in groups and indicate atrial irritability. An isolated SVEB is not significant but a high frequency suggests a higher risk in the patients. They are followed by an incomplete or non-compensatory pause, which is caused due to SA node depolarization by ectopic impulse. It usually lasts less than twice the duration of the normal P-P cycle. An increasing trend in SVEBs may be an indicator or sign of atrial fibrillation, which may lead to heart attack or stroke.
  13. 13. ECG Criteria of SVEBs: Sample ECG Analysis
  14. 14. Ventricular Ectopic Beats (VEB) Ventricular ectopic beats are early heartbeats that begin in the ventricles. They are characterized by wide and bizarre QRS complex due to early initiation of impulse in one of the ventricles, which spreads to the other ventricle with some delay. This delay occurs due to slow conduction of an impulse through the ventricles than through the normal conduction pathway. The QRS complex tends to be followed by a compensatory pause. In VEB, the QRS complex is not always preceded by a P wave. The P wave may occur directly before or after the QRS complex but it does not bear any relationship to it. Ventricular ectopics may be isolated or may be few in a row, bigeminal or trigeminal pattern, or in couplets or triplets (rapid succession of three or more VEBs with a heart rate of more than 100bpm). If more than six ventricular ectopics are present in a row, it indicates ventricular tachycardia.
  15. 15. Isolated VEBs have little effect on the pumping action of the heart and usually do not cause symptoms unless they are frequent. The primary symptom reported by patients with isolated VEBs is a feeling of the heart 'skipping a beat. This symptom may not be dangerous for people who do not have a heart disorder, but it may be followed by a life threatening arrhythmia such as ventricular tachycardia or ventricular fibrillation in people with a structural heart disorder. Ventricular ectopics may be positive or negative complexes. To check if the VEB is positive or negative, you need to view the ECG pattern of the patient in lead V1. If the QRS complex in lead V1 is positive, it indicates that the impulse is coming from the left and it is traveling towards the right. If the QRS complex in lead V1 is negative, it indicates that the impulse is coming from the right and it is traveling towards left. If some ventricular ectopics on the rhythm strip are positive and some are negative, they are collectively referred to as multifocal ectopics. If the ventricular ectopic falls so early that it interrupts the T-wave of the preceding complex, then it causes a high risk of ventricular tachycardia or fibrillation.
  16. 16. Types of Ventricular Ectopic:
  17. 17. ECG Criteria of Ventricular Ectopic:
  18. 18. Sample ECG Analysis:
  19. 19. In the given ECG strip, lead II has premature ventricular contractions, which are caused by an early ectopic impulse within the ventricles. They occur after a sinus P wave before a normal QRS complex, below the bundle of His, which extends depolarization resulting in a wider QRS complex that is often bizarre in shape, or between two consecutive sinus beats. The ECG strip has wide QRS complex (greater than 5 small squares) as the impulses are generated from the ventricles, and action potentials travel slowly from one myocyte to another. You can also find a compensatory pause between two QRS complexes showing a PVC, and a duration twice the distance of other R-R intervals.
  20. 20. Supraventricular Tachyarrhythmia's Arrhythmias are categorized into supraventricular and ventricular depending on their origin. Supraventricular arrhythmias originate in the atria or conducting system not in the ventricle, whereas ventricular arrhythmias originate in the ventricles. Supraventricular tachyarrhythmias are relatively more common and occur in patients of all ages, with or without structural heart disease. They can be further divided into two categories- atrial and atrioventricular (AV) junction tachyarrhythmia. Atrial tachyarrhythmias require only atrial tissue and AV junctional tachyarrhythmia need AV junctional tissue.
  21. 21. Atrial Tachyarrhythmias SINUS TACHYCARDIA: Sinus tachycardia (ST) is a dysrhythmia that originates in the sinus node and follows the normal conduction pathways through the heart, producing normal depolarization and a normal ECG pattern. It is associated with a higher heart rate usually 100 to 180 beats/minute. Cause: The sinus node is innervated by the sympathetic and vagal nerve endings. Sympathetic stimulation, as well as vagal withdrawal, increase the sinus rate. Circulating catecholamines also affect the sinus rate. Some of the common causes of ST are listed below: Physiologic factors: Fever, hypoxia, hemorrhage, hypotension, anemia, pain, anxiety and injury to any body part accelerates the heart rate and causes ST  Medications: Atropine, quinidine sulfate, aminophylline, epinephrine, dopamine, thyroid hormones, and glucagon can increase the heart rate and general metabolism of the body.  Damage to heart tissue: Acute injury as myocardial infarction, trauma, infection, congestive heart failure or cor pulmonale can increase the heart rate.
  22. 22. Symptoms:  Dizziness  Syncope  Weakness  Weak pulse  Disorientation  Chest tightness  Shortness of breath  Increased heart rate  Occasional palpitations
  23. 23. ECG changes:
  24. 24. Sample ECG Analysis:  Heart rate: The heart rate can be calculated by using the 10-second rule method. In lead II, there is 19 QRS complex in a 10 second period. So, the heart rate is 19 x 6 = 114 beats/min.  Rhythm: The R-R interval is same across the strip indicating that the patient has a regular rhythm.  QRS interval: Normal  P wave: Normal, upright and consistent  P: Q ratio: 1:1, Each P wave is followed by a QRS Interpretation: The given ECG strip indicates that the patient has a normal rhythm and a heart rate > 100 beats/min. The waveforms are normal with upright P waves in the lead II recordings. Each P wave is followed by a QRS complex indicating that the impulse is coming from the sinus node and not from other regions of the heart. These findings suggest that the patient has sinus tachycardia.
  25. 25. Atrial Tachycardia Atrial tachycardia (AT) is formed by a rapid succession of three or more atrial ectopic. It is characterized by an increased atrial rate (150 to 250 beats/minute) and has similar features to the single atrial ectopic beat. It is usually faster than sinus tachycardia. The rapid atrial heart rate shortens the diastole, resulting in a loss of atrial kick, reduced cardiac output, reduced coronary perfusion, and ischemic myocardial changes. As the tachycardia's do not involve the AV node, vagal maneuvers or AV nodal blockers are ineffective in terminating the tachycardia. Causes: One area in the atria becomes very irritable and initiates impulses rapidly one after another, taking over the pacemaker function from the SA node. All the impulses are conducted through the atrioventricular node to the ventricles through normal conduction pathways.
  26. 26.  MI  Cardiomyopathy  Congenital anomalies  Wolff-Parkinson-White syndrome  Valvular heart disease Symptoms:  Dizziness  Syncope  Weakness  Weak pulse  Disorientation  Chest tightness  Shortness of breath  Increased heart rate  Chest palpitations
  27. 27. ECG changes:
  28. 28. Sample ECG analysis:
  29. 29.  Heart rate: 120 beats /min  Rhythm: Regular  QRS Complex: Normal  P wave: Abnormal; It is upright in lead V1 and inverted in leads II, III, and aVF.  P: Q ratio: 1:1; Each QRS complex is preceded by a P wave  Interpretation: A heart rate of 120bpm and abnormal P wave indicates that the patient has atrial tachycardia Atrial tachycardia is sub classified based on the mechanism. Let us now learn about the three forms of atrial tachycardia:  Atrial tachycardia with block  Multifocal atrial tachycardia  Paroxysmal atrial tachycardia
  30. 30. Atrial Tachycardia with Block It is caused due to increased automaticity of the atrial tissue. A 2:1 block occurs when the atrial rate speeds up and the atrioventricular (AV) conduction becomes impaired. The ECG characteristics of atrial tachycardia with a block are:
  31. 31. Multifocal Atrial Tachycardia Multifocal atrial tachycardia is caused due to increased automaticity by an intermittent firing of numerous atrial foci. It is characterized by a high atrial rate (100 to 130 bpm) and abnormal P wave morphology. It is most common in patients with the chronic pulmonary disease. Most atrial tachycardias except multifocal atrial tachycardia are treated using radiofrequency ablation. Treatment for multifocal atrial tachycardia depends on the underlying pulmonary illness. The ECG characteristics of multifocal atrial tachycardia are:
  32. 32. The ECG strip given above indicates that the patient has a rapid irregular rhythm with a heart rate > 100 bpm. The arrow marks in the ECG points the P waves with three distinctive morphologies, which is a characteristic feature of multifocal atrial tachycardia.
  33. 33. Paroxysmal Atrial Tachycardia (PAT) The mechanism of paroxysmal atrial tachycardia (PAT) is similar to atrial tachycardia expect that it starts suddenly and often ends suddenly as a result of the rapid firing of an ectopic focus. PAT is sometimes faster than atrial tachycardia. The ECG characteristics of atrial tachycardia with block are:
  34. 34. Atrial Fibrillation Atrial Fibrillation (AF) is defined as chaotic, asynchronous, electrical activity in atrial tissue. It results from the firing of multiple impulses from numerous ectopic pacemakers in the atria. It is the most common sustained tachyarrhythmia, which is characterized by the absence of P waves and an irregularly irregular ventricular rhythm. The rate of atrial fibrillation cannot be measured, as it often exceeds 300 to 600 beats/minute producing a chaotic baseline. The ECG contains uneven baseline fibrillatory waves, or f waves rather than clear distinguishable P waves. The irregular fibrillatory waves are usually easy to recognize and are referred to as coarse atrial fibrillation.
  35. 35. When some ectopic sites in the atria initiate impulses, depolarization cannot spread in an organized manner. Small sections of the atria are depolarized individually, resulting in the atrial muscle quivering, and there is no organized atrial contraction. Mural thrombi are common consequences of long-term atrial fibrillation. In atrial fibrillation, the AV node is bombarded by hundreds of atrial ectopics at varying rates and amplitudes. The AV node therapeutically and randomly conducts impulses at a varying rate of speed, so the ventricular response is irregular. When a patient first experiences atrial fibrillation, the atrial rates are immeasurable, and the ventricular rhythm is irregular and very rapid. The ventricles respond only to impulses conducted through the AV node, hence the characteristic, wide variation in RR intervals can be seen in patients with AF. A rapid ventricular rate may be life-threatening. A normal ventricular response is defined as 60 to 100 beats /minute, so when the ventricular response rate drops below 100, atrial fibrillation is considered under control. A ventricular response rate of > 100 beats/minute indicates fast or uncontrolled AF.
  36. 36. Characteristics of 'f Waves':  f waves are often coarse (> 2 mm) in recent A.  f waves are usually fine (< 1 mm) in AF of greater duration.  f waves are of greater amplitude when there is hypertrophy or left atrial myocardium and become smaller with increasing atrial scarring and fibrosis.  The amplitude of f waves does not correlate with actual atrial size.
  37. 37. Sample ECG Analysis:
  38. 38. The given ECG strip consists of coarse fibrillatory waves in lead V1. The heart rate is 132 beats/minute, which is an indication of rapid ventricular response. The rhythm is irregularly irregular as two subsequent RR intervals have the same duration. In lead V1- the QT interval cannot be measured as the T waves are not clearly detectable. The duration of QRS complex is less than 0.1 sec. Therefore, these findings suggest that the patient has AF with a rapid ventricular response. Atrial Flutter Atrial flutter is characterized by an atrial microreentrant circuit (typically in the right atrium) leading to regular atrial depolarizations at a rate of 250 to 350 beats/minute. There is typical 2:1 conduction through the atrioventricular node, resulting in heart rates close to 150 beats/min.
  39. 39. Atrial flutter results from one of the two mechanisms:  An atrial ectopic focus similar to atrial tachycardia but with a much faster atrial rate  A self-perpetuating circular path of atrial depolarization that typically forms a continuous circuit between the inferior and superior vena cava within the right atrium. The atrial muscles respond to this rapid stimulation by producing waveforms that resemble the teeth of a saw. The sawtooth deflections are called flutter waves (F waves). The typical atrial flutter wave consists of an initial negative component followed by a positive component producing a V-shaped waveform with a sawtooth appearance. The sawtooth waves affect the whole baseline to the extent that there is no isoelectric line between the F waves, and the T wave is partially or completely eclipsed by the flutter waves. Flutter waves in the lead V1 may resemble P waves. Flutter waves can be best seen in leads II, III, aVF.You can easily identify the F waves in an ECG strip by turning it upside down!
  40. 40. The QRS complexes are usually normal as long as conduction through the ventricles is normal. In atrial flutter, the ventricular rate is slower than the atrial rate. The ventricular the rate depends on the number of impulses conducted through the AV node to the ventricles. The ventricular rate is a fraction of the atrial rate, e.g.  2:1 block = 150 bpm  3:1 block = 100 bpm  4:1 block = 75 bpm During the early stages of atrial flutter, there is typically 2:1 conduction through the atrioventricular node that results in a ventricular rate close to 150 beats/minutes. In other words, every other atrial impulse is conducted through to the ventricles. If the AV conduction ration remains constant (2:1), the ventricular rhythm will be regular, and the rhythm is described as atrial flutter with 2:1 AV conduction. If the conduction ratio varies from 4:1 to 2:1 to 6:1, the ventricular rhythm will be irregular and the rhythm is described as atrial flutter with variable AV conduction.
  41. 41. Atrial flutter with 2:1 block can be misdiagnosed as sinus tachycardia. Here are some clues that will help you to distinguish 2:1 atrial flutter with sinus tachycardia: In sinus tachycardia, the P and T waves are usually distinctly different from each other. Another clue to differentiate sinus tachycardia at 150 beats/min from atrial flutter with 2:1 AV block is finding the P' midway between the QRS complexes. Distortion of the QRS by suspected P' is called Ta distortion. Further, the patient with atrial flutter may complain of a sudden onset of rapid heart rate, feeling of weakness and dread. However, these symptoms are less likely to occur in patients with sinus tachycardia.
  42. 42. Classification of Atrial Flutter:
  43. 43. Sample ECG Analysis:
  44. 44. The given ECG strip contains inverted flutter waves in leads II, III, and aVF with an atrial rate nearly 300 bpm. The flutter waves present in lead V1 resemble the upright P waves. The rhythm is regular. There is a 2:1 AV block resulting in a ventricular rate of 150 bpm. Occasional irregularity with a 3:1 cycle is seen in V1-3. It is an example of anticlockwise flutter. Difference between atrial flutter and atrial fibrillation:
  45. 45. Supraventricular Tachycardia Supraventricular tachycardias (SVT) involve at least some part of the atrium or atrioventricular junction. SVT is a very common group of arrhythmias, which develop as a result of abnormal automaticity, triggered activity or reentry mechanism. It is characterized by a rapid heart rate (120-200bpm) and a rhythmic succession of QRS complex. The QRS complex duration is typically narrow (<120ms), reflecting conduction over the AV node and His-Purkinje system, but sometimes can have a wide QRS complex due to pre-existent or rate-dependent bundle branch blocks or other aberrant interventricular conduction disturbances. Both atrial flutter and atrial fibrillation are supraventricular tachycardias but because of the differences in their mechanisms and clinical manifestations, they are grouped separately from other types of supraventricular tachycardias, commonly referred to as paroxysmal supraventricular tachycardia (PSVT).
  46. 46. Classification: Based on the ECG criteria supraventricular tachycardia can be classified into the two types:  Short RP/long PR interval tachycardia  Long RP/Short PR interval tachycardia Short RP/Long PR Interval Tachycardia A short RP tachycardia demonstrates a short RP pattern with P waves embedded within or occurring closely after the preceding QRS complex. The RP interval reflects the retrograde conduction time for an impulse to travel from ventricular to atrial tissue. A short RP tachycardia occurs with reentrant supraventricular tachycardia when the retrograde VA conduction time is shorter than the anterograde AV conduction time. In general, atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) are short RP tachycardia.
  47. 47. Atrioventricular Nodal Reentrant Tachycardia (AVNRT) AVNRT is the most common paroxysmal supraventricular tachycardia in adults. It is more common in women than in men. In patients with AVNRT, the atrioventricular junction has two or more functionally discrete pathways – the fast and slow pathway. The "fast pathway "conducts impulses rapidly but has a relatively long effective refractory period. The "slow pathway" has a slower conduction velocity but a shorter effective refractory period than the fast pathway. AVNRT is a reentrant tachycardia that involves the AV node. The retrograde conduction typically occurs along the fast pathways. As a result, the atria are reactivated during or shortly after ventricular activation. During typical AVNRT, the P wave falls on the ST segment or within the terminal part of the QRS complex. (In most cases, the interval between ventricular and atrial activation—the V-A intervals thus < 70 ms)
  48. 48. Based on the contribution of the fast and slow pathways in the antegrade and retrograde limbs of the tachycardia circuit, AVNRT is classified into typical and atypical forms. Typical AVNRT: In typical AVNRT, a premature atrial depolarization (PAD) conducts to the atrioventricular junction through the atrium. The PAD arrives at the AV node when the fast pathway is in a refractory state. Therefore, the impulse conducts antegradely via the slow pathway with a shorter refractory period. When the impulse reaches the end of the slow pathway, the fast pathway is ready for retrograde conduction. Therefore, typical AVNRT is also called "Slowfast“ AVNRT. In typical AVNRT, the RP interval is very short, and the P wave is usually hidden within the QRS complex or appears at the end of QRS complex because of the simultaneous atrial and ventricular activation. It may be present as' pseudo r' in leads V1 or aVR and as 'pseudo s' in inferior leads or notching at the end of aVL.
  49. 49. Atypical AVNRT: In atypical AVNRT, a premature atrial depolarization conducts to the atrioventricular junction through the atrium. It occurs when the antegrade conduction to the ventricle occurs via the fast pathway, while the retrograde conduction to the atrium is through the slow pathway. Therefore, atypical AVNRT is commonly called as "fast-slow" AVNRT. In atypical AVNRT, the RP interval is longer, and P waves are manifested as negative deflections within the ST segment or shortly before the next QRS complex in the inferior leads. ECG Characteristics: Typical and atypical AVNRTs usually have a narrow QRS complex, however concomitant bundle branch block (BBB) can rarely create a wide QRS complex. Several differences in ECG characteristics will help you to distinguish between typical and atypical AVNRTs.
  50. 50. P Wave: While analyzing the ECG of a patient with suspected AVNRT, you should first check the P-wave morphology, width, location, and mechanism of initiation. The P wave axis is similar for both typical and atypical AVNRT. The P wave is inverted in inferior leads II, III, and aVF in both the types of AVNRT as the activation of the atria occurs in an inferior-to-superior direction. In lead V1 the P wave is upright as the AV node which is located posteriorly causes posterior-to-anterior activation of the atria. The width of the P wave is different in two forms of AVNRT. In typical AVNRT, the P wave tends to be narrow, whereas in atypical AVNRT it is wider because of the difference in anatomical location of the fast and slow conducting pathways that activate the atria. In typical AVNRT, P wave is rarely visible on the ECG due to simultaneous conduction of the ventricles through the slow pathway anterogradely and atria through the fast pathway retrogradely. Due to this, the P waves are inscribed in the QRS complex or occur near the QRS creating a short RP interval (RP interval is less than half the RR interval). This can sometimes manifest as a "pseudo-S wave" in the inferior leads II, III, and aVF, and "pseudo-R wave" in lead V1.
  51. 51. In atypical AVNRT, P waves are clearly visible. Due to retrograde conduction through a slow pathway, the presence of the P wave occurs later than QRS complex, resulting in an RP interval that is frequently longer than half the RR interval. The mode of initiation of the reentrant circuit is another ECG feature that helps you to distinguish typical from atypical AVNRT. An initiating atrial premature beat is commonly associated with typical AVNRT. On the other hand, a ventricular premature beat is more likely to precipitate an atypical AVNRT.
  52. 52. Atrioventricular Reentrant Tachycardia (AVRT) AVRT is the second most common form of paroxysmal supraventricular tachycardia. AVRT is more common in males than in females. It is narrow complex tachycardia with a short PR interval. An accessory pathway connects the atria to the ventricles. The tachycardia is caused due to the reentry of impulses from the ventricles back to the atria, creating a self- sustained circuit. The accessory pathway forms one arm of the reentry circuit and the usual AV nodal pathway forms the other arm of the circuit. The reentry circuit of AVNRT is larger than ANRT as the accessory pathway is located away from the AV node. Delta waves are the pathological waves that can be seen as a slurred upstroke at the beginning of the QRS complex. They are formed when the accessory pathway conducts the atrial impulse to the ventricle.
  53. 53. Wolff-Parkinson-White (WPW)syndrome is a classic example of AVRT. WPW syndrome is characterized by the presence of delta wave, short PR interval (<120ms) and wide QRS complex. Delta waves are the slurred upstroke in the QRS complex. They are often associated with a short PR interval. It is most commonly associated with a preexcitation syndrome such as WPW.
  54. 54. The two types of AVRT are:  Orthodromic AVRT  Antidromic AVRT Orthodromic AVRT: It occurs when an impulse is conducted through the AV node and then through the accessory pathway in a retrograde direction. In this condition, AVRT is associated with narrow QRS complexes that have a normal morphology. Sometimes a rate-related aberration may be present, during which the QRS complexes will have a typical right or left bundle branch block (BBB) morphology or an intraventricular conduction delay. The ECG characteristics of orthodromic AVRT are:  Presence of distinct P wave after the QRS complex, which allows us to differentiate between AVRT and AVNRT (during AVNRT the P wave is hidden within, partly merging with or close to the QRS complex).  Presence of retrograde P wave, which is closer to the preceding QRS complex than to the following QRS complex due to rapid conduction to the atria.  RP interval < PR interval
  55. 55. Antidromic AVRT: It occurs when the impulse is conducted antegrade down the bypass tract. A direction myocardial activation occurs in antidromic AVRT as ventricular activation is done through the accessory pathway and the normal His-Purkinje system. Therefore, wide and abnormal QRS complexes that do not have either a typical right or left BBB morphology are associated with antidromic AVRT. In this condition, the QRS complexes resemble the pre-excited complexes during the sinus rhythm. The ECG characteristics of antidromic AVRT are: QRS complexes are usually broader than during sinus rhythm and may resemble ventricular tachycardia due to slow conduction of impulse from one fiber to another QRS complexes are followed by retrograde P-waves.
  56. 56. Long RP/Short PR Interval Tachycardia Long RP tachycardia is characterized by an RP interval, which is longer than the next PR interval during tachycardia. This pattern occurs when the retrograde VA conduction time in reentrant arrhythmias is long due to a slowly conducting retrograde pathway during tachycardia. It consists of negative P waves in the inferior leads. It consists of the permanent form of junctional reciprocating tachycardia (PJRT).
  57. 57. Junctional Tachycardia Junctional tachycardia is an ectopic beat which, begins in the pacemaker cells found in the atrioventricular bundle (bundle of His). Junctional tachycardias can be regular or irregular with variable conduction to the atria. Types of Junctional tachycardia: Permanent form of Junctional Reciprocating Tachycardia (PJRT): A PJRT may start without any particular trigger, from sinus rhythm. It may terminate and reinitiate, such that throughout the day the patient has predominant PJRT rhythm, with brief, interspersed intervals of sinus beats. It occurs mostly in infants and children. It is often incessant with occasional interruptions by sinus beats. It does not require premature beats or PR prolongation for its initiation and may be initiated by a modest increase in sinus rate.
  58. 58. The typical ECG characteristics of PJRT are:  It has a long RP interval with negative wave in leads II, III, and aVF.  The rhythm is typically very regular.  The QRS complex is narrow.  The heart rate is 90 to 250 bpm Nonparoxysmal junctional tachycardia: Nonparoxysmal (i.e., gradual onset) junctional tachycardia is a benign dysrhythmia that is usually associated with a gradual increase in rate to more than 100 beats/min. It rarely exceeds 120 beats/min. It is a marker for potentially serious heart disease or digitalis intoxication. It may be due to enhanced automaticity or triggered activity. It may show AV dissociation or retrograde ventricular conduction.
  59. 59. Paroxysmal junctional tachycardia: Paroxysmaljunctional tachycardia, also known as focal or automatic junctional tachycardia, is an uncommon dysrhythmia. As it has a sudden onset and ends abruptly it is called as paroxysmal junctional tachycardia. It is often precipitated by a PJC. The ventricular rate for paroxysmal junctional tachycardia is generally faster, at a rate of 140 beats/min or more. When the ventricular rate is > 150 beats/min, it is difficult to distinguish junctional tachycardia from other supraventricular tachycardias. AV dissociation is common but there may be retrograde ventriculoatrial conduction with varying degree of retrograde block. The tachycardia does not require the atrium or the ventricle for its prorogation. When incessant it can cause a tachycardia dependent cardiomyopathy with heart failure.
  60. 60. The ECG characteristics of junctional tachycardia include the following:  Rhythm: Ventricular rhythm may be regular or irregular  Heart rate: 101 to 180 beats/min  P waves: Occurs before, during, or after QRS complex P wave is inverted in leads II, III, and aVF  PR interval: 0.12 sec or less; if P wave does not occur before the QRS complex then you cannot measure PR interval  QRS duration: 0.11 sec or less
  61. 61. Differential Diagnosis of the Narrow-QRSComplex Tachycardias An essential component in the differential diagnosis of tachycardias is to distinguish between tachycardias with normal QRS complex and abnormal QRS complex. The first step to distinguishing narrow-complex tachycardias from one another is to assess the R-R interval to check the rhythm. If the rhythm is irregular, then it may be atrial fibrillation or atrial flutter. If the rhythm is regular, then you should check the P waves. The next step is to check the morphology and position of P waves about the QRS complex. It helps to determine the relationship between the atrial and ventricular activity. A P wave morphologically identical to that seen in sinus rhythm probably means that the tachycardia is originating somewhere near the SA node, regardless of the mechanism. When the QRS complexes are preceded by P waves, which have a different configuration from sinus P wave, and have a longer or equal PR interval than sinus P wave, it indicates that the atrial tachycardia is arising from an ectopic focus. Check if the atrial rate and ventricular rate. If the atrial rate is greater than the ventricular rate, it indicates atrial flutter or atrial tachycardia. If not, then check RP interval.
  62. 62. The third step is to analyze the RP interval, if the RP interval is longer than PR interval, it indicates atrial tachycardia, PJRT, or Atypical AVNRT. If the RP is shortened than PR interval, then check if the RP interval is shortened than 0.07 sec which indicates AVNRT. If the RP interval is longer than 0.07sec, then it indicates AVRT, AVNRT, and atrial tachycardia. The flow chart given below depicts the procedure of differential diagnosis of the narrow-QRS-complex tachycardias:
  63. 63. Ventricular Arrhythmia Ventricular arrhythmias originate in the ventricles below the bifurcation of the bundle of His. These arrhythmias occur when electrical impulses depolarize the myocardium using a different pathway from normal impulse conduction. The ECG characteristics of ventricular arrhythmia are: The QRS complex is wider than normal due to prolonged conduction time through the ventricles and abnormal depolarization of the ventricles.  The deflection of the T wave and QRS complex are in opposite directions due to abnormal ventricular repolarization and depolarization  The P wave is absent in most of the ventricular arrhythmias because atrial depolarization doesn't occur. If a P wave is present, it originates in the sinus node, causing it to be dissociated from the ventricular rhythm.  The atrial rate is usually slower than the ventricular rate, as it originates at the sinus node
  64. 64. Fusion and capture beats may be present, which helps in distinguishing ventricular tachycardia from other broadcomplex tachycardia. Fusion beats: They occur when a normal supraventricular stimulus causes ventricular activation which fuses with the complex originating in the ventricle and produces a hybrid complex. The resulting hybrid QRS complex looks partly like a normal QRS complex and partly like a ventricular ectopic beat. Capture beats: They occur when an atrial stimulus arrives at a non-refractory AV node and is conducted normally in the ventricles. This results in a normal P wave followed by a normal QRS complex in the middle of a series of wide QRS complexes.
  65. 65. When the electrical impulses come from the ventricles instead of the atria, the atrial kick is lost, and the cardiac output decreases as much as 30%. As a result, the patient with ventricular arrhythmia may show signs and symptoms of reduced cardiac output, including:  Hypotension  Agina  Syncope  Respiratory distress
  66. 66. Although ventricular arrhythmias may be benign, they may also be life- treating as the ventricles are mainly responsible for cardiac output. Early recognition and treatment of ventricular arrhythmias will increase the chances of survival. Ventricular arrhythmias are classified into the following types based on the tachycardia morphology:  Monomorphic ventricular tachycardia  Polymorphic ventricular tachycardia  Ventricular fibrillation  Accelerated idio-ventricular tachycardia  Ventricular Flutter
  67. 67. Monomorphic Ventricular Tachycardia It is the most common form of ventricular tachycardia. The ventricular complexes have a uniform appearance (monomorphic), and each episode of ventricular tachycardia continues for a variable time, usually terminating in a long pause before sinus rhythm returns. Each paroxysm of tachycardia starts with a ventricular ectopic beat, which occurs at the same fixed interval from the previous QRS complex.
  68. 68. Polymorphic Ventricular Tachycardia (PVT) It consists of polymorphic QRS complexes which undulate around the isoelectric line, with a marked change of amplitude occurring every 5 to 30 beats, changing from one direction to another and back again.
  69. 69. Torsades-de-pointes Torsades-de-pointes (turning of points) is a dangerous form of polymorphic ventricular tachycardia characterized by paroxysms of ventricular tachycardia when the QT interval is prolonged during sinus rhythm, and prominent U waves may be seen. Prolongation of the QT interval implies prolongation of repolarization. While this may affect the whole myocardium, polymorphic ventricular tachycardia is more likely to occur when different regions of the myocardium repolarise at different rates. Transient prolongation of the QT interval may occur in the acute phase of myocardial infarction but, more commonly, this is due to the administration of drugs that prolong the QT interval such as class 1 antidysrhythmic agents or electrolyte imbalance.
  70. 70. Episodes of torsades-de-pointes usually terminate spontaneously but may precede ventricular fibrillation. Antidysrhythmic drugs should be stopped, and it may be necessary to increase the heart rate to over 100 beats/minute by pacing to prevent recurrence until the precipitating drugs are metabolized or electrolyte imbalance has been corrected. PVT unassociated with QT prolongation are uncommon but have the ECG characteristics of torsades-de-pointes. If the QT interval in the sinus is normal, management is that of monomorphic ventricular tachycardia.
  71. 71. Ventricular Fibrillation Ventricular fibrillation is a disorganized, chaotic, electrical focus in the ventricles that take over control of the heart. The ventricles do not beat in a coordinated fashion but, instead, quiver asynchronously and ineffectively, just as the atria respond in atrial fibrillation. The ECG tracings show an undulating, wavy baseline composed of irregular waveforms that vary in amplitude and morphology. The ventricular waves represent chaotic, incomplete, and haphazard depolarization of small groups of muscle fibers in the ventricles. P waves and QRS complexes are absent due to lack of organized depolarization of atria and ventricles. Coarse ventricular fibrillations indicate a more recent onset and are more likely to be reversed by defibrillation alone. Whereas, fine ventricular fibrillation indicates that the arrhythmia has been present longer and may require therapy first, then defibrillation. If defibrillations do not restore the cardiac rhythm, then the fine ventricular fibrillation progresses to ventricular asystole.
  72. 72. ECG characteristics:
  73. 73. Accelerated Idio-ventricular Tachycardia When escape rhythms arise in the ventricles or His-Purkinje system, they are called idio-ventricular rhythms. They often occur in association with successful thrombolysis. It is benign and requires no treatment. The rate is usually slow, at about 60 beats/minute. Sometimes referred to as 'slow VT'. After about 30 beats, sinus rhythm often takes over. Occasionally, the rhythm accelerates but the rate does not exceed 120 beats/minute. Rarely, sustained ventricular tachycardia or ventricular fibrillation may be replaced by idio-ventricular tachycardia.
  74. 74. Ventricular Flutter It is characterized by a rapid ventricular rate of 180-250 beats/minute, in which it is not possible to differentiate the QRS complexes from the ST segment or T waves. It appears on the ECG as rows of hairpins or as a sine wave which, is characterized by regular, large oscillations. It often precedes ventricular fibrillation.
  75. 75. References  Hatfield, A. (2014). The complete recovery room book. OUP Oxford.  Heidbuchel, H. (2002). Management of cardiac arrhythmias, edited by Leonard I. Ganz. ACTA CARDIOLOGICA, 57(4), 315-315.  Lewis, K. M. (2000). Sensible Analysis of the 12-lead ECG. Cengage Learning.  Lilly, L. S. (2012). Pathophysiology of heart disease: a collaborative project of medical students and faculty. Lippincott Williams & Wilkins  Model, D. (2006). Making Sense of Clinical Examination of the Adult Patient: Hands-on Guide. CRC Press.