SUPRAVENTRICULAR TACHYCARDIA - SVT

SVT
SUPRAVENTRICULAR TACHYCARDIA
VENTRICULAR TACHYCARDIA

1. SVT PRESENTOR- DR PINKESH MODERATOR- DR DEBASIS SIR DR SAMEER SIR DR HIREN SIR

2. DEFINITION S upraventricular tachycardia (SVT ), defined as a tachycardia in which the driving circuit or focus originates, at least in part, in tissue above the level of the ventricle (i.e., sinus node, atria, AV node, or His bundle ). In the absence of a bundle branch block, there is intact conduction to the ventricles via the right and left bundles leading to a narrow and normal-appearing QRS. Therefore, these arrhythmias are also often called narrow complex tachycardias .

3. PATHOPHYSIOLOGY Tachyarrhythmias occur as a result of three main mechanisms: reentry, which is most common; enhanced or abnormal automaticity; and triggered activity

4. PATHOPHYSIOLOGY Reentrant arrhythmias sustain themselves by repetitively following a revolving pathway comprising two limbs, one that takes the impulse away from and one that carries it back to the site of origin. For reentry to exist, an area of slow conduction must occur, and each limb must have a different refractory period. In this situation, pacing (by inducing refractoriness in one limb of the circuit) can initiate a reentrant tachycardia. Once established, pacing can also terminate the tachycardia by interfering with impulse propagation in one of the limbs.

5. PATHOPHYSIOLOGY The second mechanism, automaticity, refers to spontaneous and, often, repetitive firing from a single focus , which may either be ectopic or may originate in the sinus node. This mechanism comprises two subcategories . Enhanced automaticity is defined as a focus that fires spontaneously and may originate in the sinus node, subsidiary pacemakers in the atrium including the Eustachian ridge, Bachmann bundle, coronary sinus and AV valves, the AV node, His-Purkinje system, and the ventricles. Abnormal automaticity is usually secondary to a disease process causing alterations in ionic flow that produces a less negative resting diastolic membrane potential. Threshold potential is therefore more easily attained, thereby increasing the probability of a sustained arrhythmia.

6. PATHOPHYSIOLOGY The third mechanism, triggered arrhythmias, depends on oscillations in the membrane potential that closely follow an action potential. In the absence of a new external electrical stimulus, these oscillations, or after-depolarizations, cause new action potentials to develop. Thus, each new action potential results from the previous action potential. These arrhythmias can be produced by early or late afterdepolarization, depending on the timing of the first after-depolarization relative to the preceding action potential (the one that spawned the triggered activity).

7. Sinus Tachycardia ESSENTIALS OF DIAGNOSIS Onset and termination: gradual. Heart rate: 100 to (220 – age) bpm. P wave: identical to normal sinus rhythm P wave. R-P relationship: long.

8. Sinus Tachycardia Sinus tachycardia is usually a physiologic response, activated when the body requires a higher heart rate to meet metabolic demands or maintain blood pressure. Common causes are exercise, hypotension, hypoxemia , heart failure, sepsis, fever, hyperthyroidism, fluid depletion, and blood loss .

9. Sinus Tachycardia Inappropriate sinus tachycardia Heart rate >100/min P wave morphology identical to sinus rhydhm Exclusion of secondary causes of sinus tachycardia Exclusion of atrial tachycardias Symptoms clearly related to resting or easily provoked sinus tachycardia

10. Sinus Tachycardia In postural orthostatic tachycardia syndrome (POTS), a related syndrome consisting of orthostatic hypotension and sinus tachycardia, the cause of the orthostatic decrease in blood pressure is not hypovolemia or drugs . Both syndromes can result from autonomic neuropathy, either peripheral, as in diabetic patients, or central , from spinal cord injury.

11. Sinus Tachycardia Treatment Attempting to slow the heart rate pharmacologically can be detrimental because it counteracts the compensatory mechanism provided by the tachycardia. Therefore, management is usually focused on treating the underlying cause of the sinus tachycardia . B-blockers, CCBs, ivabradine in case of inappropriate sinus tachycardia In severe cases, sinus node radiofrequency (RF) or surgical ablation may be indicated

12. Sinus Node Reentry ESSENTIALS OF DIAGNOSIS Onset and termination: sudden. Heart rate: 100–160 bpm. P wave: identical to normal sinus rhythm P wave R-P relationship: long.

13. Sinus Node Reentry This uncommon rhythm accounts for less than 5% of SVTs. It uses the sinus node or perinodal tissue as a critical part of the reentrant circuit, producing P waves identical to those seen during normal sinus rhythm . Unlike sinus tachycardia, sinus node reentry is initiated by an ectopic beat rather than a physiologic stimulus and possesses the characteristics typical of a reentrant circuit. Therefore , it begins and ends abruptly and responds to vagal maneuvers and pharmacologic interventions by terminating rather than slowing.

14. Sinus Node Reentry Treatment The arrhythmia can be terminated quickly with intravenous adenosine, verapamil, or diltiazem, or via carotid massage. Long-term treatment uses β-blockers and calcium channel blockers.

15. ATRIAL FLUTTER ESSENTIALS OF DIAGNOSIS Onset and termination: sudden . P waves: flutter waves at 250–340 bpm . Saw tooth pattern R-P relationship: undefined due to flutter waves. Prominent neck vein pulsations of about 300/min Loss of the isoelectric baseline

16. Atrial flutter is usually associated with organic heart disease and is the second most common arrhythmia after atrial fibrillation in post–coronary artery bypass surgery patients, with an incidence of up to 33 %. Unlike atrial fibrillation, the ventricular impulses are transmitted at some integer fraction of the atrial rate. In rare circumstances, 1:1 conduction may occur. Fixed 2:1, 3:1, or 4:1 block is the usual scenario. However, variable block can also occur. If atrial flutter is suspected but F waves are not clearly visible, vagal maneuvers or pharmacologic agents, such as adenosine, can help unmask the flutter waves by enhancing the degree of AV block.

17. Atrial flutter is the prototypic macroreentrant atrial rhythm. The typical atrial flutter is a reentrant rhythm in the right atrium that is constrained anteriorly by the tricuspid annulus and posteriorly by the crista terminalis and eustachian ridge. The flutter can circulate in a counterclockwise direction around the tricuspid annulus in the frontal plane ( counterclockwise flutter) or in a clockwise direction ( clockwise or reverse flutter). Both are typical flutters because they use the cavotricuspid isthmus.

18. The counterclockwise flutter is recognized electrocardiographically by negative F waves in leads II, III, and aVF and positive F waves in lead V1 . Clockwise flutter, on the other hand, has positive F waves in leads II, III, and aVF and negative F waves in lead V1.

19. ATRIAL FLUTTER - CONVERSION Cardioversion is usually the initial treatment of choice for atrial flutter because it promptly and effectively restores sinus rhythm Cardioversion can be accomplished with synchronous direct current (DC), which often requires relatively low energy (approximately 50 J). If the electrical shock results in atrial fibrillation (AF), a second shock at a higher energy level is used to restore sinus rhythm, or depending on clinical circumstances, the AF can be left untreated and can revert to atrial flutter or sinus rhythm.

20. ATRIAL FLUTTER - CONVERSION Rapid atrial pacing is another method that may terminate the arrhythmia. Pacing is best performed in the right atrium at a rate faster than the flutter rate, which allows the circuit to be entered by the pacing impulse. If the patient has a pacemaker or implantable cardiac defibrillator with an atrial lead, pace termination can be done painlessly via the device. An alternative method uses a swallowed transesophageal electrode.

21. ATRIAL FLUTTER - CONVERSION rapid pharmacologic cardioversion can be considered with intravenous agents such as ibutilide . Ibutilide is a unique class III antiarrhythmic agent with a rate of conversion of approximately 60 % in patients with atrial flutter of less than 45 days in duration. Cardioversion can be expected within 30 minutes of administration. The major complication with this agent is the development of torsades de pointes , which can occur in up to 12.5% of patients, with 1.7% requiring cardioversion for sustained polymorphic ventricular tachycardia.

22. ATRIAL FLUTTER – RATE CONTROL In general, controlling the ventricular rate in atrial flutter is more difficult than in atrial fibrillation. β- Blockers and calcium channel blockers are moderately effective in controlling the rate. Digoxin is less helpful because it only weakly blocks AV node conduction. Intravenous amiodarone, which has some β- blocking effect, has been shown to be at least as efficacious as digoxin.

23. ATRIAL FLUTTER - ABLATION Ablation in the isthmus region interrupts the reentrant circuit and has been shown to be highly successful (90–100%) in permanently eliminating atrial flutter . Non–isthmus-dependent atypical atrial flutters can be more difficult to ablate. However, with current three-dimensional mapping systems, even these types of atrial flutter are being ablated with high success rates.

24. ATRIAL FLUTTER – STROKE PROPHYLAXIS No prospective data looking at incidence of thromboembolic events The current recommendation is to treat patients with atrial flutter just as atrial fibrillation in terms of stroke prophylaxis.

25. ATRIAL TACHYCARDIA ESSENTIALS OF DIAGNOSIS Onset and termination: sudden. Heart rate: 100–180 bpm. P wave: distinct P waves that differ from sinus P waves . Characteristic isoelectric intervals between P waves. Analysis of P wave configuration during tachycardia indicates that a positive or biphasic P wave in V1 predicts a left atrial focus, whereas a negative P wave in V1 predicts a right atrial focus. R-P relationship: long.

26. ATRIAL TACHYCARDIA In patients with paroxysmal sustained atrial tachycardia, there is a higher likelihood of associated organic heart disease, including coronary artery disease, valvular heart disease, congenital heart disease, and other cardiomyopathies. Frequently , a transient automatic atrial tachycardia will be present, the cause of which can usually be determined from the associated clinical setting. Some of the most frequent causes include acute myocardial infarction (in which case, it is seen in 4–19% of patients), electrolyte disturbances (especially hypokalemia), chronic lung disease or pulmonary infection, acute alcohol ingestion , hypoxia, and use of cardiac stimulants (theophylline, cocaine).

27. ATRIAL TACHYCARDIA Depending on the clinical situation, a beta blocker or a calcium channel blocker can be administered to slow the ventricular rate; if AT is still present, class IA, IC, or III drugs can be added. Catheter ablation procedures are generally effective in eliminating the AT, depending on the mechanism and underlying heart disease with reported success rates between 77 % and 100%

28. MULTIFOCAL/CHAOTIC ATRIAL TACHYCARDIA ESSENTIALS OF DIAGNOSIS Heart rate: up to 150 bpm. P waves: three or more distinct P waves in a single lead. Variable P-P, P-R, and R-R intervals.

29. MULTIFOCAL ATRIAL TACHYCARDIA It is related to pulmonary disease in 60–85% of cases, with chronic obstructive pulmonary disease ( COPD) exacerbation being the most common. In addition, MAT is precipitated by respiratory failure, acute decompensated cardiac function, and infection. It has also been reported to be associated with hypokalemia , hypomagnesemia, hyponatremia, pulmonary embolism, cancer, and valvular heart disease, and can also occur in the postoperative setting.

30. MULTIFOCAL ATRIAL TACHYCARDIA Management is directed primarily toward the underlying disease. AADs are frequently ineffective in slowing either the rate of the AT or the ventricular response. Beta adrenoceptor blockers should be avoided in patients with bronchospastic pulmonary disease but can be effective if tolerated. Verapamil and amiodarone have been useful.

31. JUNCTIONAL TACHYCARDIA ESSENTIALS OF DIAGNOSIS Onset and termination: gradual. Heart rate: 70–120 bpm. P waves: retrograde. R-P relationship: short, if P waves visible.

32. JUNCTIONAL TACHYCARDIA Usually seen in the setting of organic heart disease, the cause of this rhythm is almost always identifiable. Digoxin excess Acute inferior infarction accounts for 20% of junctional tachycardias Junctional tachycardia may follow open heart surgery (valve replacement more often than bypass surgery), or it can be caused by myocarditis (especially rheumatic) and, rarely, congenital heart disease .

33. ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA ESSENTIALS OF DIAGNOSIS Onset and termination: sudden. Heart rate: usually 120–200 bpm but can be faster; neck pulsations (Brugada phenomenon ) correspond to heart rate. P waves: retrograde P waves; P waves not visible in 90% of cases. R-P relationship: short, if P waves visible QRS complexes usually narrow (< 120 ms) unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. ST-segment depression may be seen with or without underlying coronary artery disease. QRS alternans – phasic variation in QRS amplitude associated with AVNRT and AVRT

34. AVNRT Atrioventricular nodal reentrant tachycardia (AVNRT) is more common in women than in men. Heart rates usually fall in the range of 120–200 bpm, although rates up to 250 bpm have been recorded. Palpitations are almost universally reported. A feeling of diuresis, noted with other supraventricular arrhythmias , is significantly more common in AVNRT and has been correlated with elevated right atrial pressures and elevated atrial natriuretic peptide. Neck pulsations are common (Brugada phenomenon) and are secondary to simultaneous contraction of the atria and ventricles against closed mitral and tricuspid valves . Dizziness and lightheadedness can occur, but frank syncope is very unusual. Sudden death has been reported but is extremely rare

35. AVNRT In AVNRT, there are two pathways within the AV node: The  slow pathway  ( alpha ): a slowly-conducting pathway with a short refractory period. The  fast pathway  ( beta ): a rapidly-conducting pathway with a long refractory period.

36. AVNRT Subtypes of AVNRT Different subtypes vary in terms of the dominant pathway and the  R-P interval.  The RP interval represents the time between anterograde ventricular activation (R wave) and retrograde atrial activation (P wave). Slow-Fast AVNRT (common type) Fast-Slow AVNRT (Uncommon AVNRT) Slow-Slow AVNRT (Atypical AVNRT )

37. AVNRT 1. Slow-Fast AVNRT (common type) Accounts for 80-90% of AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction. The retrograde P wave is obscured in the corresponding QRS  or  occurs at the end of the QRS complex as pseudo r’ or S waves ECG features: P waves are often hidden – being embedded in the QRS complexes. Pseudo R’ wave may be seen in V1 or V2. Pseudo S waves may be seen in leads II, III or aVF. In most cases this results in a ‘typical’ SVT appearance with absent P waves and tachycardia

38. AVNRT 2. Fast-Slow AVNRT (Uncommon AVNRT) Accounts for 10% of AVNRT Associated with Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway for retrograde conduction. Due to the relatively long ventriculo-atrial interval, the retrograde P wave is more likely to be visible after the corresponding QRS. ECG features: QRS-P-T complexes. Retrograde P waves are visible between the QRS and T wave.

39. AVNRT 3. Slow-Slow AVNRT (Atypical AVNRT) 1-5% AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Slow left atrial fibres as the pathway for retrograde conduction. ECG features: Tachycardia with a P-wave seen in mid-diastole… effectively appearing “before” the QRS complex. Confusing as a P wave appearing before the QRS complex in the face of a tachycardia might be read as a sinus tachycardia.

40. MANAGEMENT Vagal maneuvers, including carotid sinus massage, the Valsalva, gagging, and occasionally exposure of the face to ice water, serve as the first line of therapy . If vagal maneuvers fail, adenosine, 6 to 12 mg administered rapidly intravenously, is the initial drug of choice and successfully terminates (within 1 minute ) the tachycardia in about 90% of cases. CCBs – Diltiazem and Verapamil Beta receptor blockers can be effective but are not generally used as first-line therapy because adenosine, verapamil, and diltiazem are more effective and faster acting.

41. MANAGEMENT Rarely, if AVNRT results in hemodynamic compromise and is refractory to adenosine, DC cardioversion may be indicated with energy in the range of 10 to 50 J .

42. PREVENTION OF RECURRENCE If the attacks are infrequent, well tolerated, and short and either terminate spontaneously or are easily terminated by the patient, no prophylactic therapy may be necessary. Longer and more frequent attacks can be treated with drugs, although ablation is an effective first-line alternative. In patients with syncope or near-syncope, ablation should be considered as first-line therapy. A long-acting calcium antagonist or a long-acting beta adrenoceptor blocker is a reasonable initial choice for drug therapy.

43. PREVENTION OF RECURRENCE RF ablation achieves long-term cure in more than 95%, with a low incidence of complications, and should be considered early in the management of patients with symptomatic recurrent episodes of AV nodal reentry, especially for patients who do not want to take drugs, who are drug intolerant, or in whom drugs are ineffective.

44. Atrioventricular Reentry Tachycardias (AVRT ) AVRT is a form of paroxysmal supraventricular tachycardia. A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit. AVRT often triggered by premature atrial or premature ventricular beats. AVRT are further divided in to  orthodromic  or  antidromic  conduction based on direction of reentry conduction and ECG morphology.

45. AVRT with Orthodromic Conduction ECG features of AVRT with orthodromic conduction are: Rate usually 200 – 300 bpm P waves may be buried in QRS complex or retrograde QRS Complex usually <120 ms unless pre-existing bundle branch block, or rate-related aberrant conduction QRS Alternans – phasic variation in QRS amplitude associated with AVNRT and AVRT T wave inversion common ST segment depression

46. AVRT with Antidromic Conduction ECG features of AVRT with antidromic conduction are: Rate usually 200 – 300 bpm. Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.  Much less common than orthodromic AVRT occurring in ~5% of patients with WPW.

47. TREATMENT Treatment of AVRT is based on the presence of haemodynamic instability e.g. hypotension, altered mental state, or pulmonary oedema. In patients who are haemodynamically stable vagal manoeuvres may be successful, followed by adenosine or calcium-channel blockers, and DC cardioversion may be considered if non-repsonsive to medical therapy. In a haemodynamically unstable patient urgent synchronised DC cardioversion is required.

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