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TACHYARRTHYMIA.pptx

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Mohamad Yaakub

This document provides an overview of various tachyarrhythmias including their conduction pathways, pathophysiology, ECG characteristics, and treatment approaches. Key points covered include: - The conduction system of the heart and action potentials across cardiac tissues. - Causes of tachyarrhythmias including increased automaticity, triggered activity, and reentry. - Algorithm for evaluating and treating stable vs. unstable tachyarrhythmias. - Characteristics and management of common tachyarrhythmias like atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and ventricular tachycardia. - Use of synchronized cardioversion for unstable rhythms

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TACHYARRHYTHMIAS ALS GUIDELINE CME 23/12/22 MOHAMAD YAAKUB 1
CONTENT Conduction pathway Pacemaker and myocardium action potential Pathophysiology of tachyarrhythmia Tachyarthymia algorithm Synchronised cardioversion Common tachyarrhythmia Atrial fibrillation Atrial flutter Atrial tachycardia AVNRT, AVRT VT 2
Conduction system of heart SA Node is the pacemaker because its cells have the quickest rate of spontaneous depolarization. 3
4
ACTION POTENTIAL ACROSS CARDIAC TISSUES 5
6
Automaticity - Depolarizes spontaneously about 70 times per minute> thus HR 70 - Controlled by sympathetic and parasympathetic - No RMP , means the SA node fires continuously to maintain CO. 7
8
Basis of synchronised cardioversion 9
Pathophysiology of tachyarrhythmia 1. Increased Automaticity Autonomic nervous system (sympathetic) Drugs sympathomimetics : methamphetamine, cannabis, cocaine 2. Triggered Activity Early after depolarization (during phase 3) Delayed after depolarization (during phase 4) LQTC , TdP 3. Rentry AF/AFL AVNRT functional reentry AVRT anatomical reentry Wolf Parkinson white syndrome 10
Tachycardia : heart rate above 100 beats per minute symptomatic tachycardia generally involves rates over 150 beats per minute unless underlying ventricular dysfunction exists The fundamental approach First, determine if the patient is unstable. UNSTABLE ARRYTHMIA Hypotension Altered mental status Sign of shock cool peripheries, poor pulse volume, crt>2sec Ischemic chest pain Acute Heart Failure symptoms If instability is present and appears related to the tachycardia, treat immediately with synchronized cardioversion unless the rhythm is sinus tachycardia. IF STABLE DO 12 LEAD ECG FOR correct identification of the arrhythmia 11
12
13
SYNCHRONISED CARDIOVERSION LOW ENERGY SHOCK that uses a sensor to deliver electricity that is synchronized with the peak of the QRS complex (the highest point of the R-wave). When shock button pushed, there will be a delay in the shock. During this delay, the machine reads and synchronizes with the patients ECG rhythm. This occurs so that the shock can be delivered with or just after the peak of the R-wave in the patients QRS complex. Synchronization avoids the delivery of shock during cardiac repolarization (t-wave). If the shock occurs on the t-wave (during repolarization), there is a high likelihood that the shock can precipitate VF. 14
15 PSA SHOULD BE GIVEN BEFORE CARDIOVERSION MIDAZOLAM 0.1MG/KG FENTANYL 1 MCG/KG
16
ECGs 17
Sinus Tachycardia P wave present followed by QRS Regular rhythm with ventricular rate >100 beats per minute. Many precipitating event 18
Secondary Sinus tachycardia : Principle of mx : treat the underlying causes 19 Sinus Tachycardia Normal (physiologic) sinus tachycardia: automaticity in the sinoatrial node is increased due to increased in sympathetic input (leading to stimulation of beta-adrenergic receptors) and parasympathetic withdrawal.
Atrial Fibrillation Absent of P wave Irregular RR interval Due to multiple re-entrant wavelets conducted Many precipitating event HR 60-100 RATE CONTROLLED AF HR 100-149 AF WITH Rapid ventricular response (RVR) HR>150 FAST AF 20
AF with rapid ventricular response Irregular narrow-complex tachycardia at ~135 bpm Coarse fibrillatory waves in V1 21
22 Fast AF Irregular narrow-complex tachycardia at ~170 bpm Coarse fibrillatory waves in lead ii
Electrical chaos in the atria due to simultaneous existence of multiple re- entry circuits that generate impulse waves which propagate through the atria. These impulse waves collide with each other and with refractory cells, which fragments the waves and causes additional chaos. Initiation of AF Needs Trigger Driver (maintenance) Multiple Risk factors esp aging, leads to degeneration of the myocardium and conduction cells. that promote triggers and drivers. Paroxysmal/new AF are due to one or a few ectopic foci which can be ablated. Long standing AF > more foci > more trigger/driver > atrial remodeling > Chronic AF. (ablation less effective) 23
Identify and treat underlying causes 24
25
26
Direct suppression of the AV node conduction to increase effective refractory period and decrease conduction velocity - positive inotropic effect, enhanced vagal tone, and decreased ventricular rate to fast atrial arrhythmias. 27
28
29
30
31
32
Pre -excited AF Rate > 200 bpm Irregular rhythm, with extremely high rates in some places up to 300 bpm (this is too rapid to be conducted via the AV node) Wide QRS complexes due to abnormal ventricular depolarisation via AP variation in QRS morphology 33
34
inverted flutter waves in leads II, III, aVF Atrial Flutter with 2:1 Block for every two atrial beats, there is one ventricular beat indicated by the QRS complex. Therefore, the atrial flutter in the electrocardiogram is 2:1 ATRIAL FLUTTER 35
36
37
In some cases, presenting with 2:1 AV block, the diagnosis of atrial flutter may not be obvious on the ECG. In these situations, i.v. adenosine may increase the degree of AV block and reveal the typical ECG pattern. However, adenosine can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF. Thus, it should only be used if deemed necessary for diagnosis and resuscitation equipment is available. Rate control should be the first step in very symptomatic patients with rapid ventricular rates. 38
39
ABSENT OF P WAVE REGULAR 40 AV Nodal Re-entry Tachycardia (AVNRT)
AV Nodal Re-entry Tachycardia (AVNRT) This is the commonest cause of palpitations in patients with structurally normal hearts paroxysmal ,occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines) Regular 41
42
43
Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~ 150 bpm No visible P waves There are pseudo R waves in V1-2
Fast-Slow (Uncommon) AVNRT: Narrow complex tachycardia ~ 120 bpm. Retrograde P waves are visible after each QRS complex most evident in V2-3.
Fast-Slow AVNRT: Narrow complex tachycardia ~ 135 bpm. Retrograde P waves following each QRS complex upright in aVR and V1; inverted in II, III and aVL.
Mx of AVNRT Vagal maneuvers are techniques used to increase vagal parasympathetic 1. Carotid sinus massage increase firing of carotid sinus baroreceptor This action triggers the baroreceptor reflex, which results in increased parasympathetic output to the heart via the vagus nerve (cranial nerve X). Avoid in carotid bruit > STROKE 2. Modifies Valsava maneuver ADENOSINE 6mg >12mg > 18mg SYNCHRONISED CARDIOVERSION 47
37 (17%) of 214 standard Valsalva manoeuvre achieved sinus rhythm compared with 93 (43%) of 214 in the modified Valsalva manoeuvre group 48
- Depressing sinoatrial node automaticity and atrioventricular node conduction - extremely short half-life - injected as rapidly as possible into a proximal vein followed immediately by a 20 mL saline flush and elevation of the extremity to ensure the drug enters the central circulation before it is metabolized. Adenosine has very short plasma half-life due to enzymatic deamination to inactive inosine being achieved in seconds, with clinical effects complete within 20-30s. Thus, repeat administration is safe within 1 min of the last dose. 49
50
TACHYARRTHYMIA.pptx
52
Most common due to underlying WPW syndrome AVRT happens in patient with underlying AP such as WPW Anatomical rentry point Two types Orthodromic avrt most common Antidromic avrt diificult to diff between VT 53 AV Re-entry Tachycardia (AVRT)
WPW Sinus rhythm with a very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complex the delta wave Tall R waves and inverted T waves in V1-3 changes are due to WPW 54
WolffParkinsonWhite syndrome AV node connects the atria and the ventricles , accessory pathway(AP) is found in approximately 1 in 1000 persons. In normal heart AV node delays transmission of impulse from sa node, however in WPW impulse travels fast thru AP. location of the AP 53% left free ventricular wall 36% posteroseptal 8% right free ventricular wall 3% anteroseptal 55
SHORT PR INTERVAL FAST CONDUCTION THRU AP DELTA WAVE + WIDE QRS COMPLEX DUE TO SLOW CONDUCTION via direct muscle-to-muscle (slow) conduction, producing an initial slurred delta wave and wide QRS 56 NO DELTA WAVE AND QRS NORMAL AS IMPLUSE DOWN THRU AV NODE NOT THRU AP RETROGRADE P WAVE DELTA WAVE + WIDE QRS AS IMPULSE TRHU AP P NOT ALWAYS VISIBLE
57
Orthodromic AVRT Regular, narrow complex tachycardia at 180 bpm The QRS complexes are narrow because impulses are being transmitted in an orthodromic direction (A -> V) via the AV node Retrograde P waves are visible in V1 (see first beat), and quite clearly in lead III (notch at beginning of T wave), with a long RP interval 58
Post adenosine WPW pattern 59
Regular WCT DDX : Monomorphic VT , Antidromic AVRT witH WPW, SVT with aberrancy 60
Post syn cardioversion due to unstable Regular WCT Sinus rhythm with a very short PR interval and widespread delta waves. This confirms the initial ECG was antidromic reciprocating tachycardia. 61
62
63
MULTIFOCAL AT 64 ATRIAL TACHYCARDIA FOCAL AT single ectopic focus Regular rhythm Unifocal, identical P waves Atrial rate > 100 bpm Abnormal P wave morphology and axis (e.g. inverted in inferior leads) due to ectopic origin multiple ectopic foci within the atria. rapid, irregular rhythm with at least three distinct morphologies of P waves on the surface ECG. difficult to distinguish multifocal AT from AF on the rhythm strip, so a 12 lead ECG is indicated to confirm the diagnosis.
NC REGULAR TACHYCARDIA Each QRS complex is preceded by an abnormal P wave biphasic in V1; inverted in the inferior leads II, III and aVF; and inverted V3-V6 P wave morphology is consistent throughout 65 FOCAL AT
NC IRREGULAR TACHYCARDIA Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the rhythm strip). Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right ventricular hypertrophy due to cor pulmonale. 66 MULTIFOCAL AT
67
Accelerated ventricular rhythm (idioventricular rhythm) Regular rhythm with rate at 60100 beats per minute. As in ventricular rhythm the QRS complex is wide with discordant ST-T segment and the rhythm is regular (in most cases). Idioventricular rhythm starts and terminates gradually. primarily seen after reperfusion in an occluded coronary artery. Fusion and capture beats Usallly self limiting 68
69
idioventricular rhythm with AV dissociation and wide QRS complexes occurring at a rate faster than the sinus rate but slower than 100 bpm Regular rhythm Rate typically 50-120 bpm Three or more ventricular complexes; QRS duration > 120ms Fusion and capture beats 70
Junctional tachycardia impulses are occasionally discharged in the atrioventricular node or by cells near the node. The cells in the atrioventricular node itself may start discharging impulses during ischemia or when sa node impulses blocked The atria will be activated in the opposite direction, which is why the P-wave will be retrograde. 71
Junctional Tachycardia Narrow complex tachycardia at 115 bpm Retrograde P waves inverted in II, III and aVF; upright in V1 and aVR Short PR interval (< 120 ms) indicates a junctional rather than atrial focus 72
Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. VT can degenerate into ventricular fibrillation. 73 Ventricular Tachycardia
74
BRUGADA FORMULA TO DIFFERENTIATE SVT AND VT AS MX DIFFFERENT SVT RESPONDS TO AV NODAL BLOCKERS SUCH AS ADENOSINE HOWEVER, ADENOSINE MAY PRECIPITATE HEMODYNAMIC INSTABILITY IN VT > VFIB 75
Ventricular Tachycardia WC Positive/ Negative Concordance (in V1-V6) negative concordance likely VT Extreme Axis Deviation Dominant initial R wave in Avr Capture Beat + Fusion Beat Complete AV Dissociation Josephson Sign/Brugada Sign Rabbit ear sign (in V1/V2) 76
77 Capture beats. A capture beat (once called Dressler beat) is a normal QRS complex, identical to the sinus QRS complex, occurring during the VT at a rate faster than the VT. The term capture beat indicates that the normal conduction system has momentarily captured control of ventricular activation from the VT focus . Fusion and capture beats are more commonly seen when the tachycardia rate is slower. These beats do not alter the rate of the VT, although a change in the preceding and subsequent RR intervals is frequently observed.
78
79
Monomorphic VT: Classic monomorphic VT with uniform QRS complexes Indeterminate axis Very broad QRS (~200 ms) Notching near the nadir of the S wave in lead III = Josephsons sign 80
Monomorphic VT: Very broad QRS complexes (~ 200 ms) with uniform morphology Fusion and capture beats are seen in the rhythm strip Brugadas sign is present: the time from the onset of the QRS complex to nadir of S wave is > 100 ms (best seen in V6) 81
Aberanncy Aberrant conduction is not a mechanism of arrhythmia; it is a ventricular conduction disturbance. cardiac cells must repolarize rapidly in order to be excitable by the time the next action potential arrives. if component of the ventricular conduction system not have repolarized by the time the next impulse reaches the ventricles, the impulse will be blocked there and give rise to aberrant conduction Aberrant conduction occurs when the length of the cardiac cycle is changed without a compensatory change in the length of the refractory period. 82
VT vs SVT with aberrancy WCT should be presumed to be VT in the absence of contrary evidence. This conclusion is appropriate both because VT accounts for up to 80% of cases of WCT and because making this assumption guards against inappropriate and potentially dangerous therapy. As noted, the IV administration of drugs used for the treatment of SVT (verapamil, diltiazem, or beta-blockers) can cause severe hemodynamic deterioration in patients with VT and can even provoke VF and cardiac arrest. Therefore these drugs should not be used when the diagnosis is uncertain. Treat as SVT with aberrancy ONLY when diagnosis is certain. 83
84
85
86
87
88
89
Torsades De Pointes polymorphic VT 90
A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction. This prolonged repolarisation period also gives rise to early after-depolarisations (EADs) TdP is initiated when a PVC occurs during the preceding T wave, known as R on T phenomenon. 91
1. Congenital long QT syndromes caused by mutations in cardiac ion channels. 2. Acquired long QT syndrome due to secondary causes. 92
Principle Management of TdP 93 1. 2. Discontinue drug or treat condition that prolonged qtc
94 RECAP
RECAP 95
QUIZ 96
Unstable fast AF Syn cardioversion 200j 62 y/o female u/l IHD. Presented with palpitation and presyncope. o/e drowsy Bp 82/55 HR 180 Diagnosis and mx ? 97 QUIZ 1
55 female presented with fever , palpitation and GI losses. She also complains for neck swelling for few years and defaulted treatment. o/e agitated ,febrile ,irregular good pv T 39 Bp 145/70 hr 110-120 Lungs clear, no edema 98 QUIZ 2
1. WHAT IS ECG SHOWING? 2. CLINICAL DIAGNOSIS ? 3. MANAGEMENT ? 4. NAME ANTI-ARRHYTHMIAC DRUG THAT SHOULD BE AVOIDED IN THIS PATIENT? 99 1. AF RVR HR 100 2. THYROID STORM BW SCORE :70 3. IV HCT 200MG PTU 1000MG LUGOLS IOIDINE 10 DROPS (1 HR AFTER PTU) IV PROPRANOLOL / IV ESMOLOL 4. AMIODARONE
quiz 3 42 y/o male p/w palpitation and presyncope Bp 80/35 Hr 120-130 Spo2 98 Diagnosis? Mx? Wht went wrong? 100
Idiopathic Fascicular VT: Broad-complex complex tachycardia with modest increase in QRS width (~120 ms) RBBB morphology (RSR in V1) Left axis deviation (-90 degrees) Narrow-complex capture beat (complex #6) Several dissociated P waves are seen in the lead II rhythm strip (associated with the 3rd, 10th, 14th, 18th and 22nd QRS complexes) VERAPAMIL SENSITIVE VT 101 Diagnosis? QUIZ 4
102
RVOT VT Regular broad complex tachycardia LBBB-like morphology with rS complex in V1 and R complex in V6 Precordial transition at V3 Inferior axis (+ 90 degrees) 103
104 Thank you
105
106

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TACHYARRTHYMIA.pptx

  • 2. CONTENT Conduction pathway Pacemaker and myocardium action potential Pathophysiology of tachyarrhythmia Tachyarthymia algorithm Synchronised cardioversion Common tachyarrhythmia Atrial fibrillation Atrial flutter Atrial tachycardia AVNRT, AVRT VT 2
  • 3. Conduction system of heart SA Node is the pacemaker because its cells have the quickest rate of spontaneous depolarization. 3
  • 4. 4
  • 5. ACTION POTENTIAL ACROSS CARDIAC TISSUES 5
  • 6. 6
  • 7. Automaticity - Depolarizes spontaneously about 70 times per minute> thus HR 70 - Controlled by sympathetic and parasympathetic - No RMP , means the SA node fires continuously to maintain CO. 7
  • 8. 8
  • 9. Basis of synchronised cardioversion 9
  • 10. Pathophysiology of tachyarrhythmia 1. Increased Automaticity Autonomic nervous system (sympathetic) Drugs sympathomimetics : methamphetamine, cannabis, cocaine 2. Triggered Activity Early after depolarization (during phase 3) Delayed after depolarization (during phase 4) LQTC , TdP 3. Rentry AF/AFL AVNRT functional reentry AVRT anatomical reentry Wolf Parkinson white syndrome 10
  • 11. Tachycardia : heart rate above 100 beats per minute symptomatic tachycardia generally involves rates over 150 beats per minute unless underlying ventricular dysfunction exists The fundamental approach First, determine if the patient is unstable. UNSTABLE ARRYTHMIA Hypotension Altered mental status Sign of shock cool peripheries, poor pulse volume, crt>2sec Ischemic chest pain Acute Heart Failure symptoms If instability is present and appears related to the tachycardia, treat immediately with synchronized cardioversion unless the rhythm is sinus tachycardia. IF STABLE DO 12 LEAD ECG FOR correct identification of the arrhythmia 11
  • 12. 12
  • 13. 13
  • 14. SYNCHRONISED CARDIOVERSION LOW ENERGY SHOCK that uses a sensor to deliver electricity that is synchronized with the peak of the QRS complex (the highest point of the R-wave). When shock button pushed, there will be a delay in the shock. During this delay, the machine reads and synchronizes with the patients ECG rhythm. This occurs so that the shock can be delivered with or just after the peak of the R-wave in the patients QRS complex. Synchronization avoids the delivery of shock during cardiac repolarization (t-wave). If the shock occurs on the t-wave (during repolarization), there is a high likelihood that the shock can precipitate VF. 14
  • 15. 15 PSA SHOULD BE GIVEN BEFORE CARDIOVERSION MIDAZOLAM 0.1MG/KG FENTANYL 1 MCG/KG
  • 16. 16
  • 18. Sinus Tachycardia P wave present followed by QRS Regular rhythm with ventricular rate >100 beats per minute. Many precipitating event 18
  • 19. Secondary Sinus tachycardia : Principle of mx : treat the underlying causes 19 Sinus Tachycardia Normal (physiologic) sinus tachycardia: automaticity in the sinoatrial node is increased due to increased in sympathetic input (leading to stimulation of beta-adrenergic receptors) and parasympathetic withdrawal.
  • 20. Atrial Fibrillation Absent of P wave Irregular RR interval Due to multiple re-entrant wavelets conducted Many precipitating event HR 60-100 RATE CONTROLLED AF HR 100-149 AF WITH Rapid ventricular response (RVR) HR>150 FAST AF 20
  • 21. AF with rapid ventricular response Irregular narrow-complex tachycardia at ~135 bpm Coarse fibrillatory waves in V1 21
  • 22. 22 Fast AF Irregular narrow-complex tachycardia at ~170 bpm Coarse fibrillatory waves in lead ii
  • 23. Electrical chaos in the atria due to simultaneous existence of multiple re- entry circuits that generate impulse waves which propagate through the atria. These impulse waves collide with each other and with refractory cells, which fragments the waves and causes additional chaos. Initiation of AF Needs Trigger Driver (maintenance) Multiple Risk factors esp aging, leads to degeneration of the myocardium and conduction cells. that promote triggers and drivers. Paroxysmal/new AF are due to one or a few ectopic foci which can be ablated. Long standing AF > more foci > more trigger/driver > atrial remodeling > Chronic AF. (ablation less effective) 23
  • 24. Identify and treat underlying causes 24
  • 25. 25
  • 26. 26
  • 27. Direct suppression of the AV node conduction to increase effective refractory period and decrease conduction velocity - positive inotropic effect, enhanced vagal tone, and decreased ventricular rate to fast atrial arrhythmias. 27
  • 28. 28
  • 29. 29
  • 30. 30
  • 31. 31
  • 32. 32
  • 33. Pre -excited AF Rate > 200 bpm Irregular rhythm, with extremely high rates in some places up to 300 bpm (this is too rapid to be conducted via the AV node) Wide QRS complexes due to abnormal ventricular depolarisation via AP variation in QRS morphology 33
  • 34. 34
  • 35. inverted flutter waves in leads II, III, aVF Atrial Flutter with 2:1 Block for every two atrial beats, there is one ventricular beat indicated by the QRS complex. Therefore, the atrial flutter in the electrocardiogram is 2:1 ATRIAL FLUTTER 35
  • 36. 36
  • 37. 37
  • 38. In some cases, presenting with 2:1 AV block, the diagnosis of atrial flutter may not be obvious on the ECG. In these situations, i.v. adenosine may increase the degree of AV block and reveal the typical ECG pattern. However, adenosine can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF. Thus, it should only be used if deemed necessary for diagnosis and resuscitation equipment is available. Rate control should be the first step in very symptomatic patients with rapid ventricular rates. 38
  • 39. 39
  • 40. ABSENT OF P WAVE REGULAR 40 AV Nodal Re-entry Tachycardia (AVNRT)
  • 41. AV Nodal Re-entry Tachycardia (AVNRT) This is the commonest cause of palpitations in patients with structurally normal hearts paroxysmal ,occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines) Regular 41
  • 42. 42
  • 43. 43
  • 44. Slow-Fast (Typical) AVNRT: Narrow complex tachycardia at ~ 150 bpm No visible P waves There are pseudo R waves in V1-2
  • 45. Fast-Slow (Uncommon) AVNRT: Narrow complex tachycardia ~ 120 bpm. Retrograde P waves are visible after each QRS complex most evident in V2-3.
  • 46. Fast-Slow AVNRT: Narrow complex tachycardia ~ 135 bpm. Retrograde P waves following each QRS complex upright in aVR and V1; inverted in II, III and aVL.
  • 47. Mx of AVNRT Vagal maneuvers are techniques used to increase vagal parasympathetic 1. Carotid sinus massage increase firing of carotid sinus baroreceptor This action triggers the baroreceptor reflex, which results in increased parasympathetic output to the heart via the vagus nerve (cranial nerve X). Avoid in carotid bruit > STROKE 2. Modifies Valsava maneuver ADENOSINE 6mg >12mg > 18mg SYNCHRONISED CARDIOVERSION 47
  • 48. 37 (17%) of 214 standard Valsalva manoeuvre achieved sinus rhythm compared with 93 (43%) of 214 in the modified Valsalva manoeuvre group 48
  • 49. - Depressing sinoatrial node automaticity and atrioventricular node conduction - extremely short half-life - injected as rapidly as possible into a proximal vein followed immediately by a 20 mL saline flush and elevation of the extremity to ensure the drug enters the central circulation before it is metabolized. Adenosine has very short plasma half-life due to enzymatic deamination to inactive inosine being achieved in seconds, with clinical effects complete within 20-30s. Thus, repeat administration is safe within 1 min of the last dose. 49
  • 50. 50
  • 52. 52
  • 53. Most common due to underlying WPW syndrome AVRT happens in patient with underlying AP such as WPW Anatomical rentry point Two types Orthodromic avrt most common Antidromic avrt diificult to diff between VT 53 AV Re-entry Tachycardia (AVRT)
  • 54. WPW Sinus rhythm with a very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complex the delta wave Tall R waves and inverted T waves in V1-3 changes are due to WPW 54
  • 55. WolffParkinsonWhite syndrome AV node connects the atria and the ventricles , accessory pathway(AP) is found in approximately 1 in 1000 persons. In normal heart AV node delays transmission of impulse from sa node, however in WPW impulse travels fast thru AP. location of the AP 53% left free ventricular wall 36% posteroseptal 8% right free ventricular wall 3% anteroseptal 55
  • 56. SHORT PR INTERVAL FAST CONDUCTION THRU AP DELTA WAVE + WIDE QRS COMPLEX DUE TO SLOW CONDUCTION via direct muscle-to-muscle (slow) conduction, producing an initial slurred delta wave and wide QRS 56 NO DELTA WAVE AND QRS NORMAL AS IMPLUSE DOWN THRU AV NODE NOT THRU AP RETROGRADE P WAVE DELTA WAVE + WIDE QRS AS IMPULSE TRHU AP P NOT ALWAYS VISIBLE
  • 57. 57
  • 58. Orthodromic AVRT Regular, narrow complex tachycardia at 180 bpm The QRS complexes are narrow because impulses are being transmitted in an orthodromic direction (A -> V) via the AV node Retrograde P waves are visible in V1 (see first beat), and quite clearly in lead III (notch at beginning of T wave), with a long RP interval 58
  • 59. Post adenosine WPW pattern 59
  • 60. Regular WCT DDX : Monomorphic VT , Antidromic AVRT witH WPW, SVT with aberrancy 60
  • 61. Post syn cardioversion due to unstable Regular WCT Sinus rhythm with a very short PR interval and widespread delta waves. This confirms the initial ECG was antidromic reciprocating tachycardia. 61
  • 62. 62
  • 63. 63
  • 64. MULTIFOCAL AT 64 ATRIAL TACHYCARDIA FOCAL AT single ectopic focus Regular rhythm Unifocal, identical P waves Atrial rate > 100 bpm Abnormal P wave morphology and axis (e.g. inverted in inferior leads) due to ectopic origin multiple ectopic foci within the atria. rapid, irregular rhythm with at least three distinct morphologies of P waves on the surface ECG. difficult to distinguish multifocal AT from AF on the rhythm strip, so a 12 lead ECG is indicated to confirm the diagnosis.
  • 65. NC REGULAR TACHYCARDIA Each QRS complex is preceded by an abnormal P wave biphasic in V1; inverted in the inferior leads II, III and aVF; and inverted V3-V6 P wave morphology is consistent throughout 65 FOCAL AT
  • 66. NC IRREGULAR TACHYCARDIA Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the rhythm strip). Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right ventricular hypertrophy due to cor pulmonale. 66 MULTIFOCAL AT
  • 67. 67
  • 68. Accelerated ventricular rhythm (idioventricular rhythm) Regular rhythm with rate at 60100 beats per minute. As in ventricular rhythm the QRS complex is wide with discordant ST-T segment and the rhythm is regular (in most cases). Idioventricular rhythm starts and terminates gradually. primarily seen after reperfusion in an occluded coronary artery. Fusion and capture beats Usallly self limiting 68
  • 69. 69
  • 70. idioventricular rhythm with AV dissociation and wide QRS complexes occurring at a rate faster than the sinus rate but slower than 100 bpm Regular rhythm Rate typically 50-120 bpm Three or more ventricular complexes; QRS duration > 120ms Fusion and capture beats 70
  • 71. Junctional tachycardia impulses are occasionally discharged in the atrioventricular node or by cells near the node. The cells in the atrioventricular node itself may start discharging impulses during ischemia or when sa node impulses blocked The atria will be activated in the opposite direction, which is why the P-wave will be retrograde. 71
  • 72. Junctional Tachycardia Narrow complex tachycardia at 115 bpm Retrograde P waves inverted in II, III and aVF; upright in V1 and aVR Short PR interval (< 120 ms) indicates a junctional rather than atrial focus 72
  • 73. Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. VT can degenerate into ventricular fibrillation. 73 Ventricular Tachycardia
  • 74. 74
  • 75. BRUGADA FORMULA TO DIFFERENTIATE SVT AND VT AS MX DIFFFERENT SVT RESPONDS TO AV NODAL BLOCKERS SUCH AS ADENOSINE HOWEVER, ADENOSINE MAY PRECIPITATE HEMODYNAMIC INSTABILITY IN VT > VFIB 75
  • 76. Ventricular Tachycardia WC Positive/ Negative Concordance (in V1-V6) negative concordance likely VT Extreme Axis Deviation Dominant initial R wave in Avr Capture Beat + Fusion Beat Complete AV Dissociation Josephson Sign/Brugada Sign Rabbit ear sign (in V1/V2) 76
  • 77. 77 Capture beats. A capture beat (once called Dressler beat) is a normal QRS complex, identical to the sinus QRS complex, occurring during the VT at a rate faster than the VT. The term capture beat indicates that the normal conduction system has momentarily captured control of ventricular activation from the VT focus . Fusion and capture beats are more commonly seen when the tachycardia rate is slower. These beats do not alter the rate of the VT, although a change in the preceding and subsequent RR intervals is frequently observed.
  • 78. 78
  • 79. 79
  • 80. Monomorphic VT: Classic monomorphic VT with uniform QRS complexes Indeterminate axis Very broad QRS (~200 ms) Notching near the nadir of the S wave in lead III = Josephsons sign 80
  • 81. Monomorphic VT: Very broad QRS complexes (~ 200 ms) with uniform morphology Fusion and capture beats are seen in the rhythm strip Brugadas sign is present: the time from the onset of the QRS complex to nadir of S wave is > 100 ms (best seen in V6) 81
  • 82. Aberanncy Aberrant conduction is not a mechanism of arrhythmia; it is a ventricular conduction disturbance. cardiac cells must repolarize rapidly in order to be excitable by the time the next action potential arrives. if component of the ventricular conduction system not have repolarized by the time the next impulse reaches the ventricles, the impulse will be blocked there and give rise to aberrant conduction Aberrant conduction occurs when the length of the cardiac cycle is changed without a compensatory change in the length of the refractory period. 82
  • 83. VT vs SVT with aberrancy WCT should be presumed to be VT in the absence of contrary evidence. This conclusion is appropriate both because VT accounts for up to 80% of cases of WCT and because making this assumption guards against inappropriate and potentially dangerous therapy. As noted, the IV administration of drugs used for the treatment of SVT (verapamil, diltiazem, or beta-blockers) can cause severe hemodynamic deterioration in patients with VT and can even provoke VF and cardiac arrest. Therefore these drugs should not be used when the diagnosis is uncertain. Treat as SVT with aberrancy ONLY when diagnosis is certain. 83
  • 84. 84
  • 85. 85
  • 86. 86
  • 87. 87
  • 88. 88
  • 89. 89
  • 90. Torsades De Pointes polymorphic VT 90
  • 91. A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction. This prolonged repolarisation period also gives rise to early after-depolarisations (EADs) TdP is initiated when a PVC occurs during the preceding T wave, known as R on T phenomenon. 91
  • 92. 1. Congenital long QT syndromes caused by mutations in cardiac ion channels. 2. Acquired long QT syndrome due to secondary causes. 92
  • 93. Principle Management of TdP 93 1. 2. Discontinue drug or treat condition that prolonged qtc
  • 97. Unstable fast AF Syn cardioversion 200j 62 y/o female u/l IHD. Presented with palpitation and presyncope. o/e drowsy Bp 82/55 HR 180 Diagnosis and mx ? 97 QUIZ 1
  • 98. 55 female presented with fever , palpitation and GI losses. She also complains for neck swelling for few years and defaulted treatment. o/e agitated ,febrile ,irregular good pv T 39 Bp 145/70 hr 110-120 Lungs clear, no edema 98 QUIZ 2
  • 99. 1. WHAT IS ECG SHOWING? 2. CLINICAL DIAGNOSIS ? 3. MANAGEMENT ? 4. NAME ANTI-ARRHYTHMIAC DRUG THAT SHOULD BE AVOIDED IN THIS PATIENT? 99 1. AF RVR HR 100 2. THYROID STORM BW SCORE :70 3. IV HCT 200MG PTU 1000MG LUGOLS IOIDINE 10 DROPS (1 HR AFTER PTU) IV PROPRANOLOL / IV ESMOLOL 4. AMIODARONE
  • 100. quiz 3 42 y/o male p/w palpitation and presyncope Bp 80/35 Hr 120-130 Spo2 98 Diagnosis? Mx? Wht went wrong? 100
  • 101. Idiopathic Fascicular VT: Broad-complex complex tachycardia with modest increase in QRS width (~120 ms) RBBB morphology (RSR in V1) Left axis deviation (-90 degrees) Narrow-complex capture beat (complex #6) Several dissociated P waves are seen in the lead II rhythm strip (associated with the 3rd, 10th, 14th, 18th and 22nd QRS complexes) VERAPAMIL SENSITIVE VT 101 Diagnosis? QUIZ 4
  • 102. 102
  • 103. RVOT VT Regular broad complex tachycardia LBBB-like morphology with rS complex in V1 and R complex in V6 Precordial transition at V3 Inferior axis (+ 90 degrees) 103
  • 105. 105
  • 106. 106