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Electrical Instability in ACS

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Dr. Irwan, SpJP, FIHA. 3rd Pekanbaru Cardiology Update, August 25th, 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com

Dr. Irwan, SpJP, FIHA. 3rd Pekanbaru Cardiology Update, August 25th, 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com

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  • 1. Electrical Intability in ACS Dr. Irwan, SpJP-FIHA Department of Cardiology and Vascular Medicine Faculty of Medicine, Riau University Arifin Achmad Hospital - Pekanbaru
  • 2. Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS) Acute Coronary Syndromes* 1.57 Million Hospital Admissions - ACS UA/NSTEMI† STEMI 1.24 million Admissions per year .33 million Admissions per year Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
  • 3. Introduction • Cardiac arrhythmias routinely manifest during or following an ACS • Incidence of arrhythmia is directly related to the type of ACS • 90% of patients who AMI develop some cardiac rhythm abnormality & 25% have a cardiac conduction disturbance within 24 hours of infarct onset • VF (4.5%) in the first hour of an AMI & declines rapidly thereafter Perron AD, Swennney T: Arrhytmic Complication of ACS, Pubmed 2007
  • 4. Complications of MI Myocardial Infarction Ventricular thrombus Contractility Electrical instability Tissue necrosis Pericardial inflammation Embolism Arrhythmias Pericarditis Papillary muscle infarction/ ischemia Ventricular septal defect Ventricular rupture Mitral regurgitation Congestive heart failure Coronary perfusion pressure Ischemia Hypotension Cardiogenic shock Cardiac tamponade
  • 5. Blood Supply in the Conduction System • SA node - RCA (70% of patients) • AV node - RCA (85% of patients) • Bundle of His - LAD (septal branches) • RBB - Proximal portion by LAD - Distal portion by RCA • LBB Left anterior fascicle - LAD Left posterior fascicle - LAD and PDA Conduction Pathway Primary Arterial Supply
  • 6. Arrhythmias in Acute MI • Sinus Bradycardia - Vagal tone - SA nodal artery perfusion • Sinus Tachycardia - CHF - Volume depletion - Pericarditis - Chronotrophic drugs (e.g. Dopamine) • APB’s, atrial fib, - CHF VPB’s, VT, VF - Atrial Ischemia - Ventricular ischemia - CHF • AV block (1o , 2o , 3o ) - IMI: Vagal tone and AV nodal artery flow - AMI: Extensive destruction of conduction tissue Rhythm Cause
  • 7. How is electricity generated? By action potentials (view on own) Na, K and Ca very important for this • Na K pump • Calcium channels • Depolarization • Repolarization • ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells
  • 8. Depolaization Ventricular contraction Cardiac Action Potential
  • 9. Cardiac Cycle
  • 10. Normal Impulse Formation • Cardiac Conduction System ~ Specialized Cardiac Cells – SA Node – AV Node – Bundle of His – Purkinje • All cardiac conduction system have Automaticity – Cell’s ability to depolarize itself so that spontaneous potential action are generated – Pacemaker Cell
  • 11. Normal Impulse Formation • Native Pacemaker (SA Node) has the fastest rate – SA Node set the Heart Rate – Latent Pacemaker (AV node, Bundle of His & Purkinje) are suppressed • SA Node – Wall of RA, near the entrance of superior vena cava (SVC) • AV Node – Posteroinferior region of the atrial septum
  • 12. Normal Impulse Conduction • All cardiac cells can spread the potential action – Myocard Cell Slow conduction – Cardiac Conduction System Faster conduction • Normal Impulse Conduction – SA node generates potential action – Potential action reach AV Node & atrial myocard – Delay in AV node ~ Atrial contraction – AV Node to Bundle of His – Bundle of His to Left Bundle Branch & Right Bundle Branch – Bundle Branch to Purkinje – Purkinje to ventricular myocard – Ventricular contraction
  • 13. Normal Impulse Conduction
  • 14. Abnormal Impulse Formation 1. Altered automaticity – Altered SA node automaticity • SA Node automaticity Heart Rate • SA Node automaticity Heart Rate • Influenced by Sympathetic/Parasympathetic stimulation – Escape Rhythm • Impaired SA node automaticity • Latent Pacemaker take control of the cardiac rhythm – Altered Latent Pacemaker • Latent pacemaker automaticity • Latent Pacemaker take control of the cardiac rhythm
  • 15. Abnormal Impulse Formation 2. Abnormal automaticity – Only cardiac conduction system have automaticity – Injured Myocard cell may develop automaticity (ectopic foci) – Injured Myocard cell may take control of the cardiac rhythm 3. Triggered activty – Caused by afterdepolarization triggered by previous potential action – Self-perpetuating and leads to a series of depolarization – Triggered activity may take control of the cardiac rhythm
  • 16. Altered Impulse Conduction 1. Conduction Block – When an impulse fail to spread potential action because it encounters unexcitable region of the heart 2. Reentry – Developed under 2 main criteria • Unidirectional Block • Slowed conduction in the reentry pathway – The impulse circulate the reentry pathway repeatedly
  • 17. Rhythm Identification (ECG) • Examined best in lead II (Alternatively in V1) – At least 6 second duration
  • 18. Normal Rhythm (Sinus)
  • 19. Sinus Tachycardia
  • 20. Sinus Bradycardia
  • 21. Cardiac Arrhythmias • Bradyarrhythmias • Tachyarrhythmias – Supraventricular – Ventricular
  • 22. Sinus Bradycardia/Junctional Escape Rhythm • 4444----5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia • Sinus node ischemiaSinus node ischemiaSinus node ischemiaSinus node ischemia--------Blood supply to SA node is:Blood supply to SA node is:Blood supply to SA node is:Blood supply to SA node is: 65% RCA, 25% LCX, 10% dual supply65% RCA, 25% LCX, 10% dual supply65% RCA, 25% LCX, 10% dual supply65% RCA, 25% LCX, 10% dual supply • Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s. • Often induced by vagal reaction that may beOften induced by vagal reaction that may beOften induced by vagal reaction that may beOften induced by vagal reaction that may be protectiveprotectiveprotectiveprotective
  • 23. Location of Pathology
  • 24. How to Identify Arrhythmia • QRS rate Regular / Irregular? • QRS complex Narrow / Wide? • P wave? • Relationship between P wave & QRS complex?
  • 25. Bradyarrhythmias • Escape Rhythm – Impulse generated not from SA node • Junctional escape rhythm (from AV Node) • Ventricular escape rhythm (From his/purkinje) – ECG • No P wave / Retrograde P wave • QRS rate < 60x/min
  • 26. Atrioventricular Block • First-Degree: Usually the RCA and does not require treatment. Hold the B-blocker for PR>240 ms • Second-Degree: Usually RCA disease and does not require treatment unless HR less than 50 and arrhythmia or symptoms. Otherwise, atropine or pace • Third-Degree: Can be from any location of infarct. Can be preceded by Mobitz II Block – Pace for symptoms and for hemodynamic support. Usually not needed in inferior MI’s as block is transient (pace for HR<40-50)
  • 27. AV Block • Impulse are not spread because of blockage in AV node • 1st degree AV Block – Prolong PR interval is the only abnormality – Every P wave for every QRS complex is maintained
  • 28. AV Block • 2nd degree AV Block – Type 1 (Mobitz) • Progressive increased PR interval (gradually) until there is a P wave which is not followed by QRS complex
  • 29. AV Block • 2nd degree AV Block – Type 2 (Mobitz) • No progressive increased of PR interval • Suddenly there is a p wave which is not followed by QRS complex
  • 30. AV Block • 3rd degree AV Block – No communication between P wave and QRS Complex – P wave rate is different than QRS rate
  • 31. Recomendation for Treatment of Atrioventricular & Interventricular Conduction Disturbance During STEMI Guidlenes Recommendation for STEMI 2004, ACC-AHA
  • 32. Tachyarhythmias • Supraventricular – Supravetricular Extrasystole – Atrial Flutter – Atrial Fibrillation – Paroxysmal Supraventricular Tachycardia (SVT) • Ventricular – Ventricular Extrasystole – Ventricular Tachycardia – Torsade de Pointes – Ventricular Fibrillation
  • 33. Supraventricular Extrasystole • Caused by automaticity (ectopic foci) in atrial region other than SA node • ~ Atrial Premature Beat / Premature Atrial Contraction • ECG – Normal cardiac rhythm (sinus rhythm) – There is an earlier p wave generated – Followed by Narrow QRS complex
  • 34. Atrial Flutter • Caused by reentry over a large anatomical circuit • ECG – Irregular QRS rate – Narrow QRS complex – Multiple P wave for every QRS complex • Sawtooth phenomenon
  • 35. Atrial Fibrillation • Caused by either – Wandering Reentrant circuit within atria – Rapid firing of ectopic foci in atrial myocard • ECG – Irregular QRS rate – Narrow QRS complex – P wave Can not be identified
  • 36. Supraventricular Tachycardia • Caused by Reentry over AV node or Accessory Pathway • ECG – QRS rate Regular – Narrow QRS complex – P wave usually can not be identified • Hidden within QRS complex or T wave
  • 37. Ventricular Extrasystole • Caused by automaticity (ectopic foci) in ventricular region • ~ Ventricular Premature Beat / Premature Ventricular Contraction • ECG – Normal Cardiac Rhthm – Anomaly ECG wave • Wide QRS complex • No P wave
  • 38. Ventricular Extrasystole • Couplet • Triplet
  • 39. Ventricular Extrasystole • Bigeminy • Trigeminy
  • 40. Ventricular Extrasystole • Multifocal • R on T
  • 41. Ventricular Tachycardia • A series of 3 or more VES • Caused by either – Structural abnormality (Most commonly scar tissue due to infarction) that induce reentry – Multiple ectopic foci which makes continually changing reentry circuit • ECG – QRS rate regular – Wide QRS complex – No P wave – Similar QRS complex ~ Monomorphic VT – Vary QRS complex ~ Polimorphic VT
  • 42. Ventricular Tachycardia • VT Monomorphic • VT Polimorphic (torsade de pointes)
  • 43. Ventricular Fibrillation • Disordered stimulation of the ventricle with no coordinated contraction • Caused by multiple small wave of reentry that wander through myocardium • ECG – No discrete QRS waveforms
  • 44. Not So Benign Rhythm •Ischemic VT is often polymorphic; HR>100-110 BPM •Higher risk with more LV damage and in first 2 days after MI • Treat: DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers
  • 45. If That Didn’t Make You Nervous… Primary VF: Sudden event with no warning--10% STEMI patients before lytics. MUCH MUCH less now Secondary VF: Occurring in setting HF or shock Late VF: >48 hrs after MI-->Increased risk with IVCD, anterior wall MI, persistent SVT early in course, and RV infarction requiring pacing ***Have to worry about structural complication (free wallrupture) /ischemia Treat: Non-synced DCCV, electrolyte correction
  • 46. Why get worked up about electrolytes? Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 50:525, 1983. NOTE: Pre-lytic study
  • 47. Conclusion • Cardiac arrhythmias routinely manifest during or following an ACS • Incidence of arrhythmia is directly related to the type of ACS • Ischemic event in ACS can influenced electrical instability in the heart rhythm • treat the ischemic event &correction of imbalanced electrolit can improve the electrical instability in acs
  • 48. Thank You... Treat The Patient, Not The Monitor