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

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

10. Cardiac Cycle

11. 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

12. 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

13. 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

14. Normal Impulse Conduction

15. 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

16. 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

17. 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

18. Rhythm Identification (ECG)
• Examined best in lead II (Alternatively in V1)
– At least 6 second duration

19. Normal Rhythm (Sinus)

20. Sinus Tachycardia

21. Sinus Bradycardia

22. Cardiac Arrhythmias
• Bradyarrhythmias
• Tachyarrhythmias
– Supraventricular
– Ventricular

23. 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

24. Location of Pathology

25. How to Identify Arrhythmia
• QRS rate Regular / Irregular?
• QRS complex Narrow / Wide?
• P wave?
• Relationship between P wave & QRS complex?

26. 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

27. 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)

28. 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

29. 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

30. 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

31. AV Block
• 3rd degree AV Block
– No communication between P wave and QRS
Complex
– P wave rate is different than QRS rate

32. Recomendation for Treatment of Atrioventricular & Interventricular
Conduction Disturbance During STEMI
Guidlenes Recommendation for STEMI 2004, ACC-AHA

33. Tachyarhythmias
• Supraventricular
– Supravetricular Extrasystole
– Atrial Flutter
– Atrial Fibrillation
– Paroxysmal Supraventricular Tachycardia (SVT)
• Ventricular
– Ventricular Extrasystole
– Ventricular Tachycardia
– Torsade de Pointes
– Ventricular Fibrillation

34. 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

35. 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

36. 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

37. 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

38. 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

39. Ventricular Extrasystole
• Couplet
• Triplet

40. Ventricular Extrasystole
• Bigeminy
• Trigeminy

41. Ventricular Extrasystole
• Multifocal
• R on T

42. 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

43. Ventricular Tachycardia
• VT Monomorphic
• VT Polimorphic (torsade de pointes)

44. 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

45. 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

46. 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

47. 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

48. 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

49. Thank You...
Treat The Patient, Not The Monitor