Electrical Intability in ACS

Dr. Irwan, SpJP-FIHA

Department of Cardiology and Vascular MedicineFaculty of Medicine, Riau UniversityArifin Achmad Hospital - Pekanbaru

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 millionAdmissions per year

.33 millionAdmissions 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.

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

Complications of MI

Myocardial Infarction

Ventricularthrombus

Contractility Electricalinstability

Tissuenecrosis

Pericardialinflammation

Embolism Arrhythmias Pericarditis

Papillarymuscleinfarction/ischemia

Ventricularseptaldefect

Ventricularrupture

Mitralregurgitation

Congestiveheart failure

Coronaryperfusionpressure

Ischemia Hypotension

Cardiogenicshock

Cardiactamponade

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

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

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

Depolaization

Ventricular contraction

Cardiac Action Potential

Cardiac Cycle

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

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

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

Normal Impulse Conduction

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

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

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

Rhythm Identification (ECG)

• Examined best in lead II (Alternatively in V1)

– At least 6 second duration

Normal Rhythm (Sinus)

Sinus Tachycardia

Sinus Bradycardia

Cardiac Arrhythmias

• Bradyarrhythmias

• Tachyarrhythmias

– Supraventricular

– Ventricular

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 be Often induced by vagal reaction that may be Often induced by vagal reaction that may be Often induced by vagal reaction that may be protectiveprotectiveprotectiveprotective

Location of Pathology

How to Identify Arrhythmia

• QRS rate Regular / Irregular?

• QRS complex Narrow / Wide?

• P wave?

• Relationship between P wave & QRS complex?

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

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)

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

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

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

AV Block

• 3rd degree AV Block

– No communication between P wave and QRS

Complex

– P wave rate is different than QRS rate

Recomendation for Treatment of Atrioventricular & Interventricular Conduction Disturbance During STEMI

Guidlenes Recommendation for STEMI 2004, ACC-AHA

Tachyarhythmias

• Supraventricular

– Supravetricular Extrasystole

– Atrial Flutter

– Atrial Fibrillation

– Paroxysmal Supraventricular Tachycardia (SVT)

• Ventricular

– Ventricular Extrasystole

– Ventricular Tachycardia

– Torsade de Pointes

– Ventricular Fibrillation

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

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

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

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

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

Ventricular Extrasystole

• Couplet

• Triplet

Ventricular Extrasystole

• Bigeminy

• Trigeminy

Ventricular Extrasystole

• Multifocal

• R on T

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

Ventricular Tachycardia

• VT Monomorphic

• VT Polimorphic (torsade de pointes)

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

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

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

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

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

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