Professional Documents
Culture Documents
* Based on data from the ARIC study of the National Heart, Lung, and Blood Institute, 1987-1994. Includes
Americans hospitalized with definite or probable MI or fatal CHD, not including silent MIs. ACS indicates acute
coronary syndrome; MI, myocardial infarction; ARIC, Atherosclerotic Risk in Communities; and CHD, coronary
heart disease. From American Heart Association. Heart Disease and Stroke Statistics2003 Update.
Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at:
www.theheart.org.
Atherothrombosis* is the
Leading Cause of Death Worldwide1
Pulmonary Disease 6.
3
Injuries 9
AIDS 9.7
Cancer 12.6
Atherothrombosis* 22.3
0 5 10 15 20 25 30
Causes of Mortality (%)
Reprod.with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
LOGO
LOGO
THE EVOLUTION OF THE ATHEROSCLEROTIC PLAQUE
The Longitudinal Section Of An Artery Depicts The
Timeline Of Atherogenesis
Adapted with permission from Falk E, et al. Circulation. 1998;92:657-671. Slide reproduced with
permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
Characteristics of Unstable and
Stable Plaque
Unstable Stable
Lack of
Inflammatory inflammatory
Thin cells Thick cells
Few fibrous cap More fibrous cap
SMCs SMCs
Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells
Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with
permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
Timeline Acute Coronary Syndrome
Vulnerable Plaque
Thrombus Formation
Old
Terminology: UA NQMI STE-MI
+
+ +
In-Hospital
II
III
aVR
aVL
aVF
V1-2
V3-4
V5-6
A B C D E
Cardiac Marker - Release Kinetics
Cardiac Spesificity Increase Peak Returns
Duration to
of action
Marker Specificity Appears At Peaks At Normal
Myoglobin Non-specific 1- 3 hours 6 - 9 hours 24 hours
CK-MB Moderately 4 - 6 hours 12 - 24 hours 72 hours
Troponin I Specific 4 - 6 hours 12 - 24 hours 5- 10 days
6
Blood 5
Myoglobin
CK-MB
level of Troponin I
Marker 4
above
upper 3
limit of
normal
2
1
0 4 8 12 16 20 24 48 72 96 120
Time After
TimeOnset Post post
of onset AMI MCI
( Hours )
(hours)
( Peter ,2001 )
Complications of MI :
- ARITMIA :
Gangguan pembentukan dan atau
penghantaran impuls
- IRAMA SINUS normal : 60 100x/menit
- PEMBAGIAN :
- Gangguan pembentukan impuls : sinus ,
atrium penghubung AV ,ventrikel
- Gangguan penghantaran impuls :
blok SA, AV, intra ventrikel
- PEMBAGIAN SECARA KLINIS :
- Taki, bradi, bradi-taki-aritmia
The Cardiac Conduction System
Normal sinus rhythm
Sinoatrial node is cardiac
pacemaker
Normal sinus rhythm 60-100
beats/min
Depolarisation triggers
depolarisation of atrial
myocardium (forest fire)
Conducts more slowly
through AV node
Conducts rapidly through
His bundles and Purkinje
fibres
Clinical classification of
arrhythmias
Heart rate (increased/decreased)
Heart rhythm (regular/irregular)
Site of origin
(supraventricular/ventricular)
QRS complexes on ECG
(narrow/broad)
Mechanisms Responsible
for Arrhythmias
Abnormalities of impulse generation
A. Alterations of normal automaticity
B. Abnormal automaticity
C. Triggered activity
Early/Delayed afterdepolarization
Abnormalities of impulse conduction
A. Reentry: 1. Unidirectional block; 2. Anatomic or
functional reentrant circuit ; 3. wavelength
B. Conduction block
Combined abnormalities of impulse generation and
conduction
Transmembrane Potentials of
Myocardial Cells
A: Contractile cell
B: Autorhythmic cell:
spontaneous depolarization at phase 4
Alterations of normal
automaticity
Autonomic neurotransmitters
Triggered activity:
Early/Delayed
afterdepolarization
Re-Entry Mechanism
EKG ,hemodinamika
Takiaritmia Bradiaritmia
Cardiac arrest
Sinus bradikardi Asistol
Henti kardiopulmoner
Blok AV/Frekw.ventr lambat
Fibrilasi ventrikel (VF)
QRSsempit
QRS lebar
Reguler Irreguler Reguler Irreguler
1. VT 1. AF + WPW 1. Sinus takikardi 1. AF
2. SVT+RBBB 2. Torsade depointes
2. A. fluter 2. A. fluter
3. LBBB 3. TSVP (PAT)
Vaughan Williams classification
of antiarrhythmic drugs
Class I: block sodium channels
Ia (quinidine, procainamide,
disopyramide) AP
Phase 1
Ib (lignocaine) AP IV
Ic (flecainide) AP Phase 2
0 mV
Class II: -adrenoceptor
antagonists (propranolol, sotalol)
Phase 0 I III
Class III: prolong action potential Phase 3
and prolong refractory period
(suppress re-entrant rhythms)
(amiodarone, sotalol) -80mV Phase 4
Class IV: Calcium channel II
antagonists. Impair impulse
propagation in nodal and damaged
areas (verapamil, diltiazem)
Atrial fibrillation:
Common Causes
Coronary artery disease
Hypertensive heart disease
Valvular heart disease, mitral stenosis
Cardiomyopathy
Thyrotoxicosis
Occasionally, no structural heart
disease, especially paroxysmal atrial
fibrillation
Atrial Fibrillation:
ECG Characteristics
Absence of P waves
Very irregular baseline, f waves, with a rate of
350-600 bpm, best seen in V1,
Irregular QRS complex rate, usually normal
shape
Atrial Fibrillation
Atrial Fibrillation:
Auscultation Features
Variation in the intensity of S1
Extremely irregular heart rate
Pulse deficit (because each contraction
is not sufficiently strong to open the
aortic valve or transmit an arterial
pressure wave through the peripheral
arteries)
Atrial fibrillation:
Clinical Considerations
Decreased hemodynamic functions
rapid ventricular rates
the loss of atrial contraction
Risk of systemic embolism
5 to 7 times greater than that in
controls
Atrial fibrillation: Classification
and Management Strategies
Abnormal connection
between the atrium and
the ventricle
Pre-excitation syndrome
ECG Features
Short PR interval
Slurred upstroke of
QRS complexes (the
delta wave)
broad QRS complexes
Secondary ST-T
abnormalities
(reflecting modified
ventricular
repolarization
secondary to
abnormal
depolariozation
Pre-excitation Syndrome (WPW)
Paroxysmal SVT:
Treatment
Vagal maneuvers: Valsalva maneuver or
carotid sinus massage
First choice of drugs: adenosine 6-12 mg iv,
or verapamil 5 mg iv
Preferred choice of drugs: propafenone 70
mg iv; cedilanid 0.4-0.6 mg iv
Synchronized DC cardioversion (shock
delivery that is timed within the QRS complex
Radiofrequency catheter ablation
Radiofrequency
Catheter Ablation
Radiofrequency
Catheter Ablation
Premature Beats
Atrial
AV junctional
Ventricular
Clinical considerations
ECG features
Management strategies
Normal AP Conduction in
Ventricles
Initiation site
Defibrillator:
used to "shock" the heart from an abnormal
rhythm pattern back into a normal rhythm
Ventricular Fibrillation
Ventricular Fibrillation
Sick Sinus Syndrome (SSS)
Definition:characterized by intrinsic
inadequacy of sinus node pacemaking and
/or conduction failure between sinus node
and the rest of the atrium
Etiology: coronary heart disease,
degenerative process, cardiomyopathy
Clinical manifestations: insufficiency of
blood supply to important organs
Sick Sinus Syndrome (SSS)
ECG Features
Marked sinus bradycardia
< 50 bpm measured as
SNRT, SACT and IHR
Sinus arrest / sinoatrial
block Holter
recording
Bradycardia-tachycardia
syndrome atrial
tachyarrhythmias
Probable coexistence with
atrioventricular block
Sick Sinus Syndrome (SSS)
Sick Sinus Syndrome (SSS)
Atrioventricular Block
Atrioventricular Block
Pacemaker Implantation