Download Acute Coronary Syndromes

Acute Coronary Syndromes
Pathophysiology &
Clinical Presentations
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Ischemic Heart Disease - Overview
Parameters
Pathophysiology
Anatomy: Atheroma / Atherothrombosis
Atherosclerosis
Epicardial &
Microvascular Spam
Subjective: Angina
Objective:
EKG T wave ST seg
changes
Chemistry:
Cardiac serum
biomarkers:
CPK, CK-MB,
Troponins
Atherothrombosis
Silent ischemia
Stable angina
Acute Coronary
Syndromes
Clinical Presentations
Prevalence & severity of
stenosis
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Events During Atherogenesis
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Wall Stress =
Pxr
2h
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ISCHEMIC CASCADE
•Flow Maldistribution
•Biochemical metabolic actions
Nuclear
•Hypoperfusion
•
•
Echo
Predictable sequence of
pathophysiologic events post
myocardial supply/demand imbalance
•(S4)
Compliance
LVEDP
•
TIME FROM ONSET OF IS
•(Rales)
Contractility
•
EF
EKG
± 45 sec.
Angina / SI
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Effect of Fixed Stenosis on Myocardial Blood Flow
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Progression of coronary plaque over time Clinical Findings
Acute Coronary Syndromes
Sudden Cardiac Death
Endothelial dysfunction
Atherogenic
risk factors
Acute silent
occlusive
process
Angina
pectoris
Thrombogenic
risk factors
Age
20 years
60 years
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IHD – Clinical Spectrum
Chronic
Stable Angina
Silent Ischemia
Mixed Angina
Microvascular Angina
(Syndrome X)
Stunned & Hibernating
Acute
Unstable Angina
Acute Myocardial
Infarction (NSTEMI,
STEMI)
Sudden Cardiac Death
Prinzmetal Angina
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Clinical Classification of Chest Pain
Typical angina (define)
1.Substernal chest discomfort with a characteristic
quality and duration that is
2.Provoked by exertion or emotional stress and
3.Relieved by rest or nitroglycerin
Canadian Cardiovascular Society
Classification ( CCSC)
Class
Activity
evoking
angina
I
Prolonge None
d
exertion
II
Walking
>2
blocks
Slight
III
Walking
<2
blocks
Marked
IV
Minimal
or rest
Severe
Atypical angina ( probable)
Meets 2 of the above characteristics
Noncardiac chest pain
Meets one or none of the typical angina
characteristics
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN
Cardiovascular: Pericarditis, Aortic Valve Disease,
Aortic Dissection, Pulmonary Embolism, Mitral
Valve Prolapse
Gastrointestinal: Esophageal, Biliary, Peptic ulcer,
Pancreatitis
Pulmonary: Pneumothorax, Pneumonia, Pleuritis
Chest Wall: Costochondritis, Rib fracture, Herpes
zoster
Psychological: Anxiety disorders
*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II
ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV
Limits to
normal
activity
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CAD - Clinical Spectrum
Chronic
ischemic heart disease
Ischemia precipitated by increased myocardial oxygen demand
in the setting of a fixed, not vulnerable atherosclerotic lesion. It is
called Stable Angina when the clinical characteristics (Angina
attacks) do not change in frequency, duration, precipitating causes,
or easy with the angina is relieved, for at least 60 days.
-Silent Ischemia, -Mixed Angina -Syndome X
Stunning & Hibernating.
Acute Coronary Syndromes (ACS)
-
Ischemia or infarction are caused from a primary reduction in
coronary flow, precipitated by plaque disruption and subsequent
thrombus formation:
Unstable Angina, NSTEMI, STEMI
Prinzmetal Angina
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Stable Plaque
Vulnerable Plaque
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Plaque Disruption
UA
NSTEMI
STEMI
+ S. Markers
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Distinguishing Features of Acute Coronary Syndromes
Unstable Angina
Myocardial Infarction
NSTEMI
Anginal
•Rest angina - Rest or nocturnal
Presentation Angina ≥ 20 minutes occurring
s
within a week of presentation.
•New onset angina - ( < 2 months )
exertional angina progressing to
CCSA III
•Crescendo angina - < 2 moths
acceleration of previously stable
angina to at least CCSA III.
•Within
STEMI
Prolonged ( > 30 min )
crushing, strangling
chest pain more severe
and wider radiation than
usual angina
30 day post MI, PCI or
CABG
EKC initial
findings
Cardiac
Serum
Biomarkers
Dynamic, transiet < 24 hours
depression
ST depression
and/pr T Wave
inversion
ST elevation (
and Q waves
later)
Negative (-)
Positive (+)
Positive (+)
T-wave inversion and/or ST seg
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Acute Coronary Syndromes
Coronary Atherothrombosis
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-RCA, 1yr. Before of
the acute MI (B)
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Acute MI
Typical rise and gradual
fall (troponin) or more
rapid rise and fall of CKMB, markers of
myocardial necrosis,
with at least one of the
following:
•Ischemic symptoms
•EKG changes indicative
of ischemia (ST-seg
elevation or depression)
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T Wave – ST seg. changes
T-wave ∆
ST-seg ∆
Zone of ischemia
Path. Q waves
Zone of injury
Zone of necrosis
Lateral
Inferior
Septal Anterior
>0.03 seconds
>1/3 the total of
QRS
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“ Time is muscle”
Myocardial Infarction is a true
emergency in cardiac care.
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If the clinical picture is consistent with acute STEMI
(including True Posterior MI) or new left bundle branch block
(LBBB) is present in EKG, select and implement reperfusion
therapy, Fibrinolysis or PCI as quickly as possible within 12
hours of symptoms onset to obtain and sustain optimal flow
in the infarct-related artery (IRA). Do not wait for serum
cardiac biomarkers result before implementing reperfusion
strategy !
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ACS Treatment
 Revascularization


Mechanical: PCI, CABG
Pharmacologic: Thrombolytics
 Stabilization






of Vulnerable Plaque Aspirin
Antithrombotics
Beta-Blockers
ACE-Inhibitors
Lipid-Lowering Agents (+stantins)
Antioxidants
Aggressive Risk Factors Modifications
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Complications of Ml
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COMPLICATIONS OF INFARCTION
Papillary Muscle Rupture
Left Ventricular Thrombus
Ventricular Septal Rupture
Ventricular Free Wall Rupture
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