Acute Miocard Infark
Acute Miocard Infark
Acute Miocard Infark
EPIDEMIOLOGI
PATHOGENESIS
The hallmark is the sudden imbalance between myocardial oxygen
consumption (MVO2) and demand,which is usually the result of
coronary artery obstruction.
The imbalance may also be caused by other conditions, including
excessive myocardial oxygen demand in the setting of a stable flowlimiting lesion; acute coronary insufficiency due to other causes (e.g.,
vasospastic, angina, coronary embolism, coronary arteritis);
Noncoronary causes of myocardial oxygen supply-demand mismatch
(e.g. hypotension, severe anemia, hypertension, tachycardia,
hypertrophic cardiomyopathy, severe aortic stenosis);
Nonischemic myocardial injury (e.g., myocarditis, cardiac contusion,
cardiotoxic drugs); and multifactorial
Causes that are not mutually exclusive (e.g., stress cardiomyopathy
,pulmonary embolism, severe heart failure [HF], sepsis).
Family Historyevent
in first degree relative
>55 male/65 female
CLINICAL PRESENTATION
Chest pain is the usual symptom which brings these patients
to medical attention. Pain is severe, diffuse, retrosternal and
radiates to arms or from jaws to umbilicus. Pain does not get
relieved with sublingual nitrates or usual pain killers. It is often
associated with eructations and retrosternal burning.
Commonly patients mistake it for acid peptic symptoms and
waste precious time with antacids. It is accompanied with
vomiting, sweating
and breathlessness. About 15-20% of infarcts can be painless
specially in elderly and diabetics. Equal number may have less
characteristic pain than described above. The pain needs to be
distinguished from other causes of acute severe chest pain
which can bring patients to emergency room.
Pandey et al, 2011
Electrocardiography
ECG is generally the first investigation available for
making a diagnosis in a patient presenting with acute
severe chest pain.
Tall T waves and ST elevation are the hallmarks of
early presentation within minutes of onset of pain.
The third change appearance of Q waves, is
delayed and seen after 6 hours of onset. Q waves
denote significant myocardial necrosis.
The initial changes of upright and tall T wave with
concave upward ST segment elevation subsequently,
gives way to T wave inversion and ST coving with
convexity upwards over one day to one week.
Pandey et al, 2011
Echocardiography
Echocardiography is helpful in the
evaluation of chest pain, especially
during active chest pain.
The absence of LV wall motion
abnormalities during chest pain usually
but not always excludes myocardial
ischemia or infarction, and the presence
of regional wall motion abnormalities
helps in confirming the diagnosis
Pandey et al, 2011
CARDIAC BIOMARKERS
Cardiac biomarkers have conventionally being
used for diagnosis of acute myocardial infarction.
These have also been used in patients with
NSTEMI and unstable angina for finding high risk
individuals.
Elevation of CPK, CPK-MB and Troponins I and T
occurs in all patients with myocardial necrosis
that is seen in myocardial infarction.
Serial CK-MB estimations were done earlier for
estimation
of
infarct
size
before
echocardiography.
Pandey et al, 2011
Cardiac markers
Troponin ( T, I)
Very specific and more
sensitive than CK
Rises 4-8 hours after
injury
May remain elevated
for up to two weeks
Can provide prognostic
information
Troponin T may be
elevated with renal dz,
poly/dermatomyositis
CK-MB isoenzyme
Rises 4-6 hours
after injury and
peaks at 24 hours
Remains elevated
36-48 hours
Positive if CK/MB
> 5% of total CK
and 2 times
normal
Elevation can be
predictive of
mortality
Chest Pain
History, Physical
EKG
STEMI
UA/NSTEMI/
High Risk
Mod Risk
Low Risk
Definite
Non-Cardiac
Risk Stratification
YES
STEMI
Patient?
- Assess for
reperfusion
- Select &
implement
reperfusion
therapy
- Directed medical
therapy
Based on initial
Evaluation, ECG, and
Cardiac markers
NO
UA or NSTEMI
- Evaluate for
Invasive vs.
conservative
treatment
- Directed medical
therapy
Fibrinolysis preferred
if:
PCI available
Door to balloon <
90min
Door to balloon
minus door to needle
< 1hr
Fibrinolysis
contraindications
Late Presentation >
3 hr
High risk STEMI
Killup 3 or higher
Medical Therapy
Morphine
Analgesia
Reduce pain/anxietydecrease sympathetic
tone, systemic vascular resistance and
oxygen demand
Careful with hypotension, hypovolemia,
respiratory depression
Oxygen
Up to 70% of ACS patient demonstrate
hypoxemia
May limit ischemic myocardial damage by
increasing oxygen delivery/reduce ST
elevation
2008 by the European Society of Cardiology,
Nitroglycerin
Analgesiatitrate infusion to keep patient
pain free
Dilates coronary vesselsincrease blood
flow
Reduces systemic vascular resistance and
preload
Careful with recent ED (erectile dysfunction)
meds, hypotension, bradycardia,
tachycardia, RV infarction
Aspirin
Beta-Blockers
14% reduction in mortality risk at 7 days at
23% long term mortality reduction in STEMI
Approximate 13% reduction in risk of
progression to MI in patients with
threatening or evolving MI symptoms
Be aware of contraindications (CHF, Heart
block, Hypotension)
Reassess for therapy as contraindications
resolve
ACE-Inhibitors / ARB
Start in patients with anterior MI, pulmonary
congestion, LVEF < 40% in absence of
contraindication/hypotension
Start in first 24 hours
2008 by the European Society of Cardiology,
ARB as substitute for patients
unable to use
Heparin
LMWH or UFH
Unstable angina/NSTEMI
care
cardiac
Low
High
Intermediate
INTERMEDIATE
likelihood of ACS in
absence of highlikelihood findings
in absence of high- or
intermediate-likelihood
findings
History
Probable ischemic
symptoms
Recent cocaine use
Physical
examination
Extracardiac vascular
disease
Chest discomfort
reproduced by palpation
ECG
Fixed Q waves
Abnormal ST segments or
T waves not documented
to be new
T-wave flattening or
inversion of T waves in
leads with dominant R
waves
Normal ECG
Serum cardiac
markers
Normal
Normal
LOW
RISK
INTERMEDIAT
E RISK
HIGH RISK
Chest Pain
center
Conservati
ve therapy
Invasive
therapy
Surveillence in hospital
Serial ECGs
Serial Markers