Internal Medicine
STEMI (Myocardial Infarction)
EPIDEMIOLOGY:
DOH, 2010
RISK FACTORS:
 Tobacco/Cigarette Smoking
 Diet
o With regard to cardiovascular disease, a key element
of dietary change is an increase in intake of
saturated animal fats and hydrogenated
vegetable fats, which contain atherogenic trans -
fatty acids, along with a decrease in intake of plant-
based foods and an increase in simple
carbohydrates.
 Physical inactivity
 Lipid levels
o high cholesterol levels are estimated to cause 56%
of ischemic heart disease and 18% of strokes
o Plasma cholesterol levels tend to be higher among
urban residents than among rural residents.
 This shift is driven largely by greater
consumption of dietary fats—primarily from
animal products and processed vegetable
oils—and decreased physical activity.
 Hypertension
 Obesity
 Diabetes mellitus
PATHOPHYSIOLOGY:
 STEMI usually occurs when coronary blood flow decreases
abruptly after a thrombotic occlusion of a coronary artery
previously affected by atherosclerosis.
 Slowly developing, high-grade coronary artery stenoses do not
typically precipitate STEMI because of the development of a
rich collateral network over time.
 Instead, STEMI occurs when a coronary artery thrombus
develops rapidly at a site of vascular injury
o This injury is produced or facilitated by factors such
as cigarette smoking, hypertension, and lipid
accumulation.
 In most cases, STEMI occurs when the surface of an
atherosclerotic plaque becomes disrupted (exposing its
contents to the blood) and conditions (local or systemic) favor
thrombogenesis.
 After an initial platelet monolayer forms at the site of the
disrupted plaque, various agonists (collagen, ADP,
epinephrine, serotonin) promote platelet activation.
 After agonist stimulation of platelets, thromboxane A 2(a
potent local vasoconstrictor) is released, further platelet
activation occurs, and potential resistance to fibrinolysis
develops.
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CLINICAL MANIFESTATIONS:
History:
 Pain
o is the most common presenting complaint in patients
with STEMI.
o The pain is deep and visceral; adjectives commonly
used to describe it are heavy , squeezing , and
crushing , although, occasionally, it is described as
stabbing or burning
o It is similar in character to the discomfort of angina
pectoris but commonly occurs at rest, is usually
more severe, and lasts longer.
o the pain involves the central portion of the chest
and/orthe epigastrium, and, on occasion, it radiates
to the arms.
o Less common sites of radiation include the
abdomen, back, lower jaw, and neck.
o The pain of STEMI may radiate as high as the
occipital area but not below the umbilicus
o It is often accompanied by weakness, sweating,
nausea, vomiting, anxiety, and a sense of impending
doom.
o Radiation of discomfort to the trapezius is not seen in
patients with STEMI
o However, pain is not uniformly present in patients
with STEMI. The proportion of painless STEMIs is
greater in patients with diabetes mellitus, and it
increases with age.
The combination of substernal chest pain persisting for >30 min and
diaphoresis strongly suggests STEMI.
 Physical findings:
o anxious and restless
o Pallor associated with perspiration and coolness of
the extremities occurs commonly
o anterior infarction have manifestations of
sympathetic nervous system hyperactivity
(tachycardia and/or hypertension)
o inferior infarction show evidence of
parasympathetic hyperactivity (bradycardia and/or
hypotension)
o signs of ventricular dysfunction include fourth and
third heart sounds, decreased intensity of the first
heart sound, and paradoxical splitting of the second
heart sound
LABORATORY FINDINGS:
Myocardial infarction (MI) progresses through the following
temporal stages:
 acute (first few hours–7 days)
 healing (7–28 days)
 healed (≥29 days)
ELECTROCARDIOGRAM
o During the initial stage, total occlusion of an epicardial coronary
artery produces ST-segment elevation.
o Among patients presenting with ischemic discomfort but
without ST-segment elevation, if a serum cardiac biomarker of
necrosis is detected, the diagnosis of NSTEMI is ultimately
made
SERUM CARDIAC BIOMARKERS
o are released from necrotic heart muscle after STEMI
o Cardiac biomarkers become detectable in the peripheral blood
once the capacity of the cardiac lymphatics to clear the
interstitium of the infarct zone is exceeded and spillover into
the venous circulation occurs.
now the preferred
o Cardiac-specific troponin T
o Cardiac-specific troponin I biochemical markers for
MI
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Troponin T and Troponin I
o are particularly valuable when there is clinical suspicion of
either skeletal muscle injury or a small MI that may be below
the detection limit for creatine phosphokinase (CK) and its MB
isoenzyme (CKMB) measurements
o may remain elevated for 7–10 days after STEMI
CKMB
o CK (creatinine kinase) rises within 4–8 h and generally returns
to normal by 48–72h
o An important drawback of total CK measurement is its lack of
specificity for STEMI, as CK may be elevated with skeletal
muscle disease or trauma, including intramuscular injection.
o The MB isoenzyme of CK has the advantage over total CK that
it is not present in significant concentrations in extracardiac
tissue and, therefore, is considerably more specific.
o A ratio (relative index) of CKMB mass: CK activity ≥2.5
suggests but is not diagnostic of a myocardial rather than
a skeletal muscle source for the CKMB elevation.
CARDIAC IMAGING
o Abnormalities of wall motion on two-dimensional
echocardiography are almost universally present.
o 3) increased risk for cardiogenic shock
o 4) other relative contraindications to beta blockade
(PR interval greater than 0.24 seconds, second- or
third-degree heart block, active asthma, or reactive
airway disease).
o A commonly employed regimen is metoprolol, 5 mg
every 2–5 min for a total of 3 doses, provided the
patient has a heart rate >60 beats per minute (bpm),
systolic pressure >100 mmHg, a PR interval <0.24 s,
and rales that are no higher than 10 cm up from the
diaphragm.
COMPLICATIONS:
 CHF
 Arrhythmia

MANAGEMENT:
 Aspirin is essential in the management of patients with
suspected STEMI and is effective across the entire spectrum of
acute coronary syndromes.
o Rapid inhibition of cyclooxygenase-1 in platelets
followed by a reduction of thromboxane A2 levels is
achieved by buccal absorption of a chewed 160–
325-mg tablet in the Emergency Department.
o This measure should be followed by daily oral
administration of aspirin in a dose of 75–162 mg.
 In patients whose arterial O2 saturation is normal,
supplemental O2 is of limited if any clinical benefit and
therefore is not cost-effective.
o However, when hypoxemia is present, O2should be
administered by nasal prongs or face mask (2–4
L/min) for the first 6–12 h after infarction
 Sublingual nitroglycerin can be given safely to most patients
with STEMI.
o Up to three doses of 0.4 mg should be administered
at about 5-min intervals.
o nitroglycerin may be capable of both decreasing
myocardial oxygen demand (by lowering preload)
and increasing myocardial oxygen supply (by dilating
infarct-related coronary vessels or collateral vessels)
o Therapy with nitrates should be avoided in patients
who present with low systolic arterial pressure (<90 Pag nag cardiac arrest? You know what to do! 
mmHg) or in whom there is clinical suspicion of right
ventricular infarction
o Nitrates should not be administered to patients who
have taken the phosphodiesterase-5 inhibitor
sildenafil for erectile dysfunction within the preceding
24 h, because it may potentiate the hypotensive
effects of nitrates
 Morphine is a very effective analgesic for the pain associated
with STEMI.
o Morphine is routinely administered by repetitive
(every 5 min) intravenous injection of small doses
(2–4 mg)
 Intravenous beta blockers are also useful in the control of the
pain of STEMI.
o These drugs control pain effectively in some patients,
presumably by diminishing myocardial O2demand
and hence ischemia.
o More important, there is evidence that intravenous
beta blockers reduce the risks of reinfarction and
ventricular fibrillation
 Oral beta-blocker therapy should be initiated in the first 24 h
for patients who do not have any of the following:
o 1) signs of heart failure
o 2) evidence of a low-output state

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