INTRODUCTION

Acute coronary syndrome (ACS) is a term used to describe three subconditions associated with cardiac ischemia; they are, unstable angina (UA), non STsegment myocardial infarction (NSTEMI) and ST-segment myocardial infarction
(STEMI).
As the treatments for ACS have changed over the years, so has the terminology. A
NSTEMI has also been referred to as a non-transmural or non Q-wave MI. In the
same manner, STEMI was referred to as transmural or Q-wave MI (Clark, D. S,
2010).
ACS can occur if there are embolic clots in the circulation; for example, caused by
clots formed in the heart during atrial fibrillation. Arterial inflammation (infection) or
vasospasm can also cause transient and/or sustained ischemia. Potentially, coronary
arteries can spasm from the use of cocaine or methamphetamines; or increased
cardiac workload secondary to thyrotoxicosis, anemia, hypoxemia
or fever.
ACS is still the #1 killer for both men and women. An estimated 38% of all people will
not survive their myocardial infarction (MI) (Berra, 2011).
ACS is responsible for more than 1.5 million admissions to a hospital every year
(Berra, 2011).
It is estimated the patients who are 40 years or older, 18% of males and 23% of
females, die within the first year of a myocardial infarction (Devabhakthuni & Seybert,
2011).

DEFINITIONS
Chest Pain A symptom complex that is categorized as typical angina, atypical angina
or nonanginal chest pain. Typical anginal chest pain is 1) substernal, 2) provoked by
exercise and/or emotion, and 3) relieved by rest and/or nitroglycerin. Atypical anginal
chest pain has two of the three features listed for typical angina. Nonanginal chest
pain may be caused by a range of sources including cardiac, chest wall, pulmonary,
gastrointestinal, psychogenic.
Myocardial Ischemia A condition in which oxygen delivery to and metabolite
removal from the myocardium fall below normal levels,
with oxygen demand exceeding supply. Ischemia is usually diagnosed indirectly
through techniques that demonstrate reduced myocardial blood flow or its
consequences.
Acute Myocardial Infarction (AMI) An acute process of myocardial ischemia with
sufficient severity and duration to result in permanent myocardial
damage. The diagnosis is made when there is a characteristic rise and fall in cardiac
biomarkers indicative of myocardial necrosis that may or may not be accompanied by
the development of Q waves on the ECG.
Angina A generic term used to describe a clinical syndrome typically characterized
by a deep, poorly localized chest, jaw, shoulder, back or arm discomfort that is
reproduced with physical exertion or emotional stress and relieved promptly by rest
or sublingual nitroglycerin (NTG). Angina is further classified as stable or unstable.
Stable Angina Chest discomfort that occurs predictably at a certain level of exertion
and is consistently relieved by rest or nitroglycerin.
Unstable Angina (UA) Chest discomfort with all the qualities of typical angina except
episodes are more severe and prolonged and may occur at rest with an unknown
relationship to exertion or stress. In most patients these symptoms reflect myocardial
ischemia resulting from underlying CAD but the CAD is not severe or long enough to
cause myocardial necrosis. Patients with UA typically do not present with STsegment elevation on the ECG and do not release markers indicative of myocardial
necrosis into the blood.

Non-ST-segment elevation MI (NSTEMI) NSTEMI is an acute process of

myocardial ischemia with sufficient severity and duration to result in myocardial
necrosis. The initial ECG does not show ST-segment elevation and most patients do
not develop new Q-waves and are ultimately diagnosed as having a NQMI.
ST-segment elevation MI (STEMI) STEMI is an acute process of myocardial
ischemia with sufficient severity and duration to result in myocardial necrosis. The
ECG does show ST-segment elevation and most patients do develop new Q-waves.
Variant (Prinzmetals) Angina A clinical syndrome of pain at rest and reversible STsegment elevation without subsequent enzyme evidence of AMI. The cause is
usually coronary vasospasm but there may also be significant CAD. Unlike typical
angina, it
nearly always occurs when a person is at rest and usually between midnight and 8
am.
Acute Coronary Syndrome (ACS) ACS encompasses any constellation of signs or
symptoms suggestive of AMI or UA. ACS includes AMI, STEMI, NSTEMI, enzymediagnosed MI, UA and sudden cardiac death. The term is useful to refer to patients
before their specific diagnosis is confirmed as all of these diagnoses occur from a
coronary artery occlusion of varying degrees. (Braunwald et al., 2002)

SYMTOMATOLOGY
Chest pain or pressure, or a

discomfort from lack of blood flow, but

there is no damage to the heart muscle.

strange feeling in the chest.

It often happens when you are at rest

.
Sweating
unable to pump enough blood to supply
oxygen to your body. If your brain,

Shortness of breath.

muscles, or other body organs do not get

enough oxygen, a sense of
breathlessness may occur.
Nausea or vomiting.

Lightheadedness or sudden weakness

a disruption of the systems bodily

functions due to inadequate nutrition or

A fast or irregular heartbeat

other problems
Narrowing of the coronary arteries that
why ECG is done to check the severity.

MEDICAL MANAGEMENT
DIAGNOSTIC TEST
CK MB

NORMAL VALUES
NormalValues:

IMPLICLATION
Serum CPK/CK will be

male:5- elevated
35ug/ml(mcg/ml);

in

skeletal

muscle disease, in acute

female:5-25ug/ml MI, in cerebral vascular

newborn: 10-300 IU/L

disease,

vigorous

exercise,

IM

injections,

electrolyte imbalance, and

hypokalemia.
three

CPK

has

isoenzymes

as

presented

earlier.

Fractionation

and

measurement
three

of

these

distinct

CPK

isoenzymes have replaced

the use of total CK (or
CPK) levels to accurately
localize

the

site

increased

of

tissue

destruction.

CK-BB

is

most often found in brain

tissue. CK-MM and CKMB are found primarily in
skeletal and heart muscle.
In addition, subunits of
CK-MB

and

called

isoforms

isoenzymes,

CK-MM,
can

or
be

assayed to increase the

test's sensitivity.
- When the isoenzyme
CPK-MB

is

elevated,

greater than 5%, it could

strongly indicate damage
to the myocardial cells.
The

CPK-MB

elevates

within 4-6 hours after an

acute MI; peaks in 18-24
hours; it then returns to

\MYOGLOBIN

normal within 3-4 days

Normal Values: 30 to 90 This test measures serum
NG/ml

levels of myoglobin, an
oxygen-binding
protein,

muscle

similar

to

hemoglobin. Myoglobin is
normally found in skeletal
muscle

and

cardiac

muscle, and is released

into the bloodstream after
muscle injury. Thus, serum
myoglobin levels help to
estimate the amount of
muscle damage. However,
because myoglobin does
not indicate the site of the
damage, this test is used
only to CONFIRM other
tests such as CPK, CPKMB,

and

results

others.

must

correlated
patient's
SGOT

Test

also

be

with

the

signs

and

symptoms.
ormal Values: 5-40 U/ml Serum

Glutamic

(Frankel) 4-36 IU/L; or 16-

Oxaloacetic

60 (Karmen) U/ml U/L at

Transaminase,

called:

30 degrees C; or 8-33 (SI AST,

units) at 37 degrees C.

(Aspartate
Aminotransferase) A blood
chemistry test for the level
of SGOT in blood (is
released

with

tissue

necrosis).
- This enzyme shows an
elevation 8-12 hours after
infarction. Peak levels are

reached 24-48 hours after

the MI. This enzyme is not
particularly indicative of an
MI. Other conditions can
also cause a rise in the
levels.

High

levels

of

SGOT may be obtained

with trauma to the skeletal
muscles, in liver disease,
pancreatitis

and

others.

SGOT is found in: heart

muscle, liver, some also in
skeletal muscle, kidneys
SODIUM (Na serum

adult:

135-145

(same

and the pancreas.

mEq/L Decreased levels
forchild) (hyponatremia) may be

infants: 134-150 mEq/L

caused by: vomiting,

diarrhea, gastric suction,
excessive perspiration,
continuous IV 5%
Dextrose/water; lowsodium diet, burns,
inflammatory reactions,
tissue injury, others.
Increased sodium can
mean: dehydration, severe
vomiting & diarrhea, CHF,
Cushing's disease, hepatic
failure, high-sodium diet,
and others.

POTASSIUM

3.5-5.0 mEq/L

Hypokalemia

can

caused

decreased

intake,
vomiting,

by

be

protracted
renal

cirrhosis and others.

loss,

Hyperkalemia

can

be

caused by renal failure

and other causes. The
nurse must carefully check
vital signs of any patients
in the above risk groups,
especially
TROPONIN TEST

status
The

the

cardiac

troponin

test

measures the levels of

certain

proteins

called

troponin T and troponin I

in

the

blood.

proteins

These

are released

when the heart muscle

has been damaged, such
as a heart attack. The
more damage there is to
the heart, the greater the
amount of troponin T and I
there will be in the blood.
Cardiac troponins are the
most

specific

determining
injury.

tests

for

myocardial

Troponins

are

located on the contractile

apparatus in muscle tissue
and released in response
to injury. There are 3
isoforms: 2 found in both
cardiac

and

skeletal

muscle (cTnT, cTnC) and

one specific to myocardial
fibers

(cTnI).

Troponins

rise early at 4 to 6 hours,

and remain elevated for

up to 10 days, which
allows for both early and
late diagnosis (Futterman,
2002). However, the long
duration makes it difficult
to estimate the exact time
of the acute MI.
ECG

ECG changes that may

be seen during anginal
episodes

Transient ST
segment elevations
Dynamic T-wave
changes: Inversions,
normalizations, or
hyperacute changes

ST depressions:
These may be
junctional,
downsloping, or
horizontal

CHEST X RAY

Patients with ACS may

have a portable chest Xray performed in order to
differentiate

AMI

from

or

other

aortic
dissection

alternative causes of chest

ECG STRESS TESTING

pain.
is the standard mode of
stress

testing

for

the

assessment of ischemia,
functional

capacity,

and

prognosis in patients with

a normal resting ECG who
are not taking digoxin. It is
simple,

affordable

applicable

and

to

most

patients. However, it is not

the

most

accurate,

especially for patients on

digoxin or those who have
marked

ST-T

wave

abnormalities, LBBB, or
pacemakers.

Exercise

testing can help to identify

a high-risk patient but it
does

not

accurately

localize site or extent of

STRESS

myocardial ischemia.
Two-dimensional

ECHOCARDIOGRAPHY

echocardiography

(2-D

Echo) detects wall motion

abnormalities

that

indicate

physiologic

may

change in response to
ischemia.

2-D

Echo

is

better than ECG testing in

identifying a culprit
lesion. In addition, it can
help to assess myocardial
viability prior to
revascularization.

Stress

echocardiography can be
performed with exercise
or a pharmacologic agent
if the patient has physical
limitations. The

advantages of 2-D echo

over stress ECG testing
include

the

ability

to

assess
multiple parameters such
as

ventricular

wall

function. , chamber size,

wall
thickness

and

function.

valvular

The

main

disadvantage is that the

interpretation is subjective
and in some patients (for
example: barrel-chested
or obese) there is no
acoustic window to allow
accurate imaging
(Williams, 2009).

MEDICATIONS
Beta Blockers
METOPROLOL

The cardioselective beta-blockers work

primarily by blocking catecholamines on
the Beta1-adrenergic receptors in the
myocardium.
symptoms

by

They

relieve

inhibiting

anginal

sympathetic

stimulation to the heart, reducing heart

Calcium antagonists

rate and contractility,

act by preventing calcium entry into

NIFEDIPINE

vascular

smooth

muscle

cells

and

AMLODIPINE

myocytes. These effects cause coronary

VERAPAMIL

and peripheral vasodilation, decreased

DILTIAZEM
Anti Platelet
ASPIRIN

AV conduction, and reduced contractility.

inhibits the formation of thromboxane,
thereby diminishing platelet aggregation
and clot formation. All patients with
unstable angina should receive regular
ASA as soon as possible unless
contraindicated. ASA has significant
benefits including reducing mortality and
MI rates by 50% or more.
Contraindications include evidence or
significant risk of life-threatening
hemorrhage or a hypersensitivity to
ASA. Stomach irritation is the most
common side effect, therefore, enteric
coating is helpful.

NITRATES
NITROGLYCERINE

The major therapeutic benefit is probably

related to the venodilator effects that
lead to a decrease in myocardial preload
and LV end-diastolic volume, resulting in
a decrease in myocardial oxygen
consumption. In addition, nitrates dilate
normal as well as atherosclerotic
coronary arteries and increase coronary

ANTICOAGULANT DRUG
HEPARIN

collateral flow.
the ability of the blood to clot
(coagulation means clotting). This is
necessary if the blood clots too much, as
blood clots can block blood vessels and
lead to conditions such as a stroke or a
heart attack.