ACUTE CORONARY SYNDROME

By Ns. Retno Setyawati, M.Kep.,

SpKMB
Coronary Anatomy: The Coronary Arteries 

 There are two main coronary arteries

which impact the circulation to the
heart: the right and the left. 
 The four coronary arteries are: left main
coronary artery (LCA), left anterior
descending (LAD) artery, left circumflex
(LCX) artery, and the right coronary
artery (RCA) 
Anatomy of the Coronary Arteries 
 Coronary arteries are made up of three distinct layers: the intima, media, and
adventitious layers. 
 The intima, the inner most lining of the artery, has a thin lining of endothelium
which contains epithelial cells. In a normal artery, blood flows smoothly through the
arterial walls. In ACS, the endothelium is damaged by plaque, microvascular
bleeding and clotting takes place and narrows the diameter of the coronary artery. 
 The media is made up of smooth
muscle and elastic connective
tissue which allows for dilation
and constriction of the vessel. 
 The adventitia is designed to
protect the vessel and connect
it to other vascular structures. 
Acute Coronary Syndrome (ACS)
is a term used as a working
diagnosis to cover a spectrum of
myocardial ischaemia, including
• ST-segment elevation
myocardial infarction (STEMI),
in which there is complete
blockage of a coronary artery,
and
• non-ST elevation myocardial
infarction (NSTEMI) and
unstable angina (UA), where a
partial blockage of the artery
occurs.
Based on the electrocardiogram (ECG), two groups of patients should be
differentiated:
 Patients with acute chest pain and persistent (>20 min) ST-
segment elevation.
 Most patients will ultimately develop ST-segment elevation
myocardial infarction (STEMI).
 The mainstay of treatment in these patients is immediate
reperfusion by primary Percutaneous Coronary Intervention
(PCI) or, if not available in a timely manner, by fibrinolytic
therapy.
 Patients with acute chest discomfort but no persistent ST-segment
elevation [non-ST-segment elevation ACS (NSTEACS)] exhibit ECG
changes that may include:
transient ST-segment elevation, persistent or transient ST-
segment depression, T-wave inversion, flat T waves, or
pseudonormalization of T waves; or the ECG may be normal.
ETIOLOGY

• Acute coronary syndrome (ACS) is caused primarily by

atherosclerosis. Most cases of ACS occur from disruption
of a previously nonsevere lesion (an atherosclerotic lesion
that was previously hemodynamically insignificant yet
vulnerable to rupture)
• Elevated demand can produce ACS in the presence of a
high-grade fixed coronary obstruction, due to increased
myocardial oxygen and nutrition requirements, such as
those resulting from exertion, emotional stress, or
physiologic stress (eg, from dehydration, blood loss,
hypotension, infection, thyrotoxicosis, or surgery)
 MANIFESTATIONS
• Palpitations
• Pain, which is usually described as pressure,
squeezing, or a burning sensation across the
precordium and may radiate to the neck,
shoulder, jaw, back, upper abdomen, or either
arm
• Exertional dyspnea that resolves with pain or
rest
• Diaphoresis from sympathetic discharge
• Nausea from vagal stimulation
• Decreased exercise tolerance
Physical findings can range from normal to any of
the following:
• Hypotension: Indicates ventricular dysfunction
due to myocardial ischemia, myocardial
infarction (MI), or acute valvular dysfunction
• Hypertension: May precipitate angina or reflect
elevated catecholamine levels due to anxiety or
to exogenous sympathomimetic stimulation
• Pulmonary edema and other signs of left heart
failure
• Extracardiac vascular disease
Physical findings…..Continue…..
• Jugular venous distention
• Cool, clammy skin and diaphoresis in patients
with cardiogenic shock
• A third heart sound (S3) and, frequently, a fourth
heart sound (S4)
• A systolic murmur related to dynamic
obstruction of the left ventricular outflow tract
• Rales on pulmonary examination (suggestive of
left ventricular dysfunction or mitral
regurgitation)
Potential complications
include the following:
• Ischemia: Pulmonary edema
• Myocardial infarction:
Rupture of the papillary
muscle, left ventricular free
wall, and ventricular septum
DIAGNOSIS

In the emergency setting, electrocardiography (ECG) is the most important

diagnostic test for angina. ECG changes that may be seen during anginal
episodes include the following:
 Transient ST-segment elevations
 Dynamic T-wave changes: Inversions, normalizations, or hyperacute
changes
 ST depressions: These may be junctional, downsloping, or horizontal
 DIAGNOSIS…Continue….
Laboratory studies that may be helpful
include the following:
 Creatine kinase isoenzyme MB (CK-MB)
levels
 Cardiac troponin I/T levels
 Myoglobin levels
 Complete blood count
 Basic metabolic panel
Diagnostic imaging modalities that may be
useful include the following:
 Chest radiography
 Echocardiography
 Myocardial perfusion imaging
 Cardiac angiography
 Computed tomography, including CT
coronary angiography and CT coronary
artery calcium scoring
MANAGEMENT
Initial therapy focuses on the following:
 Stabilizing the patient’s condition
 Relieving ischemic pain
 Providing antithrombotic therapy

Pharmacologic anti-ischemic therapy includes the following:

 Nitrates (for symptomatic relief)
 Beta blockers (eg, metoprolol): These are indicated in all patients
unless contraindicated
MANAGEMENT
Pharmacologic antithrombotic therapy (Adenosine diphosphate/ADH
receptor antagonists) includes the following:
 Aspirin
 Clopidogrel
 Prasugrel Adenosine diphosphate/ADH receptor antagonists
 Ticagrelor
 Glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban)

Pharmacologic anticoagulant therapy includes the following:

 Unfractionated heparin (UFH)
 Low-molecular-weight heparin (LMWH; dalteparin, nadroparin,
enoxaparin)
 Factor Xa inhibitors (rivaroxaban, fondaparinux)
MANAGEMENT
Additional therapeutic measures that may be indicated include the
following:
 Thrombolysis
 Percutaneous coronary intervention (preferred treatment for ST-elevation
MI)

Current guidelines for patients with moderate- or high-risk ACS include the
following:
 Early invasive approach (PCI/Percutaneous Coronary Intervention)
 Concomitant antithrombotic therapy, including aspirin and clopidogrel,
as well as UFH or LMWH
UNSTABLE ANGINA (UA)
is chest pain that is new in onset,
occurs at rest, or has a
worsening pattern.
 The patient with chronic stable
angina may develop UA, or UA
may be the first clinical sign of
CAD.
 It occurs with increasing
frequency and is easily
provoked by minimal or no
exertion, during sleep, or even
at rest.
Acute Myocardial Infarction
(AMI)
• cardiomyocyte necrosis in a
clinical setting consistent
with acute myocardial
ischaemia.
• is the irreversible death
(necrosis) of heart muscle
secondary to prolonged lack
of oxygen supply (ischemia).
A combination of criteria is required to meet the
diagnosis of AMI, namely the detection of an increase
and/or decrease of a cardiac biomarker, preferably
high-sensitivity cardiac troponin (hs-cTn) T or I, with at
least one value above the 99th percentile of the upper
reference limit and at least one of the following:
1) Symptoms of myocardial ischaemia.
2) New ischaemic ECG changes. New or presumed new
significant ST-segment-T wave (ST-T) changes or new left
bundle branch block (LBBB)
3) Development of pathological Q waves on ECG.
4) Imaging evidence of loss of viable myocardium or new
regional wall motion abnormality in a pattern consistent with
an ischaemic aetiology.
5) Intracoronary thrombus detected on angiography or autopsy.
If circulation to
the MIOCARDIAL INFARCTION
affected
myocardium is
not promptly
restored,
lead to
cardiogenic
shock and
loss of
death.
functional
myocardium
affects the
heart’s ability to
maintain an
effective
cardiac output.
RISK FACTORS

 Age, gender, heredity, race, smoking, obesity,

hyperlipidemia, hypertension, diabetes, sedentary
lifestyle, diet, and others.
 In general, about 50-85% of the risk of coronary
atherosclerosis is secondary to acquired conditions.
 The remainder is secondary to genetic polymorphisms,
which involve pathways of inflammation, lipid
metabolism, coagulation, the renin-angiotensin-
aldosterone system, and other components of
atherogenesis.
Types of MI
The Joint ESC/ACCF/AHA/WHF Task Force further classified MI into 5 types on the basis
of the underlying cause :

 Type 1 (spontaneous MI): Related to atherosclerotic plaque rupture,

ulceration, fissuring, erosion, or dissection with intraluminal thrombus
in one or more of the coronary arteries, leading to decreased
myocardial blood flow or distal platelet emboli and thereby resulting in
myocyte necrosis. The patient may or may not have underlying
obstructive coronary artery disease (CAD).

 Type 2 (MI secondary to an ischemic imbalance): MI consequent to

increased oxygen demand or a decreased supply (eg, coronary
endothelial dysfunction, coronary artery spasm, coronary artery
embolus, tachyarryhthmias/bradyarrhythmias, anemia, respiratory
failure, hypertension, or hypotension).
 Type 3 (MI resulting in death when biomarker values are unavailable): 
Sudden, unexpected cardiac death before blood samples for biomarkers could be
drawn or before their appearance in the circulation.

 Type 4a (MI related to percutaneous coronary intervention [PCI]): 

Elevation of biomarker values (cTn is preferred) to more than 5 times the
99th percentile of the URL in patients with normal baseline values (< 99th percentile
URL) or a rise of values over 20% if the baseline values are elevated but stable or
falling. In addition, any of the following are required:
(1) symptoms suggestive of myocardial ischemia;
(2) new ischemic ECG changes or new BBB;
(3) angiographic loss of patency of a major coronary artery or a side branch or
persistent slow flow or no flow or embolization; or
(4) demonstration of  the new loss of viable myocardium or new regional wall
motion abnormality by cardiac imaging.
 Type 4b (MI related to stent thrombosis): MI associated with stent
thrombosis as detected by coronary angiography or autopsy in the
setting of myocardial ischemia in combination with a rise and/or fall of
cardiac biomarkers with at least one value above the 99 th percentile
URL.

 Type 5 (MI related to coronary artery bypass grafting

[CABG]): Elevation of cardiac biomarker values more than 10 times the
99 th percentile URL in patients with normal baseline cTn values. In
addition, either
(1) new pathologic Q waves or new BBB,
(2) angiographic-documented new graft or native coronary artery
occlusion, or
(3) evidence of new loss of viable myocardium or new regional wall
motion abnormality by cardiac imaging is required.
SIGNS AND SYMPTOMS

Patients with typical MI may have the following

symptoms in the days or even weeks preceding the
event (although typical STEMI may occur suddenly,
without warning):
 Fatigue
 Chest discomfort
 Malaise
SIGNS AND SYMPTOMS

Typical chest pain in acute MI has the following

characteristics:
 Intense and unremitting for 30-60 minutes
 Substernal, and often radiates up to the neck, shoulder,
and jaw, and down the left arm
 Usually described as a substernal pressure sensation
that also may be characterized as squeezing, aching,
burning, or even sharp
 In some patients, the symptom is epigastric, with a
feeling of indigestion or of fullness and gas
CHEST PAIN PATTERN WITH MI
When considering the
clinical utility of cardiac
biomarkers for the early
diagnosis of MI, it is of
utmost importance to
interpret them only in the
appropriate clinical setting
of suspected MI and always
in conjunction with detailed
clinical assessment and
thorough interpretation of
the ECG.
DIAGNOSIS
• Creatine kinase is an important enzyme for cellular function found
principally in cardiac and skeletal muscle and the brain.
• CK-MB (also called MB-bands) is a subset of CK specific to cardiac
muscle. This isoenzyme of CK is considered the most sensitive
indicator of MI. Elevated CK alone is not specific for MI; elevated
CK-MB greater than 5% is considered a positive indicator of MI.  
• Cardiac muscle troponins, cardiac-specific troponin T (cTnT)  and
cardiac-specific troponin I (cTnI) , are proteins released during
myocardial infarction that are sensitive indicators of myocardial
damage.
• Myoglobin is one of the first cardiac markers to be detectable in
the blood after an MI. It is released within a few hours of symptom
onset.
DIAGNOSIS • Complete blood count (CBC) shows an elevated WBC count due to
inflammation of the injured myocardium.
• Erythrocyte Sedimentation Rate (ESR) also rises because of
inflammation.
• Arterial blood gases (ABGs) may be ordered to assess blood oxygen
levels and acid–base balance.
• The electrocardiogram  reflects changes in conduction due to
myocardial ischemia and necrosis. Classic ECG changes seen in AMI
include T-wave inversion, ST-segment elevation, and formation of a Q
wave. Ischemic changes in the heart are seen as depression of the ST
segment or inversion of the T wave
• Echocardiography is done to evaluate cardiac wall motion and left
ventricular function.
• Radionuclide imaging may be done to evaluate myocardial perfusion.
• Hemodynamic monitoring may be initiated when AMI significantly
affects cardiac output and hemodynamic status.
Electrocardiogram indicators of risk in patients with non-ST-segment elevation acute coronary syndrome.
ECG = electrocardiogram
Electrocardiogram indicators of risk in patients with non-ST-segment elevation acute coronary syndrome.
LAD = Left Anterior Descending
Electrocardiogram indicators of risk in patients with non-ST-segment elevation acute coronary syndrome.
LAD = Left Anterior Descending
MANAGEMENT

Prehospital care
For patients with chest pain, prehospital care includes the
following:
 Intravenous access, supplemental oxygen if SaO2 is less
than 90%, pulse oximetry
 Immediate administration of nonenteric-coated
chewable aspirin
 Nitroglycerin for active chest pain, given sublingually or
by spray
 Telemetry and prehospital ECG, if available
MANAGEMENT

Emergency department and inpatient care

 Initial stabilization of patients with suspected MI and ongoing
acute chest pain should include administration of sublingual
nitroglycerin if patients have no contraindications to it.
 The American Heart Association (AHA) recommends the
initiation of beta blockers to all patients with STEMI (unless beta
blockers are contraindicated).
 If STEMI is present and the patient is within 90 minutes of a
PCI-capable facility, the patient should undergo emergent
coronary angiography and primary PCI. If the patient is longer
than 120 minutes from a PCI-capable facility, fibrinolysis should
be considered.
MANAGEMENT

Emergency department and inpatient care

 Although patients presenting without ST-segment
elevation (non-STE-ACS) are not candidates for
immediate administration of thrombolytic agents, they
should receive anti-ischemic therapy and may be
candidates for PCI urgently or during admission.
 Coronary care units have reduced early mortality rates
from acute MI by approximately 50% by providing
immediate defibrillation and by facilitating the
implementation of beneficial interventions.
12 LEAD ECG
 As stated earlier, the 12-lead ECG
should be completed and interpreted
within the first 10 minutes. When the
patient is triaged in the field by
emergency medical services (EMS)
personnel, a 12-lead ECG should be
completed as soon as possible for those
patients having signs and symptoms of
ACS. 
 Any ST-segment depression or elevation
indicate some type of ischemia and
should be considered a “red flag.” 
12 LEAD ECG
 ST-segment depression shows a smaller
degree of blood supply deficit compared to
ST-segment elevation which encompasses a
larger ischemic area. In either ST-segment
depression or elevation requires immediate
medical evaluation. 
 Other changes in the ECG which signify
cardiac ischemia are T-wave inversions,
peaked positive T-waves, or Q waves. 
Case - Presentation ECG
Assessment and Diagnostic Findings
 The diagnosis of ACS is generally based on the presenting symptoms
(Chart 28-6) in above slide;
 the 12-lead ECG and laboratory tests (eg, serial cardiac biomarkers) are
performed to clarify whether the patient has unstable angina, NSTEMI,
or STEMI.
 The prognosis depends on the severity of coronary artery obstruction
and the presence and extent of myocardial damage. Physical
examination is always conducted, but the examination alone does not
confirm the diagnosis.

Patient History
The patient history includes the description of the presenting symptom
(eg, pain), the history of previous cardiac and other illnesses, and the
family history of heart disease. The history should also include information
about the patient’s risk factors for heart disease.
Assessments Post Heart Catheterization 
The nurse needs to:
 Assess the catheter insertion site, which may be a groin or wrist,
depending on the type of catheterization done.
 At the puncture site it is important to assess for tenderness, pain,
swelling, bleeding and new bruits. These signs and symptoms are
indicative of bleeding within the site that needs to be addressed quickly. 
Assessments of Peripheral Pulses 
A nurse should always assess peripheral pulses. There should always be a
pulse, even if a compression device is used. 

The peripheral leg or arm should appear blanchable and warm to the touch. 
Nursing Diagnoses
Based on the clinical manifestations, history, and diagnostic
assessment data, major nursing diagnoses may include:
 Ineffective cardiac tissue perfusion related to reduced
coronary blood flow
 Risk for imbalanced fluid volume
 Risk for ineffective peripheral tissue perfusion related to
decreased cardiac output from left ventricular dysfunction
 Death anxiety related to cardiac event
 Deficient knowledge about post-ACS self-care