Acute

Coronary
Syndrome
Introduction Outline
Diagnostic
procedures
Definition

Pathophysiology Treatment and

and clinical prevention
manifestation

Nursing
process
 Introduction
Cardiovascular disease (CVD) is a group of
diseases that include both the heart and blood
vessels , thereby including coronary heart
disease (CHD) and coronary artery disease
(CAD), and acute coronary syndrome (ACS)
among several other conditions. Although
health professionals frequently use both terms
CAD and ACS interchangeably, as well as
CHD, they are not the same. ACS is a
subcategory of CAD
 Definition

Acute coronary syndrome (ACS) is an emergent situation

characterized by an acute onset of myocardial ischemia
that results in myocardial death (i.e., MI) if definitive
.interventions do not occur promptly

Although the terms coronary occlusion, heart attack, and

myocardial infarction are used synonymously, the
preferred term is myocardial infarction.) The spectrum of
ACS includes unstable angina, NSTEMI, and ST-segment
elevation myocardial infarction (STEMI)
epidemiology

AC
S

AL
LD
Pathophysiology
and clinical
manifestation
 Pathophysiology

In unstable angina, there is reduced blood flow in a coronary

artery, often due to the rupture of an atherosclerotic plaque. A
clot begins to form on top of the coronary lesion, but the artery is
not completely occluded. This is an acute situation that can result
in chest pain and other symptoms that may be referred to as pre
infarction angina because the patient will likely have an MI if
prompt interventions do not occur
In an MI, plaque rupture and subsequent thrombus formation result
in complete occlusion of the artery, leading to ischemia and necrosis
of the myocardium supplied by that artery. Vasospasm (sudden
constriction or narrowing) of a coronary artery, decreased oxygen
supply and increased demand for oxygen (from a rapid heart rate,
thyrotoxicosis, or ingestion of cocaine) are other causes of MI. In
each case, a profound imbalance exists between myocardial oxygen
supply and demand. The area of infarction develops over minutes to
hours. As the cells are deprived of oxygen, ischemia develops,
cellular injury occurs, and the lack of oxygen results in infarction, or
the death of cells.
The expression “time is muscle” reflects the urgency of
appropriate treatment to improve patient outcomes.
Approximately every 43 seconds, a patient will have an
MI and many of these people will die as a result. Early
recognition and treatment of patients presenting with an
MI will improve their chances of survival. Various
descriptions are used to further identify an MI: the type
(NSTEMI, STEMI), the location of the injury to the
ventricular wall (anterior, inferior, posterior, or lateral
wall), and the point in time within the process of
infarction (acute, evolving, or old).
The differentiation between NSTEMI and STEMI is
determined by diagnostic tests and is explained later in
this presentation. The 12-lead ECG identifies the type
and location of the MI, and other ECG indicators, such as
a Q wave and patient history, identify the timing.
Regardless of the location, the goals of medical therapy
are to relieve symptoms, prevent or minimize myocardial
tissue death, and prevent complications.
 Clinical Manifestations
Chest pain that occurs suddenly and continues despite
rest and medication is the presenting symptom in most
patients with ACS

indigestion, nausea,
.and anxiety
chest pain

shortness of breath

heart rate and respiratory rate may be

faster than normal cool, pale,
and moist
skin
• Chest pain occurs suddenly and continues despite rest and medication.
• Some patients have prodromal symptoms or a previous diagnosis of CAD
• Patients may present with a combination of symptoms, including chest pain,
shortness of breath, indigestion, nausea, and anxiety.
• Also, cool, pale, and moist skin. Increase HR & RR
• The signs and symptoms of MI cannot be distinguished from those of unstable
angina; hence, the evolution of the term acute coronary syndrome.
 -:Risk Factors

Non-modifiable Risk Factors: :Modifiable Risk Factors

Hyperlipidemia
Family history of CAD (first-degree relatives) Cigarette smoking, tobacco use
Increasing age (male>45, female>55) Hypertension
Diabetes
Gender (men are more) Metabolic syndrome (Insulin resistance, Central
Race (African American than Caucasian) obesity,..)
Obesity
Physical inactivity
 Assessment
and
Diggnostic finding
 Assessment and
Diggnostic finding

The diagnosis of ACS is generally based on the presenting symptoms

the 12-lead ECG and laboratory tests 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

(e.g., 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.
 Electrocardiogram
1) Unstable angina: The patient has clinical manifestations of coronary ischemia,
but cardiac biomarkers show no evidence of acute MI But show depression of
ST- segment, it’s a sign of ischemic

2) STEMI: The patient has ECG evidence of acute MI with characteristic changes
in two contiguous leads on a 12-lead ECG. In this type of MI, there is
significant damage to the myocardium.

3) NSTEMI: The patient has elevated cardiac biomarkers (e.g., troponin) but no
definite ECG evidence of acute MI. In this type of MI, there may be less
damage to the myocardium.
 Laboratory Tests

 Troponin:
• Both troponin T & I, are released and are highly specific to cardiac tissue.​
• Normal value:​
• 0.5- 2.3 mcg/l​
• Timing: ​
• Increase within a few hours (4-6) hours​
• Peaks within 10-24 hours of an infarct.​
• Lasts up to 10-14 days.​
 Laboratory Tests
 Creatine Kinase:
• Found in heart, skeletal muscle, & brain​

• CK-MB is the isoform found primarily in cardiac muscle​

• Normal values​

• - 4%-6% of total CK level.​

• Timing​

• Increase within a few hours (3-6) hours​

• Peaks within 12-24 hours of an infarct.​

• Lasts up to 12-48 hours

 Laboratory Tests

 Myoglobin ​:

• Is a heme protein that helps transport oxygen​

• Starts to increase within 1 to 3 hours​

• Within 12 hours after the onset of symptoms​

• An increase in myoglobin is not very specific in indicating an acute cardiac event​

• Normal value: M:15.2-91.2 mcg/l​

F: 11.1-57.5 mcg/l​
Assessing for Acute
Coronary Syndrome
Cardiovascular.
Chest pain or discomfort not relieved by rest or nitroglycerin; palpitations. Heart
sounds may include S3, S4, and new onset of a murmur.

Increased jugular venous distention may be seen if the myocardial

infarction (MI) has caused heart failure.

Blood pressure may be elevated because of sympathetic stimulation or

decreased because of decreased contractility, impending cardiogenic
shock, or medications

In addition to ST-segment and T-wave changes, the electrocardiogram

may show tachycardia, bradycardia, or other dysrhythmias.
Assessing for Acute
Coronary Syndrome
Respiratory
Shortness of breath, dyspnea, tachypnea, and crackles if
MI has caused
.pulmonary congestion. Pulmonary edema may be present

Genitourinary
Decreased urinary output may indicate cardiogenic shock

Neurologic
Anxiety, restlessness, and lightheadedness may indicate
increased sympathetic stimulation or a decrease in
contractility and cerebral oxygenation. The same
symptoms may also herald cardiogenic shock
Treatment
and
Prevention
Treatment Guidelines for
Acute Myocardial Infarction
• Use rapid transit to the hospital
• Insert two IV lines
• Obtain a 12-lead electrocardiogram to be read within 10 minutes
• Obtain laboratory blood specimens of cardiac biomarkers
• Obtain other diagnostics to clarify the diagnosis.
• Begin routine medical interventions: (Oxygen, Nitroglycerin,
Morphine, Aspirin, Beta-blocker, ACE inhibitors within 36 hours,
Anticoagulant, statin).
• Evaluate for indications for reperfusion therapy:
• Percutaneous coronary intervention
• Thrombolytic (fibrinolytic) therapy
• Continue therapy as indicated
 Morphine

Routine
medical
Oxygen

interventions
MONA

Nitroglycerin
 Pharmacologic Therapy​
 Nitroglycerin: vasodilator that improves blood flow to the heart muscle and
relieves pain (PO, IV).​

 Beta-Adrenergic Blocking Agents: reduce myocardial oxygen consumption by

blocking beta-adrenergic sympathetic stimulation to the heart (reduce H,
decrease BP, and reduce the myocardial contractility). ​
Metoprolol (Lopressor)​and Atenolol (Tenormin)​

 Calcium Channel Blocking Agents: decrease atrioventricular node conduction

(decrease HR, decrease the strength of myocardial contraction)​
Amlodipine (Norvasc)​and Diltiazem ​

 Antiplatelet and Anticoagulant Medications: to prevent platelet aggregation

and subsequent thrombosis.​
Aspirin​, Clopidogrel (Plavix)​and Prasugrel (Effient)​

 Anticoagulant: prevention of thrombus formation​

Heparin​and Low- molecular-weight heparin (Enoxaparin, Dalteparin) ​
Percutaneous Coronary Interventions

 Percutaneous Transluminal Coronary Angioplasty:

• The purpose of PTCA is to improve blood flow within a coronary
artery by compressing the atheroma.
• Angiography is performed using injected radiopaque contrast
agents.
• A balloon-tipped dilation catheter is passed through the sheath and
positioned over the lesion.
 Coronary Artery Stent:
• A stent is a metal mesh that provides structural support to a vessel
at risk of acute closure.
• Some stents are coated with medications to minimize the formation
of thrombi or scar tissue within the coronary artery lesion.
Surgical Procedures: Coronary Artery
Revascularization

 Coronary artery bypass graft (CABG): is a surgical procedure in which a

blood vessel is grafted to an occluded coronary artery so that blood can
flow beyond the occlusion; it is also called a bypass graft.
• CABG is performed less frequently in women.
• The coronary arteries to be bypassed must have at least a 70% occlusion, or
at least a 50% occlusion if in the left main coronary artery.
• Arterial grafts are preferred to venous grafts because they do not develop
atherosclerotic changes as quickly and remain patent longer.
• A vein commonly used for CABG is the greater saphenous vein, followed
by the lesser saphenous vein.
• Lower extremity edema continues to be a common adverse effect of vein
removal.
• The degree of edema varies and usually diminishes over time.
 Prevention
1. Controlling Cholesterol Abnormalities:​

• LDL cholesterol less than 100 mg/dL (less than 70 mg/dL for very high-risk patients)​.

• Total cholesterol less than 200 mg/dL ​.

• HDL cholesterol greater than 40 mg/dL for males and greater than 50 mg/dL for females. (it transports other
lipoproteins such as LDL to the liver). a high HDL level is a strong negative risk factor for heart disease (i.e., it
protects against heart disease).​

• Triglyceride less than 150 mg/dL​.

​
 Prevention
2. Dietary Measures​.

3. Physical Activity​.

4. Medications​.

5. Promoting Cessation of Tobacco Use.​

6. Managing Hypertension​.

7. Controlling Diabetes​.

​
Nursing process
1) Acute Pain related to increased myocardial oxygen demand and
decreased myocardial oxygen supply​

Possibly evidenced by:

 Reports of chest pain with/without radiation
 Facial grimacing
 Restlessness, changes in the level of consciousness
 Changes in pulse, BP

Outcomes#
Verbalize relief/control of chest pain within appropriate
time frame for administered medications.
Display reduced tension, relaxed manner, ease of
movement.
Nursing Interventions
​

 Balancing myocardial oxygen supply with demand​​

 administering medications as described​​

​
 evaluating the patient’s response to therapy​​

 Oxygen should be given along with medication therapy (2-4 L/min)​​

 Vital signs are assessed frequently​​

 Physical rest in bed with the head of the bed elevated​

2) Activity intolerance related to Imbalance between myocardial
oxygen supply and demand
Possibly evidenced by:
 Alterations in heart rate and BP with activity
 Development of dysrhythmias
 Changes in skin color/moisture

Demonstrate measurable/progressive increase in tolerance for

activity with heart rate/rhythm and BP within patient’s normal
limits and skin warm, pink, dry.
Report absence of angina with activity.
Nursing Interventions
 Document heart rate and rhythm and changes in BP before,
during, and after activity. Correlate with reports of chest pain
or shortness of breath.

 Instruct patient to avoid increasing abdominal

pressure (straining during defecation).

 Explain the pattern of graded increase of activity

level: getting up to commode or sitting in a chair,
progressive ambulation, and resting after meals.

 Review signs and symptoms reflecting intolerance of

present activity level or requiring notification of nurse
or physician.

 Refer to cardiac rehabilitation program.

3) Risk for Decreased Cardiac Output Risk factors may include ‘
 Changes in rate, rhythm, electrical conduction
 Reduced preload/increased SVR
 Infarcted/dyskinetic muscle, structural defects, e.g., ventricular aneurysm, septal defects

Maintain hemodynamic stability, e.g., BP, cardiac output within normal range,
adequate urinary output, decreased frequency/absence of dysrhythmias.
Report decreased episodes of dyspnea, angina.
Demonstrate an increase in activity tolerance.
Nursing Interventions
 Auscultate BP. Compare both arms and obtain lying,
sitting, and standing pressures when able.
 Evaluate the quality of pulses on both pulse points.

 Note development of S3

 Auscultate breath sounds.

 Monitor heart rate and rhythm. Document

dysrhythmias via telemetry.

 Note the response to activity and promote rest

appropriately.
 Monitor laboratory data: cardiac enzymes, ABGs,
electrolytes.
 Provide small and easily digested meals. Limit
caffeine intake and caffeine-containing products.
COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS​:
 Acute pulmonary edema.
 ​Heart failure ​.
 Cardiogenic shock.
 ​Dysrhythmias and cardiac arrest ​Pericardial effusion
and cardiac tamponade.
 Promoting Health After Acute Coronary
Syndromes

Adaptation to an ACS is an ongoing process and usually requires some modification of lifestyle.
Educate patients to make the following specific modifications:

• Avoid any activity that produces chest pain, extreme dyspnea, or undue fatigue.
• Avoid extremes of heat and cold and walk against the wind.
• Lose weight, if indicated.
• Stop smoking and the use of tobacco; avoid secondhand smoke.
• Develop heart-healthy eating patterns, avoid large meals, and Hurry while eating.
• Modify meals to align with the Therapeutic Lifestyle Changes (TLC) Or other recommended diets.
• Adhere to a medical regimen, especially in taking medications.
• Follow recommendations that ensure that blood pressure and blood glucose are in control.
• Pursue activities that relieve and reduce stress.
 References
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