ACUTE

CORONARY
SYNDROME
Prepared by:
Sahr Anne Pilar B. Parreno
 Acute Coronary Syndrome (ACS)

ACS is associated with deterioration of a once

stable atherosclerotic plaque.

ACS develops and encompasses the spectrum

of Unstable Angina (UA), non-ST-segment-
elevation myocardial infarction (NSTEMI), and
ST-segment-elevation myocardial infraction
(STEMI).
 Coronary Artery Disease

Chronic stable angina Acute Coronary Syndrome

• Unstable angina
ST- segment-
• Non-St-segment-
elevation MI
elevation MI
 Unstable Angina

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 manifestation of CAD. Unlike
chronic stable angina, UA is unpredictable and represents an emergency. The patient with previously
diagnosed chronic stable angina will describe a significant change in the pattern of angina. It will occur with
increasing frequency and is easily provoked by minimal or no exertion, during sleep, or even at rest. The
patient without previously diagnosed angina will describe anginal pain that has progressed rapidly in the last
few hours, days, or weeks, often culminating in pain at rest.
 A myocardial infarction (MI) occurs because of
sustained ischemia, causing irreversible myocardial cell
death. Eighty percent to 90% of all acute MIs are
secondary to thrombus formation.
01

Contractile function of the heart stops in the necrotic area(s).

02 The degree of altered function depends on the area of the heart
involved and the size of the infarction. Most MIs involve some
portion of the left ventricle.
 Clinical
Manifestations of
Myocardial
Infarction

PAIN
Severe, immobilizing chest pain not
relieved by rest, position change, or
nitrate administration is the hallmark Clinical
of an MI. Persistent and unlike any Manifestations of
other pain, it is usually described as a
heaviness, pressure, tightness, burning,
Myocardial
constriction, or crushing. Common Infarction
locations are substernal, retrosternal, or
epigastric areas. The pain may radiate
to the neck, jaw, and arms or to the
back
SYMPATHETIC NERVOUS SYSTEM
STIMULATION
Sympathetic Nervous System
Stimulation. During the initial phase
of MI, the ischemic myocardial cells
release catecholamines
(norepinephrine and epinephrine) that
are normally found in these cells. This
results in release of glycogen, dia-
Phoresis, and vasoconstriction of
peripheral blood vessels on Physical
examination, the patient's skin may be
ashen, clammy, and cool to touch.
CARDIOVASCULAR MANIFESTATIONS
In response to the release Of
catecholamines, BP and HR may
be elevated initially. Later, the BP
may drop because of decreased
cardiac output (CO). If fevere
enough, this may result in
decreased renal perfusion and
withe output.
NAUSEA AND VOMITING
The patient may be nauseated and
vomit. Nausea and vomiting can result
Clinical from reflex stimulation of the
Manifestations of vomiting center by the severe pain.
These symptoms can also result from
Myocardial
vasovagal reflexes initiated from the
Infarction area of the infarcted myocardium.
 Fever

The temperature may increase within the

first 24 hours up to 100.4° F (38° C).
The temperature elevation may last for
as long as 1 week. This increase in
temperature is a systemic manifestation
of the inflammatory process caused by
myocardial cell death.
HEALING PROCESS
Complications of
Myocardial
Infarction
 DYSRTHYTHMIAS HEART FAILURE

The most common complication after an Heart failure is a complication that

MI is dysrhythmias, which are present in occurs when the pumping power of the
80% of patients. Life-threatening heart has diminished. Depending on the
dysrhythmias occur most often with
Complications of
severity and extent of the injury, HF
anterior wall infarction, HE, or shock. Myocardial occurs initially with subtle signs such as
Complete heart block develops when key Infarction mild dyspnea, restlessness, agitation, or
portions of the conduction system are slight tachycardia.
infarcted. Life-threatening ventricular
dysrhythmias must be treated
immediately.
 CARDIOGENIC SHOCK
Cardiogenic shock occurs when oxygen
and nutrients supplied to the tissues are
inadequate because of severe left
Complications of
ventricular failure. Cardiogenic shock
occurs less often since the institution of Myocardial
early and rapid treatment of MI with PCI Infarction
and fibrinolytic therapy.
Papillary Muscle Dysfunction
Papillary muscle dysfunction causes
mitral valve regurgitation, which
increases the volume of blood in the left
atrium. This condition aggravates an
already compromised left ventricle by
reducing CO even further. Papillary
muscle rupture is a rare and life-
threatening complication causing massive
mitral valve regurgitation, which results
in dyspnea, pulmonary edema, and
decreased CO.

VENTRICULAR ANEURYSM
Ventricular aneurysm results when the
infarcted myocardial wall is thin and
bulges out during con-traction. The
Complications of
patient with a ventricular aneurysm may
experience HE, dysrhythmias, and Myocardial
angina. Besides ventricular rupture, Infarction
which is fatal, ventricular aneurysms
harbor thrombi that can lead to an
embolic stroke.
Pericarditis
Acute pericarditis, an inflammation of the
visceral and/or parietal pericardium, may
result in cardiac compression, decreased
ventricular filling and emptying, and HF.
It occurs 2 to 3 days after an acute MI as
a common complica. tion of the
infarction.
 Dressler Syndrome

Dressler syndrome is pericarditis with

effusion and fever that develops 4 to 6
weeks after MI. It mar also occur after
cardiac surgery. It is thought to be caused
by an antigen-antibody reaction to the
necrotic myocardium. The patient
experiences pericardial pain, fever, a
friction rub, pericardial effusion, and
arthralgia.
 DIAGNOSTIC
STUDIES ACUTE
CORONARY
SYNDROME
 ELECTROCARDIOGRAM FINDINGS Serum Cardiac Markers

The ECG is one of the primary tools to Certain proteins, called serum cardiac
rule out or confirm UA or an MI. markers, are released into the blood from
Diagnostic Studies necrotic heart muscle after an MI. These
markers, specifically serum cardiac
Acute Coronary
enzymes and troponin, are important in
Syndrome the diagnosis of MI.
 Coronary Angiography

The patient with UA or NSTEMI may

undergo coronary angiography to
evaluate the extent of the disease and to
determine the most appropriate
therapeutic modality.
COLLABORATIVE
CARE ACUTE
CORONARY
SYNDROME

Establish an IV route to provide an
access for emergency drug therapy.
Initiate oxygen by nasal cannula at a rate
of 2 to 4 L/min and ECG monitoring.
Sublingual NG and aspirin (chewable)
are given if they have not been given by
emergency medical personnel before
arrival at the ED. Morphine sulfate is
given IV for pain unrelieved by NIG.
Emergent PCI
Emergent PCI is the first line of treatment for patients
with confirmed MI.In this situation, the patient will
undergo a cardiac catheterization to locate the
blockage(s), assess the severity of the blockage(s),
determine the presence of collateral circulation, and
evaluate left ventricular function. The advantages of
COLLABORATIVE PCI include the following:
CARE ACUTE (1) it provides an alternative to surgical intervention;
(2) it is performed with local anesthesia;
CORONARY (3) the patient is ambulatory 24 hours after the
procedure;
SYNDROME (4) the length of hospital stay is approximately 1 to 3
days compared with the 4- to 6-day stay with CABG
surgery, thus reducing hospital costs; and
(5) the patient can return to work approximately 5 to 7
days after PCI instead of requiring a 6- to 8-week
convalescence after CABG.
Fibrinolytic Therapy

Treatment of MI with fibrinolytic therapy aims

to stop the infarction process by dissolving the
thrombus in the coronary artery and
reperfusing the myocardium.
 CORONARY SURGICAL
REVASCULARIZATION
Coronary revascularization with CABG
surgery is recommended for patients who
(1) fail medical management, (2) have left
main coronary artery or three-vessel
disease, (3) are not candidates for PCI
and the myocardium distal to the
(e.g., lesions are long or difficult to
access), (4) have failed PCI with ongoing
chest pain, or (5) have diabetes mellitus.
CORONARY ARTERY MINIMALLY INVASIVE
BYPASS GRAFT SURGERY. DIRECT CORONARY
ARTERY BYPASS.
Minimally invasive direct
CABG surgery consists of the coronary artery bypass
placement of new vessels to (MIDCAB is a technique that
offers patients requiring only one
transport blood between the
or two bypasses in one or two
aorta, or other major arteries,
coronary arteries located on the
anterior surface of the heart an
obstructed coronary artery (or approach to surgical treatment
arteries). that does not involve a
sternotomy and CPB.

OFF-PUMP CORONARY
ARTERY BYPASS.
The off-pump coronary artery bypass
(OPCAB) procedure uses full or partial
sternot. omy to enable access to all
coronary vessels. OPCAB is also
performed on a beating heart using
mechanical stabilizers and without CPB.
ROBOT ASSISTED
CARDIOTHORACIO SURGERY.
This technique incorporates the
use of a robot in performing
CABG or mitral valve
replacement.
TRANSMYOCARDIAL LASER
REVASCULARIZATION.
The procedure involves the use of
a high-energy laser that is
triggered electrocardiographically
to create channels between the
left ventricular cavity and the
coronary microcirculation
(ventriculocoronary
anastomoses).
 Drug Therapy
IV Nitroglycerin.

-IV NTG (Tridil) is used in the initial treatment of the patient with ACS. The goal of
therapy is to reduce anginal pain and improve coronary blood flow.

Morphine Sulfate.

-Morphine sulfate is the drug of choice for chest pain that is unrelieved by NTG.
As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen,
and consumption.

B- Adrenergic blockers
-It decreases myocardial oxygen demand by reducing HR, BP, and
contractility.
 Drug Therapy
Angiotensin-Converting Enzyme
Inhibitors.
-The use of ACE inhibitors can help prevent ventricular remodeling
and prevent or slow the progression of HE.

Antidysrhythmia Drugs.
-Dysrhythmias are the most common complications after an MI. In
general, they are self-limiting and are not treated aggressively unless
they are life threatening.

Cholesterol-Lowering Drugs.

-It decreases myocardial oxygen demand by reducingA fasting lipid panel is

obtained on all patients admitted with ACS. All patients with elevated
triglycerides and LDL cholesterol should receive cholesterol-lowering drugs.
Stool Softeners.

After an MI, the patient may be

predisposed to constipation because of
bed rest and opioid administration.
Stool softeners (e.g., docusate sodium
[Colace]) are given to facilitate and
promote the comfort of bowel
evacuation.
 TO BE
CONTINUED