d.

Synthesis of the Disease (client - based)

Acute Coronary Syndrome Non ST- Elevation Myocardial

Infarction

i. Definition of the disease

Acute coronary syndrome Non ST Elevation Myocardial Infarction

defined as a series of a transient coronary occlusion and reperfusion
leading to myocardial cellular injuries and the appearance of markers of
myocardial cellular injury. These transient coronary occlusions is brought
about by either as a result of an atherosclerotic plaque formation or plaque
rupture leading to clot formation which are not big enough to totally
occlude the artery (see figure 1 and 2), other reasons include coronary
vasoconstriction, progressive mechanical obstruction and secondary
unstable angina. (Vidya Banka, 2008)

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 normal response of the body, chemical mediators would be released thus
activating thrombosis promoting repair of the ruptured plaque wherein
endothelium would be replaced with fibrotic tissues which contributes to
narrowing of the artery and loss of its elasticity which may eventually
result in another episode of occlusion (figure 3). This transformation of an
atherosclerotic plaque to an unstable lesion follows the different stages in
platelet activation and aggregation. Rupture or ulceration of an
atherosclerotic plaque exposes the subendothelial matrix (primarily
composed of collagen and tissue factor) to circulating blood. This
particular event will result to platelet adhesion through the binding of
platelet glycoprotein (GP) Ib to von Willerbrand factor and GP VI binding
to collagen. Platelet activation ensues leading to a (1) change in shape of
the platelet (from smooth discoid to spiculated form) which increases the
surface area on which thrombin generation can occur, (2) degranulation of
the platelet alpha and dense granules, releasing thromboxane A2,
serotonin and other platelet aggregatory and chemoattractant agents; and
(3) increased expression of GP IIb/IIIa which enhances affinity to
fibrinogen. Lastly platelet aggregation takes place wherein fibrinogen
binds to activated platelet GP IIb/IIIa, creating a growing platelet
aggregate. This process continuously happening which decreases the
arterial lumen in the long run. In line with this, secondary hemostasis
happens wherein plasma coagulation system is activated. Tissue factor
will cause the activation of Factor X changing it to Factor Xa which leads
to formation of thrombin (factor IIa) which play a central role in arterial
thrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombin
powerfully stimulates platelet aggregation; and (3) it activates factor XIII
leading to cross ± linking and stabilization of fibrin clot. Thrombin
molecules will eventually incorporated to coronary thrombi forming the
nidus of rethrombosis.

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 ii. Risk Factors

Risk factors are characteristics or conditions that are statistically

associated with a high incidence of a disease. Incidences of Acute
Coronary Syndrome Non ST Elevation Myocardial Infarction are
influenced by the following:

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Age, Gender, Ethnicity ± the patient was 68 y/o, male and a pacific
islander which according to Braunwald, has an increased risk due
to the degenerative processes of the body.

Familial history± Mr. Dela Cruz¶ parents died of heart attack

predisposing him to an increased vulnerability to suffer from heart
diseases.

 
   

Elevated serum lipids ± The patient has elevated serum lipids prior
to admission and suffering from ACS NSTEMI as according to the
patient he is taking simvastatin as his maintenance drug.

Hypertension ± The patient was diagnosed of Hypertensive

Cardiovascular Disease 5 years ago. Hypertension increases the
risk of plaque rupture by exerting too much effort on the arterial
wall.

Sedentary lifestyle± The mechanism why physical inactivity

contribute to development of CAD and other cardiovascular disease

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 is unknown though literatures suggest that exercise increases HDL
levels, enhances fibrinolytic activity thus reducing clot formation.

Diabetes mellitus ±The patient was diagnosed of DM type 2 5 years

ago together with HCVD, he was then maintaining OHAs for his
DM. It is believed that patients with DM have an increased
tendency toward connective tissue degeneration and endothelial
dysfunction which is believed that this contributes to atheroma
development. Clients with DM tend to have alteration in lipid
metabolism thus increasing cholesterol and triglyceride levels.

Psychologic states ± Emotional stress stimulates SNS activity

increasing the Cardiac Workload, according to the patient he had a
small quarrel with his wife prior to the attack.

Increased consumption of Fatty, Sweet and salty foods ± increased

dietary sources of fats, and glucose further increases the glucose
and lipid level in the blood. On the other hand, an increased
amount of dietary sodium consumption contributes to elevated
blood pressure by increasing the osmolality of the blood thus
attracting more fluids to the intravascular spaces.

iii. Signs and symptoms

ACS NSTEMI presents the following signs and symptoms:

’ Pain in the chest which may radiate down the left arm or both arms
and/ or in the jaw is due to lactic acid accumulation in the
myocardium as a by- product of anaerobic respiration as a
compensatory mechanism of the body to the decreased perfusion
of the myocardium. This is often described as:
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 × a tightness
× indigestion like pain
× µlike someone sitting on my chest¶.

’ Pain may be accompanied by:

× Sweating ± pain is considered as a stressor and sweating is
induced by stress.

’ Elevated Troponin T and CK ± MB ± Troponin T and CK ± MB are

enzymes found inside the cells of the myocardium, when the
myocardium is damaged or injured, these enzymes are released in
the blood stream.

’ Crackles on lung examination ± this is brought about by pulmonary

congestion secondary to ineffective circulation of the blood going to
the aorta thus the blood goes back to the lungs causing congestion.

’ Hypertension initially followed by hypotension ± hypertension is

manifested as a compensatory mechanism of the body in attempt
to deliver blood among the major organs of the body to improve
perfusion. Eventually due to the increasing oxygen demand of the
heart muscles due to its increased workload, it will eventually slow
down causing hypotension.

’ ST segment deviation/depression ± ST segment deviation or

depression is associated with ischemia.

’ Tachycardia or dysrrhytmias ± tachycardia or dysrrhythmias are

compensatory mechanism of the body in attempt to pump the blood
to the systemic circulation.
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 ’ diminished left ventricular function ± the most affected part during
ischemic attack on the myocardium is the muscles on the left
ventricles as the left ventricles has the greater workload as to
compare with the right ventricle thus needing more oxygen. Due to
damage of the left ventricle, the function of the left ventricle is also
diminished.

’ Hyperglycemia- this is due to the increased glucose in the blood.

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