Running head: MYOCARDIAL INFARCTION 1

Evidence-Based Practice: Myocardial Infarction

Jennifer Barnett
University of South Florida

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Evidence Based Practice: Myocardial Infarction
When a sudden coronary obstruction occurs that is caused by thrombus formation over
ulcerated or ruptured atherosclerotic plaque, acute coronary syndromes result (Huether &
McCance, 2012). A myocardial infarction (MI) is an example of an acute coronary syndrome.
These take place when there is prolonged ischemia that causes irreversible damage to the
myocardium, the muscle of the heart. Myocardial infarctions are separated into two categories;
non ST elevation myocardial infarctions (non-STEMI) and ST elevation myocardial infarctions
(STEMIs). If the thrombus disintegrates before complete tissue necrosis occurs, then this
specific infarction will involve the myocardium only directly beneath the endocardium known as
a subendocardial MI (Huether & McCance, 2012). This type of infarction, a non-STEMI, will
usually result in ST segment depression, T wave inversion, and no Q waves. It is important for
these patients and those caring for them to recognize that recurrent clot formation of the
previously disrupted atherosclerotic plaque is likely.
Cellular injury occurs in the myocardium after 8 to 10 seconds of decreased blood flow
which in turn causes the affected area to become cooler (Huether & McCance, 2012). When the
flow has been disrupted, myocardial reserves are used up quickly, and anaerobic metabolism
begins as glycogen stores decrease. This process can only supply up to 65% to 70% of the total
myocardial energy required, and produces less adenosine triphosphate (ATP) than the aerobic
process can (Huether & McCance, 2012). A build up of lactic acid and hydrogen ions will then
take place which further compromises the myocardium. The decreased oxygenation of the heart
is also accompanied by electrolyte imbalances. Potassium, calcium, and magnesium are all lost
from the cells, and along with oxygen deprivation, contractility of the heart is affected,
diminishing its pumping ability. Catecholamines, which mediate the release of glucose,
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glycogen, and stored fat, are released by myocardial cells during ischemia (Huether & McCance,
2012). This can predispose an individual to dysrhythmias, heart failure, and cause grave
imbalances in the function of the
parasympathetic and sympathetic systems. Due to the release of catecholamines, plasma
concentrations of free fatty acids and glycerol rise one hour after the onset of the infarction
which can have a harmful effect on cell membranes (Huether & McCance, 2012). Blood glucose
levels rise because of the suppression of the beta cells in the pancreas and increase in
norepinephrine through the stimulation of skeletal muscle and liver cells. Hyperglycemia can be
detected about 72 hours after an acute MI, which can increase the risk of death, so close glucose
monitoring is extremely important (Huether & McCance, 2012). Angiotensin II is also released
during a MI. This results in peripheral vasoconstriction and fluid retention, increasing the
workload of the heart. Angiotensin II is a growth factor for certain cells of the heart that
consequently results in structural changes of the organ. The cardiac cells only allow for about 20
minutes of ischemia before irreversible damage and death of the tissue results (Huether &
McCance, 2012). When this point is reached, intracellular enzymes such as creatine
phosphokinase-myocardial band (CPK-MB) are released into the bloodstream where they can
then be detected by laboratory testing. These structural and functional changes caused by the MI
can be limited through rapid restoration of coronary flow and the use of angiotensin-converting
enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBS) and beta-blockers after the
infarct (Huether & McCance, 2012). For the purpose of this paper, I will be focusing on a
patient of mine who was diagnosed with a non-STEMI.
My patient, a 59 year old African American female, presented to the emergency room
with sub-sternal chest pain that was only relived with four nitroglycerins. She has a history of
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diabetes type II, lupus, and pulmonary embolism. Upon arrival to the hospital, her vital signs
were as follows; a temperature of 98.9, respiratory rate of 19, blood pressure 123/83, heart rate
87, pulse oximetry 96% on 2 liters nasal cannula, and a blood glucose level of 187. A blood test
was then performed to examine her cardiac enzymes. Her CPK-MB was 21.5 (normal range is
<3.8 for females), troponin 3.57 (normal <0.4), and brain natriuretic peptide (BNP) 422 (normal
0-100). She was diagnosed by the physician with a non-STEMI and was scheduled to go to the
cardiac catheterization lab the next morning.
All hospitals are required to have core measures for myocardial infarctions. My hospitals
core measures include; aspirin taken by the patient within 24 hours of arrival, a lipid panel done
during admission, completion of an echocardiogram to determine the patients ejection fraction,
if the ejection fraction reads <40% then the patient should be discharged on an ACE inhibitor or
ARB, smoking cessation education, discharge on a beta-blocker and aspirin, as well as a statin if
the low-density lipoprotein (LDL) level is >100. In many cases, the patient will have to undergo
a cardiac catheterization as well.
In a study done by Honeig, Aroney, and Scott they looked at early invasive (cardiac
catheterization) vs. conservative approaches (medications, stress tests, etc.) for treating patients
with unstable angina and non-STEMIs. In patients who underwent cardiac catheterizations, it
reduced the incidence of further chest pain and rehospitalizations as well as reduced the risk of
having a heart attack in the 3 to 5 years following the cardiac cath by 22% (Honeig, Aroney, &
Scott, 2010). The invasive strategy is not without risk though. This strategy is also associated
with a higher risk of procedure-related heart attacks and increased risk for bleeding (Honeig,
Aroney, & Scott, 2010). The researchers concluded that the invasive strategies may particularly
benefit those patients who are at high risk of recurrent problems, and those with a lower risk for
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recurrent events may benefit more from the conservative strategy (Honeig, Aroney, & Scott,
2010). Another group of researchers, Greenhalgh et al., studied the impact on drug-eluting stents
vs. bare metal stents for treating patients with acute coronary syndromes. After close observation
of over 14,500 patients, it was concluded that there was no statistically significant difference in
amount of deaths or recurrent MIs that took place after each type of stent was put in (Greenhalgh
et al., 2009).
The protocols and core measures that have been implemented for myocardial infarction
are essential to help keep our patients well. It is important for healthcare staff to be educated and
aware of the best and most up to date evidence based practice, to ensure our patients are having
the greatest outcomes possible. Following and keeping up with new research and techniques
associated with myocardial infarction will help us keep our patients healthy and educated so
hopefully this does not happen to them again in the future.


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References
Greenhalgh, J., Hockenhull, J., Rao, N., Dundar, Y., Dickson, R.C., & Bagust, A. (2009). Drug-
eluting stents versus bare metal stents for angina or acute coronary syndromes. Cochrane
Database of Systematic Reviews,5. DOI: 10.1002/14651858.CD004587.pub2.
Hoenig, M.R., Aroney, C.N., & Scott, I.A. (2010). Early invasive versus conservative strategies
for unstable angina and non-ST elevation myocardial infarction in the stent era. Cochrane
Database of Systematic Reviews, 3. DOI: 10.1002/14651858.CD004815.pub3.
Huether, E.S., & McCance, L.K. (2012). Understanding Pathophysiology. (5
th
ed.). St. Louis,
Missouri: Elsevier Mosby.