Explainations regarding question and answer
In regards to Q.2. you must link the signs and symptoms to the Pathophysiology.
� This means you need to research how it links to the symptom e.g. Chest pain.
� Why does that patient experience this?
� What is going on in the heart for them to experience this and must be supported by EBP
literature.
In regards to Q 3
”Describe two (2) common classes of drugs used for patients with the identified condition “
therefore any two classes of drugs not necessarily the ones mentioned in case study, you can use
any 2 classes of drugs related to patients conditions
Question 3 refers to your patient’s condition and why certain drug classes are used in the
treatment and what physiological effects the drug class have on the patient’s condition which
includes there mode of action.
In regards to Q 4
Identify and explain, in order of priority the nursing care strategies you, as the registered nurse,
should use within the first 24 hours post admission for this patient”. Therefore it has not stated
ED so it means in CCU the first 24 hours of admission to the hospital.
Causes of Myocardial Infarction
Research indicates that coronary artery disease is one of the most common causes of
myocardial infarction. This is a condition where by the coronary arteries harden and narrow due
to the buildup of atheromas or fatty plaques in the walls of the arteries a condition referred to
as atherosclerosis. The atheromas consist of platelets, cholesterol, and clots. Over time,
resistance of blood occurs in the vessels reducing blood flow or in severe cases causes when a
blood clot forms complete obstruction occurs. Sudden severe spasm or tightening of coronary
arteries can also cause myocardial infarction. This condition occurs regardless of whether the
coronary artery disease is present or not. Some of the documented causes of coronary spasms
include cigarette smoking, emotional stress, and exposure to extreme cold.
Risk Factors of Myocardial Infarction
The risk factors of myocardial infarction can be classified as modifiable risk factors and
non-modifiable risk factors. Some of the modifiable risk factors include age whereby men that
are over 45 year and women that are over 55 years are predisposed. Particular ethnicities such as
African-Caribbean and African, family history, and a history of angina and other cardiac diseases
are can also predispose an individual to develop myocardial infarction. Modifiable risk factors
include obesity, smoking, diabetes, hypertension, lack of physical activity, and
hypercholesterolemia.
Impact on Patient and Family
Myocardial Infarction (MI) makes patients to undergo extreme agony due to the
severe chest pain it causes. It also deteriorates the quality of life of the patient who may lose
weight due to the lack of appetite, nausea, and vomiting that are accompanied with this
condition. The family members of the patient are also affected because they are forced to change
their lifestyle and take on some of the patient’s duties. If a man who is the primary provider of
his family develops myocardial infarction, his wife may be forced to return to work and increase
her hours of working and spending limited time with her kids. Family members are also
required reschedule their plans and start making frequent hospital trips to visit the loved one in
case he/she is admitted.
Question 2
Patients suffering from myocardial infarction are likely to present with dyspnea.
Research indicates that dyspnea is related to the degree of reflex stimulation of the command
output in the central motor. It is also related to the intensity at which the activity of the
respiratory muscles is hindered by mechanical abnormality such as restriction or obstruction.
Myocardial infarction, weakens the pumping force of the cardiac muscles hence little blood
accesses the lungs for oxygenation. This elevates the partial pressure of CO 2 in the arteries
triggering the release of chemoreceptors which in turn cause intense reflex stimulation on
respiratory muscles causing dyspnea.
Angina pectoris is among the most common manifestation of myocardial infarction.
This is a condition that is characterized with pressure sensation in the chest or chest pain.
Occasionally, the pain radiates to the left shoulder or the jaw. This symptom arises when there
is an increase in resistance of blood flow in the epicardial arteries due to the development of
atherosclerotic plaques. The resistance causes cardiac muscles to develop ischemia prompting
the heart to react by sending pain signals.
Arrhythmias are also common presentation in patients with myocardial infarction. MI
causes ischemia which in turn initiates cardiac automaticity that develops multiple arrhythmias
both ventricular and atrial. The enhanced activity arises due to delayed after depolarization and
early after depolarization which triggers several spontaneous depolarizations that precipitate
arrhythmias in the ventricles.
During physical examination, patients with MI report of having fatigue. Myocardial
infarction is associated with an increase in sympathetic cardiac drive which arises due to the
release of sympathetic neurotransmitters such as noradrenaline and neuropeptide Y. An
increase in sympathetic activity causes utilization of essential glucose in the body hence the
patient cannot generate sufficient energy to perform physiological functions.
Sweating also occurs in patients with MI. This is as a result of over-activation of the
sympathetic nervous system, a body system that is in charge of the “fight” or “flight”
response. The pain sensation in myocardial infarction causes the release of hormones such as
adrenaline which trigger the sino atrial node and increase blood pressure consequently causing
sweating.
Treatment
Thrombolytic Agents
More heart tissue dies with each passing minute after myocardial infarction. One way
used to stop progression of cardiac damage is through restoration of blood flow as soon as
possible. This can be achieved through breaking down the formed blood clots. In myocardial
infarction, thrombolytic agents are administered to aid in dissolving of the thrombi (blood clots).
They do this through activation of plasminogen, a product that is cleaved to form another product
known as plasmin. Plasmin is a an enzyme that lyses proteins, and therefore, it has the capacity
of disintegrating cross-links between fibrin molecules that offer the primary structural integrity
of the thrombi. It is of great importance for clinicians to note that the efficacy of these
fibrinolytic agents relies on the age of the thrombi. This is because older clots have more cross-
link fibrin and are compacted hence they are quite difficult to lyse. In patients with acute
myocardial infarction, the plasminogen activators should be given within a period of less than 2
hours. However, beyond this duration the efficacy of the drugs diminishes prompt administration
of higher doses to attain the desired outcomes. Examples of fibrinolytic drugs include alteplase,
streptokinase, retaplase, urokinase, and tenecteplase,
Beta-Blockers
This is another important class of pharmaceutical agents that is prescribed to patients
with myocardial infarction. These drugs act by binding to the beta-adrenoceptors inhibiting the
binding of epinephrine and norepinephrine to these receptors hence inhibiting physiological
sympathetic activity that occurs through the receptors. In myocardial infarction, these agents
have anti-anginal activity due to their hypotensive and cardiodepressant effects. By reducing
contractility, heart rate, and arterial pressure beta antagonists reduce the heart’s work as well as
oxygen demand. This in turn improves the oxygen supply/demand ratio in the heart which
relieves the patient of anginal pain that arises due to low oxygen supply to the cardiac cells.
These agents also aid in inhibiting subsequent remodeling of the heart that has been shown to
increase mortality among patients with myocardial infarction.
In addition, beta blockers have been shown to possess antiarrhythmic properties. It has
been shown that activation of sympathetic activity increases automaticity of the sino atrial node.
It also increases the velocity of cardiac conduction and activates ectopic pace makers. These are
the effects that elicit cardiac arrhythmias. However, administration of beta blockers inhibits
sympathetic activity hence reducing the occurrence of cardiac arrhythmias.
Question 4
Normally, the mortality of myocardial infarction rises when treatment is delayed and
approximately half of patients die before hospitalization, within the first hour of onset of
symptoms. However, the prognosis of this condition improves tremendously whenever clinical
interventions are put in place. Some of the strategies a registered nurse should consider when
taking care of a patient with acute myocardial infarction include;
Management of acute pain
After admission, a nurse should monitor and document the pain characteristics. The
registered nurse should obtain a full description of the pain from the patient including the
intensity, location, characteristic, duration, and assist the patient in quantifying the pain by using
other experiences in comparing it. This is an essential strategy because pain is subjective and
clinicians should obtain proper description which provide a baseline for determine an effective
therapy. The nurse should also instruct the patient to report pain as soon as possible and offer the
patient with a quiet environment, comfort measures, and calm activities. In management of
angina, the patient should be advised to do relaxation techniques such as breathing deeply and
slowly, engaging in distractive behavior, guided imagery, and visualization. This will be
important since it will help in decreasing the perception and pain response. More importantly, the
health care provider should administer appropriate medication such as nitroglycerin to aid in
reducing angina pain.