Myocardial infarction

Myocardial infarction with history of stable angina and mitral valve stenosis
Mr Tupa Savea is a 54 year old male who has been transferred to the coronary care unit (CCU)
from the emergency department for management of episodic chest pain. He has a history of
stable angina and mitral valve stenosis. Mr Savea is of Samoan background and has lived in
regional Queensland for the last 20 years with his wife and children. He was brought in by
ambulance having had chest pain and shortness of breath. He reports having similar symptoms
on and off for the past two months but did not visit his GP as he assumed the discomfort was due
to indigestion. Mr Savea is an ex-smoker, tobacco free for the last six months and a social
drinker (approx. 10 units/week). He works full-time as an orderly at a local hospital and is active
in the Samoan support community.
On assessment Mr Savea’s vital signs are: PR 90 bpm and irregular; RR 12 bpm; BP
150/100mmHg; Temp 36.9’C; SpO2 98% on oxygen 8L/min via Hudson mask. He has a body
mass index (BMI) of 35 kg/m2 indicating clinical obesity. Blood test results show elevated
cardiac enzymes and troponin levels and cholesterol level of 8.9mmol/L. His ECG indicates that
he has a ST segment elevated myocardial infarction. Mr Savea was administered sublingual
glyceryl trinitrate followed by morphine 2.5 mg IV for pain in the emergency department. He
reports being pain free on admission to CCU.
Questions to be answered
** The following questions must be answered for your chosen case study **
The following questions relates to the patient within the first 24 hours since admission to the
emergency department (ED):

  1. Outline the causes, incidence and risk factors of the identified condition and how it can impact
    on the patient and family (400 words)
  2. List five (5) common signs and symptoms of the identified condition; for each provide a link
    to the underlying pathophysiology (350 words)
    a. This can be done in the form of a table – each point needs to be appropriately referenced
  3. Describe two (2) common classes of drugs used for patients with the identified condition
    including physiological effect of each class on the body (350 words)
    a. This does not mean specific drugs but rather the class that these drugs belong to.
  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 (500 words).

Myocardial Infarction: Case Study

Causes, Incidence, and Risk Factors for Myocardial Infarction
Myocardial infarction (MI) is an impairment of heart functioning characterized by
diminished blood supply to cardiac muscles following myocardial ischemia (Wong et al., 2012).
Myocardial cells are destroyed but not repaired as the rate of their degeneration exceeds the
capacity of repair mechanisms which are usually slowed by poor blood supply (Burges, 2012).
The causes of MI include myocardial ischemia that results when metabolic needs of the heart are
too high and exceeding a certain threshold or ischemia that results after the coronary circulation
is inefficient and affecting oxygen and nutrient delivery to heart muscles (Wong et al., 2012). In
some cases, the two causes may co-occur and eventually result in MI.
The prevalence of MI in Australia is significantly high with data indicating a correlation
between disease occurrence and age and sex(Wong et al., 2013).The Heart Foundation reported
that in Australia, the disease has higher prevalence among older persons, with more than 3,800

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cases of male patients 85 years and above having been reported in 2011. On the other hand,
about 11 cases of female patients of ages between 25 and 34 were recorded on the same year.
Nevertheless, MI prevalence in Australia was reported to have been decreasing between the
years 2007 and 2011 (2014).
Studies indicate that risk factors for MI are those that also increase people’s susceptibility
to atherosclerosis (Wong et al., 2012). These include tobacco use, being of the male gender, a
positive family history for the condition, and pre-occurring conditions such as diabetes mellitus
(DM), hypertension, and hyperlipidemia (Gehani et al., 2015). The risk of MI is highest in
persons with multiple predisposing factors.
In the case of Mr. Savea, several factors could have predisposed him to MI. These
include his history of tobacco use, being clinically obese, having high blood pressure, being at a
considerably advanced age, and of course being a male. Research links components of tobacco to
damage of blood vessels hence increasing the risk of atherosclerosis and MI (Wong et al., 2012).
Obesity is also linked to diabetes and hyperlipidemia, both which are risk factors for MI (Gehani
et al., 2015). Age and gender are unavoidable risk factors for MI.Since MI prevalence has been
linked to genetics, Mr. Savea’s family may also be susceptible to the disease. As Gehani et al.
(2015) wrote, people whose family members have been victims of MI stand elevated chances of
getting the condition.

5 Common Signs and Symptoms of MI

Signs and symptoms of MI Underlying pathophysiology
Chest pain likened to a
sensation of squeezing
caused by application of
pressure at the mid-thorax
(Haasenritter et al., 2012)

Caused by hypoxia and ischemia result in MI. Impaired cardiac
function also contributes to pain as muscles in other body parts
do not get sufficient supply of oxygen and nutrients hence
becoming weak and unable to contract and relax normally.
Reduced cardiac output also contributes to dyspnea hence
causing the squeezed sensation (Heart Foundation, 2015a).

Loss of consciousness (Heart
Foundation, 2015a)

Patients of MI may become unconscious due to poor blood
supply to the brain as manifested in the disease. The occurrence
results from cardiogenic shock whereby the heart is unable to
pump blood efficiently since cardiac muscles are damaged
(McSweeney et al., 2010).

Tachycardia and
hypertension (McSweeney et
al., 2010)

Patients with MI often present with tachycardia and
hypertension. The phenomena are linked to anxiety and pain that
patient experience when they get other symptoms of the disease.
The anxiety and pain stimulates the sympathetic system hence
causing cardiac activation and vascular constriction. As a result,
patients develop hypertension and tachycardia as secondary
manifestations (McSweeney et al., 2010).

Shortness of breath and
dyspnea (Heart Foundation,
2015a)

The symptom is associated with the damage and impairment of
heart muscles that occur in MI. The functioning of the left
ventricle is affected hence reducing its pumping ability.
Consequently, ventricular failure precedes pulmonary edema.
Accumulation of fluid in the lungs inturn reduces the pulmonary
volume, and hence causes difficulties in breathing (Heart
Foundation, 2015a).

Increased perspiration (Heart Diaphoresis that characterizes MI is due to the activation of the

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Foundation, 2015a) sympathetic pathway. Usually, the pathway is activated as a
counter mechanism for the maintenance of arterial pressure
which is usually high in patients with MI. The activation of the
pathway is a compensatory mechanism effected via baroreceptor
response following decreased cardiac output (Haasenritter et al.,
2012).
Pharmacological Treatment of MI

Several classes of drugs have been approved for the treatment of MI in Australia. These
include beta blockers and angiotensin converting enzyme inhibitors (ACEIs) (National
Prescribing Service, 2010). Drugs in the same class often work in a similar mechanism in MI
treatment.
ACEIs
The pharmacodynamics of these drugs in treating MI includes causing vascular dilation
hence reducing the myocardial afterload (Clauss et al., 2015). Song et al. reported that so as to
attain optimal effectiveness, treatment is initiated with a low dose of an ACEI that has a short
half-life. The dose is then titrated upwards until a stable maintenance dose is achieved within 24
to 48 hours. The short-acting agent may then be continued at the maintenance dose or replaced
with a longer-acting agent (2015). Angiotensin receptor blockers (ARB) may be co-administered
with ACEIs if the patient is intolerant to the latter (Gadzhanova et al., 2016). ACEIs are
recommended for diabetic and hypertensive patients while contraindicated for those with low
blood pressure or patients of kidney failure (Blood Pressure Lowering Treatment Trialists’
Collaboration, 2014). Some of the commonest ACEIs used in the management of MI include
captopril, lisinopril, and ramipril (Monroy et al., 2014). Patient data collected in Mr. Savea’s
case suggest high applicability of ACEIs.
Beta Blockers
The physiological effects of beta blockers include decreasing the force and rate of
myocardial contraction and subsequent reduction of oxygen demand in cardiac muscles (Atrial
Fibrillation Association Australia, 2014). The medication should be administered the earliest
possible after the onset of symptoms, preferably within the first 12 hours of diagnosis (Scot,
2010). Early treatment with beta blockers does not only reduce the incidence of re-infarction,
recurrent ischemia, and ventricular arrhythmias, but it also decreases the size of the infarct and
so the chances of short-term death (Scot, 2010). The medications are particularly essential when
the disease condition is characterized by poor oxygen supply owing to the drugs’ effects on
reducing oxygen demand in the myocardia (Burges, 2012). Common beta blockers used in MI
management include carvedilol, atenolol, and metoprolol (Martin et al., 2014). The drugs are
also associated with hypotensive effects, and therefore, their use is safe in the case of Mr. Savea.

Post-Admission Nursing Care Strategies for Mr. Savea

Nursing care for the presented patient should prioritize on patient comfort and safety
(Martin et al., 2014). Measures that should be taken to ensure safety for the patient include
facilitating the accessibility of intravenous drug therapy services (Branson &Johannigman,
2013). Safety should also be promoted by ensuring that the patient has the access of resuscitation
facilities, and he can be easily monitored and supervised.On the other hand, measures to increase
the comfort of the patient include early administration of oxygen therapy, pain relievers,
vasodilators, and anti-emetic medications(Branson &Johannigman, 2013).
Oxygen Therapy

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MYOCARDIAL INFARCTION
The registered nurse should ensure that Mr. Savea receives oxygen therapy so as to avert
arterial hypoxaemia that could occur within 24 hours of admissions Martin et al. (2014) warned.
The strategy would also facilitate the applicability of medications such as opioid analgesics
whose use could cause hypoxia (Martin et al., 2014). Research also indicates that administration
of oxygen to patients of MI would counter the development of infarcts hence reducing the
possibility of short-term mortality, and subsequently increasing survival chances for the victims
(Burgess, 2012).
Pain and Emesis Management
Mr. Savea presents with severe chest and abdominal pain, and therefore, the registered
nurse should prioritize on relieving the pain. Opioids such as diamorphine would be applicable in
analgesia as they are considerably highly potent (Haasenritter et al., 2012). However, such drugs
could induce emesis, and it would be necessary to counter the side effect using anti-emetic
agents. Such drugs include metoclopramide and cyclizine (Department of Health and Human
Services, 2012). The hypoxaemic effects of opioid analgesics should be countered by the use of
oxygen therapy (Burges, 2012).
Venodilation
The nurse should also prioritize on increasing blood flow to the heart by using
vasodilators. Nitrates would be an applicable class of drugs as they would reduce myocardial
oxygen demand by decreasing both the preload as well as the afterload (Branson &Johannigman,
2013). By promoting cardiac blood flow, the drugs would also help in reducing pain associated
with ischemia (National Prescribing Service, 2010).
Administration of Anti-Clotting Agents
After stabilizing the patient, the nurse should proceed with long-term measures to protect
the victim’s myocardia. The approach involves re-canalizing the affected blood vessels so as to
promote cardiac function (National Prescribing Service, 2010). Drugs that may be used for this
case include aspirin (Heart Foundation, 2014). The patient should take the drug at a low dose on
a daily basis if he can tolerate it. The Heart Foundation advised that thrombolytic agents may
also be used for the protection of the myocardium. The agency illustrated that streptokinase is an
example of an intervention that is thrombolytic and applicable in the management of MI (2015b).

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References

Atrial Fibrillation Association Australia. (2014). Beta blockers.
Blood Pressure Lowering Treatment Trialists’ Collaboration. (2014). Effects of blood pressure
lowering on cardiovascular risk according to baseline body-mass index: a meta-analysis
of randomised trials. The Lancet, 385(9571), 867-874.
Branson, R. D., &Johannigman, J. A. (2013).Pre-hospital oxygen therapy. Respiratory Care,
58(1), 86-97.
Burgess, S. (2012). Oxygen therapy for myocardial infarction. Australian Journal of
Paramedicine, 8(2), 1-3.
Clauss, F., Charloux, A., Piquard, F., Doutreleau, S., Talha, S., Zoll, J., & Geny, B.
(2015).Angiotensin-converting enzyme inhibition prevents myocardial infarction-induced
increase in renal cortical cGMP and cAMPphosphodiesterase activities. Fundamental &
Clinical Pharmacology, 29(4), 322-361.
Department of Health and Human Services. (2012). About medicines of nausea and vomiting.

Gadzhanova, S., Roughead, S., & Bartlett, L. (2016).Long-term persistence to mono and
combination therapies with angiotensin converting enzymes and angiotensin II receptor
blockers in Australia.European Journal of Clinical Pharmacology, 2016(1), 1-7.
Gehani, A., Hinai, A, Zubaid, M., Almahmeed, W., Hasani, M., Yusufali, A., & … Yusuf, S.
(2015). Association of risk factors with acute myocardial infarction in Middle Eastern
countries: the INTERHEART Middle East study. Preventive Cardiology, 21(4), 400-410.
Haasenritter, J., Stanze, D., Widera, G., Wilimzig, C., Abu Hani, M., Sönnichsen, A. C., Donner-
Banzhoff, N. (2012). Does the patient with chest pain have a coronary heart disease?
Diagnostic value of single symptoms and signs – a meta-analysis.Croatian Medical
Journal, 53(5), 432–441.
Heart Foundation. (2014). Australian Heart Disease Statistics.
Heart Foundation. (2015). Australian acute coronary syndromes capability.

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Heart Foundation. (2015a). Will you recognize your heart attack?
Martin, L., Murphy, M., Scanlon, A., Naismith, C., Clark, D., & Faraoukwe, O. (2014).Timely
treatment for acute myocardial infarction and health outcomes: An integrative review of
the literature. Australian Critical Care, 27(3), 111-118.
McSweeney, J. C., Cleves, M. A., Zhao, W., Lefler, L. L., & Yang, S. (2010). Cluster Analysis
of Women’s Prodromal and Acute Myocardial Infarction Symptoms by Race and Other
Characteristics. The Journal of Cardiovascular Nursing, 25(4), 311–322.
Monroy, F., Ferrario, C. M., Hernandez, C., & Martinez, L. (2014).Comparative Effects of a
Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma
Angiotensins after Myocardial Infarction.Pharmacology, 94(2), 21-28.
National Prescribing Service. (2010). Ischemic heart disease.
Song, P. S., Seol, S., Seo, G., Kim, D., Kim, K., Yang, J. &. . . Kim, D. (2015). Comparative
study of angiotensin 2 receptor blockers.Journal of Cardiovascular Drugs, 12(4), 43-54.
Wong, C. X., Sun, M. T., Lau, D. H., Brooks, A. G., Sulivan, T., Worthley, I. M., & Sanders, P.
(2013).Nationwide Trends in the Incidence of Acute Myocardial Infarction in Australia,
1993–2010. AJC, 112(2), 169-173.
Wong, C., Brooks, A., Leong, D., Thompson, K., & Sanders, P. (2012). The Increasing Burden
of Atrial Fibrillation Compared With Heart Failure and Myocardial Infarction: A 15-Year
Study of All Hospitalizations in Australia. Arch Intern Med, 172(9), 739-742.

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