Myocardial Infarction: Case Study

Myocardial Infarction
Myocardial Infarction

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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. 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, age and sex (Wong et al., 2013). Statistics indicate higher prevalence among older persons, with more than 3,800 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 (Heart Foundation, 2014).

Studies indicate that risk factors for MI are those that also increase people’s susceptibility to atherosclerosis. 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. 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.  

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5 Common Signs and Symptoms of MI

Signs and symptoms of MIUnderlying 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.
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.
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.
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 in turn reduces the pulmonary volume, and hence causes difficulties in breathing.
Increased perspiration (Heart Foundation, 2015a)Diaphoresis that characterizes MI is due to the activation of the 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.

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). Drugs in the same class often work in the same mechanism in MI treatment.


The pharmacodynamics of these drugs in treating MI includes causing vascular dilation, hence reducing the myocardial afterload (Clauss et al., 2015). So as to attain optimal effectiveness, treatment is initiated with a low dose of an ACEI that has a short half-life (Song et al., 2015). 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.

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. 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. 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.

Oxygen Therapy

The registered nurse should ensure that Mr. Savea receives oxygen therapy so as to avert arterial hypoxaemia that could occur within 24 hours of admission (Martin et al., 2014). The strategy would also facilitate the use of medications such as opioid analgesics whose use could cause hypoxia. 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. 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.


The nurse should 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. The patient may take the drug at a low dose on a daily basis if he can tolerate it. Thrombolytic agents may also be used for the protection of the myocardium. Streptokinase is an example of an intervention that is thrombolytic and applicable in the management of MI (Heart Foundation, 2015b). 


Atrial Fibrillation Association Australia. (2014). Beta blockers. Retrieved from

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 cAMP phosphodiesterase activities. Fundamental & Clinical Pharmacology, 29(4), 322-361.

Department of Health and Human Services. (2012). About medicines of nausea and vomiting. Retrieved from

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. Retrieved from

Heart Foundation. (2015). Australian acute coronary syndromes capability. Retrieved from

Heart Foundation. (2015a). Will you recognize your heart attack? Retrieved from

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. Retrieved from

Scot, I. (2010). Up the dose of beta blockers after MI. Medical Journal of Australia, 2010(160), 435-442.

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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