CASE STUDY 3
Introduction
Carl is a 54 year old man living with his wife and three children. The need for medical attention was first noticed when the patient suddenly became short of breath, pale and sweaty while he was playing with his children. When he as taken to the Royal Flying Doctor Service, the primary assessment suggested potential related cardiac (Myocardial Infarction).After he was referred to a metropolitan hospital, his past medical history was significant for coronary artery disease, hypertension, hyperlipidemia. Carl was also identified to be a heavy smoker and takes lot of alcohol. He also has a family history of parents who died from a possible cardiac related condition. At the critical care unit some of the significant examination and tests include, serial ECG’s, Troponin, Echocardiogram. The health care providers began on immediate management of the condition by administering Heparin 5000u S/C BD, Aspirin 300mg, Atorvastatin 80mg nocte and Metoprolol 50mg PO BD.
Critical Questions and Rationale
Critical questions
Some of the queries that need to be addressed in the case study include what is the connection between Carl’s lifestyle and potential myocardial infarction? Is there connection between his signs and symptoms and myocardial infarction? What was the relevance of conducting tests such as Troponin, serial ECG and Echocardiogram and finally was the relevance of administering Heparin, Aspirin, and Atorvastatin?
Rationale
The rationale for conduction the 12 lead ECG was to rule out the possibility of Acute Myocardial infarction. History about smoking was relevant since smoking causes about 36% of coronary artery disease. On the other hand the patient has been identified to be obese and researchers have identified that obesity accounts for about 20% of coronary heart diseases. The signs and symptoms of myocardial infarction are mostly gradual and rapid in onset. Angina pectoris in most common as a result of myocardial ischemia.
Review of Current and New Knowledge
Theoretical Principles
Myocardial infarction commonly presents as ischemic heart disease/coronary artery disease. In 2004World Health Organization estimated, that 12.2% of worldwide deaths occurred as a result off ischemic heart disease (World Health Organization 2008). With it being the leading cause of death in high or middle income countries and second only to lower respiratory infections in lower income countries. Myocardial infarction occurs when blood impedes flowing properly to various regions of the heart and the heart muscle is damaged due to lack of sufficient oxygen supply. Generally, this is due to one of the coronary arteries that supplies blood to the heart and caused a blockage as a result of unstable buildup of white blood cells, cholesterol and fat. The event is called “acute” if it is sudden and serious.
Cultural perspectives and Health behaviors
Some health behaviors and Cultural perspectives predispose individuals to heart related abnormalities. For instance, smoking leads to artherosclerosis that eventually causes heart diseases. Obesity, lack of exercise and emotional stress predisposes individuals to myocardial infarction. Family history of ischaemic heart disease or myocardial infarction predominantly if one has a first-degree relative (father, brother, mother, sister) who endured a ‘premature’ myocardial infarction
Pathophysiological process
Myocardial infarction is a subtype of acute coronary syndrome, that is non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which in most occasions (but not always) a manifestation of coronary artery disease (Moe et al ,2010).The most identified triggering event is the interruption of an atherosclerotic plaque in an epicedial coronary artery, which then forms a clotting cascade, at times causing complete occlusion of the artery. Atherosclerosis refers to the steady accumulation of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries, typically over decades (Woollard et al, 2010). Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a consequence of decades of progressing atherosclerosis. Plaques can turn out to be unbalanced, rupture, and additionally endorse a thrombus (blood clot) that occludes the artery; this can occur within a short while. When a rigorous enough plaque rupture occurs in the coronary vasculature, eventually causes myocardial infarction (necrosis of downstream myocardium).
When impaired blood flow to the heart lasts for a substantial amount of time, it prompts a process known as ischemic cascade; the heart cells in the region of the occluded coronary artery die mainly through necrosis and do not rejuvenate. A collagen scar forms in its place. Current studies have revealed that another form of cell death known as apoptosis also plays significant role in the process of tissue necrosis following to myocardial infarction (Krijnen,2009). Due to this fact, the patient’s heart becomes undyingly injured. The myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may eventually cause formation of a ventricular aneurysm that can rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more gradually than standard heart tissue. The disparity in conduction velocity between injured and uninjured tissue can prompt re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an exceptionally rapid and chaotic heart rhythm that is the leading cause of unexpected cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. On the other hand, ventricular tachycardia more often than not results in rapid heart rates that thwart the heart from pumping blood effectively. Cardiac output and blood pressure is likely to drop to precarious levels, which can cause further coronary ischemia and extension of the infarct(Jenkins et al, 2008)
New Knowledge
Research has shown that when patients are given stem cell treatment by coronary artery injections of stem cells obtained from their own bone marrow subsequent to a myocardial infarction (MI) demonstrate progress in left ventricular ejection fraction and end-diastolic volume not seen with placebo. The bigger the primaries size of the infarct, the larger the impact of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to ST elevation MI are proceeding (Schachinger et al, 2006).
Currently there are three biomaterial and tissue engineering advances for the treatment of post-Myocardial infarction conditions, but these are in an even earlier stage of medical research. However, numerous questions and concerns need to be addressed before they can be applied to patients. The firstly, the polymeric left ventricular restraints in the prevention of heart failure. The secondly, the uses of in vitro engineered cardiac tissue, which is afterward implanted vivo. And finally, injection of cells and/or a scaffold into the myocardium to create in situ engineered cardiac tissue (Christman & Lee ,2006)
Nursing Management Strategies
An MI call for instant medical attention. Treatment aims at salvaging as much myocardium as possible and to prevent additional complications, hence the phrase “time is muscle” (Jenkins et al, 2008 )Oxygen, aspirin, and nitroglycerin may be administered. The immediate concerns for a person with suspected myocardial infarction should aim at ensuring their safety and comfort. Intravenous access must be available for efficient administration of emergency drug therapy followed by swift relocation to areas with a high level of supervision and resuscitation facilities. Improving the comfort of the patient involves administration of oxygen, analgesia, anti-emetics and nitrates. An ECG should be arranged hurriedly. Assessment and treatment need to be quickly instituted: acute myocardial infarction is a medical emergency where a small amount of time can cause a difference. Development of the index case through stages of care pathway is necessary since a malignant ventricular arrhythmia is a chief and reversible cause of death in the early hours after the onset of infarction.
It’s important to conduct Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography in order to rule out diagnosis since the patient’s history, physical exam, ECG and cardiac biomarkers imply the likelihood of cardiac disorder. Moreover some of the nursing interventions that can be employed are cardiac defibrillators. This is a device that is explicitly designed to stop these potentially fatal arrhythmias. It works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect “rebooting” the heart. However, the therapy is time dependent, and the odds of triumphant defibrillation decline rapidly after the onset of cardiopulmonary arrest.
Conclusion
There are a number of risk factors related to myocardial infarction. These are such as previous history or a family history of cardiovascular diseases, old age, smoking, obesity and high amounts of cholesterol in the blood, kidney diseases. Therefore is best to attempt to stay fit so as to keep the likelihood of heart diseases minimized each moment. Morbidity and mortality from myocardial infarction are considerably decreased if patients and by standers identify symptoms early, stimulate the emergency medical service (EMS) system, and thereby cut down the time to definitive treatment. Trained pre-hospital personnel can offer life-saving interventions incase the patient develop cardiac arrest. The primary approach to improved survival is the availability of early defibrillation. Around 1 in every 300 patients with chest pain transported to the emergency department by private vehicle goes into cardiac arrest en route. A number of studies have established that patients with STEMI usually do not call 911; in one study, only 23% of patients with a confirmed coronary event used EMS.
The primary goal for healthcare professionals is to diagnose in the quickest manner whether the patient is having non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most recurrently (but not always) a demonstration of coronary artery disease since therapy vary between the 2 types of myocardial infarction. Specific considerations and distinctions involve the urgency of therapy and scale of proof concerning dissimilar pharmacological alternatives. As a general rule, original therapy for acute myocardial infarction is aimed towards restitution of perfusion as soon as probable to recover as much of the expose myocardium as possible. This may be accomplished through medical or mechanical means, such as PCI or CABG.
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