Myocardial Infarction Process and Nursing Priorities - Assignment Example

Complex Care Assignment Question 1 Angina pectoris (or simply Angina) is a medical condition brought about by decreased supply of blood to the heart because of the reduced size of coronary arteries supplying blood to the heart. It is a major sign of coronary artery disease presented as acute chest pain. MI is caused by arteries through blood clot thereby inhibiting blood from getting to a certain muscle of the heart (Mommersteeg et al., 2013). There are numerous similarities in the presentation of both Angina and myocardial infarction. Angina and MI share symptoms (Mommersteeg et al., 2013). This makes diagnosis between the two a bit challenging since on can be mistaken for the other. When diagnosing for either angina pectoris or myocardial infarction, several questions must be asked to determine which of the two the patient is suffering from. These questions include; 1. How is the feeling; is it a sharp stabbing pain, is it tightness or pressure on the chest? 2. When was the first time you had such a feeling? 3. Was there anything that could have stimulated the pain? 4. Is the pain from a specific area or its general? 5. What duration can an attack take, few seconds, few minutes or more than five minutes? 6. How does the pain come, does it commence slowly or it comes all at once? 7. Is the pain accompanied by other symptoms such as nausea, numbness or even tingling? 8. Do you feel like the pain is spreading out to the neck or jaws? 9. Which activities worsen the situation such as sudden movements of the body, physical activities like exercising or even breathing? 10. Do you experience discomfort and pain when swallowing? 11. What undertaking eases the pain such as resting, taking deep breathes or just sitting up? 12. Is there a family history of heart diseases or personal predisposition when it comes to cardiac related illness? 13. Have you ever smoked cigarettes or exposed to secondary smoking? 14. Do you have a history of previous medication and allergies? Physical examination; Pay attention to the heart and lungs. Then you should feel the heart via the chest cavity for any anomalies. Tests performed in diagnosis of angina pectoris include; Electrocardiogram (ECG)- This is used to measure the impulse produced by the heart. The impulse produced is then represented by a pattern that shows the dysfunction ie whether it is total obstruction (Mi) or partial (angina).for many angina patients, the ECG is usually normal.ECG is only carried out on patients with stable angina. Echocardiogram is where sound waves are utilized to check for the condition of the heart. The waves produce images that are then used to visualize whether there are blockages or damages to the heart arterials. Cardiac CT scan utilizes x ray machines that produce images of the heart with its arteries either enlarged or narrowed Chest x ray This is commonly used and its used to visualize the chest cavity. It produces images of the heart and its malfunctioned parts. Coronary angiography This depends on the x ray imaging. It is part of cardiac catheterization used in checking for blood vessels in the heart. This has also been used in evaluation of the lungs where there is accumulation of fluids in chest cavity. Nuclear stress test Measures flow of blood to myocardium at rest and during stress. This resembles regular stress test but in nuclear, a radioactive component is injected to the bloodstream (Mommersteeg et al., 2013). A scanner is used for detecting and creating images of the heart muscle. Deficient flow is indicated by light spots on the images. Cardiac MRI A machine with long tubes is used to produce images of the heart. Treatment Lifestyle changes –mostly in mild angina, they include; Stop tobacco use. Cigarette smoking is a major risk factor in angina, weight loss in cases where patients are overweight, controlling diabetes and moderate exercise. Drugs used include; nitrates such as nitroglycerin which is administered sublingually. Aspirin reduces blood clotting ability. Beta blockers block the effects of hormone epinephrine such as adrenaline while prasugrel and ticagrel prevent blood from clotting, On the other hand, statins cholesterol levels in blood. Calcium channel blockers which relax and widens blood vessels (Mommersteeg et al., 2013). Angiography Question 2 A description of symptoms women suffer during a myocardial infarction. 1. Excruciating pain in the back and neck. It may sometimes extend to the arms and even jaws. It comes in a gradual sequence or can be felt suddenly (Simpson et al., 2013). 2. Shortness of breath and lightheadedness. It can also be accompanied by nausea and vomiting. 3. Fatigue and extreme tiredness. Most women with MI will complain of excessive tiredness particularly around the chest. 4. There are chest pains that occur inform of tightness on the chest or squeezing pressure that can present as a stab. 5. Abdominal pains. Some women may confuse this with flu infections or ulceration of the stomach. 6. Sweating as well as cool, clammy skin is also common in women suffering from MI and paleness of the skin may sometimes be experienced. 7. There other symptom of not feeling comfortable in the upper part of the body, especially around the shoulder accompanied with rapid or irregular pulse (Simpson et al., 2013). Question 3 How Myocardial Infarction might progress to Acute Pulmonary Oedema. Acute pulmonary oedema is caused by high hydrostatic pressure in the capillaries as a result of increased pulmonary pressure in the veins. Myocardial infarction causes accumulation of fluids in the alveoli of the lungs. These fluids have low concentrations of proteins and can also be found in the interstitium. There is always frequent complaint of cough as well as pink, frothy sputum. Moreover, there may be hoarseness caused by recurrent laryngeal nerve palsy from mitral stenosis and perhaps chest pain that alerts physicians to the likeliness of acute myocardial infarction. In addition, there may be other clinical manifestations such as tachycardia, orthopnea, distended jugular veins, noisy wet respirations as well as cough with frothy, blood tinged sputum. Generally, APO may be caused by congestive heart failure, severe arrhythmias, hypertensive crisis and fluid overload due to kidney failure. Question 4 Management of APO patients may either be medically or through life style management. It is required that the immediate treatment should improve oxygenation and reduce pulmonary congestion knowing that treatment of APO is regarded as an emergency. Another important issue is to identify and correct precipitating aspects and given conditions in order to reduce recurrence (Ford, 2010). Different kinds of therapies should also be maintained in the management of APO such as oxygen therapy, high fowler’s position, diuretic therapy, contractility enhancement and vasodialator therapy (Luscher, 2008). Clear Airway should be observed while Breathing and Circulation of blood be monitored at all times. Adequate supply of oxygen must be provided to the patients (Ford, 2010). Medical management of APO is supported by reduction of systemic vascular resistance, pulmonary venous return, and Inotropic aid. -reducing pulmonary venous return helps in lowering hydrostatic pressure of the capillaries there by reducing seeping of the fluid into the alveoli. -Reducing vascular system resistance enhances perfusion but the renal system. -inotropic support is required for patients with acute valvular disorders who may present with hypotension. Nursing Management Oxygen therapy-maximum oxygen flow by ETT intubation or mechanical ventilation is what is involved in nursing management of APO. Vasodilator therapy-this helps in reducing blood amounts going back to the heart hence reducing the pumping force which the heart uses. This is best done using nitroglycerin (Luscher, 2008). Admission of aminophylline helps in preventing bronchospasms that accompany pulmonary congestion. After admission of ammophylline, elevation of the head side is carried out prior to cardiac monitoring. Question 5 Pathophysiology a. Reduced blood flow leading to acute pulmonary oedema. b. Occurs mostly as a inference of heart affection such as coronary artery disease. Classification; Cardiogenic pulmonary oedema and Non cardiogenic pulmonary oedema Cardiogenic is a result of direct damage to tissues or malfunctioning of the cardiovascular system and it may be caused by hypertensive crisis, acute arrhythmias or congestive heart failure. Moreover, it can result from overflow of fluid into the interstitium of lungs (Vitry et al., 2012). Non cardiogenic pulmonary oedema is the radiographic evidence of accumulation of fluids in the alveolar with not show of cardiogenic origin. It may be caused by aspiration, severe infections or multiple blood transfusions. In addition, it can result from inhalation of toxic gases (Vitry et al., 2012). Etiology is commonly observed in myocardial infarction with its cause being pulmonary infection. Risk constituent embody smoking, obesity, and diabetes, past predisposing or patronymic narration. It has been approximated that 1.1 million suffer APO related illness in the United States annually. It has also been seen as the leading cause of death in South American countries and the Hispania’s. Care setting; care can be provided for at the intensive care unit (ICU), emergency rooms is critical care unit (CCU) Nursing priorities Nursing priorities elevation of the head side or keep in a sitting position and supplying oxygen using the face mask. Nursing should also monitor signs of myocardial infarction, catheter and pulse oxymetry. There is also monitor ABG results for presence of hypoxemia and monitor ECG for dysrrhythmia as well as close monitoring of I/O chart (Vitry et al., 2012). Looking at discharge goals, patient can practice basic self care and reduction of anxiety. References Ford, L. E. (2010). Acute hypertensive pulmonary edema: a new paradigm. Canadian Journal Of Physiology & Pharmacology, 88(1), 9-13. Retrieved from http://eds.a.ebscohost.com/ehost/detail/detail?vid=7&sid=d1940cc3-ec2e-4162-9347-c4d43c81bb98%40sessionmgr4003&hid=4102&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d##db=aph&AN=47800195 Luscher, T., F. (2008). European Heart Journal. European Society of Cardiology, etrieved from Rhttp://eurheartj.oxfordjournals.org/content/29/23/2909.full Mommersteeg, P. M., C., Pot, I., Aarnoudse, W., Denollet, J., & Widdershoven, J. W. (2013). Type D personality and patient-perceived health in nonsignificant coronary artery disease: The TWeesteden mIld STenosis (TWIST) study. Quality of Life Research, 22(8), 2041-50. Simpson, E. L., Fitzgerald, P., Evans, P., Tappenden, P., Kalita, N., Reckless, J. P. D., & Bakhai, A. (2013). Bivalirudin for the treatment of ST-segment elevation myocardial infarction: A NICE single technology appraisal. PharmacoEconomics, 31(4), 269-75. Vitry, Agnes I,PharmB., Roughead, Elizabeth E,PharmB., Ramsay, Emmae N, BSc,G.DipAppStats, M.ClinEpi, Ryan, Philip,B.Sc, Caughey, Gillian, E, Esterman, A., . . . McDermott, Robyn,M.B.B.S. (2012). Chronic disease management: Does the disease affect likelihood of care planning? Australian Health Review, 36(4), 419-23. Read More