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1. What do you think are the factors which predisposed Mrs. Mendoza into experiencing acute myocardial infarction? Explain the rationale behind each predisposing factor. Age Sex: At any given age, men are more at risk than women, particularly before menopause, but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women. Diabetes mellitus (type 1 or 2) High blood pressure Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides Tobacco smoking, including secondhand smoke Family history of ischaemic heart disease or MI, particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women) Obesity (defined by a body mass index of more than 30 kg/m, or alternatively by waist circumference or waist-hip ratio). Lack of physical activity Psychosocial factors including, low socioeconomic status, social isolation, negative emotions and stress increase the risk of and are associated with worse outcomes after MI. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI. Alcohol prolonged exposure to high quantities of alcohol can increase the risk of heart attack. Oral contraceptive pill women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking. Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis, whether elevated homocysteine in the normal range is causal is contentious 2. Aside from the manifestations experienced by Mrs. Mendoza, what are the other clinical manifestations of acute MI? Chest pain that occurs suddenly and continues despite rest and medication is the primary presenting symptoms Patients may present with a combination of symptoms, including chest pain, shortness of breath, indigestion, nausea and anxiety.

Patient may have cool, pale and moist skin; heart rate and respiratory rate may be faster than normal. These symptoms, which are caused by stimulation of the sympathetic nervous system, may be present for only short time or may persist.

3. Differentiate angina pectoris from acute myocardial infarction in terms of its pathophysiology, chest pain, manifestation and diagnosis. ANGINA PECTORIS MYOCARDIAL INFARCTION Myocardial cells become Complete of nearly complete PATHOPHYSIOLOGY ischemic within 10 sec. of occlusion of coronary artery (due coronary artery occlusion -> to rupture of atherosclerotic decrease pumping action of the plaque -> thrombus or embolus ; heart (after several mins.) -> vasospasm; decrease oxygen decrease blood supply (glucose supply; or increase demand of and oxygen) -> decrease ATP oxygen) -> profound imbalance production -> anaerobic between oxygen supply and metabolism -> production of demand -> ischemia -> infarction lactic acid (acidosis) -> pain (cell death) after 15 mins. Squeezing, pressing and Severe, sudden in onset, crushing, CHEST PAIN burning at the left retrosternal heaviness and tightness at the or substernal area radiating to substernal area radiating to arms, arms and shoulders . jaw and neck. Not relived by nitroglycerin Weakness, numbness (arms, Dyspnea, tachypnea, crackles MANIFESTATION wrists and hands), shortness of (pulmonary congestion), pallor breath, pallor, diaphoresis, diaphoresis, decrease urinary dizziness, nausea and vomiting, output, increase PR, dizziness, severe apprehension and restlessness, anxiety and feelings of impending death. impending doom. 4. Discuss the management of clients suffering from AMI. Include the pharmacologic management, treatments or other invasive procedures with their corresponding nursing considerations. Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent MI. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, but the risk of hemorrhage is increased. Beta blocker therapy such as metoprolol or carvedilol should be commenced.[78] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. -Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 2448 hours after MI in hemodynamically stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence

of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling. Statin therapy has been shown to reduce mortality and morbidity. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids. The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death after MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone, another option, is sometimes preferable to eplerenone due to cost. Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.

An MI requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit. Early treatment of heart attack patients with an inexpensive beta-blocker drug called metoprolol, while in transit to the hospital, can significantly reduce damage to the heart during an MI. STEMI Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner. If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended. If after fibrinolysis, significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes occurs, then rescue PCI is indicated emergently. After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).

5. Explain the rationale behind the administration of streptokinase, heparin and nitroglycerin when giving these medications? Streptokinase: promotes fibrinolytic mechanism by converting plasminogen to plasmin that destroys the fibrin in the blood clot. It should be administered within 4-6 hours after acute MI. Heparin: This medication is used to prevent and treat blood clots. It is also known as anticoagulant. It is started before terminations of thrombolytics. Monitor aPTT. Nitroglycerin: prevent angina caused by coronary disease. This medicine is also to relieve an angina attack that is already occurring.

6. When AMI becomes severe there might be a need for the client to undergo coronary artery bypass graft (CABG). Postoperatively after CABG, client are at risk for developing cardiac tamponade. Discuss the pathophysiology and management of cardiac tamponade. The outer layer of the heart is made of fibrous tissue which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase.If fluid continues to accumulate, then with each successive diastolic period, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to decreased stroke volume. This causes obstructive shock to develop, and if left untreated then cardiac arrest may occur (in which case the presenting rhythm is likely to be pulseless electrical activity). Pre-hospital care Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. A number of the Helicopter Emergency Medical Services (HEMS) in the UK, which have doctor/paramedic teams, have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury. Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action. Hospital management Initial management in hospital is by pericardiocentesis. This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium. In heart surgery patients post op, the nurses monitor the amount of chest tube drainage. If the drainage volume drops off, and the blood pressure goes down, this can suggest tamponade due to chest tube clogging. In that case, the patient is taken back to the operating room for an emergency reoperation. If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility.