Diploma of Nursing: HLT51612
Analyse Health Information: HLTAP501C
Assessment Task 1: Case Study
Case Study One
Mr. Bellows is an overweight, 51-year-old with a long history of angina. He is known to your hospital and arrives in an ambulance with more severe symptoms than previous admissions. Mr. Farmer informs the ambulance crew, the Anginine tablets he has taken, have not provided any symptom relief.
He presents at Emergency Department (ED) with crushing central chest pain, which radiates down his left arm. On arrival to ED, Mr. Farmer receives 300mg aspirin, followed by IV morphine sulphate. A 12 lead ECG and blood tests reveal he has suffered an AMI.
Mr. Farmer on Day 5, is discharged home and recommended to take daily exercise and improve his diet. Mr. Farmer had previously consumed regular take-away food, smoker of 35years and led a sedentary lifestyle. Discharge medications prescribed include aspirin, metoprolol, an ACE inhibitor (perindopril) and a statin (simvastatin)
Question 1
Clearly differentiate the pathophysiology of angina and myocardial infarction, including signs and symptoms. (5 marks)
Angina Pectoris
Angina Pectoris is a disorder described by episodes of pain when the supply of oxygen to the heart is inadequate to meet the needs of the heart (Bruyninckx 2011). Hypoxia can be the result of three types of cardiac stressors:
• Ischemia caused by coronary blood vessel obstruction as a result of vasospasm, thrombosis or atherosclerosis. Ischemia can also
Mr. Howard was evaluated by his family physician after a prolonged episode of chest pain. The results of an electrocardiogram (ECG) were unremarkable; however, in view of the progression of his symptoms, he was referred to a cardiologist. Mr. Howard underwent a stress treadmill
Mr. S is a 29-year-old male with past medical history of (PMH) hypertension (HTN) and obesity who presented to local emergency room (ER) with headache and chest and back pain. Mr. s had been seen at urgent care three days prior for a headache and near syncope and was told to hold his metoprolol due to bradycardia. Due to health insurance related problem, he has been off amlodipine and lisinopril for a month.
“The patient is Adam Rudd, a 78 y/o white male with a history of hypertension. He has been diagnosed with hypertension past 15 years and is on anti-hypertensive medications and aspirin. He is very weak and short of breath. He is accompanied with his longtime friend Jennifer, who reports that Rudd was looking very weak and was complaining of severe headache and blurred vision before coming to the hospital. He is 5’9” and weighs 270 lb. Vital signs recorded were: oral temperature 98.20 F, BP 224/120 mm Hg with a heart rate of 102 beats/minute and respiration of 24 breaths per minute. The pulse oximetry reading was 94% on room air. He is complaining of severe headache and blurred vision. Rudd said that he did not take his antihypertensive medication or aspirin since he ran out of pills. He has not been taking his medication for past 15 days. He reports no known allergies to any medications or other substances.”
In the emergency room, Rudd was connected to the cardiac monitor, labs were drawn and a 20-guage peripheral IV was started in the right arm. An IV infusion of nitroprusside was started and vital signs were recorded periodically. The Pain was assessed using a PQRST pain assessment method and Rudd rates throbbing pain bilaterally in the head with a pain score of 8 that aggravates with moving and does not radiate to elsewhere other than the head. The orthostatic BP shows no changes. The E.D physician decides to admit Rudd in CCU to further monitor his blood pressure and watch for any signs of organ damage. The E.D physician writes an order for pain management and transfer to CCU. The ER nurse
Mr. Thomas’ has been diagnosed with an acute myocardial infarction (MI). A myocardial infarction is an “infarct of heart muscle caused by occlusion of one or more of coronary arteries” (Frucht, 2012 P.125). The common name for Mr. Thomas’ condition is a heart attack. A heart attack occurs if the flow of oxygen-rich blood to a section of heart muscle suddenly becomes blocked ( ). If the blood flow is not restored quickly, then that section of the heart muscle begins to die. Heart attacks have become the leading killer of both men and women in the United States. The main cause of heart attacks has
Mr. Bishop is here for routine followup of his chronic illness. He is treated with Alvesco 160 mcg two puffs twice daily, Atrovent two puffs three times daily and Ventolin as needed for his COPD. He reports good compliance and uses these inhalers as prescribed. He generally uses his Ventolin with exercise. He reports that he is running 1-2 miles a day and also doing a step tape daily and reports good exercise tolerance. He does not wake at night coughing or feeling short of breath. For his hypertension, he takes hydrochlorothiazide 25 mg, and amlodipine 5 mg, and simvastatin 20 mg for his hyperlipidemia. He takes these as prescribed and denies any side effects. He denies
To treat properly, a key component of care is to determine the cause to reduce risk of decreased cardiac output and tissue perfusion. Clinical Presentation John Smith is a 70-year-old Caucasian male. He is married, with no known allergies, and he is a full code. This morning, his wife became worried when she noticed an increase of dyspnea on exertion and dependent edema. She drove him to the emergency room where he was admitted for dyspnea and suspicion of
A 68 year old male presented to the emergency department at 0800 hours via ambulance after experiencing chest discomfort and intermittent palpitations since 0500 hours. Prior to presentation, the patient stated he
The pathophysiology of ACS includes the stable plaque forms get converted into unstable plaque forms.2 These unstable plaque forms have numerous thin fibrous cap cells, inflammatory cells, activated macrophages, and smooth muscle cells. Sympathetic activity increases myocardial contractility, pulse rate, blood pressure, and coronary blood flow which leads to plaque rupture or fissure. As the artery ruptures, it causes thrombus formation and ischemia in this particular artery. Depending on the condition, different thrombi could form. The unstable angina forms a small thrombus formation, NSTEMI forms a partial thrombus formation, and STEMI forms a complete and persistent thrombus. The risk factors involved in ACS are age, physical inactivity, and history of hypertension, diabetes, or angina. The signs of acute coronary syndromes are an acute heart failure, tachycardia, bradycardia, or heart blockage, and the symptoms of ACS consist of chest pain, pain in the extremities, nausea, shortness of breath, heavy
Nevertheless, there is an understandable and noticeable link between circulatory related diseases and lifestyle diseases, such as Coronary Heart Disease. Coronary heart disease can occur when fatty acids, such as cholesterol in an inadequate diet, build up in the walls of the coronary artery. These fatty deposits collect minerals and harden to become a plaque. Eventually, this plaque grows and can swells up, forming an aneurism. In some cases, this aneurism may burst leading to instant death. As it continues to grow and swell up, it finally blocks the artery completely and forms blood clots. This is known as coronary thrombosis. A myocardial infarction, or in other words as heart attack, occurs when no oxygen is able to reach the coronary artery and thus it is unable to fulfil its role in providing the heart muscle with a sufficient supply of blood. Heart attacks are very common in the society nowadays, especially occurring in smokers or obesity related diseases (Millar, June 2014)
Coronary endothelial dysfunction is associated with various pathological impairments, such as the disruption of cardiovascular homeostasis, poor blood circulation, myocardial injury, the accumulation and adhesion of platelets and monocytes, the increase in vasoconstriction, increased expression of inflammatory factors, and impairment in vascular regeneration which increase the risk of atherosclerosis.
Mr. Wilson, a fifty-three-year-old utility worker earns 73,000 dollars a year. At the time of his heart attack he mistook it for a heart burn, despite being the second time having one. When his wife called the ambulance he was given two options for hospitals, the city hospital or to the Brooklyn hospital. He chose the Brooklyn hospital, knowing that the city hospital would not treat him as fast. At the Brooklyn hospital he was given a drug to break up the clot blocking the artery to his heart. The medicine worked at first, however the clot reformed. He needed an angioplasty, but had to go to a different facility because the Brooklyn hospital didn’t have the resources the test there. In comparison to Mr. Miele who was also required to do an angioplasty and was done in
The most common physiological process leading to a myocardial infarction is the occlusion of coronary arteries by a process known as atherosclerosis. In fact, atherosclerosis is present in more than 90% of persons with coronary heart disease.1
A Myocardial Infarction also known as a “heart attack” or acute coronary syndrome is a medical emergency that requires immediate intervention to prevent extenuating damage or death to the muscle that pumps the human body with oxygen therefore, life. Many of those who’ve suffered damage from a heart attack and survived are able to go back to enjoying a normal life if damage is limited with proper treatment and preventive lifestyle changes. This paper will encompass the pathophysiology that is a Myocardial Infarction, and discuss its warnings, treatment, prevention as well as where a patient could find communal support after discharge.
Cardiogenic shock, according to Werden et al. (2012), is the most common cause of death from an acute myocardial infarction (AMI) and has a chance of mortality from thirty percent to eighty percent. Infarction-related cardiogenic shock (ICS) complicates approximately five to ten percent of acute myocardial infarctions (AMI) and remains the leading cause of death in patients hospitalized from an AMI (Kolte et al., 2014). Kolte et al. (2014) also states that the incidence of cardiogenic shock is higher in patients over the age of seventy-five, and has higher prevalence in women, Caucasians, Asians, and Pacific islanders. This paper will discuss the pathophysiology, clinical manifestations, tools used to diagnose, and therapeutic management of cardiogenic shock.