...angioplasty is a procedure to open an area of the arterial blockage in the heart that has become narrowed. This allows better blood flow through the artery and to the heart muscle. It is often done with a catheter that has an inflatable small sausage-shaped balloon at its tip. Coronary angioplasty is being increasingly used as a treatment for coronary artery disease; the proper evaluation and management of patients after the procedure are important issues. Although coronary angioplasty is a complex technical procedure, the methods routinely used to evaluate its results have many limitations. The management of the patient during the first 24 hours after angioplasty should focus on the prevention, detection, and if necessary treatment of acute vessel closure. Assessment: When the patient returns from the cardiac catheterization laboratory, the stability of the patient should be established initially. This will include, but is not limited to, EKG, vital signs, oxygenation level, urine output, cardiac, respiratory, pulmonary, gastrointestinal, and gentle urinary assessment. Particular attention must be paid to the peripheral vascular assessment of the lower extremities. Often the patient may return from the cardiac catheterization laboratory with a sheath in place. If this is the case, the institutional procedures for caring for sheaths should be applied. Some institutions, may allow the nurse to remove that sheath. Other institutions require that the physician removes the sheath...
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...intake. The genomic effect of aldosterone increases renal sodium transport, but the administration of large doses of aldosterone to normal individuals does not cause edema, relating to the phenomenon of "aldosterone escape"; however, in edematous disorders including cardiac failure, cirrhosis, and nephrotic syndrome, impaired aldosterone escape leads to renal sodium retention and edema formation. There is now considerable evidence for the nongenomic effects of aldosterone in several important diseases. Thus, low dosages of mineralocorticoid antagonists, with little or no effect on urinary sodium excretion, have been shown to afford a beneficial effect on morbidity and mortality in patients with advanced cardiac failure and after acute myocardial infarction. Three-drug-resistant hypertension has also been found to respond to spironolactone in modest dosages. The combination of an angiotensin converting enzyme inhibitor (ACEI) with spironolactone to treat such resistant hypertension may be more effective than adding an angiotensin receptor blocker to an ACEI. The role of spironolactone has also been shown to decrease albuminuria in chronic kidney disease including diabetic nephropathy in the presence of maximal dosages of ACEI. The effect of aldosterone in metabolic...
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...Myocardial Infarction Cardiovascular disease is the leading cause of death in the United States; approximately 500,000-700,000 deaths related to the coronary artery occur each year. Approximately 1.5 million cases of myocardial infarction occur annually in the United States. Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. Patients with typical myocardial infarction may have the following prodromal symptoms: Intense sharp chest pain, radiation of chest pain up to neck, shoulder, jaw and down left arm, ventricular tachycardia, atrial fibrillation or flutter, Coughing, wheezing, Fever, Fatigue, chest discomfort, and Malaise. Atherosclerosis is the disease primarily responsible almost 90% of myocardial infarctions that result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary thrombosis and occlusion. The damage in the myocardium is essentially the result of a tissue response that...
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...CASE STUDY 1 Acute coronary syndrome Patrick Gallagher Case outline Peter Brown is a 58-year-old gentleman who has experienced an episode of crushing central chest pain while at work. Peter works as a taxi driver and a colleague has taken him to the Accident and Emergency Department. On admission, Peter is sweaty, clammy, nauseated and short of breath. He is complaining of chest pain radiating to his left arm. This is Peter’s first presentation to hospital and he has no relevant past medical history. Peter smokes approximately 20–30 cigarettes per day and takes alcohol at weekends only. Peter is anxious and is concerned that his wife and children are informed. He also states his father died suddenly following a heart attack a number of years ago. Peter is immediately triaged and taken to the resuscitation room. You are the receiving nurse. Observations on admission include: Respiratory rate: 18 breaths per minute Oxygen saturations: 95% Blood pressure: 150/90 mmHg Pulse: 94 beats per minute Temperature: 37ºC. On admission to hospital an electrocardiograph (ECG) has been undertaken. Peter has been diagnosed with an anterior ST segment elevation myocardial infarction (anterior STEMI). Blood samples have also been drawn for urea and electrolytes (U&E), full blood picture (FBP) and highly sensitive troponin T. 1 Discuss Peter’s immediate problems and explain these using your knowledge of pathophysiology. A On admission to Accident and Emergency...
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...Back Ground: Despite impressive strides in diagnosis and management of acute myocardial infarction in the past three decades, acute myocardial infarction continues to be a major health problem. About 50% of death from acute myocardial infarction occur within 1hr of the event and are attributable to arrhythmias most often ventricular fibrillation. Ischaemic injury can produce conduction blocks at any level of the atrioventricular or Intraventricular conduction systems. Such conduction block can occur in the atrioventricular node producing various grades of AV block. Conduction block can occur in either main bundle branch producing right or left bundle branch block or in the anterior and posterior fascicle of left bundle branch, producing left anterior &left posterior...
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...Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study Summary Background Although more than 80% of the global burden of cardiovascular disease occurs in low-income and middle-income countries, knowledge of the importance of risk factors is largely derived from developed countries. Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown. Methods We established a standardised case-control study of acute myocardial infarction in 52 countries, representing every inhabited continent. 15152 cases and 14820 controls were enrolled. The relation of smoking, history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, blood apolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their 99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) were calculated. Findings Smoking (odds ratio 2·87 for current vs never, PAR 35·7% for current and former vs never), raised ApoB/ApoA1 ratio (3·25 for top vs lowest quintile, PAR 49·2% for top four quintiles vs lowest quintile), history of hypertension (1·91, PAR 17·9%), diabetes (2·37, PAR 9·9%), abdominal obesity (1·12 for top vs lowest tertile and 1·62 for middle vs lowest tertile, PAR 20·1% for top two tertiles vs lowest tertile), psychosocial...
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...Running Head: ANXIETY IN SMOKERS AND NONSMOKERS Research Critique: Anxiety in Smokers and Nonsmokers with Acute Myocardial Infarction Research Critique: Anxiety in Smokers and Nonsmokers In November 2006 the American Journal of Critical Care published a research article comparing anxiety between smokers and nonsmokers with acute myocardial infarction. This study compared various demographic areas to various treatment modalities pertaining to both smokers and nonsmokers admitted with a diagnosis of acute myocardial infarction (AMI). Background The background section of this study was clearly identified. There were clear statistics listed within the background that gave specific numbers of persons affected by acute myocardial infarctions. This study was chosen because “no studies comparing anxiety levels between smokers and nonsmokers hospitalized for an AMI have been reported” (Sheahan, et al., 2006). This study is important to nursing due to the fact that anxiety levels are inherently increased when patients are faced with difficult situations, however when a person who is more prone to anxiety faces a difficult situation the anxiety level is increased over normal values. There were several articles over five years old however they appear to be focused on aspects directly linked to this study. The specific research questions addressed in this study were clearly and directly stated in understandable language. These questions and...
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...on October 20, 2002 due to myocardial infarction. Respondent filed with petitioner a claim for death benefits under PD 626, as amended. Petitioner denied the claim on the ground that the cause of death was not work-connected. The ECC upheld petitioner. On appeal, however, the CA reversed petitioner and the ECC and held that myocardial infarction, a cardiovascular disease, was a compensable occupational disease. Thus, this petition. Is respondent entitled to compensation for her husband’s death? Yes, she is. Under PD 626, the beneficiaries of an employee are entitled to death benefits under the system if the cause of death of the employee is a sickness listed as an occupational disease by the ECC or any other illness caused by employment, subject to proof that the risk of contracting the same is increased by the working conditions. The CA correctly ruled that myocardial infarction was considered as an occupational disease because it was included under the classification “cardiovascular disease,” a compensable occupational disease under ECC Resolution No. 432 (dated July 20, 1977) subject to substantial evidence proving any of the following conditions: (a) If the heart disease was known to have been present during employment, there must be proof of an acute exacerbation clearly precipitated by the unusual strain by reason of the nature of this work. (b) The strain of work that brings about an acute attack...
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...Pathology: Myocardial Infarction Name University Objectives 1. Discuss myocardial infarction and its pathogenesis. 2. Describe the sequence of changes involved in myocardial infarction. 3. List the major physiologic and morphologic complications of myocardial infarction. 4. Describe management of myocardial infarction. 5. Discuss patient teaching of myocardial infarction. Definition Myocardial infarction (MI), commonly known as a heart attack, is an irreversible necrosis of the heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. (Zafari, 2011) Etiology The etiology of MI is predominantly from atherosclerosis i.e. coronary artery narrowing due to plaque formation. Non-modifiable risk factors for atherosclerosis includes: age, sex, family history of premature coronary heart disease, etc. Modifiable risk factors for atherosclerosis includes: smoking or other tobacco use, diabetes mellitus, hypertension, hypercholesterolemia, hypertriglyceridemia, obesity, sedentary lifestyle and/or lack of exercise, psychosocial stress, poor oral hygiene, etc. Non-atherosclerotic causes of MI include the following: • Coronary occlusion secondary to vasculitis • Ventricular hypertrophy (e.g., left ventricular hypertrophy, idiopathic hypertrophic...
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...Myocardial Infarction Mortality 1.0 Introduction In the UK, about 838,000 men and 394,000 women have had a myocardial infarction (MI) at some point in their lives, (NICE clinical guideline 48, 2007). The latest statistics from the British Heart Foundation state that approximately 227,000 people suffer from an acute MI (heart attack) each year (British Heart Foundation Statistics Website). To put this figure in to perspective this equates to one person every 2 minutes. Mortality is at approximately 30% which is 68,100 deaths in the UK per year. The National Service Framework (NSF) for Coronary Heart disease (CHD) is a 10-year programme published by the Department of Health in 2000 and has set key standards for the prevention and treatment of CHD. Access to the right treatment for those who suffer from an AMI, is essential to reduce morbidity and mortality and improve clinical outcomes. People with diabetes mellitus constitute a group of patients who have a higher risk of having an MI and also a poorer prognosis post infarction. The higher death and complication rates appear to be multifactorial but a significant finding in the Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) Trial showed to reduce one year mortality by 30% (Malberg et al., 1995). It’s recommended 1.1 Primary Objective To determine the relationship between HbA1c and prognosis of patients in East Lancashire having a myocardial infarction. 1.2 Secondary Objectives To assess...
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...Beta Blockers After Myocardial Infarction Clinical Scenario The acute care nurse practitioner on the cardiology service treats a 67 year-old-male admitted after recovering from an acute ST-Elevation Myocardial Infarction (STEMI). His risk factors include obesity, Type II diabetes mellitus, and family history. Upon exam the patient asks why he has not been started on a beta blocker yet. He explains further that when his brother had a “heart attack” in 2005, he was immediately placed on a beta blocker because the cardiologist reported how beta blockers reduce mortality after myocardial infarction (MI). The patient wants to know if a beta blocker would reduce his chance of mortality? Using the Patient-Intervention-Comparator-Outcome (PICO) format we formulated the following question. In a 67-year-old male with multiple co-morbidities with MI (P), does treatment with a beta blocker (I), compared with no beta blocker or placebo (O), reduce mortality rate (O)? Risk Factors, Incidence and Prevalence of Disease * US incidence rates of cardiovascular disease, including MI, are seen in men more than women (Alexander et al., 2007). This trend is also true in Utah ("Impact of heart," 2007). * The incidence rates of cardiovascular disease increase with age (Alexander et al., 2007). * Risk factors for cardiovascular disease include not eating enough fruits and vegetables, lack of physical exercise, smoking cigarettes and the co-morbidities of diabetes, hypertension, hyperlipidemia...
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...For the purpose of this assignment the author will discuss the pathophysiology of a myocardial infarction and will give an in-depth discussion of one central aspect of care and in this assignment the author has chosen the management of anxiety. Due to word restrictions a brief mention will be given to the other aspects of care. Ischaemia is a term which is used to describe the deficiency in blood supply to any part of the body. In ischaemic heart disease there is a deficiency in the blood supply to the heart muscle which can be caused by an obstruction to, or even a narrowing of the coronary arteries. This in turn reduces the supply of nutrients and oxygen to the heart muscle. Without an optimum oxygen supply the heart muscle is unable to function efficiently.(Boersma et al 2003) There are three ways in which an infarction may develop. 1) The narrowing and hardening of arteries is caused by degenerative changes and also the build up of cholesterol and other fatty deposits which occur in the vessel wall. Plaques which then develop and subsequently become ‘calcified or fibrotic’ is through a process known as atherosclerosis. The atherosclerotic plaque slowly builds up in the inner lining of a coronary artery. The presence of the plaques causes the linings of the artery walls to become roughened and this in turn reduces the size of the lumen and eventually occludes it. As circulation slows down there is a strong possibility of thrombus formation. Should a coronary artery become...
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...ACSC41 23/10/03 5:42 PM Page 88 41 Pathophysiology of acute myocardial infarction Start here Macrophages and T-lymphocytes Stunned myocardium Fibrous cap 24 h Lipid core Plaque rupture, platelet aggregation Mainly dead myocytes and neutrophils Transmural necrosed zone Infarct appears pale, most cells dead, neutrophils present— coagulation necrosis Granulation tissue moves inward and replaces dead tissue with scar tissue 2h 5–7 days Subendocardial necrosed zone Cellular damage progressing, but still partially reversible with reperfusion Thrombus propagates into and along coronary artery Endocardium Cross-section of ventricular wall served by thrombosed artery Scar thin firm grey Mixture of living and dead myocytes; substrate for re-entrant arrhythmias 0h > 3 months Finish here 41.1 Infarction is tissue death caused by ischaemia. Acute myocardial infarction (MI) occurs when localized myocardial ischaemia causes the development of a defined region of necrosis. MI is most often caused by rupture of an atherosclerotic lesion in a coronary artery. This causes the formation of a thrombus that plugs the artery, stopping it from supplying blood to the region of the heart that it supplies. Role of thrombosis in MI Pivotal studies by DeWood and colleagues showed that coronary thrombosis is the critical event resulting in MI. Of patients presenting within 4 h of symptom onset with ECG evidence of transmural...
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...to explore an acute deterioration in the health of an adult I have encountered during a clinical placement, in an acute care setting. The essay will begin with a definition of acute care, followed by the introduction of my patient and predisposing factors. This essay will include an explanation of the significant pathophysiological changes and related clinical manifestations and a critical analysis of the nursing interventions implemented during the acute episode of care, focusing on holistic care, rationale and evidence base. It will then describe the actual deterioration in the patient’s condition, and discuss the nurse’s role in the recognition and assessment of the actual deteriorating condition following the trusts policies. Assessment tools, monitoring, detecting and reporting will be considered. Finally this essay will include a discussion of the importance of multidisciplinary team collaboration in the diagnosis and provision of care during the acute episode, and a discussion on whether the deterioration could have been prevented by identifying any areas of practice which could change in relation to evidence based practice. For the purposes of privacy and confidentiality, in accordance with NMC (2008) code of conduct, the name of the patient will be changed to Peter and the placement area will remain as an acute care setting. According to McFerran (2008) the term “acute” is described as a disease of rapid onset, severe symptoms, and brief duration. Acute Care refers to...
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...Cardiovascular disease is one of the leading causes of death for both men and women worldwide. Acute coronary syndrome occurs when the heart muscle does not get enough oxygenated blood. As a result of this, heart muscle experience symptoms such as pain, pressure or tightness to alert the severity and progression of the disease. If the symptoms are left untreated, it can be life threatening. Acute coronary syndrome includes myocardial infarction (MI), also known as a heart attack, and unstable angina, which is a sudden severe chest pain that typically occurs when a person is at rest. Every year, acute coronary syndrome affects an estimated 1.4 million people in the United States and another 1.4 million people in Europe ("Heart Disease: Symptoms,...
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