Care, rationale and outcome in Coronary Care Unit

Care, rationale and outcome in Coronary Care Unit Nurses are required to continue education and upgrading of skills to ensure their patients receive the best possible nursing care. Cardiac nursing is a dedicated nursing practice that gives focused and precise nursing interventions, that are governed by the best practice nursing standards using latest research based facts. Nurses need to have good technique and skill when performing health history and physical assessments to enable them to look after the person as a whole. When nursing patients, nurses need to understand the care they give and reasoning of why they deliver the cares in a certain way. A sound knowledge of assessment and observations help nurses plan, initiate and deliver health care. Without knowledge and rationales the nurse may not deliver cares in the correct manner or have the ability to know when to initiate them. Myocardial infarction is a common cause for admission into the Coronary Care Unit and this case study follows cares, rationales and outcomes in this se tting. Mr Smith (synonym for confidentiality) is a retired 58 year old man that was admitted to a Coronary Care Unit (CCU) via the Emergency Department (ED) of the Atherton Hospital. His admission diagnosis was an Anterior ST Elevated Myocardial Infarction (STEMI), which had already been treated with thrombolytic therapy. On the morning of his admission, he drove himself to the ED with chest pain. He presented with left sided chest pain that radiated to his left jaw and left arm which he scored 10/10 and described as crushing. He was diaphoretic and hypertensive with nausea and vomiting. An ECG showed sinus bradycardia, rate of 60 bpm with hyperacute T waves in V2-V4, that progressed to ST Elevation. Thrombolytic therapy was administered 1 hour of his presenting to ED and within 2 hours of the initial chest pain that commenced at home. His ST segment was elevated approximately 8mm and continued to increase until 70 minutes post thrombolytic when he had 50% resolution of the ST elevation. When he presented to the ED he was given oxygen, morphine, anginine, aspirin, clopidigrel and enoxaparin as first line pharmaceutical treatments. He was transferred that afternoon to Townsville. Mr Smith was not managed in Atherton due to the lack of cardiac catheter services and was transferred for a Percutaneous Coronary Intervention (PCI) the next day where he had a stent placed in his proximal area of his Left Anterior Descending Coronary Artery (LAD). Anterior MIs affect a large surface of the heart, thrombolytic therapy and PCI are the most effective way to treat them (Evans-Murray, 2008 ). His medical history includes a previous STEMI and PCI in 1997, hypercholesterolemia, depression, a ruptured bowel and neck injury from a Motor Vehicle Accident in 1977. Upon further questioning Mr Smith admitted to recently becoming very short of breath whilst mowing the lawn. His risk factors include ex-smoker ceasing in 1993, hypercholesteremia, and stress of brother dying 3 weeks previous. His current medications were aspirin 100mg daily, atorvastatin 20 mg daily and zoloft 200mg daily. Upon arrival to a Townsville Coronary Care Unit (CCU), Mr Smith was pain free. He was connected to continuous cardiac monitoring and admission workup was attended, this includes admission paperwork, ECG, vital signs, mobile Chest x-ray and pathology tests. He was ordered and given stat doses of aspirin, clopidigrel and IV lasix. Mr Smith had an IVT running in his Left hand and an IVC in his Right hand. During the next few days Mr Smith remained febrile 37.6 ° with only a small elevation in white cell count (Huszar, 2007). Four days post infarction, Mr Smith became short of breath (SOB) in the shower and felt light headed; he was monitored in Sinus Rhythm with SaO2 of 95% on 3lpm via nasal cannula. On auscultation, crackles were heard in his lower bases. He was commenced on lasix 20mg daily. This was an indication that his Left Ventricle may not have been functioning adequately. An Echocardiogram was performed to see if the heart wall motion and valves were performing to their best ability (Kern, 2003). The report showed extensive akinesis of the septal, anterior and apex left ventricle wall. His Left Ventricle Ejection Fraction (LEVF) was 35%. Normal values for (LVEF) are 60-65% (Moser Riegel, 2008). He was commenced on a Beta Blocker Cavedilol 6.25mg and Ramipril, which was commenced post PCI and decreased from 2.5mg to 1.25 mg. Use of these medications follow the criteria of the Reducing Risk in Heart Disease (Heart Foundation, 2007). He was sent to the cardiothoracic unit on day 5 with telemetry, to monitor for any changes in his cardiac condition (Jayasekara, 2009) and discharged two days later. A systematic approach should be taken when attending to health history and physical assessment. Throughout the assessment, skin temperature, body odour, mood and appearance are observed. Patients need to feel comfortable with nurses so Mr Smith had the physical assessment explained to him and the reasons for performing it. (Brown, 2007) Mr Smiths physical assessment was completed in the morning prior to his PCI. He seemed relaxed with a jovial manner but at times did appear nervous. He was of a clean well kept appearance and looked younger than his 58 years. Neuro intact. Orientated to time, person and place, GCS 15 and PEARLA. He had a good memory of the event. Cardiovascular monitored in sinus rhythm with frequent PVCs and runs of bigeminy. ECG attached. Febrile- low grade 37.4  °, Pulse 70 bpm, blood pressure 102/69, no peripheral oedema. Jugular venous pressure was approximately 4 cms. Initially I could not palpate the apical pulse but when patient positioned onto his left side it was felt 5th ICS MCL. The reason it is felt is due to the apex of the heart comes into contact with the chest wall (Marieb Hoehn, 2010) No thrills or heaves heard. Mr Smith was warm to touch but not diaphoretic. Upon auscultation of the carotid arteries no bruits were heard. Normal S1 and S2 heart sounds were heard upon auscultation. Good radial, carotid and femoral pulses, Normal 2+ according to pulse volume scale (Lewis, 2007). Mr Smith did look pale and his haemoglobin was 121g/L. Respiratory rate of 18 per minute. Sao2 94% on 2lpm via Nasal cannula. Inspection of the thorax area revealed equal shape, size and symmetry of chest with nil use of accessory muscles. Trachea was midline. Lips and nail beds showed no signs of cyanosis. Diaphragmatic excursion was equal at 4 cms. Anterior, lateral and posterior areas revealed equal air entry, bilaterally in high and mid thoracic zones. Basal zones of thorax areas were bilaterally dull. No adventious sounds heard. Chest X-ray noted that some consolidation in bilateral bases which corresponds to the decreased air entry heard in the bases (Wang, Baumann, Slutsky, Gruber, Jean, 2010). Gastrointestinal revealed an old scar midline under the umbilicus from previous MVA. Bowel sounds heard in all 4 quadrants. Abdomen was soft with no distension. Mr Smiths upper and lower limbs and nail beds showed no signs of cyanosis or clubbing, ulceration or varicose veins. Capillary refill was normal less than 3 seconds in all limbs. Range of motions and strength were bilaterally equal and normal in all 4 limbs. Dorsalis pedis and posterior tibial veins were felt on palpation and scored 2+ bilaterally (Lewis, 2007). Acute coronary syndrome is a common cause of death. Myocardial infarction can have a good mortality rate if treated early. Treatment can be as basic as oxygen, ECG, observations, nitroglycerine through to thrombolytic therapy or a rescue angiogram/angioplasty (Overbaugh, 2009). One is not more important than the other and the patients prognosis is the main concern. Patients complain of chest pain due to myocardial oxygen demand and supply mismatching. The coronary arteries supply the myocardium with blood supply, if the supply is interrupted by a clot, spasm or atherosclerotic plaque the myocardial oxygen requirement (demand) is not met which causes myocardial cells to starve for oxygen supply. This causes the depolarization of the cells to be interrupted and changes will occur on the ECG. (Woods, 1995) Ischemia is shown on the ECG by ST segment elevation. This is primarily an emergency situation as the first 6 hours post infarction is when myocardial damage becomes irreversible (Thelan, 1994). In this time many interventions can be attended to resupply the myocardium with oxygen enriched blood supply. Oxygen is administered for at least the first 48 hours post MI so that tissue hypoxia does not become evident. At times chest pain can be relieved by applying oxygen.(Swearingen Keen, 2001) Vital signs are attended to frequently in CCU, usually hourly, which enables nurses to see any changes in hemodynamic monitoring. Complications of infarctions are heart failure and arrhythmias, due to the large area of heart wall damaged. When Mr Smith suddenly became SOB and adventious breath sounds were heard on auscultation, it alerted medical staff that his left side of the heart was congested and not efficiently pumping. Early indications of Left ventricular failure are shortness of breath (SOB) and intolerance of beta blockers, nitrates, or ACE inhibitors. Mr Smith showed signs of SOB and lightheadedness, which may be due to Ramipril ( ACE inhibitor) that was then decreased in dose (Schell Puntillo, 2006). Continuous cardiac monitoring enables nurses to keep constant checks on heart rates and rhythms, it gives nurses the ability to act on any life threatening rhythms immediately or enables them with the knowledge of impending problems that could arise (Drew, 2004). Premature Ventricular Contractions (PVC), Ventricular Tachycardia (VT) or Ventricular Fibrillation(VF) are the most likely rythyms to be noted due to the scarring or necrotic myocardial tissue (Aehlert eInstruction Corp., 2011). Mr Smith was noted to have occasional PVCs that became more frequent until he was monitored in bigeminy, which can lead to runs of VT (Huszar, 2007). Monitored patients can be observed in pulseless VT/ VF via the central monitor at the nurses station and can be immediately defibrillated, whereas if a ward patient collapses a monitor needs to be attached before the heart rhythm can be established and treatment given (McDonough, 2009). ST Segment monitoring shows significant changes in monitoring that can indicate ischemia or infarction. Central monitors should have regular nurse surveillance, will alarm if there is a significant change to the ST segment. Changes occur with or without complaints of chest pain or shortness of breath, indicating myocardial oxygen mismatch (Smith, 2008). Patients need to advised to tell staff of chest pain whilst being monitored. Some patients assume nursing staff know from the monitor when they are experiencing chest pain. (Swearingen Keen, 2001) An ECG can be performed to show any significant changes of the heart. Mr Smith showed ST segment changes in his anterior /septal (V3 V4 position) aspect of his left ventricle. This area is supplied by the Left Anterior Descending Coronary Artery. Treatment does not differ depending on which area of the heart is affected. All areas require oxygen supply. While in hospital Mr Smith was ordered serial ECGs, these are taken daily to show any changes. Expected changes expected post MI are the development of a pathological Q wave. Q waves indicate the necrosis of myocardial tissue and specifically in V1 to V4 indicates anteroseptal infarction (Dubin, 2000) Mr Smith was initially given morphine, an opioid that relieves pain by decreasing myocardial oxygen demand by decreasing the Autonomic Nervous System and decreasing anxiety (Lewis, 2007). Nitro-glycerine, was ordered as a smooth muscle relaxant that vasodilates the vessels to restore blood supply if the mismatch is due to a coronary spasm(Yassin, 2007). Aspirin is given daily indefinitely as it is a antiplatelet aggregation inhibitor that Hung, 2008 states is proven for secondary prevention of myocardial infarction, stroke and cardiovascular death in both men and women. He also discusses the combined use of clopidigrel and aspirin to reduce subacute stent thrombosis after PCIs (Hung, 2008). Thrombolytic therapy is given within the first 6 hours of chest pain.(Levin, 2008) Tenecteplase 90mg was given. Thrombolytic Therapy is given to dispel the clot and allow blood flow to the affected area. It can take up to 90 minutes for full resolution to occur (Goldberger,2010). There are certain considerations that medical staff must ensure prior to administration of this therapy, these include an absence of CVA/TIAs or surgery in the last 12 weeks (Gibson, 2009). Once administered ECGs are taken in 15-30 min intervals to see changes of ST segment, showing that myocardial blood supply and depolarization being restored. Cardiac markers are Pathology tests that also give evidence of myocardial damage. When cardiac cells are damaged the membrane walls leak these substances into the blood stream (Aehlert eInstruction Corp., 2011). Myoglobin, Creatine kinase (CK), Troponin T and Troponin I are myocardial specific and along with ST elevation can be evident of a STEMI. Ëarly in ischaemia the ST segment may lose the ST-T wave slope and appear straight. Then as the T wave broadens and the ST segment rises, the segment loses its concave form and becomes upwardly convex with elevations (Moser Riegel, 2008). Non STEMI do not have a significant change on the ECG only cardiac markers alter. These markers usually peak between 15-24 hours post infarction and remain elevated for 2-3days (Huszar, 2007) Creatine Kinase has normal value of 45-250 U/L and Mr Smiths on admission was 4290 U/L decreasing to 800 U/L, 2 days post. Troponin T normal values are à ¢Ã¢â‚¬ °Ã‚ ¤0.03ug/L but Mr Smiths ranged from 14.20ug/L at 2200hours on the day of MI, to 4.39ug/L 2 days later. Serial pathology tests are taken usually every 6 hours for the first 24 hours. Mr Smith was taken for a PCI the day after his MI. He had a stent put in his proximal area of his Left anterior descending coronary artery (LAD) in the Cardiac Catheter Lab. Mr Smiths had a PCI even though his blood supply looked like it had been reinstated, the stent will prevent clot formation again and reocclussion (Cannon, 2010). He was then transferred back to CCU and remained RIB overnight. He had a femoseal deployed into his groin to occlude the opening of the femoral vessel used for this procedure. Nurses need to do regular neurovascular and pedal pulse observations to check for bleeding or vessel occlusion (Shoulders-Odom, 2008). Mr Smith needed to be educated on his procedure pre and post operative. He has previously been for this procedure but needed re-education. It must be a daunting experience to be given twilight sedation whist having the PCI. Mr Smiths last procedure was 13 years ago which would see many new techniques being practiced that he was not familiar with. His post op education included the importance of keeping his affected leg still and care of his affected groin.(Moser Riegel, 2008) Myocardial Infarction education can be given to him at the same time but this is information that needs to be reiterated continually during his hospitalization(Lewis, 2007). He and his family need to be aware of the risk of reinfarction especially in the next 2 weeks post MI as the heart muscle is still weak and irritable and increase in activity can cause another MI. This is the time that patients start to resume their normal daily activities after hospitalization and are at the most risk. (Douglas, 2010) Documentation is very important and needs to be filled out correctly as it is a legal document (Lewis, 2007). The CCUs clinical pathway for infarction indicated strict rest in bed with commode privileges for the first 48 hours, this decreases the need for myocardial oxygen. This is difficult for active patients but it needs to be strictly followed. Due to immobility other medical complications can arise, pneumonia and decreased gas exchange, deep vein thrombosis or emboli are common. To prevent these patients are encouraged to attend to hourly Deep Breathing Exercises (DBE), leg exercises and triflow. Patients can also be sat in an upright position which increases venous return (Thelan, 1994). Anticoagulants prevent clot formation therefore Mr Smith was administered daily Clexane 90mg post PCI until discharge and administered Abciximab (Reopro) for 12 hours post PCI. To test the adequacy of anticoagulants, INR and APPT are taken to check patients dose is therapeutic. Problems with ad ministering the anticoagulant after thrombolytic therapy is bleeding (Yassin, 2007). Mr Smith was noted to have large traces of blood in his urinalysis and was sent for a Pelvic Ultrasound to be sure there was no other complications, the ultrasound was NAD. Prior to discharge Mr Smith was educated on his new regime of medications and the importance of medication compliance to decrease his risks of further cardiac complications (Albert, 2008). Nurses if experienced and up to date with current research and practices can work alongside medical staff and initiate nursing cares that are in the best interest of patients. Coronary Care Units must have confident and competent nurses to run the ward as most times they make significant decisions on implementation of nursing care. When Doctors have confidence in the nurse looking after their patients they will respect and listen to nurses opinions because they know they are educated and empowered with knowledge.

European Economic and Monetary Union Essay -- essays papers

European Economic and Monetary Union The Economic and Monetary Union (EMU) is a single currency area within the European Union in which people, goods, services and capital move without restriction (Europa Quest (1), 2001). Imperative to the success of the EMU is the implementation of a single European currency, the Euro, and the application of specific macro-economic policies by the EMU member states (Harris, 1999: 78). Moreover, it is the foreseeable intent of European governments to create a framework for stability, peace and prosperity through the promotion of structural change and regional development (JP Morgan, 2001). This essay will endeavor to highlight the fundamental gains likely to be accrued by the European business community as a result of EMU policy provisions. The developments and circumstances preceding the EMU formation will be examined to give insight into the functioning of a monetary union. Furthermore, it is essential to analyze the implications the EMU has for firms within both ‘Euroland†™ and other European nations. To establish a strong understanding of the intricacies of the EMU, it is essential to discuss both the antecedents and major developments in this monetary union. The origins of the EMU can be traced to the formation of the European Coal and Steel community (ECSC) in the early 1950s, which was the first attempt to harness European economic unity to achieve greater international competitiveness (Per Jacobson, 1999) (Duisenberg, 1998). The success of this venture prompted the foreign ministers of six ECSC nations to examine the possibility of further economic integration (Chulalongkorn University, 1999). Hence, in 1957 one the most significant agreements in European economics history, The Treaty of Rome, was signed. The Treaty of Rome’s fundamental goal was to provide for the creation of a common market (Kenwood & Lougheed, 1999:280). The most significant aspect of this treaty was the commitment made by such countries as Belgium, France, West Germany, the Netherlands, Italy and Luxembourg to facilitate the free movement of goods, services and factors of production. Essentially, these European governments sought to eliminate internal trade barriers, create common external tariffs and harmonies member states laws and regulations (Hill, 2001: 233). This movement towards a common European market continued with relative success ... ...gheed, 1999. The Growth of the International Economy: 1820-2000. Routledge Press: London. ï‚ · Martin, Peter, 1997. EMU’s New Horizon. www.stern.nyu.edu/nroubini/EMU/. Visited Mach 2001. ï‚ · Preston Robert, 1997. Note of Confusion on Single Currency. www.princetoneconomics.com. Visited April 2001. ï‚ · Princeton Economics, 1998. Country Analysis: United Kingdom. www.princetoneconomics.com . Visted April 2001. ï‚ · Roubini, Nouriel, 1997. Notes on Europe, the Euro and EMU. www.stern.nyu.edu/nroubini/EMU . Visited April 2001. ï‚ · Salmon, Pierre, 2000. Decentralisation and Supernationality: The Case of the EU. www.imf.org. Visited April 2001. ï‚ · Salvatore, Dominick, 1998. International Economics (Sixth Edition). Prentice Hall: New Jersey. ï‚ · Solomon, Robert, 1999. International Effects of the Euro. www.brook.edu/comm/policybriefs/ . Visited March 2001. ï‚ · Soltwedel, Rudiger, Dohse Dirk & Krieger-Boden, Christianne. 2000. European Labour Markets and the EMU Challenges Ahead. www.imf.org . Visited April 2001. ï‚ · Tett, Gillian, 1996. The Single Currency: Everything you wanted to know? . www.stern.nyu.edu/nroubini/EMU . Visited April 2001.

Is India Safe for Its Residents? Essay

In fact I think INDIA is the safest place to live in on earth for Indians.Yes I do agree that there is terror of terrorism; but then u need to firmly fight againstit. U can run off ur responsibilities by saying that India is not a safe place. Toh†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦.. do u think that settling down in foreign can make u feel secure If u think so ur definitely wrong!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! Are Indians safe in a country like AUSTRALIA,infact Indians are insultedthere and where ever we go and what ever we do†¦..there is nothing that equals our mother and mother land. violence and problems maybe a trouble for us ..but i think there will be no placewith out problems †¦. what we need to do is justto manage ourselves†¦Ã¢â‚¬ ¦Ã¢â‚¬ ¦ any ways to sum it up..INDIA IS THE SUPERIOR,THE SUPREME AND THE HEAVEN FOR INDIANS. right ______________________________________†¦ In India there has been lack of political will and assertive decision making to bring such fugitives to justice. Barely a month later, with the Delhi blasts this weekend, the NSA might have to revise his earlier estimate; his claimssound meaningless. Jammu and Kashmir is facing unrest. The Northeast is unsettled.West Bengal andTelangana are simmering, over 160 districts in 13 states are in the grip of left wing extremism. While the crime rate is growing, abductions and extortions have almost become an industry. The rangdari and supari culture is now a new brandof threat to the Indian citizen.Money laundering, hawala, small arms proliferation and human trafficking are on the rise. The debate on countering these internal threats, however,has been overwhelmed by politics, rather than deterrent action.While India seems tobe safe are Indians secure? Or are we on course to a functional anarchy? India’s current crisis of internal security has been a concern particularly since Decembe r 2001. When terrorists assaulted Parliament, they struck at India’s nerve centre; a qualitatively different target; and at variance with India’s previous experience with multiple threats of insurgencies, terrorism, left wing extremism, narcotic trafficking, religious fundamentalism and subnationalism. The Indian security apparatus and elite are largely indifferent, or have shied away from formulating an internal security doctrine. There has been no serious attempt to institutionalise a mechanism, direction or assertive policy to deal with â€Å"internal threats†; interim, ad hoc and incremental means have been the favoured methods adopted by successive governments. There is virtually no means to define coherentlythe enemy within. The continuous assault on Indian citizens and their psyche has shown clearly that the security apparatus has failed to plug the reocurrence of terrorist attacks. The intelligence fraternity gropes in the dark about the actual strength, source, capacity and logistics of the enemy’s next attack.With our domestic security apparatus going so horribly awry we can take it for granted that we will almost never apprehend the killers. Worse, these terror attacks and militancy are seen as merely a â€Å"law andorder† concern and treated as subject of state, whenever, political violence on a massive scale breaks out in a state, the police become the first responders. The police in India are trained, equipped and mentally conditioned to deal only with civil disorders.When confronted with serious threats to internal securitylike terrorism, insurgency and other proxy war situations, they find it difficult to respond effectively. In such a situation, the state seeks the expertise of paramilitary forces. Creation of fast track courts to avoid judicial delay and enactment of a deterrent anti-terror law would constitute an essential step forward. The need of the hour is toinstitutionalise, develop procedures and processesthat would boost inter institutional co-ordination, facilitate professional conduct of operations on athorough, professional policy analysis. Lack of professional mindset for informed debate, fierce expression of spite, bitterness and mutual political acrimony take place instead of constructive policy discussions

USS Antietam (CV-36) in the Korean War

USS Antietam (CV-36) in the Korean War Entering service in 1945, USS Antietam (CV-36) was one of over twenty Essex-class aircraft carriers built for the US Navy during World War II (1939-1945). Though arriving in the Pacific too late to see combat, the carrier would see extensive action during the Korean War (1950-1953). In the years after the conflict, Antietam became the first American carrier to receive an angled flight deck and later spent five years training pilots in the waters off Pensacola, FL.   Ã‚   A New Design Conceived in the 1920s and early 1930s, the US Navys  Lexington- and  Yorktown-class aircraft carriers were intended to meet the limitations laid out by the  Washington Naval Treaty. This placed restrictions on the tonnage of various types of vessels as well as installed a ceiling on each signatory’s overall tonnage. This system was further extended by the 1930 London Naval Treaty. As the global situation began to deteriorate, Japan and Italy departed the treaty structure in 1936. With the collapse of this system, the US Navy commenced efforts to design a new, larger class of aircraft carrier and one which utilized the lessons learned from the  Yorktown-class. The resulting product was longer and wider as well as utilized a deck-edge elevator system. This had been employed earlier on  USS  Wasp  (CV-7). In addition to embarking a larger air group, the new class carried a greatly enhanced anti-aircraft armament. Construction began on the lead ship,  USS  Essex  (CV-9), on April 28, 1941. Becoming the Standard With the US entry into  World War II after the  attack on Pearl Harbor, the  Essex-class soon became the US Navys standard design for fleet carriers. The initial four ships after  Essex  followed the types original design. In early 1943, the US Navy ordered multiple alterations to improve future vessels. The most visible of these changes was the lengthening the bow to a clipper design which permitted the addition of two quadruple 40 mm mounts. Other alterations included moving the combat information center below the armored deck, enhanced ventilation and aviation fuel systems, a second catapult on the flight deck, and an additional fire control director. Colloquially known as the long-hull  Essex-class or  Ticonderoga-class by some, the US Navy made no distinction between these and the earlier  Essex-class ships. Construction The first ship to move forward with the revised  Essex-class design was USS  Hancock  (CV-14) which was later re-named Ticonderoga. It was followed by additional carriers including USS Antietam (CV-36).   Laid down on March 15, 1943, construction on Antietam commenced at the Philadelphia Naval Shipyard. Named for the Civil War Battle of Antietam, the new carrier entered the water on August 20, 1944 with Eleanor Tydings, wife of Maryland Senator Millard Tydings, serving as sponsor. Construction rapidly advanced and Antietam entered commission on January 28, 1945, with Captain  James R. Tague in command.   USS Antietam (CV-36) - Overview Nation:  United StatesType:  Aircraft CarrierShipyard:  Philadelphia Naval ShipyardLaid Down:  March 15, 1943Launched:  August 20, 1944Commissioned:  January 28, 1945Fate:  Sold for scrap, 1974 Specifications: Displacement:  27,100 tonsLength:  888 ft.Beam:  93 ft. (waterline)Draft:  28 ft., 7 in.Propulsion:  8 Ãâ€" boilers, 4 Ãâ€" Westinghouse geared steam turbines, 4 Ãâ€" shaftsSpeed:  33 knotsComplement:  3,448 men Armament: 4 Ãâ€" twin 5 inch 38 caliber guns4 Ãâ€" single 5 inch 38 caliber guns8 Ãâ€" quadruple 40 mm 56 caliber guns46 Ãâ€" single 20 mm 78 caliber guns Aircraft: 90-100 aircraft World War II Departing Philadelphia in early March, Antietam shifted south to Hampton Roads and commenced shakedown operations. Steaming along the East Coast and in the Caribbean until April, the carrier then returned to Philadelphia for an overhaul. Leaving on May 19, Antietam began its voyage to the Pacific to join in the campaign against Japan. Stopping briefly in San Diego, it then turned west for Pearl Harbor.   Reaching Hawaiian waters, Antietam spent the better part of the next two months conducting training in the area. On August 12, the carrier left port bound for Eniwetok Atoll which had been captured the previous year.   Three days later, word arrived of the cessation of hostilities and Japans impending surrender.    Occupation Arriving at Eniwetok on August 19, Antietam sailed with USS Cabot (CVL-28) three days later to support the occupation of Japan. Following a brief stop at Guam for repairs, the carrier received new orders directing it to patrol along the Chinese coast in the vicinity of Shanghai. Largely operating in the Yellow Sea, Antietam remained in the Far East for most the next three years. During this time, its aircraft patrolled over Korea, Manchuria, and northern China as well as conducted reconnaissance of operations during the Chinese Civil War. In early 1949, Antietam completed its deployment and steamed for the United States.   Arriving at Alameda, CA, it was decommissioned on June 21, 1949 and placed in reserve. Korean War Antietams inactivity proved short as the carrier was re-commissioned on January 17, 1951 due to the outbreak of the Korean War. Conducting shakedown and training along the California coast, the carrier made a voyage to and from Pearl Harbor before departing for the Far East on September 8. Joining Task Force 77 later that fall, Antietams aircraft began mounting attacks in support of United Nations forces.   Typical operations included interdiction of railroad and highway targets, providing combat air patrols, reconnaissance, and anti-submarine patrols. Making four cruises during its deployment, the carrier generally would resupply at Yokosuka. Completing its final cruise on March 21, 1952, Antietams air group flew nearly 6,000 sorties during its time off the Korean Coast. Earning two battle stars for its efforts, the carrier returned to the United States where it was briefly placed in reserve.   Ã‚   A Groundbreaking Change Ordered to the New York Naval Shipyard that summer, Antietam entered dry dock that September for a major alteration. This saw the addition of a sponson on the port side which permitted the installation of an angled flight deck. The first carrier to possess a true angled flight deck, this new feature permitted aircraft that missed landings to take off again without hitting aircraft further forward on the flight deck. It also greatly increased the efficiency of the launch and recovery cycle.   Re-designated an attack carrier (CVA-36) in October, Antietam rejoined the fleet in December. Operating from Quonset Point, RI, the carrier was a platform for numerous tests involving the angled flight deck.   These included operations and testing with pilots from the Royal Navy. The result from the testing on Antietam confirmed thoughts on the superiority of the angled flight deck and it would become a standard feature of carriers moving forward. The addition of an angled flight deck became a key element of the SCB-125 upgrade given to many Essex-class carriers during the mid/late-1950s.   Later Service Re-designated an anti-submarine carrier in August 1953, Antietam continued to serve in the Atlantic. Ordered to join the US Sixth Fleet in the Mediterranean in January 1955, it cruised in those waters until early that spring. Returning to the Atlantic, Antietam made a goodwill voyage to Europe in October 1956 and took part in NATO exercises.   During this time the carrier ran aground off Brest, France but was refloated without damage. While abroad, it was ordered to the Mediterranean during the Suez Crisis and aided in the evacuation of Americans from Alexandria, Egypt. Moving west, Antietam then conducted anti-submarine training exercises with the Italian Navy. Returning to Rhode Island,  the carrier resumed peacetime training operations. On April 21, 1957, Antietam received an assignment to serve as a training carrier for new naval aviators at Naval Air Station Pensacola.    Training Carrier Home ported at Mayport, FL as its draft was too deep to enter Pensacola harbor, Antietam spent the next five years educating young pilots. In addition, the carrier served as a test platform for a variety of new equipment, such as the Bell automatic landing system, as well as embarked US Naval Academy midshipmen each summer for training cruises. In 1959, following dredging at Pensacola, the carrier shifted its home port.   In 1961, Antietam twice provided humanitarian relief in the wakes of Hurricanes Carla and Hattie.   For the latter, the carrier transported medical supplies and personnel to the British Honduras (Belize) to provide aid after the hurricane devastated the region. On October 23, 1962, Antietam was relieved as Pensacolas training ship by USS Lexington (CV-16). Steaming to Philadelphia, the carrier was placed in reserve and decommissioned on May 8, 1963. In reserve for eleven years, Antietam was sold for scrap on February 28, 1974.

California Sea Otters essays

California Sea Otters essays The California, or southern, sea otter (Enhydra lutris nereis) is the only sea otter subspecies currently listed as an endangered species under the federal Endangered Species Act. The California sea otter is also a fully protected mammal by California state law and by the Marine Mammal Protection Act. In the 1700s, the sea otters were hunted to near extinction for their fur. In the late 1930s, a small population of otters (estimated at approximately 300) was discovered along Californias Big Sur coast. The California population is estimated at a mere 2,000 as of Fall 2001. Historically, there were between 16,000 to 20,000 sea otters along the coast of California Sea otters are classified as both an umbrella species, and a keystone species. As an umbrella species, the protections made for the sea otter will essentially affect a large number of other species in their ecosystem. A keystone species is a term used to refer to the sea otters functional role within their ecosystem. The feeding habits of the sea otters have a crucial effect on their ecological system, and their actions affect many of the organisms within their food chain. The sea otters can be referred to as indicators of the health of their ecosystem. Many causes have been recognized as contributing to the population decline: shark attacks, gunshot wounds, mating activities, fishing/net line injuries, habitat degradation, lack of an adequate food supply, land and water pollution, and disease. In a 1996 report, nearly 1700 sea otter deaths had been documented. The report stated that 18.9% of the deaths were from some sort of trauma, 12% from shark attacks, 4.6% from gunshot wounds, 2.3% from mating activities, 4.6% from fishing/net line injuries, 16.5% due to dependent animals, 4% from natural causes, and 56% of the deaths were undetermined. From 1992 to 1995 the National Wildlife Heath Center had examined approximately 5 ...

Treasury Yield Curve Coursework Example | Topics and Well Written Essays - 750 words

Treasury Yield Curve - Coursework Example Inflation affects purchasing power of money and therefore has a major effect on interest rates. Therefore if inflation rate is expected to be 1% during the next year this is added to the risk free interest rate (say 3.5%) and so the Treasury bill rate will be: rT-bill = rRF = r* + IP = 3.5% + 1% = 4.5% The inflation rate is the main factor which determines the shape of the treasury yield curve. If the inflation rate is expected to increase, then the treasury yield curve will slope upwards; which is normal. On the other hand, if the inflation rate is expected to decrease, then this will cause the treasury yield curve to slope downwards. Another factor affecting the Treasury bill rate is interest rate risk. When interest rates rises the prices of treasury bonds decline sharply and since this is a regular occurrence all long term bonds including treasury bonds have an element of interest rate risk. A maturity risk premium (say 2.5%) is therefore added to the risk free rate resulting in the following formula for calculating the Treasury bill rate. rT-bill = rRF = r* + IP + MRP. = 3.5% + 1% + 2.5 = 7% This premium increases with the time to maturity. Therefore, the longer the period the higher maturity risk premium. ... This information tells me that interest rates are subject to various economic conditions that will cause it to rise or fall and that the trend does not have to be continuous as it would appear from the examples seen. This yield curve has a dip and a hump indicating that the interest rates on one year maturities are higher than interest rates on 5 year maturities. The interest rates on medium term maturities rises constantly between year 6 and year 20 and then falls resulting in interest rates on some long term maturities being much lower than the interest rates on some in the medium term. Part 2 Yield to Maturity The yield to maturity is the annualized discount rate that equates the future coupon and payments to the future coupon and principal payments to the initial proceeds received from the bond offering (Madura 2006, p157). Consider Wal-Mart bond which matures on July 2015 with coupon rate of 2.25% which is paid semi-annually. The value of a bond (Vb) is found using the following formula. Vb = 1000 = [$11.25/(1 + rd/2)1] + [$11.25/(1 + rd/2)2] + [$11.25/(1 + rd/2)3] + [$11.25/(1 + rd/2)4] + [$11.25/(1 + rd/2)5] + [$11.25/(1 + rd/2)6] + [$11.25/(1 + rd/2)7] + [$11.25/(1 + rd/2)8] + [$11.25/(1 + rd/2)9] + [$11.25/(1 + rd/2)10] + [$1,0001/(1 + rd/2)10] The PV table can be used to find the figures for each of the ten six-monthly period: where $11.25 is the half yearly coupon rate. The time to maturity is five years and so Wal-Mart 2.25% Corporate Bond Time Periods Interest Payment Maturity Payment Total cash Flow PV Factor (1.125%) PV of Cash Flow    $ $ $    $'000 0       1000 1 1000 Par Value of Bond 1 11.25    11.25 0.9889 11.1251 2 11.25    11.25 0.9779 11.0014 3 11.25    11.25 0.967 10.8788 4 11.25    11.25

Food science Essay Example | Topics and Well Written Essays - 2500 words

Food science - Essay Example Bacteria require their own chow to produce and increase. There are different kinds of bacteria, which contaminate the food. Each type of bacteria causing food poisoning would be studied along with the symptoms and treatment separately. There are approximately 74 million cases of food poisoning out of which 323,000 hospitalized and nearly 4000 die yearly in the U. S. alone. According to CDC (Centers for Disease Control and Prevention) food poisoning is common in all groups of ages but particularly the children and aged people are most vulnerable to face serious penalties from food poisoning. During 1990 to 1994 numbers of children suffering from food poisoning were approximately 73 million but during the period from1985 to 1989 number of suffering children were 81 million. According to an estimate 400 to 500 children in the U.S die annually from food poisoning. The probability of having food poisoning is in fact very small when the number of food poisoning cases in the population of 21.4 million in Australia. Exact statistics of food poisoning cases are really very difficult to gather because a lot of cases are easygoing and not reported. In the year 2003, the FSIC (Food Safety Information Council) anticipated about more than 4 million Australians experience food poisoning each year. This is obviously a very huge number and this issue needs our deep focus, it also specifies that about 0.03% of meals are infected forms of food poisoning. The most worrying thing about food poisoning is that it can be deadly. Two aged people died by eating infected beef in Victoria in Feb. 2007; another died from food poisoning in hospital this year. These kinds of incidents speed up the need to develop food safety standards. A report published in 2005 reveals that nearly 130 people die from food poisoning every year in Australia. Mostly food poisoning