Case Summary On The Effects Of Unstable Angina Nursing Essay

Case Summary On The Effects Of Unstable Angina Nursing Essay Mr AR is a 41 years old male. His calculated BMI was 20.9kg/m2. His presenting complaint was chest pain which has lasted for three days before being admitted into the hospital. His chest pain was of pressing type, it occurred even at rest and lasted for 5-10 minutes each time. It was relieved slightly by rest and it was always accompanied by numbness on his left hand. He had shortness of breath, orthopnea, headache and low effort tolerance. He complained of abdominal discomfort also. He had stopped taking all his medications for the past three days. He had a pacemaker fixed 16 years ago for his atrial fibrillation (AF), but the pacemaker stopped functioning 3 years ago. Due to financial constraint, he did not go for a new pacemaker replacement. He underwent an angiogram last year and was found that he has 2 blocked vessels. He has a history of hypertension too. Before being admitted into the hospital, he has been taking frusemide 40mg twice daily, hydrochlorothiazide 25mg once daily, perindopril 8mg once a day and amlodipine 10mg once a day for his hypertension. For his AF, he has been taking warfarin 5mg once daily and digoxin 125microgram once daily. In addition, he took simvastatin 40mg at night for the prevention of cardiovascular events. Mr AR was found to have poor compliance. He always missed the dose, took the medications at the wrong time and was unsure the reason behind taking all his medications. He was first admitted to the acute and emergency department. ECG was carried out and there was no ST-elevation. His blood pressure was found to be high, 172/126mmHg. No troponin test was done on Mr AR, the only available test results on cardiac enzymes were that of creatine kinase (CK), aspartate amino transferase (AST) and lactate dehydrogenase (LDH). All three were not elevated. Hence, he was diagnosed with unstable angina, gastritis and hypertensive urgency. He was given nifedipine 10mg, aspirin 300mg, Sublingual GTN and plavix 300mg in the acute and emergency department. His management plans were to monitor his vital signs every hourly for two hours followed by every two hourly and to carry out dextrostix test three times daily. He was given 60mg enoxaparin subcutaneously immediately and twice daily thereafter, intravenous ranitidine 50mg three times daily, sublingual glyceryl trinitrate (GTN) one tablet when required and IV frusemide 20mg twice daily. He was restricted to fliud intake of 800mL per day and started on fliud input and output monitoring. He will also be started on low salt diet for the management of his hypertension. On day 2, he no longer complained of chest pain. His potassium level was found to be slightly lower than normal range (3.3mmol/L). His BP was still high throughout the day, fluctuating at around 150/120mmHg. He was started on tablet clopidogrel 75mg once daily. On day 3, IV frusemide was changed to oral frusemide. On day 4 his blood pressure has already dropped to around 120/90 mmHg. He was planned for discharge and enoxaparin was to be stopped on that day. Disease overview and pharmacological basis of drug therapy Mr AR was diagnosed with 3 diseases. Only unstable angina will be discussed. Unstable angina (UA) is categorized under acute coronary syndrome (ACS) which is very common in the UK. According to the hospital episode statistic year 2002-2003, there were 83842 cases of UA in England and 4421 cases in Wales.1 UA happened when there is insufficient myocardial oxygen supply to meet the oxygen demand of the heart. The reduction in the oxygen supply is due to the disruption of artherosclerotic plaque, causing the formation of intracoronary thrombus and hence narrowing of artery. Abnormal vasospasm of the coronary arteries or coronary dissection may also lead to UA. UA is closely related to non-ST elevated myocardial infarction (NSTEMI) as they have the same pathogenesis and both are presented as chest pain. The only difference between them is that in NSTEMI, there is a rise in the cardiac biomarkers such as cardiac troponin or the MB isoenzyme of creatine phospokinase (CK-MB), which indicate s myocardial injury. In UA, the ischemia is not severe enough to cause damage to the myocardial cells and thus releasing these biomarkers in detectible amount. For the diagnosis of unstable, the patients history of anginal symptoms should be obtained. Physical examination like cardiac examination and vital signs monitoring may also be done. Patient with ongoing chest discomfort should have a 12-lead ECG performed within 10 minutes of onset to check if there is any ST-elevation or depression. If there is no ST elevation, STEMI will be ruled out and the level of serum cardiac biomarkers will be used to determine if the patient has UA or NSTEMI. Troponin I or T are normally the biomarker chosen for detecting myocardial cell death as it is detectable in the serum 3-6 hours after a myocardial infarction and remained raised for 14 days. If the serum troponin level is less than 0.01 Ã‚ ­g/L, then the patient will be diagnosed to have unstable angina. CK-MB may also be used when troponin test is not available. In Mr AR case, the results on the cardiac enzymes available, namely AST, CK and LDH are all non specific cardiac biomarkers as those enzy mes can also be elevated in skeletal muscle injury or liver disease. The treatment of UA can be divided into emergency treatment and secondary prevention treatment.2,3 Patients must rest in bed and ECG monitoring should be continued during the early phase of hospital stay. Sublingual glyceryl trinitrate (GTN) tablet or spray should be given for the relief of angina symptoms. GTN is a fast acting coronary vasodilators. Dilatation of veins going to the heart reduces ventricular volume and preload, while dilatation of systemic conductive arteries together with the decrease in ventricular volume causes a reduction in afterload. These effects will all reduce the myocardial oxygen demand.4 GTN also found to dilate collateral vessels, thus the areas of ischemia will receive a higher blood flow. If the chest pain is not relieved by GTN, intravenous morphine sulphate can be given to ensure patient comfort. Patient with ongoing chest pain or high risk patients should be given inravenous beta-blockers followed by oral route if there is no contraindication. Inter mediate or low risk patients can be given oral beta-blockers. If beta-blocker is contraindicated such as the in presence of uncontrolled heart failure, or the chest pain is not relieved by GTN and beta-blocker, nondihydropyridine calcium channel blocker can be given. Antiplatelet therapy should be given immediately by giving aspirin 300mg initially, followed by 75mg once daily for long term secondary prevention. In addition, clopidogrel 300mg should be given initially and 75mg daily thereafter for 3 months. Aspirin works by inhibiting the cyclooxygenase (COX) 1 enzyme on the platelet, thus preventing the production of thromboxane which stimulates platelet aggregation.5 Clopidogrel is an antiplatelet which acts by inhibiting adenosine diphosphate (ADP) from binding to its receptor, hence blocking the activation of ADP-mediated glycoprotein GPIIb/IIIa complex, a step involved in aggregation of platelets.6 Unfractionated heparin (UH) or low molecular weight heparin (LMWH) is an important antithrombotic agent in the management of UA. LMWH is normally preferred over UH as it can be given subcutaneously and no coagulation monitoring is needed. LMWH like enoxaparin should be given for 2-8 days. Heparin binds to antithrombin and the complex formed deacti vates a series of enzymes involved in the coagulation process. Thus thrombus formation will be inhibited.7 Patients with high risk of MI or death should also be given glycoprotein IIb/IIIa antagonist such as eptifibatide, tirofiban or abciximab. For the secondary prevention treatment, in addition to aspirin and clopidogrel, beta-blockers should be continued indefinitely. Statins can be started regardless of the patients cholesterol level for the preventing cardiovascular events. Statins are 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, which act by inhibiting the biosynthesis of cholesterol.8 Angiotensin converting enzyme (ACE) inhibitors are useful in patients with UA also. They work by inhibiting the production of angiotensin II which is a potent vasoconstrictor and reducing the breakdown of bradykinin which is a potent vasodilator.9 Evidence for the treatment of the conditions When the patient was admitted to the acute and emergency department, he was given clopidogrel 300mg, aspirin 300mg immediately and was then continued with long term treatment of 75mg of clopidogrel. The use of clopidogrel for the long term treatment of unstable angina was supported by two large trials. First, the CAPRIE trial which compare the beneficial effect of clopidogrel versus aspirin in patients at high risk of ischaemic event.10 In this trial, patients were either given 75mg clopidogrel once daily or 325mg of aspirin once daily. The clopidogrel group has a marginally lower risk of ischaemic stroke, myocardial infarction, or vascular death (5.32%) compared to the aspirin group (5.83%). The side effects reported were similar in both groups, indicating that clopidogrel has a comparable safety profile to that of aspirin. The second trial is the CURE Trial which investigate the beneficial effect of adding clopidogrel to aspirin therapy in patients with non-ST elevation acute coronary syndrome.11 In this trial, 12,562 patients were given either 300 mg clopidogrel innitially, then 75 mg once daily or placebo plus aspirin for 3 months to a year. It was found that there was a lower rate of death from cardiovascular causes, nonfatal MI or stroke in the clopidogrel group. However, the risk of major bleeding was significantly higher in clopidogrel group. Hence, it can be concluded that long term clopidogrel should be used in patients with acute coronary syndrome in addition to aspirin. In addition, according to a meta-analysis done by the Antithrombotic Trialists Collaboration, long term treatment of aspirin in the range of 75-150mg was found to be beneficial in patients with acute coronary syndrome. In cases where antithrombotic effect is needed immediately such as during acute attack of MI or UA, aspirin at a dose of 300mg should be given.12 In Mr AR case, only 300mg of aspirin was given in the acute and emergency department, no long term treatment of aspirin was given. This might be due to his newly diagnosed gastritis. NSAIDs were found to cause or worsen gastritis.13 According to the AHA/ACC guideline, clopidogrel will be the alternative for patients intolerant to aspirin due to gastrointestinal problems. According to a study done by Harker LA et al. where the tolerability and side effects of aspirin and clopidogrel were compared using the results from the CAPRIE trial, it was found that the group of patients receiving clopidogrel has a lower percentage of gas trointestinal side effects, with a rate 27.1% compared to 29.8% in those taking aspirin (p < 0.001).14 This finding support the reason behind clopidogrel being the only antiplatelet given to Mr AR. However, The difference in the incidence of side effects between the two treatment group was small and higher rate of occurrence of gastrointestinal problem in aspirin group might be due to the high dose of aspirin used (325mg). The policy of the ACC/AHA guideline of using clopidogrel instead of aspirin in patient with a history of GI complication was also refuted by Chan and colleagues.15 In this study, 320 patients who had recovered from aspirin-induced upper GI bleeding were given either 75 mg of clopidogrel daily or 80 mg of aspirin daily together 20mg of proton-pump inhibitor esomeprazole twice daily. When the patients were followed up after one year, it was found that patients in the aspirin group has a lower rate of recurrent upper GI bleeding compared to those receiving clopidogrel plus esomeprazole (8.6% versus 0.7%, P=0.001). No protective effect was conferred by esomeprazole in aspirin-induced lower GI bleeding. Hence, low dose aspirin is still deemed appropriate in Mr ARs case if given with a proton pump inhibitor or H2-antagonist like ranitidine. On day 1 Mr AR was given 60mg of enoxaparin immediately and twice daily thereafter. A comparison between the efficacy of UH and LMWH was carried out in the ESSENCE trial.16 In this trial, patients were allocated either subcutaneous enoxaparin plus placebo bolus and infusion or bolus and infusion unfractionated heparin plus placebo subcutaneous injection. In addition, they were all given oral aspirin. It was found that the enoxaparin group has a lower rate of recurrent angina, MI or death and also the need of revascularization process. Hence it was concluded that enoxaparin is more advantageous than UH, as there is little protein binding, longer plasma half life and more resistant to neutralisation by platelet factor IV as compared to UH. The dose given to Mr AR is justified according to a trial where the dose of enoxaparin was adjusted according to the weight of the patients. 17 It was found that giving 1mg/kg of enoxaparin to patients with UA or non-Q wave MI resulted in a lower ris k of major bleeding compared to giving a dose of 1.25mg/kg (6.5% versus 1.9%). Mr ARs weight was 59kg, thus a dose of 60mg is appropriate and evidence based. Sublingual GTN was given to Mr AR for the relief of his chest pain. According to the British Medical Journal evidence centre, no good evidence was found on the angina. There is one randomized placebo controlled study done by Karlberg et al. where they compared the effectiveness of intravenous GTN versus placebo in reducing ischaemic attack in unstable angina.18 In this trial, they found that patients given GTN have a fewer new onset of chest pain compared to placebo group. No trial was done to investigate the effectiveness of sublingual GTN in preventing ischaemic attack. However, according to a methodological study done by G Nyberg to determine the time of onset of sublingual GTN, it was found there was a significant reduction in the intensity of exercise induced chest pain and an improvement in the ST-depression when 0.5mg of GTN was given sublingually at the onset of chest pain.19 Hence, there is a consensus that sublingual GTN can be used for symptomatic control of unstable angin a. Mr ARs previous medications were continued during the hospital stay. Among those medications, perindopril, an ace-inhibitor, is also proved to be beneficial in the prevention of MI. There are two well known studies done on the effect of ace-inhibitors in preventing cardiovascular event in patients with cardiovascular disease, namely the HOPE trial and the EUROPA trial.20,21 In the HOPE trial, ramipril was chosen as the treatment drug. As for the EUROPA trial, perindopril was chosen to investigate if there is any beneficial effect in preventing MI, cardiac arrest or mortality in patients with stable coronary disease. It was found out that in the group of patients receiving perindopril, there was a 20% relative risk reduction in the primary end point as compared to the placebo group. Hence, it was concluded that perindopril should be given to all patients with coronary heart disease, including Mr AR who has unstable angina. In addition, Mr AR was continued with 40mg simvastatin once daily at night. According to a trial on simvastatin, it was found that giving simvastatin to high risk patients lowers their cholesterol level and reduces the incidence of cardiovascular events.22 In this trial, 20536 adults in the UK with high risk of getting cardiovascular event were given simavastatin 40mg daily or placebo. It was found that the simvastatin group has a lower percentage of all cause of death (12.9%) and major vascular event (19.8%) compared to the placebo group (14.7% and 25.2% respectively). There was a difference of about 1.0mmol/L in the LDL cholesterol level between the two groups after treatment regardless of the initial cholesterol level. This indicates that there is a reduction in the LDL cholesterol level in the simvastatin group which is independent on the initial cholesterol level. For patient given simvastatin, the risk reduction of the first major vascular event is similar no matter the patient s were taking ace inhibitors, aspirin, beta blockers or antihypertensive drugs or not. This shows that simvastatin provides additional benefits when added to the existing treatment with these drugs. Thus, it can be concluded that simvastatin will be beneficial to Mr AR who was taking ace inhibitor and antihypertensive drugs concurrently. Mr Ar was newly diagnosed with gastritis and was commenced on IV ranitidine. In a double blind clinical study, patients diagnosed with gastritis were given 300mg ranitidine daily for 4 weeks or placebo only.23 It was found that patients from the ranitidine group improved significantly faster than the placebo group and 80% of the patients had their symptoms completely resolved. Only 45% of the patients from placebo group achieved improvement in their symptoms while the remaining showed no change in their gastritis. Hence, it was concluded that ranitidine is an effective treatment option for gastritis. However, this trial only involved 52 patients and this small sample size renders the finding from trial inconclusive. In another trial where the effectiveness of ranitidine and sucrafate was compared, it was found out that both have a similar activity in relieving the symptoms of gastritis.24 77.6% of the patients receiving sucralfate and 79.4% from the ranitidine group had their symptom s completely resolved at the end of the study period (8 weeks). However, ranitidine was found to act faster in relieving pain compared to sucralfate. Hence, it can be concluded that the management of Mr ARs gastritis with ranitidine is justified. Mr AR was given nifedipine 10mg for the treatment of his hypertensive urgency. Even though nifedipine was found to be effective in reducing blood pressure within 20 minutes, this fast release, short-acting calcium channel blocker are not recommended in this case as Mr AR did not receive any beta-blocker before. According to the results obtained from the Holland Interuniversity Nifedipine/metoprolol Trial (HINT), monotherapy with nifedipine in patients with unstable angina naà ¯ve to beta blockers was associated with a higher risk of recurrence ischaemic attack or MI.25 The event rate ratio compared to placebo for beta blocker naà ¯ve, nifedipine only group was 1.15. As for the group receiving both nifedipine and metoprolol, the ratio was lower (0.80). Patients who were already receiving beta blockers and were added with nifedipine also showed lower rate ratio (0.68). Hence, it was concluded that nifedipine was only beneficial in patients who were treated with beta blocker at the sa me time. Moreover, it was found from the Trent study that nifedipine does not show any beneficial effect in patients with MI.26 In this trial, the death rate for patients receiving nifedipine 10mg four times daily and placebo was similar. When the number of death and MI were compared among patients taking beta blocker and not taking beta blocker among admission, it was found that the latter group has a higher rate of death and MI. This result is comparable to those from the HINT trial. Hence, the use of nifedipine in treating Mr ARs hypertensive urgency is not justified, other drug should be chosen. Conclusion The immediate treatment of UA with high dose of antiplatelet agent aspirin and clopidogrel together with the antithrombotic agent LMWH are justified as they help preventing the progression of UA to MI. Sublingual GTN on the other hand helps relieving his chest pain. As for his previous perindopril and simvastatin that were continued, these help in preventing recurrent angina also. Choosing clopidogrel for the long term prevention treatment of UA due to the presence of gastritis might not be the best option for Mr AR. Once his gastritis has resolved, life-long aspirin at the dose of 75mg should be added in with oral ranitidine 300mg twice daily prescribed as prophylaxis against NSAID induced gastritis. However, the use of nifedipine in the management of his hypertensive urgency is not justified. Instead, he should be given labetalol, atenolol or clonidine which were found to be better alternatives to nifedipine in treating hypertensive urgency.27 PATIENT MEDICATION PROFILE Patient details Name: AG Consultant: General Practitioner: Address: Gender: Male Weight: 59kg Height: 168cm Community pharmacist: Age: 41 Known sensitivities: NKDA Social history: Non-smoker, No alcohol abuse. Patient hospital stay Reason for admission Admission date: Chest pain. Discharge date: Relevant medical history Relevant drug history Date Problem description Medication Comments 1994 Pacemaker fixed Warfarin 5mg OD Atrial fibrillation 2007 Pacemaker not functioning, did not go for replacement due to financial constraint T digoxin 125mcg OD Atrial fibrillation 2007 Angiogram, 2 blocked vessels T frusemide 40mg BD Hypertension Hypertension Perindropil (coversylƒ’) 8mg OD Hypertension T amlodipine 10mg OD Hypertension Hydrochlorthiazide 25mg OD Hypertension T simvastatin 40mg ON Prevention of cardiovascular event Prescribed medication Route of administration Start Stop Nifedipine (adalat) 10mg PO Day 1 Aspirin 300mg PO Day 1 Day 1 Clopidogrel (plavixƒ’) 300mg PO Day 1 Day 1 Clopidogrel (plavixƒ’) 75mg OD PO Day 2 Enoxaparin (Clexaneƒ’) 60mg stat, BD subcutaneous Day 1 GTN 1 tablet PRN sublingual Day 1 Simvastatin 40mg ON PO Day 1 Amlodipine 10mg OD PO Day 1 Hydrochlorothiazide 25mg OD PO Day 1 Warfarin 5mg OD PO Day 1 Furosemide (Lasix) 40mg stat, BD IV Day 1 Day 3 Furosemide 40mg BD PO Day 3 Perindopril (Coversylƒ’) 8mg OD PO Day 1 Ranitidine (zantac) 50mg tds IV Day 1 Digoxin 125mcg OD PO Day 1 Clinical/ Laboratory Tests Date Results Potasium (3.5-5.0 mmol/L) Day 2 3.3 BP Day 2 150/118 Day 3 134/100 Day 4 122/86 Pharmaceutical Care Plan Care Issue Action Actual output/ Desired output Long term treatment with aspirin. Patient should be given 75mg of aspirin for the secondary prevention of UA. Patient has gastritis. He should be started on long term treatment of aspirin once his gastritis has resolved and ranitidine should be prescribed as prophylaxis against NSAIDs induced GI complications. Long term treatment with beta blockers. Beta blocker should be given to the patient as the secondary prevention treatment. Patient should be started on labetalol 100mg twice daily and titrate up to 200mg twice daily. Inappropriate use of nifedipine for the management of hypertensive urgency. Nifedipine should be substituted with labetalol 200-300mg every 3-4 hours when required. Not taken. Interaction between digoxin and diuretics when hypokalaemia occur. Potasium level should be monitored. Inform the patient on signs and symptoms of digoxin toxicity. Patients potassium level was lower than the normal range on day 2. He should be given potassium sparing diuretics or potassium supplement if the potassium level keeps going down. Monitoring should be continued. High risk of bleeding due to warfarin, aspirin, clopidogrel and enoxaparin. Bleeding tendency should be monitored. Patient should be told to inform the GP if there is any unusual bleeding like blood in the stool. Patients INR and prothrombin time were within the normal range. Monitoring was continued. Changing of IV ranitidine to oral ranitidine. Patient should be switched to oral ranitidine150mg twice daily after being discharged. Not taken. GTN for relief of angina symptoms. Patient should be prescribed GTN spray or sublingual tablet for the relief of chest pain shoul the patient has another angina attack. GTN sublingual tablet was prescribed as discharge medication. Poor patient compliance Patient should be informed on the reason behind taking his medication, the importance of compliance. Compliance aid should be given. Patient was counselled on the importance of compliance. Side effects of simvastatin -muscular side effects -liver disease Patient should be advised to report immediately any unexplained muscle pain, weakness nor tenderness. Regular LFT monitoring should be done. No monitoring of cholesterol level. Cholesterol level should be monitored suring the hospital stay so that the dosage of simvastatin can be adjusted accordingly. Cholesterol level should be maintained below 5.2mmol/L. Patient education on healthy lifestyle. Patient should be told on the importance of low salt diet for his HT and encouraged to exercise more. Patient was counselled on the importance of healthy lifestyle before being discharged.

Drag in aircrafts

There are four forces that act on an aircraft in flight: lift, weight, thrust, and drag. Aircraft’s motion in air is dependent on the relative magnitude and direction of these forces. Fig -1 below shows the direction of these forces. Fig 1 (Benson, 2006) The weight of an airplane is always directed towards the center of the earth. The thrust is normally directed forward along the center-line of the aircraft. Lift and drag are aerodynamic forces on the airplane.Drag acts in a direction opposite to the motion of the aircraft and hence is sometimes referred to as the aerodynamic friction, while lift force acts perpendicular to the motion. An aircraft is in a state of equilibrium when the thrust and drag are equal and opposite. It will continue to move forward at the same uniform speed. If thrust or drag becomes greater than the opposite force, the aircraft loses its state of equilibrium. If thrust is greater than drag, the aircraft will accelerate. If drag is greater than thrust, the aircraft will lose speed and eventually descend.When lift and weight are equal and opposite, the airplane is in a state of equilibrium. If lift is greater than weight, the aircraft will climb. If weight is greater than lift, the airplane will descend. Drag is the aerodynamic force encountered as an airplane pushes through the air, which tends to slow the airplane down. Drag is generated by the contact of a solid body with a fluid, in this case due to the interaction between the plane body and air. Drag force, which is a mechanical force, is generated by every part of the airplane including the engines.It is a vector quantity i. e. has both magnitude and direction. Drag must be overcome by thrust in order to achieve forward motion. Drag is generated by nine conditions associated with the motion of air particles over the aircraft. Although prediction of drag and wind tunnel drag measurements of models yield good results, final drag evaluation must be obtained by flight tests. Sou rces of Drag in aircrafts Drag can be thought of as aerodynamic friction, and one of the sources of drag is the skin friction between the molecules of the air and the solid surface of the aircraft.Drag can also be thought of as aerodynamic resistance to the motion of the object through the fluid. This source of drag depends on the shape of the aircraft and is called form drag. As air flows around a body, the local velocity and pressure are changed. Since pressure is a measure of the momentum of the gas molecules and a change in momentum produces a force, a varying pressure distribution will produce a force on the body. This causes pressure drag. As an aircraft approaches the speed of sound, shock waves are generated along the surface.There is a drag penalty, known as wave drag that is associated with the formation of the shock waves. The magnitude of the wave drag depends on the Mach number of the flow. Ram drag is associated with slowing down the free stream air as air is brought i nside the aircraft. Jet engines and cooling inlets on the aircraft are sources of ram drag. (Benson, 2006) There is an additional drag component caused by the generation of lift, known as induced drag, is the drag due to lift. It is also called â€Å"drag due to lift† because it only occurs on finite, lifting wings.This drag occurs because the flow near the wing tips is distorted span wise as a result of the pressure difference from the top to the bottom of the wing. Swirling vortices are formed at the wing tips, which produce a downwash of air behind the wing which is very strong near the wing tips and decreases toward the wing root. The local angle of attack of the wing is increased by the induced flow of the down wash, giving this, downstream-facing, component to the aerodynamic force acting over the entire wing. Types of Drag in aircrafts There are several types of drag: form, pressure, skin friction, parasite, induced, wave and ram.However, form, pressure, skin friction, wave and ram drags are collectively known as parasite drag. Hence, there are only two types of drag: parasite and induced Parasite drag – Profile or parasite drag is caused by the airplane pushing the air out of the way as it moves forward. The parasite drag of a typical airplane consists primarily of the skin friction, roughness, and pressure drag of the major components. Some additional parasite drag is also due to things like fuselage upsweep, control surface gaps, base areas, and other extraneous items.The basic parasite drag area for airfoil and body shapes can be computed from the following expression: f = k cf Swet, where the skin friction coefficient, cf , which is based on the exposed wetted area includes the effects of roughness, and the form factor, k, accounts for the effects of both super-velocities and pressure drag. Swet is the total wetted area of the body or surface. Computation of the overall parasite drag requires that we compute the drag area of each of t he major components (fuselage, wing, nacelles and pylons, and tail surfaces) and then evaluate the additional parasite drag components described above.Hence it is written as: CDp = S ki cfi Sweti / Sref + CDupsweep + CDgap+ CDnac_base + CDmisc, where the first term includes skin friction, and pressure drag at zero lift of the major components. cfi is the average skin friction coefficient for a rough plate with transition at flight Reynolds number. Equivalent roughness is determined from flight test data. (http://adg. stanford. edu/aa241/drag/parasitedrag. html) Induced drag – Induced drag is the part of the force produced by the wing that is parallel to the relative wind, i. e. the lift.As it is a consequence of the vortices it is sometimes called vortex drag. Induced drag is least at minimum AOA and is greatest at the maximum AOA i. e. angle of attack. Induced drag = (k ? CL? / A) ? Q ? S where A is the wing aspect ratio. (Preston, R) The magnitude of induced drag depends on the amount of lift being generated by the wing and on the wing geometry Long, thin (chord wise) wings have low induced drag; short wings with a large chord have high induced drag. An airplane must fight its way through both kinds of drag in order to maintain steady flight.. Total drag is a sum of Parasite and Induced drag. Total Drag = Parasite drag + Induced drag However, the total drag of an aircraft is not simply the sum of the drag of its components. When the components are combined into a complete aircraft, one component can affect the air flowing around and over the airplane, and hence, the drag of one component can affect the drag associated with another component. These effects are called interference effects, and the change in the sum of the component drags is called interference drag. Thus, (Drag)1+2 = (Drag)1 + (Drag)2 + (Drag)interference (Johnston, D)Generally, interference drag will add to the component drags but in a few cases, for example, adding tip tanks to a wing , total drag will be less than the sum of the two component drags because of the reduction of induced drag. Total drag and its variation with altitude The equation for total drag is: D = CD x S x ? rV2 (Preston, R) where, CD is the coefficient of drag. It must be subdivided into two parts, the Cdi (Coefficient of induced drag) and CDp (Coefficient of parasite drag. ). Therefore it can be written as: D = (Cdi + Cdp) x S x ? rV2 (Preston, R)The airplane's total drag determines the amount of thrust required at a given airspeed. Thrust must equal drag in steady flight. Lift and drag vary directly with the density of the air. As air density increases, lift and drag increase and as air density decreases, lift and drag decrease. Thus, both lift and drag will decrease at higher altitudes. Fig 1 shows the total drag curve which represents drag against velocity of the object. The fuel-flow versus velocity graph for an air graph is derived from this graph, and generally looks as shown in Fig 2 Fig – 1 (Preston, R) Fig – 2 (Preston, R) From the above drag it is seen that the total drag is minimum at a certain velocity. This occurs when the parasitic drag is equal to the induced drag. Below this speed induced drag dominates, and above this speed parasite drag dominates. Design engineers are interested in minimizing the total drag. Unfortunately many factors may conflict. For example, longer wing span reduces induced drag, but the larger frontal area usually means a higher coefficient of parasite drag. Conversely, a high wing loading (i. e.a small wing) with a small aspect ratio produces the lowest possible parasite drag but unfortunately is the produces for a lot of induced drag. In recent time it is seen that jet airliners have longer wings, to reduce induced drag, and then fly at higher altitudes to reduce the parasite drag. This causes no improvement in aerodynamic efficiency, but the higher altitudes do result in more efficient engine operation. (Preston, R) Angle of Attack (AOA), is the angle between the wing and the relative wind. Everything else being costant, an increase in AOA results in an increase in lift.This increase continues until the stall AOA is reached then the trend reverses itself and an increase in AOA results in decreased lift. The pilot uses the elevators to change the angle of attack until the wings produce the lift necessary for the desired maneuver. Besides AOA other factors also contribute to the production of lift, like relative wind velocity and air density i. e. temperature and altitude. Changing the size or shape of the wing (lowering the flaps) will also change the production of lift. Airspeed is absolutely necessary to produce lift.If there is no airflow past the wing, no air can be diverted downward. At low airspeed, the wing must fly at a high AOA to divert enough air downward to produce adequate lift. As airspeed increases, the wing can fly at lower AOAs to produce the needed lift. This is why airplane s flying relatively slow must be nose high (like an airliner just before landing or just as it takes off) but at high airspeeds fly with the fuselage fairly level. The key is that the wings don't have to divert fast moving air down nearly as much as they do to slow moving air.Air density also contributes to the wing's ability to produce lift. This is manifested primarily in an increase in altitude, which decreases air density. As the density decreases, the wing must push a greater volume of air downward by flying faster or push it down harder by increasing the angle of attack. This is why aircraft that fly very high must either go very fast e. g. Mach 3, or must have a very large wing for its weight. This is why the large passenger airplanes cruise at higher altitude to reduce drag, and hence save on the furl costs.(â€Å"Aircraft for Amateurs†, 1999) Small sized aircrafts have lower than normal Reynolds number. The drag coefficient attributable to skin friction is hence high er for the small aircraft. For this reason, the maximum lift-drag ratios characteristic of business jet aircraft tend to be lower than those of the large transports. Hence, the smaller flights can fly at relatively lower altitudes. References Books John A. Roberson & Clayton T. Crowe, 1997, Engineering fluid Mechanics, 6th ed. , John Weily & Sons Inc. , ISBN 0-471-14735-4.Clement Klienstreuer, 1997, Engineering Fluid Dynamics, Cambridge University Press, ISBN 0-521-49670-5 Websites â€Å"Aircraft for Amateurs†, 11th Jan. 1999 http://www. fas. org/man/dod-101/sys/ac/intro. htm Benson, T. , â€Å"The Beginner’s guide to Aeronautics†. , 14th March 2006 http://www. grc. nasa. gov/WWW/K-12/////airplane/ Johnston, D. , â€Å"Drag†, http://www. centennialofflight. gov/essay/Theories_of_Flight/drag/TH4. htm â€Å"Parasitic Drag†, http://adg. stanford. edu/aa241/drag/parasitedrag. html Preston, R. , â€Å"Total Drag† and â€Å"Flight Controls† , http://selair. selkirk. bc. ca/aerodynamics1/

Death as a Main Theme of Philip Larkin’s Aubade

Aubade is the last poem by Philip Larkin. This poem became the culmination of his life and work and contains basic ideas of Larkin’s philosophical and literary credo. This poem became Larkin’s profound and personal investigation of the theme of death. Published in the Times Literary Supplement for the first time, this poem became a characteristic feature of his literary work. The poem is full of symbolism. The very title, Audabe, or Morning Serenade, creates anticipations in the minds of the readers and Larkin uses contrast in order to deliver his message to the readers. His aubade turns to be anti-aubade and this sad irony only underlines contrast and irony, used by the author. He uses a popular romantic title for his poem in order to underline the loss of innocence in the perception of the world.The very first lines of the poem describe typical day of routine life of the person, who does not see any sense in his life and spends dull days and sleepless nights thinking about inevitable death.Till then I see what’s really always there: Unresting death, a whole day nearer now, Making all thought impossible but how And where and when I shall myself die (Larkin 69).The theme of death and depression is typical for the works of Larkin. The theme of death and fear of dying goes through the entire poem. Scepticism and pragmatic view on religion give special shades of meaning to the theme of death. He speaks about it without idealization and pathos but, at the same time, he does not hide his feelings of fear and despair in front of this phenomenon. His pessimistic and gloomy mood makes the poem sound accordingly. As famous Donald Hall wrote about Philip Larkin in his article, â€Å"This is the man who famously said that deprivation was for him what daffodils were for Wordsworth. Yet surely the results of this life, in the shape of his poems, are gifts, not deprivations† (Hall 117).Larkin got the reputation of a melancholy poet. His light sorr ow and gloomy intonations became a visit card of all his literary works. Mixture of wit, humour and sad irony add special zest to sad motifs of Aubade.Dread of death creates a dark background of the poem. The author thinks about things he did not accomplish yet and describes gradual extinction and the most terrible thing.The sure extinction that we travel to And shall be lost in always. Not to be here, Not to be anywhere, And soon; nothing more terrible, nothing more true (Larkin 69).He can not stop thinking about state of non-being, which will naturally become a final destination for everybody. Being away from pathetic feelings he looks for a distinct place, which would become the house for humans after death and does not find such a place. This though deprives him of sleep and fulfills all his thoughts.His vision of death is determined by his philosophical credo and religious beliefs. All Western tradition regards death as an eternal rest and, if not to turn to religious explanati ons, the death appears as a final termination of the human existence.  Ã‚  Larkin rejects this view, calling the death â€Å"unresting†. This word combination makes and oxymoron as the term â€Å"death† itself assumes rest and calmness (Webster's New World College Dictionary).   Ã‚  Finally, the theme of death as an unresting thing, which does not bring pleasure and calm, becomes one of the main themes of the poem. He also uses unresting in another shade of the meaning. He turns to the word unresting in order to show that death is a phenomenon which can not be escaped or avoided by anybody. Nobody can escape death and all people are equal in front of it. As he states in the poem, â€Å"Most things may never happen: this one will†Ã‚  (Larkin 69).The very structure of the poem serves in order to help the author to deliver this message to the readers. Somewhat unusual structure of the poem does not make logical pauses at the end of the stanzas. The parts of the poem are connected so closely that they turn to each other as a continuous process, where motion does not stop for a single second. Sentences do not end at the end of the lines. Larkin uses long sentences, which rest for several lines and even when they end, it usually happens in the middle of the line, so that the next sentence starts immediately. For example, â€Å"no sight, no sound, / No touch or taste or smell, nothing to think with, / Nothing to love or link with†Ã‚  (Larkin 69). Such structure does not let the reader rest and make poses.It reminds the readers about the flowing nature of life, when people can not stop and have a rest haunted by the unresting death. Even in the cases when there are poses at the end of the lines the sentences are not completed, and the reader can not keep long poses, since the line does not contain a terminated thought and next lines continue ideas from the previous ones. Making a pause between the lines and having a rest becomes same im possible, as having a pause in one’s life and taking time to think over important things and finish things, which are not finished.Special structure of sentences is not the only means used by Larkin in order to attract the readers’ attention to the unresting nature and inevitable character of death. Gloomy and depressive tones of the poem show this very nature of death. The author uses sad irony and light sorrow in order to show naivety of people, who try to escape thoughts about death and pretend that this will never happen to them, even despite they are surrounded by death every day of their lives. People seek for stability and guarantees but finally it turns out that death can be the only stable thing in this world.The second stanza illustrates the author’s attitude to religion. Larkin does not believe in the pictures of afterlife, created by different religious doctrines.   His pessimistic attitude towards religions does not let him accept any kind of non- rational explanation of the life after death. â€Å"Larkin’s last major poem, Aubade is to conclude his religious poetic oeuvre with an internal argument of the poetic persona on religion and what remains after death† (Lerner 183). The author spends sleepless nights thinking about death. He spends hours trying to imagine the state, where all the senses cease their existence and a person looses all connections with the existence. Larkin goes further than just philosophical reflections about the death, he thinks about physical experience of â€Å"no-being†. As he states, â€Å"This is what we fear—no sight, no sound, / No touch or taste or smell, nothing to think with, / Nothing to love or link with† ( Larkin 69).Physical nature of death becomes the focus of Larkin’s attention. Such an attitude reduces human life to physical existence and that is the reason the author becomes so desperate to find any explanations of things, which will happen t o him after death.   As states Adam Stainer, â€Å"His inability to palliate his mind’s sense of panic mirrors the other figure depicted as unresting in the poem—death itself†   (Stainer 16). And even her unresting nature of death is obvious. Looking for a possible description of the state of non-living, Larkin can not escape a thought that this state will last forever. He regards the death not as a single event, which causes transformation, but rather as a continuous process of perpetual anaesthesia, where people stay forever.Larkin uses irony to show how eternal state of nothingness can be the most terrible thing, which brings neither calm nor peace.   What is notable, even during short period of life people can not get rid of the threat of death. It surrounds them whatever they do and the author does his best to show this state of living under constant threat in his poem. Ceaseless nothingness appears to be the biggest Larkin’s fear and this thou ght does not let him fall asleep at nights and deprives him of calm and happiness when he is awake.In the next stanza he speaks about courage, which turns to be useless in the face of death. Merciless nature of death makes no distinctions between those, who are afraid of it and who are not.The last lines of the poem contain a deep metaphor, making a contrast between routing life and death, which he can not forget about even for a minute.Meanwhile telephones crouch, getting ready   to ring In locked-up offices, and all the uncaring Intricate rented world begins to rouse. The sky is white as clay, with no sun. Work has to be done. Postmen like doctors go from house to house (Larkin 69).Postmen, walking from one house to another, symbolize for Larkin inevitable approaching of the dawn, which, in its turn, symbolizes an inevitable approach of death. He compares them to doctors, who must save people’s lives but constantly fail, as nobody can overcome death. Careless world wakes up in order to make one step towards death. For Larkin this is a phenomenon he can neither escape, nor forget.  The author does not separate thoughts about his own death from the general philosophical questions. This underlines Larkin’s perception of the death as the most private and the most common and public event at the same time.Works CitedAgnes, Michael, ed. in chief, Webster's New World College Dictionary, fourth edition, MacMillan, 1999.Hall,   The New Criterion Vol. 4, No. 6, February 1986.Kirszner, Laurie G., and Stephen R. Mandell, eds. Literature: Reading, Reacting, Writing. 6th ed. Boston: Wadsworth, 2007.Larkin, Philip. Collected Poems,   Farrar Straus & Giroux, 1989.Lerner, Laurence: Philip Larkin. In Writers and Their Works series.   Plymouth: Northcote House Publishers Ltd., Plymbridge House, 1997.Steiner, Adam. Honors British Literature. Dr. Fraser. Concepts of Rest and Unrest in â€Å"Aubade†, 2005.Salwak, Dale ed. Philip Larkin: The Man and H is Work. London: MacMillan, 1989.

Summary Investigative Journalism Essay - 952 Words

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