Battle of the Bismarck Sea in World War II

The Battle of the Bismarck Sea was fought March 2-4, 1943, during World War II (1939 to 1945). Forces Commanders Allies Major General George KenneyAir Commodore Joe Hewitt39 heavy bombers, 41 medium bombers, 34 light bombers, 54 fighters Japanese Rear Admiral Masatomi KimuraVice Admiral Gunichi Mikawa8 destroyers, 8 transports, approx. 100 aircraft Background With defeat looming in the Battle of Guadalcanal, the Japanese high command began making efforts in December 1942 to reinforce their position in New Guinea. Seeking to shift around 105,000 men from China and Japan, the first convoys reached Wewak, New Guinea in January and February delivering men from the 20th and 41st Infantry Divisions. This successful movement was an embarrassment to Major General George Kenney, commander of the Fifth Air Force and Allied Air Forces in the Southwest Pacific Area, who had vowed to cut off the island from re-supply. Assessing the failures of his command during the first two months of 1943, Kenney revised tactics and embarked on a rapid training program to ensure better success against maritime targets. As the Allies set to work, Vice Admiral Gunichi Mikawa began making plans to shift the 51st Infantry Division from Rabaul, New Britain to Lae, New Guinea. On February 28, the convoy, consisting of eight transports and eight destroyers assembled at Rabaul. For additional protection, 100 fighters were to provide cover. To lead the convoy, Mikawa selected Rear Admiral Masatomi Kimura. Striking the Japanese Due to Allied signals intelligence, Kenney was aware that a large Japanese convoy would be sailing for Lae in early March. Departing Rabaul, Kimura originally intended to pass south of New Britain but changed his mind at the last minute to take advantage of a storm front that was moving along the north side of the island. This front provided cover through the day on March 1 and Allied reconnaissance planes were unable to locate the Japanese force. Around 4:00 PM, an American B-24 Liberator briefly spotted the convoy, but the weather and time of day precluded an attack. The next morning, another B-24 spotted the Kimuras ships. Due to the range, several flights of B-17 Flying Fortresses were dispatched to the area. To help reduce the Japanese air cover, Royal Australian Air Force A-20s from Port Moresby attacked the airfield at Lae. Arriving over the convoy, the B-17s began their attack and succeeded in sinking the transport Kyokusei Maru with the loss of 700 of the 1,500 men on board. B-17 strikes continued through the afternoon with marginal success as the weather frequently obscured the target area. Tracked through the night by Australian PBY Catalinas, they came within range of the Royal Australian Air Force base at Milne Bay around 3:25 AM. Though launching a flight of Bristol Beaufort torpedo bombers, only two of the RAAF aircraft located the convoy and neither scored a hit. Later in the morning, the convoy came into the range of the bulk of Kenneys aircraft. While 90 aircraft were assigned to striking Kimura, 22 RAAF Douglas Bostons were ordered to attack Lae through the day to reduce the Japanese air threat. Around 10:00 AM the first in series of closely coordinated aerial attacks began. Bombing from around 7,000 feet, B-17s succeeded in breaking up Kimuras formation, reducing the effectiveness of the Japanese anti-aircraft fire. These were followed by B-25 Mitchells bombing from between 3,000 and 6,000 feet. These attacks drew the bulk of the Japanese fire leaving an opening for low-altitude strikes. Approaching the Japanese ships, the Bristol Beaufighters of No. 30 Squadron RAAF were mistaken by the Japanese for Bristol Beauforts. Believing the aircraft to be torpedo planes, the Japanese turned towards them to present a smaller profile. This maneuver allowed the Australians to inflict maximum damage as the Beaufighters strafed the ships with their 20 mm cannons. Stunned by this attack, the Japanese were next to hit by modified B-25s flying at low-altitude. Strafing the Japanese ships, they also made skip bombing attacks in which bombs were bounced along the surface of the water into the sides of enemy vessels. With the convoy in flames, a final attack was made by a flight of American A-20 Havocs. In short order, Kimuras ships had been reduced to burning hulks. Attacks continued through the afternoon to ensure their final destruction. While the battle raged around the convoy, P-38 Lightnings provided cover from Japanese fighters and claimed 20 kills against three losses. The next day, the Japanese mounted a retaliatory raid against the Allied base at Buna, New Guinea, but inflicted little damage. For several days after the battle, Allied aircraft returned to the scene and attacked survivors in the water. Such attacks were viewed as necessary and were partially in retribution for the Japanese practice of strafing Allied airmen while they descended in their parachutes. Aftermath In the fighting at the Bismarck Sea, the Japanese lost eight transports, four destroyers, and 20 aircraft. In addition, between 3,000 and 7,000 men were killed. Allied losses totaled four aircraft and 13 airmen. A complete victory for the Allies, the Battle of the Bismarck Sea led Mikawa to comment a short time later, It is certain that the success obtained by the American air force in this battle dealt a fatal blow to the South Pacific. The success of Allied airpower convinced the Japanese that even strongly escorted convoys could not operate without air superiority. Unable to reinforce and resupply troops in the region, the Japanese were permanently put on the defensive, opening the way for successful Allied campaigns.

Nuclear Weapons During The Cold War Era Essay - 907 Words

The development and use of nuclear weapons in 1945 changed not only warfare, but how countries approach warfare as a whole. As Andrew Heywood notes in his book, Global Politics, says that there’s a tendency â€Å"for any weapons to proliferate† or spread. With that knowledge it should be assumed that many nations would want to obtain nuclear weapons after seeing what the power that they hold. A state being in possession of a nuclear weapon can deter potential enemies and make them a power on the global scale. The Cold War era and post- Cold War era both saw an in increase in the spread of nuclear weapons. During the Cold War, after the US first used a nuclear weapon in 1945, states that gained nuclear capabilities were the France, the UK, China and the Soviet Union. Post – Cold War era India, Pakistan, Israel and North Korea all gained nuclear weapons and shows the problem with proliferation of them. India and Pakistan are neighboring states and rivals which can lead to the possibility that they could be used at any moment. North Korea is a dangerous militaristic state that constantly threatens other states. This illustrates that the spread of nuclear weapons is a global problem because nuclear proliferation can possibly put WMDS, weapons of mass destruction, in the hands of rival states or extremely dangerous nations. There’s also the possibility of them falling into the hands of non state actors such as terrorists groups. Nuclear proliferation and nuclear disarmament/armsShow MoreRelatedThe Human Race Cannot Coexist with Nuclear Weapons Essay1252 Words   |  6 Pagestwo bombs ended World War II and changed the public’s view of nuclear energy. 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Responsible For Pumping Sufficient Amount †Myassignmenthelp.Com

Question: Discuss About The Responsible For Pumping An Sufficient Amount? Answer: Introducation A diagnosis has been done on Mrs. Brown with acute exacerbation of heart failure (AIHF). The symptoms of AIHF are initially caused by the pulmonary oedema due to an increased filling pressure in the left ventricle (LV) (Copstead Banasik, 2013). To meet the metabolic demand of the body, the LV is responsible for pumping an sufficient amount of oxygenated rich blood to the body. The LV becomes impaired to perform this activity, which leads to increase the blood volume and blood pressure in the LV (Gallagher, 2012). This situation results to the flowing of the blood forwarded into the body, which can cause the increased blood in the LV to revert through the pulmonary veins and left atrium, resulting to an increment in the capillary pressure (Craft Gordon, 2015). The fluid more possibly becomes to penetrate into the interstitial spaces and the lungs alveoli from the capillary walls causing a lift in the capillary hydrostatic pressure leading to pulmonary oedema, as a result of increase of the pulmonary circulation hydrostatic pressure (Fenwick, 2015). The pulmonary gas exchange function can be significantly impaired due to the increased fluid and in the alveoli and airway as the interference of the gas exchange with the lungs ventilation process. Hence, severe dyspnoea would be experienced by Mrs. Browns. Due to the movement of the air that passes through the alveolar flied, sounds of the crackles are heard from the patient having pulmonary oedema (Fenwick, 2015). It is indicated from the oxygen saturation reading that Mrs. Brown is having inadequate supply of blood in her body. The situation is resulted by the incapability of the lungs for not effective oxygenation of the blood. Therefore, while leaving the pulmonary circulation, the blood gets poorly oxygenated (Gallagher, 2012). The failing heart is responsible for not delivering the adequate oxygenated blood to reach the tissue oxygen needs, resulting into the hypoxia and reduced tissue perfusion, as stated b y Fenwick (2015). AHF is connected with a remarkable reduction in the cardiac output (CO), myocardial contractility and stroke volume. Accumulated blood pressure and tachycardia has been experienced by Mrs. Brown due to the activation o compensatory mechanism responding to the reduced CO. The activation of the symoathetic nervous system is stimulated by the decreased cardiac output to discharge the no noradrenalin and adrenaline that can be the reason for increment in vasoconstriction (McCance Huether, 2014). With the activation of the vasoconstriction, the further elevation happens in the myocardial contractility, peripheral vascular constriction and the HR. A decreased blood flow to the kidneys is caused by the decreased CO, resulting to a step down in the glomerular filtration rate, additionally (McCance Huether, 2014). Chopsted and Banasik (2013) has showed in response to the above stated situation, that, to release rennin, which transforms the angiotensinogen to angiotensin I from angiotensin II the kidneys are stimulated by the rennin-angiotensin-aldosteron. A lift in the arterial blood pressure is caused by the increase of the peripheral vasoconstriction from such situation. In addition, Gordon and Craft (2015) stated that, the release of antidiuretic hormone (ADH) is stimulated by the posterior pituitary, in response to the reduction of the cerebral perfusion pressure caused by the low CO. An important role is played by the ADH in raising the reabsorption of the water of the renal tubules, which results in increased volume of blood and the water retention. If the prescribed oxygen therapy is provided to Mrs. Brown, it will relieve the symptoms of her connected with acute hypoxia and dyspnoea. The density of oxygen in airway and the alveolar space is increased and the levels of carbon dioxide are decreased by the disposal of oxygen. Therefore, this helps the gases to spread out into the capillaries of pulmonary by crossing the membrane of the alveolar capillary (Wagner Hardin-Pierce, 2014). As the result, the function of the pulmonary gas exchange improves and the symptoms of the dyspnoea decreases.the oxygen level in the blood is increased and the requirement for the tissue perfusion is improved by the oxygen therapy (Powell, Graham, OReilly Punton, 2016). Optimally, a pulse oximetry has been used for monitoring the effectiveness of oxygen therapy disposal provided to Mrs. Brown. Mrs. Brown has been placed in the high Fowler position while her feet is dangling at the bedside, which improves the gas exchange function and the ventilation by enhancing her thoracic capacity (Gallagher, 2012). Moreover, the cardiac preload caused by the ineffective systematic circulation is decreased by this particular position. During diastole, the blood amount returning to the left ventricle gets less overfilled, as a result of the decreased return of venous (Wagner Hardin-Pierce, 2014). Consequently, this improves the LV performance. Furosemide is one of the loop diuretic drugs. The reabsorption of the chloride and the sodium ions into the interstitial fluid from the loops inhibited by the direct working of the ascending loops medullary part of Henle, which result into a hypotonic interstitial fluid environment (Bullock Manias, 2013). The reduction of the pulmonary venous pressure is helped by the Furosemide, by circulating the oedemous fluid, which can be responsible for resulting to the optimal exchange of gas. The intravascular volume is decreased by this which can lead to a reduction of return of venous to the preload and LV. This can benefit the improvement of the cardiac output by allowing the overfilled LV to constrict more effectively by the reduced venous return (Gallagher, 2012). The electrolyte imbalances and the dehydration are affected by the common adverse. The main affected electrolyte is the potassium ions and imbalances in the potassium level can lead to cardiac dysrhythmias, hypokalaemia and co nfusions in aged patients (Riley, 2013). Thus, the nurses are suggested to monitor and document the fluid and electrolyte status of the patient, prior to begin the therapy of intravenous (IV) furosemide. The IV furosemide usage on an aged patient needs to be as low dose as possible, and generally not more than 4mg per minute not to cause ototoxicity. The patient needs to be monitored frequently for dizziness, headache, dry mouth and loss of skin turgor as the signs of dehydration. For further advice, these symptoms are needed to be documented and reported to the doctors (Bullock Manias, 2013). Glyceryl trinitrate is one of the peripheral vasodilator drugs, which is absorbed by the endothelial cells of the wall of the blood vessel and transformed into nitric oxide (NO) in the vascular muscle. The activation of the second manager system depended on calcium is stimulated by the NO for releasing cyclic guanosine monophosphate thatalerts the myosins activity resulted into the dilating of the blood vessels (Gallagher, 2012). The NO levels in the vascular smooth muscle, which is responsible for the activation of the vasodilatation, is increased by the glyceryl trinitrate. This results into the systematic vascular response (SVR) and reduction of venous return that further results into decreased cardiac preload and cardiac after load. Dilating the pulmonary vasculature is acted by this which is responsible for the result of the increase in venous capacitance (Gallagher, 2012). The facial flushing, hypotension and the headache is caused by the common adverse. The blood pressure that is resulted from the reduced SVR is decreased by glyceryl trinitrate. Thus, is considered to be important to observe the blood pressure of the patient frequently, every 5 to 10 minutes for avoiding the systematic hypotension. The nurses are required to document and report to the doctors immediately, if a large reduction in the systolic blood pressure can be seen in the patient (Riley, 2013). Reference: Bullock, S., Manias, E. (2013). Fundamental of Pharmacology (7th ed.). Pearson Australia. Copstead, L., Banasik, J. (2013). Pathophysiology (5th ed.). Elsevier Astralia. Craft, J., Gordon, C. (2015). Understanding Pathophysiology (2nd ed.). Chatswood, Australia: Elsevier Australia. Fenwick, R. (2015). Mnagaement of acute heart failure in the emergency department. Emergency Nurse. 23(8), 26-35. Retrieved from https://search.proquest.com/docview/1784630412/fulltextPDF/A56CA91C5E14460PQ/1?accountid=36155 Gallagher, R. (2012). Problems of oxygenation: perfusion. In Brown, D., Edwards, H. (3rd edition.). Lewiss medical-surgical nursing: assessment and management of clinical problems. (pp. 883-898). Chatswood, NSW: Elsevier Australia. McCance, K., Huether, S. (2014). Pathophysiology: the biologic basis for disease in adults and children (7th edi.). Elsevier Australia. Powell, J., Graham, D., oReilly, S., Punton, G. (2016). Acute pulmonary oedema. Nursing Standard. 30(23),51. Retrieved from https://search.proquest.comezproxy.uws.edu.au/docview/1784938311.fulltext/71A552B44E73PQ/1?accountid=36155 Riley, J. (2013). Acute decompensate heart failure: diagnosis and management. British Journal of Nursing. 22(22), 1290-1295. Retrieved from https://web.b.ebscohost.com.ezproxy.uws.edu.au/ehost/pdfviewer?sid=c609c3a5-1919-41fc-8ff8-eac9facfea9f%40sessionmgr4009vid=5hid=4201 Wagner, K., Hardin-Pierce, M. (2014). High-acuity nursing (6th ed.). Upper saddle river, New Jersey: Pearson.

The Sound of Revenge free essay sample

Chamillionaires major album debut â€Å"The Sound of Revenge† proves he is one of the Souths hottest new artists. The previous SwishaHouse emcee knows how to step up his game. He is quick-tongued and can nab a hook with perfect timing. He may not be like Slim Thug or Mike Jones but he knows how to spit a verse and can polish it off tastefully, like in â€Å"Rain.† Cham knows how to write raps that will keep running through your head. Just listen to â€Å"Southern Takeover† or â€Å"Frontin,† one of my favorites, or when he tears the track up with Layzie Bone in â€Å"Ridin.† Despite those songs, this album isnt quite on the level of some of his independent work. Cham isnt making music on his own anymore and relies too much on his guests. Regardless, with his smoking beats and clever tongue, Chamillionaires album brings his Southern game to the multitudes. We will write a custom essay sample on The Sound of Revenge or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page