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Nursing Essay 代写:高中跌倒患者

Keywords:Nursing Essay 代写

Nursing Essay 代写:高中跌倒患者

简介该论文是说Mark‘’s 从高空中坠落后如何护理的一片学术论文,该论文用词精湛。是我们第一批辅导出来的学员作品,如果你也需要论文指导或代写论文服务请联系我们的24小时写作客服!

After Mark’s accident of felling down, firstly his skin, muscle, and other soft tissue get injury .These injury include abrasions and bruising, which can cause edema around the wounds. Even worse, the vessels and arteries of lower limbs get injured and lead to bleeding badly. At the same time, Mark have severe multiple bone fracture, which also can cause bleeding and body fluid lost.
When body loses blood over 25% of total volume, it would exceed the ability of compensation, which would cause hemorrhagic shock. In this stage, deceasing of effective circulation volume make thoadrenmodularly system excitability, catecholamine secrete into circulation. All these nervous and humeral reactions make small vessels contract especially arterioles, metarteriole and precapillary sphincter, which make true capillary network shut down.
Meanwhile, beta-adrenoceptor excitation makes arterio-venous anastomosisopen, microcirculation Non - nutritive blood flowincrease. On the one hand, the reaction of microcirculation has important meaning to whole body to compensate. On the other hand, that can cause body tissue severe. This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood.The baroreceptors in the arteries detect the resulting hypotension, and cause the release of epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.
When it come worse, at this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cell's total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.

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