Mr Jensen Case Study

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Question 1 - The Pathophysiology
Explain the pathophysiology of Mr Jensen’s post-operative hypovolemia and how some of his post-operative assessment data might have contributed to this. In addition explain how the body might compensate for this physiologically (approximately 800 words). (997 Words)

Mr George Jensen is a 65-year old male who was brought into Emergency Department with an open fracture of his right tibia and fibula after falling from his roof. Taken to theatre as an emergency case, Mr Jensen had an open reduction and external fixation of his fractures. He has returned to the ward post-operatively with hypovolemia.

Hypovolemia is a decrease in the volume of blood in the body, which can be due to blood loss or loss of body
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By analyzing Mr Jensen’s post-operative assessment data, his hypovolemia is able to be staged. By staging Mr Jensen’s hypovolemia, an indication of the amount of fluid volume loss, his body’s compensatory mechanisms, priority problems and nursing interventions are able to be identified.

Clinically, there are four stages of hypovolemia. Each stage is determined by the amount of fluid volume lost (Brown & Edwards, 2013). By looking at Mr Jensen’s post-operative vital assessment data, his hypovolemia is able to be classified as a stage two. Stage two hypovolemia is characterized by the loss of 15-30% of the total blood volume, or between 750 and 1500 mL.

By this stage, cardiac output cannot be maintained by arterial constriction, resulting in tachycardia (>100bpm), increased respiratory rate (over 20 breaths/minute) and a slight decrease in blood pressure. The patient’s pulse may become narrow and skin becomes excessively pale The patient can present symptoms of anxiety and feeling restless. The capillary refill may be delayed and the urine output is reduced to 20-30 mL/h (Brown & Edwards, 2013). Evidence of this can be seen within Mr Jensen’s post-operative assessment data. He has tachycardia of 107 bpm, his blood pressure is currently 104/55mmHg which is low, and he has an increased respiratory rate of 24 breaths per
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Decreased blood flow to the kidneys activates the renin angiotensin system. Renin is released, which activates angiotension to produce angiotensin I, which is then converted to angiotensin II. Angiotensin II is also a potent vasoconstrictor, which causes both arterial and venous vasoconstriction. Angiotensin II also stimulates the adrenal cortex to release aldosterone, which results in sodium and water reabsorption and potassium excretion by the kidneys. The increase in sodium reabsorption raises the serum osmolarity and stimulates the release the antidiuretic hormone ADH from the posterior pituitary gland. ADH works by increasing water reabsorption by the kidneys, thus further increasing blood volume. (Brown & Edwards, 2013). Decreased blood flow to the skin results in the patient feeling cool and clammy (Brown & Edwards, 2013). This can be seen in Mr Jensen. The scenario states that his right leg is cool to touch. Brown and Edwards (2013) also state that an increase in temperature represents the body 's response to injury, inflammation and infection. It may suggest the presence of an infectious process as the etiology for shock (i.e., septic

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