B httpsy IE1 Francisca Alon My Home B 81-255-B Human Physi BI255_S18EssaysE3 say
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B httpsy IE1 Francisca Alon My Home B 81-255-B Human Physi BI255_S18EssaysE3 say Questions (10 points) 1. A physiology student is hooked up to a spirometer, which is attached to a gas tank that controls oxyeen delivery, You have your track star run on a treadmill and after about 5 minutes the track consciousness Troubleshooting you notice the tank gauge is broke. Instead of delivering a gas mixture with 21% oxygen, t actually delivered 5% oxygen. Explain why it took minutes before the observed outcome. Discuss hemoglobin in your answer Explain why the patient passed out. Did passing out help and why or why not. If the track star had hyperventilated while on the treadmill, would the outcome have changed? Explain why or why not. star starts to breathing incredibly heavily and suddenly loses he tank characterized by an increase in airway resistance 2. Steve suffers from chronic obstructive pulmonary disease (COPD). This disease is and a decrease these issues. Additionally, explain wha healthy person. How would the body compensate? in lung compliance. Explain what would happen to Steve's minute ventilation in terms of tidal volume as a result of t the levels of oxygen and carbon dioxide in his arterial system would be compared to a 3. You are working in an ER and you administer a ba g of saline to a patient that is infused with a large amount of albumin. As a result earch 5 6 7 8 9 0Explanation / Answer
1.ans. The initial delay of 5 minutes is because the person in question is a star athlete.Repeated high-intensity training of an athlete incur substantial anaerobic metabolic challenges and create an acidic muscle milieu that is unfavorable for subsequent performance. Hyperventilation, resulting in respiratory alkalosis, acts as a compensatory mechanism for metabolic acidosis.The ergogenic effects of hyperventilation in trained athletes is effected by prolonged anaerobic energy supply processes mediated through phosphocreatine, glycolysis/glycogenolysis and delayed excitation/contraction failure, enabling powerful force generations to be maintained for the sprinting duration. Additionally, increased activity of respiratory and trunk muscles may serve as a diverting activity that accelerates recovery of fatigue. Attenuation of power decrement with hyperventilation suggests that a training session can be sustained under relatively higher exercise intensity to enable greater adaptive changes, and thus enhanced training efficacy.
The athlete passed out as fast-paced breathing expelled more carbon dioxide from his body than usual, causing blood's carbon dioxide level to drop and its pH to rise. As a result, the arteries constricted, causing feelings of dizziness or light-headiness. The passing out helped to allow expansion of the arteries and osmolarity of the incumbent blood gas pressure.
2.ans.The expiratory flow of patients with COPD are limited during tidal respiration. It represents the maximal possible flow they can generate at that said volume. In flow-limited patients like Robert, the time available for lung emptying (expiratory time) during spontaneous breathing is often insufficient to allow end expiratory lung volume to decline to its natural relaxation volume. This leads to lung hyperinflation.The loss of the elastic recoil in emphysema show a functional residual capacity which exceeds the predicted model.Sustained open airways and air trapping during premature closure are aspects of lung hyperinflation.When tidal volume is increased or the expiratory time is short because of a high respiratory rate, the lung cannot deflate to its usual resting equilibrium between breaths. This raise in alveolar pressure and lung volume results affect the dynamic status of the lung. Breathing takes place near the total lung capacity. Tidal breathing during an exacerbation in a patient with COPD may be shifted upwards close to the total lung capacity as a consequence of dynamic hyperinflation .
Since robert is affected with COPD, he must adopt a higher minute ventilation in order to keep alveolar ventilation constant. These adaptive mechanisms serve to maintain the partial pressure of carbon dioxide within normal limits but during times of relative disease stability, they may not be adequate to maintain gas exchange homeostasis in the face of increased physiological stress/ exercise.
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