A Friend In Need Is A Friend Indeed: A Case Study On Human R ✓ Solved

A Friend In Need Is A Friend Indeeda Case Study On Human Respiratory

A Friend in Need Is a Friend Indeed: A Case Study on Human Respiratory Physiology by William H. Cliff Department of Biology Niagara University, Lewiston, NY Ann W. Wright Department of Biology Canisius College, Buffalo, NY When Charles returned to his apartment at 5 PM in the evening, he turned on his old kerosene-fueled space heater. It had been a cold day in late spring and his third floor apartment was chilly. After spending an hour fixing dinner, he ate while watching the evening news on TV.

He noticed that his vision became progressively blurred. When he got up to go to the kitchen, he felt lightheaded and unsteady. Entering the kitchen, he became very disoriented and passed out. The next thing he remembered was waking up in the intensive care unit of the hospital. Some friends who had stopped by about 7 PM had found Charles unconscious on the kitchen floor.

They had called an ambulance, which had rushed Charles, still unconscious, to the hospital. An arterial blood sample drawn when he first arrived at the hospital showed the following values: Questions 1. The blood gas measurements show abnormalities in the partial pressure(s) of what gas(es)? Why did you choose the answer you did? 1. CO and CO2 2. CO alone 3. O2 and CO 4. O2 , CO and CO2 2. A measurement of Charles’ blood reveals that the O2 content is low (50% of normal) and hemoglobin is 50% saturated with CO (50% HbCO). The oxygen-hemoglobin saturation curve in Charles’ blood (50% HbCO) and under normal conditions (2% HbCO) is shown below. CO2 binding to hemoglobin is normal in both instances. What is the approximate % saturation of hemoglobin by O2 in normal arterial blood? How did you arrive at your answer? 1. 100% 2. 97% 3. 75% 4. 50% 5. 35% 3. What is the maximum amount of O2 (ml/ 100 ml blood) that can be carried in Charles’ arterial blood? How did you arrive at your answer? 1. 2 ml/100 ml 2. 5 ml/100 ml 3. 10 ml/100 ml 4. 15 ml/100 ml 5. 20 ml/100 ml 4. CO enhances the Bohr effect. This means that CO will cause a more pronounced shift of the hemoglobin oxygen saturation curve to the: . Explain why you chose the answer you did. 1. right 2. left 5. If the partial pressure of O2 in the body tissues is 20 mm Hg, what is the best estimate of the amount of O2 (ml/100ml) that can be released from Charles’ blood as it circulates in his systemic capillaries? How did you arrive at your answer? 1.

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Introduction

This case study examines the physiological implications of carbon monoxide (CO) poisoning in a human subject, Charles, who experienced severe hypoxia after exposure to a kerosene space heater. The analysis explores blood gas abnormalities, hemoglobin saturation, gas transport, and potential treatment strategies grounded in respiratory physiology principles.

Blood Gas Analysis and Respiratory Abnormalities

Supplied blood gas measurements indicate abnormalities predominantly involving carbon monoxide (CO) and carbon dioxide (CO2). Specifically, elevated CO levels interfere with normal oxygen transport, as CO binds extensively to hemoglobin, forming carboxyhemoglobin (HbCO). The choice of this answer is supported by the clinical context and the typical effects of CO poisoning, including hypoxia and altered blood gas values. Such abnormalities manifest as decreased partial pressure of O2 despite normal or near-normal partial pressures of CO2, consistent with CO’s high affinity for hemoglobin and its role in impairing oxygen delivery.

Oxygen Saturation and Hemoglobin Binding

The oxygen-hemoglobin saturation curve demonstrates a substantial reduction in hemoglobin oxygen saturation in Charles’ blood (50% HbCO) compared with normal conditions (2% HbCO). In normal arterial blood, hemoglobin is nearly 97-100% saturated with O2, which aligns with a typical oxygen saturation of approximately 97%. This value is derived from standard physiological data and the oxygen dissociation curve, considering that arterial partial pressures of O2 (around 100 mm Hg) correspond with high saturation levels.

Given that Charles’ hemoglobin is 50% saturated with CO, the residual saturation with O2 approximately drops to 50%, indicating significant impairment of oxygen transport capacity.

Maximum O2 Carrying Capacity of Blood

Under optimal conditions, arterial blood can carry about 20 ml of O2 per 100 ml of blood. This total capacity considers the maximal hemoglobin oxygen binding, with each gram of hemoglobin capable of binding approximately 1.34 ml O2. Assuming normal hemoglobin concentration (~15 g/dL), this maximum aligns with 20 ml O2 per 100 ml blood. The calculation involves multiplying the hemoglobin concentration, binding capacity, and considering the hemoglobin’s oxygen saturation.

Impact of CO on the Bohr Effect

The presence of CO enhances the Bohr effect, which describes how increased CO2 levels or decreased pH decrease hemoglobin’s affinity for oxygen. This results in a rightward shift of the oxygen dissociation curve, promoting oxygen release in tissues. The correct choice is a shift to the right, consistent with the physiological response to CO-induced impaired oxygen delivery.

Oxygen Release in Systemic Capillaries

At a tissue partial pressure of O2 around 20 mm Hg, the blood releases oxygen based on the position of the dissociation curve. Given the impaired oxygen-carrying capacity, the estimated amount of O2 released from Charles’ blood is approximately 1 ml per 100 ml of blood, which is adequate for cellular respiration needs under compromised conditions. The calculation considers the oxygen partial pressure gradient and hemoglobin saturation dynamics.

Hemoglobin Affinity for CO vs. O2

Despite the lower partial pressure of CO compared to O2, the hemoglobin’s affinity for CO is roughly 200-250 times higher than for O2. This high affinity explains why CO binds preferentially, displacing oxygen and reducing oxygen availability. The detectably higher binding of CO under these conditions supports this high affinity ratio, which is crucial in understanding CO poisoning severity.

Physiological Response - Chemoreceptors and Hyperventilation

Charles’ decreased O2 saturation would likely trigger chemoreceptor-mediated hyperventilation. Peripheral chemoreceptors located in the carotid and aortic bodies detect hypoxemia—low blood oxygen levels—and signal the respiratory centers to increase ventilation. Consequently, hyperventilation aims to compensate for impaired oxygen delivery, despite CO’s adverse effects. The most appropriate answer is that hyperventilation occurs because the bodies sense the decreased oxygen saturation (option 3).

Fundamental Problem in Gas Transport

Charles’ disorder primarily stems from impaired transportation of gases due to CO’s interference with hemoglobin function. The problem lies at the stage of gas transport from the alveolar capillaries to the tissues, involving hemoglobin’s binding and release of oxygen. Therefore, the most accurate answer is 'transport of gases between the alveolar capillaries and capillary beds in other tissues'.

Analogy to External Respiration Physiology

This condition closely mirrors hypoxia caused by altitude sickness, where reduced oxygen partial pressures lead to decreased oxygenation of blood. Both scenarios involve insufficient oxygen transfer from alveoli to blood or from blood to tissues. The analogy is most fitting with altitude sickness (option 2).

Treatment Strategies

An aggressive treatment plan would likely involve administering high-concentration oxygen therapy to displace CO from hemoglobin, thus restoring oxygen transport. Alkalizing the blood to increase pH, partial blood transfusions, and increasing oxygen availability are effective strategies. Conversely, administering gases with elevated CO2 is contraindicated because it worsens hypoxia, making option 4 inappropriate. Therefore, the treatment component least appropriate is option 4, as it would exacerbate the hypoxic state.

Conclusion

This case underscores the critical impact of CO poisoning on respiratory physiology, emphasizing the importance of prompt oxygen therapy, understanding hemoglobin binding dynamics, and the body's compensatory mechanisms. Comprehending these physiological principles guides effective clinical management of such toxicological emergencies.

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