Anatomy Quiz: Regulation Of Breathing Chemoreceptors
12 questions · exam conditions
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Regulation Of Breathing ChemoreceptorsQuestion 1 of 12

During a diving response, breath-holding causes blood CO₂ levels to rise from 40 mmHg to 55 mmHg while O₂ levels drop from 100 mmHg to 75 mmHg. Which chemoreceptor response pattern would be expected during this scenario?

Only peripheral chemoreceptors are activated because central chemoreceptors cannot detect changes during breath-holding
Central chemoreceptors respond strongly to CO₂ increase while peripheral chemoreceptors show minimal activity due to adequate O₂ levels
Both central and peripheral chemoreceptors are activated, with central responding to CO₂ rise and peripheral responding to both CO₂ and O₂ changes
Central chemoreceptors are inhibited by the diving response while peripheral chemoreceptors increase their CO₂ sensitivity
Peripheral chemoreceptors respond only to the O₂ decrease while central chemoreceptors respond only to the CO₂ increase
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Anatomy Quiz

Anatomy Quiz: Regulation Of Breathing Chemoreceptors

Practice Regulation Of Breathing Chemoreceptors in Anatomy with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

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This quiz focuses on Regulation Of Breathing Chemoreceptors, giving you a quick way to practice the rules, question types, and explanations that matter most for Anatomy.

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Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

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Question 1

During a diving response, breath-holding causes blood CO₂ levels to rise from 40 mmHg to 55 mmHg while O₂ levels drop from 100 mmHg to 75 mmHg. Which chemoreceptor response pattern would be expected during this scenario?

  1. Only peripheral chemoreceptors are activated because central chemoreceptors cannot detect changes during breath-holding
  2. Central chemoreceptors respond strongly to CO₂ increase while peripheral chemoreceptors show minimal activity due to adequate O₂ levels
  3. Both central and peripheral chemoreceptors are activated, with central responding to CO₂ rise and peripheral responding to both CO₂ and O₂ changes (correct answer)
  4. Central chemoreceptors are inhibited by the diving response while peripheral chemoreceptors increase their CO₂ sensitivity
  5. Peripheral chemoreceptors respond only to the O₂ decrease while central chemoreceptors respond only to the CO₂ increase
Explanation: When you encounter questions about chemoreceptors and respiratory drive, focus on understanding what triggers each type of chemoreceptor and how they work together during physiological stress. During breath-holding with rising CO₂ (40→55 mmHg) and falling O₂ (100→75 mmHg), both chemoreceptor systems activate simultaneously but respond to different stimuli. Central chemoreceptors in the medulla are exquisitely sensitive to CO₂ changes and will strongly respond to the 15 mmHg increase in CO₂. Meanwhile, peripheral chemoreceptors in the carotid and aortic bodies detect both CO₂ and O₂ changes - they'll respond to the CO₂ rise and become increasingly active as O₂ drops, though their strongest response occurs when O₂ falls below 60 mmHg. Answer choice A is incorrect because central chemoreceptors absolutely can detect CO₂ changes during breath-holding - this is actually when they're most active. Choice B fails because while central chemoreceptors do respond strongly to CO₂, peripheral chemoreceptors aren't minimally active; O₂ at 75 mmHg is getting low enough to stimulate them, plus they also respond to CO₂ increases. Choice D is wrong because the diving response doesn't inhibit central chemoreceptors - it may temporarily override their signals, but the receptors themselves remain active and sensitive. The correct answer is C because both receptor types are indeed activated, with central chemoreceptors primarily responding to the CO₂ increase and peripheral chemoreceptors responding to both the CO₂ rise and O₂ decline. Remember: Central chemoreceptors = CO₂ specialists; peripheral chemoreceptors = respond to both CO₂ and O₂, with O₂ sensitivity increasing as levels drop.

Question 2

A patient at high altitude (3000m) has been acclimatizing for 2 weeks. Compared to their initial arrival, how would you expect their chemoreceptor sensitivity to have changed?

  1. Peripheral chemoreceptor sensitivity to hypoxia decreases while central chemoreceptor sensitivity to CO₂ remains constant
  2. Both peripheral and central chemoreceptor sensitivities increase to compensate for the chronic hypoxic environment
  3. Peripheral chemoreceptor sensitivity to hypoxia increases while central chemoreceptor sensitivity to CO₂ may be reset to lower baseline levels (correct answer)
  4. Central chemoreceptor sensitivity increases while peripheral chemoreceptors become less responsive to oxygen changes
  5. Both chemoreceptor types maintain their original sensitivity levels but respiratory muscle strength increases instead
Explanation: When you encounter questions about altitude acclimatization, focus on how the body adapts its respiratory control mechanisms to chronic hypoxia over time. The key is understanding that different chemoreceptors respond differently to prolonged exposure. After two weeks at high altitude, the body undergoes specific adaptations. Peripheral chemoreceptors (located in carotid and aortic bodies) actually become more sensitive to hypoxia as part of the acclimatization process. This increased sensitivity helps maintain appropriate ventilatory responses to the persistently low oxygen environment. Meanwhile, central chemoreceptors in the medulla may reset their baseline sensitivity to CO₂ to lower levels. This occurs because chronic hyperventilation (the body's response to hypoxia) leads to respiratory alkalosis, and the central chemoreceptors adapt by becoming less sensitive to maintain a new equilibrium. Option A incorrectly states that peripheral chemoreceptor sensitivity decreases - it actually increases with acclimatization. Option B suggests both sensitivities simply increase, missing the nuanced reset mechanism of central chemoreceptors. Option D reverses the roles, incorrectly claiming peripheral chemoreceptors become less responsive when they actually enhance their sensitivity. The correct answer is C because it captures both the enhanced peripheral chemoreceptor sensitivity to hypoxia and the potential resetting of central chemoreceptor baseline sensitivity to CO₂. Remember: altitude acclimatization questions often test whether you understand that adaptation involves both enhancement of some responses (peripheral oxygen sensing) and recalibration of others (central CO₂ sensing), not just simple increases across all systems.

Question 3

A researcher measures chemoreceptor activity while gradually lowering inspired O₂ concentration. At what approximate arterial O₂ level would peripheral chemoreceptors begin to show significant activation?

  1. 100 mmHg, as chemoreceptors are most sensitive at normal oxygen levels
  2. 90 mmHg, when oxygen saturation begins to decline from its plateau
  3. 80 mmHg, corresponding to the steep portion of the oxygen-hemoglobin dissociation curve
  4. 60 mmHg, when hypoxemia becomes clinically significant and oxygen saturation drops substantially (correct answer)
  5. 40 mmHg, only when oxygen levels reach critically low values that threaten cellular function
Explanation: When you encounter questions about chemoreceptor activation, remember that peripheral chemoreceptors (located in the carotid and aortic bodies) have a unique response pattern to oxygen levels. Unlike central chemoreceptors that primarily respond to CO₂/pH changes, peripheral chemoreceptors monitor oxygen but only activate significantly during substantial hypoxemia. The key insight is that peripheral chemoreceptors remain relatively quiet until arterial oxygen pressure drops to around 60 mmHg. At this threshold, oxygen saturation falls dramatically (to about 90% or below), creating the hypoxemic conditions that trigger robust chemoreceptor firing. This activation then stimulates increased ventilation to restore oxygen levels. Choice A is incorrect because chemoreceptors are actually least active at normal oxygen levels (100 mmHg) - they're designed as emergency sensors, not routine monitors. Choice B misunderstands the oxygen-hemoglobin curve; at 90 mmHg, you're still on the relatively flat upper portion where saturation remains high (around 97%), so chemoreceptor activation is minimal. Choice C confuses the steep portion of the curve (around 40-50 mmHg tissue level) with the chemoreceptor activation threshold, and 80 mmHg still maintains adequate oxygen saturation. Choice D correctly identifies that significant chemoreceptor activation occurs around 60 mmHg, when hypoxemia becomes clinically meaningful and oxygen saturation drops substantially below normal ranges. For anatomy and physiology exams, remember this "60 mmHg rule" for peripheral chemoreceptors - they're your body's hypoxemic alarm system, not continuous oxygen monitors.

Question 4

During metabolic acidosis, arterial pH drops from 7.4 to 7.1 while CO₂ decreases from 40 mmHg to 25 mmHg due to compensatory hyperventilation. How would central chemoreceptors respond in this situation?

  1. They would be strongly stimulated because the low pH directly activates them regardless of CO₂ levels
  2. They would be inhibited because the low CO₂ level overrides any stimulation from acidosis
  3. They would be less active than expected because the decreased CO₂ reduces their stimulation despite systemic acidosis (correct answer)
  4. They would show maximum activation because both acidosis and hyperventilation stimulate central chemoreceptors
  5. They would be unaffected because metabolic acidosis does not influence central chemoreceptor function
Explanation: When you encounter questions about acid-base regulation, focus on how different chemoreceptors respond to specific stimuli. Central chemoreceptors in the medulla are primarily sensitive to CO₂ and H⁺ ions in cerebrospinal fluid, while peripheral chemoreceptors respond to blood pH, CO₂, and oxygen levels. In this metabolic acidosis scenario, you need to understand what's happening at the central chemoreceptors specifically. While the body is experiencing severe acidosis (pH 7.1), the compensatory hyperventilation has dramatically reduced CO₂ from 40 to 25 mmHg. Central chemoreceptors respond mainly to CO₂ levels because CO₂ crosses the blood-brain barrier and forms carbonic acid in the CSF. With CO₂ this low, central chemoreceptor stimulation is actually reduced compared to normal, even though systemic acidosis exists. Option A incorrectly assumes central chemoreceptors directly sense blood pH - they primarily respond to local CO₂ and CSF pH changes. Option B goes too far by saying they're completely inhibited; they're just less stimulated than you might expect. Option D wrongly suggests hyperventilation stimulates central chemoreceptors when it actually reduces their primary stimulus (CO₂). The correct answer is C because it captures this counterintuitive relationship: despite systemic acidosis, central chemoreceptors are less active due to the low CO₂ from compensatory hyperventilation. Remember: Central chemoreceptors care most about CO₂, not systemic pH. In acid-base questions, always consider which specific receptor type is being discussed and what their primary stimuli are.

Question 5

A patient with a brainstem lesion affecting the medullary chemoreceptive area shows reduced ventilatory response to CO₂ but normal response to severe hypoxia (O₂ < 50 mmHg). This pattern suggests which of the following about chemoreceptor function?

  1. Both central and peripheral chemoreceptors are damaged, but hypoxic drive overcomes the damage at low oxygen levels
  2. Central chemoreceptors are impaired while peripheral chemoreceptors remain functional for both CO₂ and O₂ detection (correct answer)
  3. Peripheral chemoreceptors are selectively damaged in their CO₂ sensitivity while retaining O₂ sensitivity
  4. The respiratory center is damaged but chemoreceptors are intact, causing delayed responses to all stimuli
  5. Central chemoreceptors are functional but their connection to the respiratory center is interrupted
Explanation: When analyzing respiratory control disorders, you need to distinguish between central chemoreceptors (in the medulla) and peripheral chemoreceptors (in carotid and aortic bodies), as they have different sensitivities and functions. The medullary chemoreceptive area contains central chemoreceptors that are primarily responsible for detecting CO₂ changes in cerebrospinal fluid. When this area is damaged, the patient loses the ability to respond appropriately to rising CO₂ levels. However, peripheral chemoreceptors in the carotid and aortic bodies remain intact and functional. Peripheral chemoreceptors serve a dual role: they respond to both severe hypoxia (O₂ < 60 mmHg) and can detect CO₂ changes, though they're less sensitive to CO₂ than central chemoreceptors. Since this patient shows normal response to severe hypoxia, the peripheral chemoreceptors are clearly functional for oxygen detection and can still contribute to CO₂ sensing, just not enough to maintain normal CO₂ responsiveness without the central chemoreceptors. Answer B correctly identifies this pattern: impaired central chemoreceptors with functional peripheral chemoreceptors. Answer A incorrectly suggests both systems are damaged. Answer C wrongly implies peripheral chemoreceptors can selectively lose CO₂ sensitivity while retaining O₂ sensitivity. Answer D mislocates the problem to the respiratory center rather than the specific chemoreceptive area. Remember this key distinction: central chemoreceptors primarily handle CO₂ detection, while peripheral chemoreceptors are your body's main oxygen sensors but also contribute to CO₂ monitoring. Medullary lesions typically affect CO₂ response more than oxygen response.

Question 6

A patient receives 100% oxygen therapy, which raises their arterial O₂ from 60 mmHg to 400 mmHg while CO₂ remains at 45 mmHg. What would be the expected effect on peripheral chemoreceptor activity?

  1. Activity increases significantly due to the high oxygen levels stimulating chemoreceptor metabolism
  2. Activity decreases dramatically as the hypoxic drive is eliminated, but CO₂ sensitivity remains intact (correct answer)
  3. Activity remains unchanged because peripheral chemoreceptors are primarily responsive to CO₂ rather than oxygen
  4. Activity increases initially then decreases as the chemoreceptors adapt to the hyperoxic conditions
  5. Activity is completely inhibited because high oxygen levels are toxic to chemoreceptor cells
Explanation: When you encounter questions about oxygen therapy and chemoreceptors, focus on understanding what triggers peripheral chemoreceptor firing and how oxygen levels affect this system. Peripheral chemoreceptors in the carotid and aortic bodies are primarily hypoxic sensors - they fire rapidly when arterial O₂ drops below about 60 mmHg, creating the "hypoxic drive" for breathing. In this scenario, oxygen therapy eliminates hypoxia by raising arterial O₂ from 60 mmHg (borderline hypoxic) to 400 mmHg (severely hyperoxic). This removes the primary stimulus for peripheral chemoreceptor activation. However, these receptors retain their ability to respond to CO₂ and pH changes, which is why the CO₂ sensitivity remains intact even though the hypoxic drive disappears. Choice A incorrectively suggests high oxygen stimulates chemoreceptor metabolism and increases activity - actually, hyperoxia suppresses peripheral chemoreceptor firing. Choice C contains a major misconception: while central chemoreceptors primarily respond to CO₂, peripheral chemoreceptors are highly sensitive to oxygen levels, especially during hypoxia. Choice D describes an adaptation pattern that doesn't occur with peripheral chemoreceptors under hyperoxic conditions - they simply remain suppressed as long as oxygen levels stay elevated. For anatomy and physiology exams, remember that peripheral chemoreceptors act like "oxygen alarms" - they're quiet when oxygen is adequate but scream when it gets dangerously low. Removing hypoxia essentially turns off this alarm system while leaving other respiratory control mechanisms functional.

Question 7

A patient with sleep apnea experiences repeated episodes where breathing stops for 30 seconds. During these episodes, CO₂ rises to 60 mmHg and O₂ falls to 70 mmHg before breathing resumes. Which statement best describes the chemoreceptor response pattern during and after these episodes?

  1. Only central chemoreceptors respond during the episode, while peripheral chemoreceptors remain inactive until O₂ drops below 50 mmHg
  2. Both chemoreceptor types are maximally stimulated throughout the episode, causing immediate arousal and breathing resumption
  3. Central chemoreceptors respond progressively to CO₂ buildup while peripheral chemoreceptors show increasing activity as O₂ falls (correct answer)
  4. Peripheral chemoreceptors are the primary drivers of arousal while central chemoreceptors are suppressed during sleep
  5. Central chemoreceptors adapt quickly to the CO₂ increase, leaving peripheral chemoreceptors as the main arousal stimulus
Explanation: When you encounter questions about respiratory control, focus on how different chemoreceptors respond to specific blood gas changes and their sensitivity thresholds. During sleep apnea episodes, both central and peripheral chemoreceptors activate, but they respond to different stimuli with distinct patterns. Central chemoreceptors in the medulla are primarily sensitive to CO₂ (and H⁺ ions). As CO₂ rises from normal levels (~40 mmHg) to 60 mmHg, these receptors show a progressive, linear increase in firing rate. Meanwhile, peripheral chemoreceptors in the carotid and aortic bodies respond to both low O₂ and high CO₂, but their O₂ response follows a steep curve that becomes significant as oxygen falls below 80 mmHg. At 70 mmHg, they're definitely active and contributing to the drive to breathe. Option A is wrong because peripheral chemoreceptors begin responding well before O₂ drops to 50 mmHg—they start increasing activity around 80 mmHg. Option B incorrectly suggests immediate arousal; if chemoreceptors responded maximally throughout, the episodes wouldn't last 30 seconds. Option D reverses the roles—central chemoreceptors aren't suppressed during sleep, and peripheral chemoreceptors, while important, aren't the sole drivers of arousal. The correct answer is C because it accurately describes the graded, progressive responses of both receptor types to their respective stimuli during the episode. Remember: Central chemoreceptors = CO₂ sensitive with linear response; peripheral chemoreceptors = O₂ and CO₂ sensitive with steep O₂ curve below 80 mmHg. Both contribute to respiratory drive during hypercapnic-hypoxic episodes.

Question 8

During exercise, a person's arterial CO₂ remains at 40 mmHg despite a 10-fold increase in CO₂ production by muscles. Which mechanism best explains how chemoreceptors contribute to maintaining this CO₂ homeostasis?

  1. Central chemoreceptors detect the increased metabolic CO₂ production directly and increase respiratory drive proportionally
  2. Peripheral chemoreceptors sense the increased oxygen consumption and automatically adjust ventilation to match CO₂ production
  3. Central chemoreceptors maintain their tonic drive while other neural mechanisms account for the ventilatory increase during exercise (correct answer)
  4. Both chemoreceptor types increase their baseline sensitivity during exercise to detect smaller changes in blood gas levels
  5. Peripheral chemoreceptors detect minor fluctuations in arterial CO₂ that occur before blood gas measurements can detect them
Explanation: When you encounter questions about respiratory control during exercise, focus on distinguishing between the mechanisms that drive normal breathing versus exercise ventilation. This is a key concept that often appears on anatomy and physiology exams. During exercise, the remarkable fact is that arterial CO₂ levels stay constant despite massive increases in CO₂ production. This happens because chemoreceptors aren't the primary drivers of increased breathing during exercise. Central chemoreceptors in the medulla respond to changes in cerebrospinal fluid pH (which reflects CO₂ levels), but since arterial CO₂ remains at 40 mmHg during exercise, these receptors maintain their normal tonic activity rather than dramatically increasing respiratory drive. The actual increase in ventilation comes from other mechanisms like neural feedforward from the motor cortex, proprioceptive feedback from moving limbs, and possibly humoral factors from working muscles. Option A is incorrect because central chemoreceptors don't detect metabolic CO₂ production directly—they respond to CO₂ levels in blood/CSF, which remain constant during exercise. Option B wrongly suggests peripheral chemoreceptors automatically match ventilation to CO₂ production based on oxygen consumption, but these receptors primarily respond to low oxygen, high CO₂, or low pH. Option D incorrectly proposes that chemoreceptor sensitivity increases during exercise, but there's no evidence for this adaptive mechanism. Remember this pattern: when arterial blood gases remain normal during a physiological challenge, look for non-chemoreceptor mechanisms driving respiratory changes. Exercise ventilation is largely controlled by neural anticipation and feedback, not chemoreceptor response to blood gas changes.

Question 9

A 45-year-old patient with diabetic ketoacidosis presents with rapid, deep breathing (Kussmaul respirations). Laboratory results show: pH 7.18, PCO₂ 22 mmHg, HCO₃⁻ 8 mEq/L, and PO₂ 95 mmHg.

Which chemoreceptor mechanism is primarily driving this patient's respiratory pattern?

  1. Peripheral chemoreceptors responding to metabolic acidosis by detecting decreased blood pH (correct answer)
  2. Central chemoreceptors responding to respiratory acidosis as CO₂ crosses the blood-brain barrier
  3. Central chemoreceptors responding to metabolic acidosis as H⁺ ions cross the blood-brain barrier
  4. Peripheral chemoreceptors responding to mild hypoxemia from the metabolic derangement
Explanation: In metabolic acidosis, peripheral chemoreceptors (carotid and aortic bodies) detect the decreased blood pH (7.18) and stimulate hyperventilation to blow off CO₂ as respiratory compensation. The low PCO₂ (22 mmHg) confirms this compensatory hyperventilation. Option B is incorrect because this is metabolic, not respiratory acidosis. Option C is wrong because H⁺ ions cannot easily cross the blood-brain barrier. Option D is incorrect because PO₂ is normal (95 mmHg).

Question 10

A patient receives supplemental oxygen therapy, raising their arterial PO₂ from 55 mmHg to 120 mmHg. Their breathing rate decreases from 24 to 18 breaths per minute. However, when a different patient with normal PO₂ (95 mmHg) receives the same oxygen therapy (raising PO₂ to 120 mmHg), no change in breathing occurs. What explains this difference?

  1. The first patient had hypoxic depression of central chemoreceptors that was reversed by oxygen therapy
  2. Peripheral chemoreceptors show a non-linear response curve, with steep sensitivity below ~80 mmHg PO₂ but minimal sensitivity above this threshold (correct answer)
  3. The first patient had developed oxygen toxicity, while the second patient's antioxidant systems prevented this response
  4. Central chemoreceptors in the first patient had adapted to use oxygen as a primary stimulus due to chronic respiratory disease
Explanation: Peripheral chemoreceptors exhibit a non-linear response to PO₂, with minimal activity at normal levels (>80 mmHg) but exponentially increasing activity as PO₂ falls below ~70-80 mmHg. The first patient at 55 mmHg was on the steep part of this curve, so increasing PO₂ to 120 mmHg significantly reduced chemoreceptor firing and breathing rate. The second patient at 95 mmHg was already above the threshold where peripheral chemoreceptors are minimally active, so further oxygen increase had no effect. Option A is incorrect because hypoxia stimulates, not depresses, chemoreceptors. Option C is wrong because oxygen toxicity doesn't occur at these levels and doesn't affect breathing rate acutely. Option D incorrectly suggests central chemoreceptors can adapt to use oxygen as a primary stimulus.

Question 11

A research study measures ventilation responses to different stimuli. When subjects breathe 5% CO₂ in air, their minute ventilation increases 4-fold. When the same subjects breathe 12% O₂ in air (equivalent to ~4300m altitude), their minute ventilation increases only 1.5-fold. What accounts for this difference in magnitude of response?

  1. Central chemoreceptors have a higher density of CO₂-sensitive neurons compared to peripheral O₂-sensitive cells
  2. CO₂ stimulates both central and peripheral chemoreceptors, while hypoxemia primarily stimulates only peripheral chemoreceptors (correct answer)
  3. The CO₂ response threshold is much lower than the O₂ response threshold, making CO₂ detection more sensitive
  4. Peripheral chemoreceptors respond linearly to O₂ changes, while central chemoreceptors respond exponentially to CO₂ changes
Explanation: CO₂ stimulates both central chemoreceptors (via H⁺ in CSF) and peripheral chemoreceptors (via H⁺ in blood), creating a dual stimulation pathway that produces a robust ventilatory response. Hypoxemia primarily stimulates peripheral chemoreceptors only, as central chemoreceptors are relatively insensitive to oxygen levels. This explains the greater magnitude of response to CO₂. Option A is incorrect - it's about location and dual stimulation, not neuron density. Option C is wrong because both systems are quite sensitive, but the 12% O₂ stimulus is above the steep part of the hypoxic response curve. Option D incorrectly describes the response patterns - peripheral chemoreceptors actually show an exponential response to hypoxemia below ~60 mmHg PO₂.

Question 12

During a high-altitude expedition, a climber's arterial blood gas shows PO₂ of 55 mmHg and PCO₂ of 28 mmHg. The climber reports feeling short of breath but is breathing rapidly. Which chemoreceptor response pattern best explains these findings?

  1. Central chemoreceptors are stimulating ventilation due to respiratory acidosis from the low PCO₂ levels
  2. Peripheral chemoreceptors are driving hyperventilation in response to hypoxemia, which secondarily lowers PCO₂ (correct answer)
  3. Both central and peripheral chemoreceptors are equally stimulated by the combined hypoxemia and hypocapnia
  4. Central chemoreceptors are inhibiting ventilation to prevent further CO₂ loss, but peripheral chemoreceptors override this signal
Explanation: At high altitude, the primary stimulus is hypoxemia (PO₂ 55 mmHg), which activates peripheral chemoreceptors in the carotid and aortic bodies. These receptors stimulate hyperventilation to increase oxygen uptake. The resulting increased ventilation blows off CO₂, causing the observed hypocapnia (PCO₂ 28 mmHg). Option A is incorrect because low PCO₂ causes respiratory alkalosis, not acidosis, and would inhibit central chemoreceptors. Option C is wrong because hypocapnia actually inhibits central chemoreceptors. Option D incorrectly suggests central chemoreceptors can 'override' - they work together but peripheral chemoreceptors dominate in severe hypoxemia.