Quiz 109 · Physiological Changes at High Altitude

Answers to Quiz 108 · Regulation of Respiration

1. The central pattern generator that sets the basic breathing rhythm is located in the:

   Answer: Pre-Bötzinger complex of the medulla

   Its pacemaker cells lie between the nucleus ambiguus and the lateral reticular nucleus, and destroying them abolishes rhythmic phrenic firing. The Bötzinger complex is the rostral, expiratory part of the VRG, and the NTS holds the DRG. Revise respiratory centers (neural control)

2. The dorsal respiratory group (DRG) of the medulla:

   Answer: Lies around the nucleus tractus solitarius and is mainly inspiratory

   The DRG sits in and around the NTS, takes in IX and X afferents and projects straight to the phrenic motor neurons. The nucleus ambiguus region is the VRG; the two pontine options describe the pneumotaxic and apneustic centers. Revise respiratory centers (neural control)

3. The pneumotaxic center is made up of the:

   Answer: Nucleus parabrachialis medialis and Kölliker–Fuse nucleus

   Both nuclei lie in the rostral pons; the center switches between inspiration and expiration and holds the apneustic center in check. The ambiguus nuclei belong to the VRG in the medulla. Revise respiratory centers (neural control)

4. In an animal, the brainstem is cut in the upper pons, just below the pneumotaxic center, and both vagi are then cut. Breathing becomes:

   Answer: Prolonged inspiratory gasps with brief expirations (apneusis)

   With the pneumotaxic center and the vagus both gone, nothing checks the apneustic center's drive to the medullary inspiratory neurons. Breathing stops only after a cut below the medulla, turns irregular after a cut just below the pons, and is unchanged after a cut above it. Revise respiratory centers (neural control)

5. Loss of vagal feedback from the lungs changes the phrenic nerve discharge in each breath by:

   Answer: Prolonging it without changing its size

   Vagal stretch afferents normally inhibit the inspiratory neurons. Without them the phrenic discharge lasts longer, so each inspiration is bigger even though the firing is no stronger. Revise respiratory centers (neural control)

6. Blood flow through the carotid body is about:

   Answer: 2 L per 100 g per min, about 40 times that of the brain

   It is the highest flow per gram in the body, so the tissue's PO₂, PCO₂ and pH stay almost those of arterial blood despite a metabolic rate three times the brain's. Revise chemical control of breathing

7. Ventilation rises only a little as arterial PO₂ falls from 100 to 60 mmHg. One reason is that:

   Answer: The extra breathing lowers PCO₂, which damps the drive

   The small rise in breathing blows off CO₂, and less saturated Hb (a weaker acid than HbO₂) lowers blood H⁺; both brake ventilation until PO₂ drops below 60 mmHg. Chemoreceptor firing starts climbing as soon as PaO₂ falls below 100 mmHg. Revise chemical control of breathing

8. A patient with carbon monoxide poisoning has a much reduced arterial O₂ content but a normal PaO₂. His breathing is barely stimulated because:

   Answer: The peripheral chemoreceptors respond to PaO₂, not to O₂ content

   The carotid bodies sense the tension of dissolved O₂, which stays normal in anemia and CO poisoning, however low the content falls. Hypoxia acts mainly through the peripheral, not the central, chemoreceptors. Revise chemical control of breathing

9. The central chemoreceptors respond quickly to a rise in arterial PCO₂ but hardly at all to a metabolic fall in blood pH because:

   Answer: CO₂ crosses into the CSF easily, while H⁺ enters the brain very slowly

   CO₂ diffuses into the CSF and is hydrated there to H⁺, the true stimulus of the central chemoreceptors, while blood H⁺ penetrates poorly. CSF is nearly protein-free, with bicarbonate as its main buffer. Revise chemical control of breathing

10. A man with long-standing COPD has a raised PaCO₂ and a low PaO₂. He is given a high concentration of O₂ alone and becomes drowsy. The most likely reason is that:

    Answer: Removing his hypoxic drive has made him hypoventilate and retain more CO₂

    In chronic hypercapnia CSF bicarbonate rises and the central drive fades, so breathing rests on hypoxia acting on the peripheral chemoreceptors. Correcting only the hypoxia removes that drive and CO₂ climbs toward narcosis; mechanical support of ventilation is the better choice. Revise chemical control of breathing

11. The Hering–Breuer inflation reflex:

    Answer: Is set off by slowly adapting stretch receptors and lengthens expiration

    Slowly adapting receptors in the airway smooth muscle fire as the lungs inflate, and their vagal input prolongs expiration or cuts inspiration short. It sets tidal volume in quiet breathing in infants; in awake adults it works only with very large breaths. Revise non-chemical control: reflexes and sleep

12. Juxtapulmonary capillary (J) receptors are:

    Answer: Unmyelinated endings beside the alveoli, most sensitive to edema and congestion

    They are the pulmonary C fibers described by A. S. Paintal, reached from the pulmonary capillary blood; their firing gives rapid shallow breathing. The other three describe slowly adapting, rapidly adapting and bronchial C fiber endings. Revise non-chemical control: reflexes and sleep

13. After a heart–lung transplant, which of these is lost?

    Answer: The Hering–Breuer reflex

    Nerves to the donor lungs never regrow, so the lung stretch reflex and cough from the small airways vanish. The trachea above the carina keeps its own nerves, so tracheal cough survives, and yawns, sighs and resting breathing stay normal. Revise non-chemical control: reflexes and sleep

14. During swallowing, breathing is briefly inhibited and the glottis closes. This protective response is carried by afferents from the:

    Answer: Viscera and diaphragm

    Visceral and diaphragmatic afferents stop breathing and shut the glottis during swallowing and vomiting, so food and vomitus cannot enter the airway. Revise non-chemical control: reflexes and sleep

15. An obese man snores loudly, wakes many times a night, and has morning headaches and daytime sleepiness. The basic fault is most likely:

    Answer: Loss of pharyngeal muscle tone in REM sleep, blocking the airway in inspiration

    This is obstructive sleep apnea: slack pharyngeal muscles close the airway, each apnea ends in an arousal, and obesity adds to it. Reduced medullary output to the phrenic motor neurons is the cause of central sleep apnea. Revise non-chemical control: reflexes and sleep

15 questions on chapter 109. Pick one answer for each, then save. Your answers stay in this browser, and the right ones are shown at the top of the next quiz.

1. Hypoxia-induced hyperventilation becomes significant only when alveolar PO₂ falls below:

40 mmHg60 mmHg70 mmHg80 mmHg

2. The hyperventilation of the first stage of compensation at high altitude is mainly due to stimulation of:

The carotid bodiesThe central chemoreceptors of the medullaThe pneumotaxic centrePulmonary stretch receptors

3. Why is the rise in ventilation small during the first stage of compensation at high altitude?

The respiratory muscles are fatigued by the coldFalling arterial PCO₂ and alkalosis blunt the hypoxic responseThe carotid bodies are not yet sensitive to hypoxiaPulmonary vasoconstriction limits ventilation

4. The renal mechanism of ventilatory acclimatization brings blood pH back toward normal in about:

3 weeks3 months3 days3 hours

5. The maximum height up to which a person can adapt, beyond which O₂ inhalation is needed for survival, is:

10000 feet18000 feet24000 feet14000 feet

6. The rise in red-cell 2,3-DPG during acclimatization helps the tissues because it:

Shifts the O₂–Hb dissociation curve to the leftShifts the O₂–Hb dissociation curve to the rightIncreases the O₂-carrying capacity of each gram of HbRaises the solubility of O₂ in plasma

7. Erythropoietin-driven erythropoiesis at high altitude begins in about:

3 hours2 months2 weeks3 days

8. Which of these is NOT among the tissue changes of acclimatization to high altitude?

Fall in myoglobin contentIncrease in the number of mitochondriaIncrease in cytochrome oxidase activityIncrease in the number of capillaries

9. Cardiac hypertrophy in a long-term high altitude resident is best explained by:

Systemic vasodilation caused by hypoxiaPolycythemia raising blood viscosity and cardiac workloadLoss of sympathoadrenal toneA permanent fall in heart rate

10. The ventilatory equivalent (VE), the preferred index of the ventilatory response to altitude, is the ratio of:

Alveolar ventilation to pulmonary blood flowTidal volume to respiratory rateExpired minute volume to O₂ consumptionCO₂ output to O₂ consumption

11. The symptoms of acute mountain sickness typically appear after arrival at high altitude within:

3 to 4 days30 minutes4 to 8 hours2 weeks

12. Which of these is NOT a feature of chronic mountain sickness (Monge's disease)?

Right ventricular hypertrophyPolycythemiaHypovolemiaPulmonary hypertension

13. In chronic hypoxia at altitude, narrowing of the pulmonary arterial lumen is caused by:

Hypertrophy and hyperplasia of pulmonary arterial smooth muscleThrombosis of the pulmonary arteriolesCollapse of arterioles by raised alveolar pressureFibrosis of the alveolar septa

14. A climber at high altitude becomes disoriented and ataxic and then lapses into coma. The coma is due to:

Herniation of the brain through the tentoriumCarbon dioxide narcosisHypoglycemia from exhaustionCerebral vasospasm from alkalosis

15. Acetazolamide is the diuretic of choice in high altitude illness because it:

Blocks the Na⁺–K⁺–2Cl⁻ pump in the loop of HenleInhibits carbonic anhydrase, increases bicarbonate excretion and reduces CSF formationBlocks calcium channels in the pulmonary arteriesAntagonizes aldosterone and spares potassium

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