Section 2 Physiology
2.1 Organ System Physiology in Sleep: Respiratory
A Medical Student Volunteers for an Experiment
1 At the beginning of the night there is initial measurement of awake minute ventilation. Compared to any stage of sleep, awake minute ventilation is:
2 The medical student has just studied neuroanatomy but knows nothing about control of breathing. He asks the researcher where the pacemaker for breathing is located. What does the researcher answer?
3 The student goes to sleep wearing a mask connected to a system that lowers his alveolar PO2 and can also transiently occlude the airway. His hypoxic ventilatory response is measured. Hypoxic ventilatory response is lowest in what sleep stage?
5 Which of the following would you expect to be an unreliable stimulus for arousal in the medical student?
6 After the first study night is over, the researcher asks the medical student if he would volunteer for an experiment in which upper airway muscle tone is measured during sleep. This test requires inserting a needle electrode into the tongue. The student respectfully declines to participate. What was the researcher expecting to find about upper airway muscle tone during sleep?
8 What change in SaO2 would be expected with a 20 mm Hg drop in his PaO2?
C A fall in SaO2 would be less than in a normal person because he is on the flat portion of the O2 dissociation curve.
11 A variety of stimuli affect breathing via receptors located throughout the body; these receptors include all of the following except:
12 Before this patient can have a sleep study, he is admitted to the hospital in hypercapnic respiratory failure. His wife states that he developed a mild upper respiratory infection for which he took a drug that contained 325 mg acetaminophen and 15 mg codeine. He took the medication at bedtime, appeared to struggle to breathe a few minutes later, and then became unresponsive. She then called 911. What is the likeliest cause of his respiratory failure?
1 D. The brain stem respiratory pacemaker receives information from three general areas: the brain, the blood, and the lungs (including airways). The brain sends information on wakefulness and sleep stages and on whether voluntary control is overriding chemical control. For example, when we speak, we override chemical control of breathing. The blood provides information regarding PaO2, PaCO2 and hydrogen ion concentration, which are sensed by the peripheral chemoreceptors. PaCO2 and hydrogen ion concentration are also sensed by the central chemoreceptors located in the medulla. The peripheral chemoreceptors located primarily in the carotid body are fast responding, whereas the central chemoreceptors located beyond the blood–brain barrier respond more slowly to changes. Information from the lungs and airways is transmitted from stretch and other receptors via the vagus nerve. During wakefulness, minute ventilation is higher than during sleep. Atlas, p 38
2 B. The main respiratory control center is located in the medulla. It is made up of the dorsal respiratory group (DRG; contains the ventrolateral nucleus of the tractus solitarius) and the ventral respiratory group (VRG; contains the pre-Bötzinger complex, the nucleus ambiguous, and the nucleus preambiguous). Output from the DRG and VRG go to the phrenic nerve and the hypoglossal nucleus. Atlas, p 37; PPSM5, p 238
3 D. REM is a “primitive” state in which homeostasis does not seem to be a priority. During REM there is less homeostatic control of heart rate (it can become irregular), blood pressure, and arterial blood gases compared to NREM. Both the hypoxic and hypercapneic chemical drives to breathe are reduced in REM. Atlas, p 39; PPSM5, p 251
4 C. Surprisingly, when the upper airway is occluded in normal people, arousal occurs more rapidly in REM than NREM sleep. This is in contrast to the situation with obstructive sleep apnea, in which arousal response to occlusion is faster in NREM sleep. PPSM5, p 252; Issa and Sullivan, 1983
5 B. Hypoxia is an unreliable arousal stimulus, which is somewhat surprising because maintenance of oxygen levels is so critical. Nevertheless, even when SaO2 falls to the 70% range (PaO2 at 40 mm Hg), normal subjects often do not wake. This is in stark contrast to the hypercapnic response during sleep. People almost always wake when PaCO2 has increased by 15 mm Hg. PPSM5, p 252
6 D. Upper airway muscle tone decreases in the transition from awake to NREM sleep and is virtually absent in REM sleep. The loss of muscle tone related to REM sleep profoundly affects all the respiratory muscles except the diaphragm. This explains why snoring occurs during sleep and not wakefulness, and why in OSA the obstructive apnea episodes are always worse in REM sleep. PPSM5, p 254
7 D. Understanding the implications of the shape of the oxyhemoglobin dissociation curve is critical in interpreting oximetry data during polysomnography. The dissociation curve can be thought of as two linear portions—a steep one and a flat one—joined by a shoulder, the latter an SaO2 of about 90% (Fig. 2.1–1). On the flat portion above 90% SaO2, a relatively large decrement in PO2 is necessary to produce a physiologically significant change in SaO2; in a normal person, PO2 has to drop by 20 to 30 mm Hg for a physiologically significant drop in SaO2. On the steep portion of the curve—representing the sleeping SaO2 for someone who has COPD and/or who is morbidly obese and/or hypoventilating—a relatively small drop in PO2 results in a physiologically significant drop in SaO2. An identical 30 mm Hg drop in PaO2 results in a much greater drop in such a patient compared to a person with a normal baseline PaO2 (Fig. 2.1–2). This well-known fact shows that a fixed requirement for scoring hypopneas—3% of 4% drop in SaO2—can have very different implications depending on where the subject started from.
8 A. This patient’s SaO2 is on the shoulder of the oxyhemoglobin dissociation curve. Therefore, compared to a normal individual with SaO2 of 98%, he will manifest a larger drop in SaO2 for a given drop in PaO2. Notice in Figure 2.1–2 that a 30 mm Hg drop in SaO2 in the patient (blue arrows) with baseline SaO2 of 90% results in a dramatically larger drop in SaO2 than in a person with a normal SaO2 (red arrows). Also, an elevated blood carbon monoxide level (from smoking) is not picked up by the standard laboratory oximeter; as result, the oximeter-measured SaO2 will always be somewhat higher than the patient’s true SaO2.
9 A. The likeliest finding in this patient is hypoventilation during sleep. Although there is an increased risk of obstructive sleep apnea (OSA) because of obesity, the lack of a snoring history makes OSA less likely.
10 D. There is a loss of tone of the accessory muscles of respiration just as there is in almost all muscles during both the tonic and phasic components of REM sleep. The effect of the loss of muscle tone seems related to the spindle density of the muscles. Muscles with a lower spindle density (e.g., the diaphragm) seem resistant to the tonic reduction in muscle tone; thus the diaphragm is not paralyzed during REM. However, during the phasic component of REM sleep there occurs additional inhibition of the respiratory motor neurons, reducing activity of the diaphragm somewhat and possibly causing hypoventilation. Hypoxemia that occurs in patients with COPD is also related to phasic REM. Thus both hypoxemia and hypoventilation are most likely to occur in phasic REM sleep (Fig. 2.1–3). PPSM5 p 243, Fig. 21-4
11 B. Breathing is controlled by metabolic factors, including blood gas changes, with PaO2 sensed by the carotid bodies and PCO2 sensed by the carotid bodies and medullary central chemoreceptors; lung function (vagal inputs from the lung, e.g., stretch receptors in the lungs); and cortical inputs (effect of arousal state and sleep stage). Atlas, pp 37-44; PPSM5, ch 20
12 D. Although answers A, B, and C are possibilities, the best choice is adverse response to the opiate codeine. Patients with respiratory disease may be exquisitely sensitive to respiratory depressants. Remember the pre-Bötzinger complex discussed in the answer to question 2? The complex is part of the respiratory pacing system in the medulla (in the ventral respiratory group of neurons), and it contains mu-opioid receptors that codeine can activate, resulting in respiratory depression. Many drugs that suppress CNS function or activate opioid receptors can cause respiratory suppression in patients who are dependent on increased respiratory drive to maintain ventilation. (Note he had prominent sternocleidomastoid muscle activity.) PPSM5, p 237
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