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Unit 5. 3 Case studies sleep and exercise KEY

Name:Date:2008

Case study # 1

Patient is a 35 year old WM who wants to run the marathon. He has a resting HR of 110BPM and a systemic BP of 156/98 mmHg. His EKG shows a sinus tachycardia at rest. His respiratory rate is 16 BPM with an I:E ratio of 1:1.5. On auscultation you hear clear BBS. His PEFR is WNL for his age. He has no history of lung or cardiac disease.

  1. Assuming his metabolism is WNL, how much 02 does he consume in a minute?
  2. 250 ml/min
  3. Assuming his metabolism is WNL, how much C02 does he produce in a minute?
  • 200 ml/ml
  1. Based on the normal V02 and VC02, calculate the respiratory quotient [RQ] for this man
  • VC02/V02= 200/250 = .8 is the RQ
  1. How much 02 [VL02 ] do we expect his lungs to diffuse within a minute
  2. 250 ml/min of 02 diffuses into the capillary from the alveoli
  3. How much C02 [VLC02] doe we expect his lungs to diffuse within a minute
  4. 200 ml/min of C02 diffuses out of the capillary into the alveoli
  5. Based on the normal VLC02/VL02 calculate his respiratory exchange ratio
  6. 200 ml/min of C02/250 ml/min of 02 = .8 is the respiratoryexchange ratio
  7. Based on what we know of this man do you think that the amount of 02 brought into the blood stream [VL02] will equals the amount of 02 [V02] consumed at the cellular level. Explain your answer.
  8. No, he may have a problem with increasing his Cardiac Out to get the tissue perfused enough to get 02 to tissue
  9. Do you think that this man will be able to create the increased CO that he needs to run a marathon? Explain your answer.
  10. No, He may have a problem with increased perfusion during exercise because of his increased systemic blood pressure and his baseline tachycardia. Increases of diastolic pressure imply increased resistance to blood flow in the blood vessels. His baseline tachycardia may be due to this or to something else. While he has no history of cardiac disease, we need to assess him further
  11. So, based on the information above, would this man’s inability to exercise be limited by his cardiovascular system or by his pulmonary status?
  • His inability to exercise would be limited by his cardiovascular system rather than his pulmonary status. With good daily exercise and watching his diet, he might be able to work up to running a marathon in the future—but not in the next few weeks.

Case study # 2

Patient is a 48 year old WM who wants to run the marathon. He has a resting HR of 67 BPM and a systemic BP of 120/62 mmHg. His EKG shows a normal sinus rhythm at rest. His respiratory rate is 26 BPM. He uses Combivent MDI about three times a day. His PEFR is 70% of predicted before bronchodilator and 85% of predicted after.

  1. Based on what we know of this man do you think that the amount of 02 brought into the blood stream [VL02] will equals the amount of 02 consumed [V02] at the cellular level.
  2. While it might at rest, his ability to pull in 02 might equal his metabolic needs, during exercise, he may not be able to keep this up
  3. Explain your answer.
  4. his decreased PEFR imply that there will be a problem with increasing his VE without significant increased WOB
  5. because he is taking a combination of short-acting Beta II drugs with cholinergic antagonist, and he still has baseline decreased PEFR, we can see that his bronchospasm is not under control
  1. Do you think that this man will be able to create the increased CO that he needs to run a marathon?
  2. Maybe, maybe not.
  3. Explain your answer:
  4. There seems to be nothing wrong with his cardiovascular system at rest, but because of his decreased PEFR we need to question him carefully about his current level of daily exercise.
  1. Do you think that he will be able to increase his VE to 100 LPM needed to run this marathon?
  2. At this point in time, we cannot be sure that he can raise his VE without a increase in WOB.
  3. He might also have exercise induced bronchospasm
  4. What would happen to his PaC02 if he is unable to raise his VE enough to keep up with the metabolism during this race?
  5. His PaC02 would rise, which would increase his ventilatory drive; he would feel SOB
  6. If this happened what would happen to his pH?
  7. The rise in PaC02 would drop the pH
  8. The point at which a person’s metabolism turns to anaerobic metabolism is called his aerobic threshold. Do you think that he will reach this point before a normal person?
  9. Yes, because his increased WOB would increase his 02 consumption and C02 production which his ventilation may not be able to match
  10. So, based on the information above, would this man’s inability to exercise be limited by his cardiovascular system or by his pulmonary status?
  11. pulmonary status, but if he becomes hypoxic enough during this run, he could trigger cardiac arrhythmias
  12. What could you recommend for this patient to do to get ready for this race?
  13. Because he is on daily beta II agonists, he needs to be started on inhaled steroids. He no longer is classified as mild, intermittent asthma.
  14. Once he’s been on steroids for a few days, try to decrease the cholinergic antagonist- it may not be necessary
  15. He will need to exercise daily to work up to this
  16. Explain how you would monitor him?
  17. After a few days of inhaled steroids we need to monitor his PEFR at rest and during exercise.
  18. He may need a puff or two of a Beta II agonist just before he runs
  19. He needs to learn how to breathe while running without triggering cholinergic bronchospasm. Breathe through the nose, not the mouth.
  20. He needs to breath regularly during exercise and inhale as his knees come up to his chest

Case study # 3

Your patient has been referred to the clinic for a work up. Although this 57 YO BM has no history of smoking, nor history of COPD, during a routine exam an ABG showed that he had chronic hypercapnia although his Pa02 was 83 mmHg at the time.

An EKG was done at the time which showed right heart hypertrophy associated with cor pulmonale.

On exam, you see an obese gentleman in no apparent respiratory distress whose BBS are clear. His capillary refill is brisk and his HR 99, RR 15 and systemic BP is 128/75 mmHg and his Sp02 while awake is 98%.

The doctor decides to send him to a sleep lab for assessment of possible sleep apnea.

  1. Why does the doctor suspect this?
  • The ABG shows s/s of chronic hypercapnia but there are no s/s of COPD so we need to investigate
  1. What would be the expected effect of non-REM sleep on the patient’s HR, RR, systemic BP and Pa02?
  2. During non-REM sleep, we expect the RR to slow and the PaC02 to rise and the Pa02 to drop, but the HR and PB both drop during non-REM sleep
  1. What would be the expected effect of REM sleep on the patient’s HR, RR, systemic BP and Pa02?
  2. Because the patient is dreaming, the HRs vary
  3. The brain stem may or may not recognize rising hypercapnia or hypoxemia
  4. The Bp tends to rise during REM sleep

The patient goes into the sleep lab and is set up with EEG, pulse oximeter, EKG and a device for measuring gas flow at the nose and at the mouth. He also has motion detector probes on his chest and belly.

  • The EEG shows the following: delta waves
  • The EKG shows the following: HR is now 85
  • The Sp02 shows the following: Sp02 drops to 95%
  • The motion detectors & gas flow probes show the following: RR drops to 9BPM and is regular
  1. At what stage of sleep is this man right now?
  2. Delta waves show up in stage 3 and 4 of non-REM sleep
  3. Are his VS constant with this stage of sleep?
  • During stage 3 and 4 of non-REM sleep you expect the RR and BP to be down
  1. Do you expect this Sp02 at this stage of sleep?
  • yes

Within 80 minutes, the patient’s:

  • EEG shows the following: slow voltage saw tooth waves.
  • EKG: HR is now sinus tachycardia with occasional PVC
  • He has several episodes of apnea lasting longer than 20 seconds alternating with rapid respirations
  • Sp02 shows the following: Sp02 drops to 85%
  • He is snoring
  • The chest wall is moving, but the gas flow probes show little gas movement
  • The motion detectors & gas flow probes show completely different respiratory rates.
  1. At what sleep stage is this patient?
  2. He is in REM sleep
  3. Are his VS and Sp02 normal for this stage of sleep?
  4. While HR are variable during this stage, we don’t expect him to have cardiac arrhythmias
  5. While the control over ventilation is damped down during this sleep stage, we don’t expect his Sp02 to drop down to an hypoxic level
  6. Explain the possible discrepancy between chest wall movement and gas flow from the mouth and nose.
  7. If there is chest wall movement, but no air flow, the patient might have increased airway resistance in the upper airways so that there is upper airway occlusion
  8. Explain why he is snoring at this point
  9. Collapse of soft tissue in the upper airways can cause snoring
  10. For what problems is he at increased risk at this point in his sleep cycle
  11. He could have cardiac arrest during sleep
  12. He could have serious hypoxia due to upper airway occlusion and if the ventilatory centers are blunted during this phase of sleep, he is at increased risk of anoxia