Case Studies

Case 2

Tom, who is 15 years old, attends his general practitioner’s (GP) asthma clinic. He has had asthma since early childhood. On two occasions, when he was 8 and 10 years old, he had attacks severe enough to require hospital admission. At present, his asthma is well controlled on regular inhaled beclometasone dipropionate, 200 μg twice daily, and inhaled salmeterol, 50 μg twice daily. Today, his peak flow is 510 L/min (predicted value for his age and height 530 L/min). On auscultation, there is vesicular breathing and no other sounds.

• 1. Is this peak flow normal? Apart from the nomogram values, can you think of any other peak flow reading with which it would be useful to compare today’s clinic reading?

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  Correct answer:
  For males, peak flow should be no more than 100 L/min below the predicted; Tom’s peak flow is therefore within the normal range for his age and size. The most useful value to compare it with would be his own best peak flow rate.

• 2. If you measured the following how would they compare with the normal for a boy of his age and size?

  • FEV₁/FVC
  • Airway resistance
  • Functional residual capacity (FRC)
  • Lung compliance
  • Arterial PO₂ and arterial PCO₂

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  Correct answer:
  All of these should be normal. Asthma, especially in the young, is reversible, and between attacks patients usually have normal airway resistance, compliance, lung volumes and blood gases. Peak flow and auscultation (but see note in Answer to Question 9) suggest little evidence of airway obstruction today.

On a school trip to a countryside park, Tom becomes breathless running across a field. His teacher is alarmed by his noisy breathing and asks you, a passing medical student, to assess whether they need to get him to hospital.

• 3. What simple observations can you make that will help you decide how severe this attack is? In his backpack he has a salbutamol inhaler, a salmeterol inhaler, a sodium cromoglycate inhaler and a beclometasone inhaler. Which should he use?

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  Correct answer:
  Simple observations that can be made in these circumstances are as follows:

  • How breathless is he? Inability to talk in complete sentences is an indication of a severe attack.
  • Respiratory rate (>25 breaths/min suggests a severe attack).
  • Cyanosis (very severe attack).
  • Pulse rate (>110 beats/min suggests a severe attack).
  • If he has his peak flow meter with him, a value of more than 50% of his best or predicted suggests severe attack.

  Even in the absence of the above signs of a severe attack, it is important to monitor the response to treatment to ensure that improvement rather than deterioration is occurring. He should use a short-acting p2-adrenoreceptor agonist (salbutamol), which relaxes bronchial smooth muscle (see Chapter 25).

• 4. If you measured the following how would they compare with the normal for a boy of his age and size?

  • FEV₁/FVC
  • Peak flow rate
  • Airway resistance
  • FRC
  • Lung compliance
  • Arterial PO₂ and arterial PCO₂

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  Correct answer:
  He now has definite bronchoconstriction; we would expect both peak flow and FEV1/FVC to be reduced. In this mild attack, he would probably be able to exhale completely, so functional residual capacity (FRC) is likely to be normal. There is at present no reason why lung compliance should be altered. Although he will be working harder than normal, he should be achieving a normal alveolar ventilation and his blood gases should be normal. A reduced arterial PCO₂ may be caused by anxiety and consequent hyperventilation.

• 5. If you had had your stethoscope with you, what would you have heard on examining his chest?

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  Correct answer:
  Expiratory rhonchi (musical sounds caused by vibration of the sides of collapsing airways).

At 18 years of age, Tom goes to college in London. He stops taking regular medication, as he feels he has ‘grown out’ of his asthma. He keeps a salbutamol inhaler in his room ‘just in case’. During the first term he is well, apart from a couple of wheezy episodes while playing football. In the second term, he develops a heavy cold, and over 24 hours he becomes progressively more breathless despite frequent puffs of salbutamol. His friends call out his GP, who finds the following: Tom is fully alert, but talking in broken sentences because he is very breathless. He is not cyanosed. He is using his accessory muscles of respiration. On auscultation, there are widespread expiratory rhonchi (wheezes). BP is 115/80 mmHg, HR 110 beats/min, respiratory rate 30 breaths/min, peak flow 200 L/min.

• 6. Which observations suggest that this is a fairly severe attack?

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  Correct answer:
  Expiratory rhonchi (musical sounds caused by vibration of the sides of collapsing airways).

• 7. If the GP had measured airway resistance, FRC, lung compliance, arterial PO₂ and PCO₂, how would they compare to the predicted values?

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  Correct answer:
  This is clearly a severe asthma attack, and airway resistance would be greatly increased. It is likely that air trapping would occur, as initially expiration is affected more than inspiration. As expiration is slowed, the subject may be forced to breathe in before the last breath has been fully exhaled, or air may be trapped behind collapsed airways. This would lead to a raised FRC. The volume–pressure curve flattens as total lung capacity (TLC) is approached (i.e. compliance is reduced). Consequently, with this severity of attack, the work of breathing is increased not only because of increased work against airway resistance, but also because of increased elastic resistance. In addition, with increased FRC, the inspiratory muscles may not be at their optimum working length and hence efficiency is impaired. Some ventilation–perfusion mismatching would be expected, as bronchoconstriction and inflammation will result in underventilation of some regions, and with the resulting shunt effect there is likely to be some degree of arterial hypoxia. Increased total ventilation will usually lower the PCO₂, resulting in a final blood gas picture of low PO₂ and low PCO₂.

His GP decides that this attack warrants hospital admission, and he calls an ambulance. Unfortunately, owing to heavy traffic it is 40 minutes before he arrives at the local Accident and Emergency department. By this time, Tom is confused, too breathless to talk and unable to produce a peak flow reading. The Accident and Emergency officer notices he is now cyanosed, although the widespread rhonchi noted in the GP’s letter have now disappeared. Arterial blood gases show arterial PO₂ = 7 kPa and arterial PCO₂ = 5.5 kPa while breathing 60% oxygen.

• 8. Discuss the features that suggest this asthma attack is life-threatening. Do the reduced rhonchi on auscultation contradict the other findings?

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  Correct answer:
  The cyanosis indicates severe hypoxia, and is probably responsible for his confused mental state. The inability to talk and produce a peak flow reading is also signs of life-threatening asthma. The disappearance of rhonchi is consistent with very poor air movement. Rhonchi are a characteristic feature of airway obstruction, but they are not a reliable indicator of severity. In life-threatening asthma, the normal vesicular breath sounds are also absent. A silent chest in an asthma attack is an ominous sign.

• 8. Discuss the features that suggest this asthma attack is life-threatening. Do the reduced rhonchi on auscultation contradict the other findings?

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  Correct answer:
  The cyanosis indicates severe hypoxia, and is probably responsible for his confused mental state. The inability to talk and produce a peak flow reading is also signs of life-threatening asthma. The disappearance of rhonchi is consistent with very poor air movement. Rhonchi are a characteristic feature of airway obstruction, but they are not a reliable indicator of severity. In life-threatening asthma, the normal vesicular breath sounds are also absent. A silent chest in an asthma attack is an ominous sign.

• 9. What is the cause of the low arterial PO₂? Was the inhaled oxygen helpful, and if so, was the correct concentration used? Is this PCO₂normal, and how does it affect your assessment of the severity of this attack?

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  Correct answer:
  The low PaO₂ is caused by ventilation–perfusion mismatching. Hypoxia is what kills in severe asthma, so it is appropriate to give high inspired oxygen, which should significantly raise alveolar oxygen tension in poorly ventilated regions of his lung, and so improve arterial oxygenation. In this patient, there is no need to worry about ventilatory drive, so as high as possible is the correct emergency treatment. With a face mask, the maximum achievable is approximately 60%. Although a PCO₂ of 5.5 kPa would usually be considered ‘normal’, in the presence of severe hypoxia it should be regarded as worrying. With this degree of hypoxia, the drive to breathing should be increased, with increased ventilation and low PCO₂. Here, the failure to raise ventilation appropriately is likely to indicate exhaustion. The patient may deteriorate rapidly – a further fall in ventilation will worsen hypoxia, and this may be fatal. In the presence of significant hypoxia, a ‘normal’ or high arterial PCO₂ should be regarded as a serious finding.