Respiratory Medicine - Stephen J. Bourke

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O 2 saturation 97% are most in keeping with: a chronic metabolic acidosisan acute on chronic metabolic acidosisan overcompensated metabolic alkalosisan acute on chronic respiratory acidosisa chronic respiratory acidosis

      4 3.4 Given arterial blood gases of pH 7.32, PCO 2 8.0 kPa, PO 2 13.0 kPa, sHCO 3 28 mmol/L, O 2 saturation 97%, one could confidently conclude that: the patient is breathing supplemental oxygenthe patient has COPDthe patient needs to be transferred to ITUthe condition is chronic and stablethe lungs are normal

      5 3.5 A 24‐year‐old woman presents to hospital as an emergency with breathlessness. Her arterial blood gases while breathing room air are pH 7.49, PCO 2 2.9 kPa, PO 2 12.5 kPa, sHCO 3 24 mmol/L, O 2 saturation 97%. This presentation is most in keeping with: pulmonary embolismanxietyopiate overdoseexcess vomitingpneumonia

      6 3.6 A 46‐year‐old man has an FEV 1 that is only 80% of the predicted value: his exercise capacity will be approximately 80% of age/height‐matched peershe will be 20% more breathless than age/height‐matched peershe has airway obstructionthis is consistent with the absence of any lung disease at allit is likely that he smoked

      7 3.7 A reduced forced vital capacity (FVC): always accompanies a reduction in FEV1can be seen in muscular weakness even when the lungs are normalcannot be present if slow (relaxed) vital capacity is normalsuggests lung fibrosisis a bad prognostic marker

      8 3.8 In diseases causing weakness of the respiratory muscles, the pattern of lung function disturbance expected would be: reduced FEV1, relatively normal FVCnormal FEV1:FVC ratio, reduced KCOreduced FEV1 and FVC, increased KCOnormal lung functionincreased FEV1:FVC ratio

      9 3.9 Transfer coefficient (KCO) would be reduced in the following conditions: obesityCOPDpulmonary haemorrhageasthmathyrotoxicosis

      10 3.10 In muscular dystrophy affecting the respiratory muscles, the following physiological findings would be expected: reduced FEV1reduced FVCreduced TLCOreduced KCOreduced TLC

      1 3.1 ASee Fig. 3.1.

      2 3.2 BThe normal FEV:VC and reduced FEV1 imply restriction. The reduced KCO suggests the cause is intrapulmonary.

      3 3.3 DThe pH is low, so this is an acidosis. The PCO2 is high, so this is a respiratory acidosis. The bicarbonate is high, suggesting there has been time to attempt to compensate (chronic). However, the pH would be in the normal range had this been a chronic stable state, so there must be an acute component. Remember, too, that physiological compensatory mechanisms don’t overcompensate.

      4 3.4 AIf you assume the patient is breathing room air (PIO2 = 21 kPa), then the alveolar–arterial gradient (see Chapter 1) will be negative (partial pressure of oxygen higher in the arterial blood than in the alveoli), suggesting the patient is a net contributor of oxygen to the environment. This seems unlikely. The inspired PO2 therefore must be greater than 21 kPa.The condition is clearly not stable; the pH is outside the normal range. As we aren’t given the PIO2, we can’t conclude the lungs are normal. The A–a gradient may be very high.

      5 3.5 AThis is a primary respiratory alkalosis, so the answer must be either anxiety‐driven hyperventilation or pulmonary embolism. The alveolar arterial gradient is increased, implying a problem within the lungs (affecting V/Q matching), which anxiety cannot explain.

      6 3.6 DAt 80% of the predicted value, the result is still well within the normal range and therefore can be found within the normal population (of course, this doesn’t mean you can conclude that there is no disease present).

      7 3.7 BMuscular weakness can inhibit the ability to fill the lungs to their capacity, therefore when the FVC manoeuvre is performed there’s less than the normal amount of air to be expelled. Although a reduced FVC may be seen in lung fibrosis, it is seen in many other conditions and therefore cannot be taken to ‘suggest’ fibrosis in isolation.

      8 3.8 CMuscle weakness is an example of an extrapulmonary restrictive defect. Therefore, FEV1 and FVC will be reduced (approximately in proportion) and the gas transfer per unit lung volume (KCO) will be elevated (see text).

      9 3.9 BIn pulmonary haemorrhage, obesity and asthma, KCO is typically elevated (see text). Thyrotoxicosis is a high cardiac output condition with more than the average amount of blood in the pulmonary circulation. There is therefore increased capacity to absorb CO (KCO may therefore be high).

      10 3.10 A,B,C,EKCO is increased in restrictive defects caused by extrapulmonary factors.

      Chest X‐ray

      The chest X‐ray has a key role in the investigation of respiratory disease. The standard view is the erect, postero‐anterior (PA) chest X‐ray taken at full inspiration with the X‐ray beam passing from back to front. A lateral X‐ray gives a better view of lesions lying behind the heart or diaphragm, which may not be visible on a PA view, and allows abnormalities to be viewed in a further dimension. Supine and antero‐posterior (AP) views are usually taken at the bedside using mobile equipment in patients who are too ill to be brought to the X‐ray department. AP films are less satisfactory in defining many abnormalities, producing magnification of the cardiac outline, for example.

      It is helpful to examine the film systematically to avoid missing useful information. The shape and bony structures of the chest wall should be surveyed and the position of the hemidiaphragms and trachea noted. The shape and size of the heart and the appearances of the mediastinum and hilar shadows are examined. The size, shape and disposition of the vascular shadows are noted and the pattern of the lung markings in different zones is carefully compared. It is advisable to focus attention on areas of the chest X‐ray where lesions are commonly missed, such as the lung apices, hila and the area behind the heart. Any abnormality detected should be analysed in detail and interpreted in the context of all clinical information. It is often helpful to obtain previous X‐rays or to monitor the evolution of abnormalities over time on follow‐up X‐rays. Some of the radiological features of the major lung diseases are shown in individual chapters. In some circumstances chest X‐ray abnormalities follow a specific pattern that allows a differential diagnosis to be outlined.

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