Respiratory Medicine - Stephen J. Bourke

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fall below this important threshold, which is marginal to the sustainability of life.

      When this occurs, hypoxia then takes up the reins as the driver to ventilation and prevents what would have been a progressive decline to death. Once an individual is dependent on this ‘hypoxic drive’, a degree of hypoxia is (obviously) necessary to drive ventilation. This is not always appreciated. At times, a ‘high‐flow’ oxygen mask may be applied to a patient by a well‐meaning doctor in an attempt to raise the PO2 to a more ‘normal’ level. But no hypoxia means no drive to breathe. The result can be catastrophic underventilation, which, if not dealt with properly, can be fatal. When treating hypoxic patients who may have chronic lung disease, until their ventilatory drive is known (from arterial blood gas analysis), oxygen should be judiciously controlled to achieve an oxygen saturation (based on pulse oximetry) between 88% and 92%. In this ‘Goldilocks’ zone, the patient will not die of hypoxia and ventilation is unlikely to be depressed to any significant degree.

      imageKEY POINTS

       The essential function of the lungs is the exchange of oxygen and carbon dioxide between the blood and the atmosphere.

       Ventilation is the process of moving air in and out of the lungs, and it depends on the tidal volume, respiratory rate, resistance of the airways and compliance of the lungs. A fall in ventilation leads to a rise in PCO2 and a fall in PO2: type 2 respiratory failure.

       Derangement in the matching of ventilation and perfusion in the lungs (which may be caused by any disease intrinsic to the lung or its vasculature) leads to a fall in PO2: type 1 respiratory failure.

       The respiratory centre in the brain stem is responsible for the control of breathing. pH and PCO2 are the primary stimuli to ventilation. Hypoxia only acts as a stimulant when PO2 < about 8 kPa.

      1 Brewis RAL, White FE. Anatomy of the thorax. In: Gibson GJ, Geddes DM, Costabel U, Sterk PJ, Corrin B, eds. Respiratory Medicine. Edinburgh: Elsevier Science, 2003: 3–33.

      2 Maynard RL, Pearce SJ, Nemery B, Wagner PD, Cooper BG. Cotes’ Lung Function. Oxford: Wiley Blackwell, 2020.

      3 Gibson GJ. Clinical Tests of Respiratory Function. Oxford: Chapman and Hall, 2009.

      4 West JB. Pulmonary Pathophysiology – The Essentials. Baltimore, MD: Williams and Wilkins, 1987.

      1 1.1 The principal muscle(s) involved in inspiration is (are):the diaphragmrectus abdoministhe scalene musclessternocleidomastoidsthe intercostals

      2 1.2 Lung compliance:is reduced as lung volume increasesis reduced in emphysemais increased in lung fibrosisis the change in pleural pressure per unit change in lung volumeis the principal factor determining forced expiratory flow

      3 1.3 In relation to airway resistance:overall airway resistance increases as lung volume increasesin health, at high lung volume, the greater part of airway resistance is situated in the central airwaysairway resistance is reduced in emphysema due to diminished retractile force on the airwayairway resistance is proportional to the cubed power of the radius of the airway (r3)forced expiratory flow is unrelated to effort

      4 1.4 In relation to ventilation (V) and perfusion (Q): the upper zones of the lungs are ventilated more than the lower zonesthe upper zones of the lungs receive more perfusion than the lower zonesV/Q is greater in the lower zonesVQ matching is essential to gas exchangereduced overall ventilation leads to a fall in PCO2

      5 1.5 In a patient breathing room air at sea level, the arterial blood gases were: pH 7.36, PCO 2 3.2 kPa, PO 2 12 kPa, aHCO 3 – 19, base excess –5. The alveolar–arterial gradient is:2.5 kPa5.0 kPa5.5 kPa6.5 kPa10.0 kPa

      6 1.6 During expiration, the diaphragm: risesremains unchangedshortensstiffenscauses a fall in intrathoracic pressure

      7 1.7 A reduction in ventilation leads to: a rise in PaCO2 and PaO2a fall in PaCO2 and PaO2a rise in PaCO2 and a fall in PaO2a fall in PaCO2 and a rise in PaO2a rise in PaCO2 and no change in PaO2

      8 1.8 VQ mismatching leads to: a rise in PaCO2 and no change in PaO2a fall in PaCO2 and PaO2a rise in PaCO2 and a fall in PaO2a fall in PaCO2 and a rise in PaO2no change in PaCO2 and a fall in PaO2

      9 1.9 In relation to the control of breathing: hypoxia is irrelevanta rise of 0.2 kPa in pCO2 is required before ventilation is driven to increasea metabolic acidosis can increase ventilation and therefore PaO2a fall in blood pH will tend to reduce ventilationa fall in pH implies there has been a reduction in ventilation

      10 1.10 In relation to airway resistance: resistance is unrelated to lung volumethe site of principal resistance moves to the smaller airways as lung volume is reducedmaximum forced expiratory flow can be achieved at mid lung volumeFEF25–75 provides accurate information on the calibre of the large airwaysFEF25–75 provides accurate information on the calibre of the small airways

      Multiple choice answers

      1 1.1 AThe diaphragm is the main muscle of inspiration; contraction forces the abdominal contents down, creating a relative vacuum in the thorax which ‘sucks’ air into the lungs.

      2 1.2 ALung compliance is the change in lung volume brought about by a unit change in transpulmonary (intrapleural) pressure. The fibrotic lung is less compliant. The emphysematous lung is more compliant. In any lung, its capacity to stretch (expand) is reduced as volume increases ie it gets less compliant.

      3 1.3 BAirway resistance in health resides principally in the central (large) airways at high lung volume (‘You only have one trachea’). As lung volume decreases, the site of greatest resistance moves peripherally to the smaller airways (their calibre diminishes). It is increased in emphysema and is proportional to r4. Increasing effort WILL lead to increased expiratory flow, but only up to a certain point, beyond which ‘peak flow’ cannot be increased no matter what the effort.

      4 1.4 DGas exchange is driven by diffusion and therefore dependent on bringing the air and blood together (V/Q matching). Most of the ventilation goes to the bases, but an even greater proportion of the perfusion goes to the bases. Poor V/Q leads to a fall in PO2 but does not affect PCO2. Reduced overall ventilation causes a rise in PCO2 and a fall in PO2.

      5 1.5 BThis is elevated, implying a problem with VQ matching within the lung.

      6 1.6 ADuring inspiration, the diaphragm contracts and stiffens, pushing the abdominal contents down and reducing pressure in the thorax, which ‘sucks’ air in. Expiration is a relatively passive reversal of the process.

      7 1.7 CReducing ventilation means less CO2 is ‘blown off’ (leading to a rise in PACO2 and PaCO2). If fresh air isn’t brought into the lungs then alveolar oxygen will not be replenished, PAO2 will fall and so must PaO2.

      8 1.8 ESee Figure 1.11.

      9 1.9 CThe sensitivity to changes in pH and pCO2 is so exquisite that adjustments are made before any measurable change can occur. Hypoxia does matter, but only has significant impact on the drive to breathe when pO2 falls significantly (approx. 8 kPa). A low pH can be caused by either reduced ventilation or a metabolic disturbance (in which case, it would lead to a rise in ventilation). Increased ventilation will increase PAO2 and therefore PaO2 though it won’t increase the oxygen content of the blood (much) as arterial blood is ordinarily close to fully saturated.

      10 1.10 BAs lung volume is reduced, the small airways narrow and the site of principal resistance moves peripherally (i.e. to the smaller airways). Resistance

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