Introduction

Respiratory physiology involves a number of areas, all of which are complex. These areas include the structure and function of the lung, the mechanics of breathing, gas exchange within the lung, oxygen uptake/transport and delivery, control of carbon dioxide and ventilation. Pathologies of the lung itself, as well as other disorders (cardiac disease, neurological disease, haematological disease, musculoskeletal disorders etc.) have varying effects on the different aspects of pulmonary physiology. In addition, advanced respiratory treatments such as mechanical ventilation may also have effects on all of these.

Respiratory terminology encompasses both anatomical and physiological descriptors, as well as terms used in investigations and respiratory management. For the non-pulmonologist or intensivist, much of this terminology may be confusing. Many of the terms sound similar and may seem to be used interchangeably. This is especially so in the case of invasive or non-invasive ventilation, where quite different modes of ventilation may share very similar language descriptors. Also, seemingly standard terms used by manufacturers in a proprietary sense to describe modes of mechanical ventilation may in fact describe very different things in different makes and models.

In addition to this, some terms have broader ‘meanings’ to the wider medical community; however, intensivists and pulmonologists may use the terminology either very specifically or otherwise. An example may be the word ‘ventilation’, which is often used as a shortened version of ‘mechanical ventilation’ but more properly means the total exchange of gas (usually air) between the lungs and the ambient environment. Many intensivists/pulmonologists would also use the term as a substitute for carbon dioxide clearance.

This chapter will not look in detail at respiratory physiology as learnt in medical school. Rather, it will look at terms used in the discussion of pulmon-ary physiology, respiratory disease and respiratory failure/support, and will focus on terms that may be encountered by the non-intensivist/pulmonologist when caring for patients with respiratory disease. The chapter is divided into sections dealing with oxygen and oxygenation, carbon dioxide and breathing, lung function and mechanical ventilation, including airway access and weaning. These distinctions, however, are mainly for convenience, and the terms may be used across the spectrum of respiratory disease. Hopefully this chapter will act as somewhat of a glossary when referring to the more specific sections of the textbook.

Purely anatomical or pathological terminology will not be discussed, nor will common terminology in general usage across medicine, for example pulmonary oedema, consolidation, atelectasis etc.

Some Basics of Respiratory Physiology

The respiratory system is designed to allow oxygen to enter the bloodstream and to remove carbon dioxide. Inspiration draws gas (humidified by the upper airway) into the alveoli, and oxygen then diffuses across the alveolar capillary membrane and into the pulmonary capillaries. At the same time, carbon dioxide diffuses from the pulmonary capillaries into the alveoli and is then exhaled. Gas exchange therefore relies upon the partial pressures of oxygen and carbon dioxide in both the blood and the alveoli, as well as the matching of alveolar gas flow and blood flow, and the integrity of the alveolar spaces and alveolar capillary membrane. Different areas of the lung have differing degrees of ventilation and perfusion matching, with upper lung units having relatively more ventilation and lower lung units relatively increased perfusion. Of every breath, a proportion remains in the large airways (dead space) and therefore does not participate in gas exchange. Following diffusion into the alveolar capillaries, oxygen is largely bound to haemoglobin and transported to the peripheries. A small amount of oxygen is transported unbound but dissolved in blood. In the tissue beds, oxygen dissociates from haemoglobin and is replaced by carbon dioxide, to be returned to the lungs and expelled. Control of breathing is complex, with central nervous system controls as well as peripheral sensors. Blood PCO₂ is the most important controller of ventilation under normal circumstances, but PO₂ is an important driver under certain circumstances, especially chronic hypoxia or at altitude.

The mechanics of breathing are complex. In order to inflate the lungs during inspiration, each breath must overcome both the natural resistance of the airways and the tendency of the lungs to collapse (elastic recoil, attributable to tissue elasticity and the surface tension within the alveoli). Inspiration is an active process, with the diaphragm being the most important muscle. The slope of the pressure/volume curve of the lung is called the lung compliance (i.e. change in volume per unit change in pressure). The chest wall and thoracic cage also play a role in the mechanics of breathing. The chest wall has a natural tendency to expand but is also elastic. This outward pull of the chest wall opposes the elastic recoil of the lung itself, preventing the lung from collapsing. At the end of a normal breath, these opposing forces are in equilibrium. Normal expiration is a passive process under most conditions, but is significantly altered in conditions such as asthma.

It can be seen from the above that conditions that affect the airways, lung parenchyma, alveoli, pulmonary vessels, pleura and chest wall, respiratory muscles, or haemoglobin will have effects on respiratory function and gas exchange. In addition to this, other pathologies that involve increasing tissue oxygen demands or carbon dioxide production will also have effects on respiratory function.

The requirement for mechanical ventilatory support is another circumstance where respiratory physiology is altered. Depending on the nature of the insult, respiratory function may be significantly altered by the underlying illness, e.g. asthma, aspiration etc. However even in the setting of otherwise normal lungs (e.g. ventilation after neurosurgery), mechanical ventilation itself has significant effects on cardiopulmonary physiology and respiratory mechanics. Positive pressure ventilation alters lung and chest wall mechanics, has effects on right ventricular function, and may be a direct cause of injury to the lungs if managed inappropriately.

Oxygen and Oxygenation

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  Partial pressure of gases: total pressure of a gas is the sum of the ‘partial pressures’ of each gas (dependent on the proportion of each), e.g. PO₂

  
  
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  Partial pressure of gas dissolved in a fluid: dependent on the concentration and the individual solubility coefficient of each gas, e.g. PaO₂ where “a” = arterial blood.

  
  
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  Diffusion: oxygen and carbon dioxide are transferred from the alveoli to the blood and vice versa via diffusion. Each gas has a different diffusing capacity, with carbon dioxide diffusing about 20 times more rapidly than oxygen. Diffusion is proportional to the membrane thickness and the concentration gradient across the membrane (see A–a gradient later).

  
  
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  Oxygen transport: transfer of oxygen to body tissues. About 97% of oxygen is transported in combination with haemoglobin, and the remaining 3% in a dissolved state.

  
  
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  Oxygen saturation (SaO₂): Most oxygen transport occurs as oxygen bound to haemoglobin. Normally, oxygen and haemoglobin associate and dissociate as the partial pressure of oxygen changes in the blood. As the PO₂ increases, the percentage of haemoglobin bound to oxygen increases too: the percentage saturation of the haemoglobin. See also Pulse oximetry.

  
  
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  Hypoxaemia: low partial pressure of oxygen in the blood. The causes of hypoxaemia are: hypoventilation, V/Q mismatch, shunt, diffusion limitation and low inspired oxygen partial pressure.

  
  
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  Oxygen/haemoglobin dissociation curve: the dissociation of oxygen and haemoglobin can be affected by factors other than PO₂. The curve may shift to the left or right based on other factors such as pH, temperature, fetal haemoglobin, etc.

  
  
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  Type I respiratory failure: also known as hypoxic respiratory failure. Characterized by low oxygen partial pressures (PaO₂) and saturations (SaO₂) with normal or low carbon dioxide levels.

  
  
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  Fraction of inspired oxygen (FiO₂): fraction of inspired oxygen expressed as a percentage of inspired gas, not a pressure per se. Air is 21% oxygen, therefore FiO₂ breathing air is 0.21. Partial pressure can be calculated by multiplying the FiO₂ by the total pressure.

  
  
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  Oxygen delivery: supply of oxygen to the tissues (DO₂). It is a product of cardiac output and the oxygen content of blood (determined by haemoglobin concentration and PaO₂):

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  Dysoxia: point at which maximal oxygen extraction from blood by the tissues is reached and exceeded (i.e. demand exceeds supply) and anaerobic cellular metabolism results.

  
  
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  Shock: failure of adequate oxygen delivery and/or utilization. May be subdivided into a number of headings, e.g. cardiogenic/obstructive/distributive, etc.

  
  
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  Ventilation/perfusion abnormalities (V/Q mismatch): for gas exchange to occur, lung units must have gas going in and out (ventilation), as well as blood flow (perfusion). A mismatch between these two will affect gas exchange.

  
  
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  Alveolar gas equation: equation to approximate the alveolar partial pressure of oxygen (P_AO₂): this allows calculation of the alveolar–arterial oxygen difference (see A–a gradient). This is important as oxygen passively diffuses from the alveolar space to arterial blood.

Because inspired air is humidified by the upper respiratory tract, the partial pressure of oxygen is calculated using barometric pressure (760 mmHg at sea-level) minus partial pressure of water vapour at body temperature (47 mmHg) multiplied by the percentage of inspired oxygen.

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  A–a gradient: gradient between alveolar and arterial oxygen partial pressures. The A–a gradient normally increases with advancing age and higher concentrations of inspired oxygen. The A–a gradient can be used as an indirect measurement of ventilation-perfusion abnormalities/gas exchange problems.

  
  
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  P/F ratio: the PaO₂/FiO₂ ratio is a simple bedside way to look at lung injury/oxygenation problems and is helpful in scoring and stratification. Calculated by dividing the measured PaO₂ by the inspired oxygen fraction, for example 100 mmHg/0.21 = 476. Often split into mild (200–300), moderate (100–200) and severe (<100) categories. See ARDS later.

  
  
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  Oxygen index (OI): measure of severity of lung injury when receiving mechanical ventilation (different from P/F ratio in that it incorporates the airway pressure). Used as a stratification tool.

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  Oxygen consumption (VO₂): A measure of how much oxygen is being used by the tissues. Often approximated by using central venous oxygen saturations (ScVO₂) or mixed venous oxygen saturations (SVO₂).

  
  
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  Mixed/central venous oxygen saturation (SVO₂/SCVO₂): can be used as a measure of oxygen delivery and consumption. SCVO₂ is sampled from a central line, whereas SVO₂ is taken from a pulmonary artery catheter, ensuring complete venous admixture from superior and inferior vena cavae and coronary sinus.

  
  
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  Pulse oximetry (SpO₂): A non-invasive way of measuring arterial oxygen saturations. Works by absorbance of light from two different wavelengths (660 nm and 940 nm). May not always correlate with SaO₂ and has potential errors (such as reading falsely high with carbon monoxide exposure).

  
  
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  Intrapulmonary shunt: an area of lung that is perfused but not ventilated, resulting in zero gas exchange and effectively transfer of deoxygenated blood from the right heart to the left heart. Can be thought of as an extreme form of V/Q mismatch (see Dead space). Shunts may also occur outside the lung (e.g. intracardiac shunt).