The primary function of the lungs is to enable gas exchange between inspired air that reaches the alveoli and the blood of the pulmonary capillaries. This process of gas exchange is crucial for homeostasis and is interdependent with the circulatory system’s prime role of blood transport. To enable adequate gas exchange it is crucial that oxygen and carbon dioxide move between air and blood by simple diffusion across the alveolar surface. More specifically, there is a balance between ventilation (V) and perfusion (Q). However, it is more complicated than this. V and Q are not evenly distributed throughout the lung (Hazinski 1999). Figure 45.2 illustrates how V increases from apex to the base of the lung and Q increases from apex to base relatively more than perfusion. During normal quiet breathing in an upright position the bases of the lung receive about 50% more ventilation than the apices. This is due to:

If oxygen is not delivered to alveolar capillaries, or the alveolar surface is damaged, oxygen and/or carbon dioxide elimination may be impaired, V and Q are not balanced and respiratory failure ensues. In a single lung unit V and Q must be matched to allow gas exchange (Fig. 45.3).

During normal inspiration the mechanical contraction of the inspiratory muscles causes the thoracic cage to enlarge in volume. This increased volume causes a pressure gradient between the lungs and the atmosphere. This pressure differential is enough to cause an in-rush of air into the lungs. The work that the inspiratory muscles perform represents the negative pressure applied. Figure 45.4a shows the changes in airway pressure in the mouth during spontaneous quiet breathing. Airway pressure during inspiration is negative, allowing air to enter the lungs, and is positive during expiration. Also, there is normally a brief pause, when airway pressure remains at atmospheric pressure. Figure 45.4b shows the upper airway pressures (measured at the mouth) during mechanical ventilation. In artificial ventilation, the ventilator must provide the inspiratory pressure provided by the inspiratory muscles in normal respiration. This is done by creating a positive intrapulmonary pressure whereby air is pushed out of the ventilator into the lungs of the patient, thus raising the pressure in the airways relative to atmospheric pressure. This resultant increase in intrapulmonary pressure forces the lungs to expand. It is important to remember that artificial ventilation fundamentally alters normal airway pressures. This fact accounts for most of its benefits and complications.

In the equation Pressure = Volume ÷ (Compliance + Resistance), compliance and resistance are assumed to remain constant and is illustrated by (a) in Figure 45.5. However, this is not the case in cardiopulmonary illness. With stiff lungs (reduced compliance) patients tend to take rapid, small breaths, to minimise elastic workload as in Figure 45.5b. With high airway resistance, for example in asthma, patients take large slow breaths (Figure 45.5c). As can be seen in Fig. 45.5, the inspiratory lung volume is low in both. Thus, their combined effect is a greater load presented to the ventilator. Pressure, volume and flow change over time in illness, therefore they are considered variable. From the equation of motion, the ventilator must control one of these variables. A mechanical ventilator will control airway pressure, inspired volume or inspired flow.

But there is more to compliance. To achieve compliance, alveolar lung units have an important lung property – they are elastic. They can be expanded by small forces and return to their resting state. Two components are responsible for their elastic behaviour:

Thus less pressure is required to inflate alveoli (Martini 1998). The lung contains a foamy phospholipid fluid commonly known as surfactant. Pulmonary surfactant is produced by type I and II alveolar pneumocytes, and is responsible for decreasing the surface tension of the lining fluid within the bronchial tree. Without surfactant, pulmonary airways become unstable and have decreased compliance. Surfactant decreases the surface tension of the alveoli in order to aid the diffusion of gases (Martini 1998). A reduction in production of surfactant will directly affect gas exchange. General causes of reduced surfactant production are:

To help understand this concept, think about blowing up a balloon. At first it is difficult and then there is a ‘give’ and the balloon inflates easily. This occurs in the same way in the lungs. The greatest workload in the respiratory cycle is in early inspiration where the pressure–volume curve is relatively flat (Fig. 45.6).

Once the steep part of the pressure–volume curve (PVC) (the P _flex) is reached, the lung suddenly inflates easily; this is the inflection point. The PVC is flattest at low lung volumes and consequently the work of breathing is highest. If the lungs were left filled with air so that the resting state is at or above the inflection point, the work of breathing is reduced considerably. Going back to our analogy, this is like letting a balloon deflate incompletely and then re-inflating it. This is the basis for positive end expiratory pressure (PEEP), which is a continuous constant pressure of gas delivered to prevent alveolar collapse (PEEP will be discussed in more detail later).

Finally, the last physiological mechanism we must consider is closing volume. In health, the lungs dangle downwards in the pleural cavity supported by a vacuum of negative pressure. As you would expect, the magnitude of this negative pressure is greater in the apices than in the bases. The effect of this is to splint the airways open at the end of the tidal volume (normal expiration) – the expiratory reserve volume (ERV) (McCance & Huether 2002) (Fig. 45.7). Apical alveoli are more inflated at rest than basal. But during inspiration, because the latter are at a steep part of the pressure–volume curve, the gas turnover (see Fig. 45.6) is greater. However, in illness, further confounded by upper airway compromise, and especially when lying supine, there is a tendency for distal, particularly basal airways to collapse in expiration. This is known as the closing volume. If this is not addressed by delivering PEEP through the ventilator, eventually the closing volume will impinge on and begin to exceed functional residual capacity (FRC) and atelectasis (alveolar collapse) will occur at the end of quiet expiration.

As we have seen, artificial ventilation is unlike normal ventilation. Positive pressure ventilation can be injurious to the lungs, which were designed as a negative pressure circuit receiving oxygen at 21%. Moreover, artificial ventilation is most often required by patients with underlying lung or cardiovascular pathology which makes the lung tissue even more susceptible to ventilator-induced lung injury and cardiovascular complications.

In response to these findings, respiratory experts have espoused the use of lung protective ventilator strategies (Kerr 1997). One strategy is to use sufficient PEEP to raise FRC above closing capacity without compromising cardiac output and as a consequence oxygen delivery. This strategy keeps alveolar units on the steep part of the compliance curve (see Fig. 45.6). Higher levels of PEEP help to maintain:

Thus, higher levels of PEEP lead to reduced end inspiratory volumes preventing shear/stretch injury.

Another strategy advocated is the use of pressure-limited ventilation and increasing mean airway pressures by permissive hypercapnia and hypoxemia (Reynolds et al 1993). There is no research evidence to dictate what acceptable oxygen or carbon dioxide levels are. The general philosophy is that an acceptable level is determined by what intensivists are willing to do to get there considering the research findings available regarding the causation of lung injury. For example, if an oxygen saturation of 95% can only be achieved through using a PEEP of 12 cmH ₂O and a FiO ₂ of 1.0 (100%) this is not acceptable in the light of the best available evidence. Both high PEEP and high inspired-oxygen concentrations are injurious to the lung. However, if achieving a carbon dioxide level of 5.4 kPa results in a peak pressure of 30 cmH ₂O, this might be acceptable as this carbon dioxide level is acceptable. In general (Parker et al 1993):

It is recognised that these limits are arbitrary in nature and no study has ever demonstrated what safe limits are (Hill 1997). These limits are made by intensivists in the context of the patient’s clinical situation and expected clinical course. Thus the overall goal of mechanical ventilation is not to achieve a target blood gas value but to maximise oxygen delivery while minimising pulmonary injury.

Inhaled nitric oxide (iNO) was originally thought to be the ‘magic bullet’ for improving V/Q mismatch in severe respiratory failure (Tibballs 1998). Given its ability to vasodilate blood vessels, be delivered as a gas (act on blood vessels that perfuse ventilated alveoli: selective pulmonary vasodilatation) and its short half-life (no systemic hypotension), it was studied with great interest. However, although iNO does improve oxygenation in acute respiratory distress syndrome, it does not improve outcome. It has more of a beneficial effect in patients with pulmonary hypertension, especially neonates with persistent pulmonary hypertension of the newborn or post-operative cardiac patients.

There are options, beyond adjusting the ventilator, which have implications for nursing. Body positioning affects ventilation/perfusion (V/Q) matching and therefore arterial oxygen levels. Accumulation of secretions and atelectasis can occur in the dependent regions of the lungs, therefore regular position changes will help to avoid problem areas developing. Position can also affect a child’s FRC. A reduction in FRC will make a child more vulnerable to atelectasis and allow more rapid hypoxia. It is important to consider which positions may help to optimise oxygenation and this is a multi-professional decision made in consultation with a respiratory physiotherapist. It is well established that atelectasis develops in the dorsal areas of the lung when patients are in a supine position for any extended period of time (Ganong 2001). ‘Prone positioning’ a patient can help re-expand these collapsed areas, improve alveolar ventilation and hence gas exchange (Ball et al 2001). Additionally, the chest wall has a more favourable compliance curve in the prone position. Most patients will usually have improved oxygenation when prone and can tolerate being prone for 20 hours at a time, with regular pressure relief. It has not been established that prone positioning improves mortality but it can be useful in the patient that is difficult to oxygenate.

In normal circumstances the upper airway warms and humidifies air, so that it reaches core temperature and 100% saturation just below the carina. This process is known as gas conditioning (Williams et al 1996). During gas conditioning inspired air is also cleaned and filtered of foreign particles by the mucociliary transport system, which extends from the nasopharynx towards the bronchioles (Estes & Meduri 1995). Thus, gas conditioning optimises gas exchange and protects delicate lung tissue. The placement of an endotracheal tube bypasses this defence mechanism and the gas exchange function of the lung. The placement of the endotracheal tube physically shifts the conditioning, and heat and moisture recovery functions, further down the airway which would not normally be required to give up heat and moisture.

Hence in the intubated patient, the mucociliary transport system is the sole remaining mechanical defence system. The mucociliary transport system’s function depends on the:

If the temperature of inspired gas is less than core temperature the beat frequency of the cilia will reduce and the gas will be heated to a suboptimal temperature causing the relative humidity of the gas to be reduced. Less than optimal humidification results in a compromised mucociliary transport and pooling of mucus in the lower airways thus restricting gas exchange and being an ideal site for bacterial colonisation (Centers for Disease Control (CDC) 1994). Furthermore, the gel layer will lose moisture and become thicker. If suboptimal humidification is allowed to continue, cell damage might occur and the process of gas conditioning will move deeper into the lung. Increased thick mucus and reduced clearance of secretions from small airways results in reduced airway patency and lung compliance (Williams et al 1996). Thus the nurse must ensure that inspired gases are maintained at core temperature and humidity. Effective humidification will also maximise lung defence by reducing exposure to contaminants invading the airways by increasing clearance of contaminants through suctioning.

The initial settings prescribed and set by the intensivist for both volume and pressure are similar. Except in volume control a tidal volume is set at usually 8–10 mL/kg and in pressure control the peak airway pressure is set. The starting peak airways pressure is set at what is needed to adequately inflate the patient’s chest and generate breath sounds and is usually 15–20 cmH ₂O above PEEP. The starting breath rate is usually one that would be physiologically appropriate for the age of the patient. Immediately after intubation patients are usually placed on a FiO ₂ of 1.0 and are weaned down as long as the oxygen saturations remain acceptable. PEEP is usually set at 5 cmH ₂O and then increased as needed to achieve acceptable oxygen saturations with a FiO ₂ less than 0.6 (Pearson 2002) (Fig. 45.12).