Asthma and COPD
Asthma is an acute generalized airway obstruction syndrome associated with bronchospasm due to hyper-reactivity of airways and the release of inflammatory mediators such as histamine.
COPD is a slow, progressive disorder characterized by airway obstruction and a reduced FEV1/FVC. There is a gradual deterioration over years with lung parenchymal destruction, an increased residual volume and hyperinflated chest. The diaphragm is flattened and the intercostal muscles are elevated to a mechanically disadvantageous position. Classically, patients breathe with small tidal volumes. A high Vd/Vt ratio (high PaCO2) and a significantly reduced inspiratory reserve volume (hinders coughing) necessitate an increase of minute volume by a faster respiratory rate. As the condition progresses, expiration is no longer passive, but requires positive pressure to overcome bronchial resistance. This positive pressure at the end of expiration causes premature small airway collapse and incomplete emptying of the lung. Intrinsic PEEP (PEEPi) develops (a measure of the adequacy of expiration and relates to the amount of air trapping during the respiratory cycle). Before inspiratory flow begins, intrapleural pressure has to be reduced by an amount equivalent to PEEPi. Increased inspiratory and expiratory muscular effort is needed to overcome PEEPi. Acute exacerbations of COPD can increase bronchial resistance and accentuate the problem. Lung impairment is often progressive, but reversibility should be assessed with bronchodilator therapy or steroids in all patients.
Ventilatory strategies in asthma and COPD
The ventilator should have a graphical real-time display of flow and pressure. The elimination of hypoxaemia can almost always be achieved by the short-term use of a high inspired oxygen concentration titrated to a PaO2 of 8–10 kPa. The minute volume should be adjusted to pH and not to the PaCO2 to avoid over-ventilation with consequent alkali loss and reduced renal compensation.
At the start of controlled ventilation in asthmatics, tidal volumes may need to be reduced to avoid high airway pressures and barotrauma. Enough time has to be allowed for expiration to reduce gas trapping. Increased respiratory rate leads to a significant increase in PEEPi as a result of a reduced expiratory time. Therefore, a low respiratory rate and a I:E ratio of 1:1.5 or 1:2 should be chosen to achieve a flow pattern as shown in Figure 13.
Whether non-invasive positive-pressure ventilation (reduces mortality and incidence of intubation in management of COPD) or conventional ventilation are used, triggered spontaneous breathing (pressure support, assisted spontaneous breathing) is the optimal mode. The use of PEEP or CPAP requires particular care but can reduce inspiratory and expiratory work. On inspiration, PEEP reduces the negative inspiratory effort needed by the patient to overcome PEEPi before gas begins to flow. On expiration, PEEP helps to splint open the airway and allow more complete exhalation (improved CO2 clearance). Optimally PEEP/CPAP should be set below PEEPi (Figure 14).
Qualitative measurement of PEEPi during positive-pressure ventilation can be obtained using the end-expiratory hold control on the ventilator. This allows equilibration of pressures between the alveoli and the ventilator and is an indication of the total PEEP. The PEEPi can then be calculated by subtracting the dialled PEEPe from the total PEEP (Figure 15).
ARDS is characterized by generalized pulmonary infiltration secondary to increased permeability resulting in interstitial and alveolar oedema. ARDS is defined by: a PaO2/ FiO2 of less than 200 mmHg; bilateral interstitial infiltrates on a chest radiograph; no evidence of LV failure with a pulmonary artery wedge pressure of less than 18 mmHg; a recognized cause of ARDS. Hypoxia is secondary to decreased compliance, increased pulmonary shunt and pulmonary hypertension. It is this pulmonary hypertension that causes an increase in microvascular pressure resulting in increased capillary leak and interstitial oedema. It may also precipitate RV failure. Poor lung compliance and attempts to ventilate with normal tidal volumes may lead to high airway pressures and possible volutrauma.
Ventilatory strategies in ARDS
The ventilator should have real-time graphical displays of flow and pressure waveforms. Protective ventilation is the key to safe and effective management. Ventilation strategies are aimed at preventing the detrimental effects of volutrauma. Strategies include pressure-controlled forms of ventilation with small tidal volumes (5–6 ml/kg) and high respiratory rates (> 25 breaths/min) to prevent over-distension. When volume-controlled ventilation is used, gas is preferentially delivered to more compliant lung units, with a risk of over-distension. The application of pressure-controlled ventilation, results in better gas distribution and less distension of non-compliant lung units (Figure 16).
Mean airway pressure (which corresponds with alveolar recruitment and improved PaO2 ) should be increased. The mean airway pressure correlates with the area under the pressure curve and can be increased by several manoeuvres.
A higher mean airway pressure for a given peak airway pressure can be achieved with pressure-controlled ventilation. The normal alveoli are more susceptible to the effects of peak airway pressure (Figure 16). High airway pressures result in volutrauma and should be limited to less than 35 cm H2O. If volume-controlled ventilation is used, it can be difficult to keep the peak airway pressure below this, in patients with non-compliant lungs.
With pressure-control modes it is possible to increase the mean airway pressure safely, by prolonging inspiratory time, without the need to increase the peak pressure. A reduction in expiratory time can induce auto-PEEP (PEEPi) where a new breath is delivered before expiratory flow is complete. The remedy for this is a reduction in the respiratory rate followed by a reduction in the I:E ratio until gas trapping just disappears on the flow waveform. This results in improved oxygenation within the pressure limit without overstretching the alveoli (Figure 13). If gas trapping develops with pressure-controlled ventilation a reduction in tidal volume with each subsequent breath follows. When volume-controlled ventilation is used for inverse ratio ventilation, the tidal volume is sustained with each breath and peak airway pressure rises. This progressively worsens gas trapping. Volume-controlled ventilation should not be used in inverse ratio mode.
The optimal PEEP level should be set from the lower inflection point on a plot of the static pressure–volume curve (Figure 8). In ARDS secondary to diffuse homogeneous lung injury the PEEP level may often be above 12–15 cm H2 O. The static curve can be constructed with pressure-control ventilation using the peak pressure value, provided the gas flow ceases before the end of expiration, or using volume-controlled ventilation and plotting the plateau pressure (no flow) against the respective tidal volumes. By randomly changing the size of the tidal volume every five breaths, a curve can be safely plotted in a compromised patient. Higher levels of PEEP ensure an FRC greater than the closing capacity and reduce the tendency towards alveolar collapse, V/Q mismatch and hypoxaemia. In ARDS associated with focal consolidation (secondary to pneumonia) new evidence suggests that high PEEP levels may be less beneficial and lead to over-distension of healthy lung units.
Protective ventilation may lead to permissive hypercapnia (a higher than normal PaCO2) particularly as an increased Vd/Vt ratio is associated with ARDS. Providing renal function is preserved, the HCO3 level increases over 2–6 hours to buffer the rise in PaCO2 and normalize pH. The benefits of protective ventilation strategies outweigh the detrimental effects of a higher PaCO2 in adult critical care.
This technique can improve oxygenation in some ARDS patients. In the supine position, ventilation is preferentially directed to the anterior part of the lung, but the optimal perfusion is in the lung bases close to the diaphragm. In addition, the weight of the mediastinum and heart together with heavy oedematous lung collapses the lung posteriorly. When prone, the compliance of the anterior chest wall is increased, the posterior chest wall is already relatively non-compliant and ventilation is preferentially directed to the bases where perfusion is optimal. The mediastinum and heart are also dependent and lung previously compressed posterior to this can expand. The benefits are essentially from improved V/Q matching, but drainage of secretions is also increased.
High frequency oscillatory ventilation (HFOV)
HFOV is a relatively new mode in adult practice. HFOV generates sub-dead space tidal volumes at high rates (4–5/s) at a constant high mean airway pressure. Lung recruitment follows with reasonable clearance of CO2. It is commonly used in neonates but there are few good adult studies.
Other treatment modalities
Other therapies include inhaled nitric oxide, inhaled prostacyclin, continuous rotation, partial liquid ventilation and extracorporeal membrane oxygenation.
© 2003 The Medicine Publishing Company Ltd