Acute Lung Injury - Treatment

Treatment

The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O₂ or volutrauma.

Pressure control ventilation (PC) is more versatile than volume control: but a volume limited strategy should be used to prevent stretch injury to the alveoli. A number of adjunct therapies are available, none have proven effective. Of these, inhaled nitric oxide and prone positioning are most frequently used. Current ventilation strategies involve using low tidal volumes with or without high levels of PEEP. The open lung approach attempts to optimize lung mechanics and minimize phasic damage by strategically placing PEEP above Pflex. Ventilator induced lung injury is caused by volutrauma and excessive use of oxygen.

Steroids may have a role in chronic ARDS in patients, without infection, with high O2 requirements days to weeks into the disease process. It was historically known as "double pneumonia".

In general tidal volumes should not exceed 6ml/kg and plateau pressure should not exceed 30 cmH₂O (2.9 kPa). However tidal volumes of 4ml/kg should be delivered irrespective of airway pressure. The management of patients with respiratory failure goes beyond ventilation strategies, requiring a holistic multisystem approach. Providers are reminded of the ABCDEFG mnemonic.

A = Airway, establish a patent airway, intubate as necessary.

B = Breathing, commence mechanical ventilation and obtain an adequate minute volume to maintain oxygen delivery.

C = Circulation: blood pressure, pulse, intravascular volume – fluid resuscitation and vasopressors as necessary

D = Diagnosis, find the underlying problem and control the source.

E = Empiric therapy, for example antimicrobials for sepsis

FG = Feed the Gut, to prevent villus atrophy and bacterial translocation

The principles of mechanical ventilation are simple:

1. Give enough oxygen to keep the PaO2 over 60 mmHg (8.0 kPa) preferably, and over 50 mmHg (6.7 kPa) at the very least.
2. Avoid volutrauma and barotrauma, by keeping the tidal volumes in the 4-6 ml/kg range and the airway plateau pressure below 30-35 cmH₂O (2.9–3.4 kPa) (the tidal volume should not be less than 4ml/kg, irrespective of airway pressure).

The PaO2 is a function of the FiO2, the PEEP level, the mean airway pressure and the minute ventilation. The tidal volume, depending on what mode of ventilation is used, is determined by the pressure control level (in pressure controlled modes) or the tidal volume dialed up on the ventilator (in volume controlled modes).

There is no clear evidence that any particular mode or strategy improves outcome in ALI, except for controlling tidal volumes and airway pressures. What follows is a suggested starting strategy:

1. Start with a high FiO2 (use the same FiO2 on the patient following intubation as before).
2. Set the CPAP/PEEP level – if the patient has a P/F ratio of 200-300 start with CPAP/PEEP of 5 cmH₂O (490 kPa), if the P/F ratio is <200, use a CPAP/PEEP of 10 cmH₂O (980 kPa).
3. For inspiratory support, use a decelerating flow pattern, with a tidal volume of 5-6 ml/kg, of if pressure control is being used, a pressure limit which gives a tidal volume of 5-6 ml/kg (1).

It is important to note that ARDS is a disease of altered lung compliance. This is reduced due to the presence of large quantities of extravascular lung water. However, chest wall compliance may also be low - in patients who are edematous, have had massive fluid resuscitation or have abdominal hypertension. In this situation, the chamber in which the lungs are inflating (the chest), bears more resemblance to a brick wall than a rib cage with muscles. Higher inflation pressures are required to inflate the lungs in these circumstances and higher PEEP is required to maintain FRC.

The choice of mode of ventilation is institution specific. The majority of intensive care units in the United States continue to use volume controlled modes of ventilation to treat ARDS. Severe hypoxemia is managed by increasing mean airway pressure by escalating levels of PEEP and rapid respiratory rates. The logic behind increasing mean airway pressure is that much of the ventilation perfusion mismatch contributing to hypoxia occurs at end expiration (click here for more information). Although the majority cases can be managed in this way, more versatile modes are available, under the pressure control umbrella.

Pressure control modes have the advantage of allowing us manipulate the mean airway pressure by prolonging inspiration, and this may improve oxygenation without increasing peak or plateau pressures . In addition, pressure control may improve gas distribution at the end of inspiration, particularly where different lung units have different resistance patterns (ALI is, after all, a heterogeneous process).

The drawback of prolonging inspiration, and, in effect, inverting the I:E ratio (2:3), is that the patient may experience a lot of discomfort, and requires deep sedation. Further, incomplete expiration tends to reduce CO₂ elimination, and the patient will develop “permissive hypercapnia” and respiratory acidosis. As we now know that ventilator induced lung injury causes much more trouble than respiratory acidosis, we do not consider the latter to be a major problem (4). Newer pressure control modes such as BiLevel / Airway Pressure Release ventilation have been developed to address the problem of patient discomfort in inverse ratio ventilation; with some success.