Introduction

The medical literature can be daunting for those at the beginning of their careers. Papers which may be straightforward to the experienced clinician or seasoned researcher can be almost unreadable to those who are less familiar with the specific vocabulary of the field.

In this paper we present a short glossary of terms which commonly appear in the literature regarding the acute respiratory distress syndrome (ARDS), including the papers in this issue of Intensive Care Medicine. Our goal is in no way to provide a comprehensive review of ARDS but rather a short guide for the perplexed (Table 1).

Table 1 ARDS glossary for beginners
Full size table

Diagnosis

Baby lung

The baby lung concept was derived from computed tomography findings in ARDS patients. The lung injury pattern in ARDS is very heterogeneous with portions of the lung that may be normally aerated, poorly aerated, overinflated, or completely consolidated (non-aerated tissue). The areas of normally aerated lung tissue have the dimensions of a 5- to 6-year-old child (300–500 g of aerated tissue) and thus have been termed “baby lungs” [1]. To prevent barotrauma to these areas of normal lung tissue, ventilator strategies with lower tidal volumes should be utilized.

Berlin definition of ARDS

In 2011, a panel of experts convened to develop an updated definition of ARDS [2]. Using a consensus process, they focused on feasibility, reliability, and validity and evaluated the objective performance of the diagnostic criteria. The Berlin definition of ARDS includes the following four criteria:

  1. A.

    Timing: ARDS develops within 1 week of a known clinical insult or new or worsening respiratory symptoms.

  2. B.

    Bilateral opacities on chest imaging that are not fully explained by effusions, lobar/lung collapse, or nodules.

  3. C.

    Respiratory failure not fully explained by cardiac failure or fluid overload. Objective assessment, such as echocardiography, is needed to exclude hydrostatic edema if no risk factor is present.

  4. D.

    Hypoxemia: ARDS was divided into three categories based on the degree of hypoxemia:

  • Mild: 200 mmHg < P/F ≤ 300 mmHg with PEEP or CPAP ≥ 5 cmH2O.

  • Moderate: 100 mmHg < P/F ≤ 200 mmHg with PEEP ≥ 5 cmH2O.

  • Severe: P/F ≤ 100 mgHg with PEEP ≥ 5 cmH2O.

Diffuse alveolar damage

Diffuse alveolar damage is the classic histological finding in ARDS patients. It is characterized by lung edema, acute inflammation, hemorrhage, hyaline membranes and alveolar epithelial injury [3]. On the basis of recent open lung biopsy or autopsy studies, diffuse alveolar damage is only present in approximately 50 % of patients who fulfill the diagnostic criteria for ARDS, though when present it is associated with a worse outcome [4, 5]. Diffuse alveolar damage can also be present in other non-ARDS conditions [6] such as organizing pneumonia, drug-induced pneumonitis, and alveolar hemorrhage syndromes.

PaO2/FiO2 ratio

This ratio is used to define the degree of hypoxemia in ARDS patients. A lower ratio is consistent with more severe hypoxemia. The P/F ratio is calculated by dividing the PaO2 by the FiO2. For example, in a patient with a PaO2 of 60 mmHg on 50 % (0.5) FiO2, the P/F ratio would be 120 (60/0.5).

Lung mechanics in ARDS

Driving pressure

The driving pressure is the change in pressure across the lung during the delivery of a tidal breath. This pressure is related to both the tidal volume (TV) and to the compliance of the respiratory system (DP = TV/CRS). Lower driving pressures have been associated with decreased mortality in ARDS [7].

Lung strain

Strain refers to the deformation of an object relative to its resting size or shape. The ideal resting conformation of the ARDS lung is unknown. Since most patients will have some level of PEEP applied to the lung, their lungs will not collapse back to the resting conformation. For this reason lung strain is not equivalent to TV and the true strain of the lung in clinical practice may be unknown.

Lung stress

In physics, stress refers to the internal forces per unit area that balance an external load. The transpulmonary pressure is the pertinent distending pressure of the lung [8]. It represents global lung stress in the face of the load placed on the lung by insufflation.

Plateau pressure

This is the pressure recorded at the airway opening during an end-inspiratory pause. Because there is no flow during this time, there is no resistance, and plateau pressure reflects the alveolar pressure.

Tidal volume

TV is the volume of gas delivered to the lung in any given breath. In volume controlled ventilation (VCV) this will be set on the ventilator by the clinician. In pressure controlled ventilation (PCV), TV will depend on the compliance of the lung. Lower TV has been shown to be beneficial in patients with ARDS [9].

Transpulmonary pressure

The actual distending pressure of the lung is the transpulmonary pressure. This is the pressure applied at the airway minus the pressure required to overcome the pressure in the pleural space (This is represented physiologically as PL = PAW–Ppl). The true pressure in the pleural space cannot be measured in clinical practice but it may be estimated using the pressure in the esophagus as a surrogate [10].

Treatment

Extracorporeal membrane oxygenation (ECMO)

In patients with severe hypoxemia (PaO2/FIO2 < 80 mmHg) when above strategies had failed, ECMO may be used in patients with a reasonable chance of survival. One randomized trial found a benefit from this strategy in a specific organizational model [11].

Neuromuscular blocking agent (NMBA)

The NMBA cisatracurium has been shown to improve survival in one placebo-controlled randomized controlled trial [12]. The mechanisms for this effect include prevention of overdistension, as indicated by the significantly lower pneumothorax rate in the NMBA group, and reduction in lung inflammation.

Nitric oxide (NOi)

Administered intratracheally, NOi selectively dilates pulmonary vessels in well-ventilated lung areas and diverts blood flow there resulting in better oxygenation. NOi also reduces pulmonary artery pressure. In previous trials NOi was not associated with better survival and might have some harmful effect on kidney function [13]. These trials were, however, performed before the era of lung-protective mechanical ventilation.

Positive end-expiratory pressure (PEEP)

It is the amount of airway pressure above atmospheric pressure at the end of expiration. PEEP increases functional residual capacity and contributes to minimize intratidal recruitment. The optimal level of PEEP to set is not known. Different strategies have been tested in randomized controlled trials. None of them was associated with increasing survival except if higher PEEP was associated with lower TV. The meta-analysis of three large trials comparing lower to higher PEEP at fixed TV of 6 ml/kg predicted body weight concluded that higher PEEP had a beneficial effect [14].

Prone position

Turning the patient face down during mechanical ventilation improves oxygenation and prevents ventilator-induced lung injury by allowing more homogeneous distribution of TV and stress and strain throughout the lung. Prone positioning has been shown to improve survival in patients with moderate to severe ARDS in a meta-analysis on individual-patient data [15] and in a single trial in a specific subgroup of patients [16].

Recruitment maneuver

It is a procedure in which the lung is inflated to a high pressure (20–40 cmH2O) for a short period of time (20–40 s). This is done to recruit collapsed alveoli and to prevent further lung injury from atelectasis. There are a number of different approaches to performing a recruitment maneuver in the literature.