**1. Diagnosing and evaluating the severe acute respiratory distress syndrome**

Acute respiratory distress syndrome is characterized by an increase of the permeability of the lungs alveolar-capillary membranes leading to the extravasation of the intravascular plasma of the lungs capillary network surrounding the alveoli to the alveolar spaces that were previously filled by air. This accumulation of liquid rich in proteins inside the alveolar spaces turns an air-filled lungs into a heavy high-osmotic pressure liquid-filled lungs and the consequent collapse of the lowermost lung regions, shunt, refractory hypoxemia, decrease in lungs compliance and increase in dead space that are more pronounced the more severe the permeability changes of the pulmonary alveoli-capillary membrane. Regarding the physiopathology of ARDS, the hallmark mechanism of injury is inflammation leading to increased endothelial and epithelial permeability and liberation of receptors for angiopoietin-2 and advanced glycation end products (RAGE) [1–4].

ARDS had higher EVLWi (severe, 19.1; moderate, 17.2; mild, 16.1; *P* < 0.05) and PVPI (3.2; 3.0; 2.7; *P* < 0.05). When the authors evaluated 495 independent measurements over three con-

/FIO<sup>2</sup>

**4. The hole of pulmonary arterial hypertension and right ventricular** 

observed an association between ARDS severity according to Berlin definition and 28-day

Hemodynamic data from the ARDSnet Fluids and Catheter Therapy Trial (FACCT) [6] that analyzed 475 patients randomized to receive a pulmonary artery catheter for ARDS management, none of the baseline measures of cardiopulmonary dysfunction distinguished survivors from nonsurvivors. When the authors measured the transpulmonary gradient (TGP), they observed that 73% of the ARDS patients monitored with the Swan-Ganz had an elevated TGP (>12 mm Hg). Patients with a TPG *>* 12 mm Hg had a significantly greater mortality rate than patients with a TPG *<* 12 mm Hg (30 vs. 19%; *P =* 0.02). In multivariate analysis, an elevated TPG and a high PVRi remained an independent predictor of an adverse outcome in this ARDS population. In a recent, prospective and observational study in an academic medical intensive care unit in France [7], 226 consecutive patients with moderate to severe ARDS ventilated who received a

O, underwent transesophageal echocardiography (TEE) within the first 3 days after the diagnosis of ARDS. Cor pulmonale (dilated right ventricle associated with septal dyskinesia), was detected in 49 patients (prevalence of 22%; 95% confidence interval, 16–27%). Patients who had cor pulmonale presented a significantly higher 28-day mortality rate (60 vs. 36%, *P* < 0.01) compared with the ARDS patients without cor pulmonale. Sepsis and higher values of driving pressure were associated with the presence of cor pulmonale that was an independent risk factor for 28-day mortality in their population. Taking these results into consideration, a subgroup of ARDS severity stratification: ARDS with right ventricular dysfunction should be proposed especially because different ventilatory strategies (prone position, low driving pressures, titrated PEEP levels), distinct pharmacologic therapy (pulmonary artery vasodilators)

should be tested in order to improve prognosis of this subgroup of ARDS patients [4].

**5. The hole of low respiratory system compliance in ARDS severity** 

Other factors that are associated with severe ARDS are respiratory system compliance of

APACHE II and SAPS II score as well as multiple organ failures (the higher the organ failures,

O, pulmonary dead space fraction greater than 0.60, as well as high

/FIO<sup>2</sup>

and PVPi (r = −0.345, *P* < 0.001 The authors

Severe Acute Respiratory Distress Syndrome http://dx.doi.org/10.5772/intechopen.77071

O and mean PEEP of 8.8 ± 3.6 cm

ratio

51

secutive days, they observed a moderative and negative correlation between PaO<sup>2</sup>

and EVLWi (r = −0.355, *P* < 0.001) and PaO<sup>2</sup>

mortality rate: severe, the odds ratio 4.167 relative to mild.

**dysfunction in ARDS severity stratification**

protective ventilation (plateau pressure less than 30 cm H<sup>2</sup>

H2

**stratification**

less than 20 mL/cm H<sup>2</sup>

the higher the patient mortality) [1–4].
