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MINISTRY OF EDUCATION AND TRAINING

MINISTRY OF DEFENCE

108 INSTITUTE OF CLINICAL MEDICAL AND PHARMACEUTICAL SCIENCES

-------------------------------------------------

NGO TRONG TOAN

RESEARCH EFFECTS OF MECHANICAL
VENTILATION WITH TIRATING POSITIVE ENDEXPIRATORY PRESSURE GUIDED BY ESOPHAGEAL
PRSSURE IN PATIENTS WITH ACUTE RESPIRATORY
DISTRESS SYNDROME

Speciality: Anesthesia Resuscitation
Code: 62723301

ABSTRACT OF MEDICAL PHD THESIS

Hanoi – 2022


THE THESIS WAS DONE IN: 108 INSTITUTE OF CLINICAL
MEDICAL AND PHARMACEUTICAL SCIENCES

Supervisor:
1. Prof. PhD. Nguyen Thi Du
2. Ass. Prof. PhD. Dao Xuan Co

Reviewer:

1. .............................................................................
2. .............................................................................
3. ..............................................................................

This thesis will be presented at Institute Council at: 108 Institute of
Clinical Medical and Pharmaceutical Sciences
Day
Month Year

The thesis can be found at:
1. National Library of Vietnam
2. Library of 108 Institute
Pharmaceutical Sciences

of

Clinical

Medical

and


1

INTRODUCTION
Acute respiratory distress syndrome (ARDS) is a syndrome with
highly prevalent rate in intensive care units. Despite recent
therapeutic advances in patients with ARDS, in-hospital mortality
rate remains unacceptably high from 14.2% to 84% according to each

study, average of 40%.
Mechanical ventilation that to secure oxygenation for patient is
very important to manage patients with ARDS. Positive endexpiratory pressure (PEEP) is an important parameter of mechanical
ventilation in treating ARDS patients. Whereas low tidal volumes are
clearly beneficial in patients with ARDS, how to choose a PEEP to
obtain the best benefit is uncertain and has many opinions.
A new approach is that ideally, mechanical ventilation should
provide sufficient transpulmonary pressure (plateau airway pressure
minus pleural pressure) to maintain oxygenation while minimizing
repeated alveolar collapse or overdistention leading to lung injury. In
critical illness, there is marked variability among patients in abdomal
and pleural pressures; thus, for a given level of PEEP,
transpulmonary pressures may vary unpredictably from patient to
patient. Pleural pressures can be estimated by using an esophageal
balloon catheter. PEEP are adjusted according to each patient’s lung
and chest-wall mechanics. In patients with high estimated pleural
pressure who are undergoing ventilation with conventional ventilator
settings, underinflation may cause hypoxemia. In such patients,
raising PEEP to maintain a positive transpulmonary pressure might
improve aeration and oxygenation without causing overdistention.
Conversely, in patients with low pleural pressure, maintaining low


2

PEEP would keep transpulmonary pressure low, preventing
overdistention and minimizing the adverse hemodynamic effects of
high PEEP.
On the world, using an esophageal balloon catheter to measure
esophageal pressures then adjusting PEEP according to measured

esophageal pressures has been studied by Talmor, Sarge, Fessler,
Yang…These researchers showed some initial benefits of adjusting
PEEP depending on esophageal pressures are
However, in Vietnam studies about esophageal pressure and its
use in treating patients with ARDS have been rare. So the thesis
“Research effects of mechanical ventilation with titrating positive
end-expiratory pressure guided by esophageal pressure in
patients with acute respiratory distress syndrome” has been
conducted with two following purposes:
1. Study change of esophageal pressure measured by adult
esophageal balloon catheter set and correlation between
esophageal pressure and lung mechanical indexes in ARDS
patients.
2. Evaluate

efficacy

about

improving

arterial

blood

oxygenation of mechanical ventilation with titrating
positive end-expiratory pressure guided by esophageal
pressure in ARDS patients.

3

Chapter 1
OVERVIEW
1.1. Acute respiratory distress syndrome
1.1.1. The Berlin definition of ARDS
ACUTE RESPIRATORY
CHARACTERISTICS
DISTRESS SYNDROME
Within 1 week of a known clinical
Timing
insult or new/worsening respiratory
symptoms
Bilateral opacities-not fully explained
Chest imaginga
by effusions, lobar/lung collapse, or
nodules
Respiratory failure not fully explained
by cardiac failure or fluid overload;
Need objective assessment (e.g.,
Origin of edema
echocardiography)
to
exclude
hydrostatic edema if no risk factor
present
200 Mild
CPAP ≥ 5 cmH2Oc
100

Oxygenationb Moderate
cmH2O
PaO2/FiO2 ≤ 100 with PEEP ≥ 5
Severe
cmH2O
a

Chest X-ray or CT scan

b

If altitude higher than 1000 m, correction factor should be made as

follows: PaO2/FiO2 x (barometric pressure/760)
c

This may be delivered non-invasively in the mild ARDS group

1.1.2. Etiology
ARDS is caused by a multitude of disorders (There are over 60 ill
disorders associating with ARDS); sepsis and pneumonia are the


4

most common. Recently, cause due to virus has been considered
especially when the world has been undergoing covid-19 pandemic.
1.1.3. Pathophysiology
Although the mechanism of the lung injury varies with cause,
widespread injured capillary-alveolar membrane is common and

leads to increased permeability of this membrane, release edema fluid
with a lot of protein into interstitial spaces and alveoli.
1.1.4. Clinical features
- Symptoms and signs are nonspecific and typically develop
within 24 to 48 hours of initial injury or illness.
- Dysnea is the primary symptom.
1.1.5. Laboratory features
- Artery blood gas:
+ PaO2 is very low and only partially responsive to O2
supplementation.
+ Alveolar-artery oxygenation difference increases.
- Chest x-ray
+ Chest x-ray shows bilateral, widespread pulmonary
infiltrates
+ Infiltrates develop rapidly.
+ Infiltrates are symmetrical or asymmetrical.
- Chest CT
Injured lung is inhomogeneous, includes 3 zones:
+ normal lung
+ ground-glass opacification
+ atelectatic lung
1.1.6. Mechanical ventilation in the acute respiratory distress
syndrome
Mechanical ventilation is essential in addressing patients with


5

ARDSD, ensures adequate oxygenation of arterial blood, provides
sufficient oxygen transport to vital organs and tissues, assists in

eliminating CO2, relieves excessive burdens placed upon the
respiratory muscles, helps maintain alveolar stability, and allows
therapeutic measures that require controlled ventilation. However,
mechanical ventilation also has the potential to inflict adverse clinical
outcomes.
PEEP is an important parameter in ventilating patients with
ARDS. Now, how to set up PEEP to obtain the best benefit is
uncertain. According to Gattinoni, ideally, a “best PEEP”
simultaneously: (1) provides appropriate gas-exchange; (2) keeps the
lungs open (prevents phasic airway collapse); (3) avoids alveolar
overdistention; and (4) does not compromise hemodynamics. Any
PEEP selected is always a compromise among these objectives.
Now, in the world, there are a variety of approaches to set up PEEP
for ARDS patients.
1.2.

Esophageal-pressure

guided

mechanical

ventilation

(EPVENT)
Transpulmonary pressure is the most important in mechanical
ventilation because it really stress on lung. Ptp (transpulmonary
pressure) = Pplat - Ppl. Two patients that have the same Pplat
(plateau airway pressure) but have different Ppl (pleural pressure)
will have different risk of VILI (ventilation-induced lung injury) and

need different PEEP. In clinical practice, Pplat is easy to measure,
but directly measuring Ppl is invasive and complicated. To resolve
this issue, correlation between Ppl and Pes is used, Pes at under third
of esophagus can be measured by an adult esophageal balloon
catheter.


6

According to Talmor, Pleural pressure varies widely and
unpredictably among patients with ARDS, likely due to factors such
as obesity, abdominal fluid accumulation and oedema, which
influence the mechanical behaviour of the chest wall and diaphragm.
This wide range of pleural pressure among individuals could
significantly

affect

lung

inflation

produced

by

mechanical

ventilation. For example, a relatively high level of PEEP of 18
cmH2O could be too low in a patient with a pleural pressure of 20

cmH2O, allowing collapse of some airspaces with each expiration
and leading to atelectrauma (end-expiratory Ptp = -2 cmH2O), but too
high in a patient with a pleural pressure of 5 cmH2O (end-expiratory
Ptp = 13 cmH2O), causing haemodynamic compromise, increased
dead space ventilation and overdistension of the lungs at endinflation. Thus, ideally, adjusting PEEP for patients with ADRS
should individualise how keeping Ptp PEEP ≥ 0 cm H2O to avoid
atelectasis at end-expiration and Ptp plat ≤ 25 cmH2O to avoid lung
over-distention at end-inspiration.
In 2014, Talmor introduced the Esophageal Pressure-Guided
Ventilation 2 (EPVent2), a new table about adjusting PEEP in
patients with ARDS based on mesuring Pes. This table is used for
sdudies about ARDS.
Table 1.6. The esophageal pressure-guided ventilation 2 (EPVent2)
Bước

1

2

3

4

5

6

7

8

9

10

11

12

13

FiO2

0.3

0.4

0.5

0.5

0.6

0.6

0.7

0.7

0.8

0.8

0.9

0.9

1.0

PtpPEEP

0

0

0

2

2

3

3

4

4

5

5

6

6


7

Chapter 2
SUBJECTS AND METHODS
2.1. STUDYING SUBJECTS
68 ARDS patients from 3 centers (Intensive Care Departement,
Emercency Department of Bach Mai Hospital and Intensive Care
Departement of Central Geriatric Hospital) were studied from July
2015 to July 2018.
2.1.1. Selection criteria for study patients
- Adults patients aged 16 years and older with moderate-to-severe
ARDS will be enrolled. The Berlin Conference definition is used to
identify patients with moderate-to-severe ARDS (see table 1.2.)
- Patients who agree to participate in the research.
2.1.2. Exclusive criteria
- Patients who did not agree to participate in the research
- Recently treated for bleeding varices, stricture, heamatemesis,
esophageal trauma, recent esophageal surgery.
- Severe coagulophathy (platelet count <5000/µL or international
normalized ratio > 4).
- History of lung or liver transplantation.
- Elevated intracranial pressure or conditions where hypercapniainduced elevations in intracranial pressure should be avoided

(including intracranial bleeding, cerebral contusion, cerebral eodema,
mass effect (midline shift on CT scan).
- Evidence of active air leak from the lung (including bronchopleural fistula, pneumothorax, pneumomediastinum or air leak from
existing chest tube).
- Neuromuscular disease that impairs ability to ventilate
spontaneously (including C5 or higher spinal cord injury, amyo-


8

trophic lateral sclerosis, Guillain-Barre syndrome or myasthenia
gravis).
- Severe chronic liver disease (Child-Pigh Score ≥ 12).
- Use of rescue therapies prior to enrolment (including nitric oxide,
ECMO, prone posisioning or high frequency oscillation), unless
therapies were used as the initial mode of ventilation.
2.1.5. Criteria for getting patients out the study
- Treating clinician refusal, or unwillingness to commit to controlled ventilation for at least 24 h.
- Patients not commited to full support.
- Inability to get informed consent from the patient or surrogate.
- Patients were unably sedated.
2.1.4. Study center
2.2. RESEACH METHODOLOGY
2.2.1. Study Design:
- In objective 1: prospective observational descriptive and analytical
study
- In objective 2: prospective, interventional, randomized and followup.
2.2.2. Study devices
- Adult esophageal balloon catheter set (USA).
- AVEA ventilator with esophageal maneuver screen (USA).

2.2.2. Sample size
- In objective 1, 34 patients with ARDS.
- In objective 2, our primary end point is average between-2 groups
difference of PaO2/FiO2. To determine sample size, we chose the
following equation:


9

n=

2
( ,  )

2S 2
2

Z2 (α, β) = 10,5 (α = 0.05, β = 0.1).
∆ = 280-191 (from 2 previous studies)
S (maxium standard diviation) = 109 (from 2 previous studies)
We have:
2 × 1092
𝑛 = 10,5
≈ 32
(280 − 191)2
Thus, minimal sample of each group is about 32.
2.2.3. Study procedure
Objective 1: 34 ARDS patients were supine with the bed at 300 head up.
An adult esophageal balloon catheter was first passed by nose or mouth into
the stomach with its tip 60 cm from the incisors or nares (placement of the

balloon in the stomach was confirmed by a transient increase in pressure
during a gentle compression of the abdomen) and then withdrawn to 40 cm
to record Pes (esophageal end-inspiratory pressure and esophageal endexpiratory pressure) during mechanical ventilation at To (before
intervention of each group), T1, T2, T3... Ppeak, PEEP, CRS (respiratory
system compliance), Ccw (chest wall compliance), Vte/kg, ect were
measured simultaneously at each time. Proper balloon position in the
esophagus was confirmed in all patients by observing an appropriate change
in the pressure tracing as the balloon was withdrawn into the thorax
(changes in pressure waveform, mean pressure, and cardiac oscillations). In
patients who were making respiratory efforts, correct balloon position could
be confirmed by the presence of nearly equal fluctuations in Paw and Pes
during inspiratory efforts against an occlusion.


10

Objective 2: ARDS patients were randomly assigned with the use of a
block-randomization scheme to the control or esophageal-pressure-guided
group (each group had 34 patients). 68 ARDS patients of both two groups
were supine, with the head of the bed elevated to 300. Airway pressure, tidal
volume, air flow and arterial blood gas were recorded during mechanical
ventilation. All patients of both two groups, while under heavy sedation or
paralysis, underwent a recruitment maneuver to standardize the history of
lung volume, in which airway pressure was increased to 40 cmH2O for 30
seconds. After the recruitment maneuver, the patient underwent mechanical
ventilation according to the treatment assignment. The patients in the
esophageal-pressure-guided group underwent mechanical ventilation with
settings determined by the initial esophageal-pressure measurements. Tidal
volume was set at 6 ml per kilogram of predicted body weight. PEEP levels
were to achieve a transpulmonary pressure of 0 to 6 cmH2O at end

expiration, according to a sliding scale based on the partial pressure of
arterial oxygen (PaO2) and the fraction of inspired oxygen (FiO2) (Table
1.6).
Patients in the control group were treated according to the low-tidalvolume stratery reported by the ARDSNet study of the National Heart,
Lung, and Blood Institute. This stratery specifies that the tidal volume is set
at 6 ml per kilogram of predicted body weight and PEEP is based on the
patient’s PaO2 and FiO2 (low PEEP table).
All measurements (arterial blood gas, indexes of lung michanics) were
repeated 5 minutes after the initiation of experimental or control ventilation
and again at 24, 48, 72 hours, ect. Measurements were also performed as
needed after changes (about 20 minutes) were made to ventilator settings
because of any clinically significant change in the patient’s condition.


11

The primary end point of the study was arterial oxygenation, as measred
by the ratio of PaO2 to FiO2 at 24, 48, 72 hours, ect after randomization. The
secondary end points included indexes of lung mechanics (respiratory
system compliance), ventilator-related complications (pneumothorax,
pneumomediastinum), as well as outcomes of the patients (the numbers of
ventilator-free days at 28 days, death within 28 days).
2.2.4. Research variables
- General characteristics of target population: Age, gender, index
body mass (BMI), risk factors of ARDS, APACHE II, SOFA,
medical history.
- Characteristics of arterial blood gas: pH, PaCO2, PaO2, HCO3,
PaO2/FiO2.
- Indexes of lung mechanics: PesENDin, PesENDex, Ptpplat,
PtpPEEP and Ppeak, Pplat, Pmean, PEEP, CRS, Vte/ideal body

weight.
- Interventional result and related undesired effects:
+ Death within 28 days.
+ Time of death.
+ Causes of death: sequential organ failure, septic shock,
respiratory failure, pneumothorax,...
+ The number of ventilator-free days at 28 days.
+ Pneumothorax, pneumomediastinum.
+ Nose bleeding, gut bleeding.
+ Changes of arterial blood pressure and ECG when adjusting
PEEP.
2.2.5. Accessment points
For objective 1
- Change of Pes:


12

+ Change of PesENDin
+ Change of PesENDex
- Correlation:
+ Correlation between PesENDin, PesENDex and BMI at baseline.
+ Correlation between PesENDin, PesENDex and CCW at baseline.
+ Correlation between PesENDex and PEEP at baseline.
+ Correlation between PesENDin and Ppeak at baseline.
+ Correlation between PtpPEEP and PEEP at baseline.
+ Correlation between Ptpplat and Vte/kg at baseline.
For objective 2
- The primary end point of the study was arterial oxygenation, as
measured by the ratio of PaO2 to FiO2 (PaO2/FiO2) after randomization.

2.3. DATA PROCESSMENT
The data was processed by medical statictic method with SPSS
16.0 software for Window.
- Continuous variables were performed as X ± SD, or median,
interquartile range.
- Percentage was compared by χ2 test (or Fisher test).
- Mean of two independent groups were compared by t - test or
Mann-Whitney test.
- Paired samples-t-test was for before-after comparison.
- Percentage was compared by χ2 test (or Fisher test).
- Pearson Correlation Coefficient was calculated to find
correlation between change of esophageal pressure and some lung
mechanical parameters and tested this correlation.
- p value < 0,05 was considered statistical significance.


13

Chapter 3
RESEARCH RESULTS
3.1. General characteristic of target population
- There were 68 moderate to severe ARDS patients enrolled this
study, mean of age was 63.3 ± 18.5 years old, oldest was 93,
youngest was 16. 63.2% (43/68) were patients from 60 years old and
over. Very elderly patients (over 80 years old) were 17.6% (12/68).
There was no significant difference of age between two groups
EPVent2 and ARDSnet.
- There were more male than female, male proportion was 58.8%.
There was no significant difference about gender distribution
between two groups EPVent2 and ARDSnet.

- There were no patients with BMI > 30. Patients with BMI from
20 to 25 met 79.1%. Patients with BMI < 18 met 3.0%. There was no
significant difference about BMI between two groups EPVent2 and
ARDSnet.
- High blood pressure is a chronic disease met with the highest
percentage was 33.8% (EPVent2 was 35.3%; ARDSnet was 32.4%),
diabetes mellitus with second percentage was 29.4% (EPVent2 was
35.3%; ARDSnet was 23.5%).
- Patients with ARDS caused by pulmonary disease was main,
met 95.5 % (EPVent2 was 97.1%; ARDSnet was 94.1%). ARDS caused
by pneumonia due to bacteria took the highest percentage in both two
groups, 85.3% for both.
- All patients in both groups were severely ill, with a mean (SD)
APACHE II score of 17.9 ± 6.3 and SOFA score of 8.2 ± 3.4. There
was no significant difference about APACHE II score and SOFA
score between two groups with p > 0.05.


14

- Characteristics of lung mechanics such as Ppeak, Pplat, Pmean,
PEEP, CRS, Vte, Vte/IBWkg, breath frequency, inspiratory time of
two groups at baseline were well matched.
3.2. Change in esophageal pressure and correlation with some
indexes of lung mechanics
3.2.1. Changes in PesENDin and PesENDex

-

PesENDin and PesENDex varied widely between different

times on the same patient and between different patients. PesENDin
and PesENDex were relatively high. PesENDin and PesENDex
averaged 16.7 ± 5.4 cmH2O ; 12.7 ± 4.5 cmH2O, respectively.
3.2.2. Correlation between esophageal pressure and some indexes
of lung mechanics
- PesENDin, PesENDex were not correlated with obesity as
assessed by body mass index, r = 0.227; p = 0.220; n = 31 (figure
3.1) and r = -0.194; p = 0.296; n = 31 (figure 3.2), respectively.
- PesENDex was not correlated with Ccw (r = 0.13; p = 0.509; n =
28). (figure 3.3)
- PesENDexTo was not correlated with PEEP at baseline (r = 0.01; p = 0.958; n = 32). (figure 3.4)
- PesENDin was significantly correlated with Ppeak at baseline (r = 0.601; p
< 0.001; n = 32). (figure 3.5). PesENDin = 4.022 + 0.415 × Ppeak.

Hình 3.1. Correlation between

Hình 3.2. Correlation between


15

PesENDin and BMI

PesENDex and BMI

Hình 3.3. Correlation between PesENDex and Ccw

Hình 3.4. Correlation between

Hình 3.5. Correlation between

PesENDex and PEEP

PesENDin and Ppeak


16

3.3. Effects of EPVent2 in comparision with ARDSnet
3.3.1. Oxygenation improvement
3.3.1.1. FiO2 level
Table 3.17. FiO2 level between two groups
EPVent2
ARDSnet
p
MinMinX ±SD
X ±SD
Max
Max
To
0.4-1 0.78±0.18 (n=32) 0,4-1 0.74±0.16 (n=34) >0.05
T1
0.5-1 0.7±0.15 (n=31)
0,5-1 0.77±0.15 (n=34) >0.05
T2
0.4-1 0.65±0.2 (n=29)
0,5-1 0.74±0.14(n=21) >0.05
T3 0.4-0.9 0.57±0.16 (n=16) 0,3-1
0.68±0.2 (n=15) >0.05

T4
0.4-1 0.62±0.22 (n=12) 0,4-1 0.67±0.19 (n=10) >0.05
p1-0 <0.05
p1-0 >0.05
p2-0 <0.01
p2-0 >0.05
p
p3-0 <0.01
p3-0 >0.05
p4-0 <0.05
p4-0 >0.05
Comment:
- FiO2 was significantly reduced (with p < 0,05) at T1, T2, T3, T4
compared with T0 in EPVent2 group.
3.3.1.2. PaO2 (mmHg)
Table 3.18. PaO2 change in two groups
EPVent2
ARDSnet
p
Min-Max
Min-Max
X ±SD
X ±SD
To
39-132 73.5±17 (n=33) 40-107 70.8±16.4 (n=34) >0.05
T1
54-354 122±63 (n=32) 46.5-123 77.5±21.7 (n=34) <0.01
T2 55-288.7 129±59 (n=30) 36.4-200 88±37 (n=21) <0.01
T3
77-315 120±58 (n=17) 38-133

89±23 (n=14) >0.05
T4

p

51.5-136

92.4±28 (n=13)

p1-0 <0.01
p2-0 <0.01
p3-0 <0.01
p4-0 <0.05

51.5-97

77±17 (n=10)

>0.05

p1-0 >0.05
p2-0 >0.05
p3-0 >0.05
p4-0>0.05

Comment:
- PaO2 at T1 and T2 in EPVent2 group was significantly higher (p
< 0.05) in comparision with ARDSnet group. Difference at T1 was
44.5 mmHg; at T2 was 41 mmHg.

17

- PaO2 at T1, T2, T3, T4 increased significantly (p < 0.01 and
0.05) in comparision with T0 in EPVent2 group. Average differences
at T1, T2, T3 and in comparision with T0 were 48.1 mmHg, 57.3
mmHg, 49.5 mmHg, 21.7 mmHg respectively.
3.3.1.3. PaO2/FiO2
Table 3.19. Change of PaO2/FiO2 in EPVent2 group and ARDSnet
group
Nhóm EPVent2
Min-Max
To
T1

56-153
54-504

T2

55-516

T3

113-525

T4

64-340

p
Min-Max
X ±SD
X ±SD
100±26 (n=32) 54-199 101±34 (n=34) >0.05
186±103 (n=32) 46.5-205 111±46 (n=34) 0.000
214± 103
45-285 125±53 (n=21) 0.000
(n=30)
221±102 (n=17) 95.4-402 161±82 (n=15) >0.05
177±85 (n=13)

p1-0 <0.01
p2-0 <0.01
p3-0 <0.01
p4-0<0.01

p

Nhóm ARDSnet

54-194

123±46 (n=10)

>0.05

p1-0 >0.05
p2-0 >0.05
p3-0 <0.05

p4-0>0.05

Comment:
- PaO2/FiO2 at T1 and T2 of EPVent2 group were significantly
higher (p < 0.001) in comparision with ARDSnet group. PaO2/FiO2
differences between EPVent2 group and ARDSnet group at T1 and T2
were 75 and 89 respectively.
- In EPVent2 group, PaO2/FiO2 at T1, T2, T3, T4 were
significantly increased (p < 0,01) in comparision with T0, increases
were 86.8, 115, 124.4, 81.8 mmHg respectively.


18

Chapter 4
DISCUSSION
4.1. General characteristic of target population
4.1.1. Age
Average age in our research was much higher than previous studies.
63.2% were patients from 60 years old and over. Very elderly
patients (over 80 years old) were 17.6%. By comparison, in Pham
Van Dong’ study, the percentage of patients over 60 years old was
only 10.8%; Do Minh Duong’s study, the percentage of patients over
60 years old was 28.5% and over 70 was only 9.5%; Le Duc Nhan’s
study, the percentage of patients over 60 years old was about 30%
and over 70 was 23%. Elderly patients usually associate with chronic
multidiseases and frailty, more death rate. According to Gong (2006),
death rate of ARDS increases 1.96 times for every 10 years of age.
4.1.2. Chronic diseases
In comparison with Le Duc Nhan’s study, our patients acquired

more chronic disease. Patient with more chronic disease usually
associate with bad outcome.
4.1.3. Risk factors of ARDS
Bacterial pneumonia is main cause of ARDS in our study (95.5
%). In Do Minh Duong’s study, Le Duc Nhan’s study, ARDSnet’s
study, bacterial pneumonia is 85.6%, 32.3% and 33% respectively.
Thus, cause of ARDS in our study is very homogeneous.
4.1.4. Arterial blood gas at the baseline
PaO2/FiO2 at the baseline in our study was quite low and similar
with studies of Do Minh Duong, Le Đuc Nhan, Tran Thi Oanh,
Grasso, Amato.
4.1.5. Desease’s serious grade at the baseline
By comparison with previous studies about ARDS is that
APACHE II in our study is higher and SOFA is lower. These
characteristics may be reason to explain why mortality rate in our
study is higher.