Intrinsic positive end-expiratory pressure in mechanically
ventilated patients with and without tidal expiratory flow
limitation
Apostolos Armaganidis, MD; Krystallia Stavrakaki-Kallergi, MD; Antonia Koutsoukou, MD;
Andreas Lymberis, PhD; Joseph Milic-Emili, MD; Charis Roussos, MD, PhD
Objective: To assess static intrinsic positive end-expiratory
pressure (PEEPi,st) and expiratory flow limitation (FL) in 32 consecutive mechanically ventilated patients with acute respiratory
failure (ARF), using a commercial ventilator with an incorporated
device that allows the application of a negative expiratory pressure (NEP).
Design: Prospective clinical study.
Setting: Multidisciplinary intensive care unit of a university
hospital.
Patients: Thirty-two consecutive ventilated patients with ARF
of various etiologies.
Interventions: Evaluation of respiratory mechanics, PEEPi,st,
and FL from pressure, flow, and volume traces provided by the
ventilator.
Measurements: Peak airway pressure, PEEPi,st, dynamic elastance, and interrupter resistance were measured in relaxed patients in a supine position. Comparison of tidal flow–volume
curves before and during the application of an NEP of 5 cm H2O
was used to assess tidal expiratory FL.
Results: Twelve of 32 patients studied exhibited tidal expiratory FL, which was detected by the absence of increase in
A
lthough static intrinsic positive end-expiratory pressure
(PEEPi,st) and dynamic hyperinflation (DH) have been reported for patients with airway obstruction as early as 1975 (1), widespread
From the Critical Care Department (Drs.
Armaganidis, Stavrakaki, Koutsoukou, Lymberis, and
Roussos), Evangelismos General Hospital, Medical
School of Athens University, Greece; and the Meakins–
Christie Laboratories (Dr. Milic–Emili), McGill University, Montreal, Quebec, Canada.
Supported, in part, by a grant from the Thorax
Foundation, Athens, Greece. Draegerwork A.G.,
Lübeck, Germany, and their distributor in Greece, N.
Papapostolou LTD, provided the Draeger Evita 2 ventilator equipped with an NEP device for assessment of
expiratory FL.
Address reprint requests to: Apostolos Armaganidis,
MD, Critical Care Department, Medical School of
Athens University, Evangelismos General Hospital,
Ipsilantou 45– 47, Athens 106 75, Greece.
Copyright © 2000 by Lippincott Williams & Wilkins
Crit Care Med 2000 Vol. 28, No. 12
expiratory flow despite application of an NEP over the entire or
part of the baseline expiratory flow–volume curve. All patients
exhibited PEEPi,st, which amounted to 1.2 ⴞ 0.9 cm H2O (mean ⴞ
SD) in the 20 non-FL patients and 7.1 ⴞ 2.8 cm H2O in the 12 FL
patients (p < 0.00001). The majority of patients with ARF resulting from underlying lung disease (11 of 13) had FL and a
PEEPi,st > 4 cm H2O, whereas in patients with ARF of extrapulmonary origin, PEEPi,st was always < 4 cm H2O and only one
grossly obese patient exhibited FL. Based on multiple regression
analysis, in non-FL patients, PEEPi,st correlated significantly only
with minute ventilation, whereas in FL patients PEEPi,st correlated
significantly with peak airway pressure.
Conclusions: Because all the patients exhibited PEEPi,st and
12 of 32 patients (38%) also had FL, the authors conclude that the
assessment of these variables at the bedside could provide useful
information concerning respiratory mechanics in mechanically
ventilated patients. (Crit Care Med 2000; 28:3837–3842)
KEY WORDS: expiratory flow limitation; mechanical ventilation;
intrinsic positive end-expiratory pressure; respiratory mechanics;
negative expiratory pressure; ventilator; flow–volume curves; dynamic hyperinflation; resistance; elastance
interest in this topic started in the 1980s
(2– 4). Since then it has been recognized
that PEEPi,st (measured by an expiratory
hold maneuver) and DH promote an increase in inspiratory work, impairment of
inspiratory muscle function, and adverse
effects on hemodynamics. DH and
PEEPi,st contribute to dyspnea (5, 6), are
the main cause of ventilatory failure (7,
8), and exercise limitation (9) in patients
with chronic obstructive pulmonary disease (COPD). The fact that in COPD patients tidal expiratory flow limitation (FL)
plays a major role in eliciting DH was
first suggested by Hyatt (10). This was
based on his observation that at-rest patients with severe COPD often breathe
tidally along their maximal flow–volume
curve. This approach to detect FL requires the use of a body plethysmograph
(11) and hence it cannot be used in mechanically ventilated patients. Further-
more, there are other factors that make
assessment of tidal FL based on comparison of tidal and maximal flow–volume
(V̇–V) curves problematic (12). Recently,
however, an alternative technique, the
negative expiratory pressure (NEP)
method, has been introduced to detect FL
during tidal breathing. This technique is
reliable and does not require body plethysmography (13). Furthermore, this
method can be used in mechanically ventilated patients (13). With NEP it has
been documented that in both spontaneously breathing (6) and mechanically
ventilated (13) COPD patients, PEEPi,st
and DH are mainly the result of the presence of tidal FL.
DH and PEEPi,st are also common in
patients with adult respiratory distress
syndrome (7, 14, 15) and cardiogenic pulmonary edema (CPE) (7). It is not known,
however, if in these instances DH and
3837
PEEPi,st are associated with FL. Indeed,
DH and PEEPi,st may also occur in the
absence of FL: A high expiratory resistance (resulting from underlying disease
and from the endotracheal tube and expiratory circuitry of the ventilator) may
impede expiration such that the next mechanical inspiration occurs before complete exhalation to the elastic equilibrium
(relaxation volume) of the respiratory
system (16). The ventilatory settings of
the ventilator (e.g., high inspiratory-toexpiratory time ratio, high ventilation)
may also elicit PEEPi,st and DH in the
absence of tidal FL (4, 17).
In the current investigation we assessed PEEPi,st by occluding the airway
at end-expiration and FL using the NEP
technique (13) in 32 consecutive patients
who required mechanical ventilation for
different etiologies. Our hypothesis was
(1) that we could demonstrate FL in most
mechanically ventilated patients with underlying airway or parenchymal lung disease but not in patients without lung
disease and (2) that PEEPi,st should be
higher in patients with lung disease as a
result of FL.
MATERIALS AND METHODS
Patients. Thirty-two consecutive patients
admitted to the department of intensive care
of Athens University Medical School and who
required mechanical ventilation for different
etiologies were recruited for the study. Their
anthropometric characteristics, baseline blood
gases, and etiology are presented in Table 1.
Patients were studied within 48 hrs from admission, after respiratory and hemodynamic
stability had been achieved. The research protocol was approved by the ethics committee of
our institution, and informed consent was obtained from the patient or next of kin.
Patients were intubated (Portex cuffed endotracheal tube with an internal diameter of
7.5–9 mm; Portex Limited, Kent, UK) and mechanically ventilated on control mode with
constant inspiratory flow with a Draeger-Evita
2 respirator (Draeger, Lübeck, Germany)
equipped with an NEP device attached to the
distal end of the expiratory circuit of the ventilator (i.e., after the expiratory valve). During
the experiments the humidifier was omitted
from the ventilator circuit. The respirator set-
tings (Table 2) and inspired oxygen fraction
(FIO2) were selected by the primary physicians
according to their clinical judgment, and no
changes were made before or during the study.
The inspiratory flow amounted to 0.85 ⫾ 0.13
L/sec (mean ⫾ SD) and the duty cycle (inspiratory time/total cycle duration [TI/TTOT]) was
0.33 (ratio of inspiration to expiration, 1:2) in
all but two patients (0.44 L/sec and 0.50 L/sec
in Patients 8 and 23 respectively). All patients
were sedated with midazolam, and some of
them were paralyzed with pancuronium bromide at the discretion of their primary physician. No patient was sedated or paralyzed because of our protocol.
Airway pressure (Paw), flow (V̇), and volume (V) were measured with the pressure
transducers and flowmeters built into the ventilator used. Built-in software was used to
monitor these variables on an Evita Screen
(Draeger) and to obtain on-line records of the
time course of Paw, V̇, and V, as well as the
V̇–V loops before and during the application of
NEP. The Paw, V̇, and V signals were also
stored at 125 Hz on an IBM-compatible personal computer (Turbo X; Plaisio Computers,
Athens, Greece) interfaced with a homemade
data acquisition program based on Test Point
Table 1. Anthropometric characteristics, blood gases, tidal expiratory flow limitation, static PEEPi, and diagnosis of patients
Patient
No.
Age
yr
Sex
Height
cm
Weight
kg
PaO2
mm Hg
PaCO2
mm Hg
FIO2
FL
% VT
PEEPi,st
cm H2O
Diagnosis
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
65
73
78
65
78
63
75
20
84
70
70
58
83
55
18
30
77
30
25
26
21
63
30
55
70
68
77
75
69
70
67
58
F
F
M
M
F
F
M
M
M
F
M
M
M
M
M
M
M
F
M
M
F
F
F
M
F
M
M
M
M
M
M
M
162
162
175
170
160
162
175
180
178
153
170
168
175
178
170
175
180
160
170
175
160
158
158
175
158
175
168
170
175
170
170
170
78
80
78
130
85
80
90
90
80
60
70
70
85
130
70
88
78
60
75
75
68
55
60
78
55
80
70
75
80
75
75
75
83
151
107
80
111
60
69
215
162
93
119
99
99
188
124
193
130
203
180
251
254
135
102
168
89
88
107
165
94
140
144
124
32
63
39
55
36
38
44
42
55
39
40
42
36
29
30
26
35
25
25
29
25
34
22
42
39
35
32
34
33
40
37
31
0.55
0.45
0.70
0.75
0.45
0.80
0.70
0.60
0.60
0.60
0.60
0.60
0.55
0.50
0.60
0.50
0.55
0.40
0.60
0.50
0.50
0.40
0.35
0.50
0.50
0.55
0.70
0.60
0.55
0.45
0.65
0.60
52
48
75
57
68
11
14
23
28
51
84
0
0
17
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
5.2
7.7
8.7
4.3
12.6
8.8
5.0
7.7
8.3
9.3
4.4
1.6
2.5
2.8
3.3
1.2
0.9
0.2
0.5
0.4
0.4
0.2
1.0
0.9
1.2
1.0
2.7
1.7
2.2
0.5
0.9
0.4
COPD
COPD
COPD
COPD, obesity, sleep apnea
Pulmonary embolism, asthma
Pneumonia, asthma
Aspiration pneumonia, atelectasis
Aspiration pneumonia, head trauma
Myasthenia, pneumonia
Pulmonary edema, pleural effusions
Cardiosurgery, pneumonia
Pneumonia, diabetic coma
Cardiogenic pulmonary edema
Obesity, sepsis, abdominal surgery
Head trauma, atelectasis
Head trauma
Head trauma
Head trauma
Head trauma
Head trauma
Head trauma
Brain tumor
Brain tumor
Intracerebral hematoma
Polyneuropathy
Myasthenia
Septic shock
Ketoacidosis, renal failure
Abdominal surgery, sepsis
Abdominal surgery
Thoracic empyema
Hemothorax
F, female; M, male; FL, tidal expiratory flow limitation; PEEPi,st, intrinsic static positive end-expiratory pressure; COPD, chronic obstructive pulmonary
disease.
3838
Crit Care Med 2000 Vol. 28, No. 12
software (version 3, Capital Equipment, Billerica, MA) for subsequent replay and assessment of respiratory mechanics. Arterial blood
gases were measured with an ABL System 610
blood gas analyzer (Radiometer, Copenhagen,
Denmark) during baseline ventilation. Heart
rate, systemic arterial blood pressure, and arterial O2 saturation were monitored continuously (Life Scope 14; Nihon Kohden, Tokyo,
Japan).
Patients were studied in the supine position at a zero positive end-expiratory pressure
(PEEP) setting on the ventilator. At this setting the ventilator actually applies a PEEP of
0.8 cm H2O. The latter was subtracted from
total PEEP to obtain PEEPi,st. Patient relaxation during the experiments was evidenced
by uniform sequential recordings of Paw, V̇,
and V, and absence of negative deflections in
Paw or other visible signs of spontaneous
breathing efforts.
In each subject respiratory mechanics,
PEEPi,st, and expiratory FL were assessed as
described in the following sections.
Respiratory Mechanics and PEEPi,st. The
total interrupter resistance (Rint) was measured by occluding the airway at end-inspiration, as described previously in detail (7, 18).
Briefly, Rint was obtained using the following
equation:
Rint ⫽ (Ppeak ⫺ P1)/V̇I
(1)
where Ppeak ⫺ P1 is the immediate drop in
P aw from peak value (Ppeak) to P1 on cessa-
tion of inspiratory flow and V̇I is the flow
immediately preceding the airway occlusion
(Fig. 1).
The dynamic elastance of the respiratory
system (Edyn,rs), which reflects the pressure
dissipation resulting from elastic recoil, viscoelastic behavior, and time constant inequality (17, 18), was obtained by the following
equation:
Edyn,rs ⫽ (P1 ⫺ PEEPi,dyn)/VT
(2)
where dynamic instrinsic PEEP (PEEPi,dyn)
was the Paw indicated on the Evita Screen
(Fig. 1) when the cursor was placed at the
onset of inspiratory flow.
Respiratory mechanics variables were measured on three subsequent breaths, and the
mean values were used for subsequent analysis.
PEEPi,st was obtained by occluding the
airway at end-expiration using the endexpiratory hold button of the respirator (2, 4,
7). When this button is activated, both inspiratory and expiratory valves are closed for a time
corresponding to the inspiratory time set on
the ventilator. Because 3 sec of end-expiratory
occlusion are required for accurate measurement of PEEPi,st (8), 3 to 4-sec occlusions
were achieved by decreasing the frequency of
the respirator to 6 cpm immediately after activation of the end-expiratory hold button
(Fig. 1). At least two end-expiratory occlusion
maneuvers were performed, and the mean
PEEPi,st value was used for subsequent analysis.
The total inspiratory work (WI) per breath
was obtained by integration of Paw with respect to inspiratory volume during baseline
ventilation. The WI included the total work
done on the respiratory system and the resistive work resulting from the endotracheal
tube. The work resulting from PEEPi,st was
obtained as a product of PEEPi,st and VT.
Work was also expressed per liter of inspired
volume (WI/VT). With constant flow inflation,
WI/VT corresponds to mean inspiratory pressure (8).
Flow Limitation. Expiratory FL was assessed using the NEP technique (13). The NEP
device incorporated into the Evita 2 ventilator
applies an NEP of ⫺5 cm H2O 8 msec after the
onset of expiratory flow, and maintains it
throughout the expiratory time set on the
ventilator. However, NEP is discontinued automatically if there is occurrence of spontaneous inspiratory efforts, as evidenced by inspiratory flow during the expiratory time of
the ventilator. The NEP device is activated by
pressing a special button on the ventilator
during inspiration—a maneuver not seen by
the patient. Using the built-in software in the
Evita Screen, the V̇–V loop of the breath with
NEP was superimposed on that of the preceding control breath. The end-expiratory volume
was reset automatically after each expiration,
Table 2. Anthropometric characteristics, blood gases, ventilatory settings, and respiratory mechanics
data of FL and non-FL patients
Parameter
Sex, M/F
Age, yr
Height, cm
Weight, kg
FIO2
PaO2, mm Hg
PaCO2, mm Hg
pH
V̇E, L/min
VT, mL
fR, breaths/min
TI, sec
TP, sec
TE, sec
TL:TTOT
Ppeak, cm H2O
PEEPi,st, cm H2O
Edyn,rs, cm H2O/mL
Rint,rs, cm H2O/L/sec
WI,rs, cm H2O/L
WI,rs/VT, cm H2O
FL
(n ⫽ 12)
Non-FL
(n ⫽ 20)
p Value
7/5
66 ⫾ 16
169 ⫾ 8
88 ⫾ 21
0.61 ⫾ 0.11
120 ⫾ 49
43 ⫾ 10
7.40 ⫾ 0.9
9.99 ⫾ 2.70
638 ⫾ 80
15.7 ⫾ 3.7
1.40 ⫾ 0.39
0.58 ⫾ 0.36
2.67 ⫾ 0.86
0.35 ⫾ 0.04
41.6 ⫾ 6.4
7.1 ⫾ 2.8
47.3 ⫾ 17.2
18.3 ⫾ 7.1
20.7 ⫾ 4.6
33.1 ⫾ 7.4
15/5
52 ⫾ 21
169 ⫾ 7
72 ⫾ 9
0.53 ⫾ 0.09
145 ⫾ 50
33 ⫾ 9
7.45 ⫾ 0.6
10.02 ⫾ 2.10
607 ⫾ 86
16.6 ⫾ 3.1
1.29 ⫾ 0.32
0.49 ⫾ 0.33
2.47 ⫾ 0.56
0.34 ⫾ 0.04
31.0 ⫾ 6.5
1.2 ⫾ 0.9
31.8 ⫾ 7.1
13.9 ⫾ 2.8
13.3 ⫾ 5.4
21.6 ⫾ 7.0
—
NS
NS
⬍0.01
NS
NS
⬍0.002
NS
NS
NS
NS
NS
NS
NS
NS
⬍0.0001
⬍0.00001
⬍0.002
⬍0.02
⬍0.0004
⬍0.0002
FL, flow limited; Non-FL, nonflow limited; M, male; F, female; V̇E, minute ventilation; VT, tidal
volume; fR, respiratory frequency; TI, inspiratory time; TP, end-inspiratory pause time; TE, expiratory
time; TTOT, total cycle duration; Ppeak, peak airway pressure; PEEPi,st, intrinsic static positive
end-expiratory pressure; Edyn,rs, dynamic elastance; Rint,rs, interrupter resistance; WI,rs, total
inspiratory work per breath; WI,rs/VT, total inspiratory work per liter of ventilation.
Values are mean ⫾ SD.
Crit Care Med 2000 Vol. 28, No. 12
Figure 1. Recordings of pressure at airway opening (Paw), flow, and volume provided by the Evita
screen. During the end-inspiratory pause there
was a rapid drop in Paw from a peak value (Ppeak)
to P1. Static, intrinsic positive end-expiratory
pressure was obtained by occluding the airway at
end-expiration and decreasing the frequency of
the respirator to 6 cpm to obtain an occlusion
time ⬎ 3 sec. Dynamic, intrinsic positive endexpiratory pressure (PEEPi,dyn) was the Paw
value at the onset of inspiratory flow. PEEPi,
static, intrinsic positive end-expiratory pressure;
TI, inspiratory time; TP, end-inspiratory pause
time; TE, expiratory time; s, seconds.
3839
and negative values of volume were not displayed by the ventilator’s software.
Patients were categorized as non-FL if NEP
elicited an increased flow over the entire range
of the control VT, as shown in Figure 2A. In
contrast, if part or the entire V̇–V curve with
NEP was superimposed on the control V̇–V
curve, FL was present (Fig. 2B). The extent of
FL (i.e., the volume over which the flow with
NEP was the same as in the preceding control
expiration) was expressed as a percent of the
control expired VT (FL, %VT) (13).
Because all measurements were made on
relaxed subjects, the mechanics data and the
NEP tests were highly reproducible in repeated measurements.
Statistical Analysis. Results are reported as
mean ⫾ SD. The conventional level of significance (p ⬍ 0.05) was used for all analyses.
Patients were divided into two groups according to the presence or absence of expiratory
FL: FL and non-FL. Differences between the
two groups were evaluated using the unpaired
Student’s t-test. In each group, regression
analysis was carried out using the least
squares method, with PEEPi,st as the dependent variable, whereas the independent variables included the anthropometric characteristics, ventilator settings, and blood gas and
respiratory mechanics data. The strongest significant contributors to PEEPi,st were selected by forward stepwise regression analysis
to form predictive equations. All statistical
analyses were performed with STATISTICA
software (version 6.0, Statsoft, Tulsa, OK).
RESULTS
The use of NEP revealed that 20 patients were non-FL and 12 were FL. Of
the latter group of patients, the FL portion of the expired volume amounted to
44 ⫾ 25% of the control VT (range, 11–
85%). PEEPi,st was present in all patients
(Fig. 3), but values were significantly
higher (p ⬍ 0.00001) in the FL patients
(7.1 ⫾ 2.8 cm H2O; range, 2.8 –12.6 cm
H2O) than in the non-FL patients (1.2 ⫾
0.9 cm H2O; range, 0.2–3.3 cm H2O). The
individual values of FL (%VT) and PEEPi,st are provided in Table 1.
The anthropometric characteristics,
arterial blood gases, ventilatory settings
used, and respiratory mechanics data of
FL and non-FL patients are shown in
Table 2. Body weight, PaCO2, and all respiratory mechanics data were significantly lower in the non-FL patients. Half
of the latter population had head trauma,
which required therapeutic hyperventilation.
According to the results of multiple
regression analysis, in the non-FL patients there was a significant relation
(p ⬍ 0.01) only between PEEPi,st and
minute ventilation VE (Fig. 4). In the FL
patients, the only significant relation was
between PEEPi,st and Ppeak (Fig. 5). The
linear regression equation was
PEEPi,st ⫽ ⫺7.4 ⫹ 0.35 Ppeak
(3)
with a standard error of regression
amounting to 1.6 cm H2O.
DISCUSSION
The main finding of the current study
is that 11 of 13 patients with acute respiratory failure (ARF) resulting from pulmonary disease (Patients 1–11 in Table 1)
exhibited tidal FL with PEEPi,st ⬎ 4 cm
H2O. In contrast, in all 19 patients in
whom ARF was of extrapulmonary origin
(Patients 14 –32 in Table 1), PEEPi,st
was ⬍ 4 cm H2O and tidal FL was absent,
except in Patient 14, who was grossly
obese.
In the non-FL group of patients, a
significant correlation was only found between PEEPi,st and VE (Fig. 4). In the
absence of FL, the rate of passive lung
deflation is determined by the elastic recoil pressure stored during the preceding
lung inflation and the opposing flow resistance offered by the respiratory system
(including the endotracheal tube and the
expiratory circuit of the ventilator). In
non-FL patients Rint,rs, which included
the resistance of the endotracheal tube,
was high (13.9 ⫾ 2.8 cm H2O/L/sec). Furthermore, the resistance of the expiratory
circuit of ventilators is also high (13).
With high resistance, the next mechanical inflation may occur before complete
exhalation to the elastic equilibrium (relaxation volume) of the respiratory system with ensuing DH and PEEPi,st (4,
14). The latter is enhanced by a high VE
(17). Accordingly, the finding of a significant correlation of PEEPi,st to VE is not
surprising. In this connection it should
be noted that our non-FL group included
10 patients with severe brain damage who
were therapeutically hyperventilated
(PaCO2 ⫽ 29 ⫾ 6 mm Hg) to produce
cerebral vasoconstriction to decrease
Figure 4. Relationship of static, intrinsic positive
end-expiratory pressure (PEEPi) to minute ventilation (V E ) in nonflow-limited patients.
PEEPi ⫽ ⫺1.2 ⫹ 0.24 V̇E; r ⫽ 0.56; p ⬍0.01.
Figure 2. Tidal flow–volume loops of breath with
negative expiratory pressure (thick lines) and
preceding control breath (thin lines) in a nonflow-limited (non-FL) patient (A) and an FL (B)
patient. Arrow indicates onset of FL in Patient 3.
See text for further explanation. FL, flow limitation; L, liter.
3840
Figure 3. Individual and mean values of static,
intrinsic positive end-expiratory pressure
(PEEPi) in flow-limited (FL) and non-FL patients.
Figure 5. Relationship of static intrinsic positive
end-expiratory pressure (PEEPi) to peak airway
pressure (Ppeak) in flow-limited patients.
PEEPi ⫽ ⫺7.4 ⫹0.35 Ppeak; r ⫽ 0.82; p ⬍0.001.
Crit Care Med 2000 Vol. 28, No. 12
M
odern ventilators allowing
on-line assess-
ment of flow limitation and
static intrinsic positive endexpiratory pressure could
provide useful information
concerning respiratory mechanics in mechanically
ventilated patients.
blood flow and brain water (19). In five
patients with severe brain damage who
were hyperventilated (PaCO2 ⫽ 30 ⫾ 4
mm Hg), Tantucci et al. (20) also observed a high flow resistance, which they
attributed to bronchoconstriction. In our
10 patients with brain damage, Rint,rs
amounted to 13.1 ⫾ 3.3 cm H2O/L/sec. In
the other 10 non-FL patients, PaCO2 was
36 ⫾ 4 mm Hg but Rint,rs was also high
(14.8 ⫾ 1.9 cm H2O/L/sec). Thus, in the
non-FL patients, PEEPi,st was the result
of the association of high Rint,rs and relatively high V̇E (Table 2).
Based on the multiple regression analysis, in the FL patients PEEPi,st correlated significantly only with Ppeak (Fig.
5). Because in our FL patients no external
PEEP was added and the ventilatory settings were relatively homogeneous (Table
2), Ppeak reflects the combined pressure
dissipation resulting from flow resistance, elastic recoil, viscoelastic behavior,
and PEEPi,st (15) (i.e., the overall severity of lung disease). Accordingly, equation
3 can be taken as an indication that in FL
patients, PEEPi,st increases with the severity of lung disease, as reflected by
Ppeak. It should be noted, however, that
the significant correlation of PEEPi,st to
Ppeak may simply reflect the fact that
PEEPi,st, which is included in Ppeak, is
actually a major determinant of Ppeak.
Tidal FL and PEEPi,st, which have
been previously reported in mechanically
ventilated patients with chronic obstructive lung disease (6, 13), were also observed in our six patients with COPD or
asthma. One of these patients (Patient 4)
as well as a patient with sepsis and abdominal surgery (Patient 14) were grossly
Crit Care Med 2000 Vol. 28, No. 12
obese (130 kg; Table 1): Tidal FL and
PEEPi,st have recently been demonstrated in healthy, supine obese patients
by Pankow et al. (21), who attributed this
to breathing at low lung volume with
concomitant reduction in expiratory flow
reserve and air trapping. Decreased expiratory flow reserve resulting from a reduction in functional lung units may also
explain the presence of tidal FL and
PEEPi,st in the four patients with pneumonia (Patients 7–9 and 11).
Tidal FL and PEEPi,st were also found
in Patient 10, who had CPE. Although
PEEPi,st has been reported previously in
patients with CPE (7), expiratory FL was
not assessed in those patients. There are
several mechanisms that could induce FL
in CPE. In patients with heart disease,
there is a reduction in maximal expiratory flows, which has been attributed to
competition for space between the airways and the pulmonary vessels (22–24).
With alveolar flooding, functional residual capacity may be reduced (25), with a
concomitant decrease in expiratory flow
reserve in the tidal volume range. Breathing at low lung volume caused by CPE
should also promote small-airway closure
and gas trapping, particularly in the supine position (26). Furthermore, Patient
10 was 70 yrs old, and old age promotes
small-airway closure (26). Increased closing volume and gas trapping have been
reported in pulmonary edema (27, 28). By
reducing the number of lung units with
patent airways, enhanced small-airway
closure should further decrease expiratory flow reserve in CPE.
In conclusion, using a new Evita 2
ventilator equipped with an NEP device,
we were able to assess tidal expiratory FL
and PEEPi,st in 32 consecutive mechanically ventilated patients. Most patients
with ARF of pulmonary origin were FL
and had a PEEPi,st ⬎ 4 cm H2O. In
contrast, all patients with ARF of extrapulmonary origin were non-FL and
had a PEEPi,st ⬍ 4 cm H2O. Modern
ventilators allowing on-line assessment
of FL and PEEPi,st could provide useful
information concerning respiratory mechanics in mechanically ventilated patients.
ACKNOWLEDGMENTS
The authors especially thank Dr. J.
Manigel from Draeger for his kind advice and support in the construction of
the NEP device. They also thank Mrs. C.
Sotiropoulou for advice on the statistical
analysis of the data, as well as the nurses
and staff of the intensive care unit of their
hospital for support and cooperation during the study.
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Crit Care Med 2000 Vol. 28, No. 12