Cardiac and respiratory effects of continuous

Transcription

Cardiac and respiratory effects of continuous positive airway
pressure and noninvasive ventilation in acute cardiac
pulmonary edema
Karim Chadda, MD; Djillali Annane, MD, PhD; Nicholas Hart, MD; Philippe Gajdos, MD;
Jean Claude Raphaël, MD; Frédéric Lofaso, MD, PhD
Objective: Continuous positive airway pressure (CPAP) is considered an effective nonpharmacologic method of treating patients with severe acute cardiogenic pulmonary edema. However,
we hypothesized that bilevel noninvasive positive-pressure ventilation (NPPV), which combines both inspiratory pressure support
and positive expiratory pressure, would unload the respiratory
muscles and improve cardiac and hemodynamic function more
effectively than CPAP.
Design: Randomized crossover study.
Setting: Critical care unit, Raymond Poincaré Hospital.
Patients: Six consecutive patients with acute cardiogenic pulmonary edema.
Interventions: Patients were sequentially treated with 5 cm
H2O CPAP, 10 cm H2O CPAP, and NPPV in a random order.
Measurements and Main Results: Cardiac and hemodynamic
function and indexes of respiratory mechanics were measured at
D
uring acute cardiogenic pulmonary edema (ACPE), resistive and elastic respiratory
loads are increased (1). The
respiratory muscles therefore have to
generate a greater pressure to initiate inspiratory flow and maintain an adequate
tidal volume. This increase in negative
intrathoracic pressure during inspiration
further aggravates the development of
pulmonary edema by increasing both
ventricular preload and afterload (2, 3).
Furthermore, the oxygen cost of breathing is increased, which can compromise
From the Service de Réanimation Médicale, Service de Physiologie–Explorations Fonctionnelles and
Centre d’Innovation Technologique, Hôpital Raymond
Poincaré, Garches, France.
Supported, in part, by the Assistance Publique des
Hôpitaux de Paris.
Address requests for reprints to: Djillali Annane,
MD, PhD, Service de Réanimation Médicale, Hôpital
Raymond Poincaré, 92380 Garches, France. E-mail:
[email protected]
Copyright © 2002 by Lippincott Williams & Wilkins
DOI: 10.1097/01.CCM.0000034691.01813.94
Crit Care Med 2002 Vol. 30, No. 11
each treatment sequence. NPPV reduced the esophageal pressure
swing and esophageal pressure-time product compared with
baseline (p < .05). There was no reduction in esophageal pressure swing or esophageal pressure-time product with CPAP. NPPV
and 10 cm H2O CPAP reduced the mean transmural right and left
atrial filling pressures without a change in cardiac index.
Conclusions: This study demonstrates that NPPV was more
effective at unloading the respiratory muscles than CPAP in acute
cardiogenic pulmonary edema. In addition, NPPV and 10 cm H2O
CPAP produced a reduction in right and left ventricular preload,
which suggests an improvement in cardiac performance. (Crit
Care Med 2002; 30:2457–2461)
KEY WORDS: heart failure; hemodynamics; noninvasive ventilation; acute cardiogenic pulmonary edema; continuous positive
airway pressure; noninvasive positive-pressure ventilation
oxygen delivery to the myocardium. Although most patients improve with diuretics, vasodilators, and oxygen, from as
early as 1936 (4), continuous positive airway pressure (CPAP) has been shown to
be an effective treatment of ACPE unresponsive to standard medical therapy (4 –
7). Many of the subsequent studies in
both acute and chronic cardiac failure
have shown that CPAP improves respiratory variables (5–7), arterial blood gas
tensions (6, 7), hemodynamic function
(5–7), and respiratory mechanics (8 –10)
and reduces the rate of endotracheal intubation (5, 7).
As inspiratory assistance combined
with expiratory pressure has been shown
to reduce work of breathing and alleviate
respiratory distress more effectively than
CPAP alone (11), a number of uncontrolled studies have investigated the effectiveness of noninvasive positivepressure ventilation (NPPV) in patients
with ACPE (12, 13). More recently, Masip
et al. (14) showed in patients with ACPE
that NPPV compared with conventional
therapy reduced endotracheal intubation
rate and time to recovery. However, the
only controlled study comparing CPAP
and NPPV was prematurely stopped as
myocardial infarction rate was observed
to be higher in the NPPV group (15).
Indeed, a meta-analysis of studies (16)
and a recent state-of-the-art communication (11) came to the conclusion that the
evaluation of NPPV efficiency in patients
with ACPE was too scanty and that 10 cm
H2O CPAP should be considered the initial therapy of choice for acute pulmonary edema, pending the publication of
more studies comparing CPAP and NPPV.
Therefore, the aim of this study was to
compare the previously proposed CPAP
level with NPPV in patients with ACPE,
and we hypothesized that NPPV would
unload the respiratory muscles and improve cardiac and hemodynamic function
more effectively than CPAP in patients
with ACPE. In addition, to avoid any of
the possible deleterious effects previously
described (15), we limited the maximum
inspiratory pressure of NPPV to be at the
same level as CPAP.
2457
METHODS
Respiratory Measurements
We performed a single-blinded, randomized crossover study in patients with ACPE
admitted to Raymond Poincaré Hospital intensive care unit. The study protocol was approved by the comité consultatif de protection
des personnes pour la recherche biomédicale
de l’hôpital Henri-Mondor. Written informed
consent was obtained from all patients before
randomization.
Breathing Pattern. Flow was measured using a Fleisch 2 pneumotachograph (Fleisch,
Lausanne, Switzerland) connected to a differential pressure transducer (Validyne MP-45,
⫾5 cm H2O, Northridge, CA). The flow signal
was electronically integrated to calculate tidal
volume and minute ventilation.
Pressure Measurements. Esophageal pressure was recorded after the insertion of a catheter-mounted transducer system (Gaeltec,
Dunvegan, Isle of Skye, UK). Appropriate
placement of the esophageal transducer was
verified with an occlusion test (18). A pressure
transducer (Validyne MP-45, ⫾14 cm H2O)
was connected between the pneumotachograph and the patient to measure the pressure
at upper airways. All signals were sampled at
128 Hz and passed to a computer using an
analogic-numeric system (MP100, Biopac System, Goleta, CA). Data were analyzed after the
completion of the study.
Dynamic Compliance. Dynamic pulmonary compliance (CLdyn, in L/cm H2O) was
calculated as the ratio of tidal volume to the
difference in transpulmonary pressure at the
start and end of inspiration. Esophageal pressure values at instants of zero flow were considered as the start and end of the inspiratory
cycle. Onset of the sharp negative deflection of
the esophageal pressure curve was taken as
the start of inspiratory effort.
Esophageal Pressure-Time Product. Average esophageal pressure-time product (in cm
H2O·sec⫺1·min⫺1) was measured from 40 consecutive breaths as the area subtended by esophageal pressure and chest-wall static recoil pressure-time curve, taking account of dynamic
intrinsic positive end-expiratory pressure over
inspiratory time (19). The chest-wall static recoil
pressure-time curve was extrapolated from normal subjects’ chest-wall static recoil pressurevolume curve, which corresponded to 4% of the
predicted vital capacity per centimeter H2O (20).
Using the theoretical chest-wall compliance may
lead to an error, but since this error would be
constant throughout the study, the results
would still be valid.
Selection of Patients
The study was subdivided into three
phases. The first phase (6 –12 hrs) was for
assessment and treatment of ACPE with standard medical therapy. The second phase was
patient recruitment, and the third phase was
the study protocol itself. Patients were only
included in the study if they met the following
criteria: 1) orthopnea, 2) an elevated jugular
venous pressure, 3) a third heart sound on
auscultation, 4) a pulmonary arterial occlusion pressure of 18 mm Hg or more, and 5) a
cardiac index below 2.80 L·min⫺1·m⫺2. Patients were excluded from the study if they had
evidence of sepsis, pneumonia, altered mental
status, acute myocardial infarction, or arrhythmias. Patients underwent the CPAP and
NPPV trial at least 6 hrs after the last dose of
diuretic and at least 1 hr after discontinuation
of vasodilator and inotropic drugs.
Study Protocol
Patients were intensively monitored during five separate study periods. Every period
lasted 20 mins. The first and fifth periods were
periods of spontaneous breathing. CPAP of 5
cm H 2 O (CPAP5), CPAP of 10 cm H 2 O
(CPAP10), and NPPV were administered between the two spontaneous breathing periods
in a random order. A resting steady state period of 10 mins was performed before the first
period. All patients were studied at the bedside
in the recumbent position. We used a full face
mask (Respironics, Murrysville, PA) to measure minute ventilation and to apply CPAP and
NPPV. During spontaneous breathing, airway
pressure was the ambient pressure (17). Patients were administered oxygen to maintain
oxygen saturation at ⬎90%. CPAP was administered with a REM⫹ device (Nellcore Puritan
Bennett, Nancy, France). This device incorporates a servo-controlled system that enables
minimization of pressure variation and work
of breathing (17). NPPV was administered
with an Onyx device (Nellcore Puritan Bennett, Nancy, France). Positive end-expiratory
pressure was 5 cm H2O and pressure support
was 5 cm H2O; inspiratory pressure was therefore 10 cm H2O.
2458
Cardiac and Hemodynamic
Measurements
Heart Rate and Blood Pressure. Systolic
and diastolic blood pressures (in mm Hg) and
heart rate were measured using an automatic
sphygmomanometer (Dinamap, Critikon,
Tampa Bay, FL). Mean arterial pressure was
calculated as follows: (systolic pressure ⫹ [2 ⫻
diastolic pressure])/3.
Intracardiac and Transmural Cardiac
Pressure. A 7-Fr pulmonary artery catheter
(Edwards Laboratories, Santa Ana, CA) was
inserted via the internal jugular vein. Right
atrial pressure (mm Hg), systolic pulmonary
arterial pressure (mm Hg), and diastolic pulmonary arterial pressure were measured.
Mean pulmonary arterial pressure was calcu-
lated as follows: (systolic pulmonary arterial
pressure ⫹ [2 ⫻ diastolic pulmonary arterial
pressure])/3. All hemodynamic measurements
were taken at end-expiration. Mean transmural right atrial pressure (mm Hg) and mean
transmural pulmonary arterial occlusion pressure (mm Hg) were calculated (21). In brief,
the mean esophageal pressure calculated over
whole breath is subtracted from intrathoracic
vascular measurements at each level of airway
pressure (21).
Cardiac Output and Derived Hemodynamic Variables. Cardiac output (L/min) was
calculated with an Edwards Model 9250 (Edwards Laboratories) as a mean of five measurements obtained by injecting 10 mL of dextrose
solution randomly during the respiratory cycle,
with exclusion of highest and lowest values. Arterial and mixed venous blood gas samples were
obtained from the radial artery and pulmonary
artery, respectively. These samples were immediately measured (Radiometer ABL 720,
Tacussel, Copenhagen, Denmark). Derived hemodynamic and blood oxygen variables, stroke
volume index, mixed venous oxygen saturation,
oxygen delivery, and oxygen uptake were calculated using standard formulas (20).
Statistical Analysis
Data are expressed as mean ⫾ SD. Differences between spontaneous breathing,
CPAP5, CPAP10, and NPPV were tested using the nonparametric Friedman test. The
5% level was chosen as significant. When a
significant difference was observed, pairwise comparisons were performed using the
Bonferroni test.
RESULTS
Population Description
Over a 2-yr period, six patients with
ACPE were recruited into the study. Three
patients had hypertensive cardiomyopathy,
two had idiopathic cardiomyopathy, and
one had ischemic cardiomyopathy. All the
patients had New York Heart Association
class III or IV heart failure. The anthrometric and treatment data of the patients are
shown in Table 1.
Respiratory Function
Breathing Pattern and Gas Exchange.
The effects of CPAP and NPPV on breathing
pattern, gas exchange, respiratory load, and
respiratory muscle unloading are shown in
Table 2. Although there was an increase in
tidal volume with CPAP5 (15%), CPAP10
(8%), and NPPV (27%) compared with
spontaneous breathing, this only reached
statistical significance with NPPV (p ⫽
.018). There was a mean increase in minute
Table 1. Patients’ characteristics
Pt. No.
Age/Sex
Weight,
kg
Height,
m
Cardiac Disease
LVEF, %
Class, NYHA
Medications
1
2
3
4
5
6
58/M
53/M
62/M
60/F
70/M
80/F
86
82
47
60
81
80
1.72
1.81
1.72
1.60
1.70
1.68
IDCM
IDCM
ISCM
HCM
HCM
HCM
43
43
28
40
40
45
IV
IV
IV
III
III
IV
VD-DR-AD
VD-BB-NI-DR
VD-DR-CA-AD
VD-NI-DR
CA-NI-DR-AD
AD-BB-CA
Pt, patient;
LVEF, left ventricular ejection fraction; NYHA, New York Heart Association; IDCM, idiopathic cardiomyopathy; ISCM, ischemic cardiomyopathy; HCM,
hypertensive cardiomyopathy; VD, vasodilators; DR, diuretics; AD, amiodarone; BB, ␤-blockers; CA, calcium antagonists.
Table 2. Respiratory and mechanics variables during spontaneous breathing (SB), 5 and 10 cm H2O continuous positive airway pressure (CPAP5 and
CPAP10), noninvasive positive pressure ventilation (NPPV), and return to spontaneous breathing (RSB)
Ventilatory Mode
SB
CPAP5
CPAP10
NPPV
RSB
p
VT, mL
RR, breaths/min
VE, L/min
VT/TI
TI/TTOT
CLdyn, L/cm H2O
⌬Pes, cm H2O
PTPes, cm H2O䡠sec/min
518 ⫾ 44
20 ⫾ 2
10.5 ⫾ 1.2
0.47 ⫾ 0.05
0.39 ⫾ 0.02
0.119 ⫾ 0.049
10.56 ⫾ 2.43
212 ⫾ 65
597 ⫾ 70
19 ⫾ 2
11.3 ⫾ 1.7
0.50 ⫾ 0.07
0.41 ⫾ 0.03
0.127 ⫾ 0.065
8.56 ⫾ 1.83
172 ⫾ 77
562 ⫾ 48
19 ⫾ 3
10.7 ⫾ 1.9
0.48 ⫾ 0.05
0.36 ⫾ 0.02
0.152 ⫾ 0.073
8.75 ⫾ 2.57
191 ⫾ 55
656 ⫾ 123a
18 ⫾ 2
13.1 ⫾ 1.8
0.54 ⫾ 0.13
0.36 ⫾ 0.02
0.153 ⫾ 0.047
6.58 ⫾ 2.60a
146 ⫾ 76a
530 ⫾ 65
20 ⫾ 2
10.1 ⫾ 1.3
0.48 ⫾ 0.05
0.38 ⫾ 0.03
0.118 ⫾ 0.047
10.86 ⫾ 2.87
203 ⫾ 68
.018
.725
.340
.225
.234
.475
.020
.001
VT, tidal volume; RR, respiratory rate; VE, minute ventilation; VT/TI, mean inspiratory flow; TI/TTOT, inspiratory duty cycle; CLdyn, dynamic pulmonary
compliance; ⌬Pes, esophageal pressure; PTPes, esophageal pressure-time product.
a
p ⬍ .05, Bonferoni test vs. SB and RSB.
ventilation of 2.6 L/min with NPPV, 0.8
L/min with CPAP 5, and 0.2 L/min with
CPAP10. In addition, we observed a mean
rise in PaO2 of 21 mm Hg with NPPV and 16
mm Hg with CPAP10 compared with baseline (Table 3). However, due to the small
numbers in this study, no significant differences in minute ventilation and in PaO2
were observed.
Lung Compliance and Respiratory
Muscle Unloading. Although there was a
mean increase in CLdyn of 33 mL/cm H2O
and 34 mL/cm H2O with NPPV and CPAP10
compared with baseline, these rises were
not significant statistically. Esophageal
pressure swing and esophageal pressuretime product decreased significantly with
NPPV (37%, p ⫽ .02, and 31%, p ⫽ .001,
respectively) compared with spontaneous
breathing. In contrast, with CPAP5 or
CPAP10, the decreases in esophageal pressure swing (19% and 17%, respectively) or
esophageal pressure-time product (19%
and 10%, respectively) compared with
spontaneous breathing were not statistically significant (Table 2).
Cardiac and Hemodynamic
Function
There were no changes in heart rate
and blood pressure during CPAP 5,
CPAP10, and NPPV (Table 3). CPAP10
and NPPV produced significant decreases
in both mean transmural right atrial
pressure (61% and 57%, respectively) and
in mean transmural pulmonary arterial
occlusion pressure (48% and 48%, respectively) when compared with spontaneous breathing. There were no significant changes in cardiac index, stroke
volume index, mixed venous oxygen saturation, oxygen delivery, and oxygen uptake with CPAP5, CPAP10, or NPPV compared with spontaneous breathing.
DISCUSSION
The main finding of this small study is
that short-term use of NPPV compared
with CPAP 10 in patients with ACPE
causes a greater reduction in respiratory
load but with similar improvements in
cardiac performance.
Critique of Method
Patient Recruitment. One of the major
limitations of this study was patient recruitment. However, this was an invasive
physiologic study that required each patient to have an esophageal pressure
monitoring catheter and a pulmonary artery catheter inserted to measure
changes in respiratory mechanics, cardiac function, and hemodynamic function during five separate study periods.
To our knowledge, the only other study
that has attempted to study patients with
ACPE so extensively in a similar setting,
albeit with CPAP alone, was by Lenique et
al. (10), and even in this study, in which
the protocol was simplified, the investigators only managed to recruit and study
eight patients. It is also noteworthy that
only one patient (patient 3) had an ischemic cardiomyopathy and a left ventricular ejection fraction of ⬍40%; the remainder of the patients had idiopathic
dilated cardiomyopathy or hypertrophic
cardiomyopathy. The behavior under
NPPV and CPAP of this patient was similar to the others as we observed both a
decrease of esophageal pressure-time
product under NPPV and a slight decrease of ⬍10% of cardiac index under
NPPV and CPAP10 compared with basal
conditions. Thus, we do not believe this
patient would change the main findings
of this study.
Comparison with Other Studies.
Lenique et al. (10) reported a reduction
in work of breathing in patients with
ACPE associated with a decrease in CLdyn
and lung resistance using CPAP10. Al2459
Table 3. Patients’ hemodynamics and arterial blood gas variables during spontaneous breathing (SB), 5 and 10 cm H2O continuous positive airway pressure
(CPAP5 and CPAP10), noninvasive positive pressure ventilation (NPPV), and return to spontaneous breathing (RSB)
Ventilatory Mode
SB
CPAP5
CPAP10
NPPV
RSB
p
HR, bpm
BP, mean, mm Hg
MRAPTM, mm Hg
PAOPTM, mm Hg
CI, L/min/m2
SVI, mL/m2
Sv៮ O2, %
pH
PaO2, torr
PaCO2, torr
ḊO2, mL/min
V̇O2, mL/min
85 ⫾ 12
86 ⫾ 05
13.0 ⫾ 3.0
29 ⫾ 04
2.34 ⫾ 0.18
29.5 ⫾ 4.1
60 ⫾ 0.05
7.39 ⫾ 0.05
71 ⫾ 05
41.2 ⫾ 5.0
348 ⫾ 37
135 ⫾ 13
82 ⫾ 13
94 ⫾ 03
8.5 ⫾ 2.4
19 ⫾ 03a
2.37 ⫾ 0.18
31.0 ⫾ 4.3
60 ⫾ 0.05
7.41 ⫾ 0.04
78 ⫾ 05
39.6 ⫾ 3.9
366 ⫾ 25
130 ⫾ 16
86 ⫾ 13
93 ⫾ 03
5.0 ⫾ 2.4a
15 ⫾ 02a
2.19 ⫾ 0.17
32.4 ⫾ 3.6
60 ⫾ 0.05
7.41 ⫾ 0.03
87 ⫾ 06
38.8 ⫾ 2.5
342 ⫾ 16
124 ⫾ 14
83 ⫾ 13
91 ⫾ 03
5.5 ⫾ 1.7a
15 ⫾ 03a
2.11 ⫾ 0.17
31.4 ⫾ 4.2
61 ⫾ 0.05
7.41 ⫾ 0.04
92 ⫾ 07
38.8 ⫾ 4.3
330 ⫾ 19
120 ⫾ 11
88 ⫾ 13
85 ⫾ 03
14.0 ⫾ 3.3
27 ⫾ 03
2.22 ⫾ 0.22
27.4 ⫾ 4.2
60 ⫾ 0.05
NA
NA
NA
NA
NA
.588
.675
.048
.019
.080
.655
.998
.778
.245
.997
.325
.287
HR, heart rate; BP, blood pressure; MRAPTM, transmural mean right atrial pressure; PAOPTM, transmural pulmonary arterial occlusion pressure; CI,
cardiac index; SVI, stroke volume index; Sv៮ O2, mixed venous oxygen saturation; ḊO2, oxygen delivery; V̇O2, oxygen consumption.
a
p ⬍ .05, Bonferoni test vs. SB and RSB.
though in our study the respiratory muscles were unloaded using NPPV, as evidenced by the decrease in esophageal
pressure swing and esophageal pressuretime product, we found no statistical increase in CLdyn with NPPV or CPAP10,
although there was a trend for the CLdyn
to increase. In fact, the mean rise in
CLdyn was greater with CPAP10 and NPPV
compared with the study by Lenique et al.
(10), but probably due to the small patient numbers in the current study, these
differences were not significant.
Significance of the Findings
Respiratory Effects. In the present
study, neither CPAP or NPPV improved
the respiratory mechanics. However
baseline values of elastic loading, CLdyn,
in our patients were higher than that in
previous reported studies (10), and this
discrepancy in the load could have contributed to the reduced improvements in
work of breathing in our study during
CPAP5 and CPAP10. The observed unloading of the respiratory muscles and
reduction in esophageal pressure swing
and esophageal pressure-time product is
probably attributable to inspiratory assistance during NPPV; thus, we hypothesize
that NPPV unloads the respiratory muscles and increases tidal volume immediately at the initiation of ventilation, before any significant alteration in
respiratory mechanics. This is therefore
in contrast to CPAP that unloads the respiratory muscles as a result of an improvement in pulmonary mechanics.
Cardiac Effects. The effects of positive
intrathoracic pressure on cardiac output
are variable and dependant on the ven2460
tricular filling pressures. In contrast to
the normal heart, the cardiac output of
the failing heart is predominantly dependent on afterload changes (9). Studies
using CPAP in patients with stable
chronic heart failure have shown that the
greatest increase in cardiac output is
found in those patients with higher filling
pressures (e.g., pulmonary arterial occlusion pressure of ⬎12 mm Hg) (22). Although we only included in this study
patients who had a pulmonary arterial
occlusion pressure of ⬎18 mm Hg, to
maximize the chances of observing an
increase in cardiac output, we did not
observe any increase in cardiac output
during either the CPAP or NPPV mode. In
fact, there was a tendency for cardiac
output to decrease during CPAP10 and
NPPV in comparison with basal conditions (p ⫽ .08). This difference could be
statistically significant with a greater
number of patients included. However,
the differences between NPPV or CPAP10
and basal conditions were ⬍10%, which
is low considering that a ⬎12% change in
cardiac output, using the thermodilution
method, is required to be of clinical relevance (23).
Clinical Implications of Findings. Until recently, NPPV was not considered effective treatment for ACPE (24). However, after two recent clinical trials in
patients with ACPE, interest in the use of
NPPV in the management of patients
with acute cardiac decompensation has
increased (14, 15). Although most patients with acute heart failure respond to
standard medical therapy without the
need for ventilatory assistance, NPPV has
been shown to be better than CPAP (15)
and conventional therapy with oxygen
(12). NPPV causes a greater improvement
in respiratory rate (15), blood pressure
(15), arterial blood gases (15), and time to
recovery (14), with a reduction in intubation rate (14). The unloading of the
respiratory muscles and increase in tidal
volume reported in this study is supportive evidence for the clinical benefits demonstrated in previous studies (14, 15).
However, there are still concerns
about managing patients with acute heart
failure with NPPV. Although Mehta et al.
(15) reported the beneficial effects of
NPPV in ACPE patients, this trial had to
be terminated prematurely because of the
high rate of acute myocardial infarction
in the NPPV group. Despite a trend toward more chest pain in the NPPV group,
which could be due to inadequate randomization, this observation raises the
possibility that bilevel pressure-support
ventilation stresses the myocardium
greater than CPAP. However, we found
no differences between CPAP and NPPV
in terms of the cardiac or hemodynamic
effects. CPAP10 and NPPV produced similar reductions in right and left ventricular preload, as evidenced by the fall in
right and left atrial transmural pressures,
without any change in cardiac output,
which has previously been suggested as
an improvement in cardiac performance
(10). In addition, in this study, none of
the patients experienced any ischemic
problems using either NPPV or CPAP.
Therefore, the advantages and pitfalls of
using NPPV in patients with ACPE need
to be appreciated, but in this study, as
with the study by Masip et al. (14) we
S
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CONCLUSION
Short-term use of NPPV has similar cardiac and hemodynamic benefits as CPAP10
in patients with ACPE. In addition, NPPV
unloads the respiratory muscles, reduces
respiratory effort, and increases tidal volume before any alterations in pulmonary
mechanics. This is in contrast to CPAP,
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muscle unloading are observed. The results
of this study favor the use of NPPV in selected patients with ACPE, and clinical trials are now warranted to compare the clinical and physiologic effects of standard
medical therapy with NPPV and CPAP.
ACKNOWLEDGMENTS
We thank the physicians and nursing
staff of the service de réanimation médicale de l’hôpital Raymond Poincaré for
valuable cooperation and Michèle Lejaille, Line Falaise, and Gilles Macadoux
for their technical assistance.
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2461
Short-term Noninvasive Pressure
Support Ventilation Prevents ICU
Admittance in Patients With Acute
Cardiogenic Pulmonary Edema*
Matteo Giacomini, MD; Gaetano Iapichino, MD; Marco Cigada, MD;
Aldo Minuto, MD; Rebecca Facchini, MD; Andrea Noto, MD; and Elena Assi, MD
Study objectives: Noninvasive ventilation, although effective as treatment for patients with acute cardiogenic pulmonary edema when prolonged for hours, is of limited use in the emergency department (ED).
The aim of the study was to determine whether a short attempt at noninvasive pressure support ventilation
avoids ICU admittance and to identify lack of response prediction variables.
Design: Prospective inception cohort study.
Setting: ED of a university hospital.
Patients: Fifty-eight consecutive patients with cardiogenic pulmonary edema who had been unresponsive
to medical treatment and were admitted between January 1999 and December 2000.
Interventions: Pressure support ventilation was instituted through a full-face mask until the resolution of
respiratory failure. A 15-min “weaning test” was performed to evaluate clinical stability. Responder
patients were transferred to a medical ward. Nonresponding patients were intubated and were admitted
to the ICU.
Main outcome measures: The included optimal length of intervention, the avoidance of ICU admittance, the
incidence of myocardial infarction, and predictive lack of response criteria.
Results: Patients completed the trial (mean [ⴞ SD] duration, 96 ⴞ 40 min). None of the responders (43
patients; 74%) was subsequently ventilated or was admitted to the ICU. Two new episodes of myocardial
infarction were observed. Thirteen of 58 patients died. A mean arterial pressure of < 95 mm Hg (odds ratio
[OR], 10.6; 95% confidence interval [CI], 1.8 to 60.8; p < 0.01) and COPD (OR, 9.4; 95% CI, 1.6 to 54.0;
p < 0.05) at baseline predicted the lack of response to noninvasive ventilation.
Conclusions: A short attempt at noninvasive ventilation is effective in preventing invasive assistance. A
15-min weaning test can identify patients who will not need further invasive ventilatory support. COPD and
hypotension at baseline are negative predictive criteria.
(CHEST 2003; 123:2057–2061)
Key words: acute cardiogenic pulmonary edema; acute myocardial infarction; endotracheal intubation; length of ventilatory
treatment; predictive failure criteria; noninvasive pressure support ventilation
Abbreviations: ACPE ⫽ acute cardiogenic pulmonary edema; AMI ⫽ acute myocardial infarction; ED ⫽ emergency
department; NIPSV ⫽ noninvasive pressure support ventilation; OR ⫽ odds ratio; PEEP ⫽ positive end expiratory pressure;
Spo2 ⫽ peripheral saturation of oxygen.
cardiogenic pulmonary edema (ACPE) may
A cute
be a rapidly reversible illness once its pathogenic
factors are controlled and the vicious circle of hypoxia/
*From the Istituto di Anestesiologia e Rianimazione dell’Università degli Studi di Milano (Drs. Giacomini, Iapichino, Cigada,
Minuto, Noto, and Assi), Azienda Ospedaliera, Polo Universitario
Ospedale San Paolo, Milan, Italy; and the Istituto di Ricerche
Farmacologiche “Mario Negri” (Dr. Facchini), Centro di
Ricerche Cliniche per le Malattie Rare “Aldo e Cele Daccò,”
Ranica, Bergamo, Italy.
Manuscript received April 9, 2002; revision accepted September
27, 2002.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:
[email protected]).
Correspondence to: Gaetano Iapichino, MD, Cattedra di Anestesiologia e Rianimazione dell’Università di Milano, Azienda Ospedaliera,
Polo Universitario Ospedale San Paolo, via A. Di Rudinı̀ 8, 20142
Milano, Italy; e-mail: [email protected]
www.chestjournal.org
heart failure/hypoperfusion has been interrupted.
The beneficial effects of positive intrathoracic pressure are well-established, and its use through a
facemask has been addressed by several authors.1– 4
Pressure support ventilation adds to the effects of
positive end-expiratory pressure (PEEP) the possibility of decreasing respiratory workload and oxygen
consumption, thus resulting in a faster restoration of
vital signs.5–9 The result can be the avoidance of
endotracheal intubation.
If the duration of treatment were short enough,
noninvasive pressure support ventilation (NIPSV)
could be applied in the emergency department
(ED), thus avoiding admittance to the ICU. However, no indications are available as to how long
NIPSV has to be continued before judging it sucCHEST / 123 / 6 / JUNE, 2003
2057
cessful or not. Noninvasive respiratory assistance is
usually applied for hours. As a result, ICU facilities
are required,6,10 –16 and possibly unavoidable invasive
ventilation can be delayed.7,10,17,18
Of note, predictive criteria for lack of response to
NIPSV for ACPE are lacking,13,16,17 and higher
incidences of acute myocardial infarction (AMI)6 and
mortality10 were reported in patients who had been
treated with NIPSV in contrast to those receiving
continuous positive airway pressure or conventional
treatment.
This uncontrolled prospective trial was performed
in the ED on patients with pure ACPE who were
unresponsive to full medical treatment. The primary
objectives were as follows: (1) to determine the
optimal duration of NIPSV (ie, whether it can be
short enough to be performed in the ED, yet
effective in avoiding intubation and ICU admittance); (2) to identify specific criteria that are predictive of lack of response; and (3) to evaluate the
effect of NIPSV on patients with AMI and its role in
the presence of AMI.
Secondary objectives were hospital length of stay
and mortality.
Materials and Methods
The setting was the ED of a university hospital. This study was
performed in accordance with the Declaration of Helsinki.
Informed consent was given by the patients in the study or by
their next of kin. All consecutive patients affected by ACPE who
required respiratory assistance after the institution of conventional medical treatment (defined as therapy with morphine
oxygen via face mask, diuretics, and vasoactive drugs) had proven
to be ineffective were eligible for the study.
The inclusion criteria were as follows: (1) pulmonary edema
confirmed by rales over both lungs and signs of pulmonary
congestion on chest radiographs within the first hour after
presentation to the ED; (2) a pulse oximetric saturation (Spo2) of
⬍ 95% despite oxygen administration at 10 L/min via a reservoir
mask; and (3) severe respiratory distress with dyspnea and use of
accessory muscles, severe cyanosis, oligoanuria, and signs of
peripheral hypoperfusion.
The exclusion criteria were life-threatening conditions (eg,
bradycardia or malignant tachyarrhythmias with severe hemodynamic impairment), end-stage renal or liver disease, severe
neurologic impairment (ie, Glasgow coma scale, ⬍ 7), and concomitant pneumonia. Demographic and anamnestic data were
collected. A gastric tube was placed to avoid stomach distension.
NIPSV was applied (Respicare SC ventilator; Dräger Medizintechnik GmbH; Lübeck, Germany) through a full-face mask.
PEEP and pressure support were initially set at 5 and 10 cm H2O
(over PEEP), respectively. This setting then was modified in the
attempt to obtain a tidal volume between 5 and 7 mL/kg. The
fraction of inspired oxygen ranged between 0.8 and 1.
Noninvasive BP, Spo2, heart rate, and respiratory rate were
monitored continuously. Arterial blood gas levels and ECG were
recorded at baseline (on a reservoir oxygen mask before the onset
of NIPSV) and just before the termination of NIPSV.
NIPSV was considered to be effective if dyspnea disappeared
and if respiratory and hemodynamic parameters improved to2058
gether with peripheral perfusion (ie, skin temperature and
diuresis). The reporting of a subjective impression of “getting
better” by the patient was also mandatory.
In the first 10 months of the study, the decision to stop NIPSV
treatment and to perform a weaning test was left to the clinical
judgment of the intensivist in charge, once the NIPSV efficacy
criteria were met. After an interim analysis, which was intended
to further reduce the duration of treatment, we decided to
perform a weaning test within 90 min of the initiation of NIPSV.
The weaning test was conducted as follows. NIPSV was
discontinued, and the patient was allowed to breath spontaneously on a reservoir oxygen mask for 15 min. If the patient
remained clinically stable (ie, Spo2 of ⬎ 95%, absence of dyspnea, and stable hemodynamic parameters), the patient was
discharged to the ward (defined as the responder group). The
wards were defined medical wards with cardiologic expertise in
which at least some beds were equipped with ECG and Spo2
monitoring equipment. If the patient did not respond to weaning,
we proceeded to invasive ventilation, and the patient was transferred to the ICU (defined as the failure group).
The need for invasive ventilation, new episodes of AMI,
hospital length of stay, and mortality were analyzed. AMI was
diagnosed when two of the following three criteria were met:
chest pain; increase in creatine phosphokinase concentration; and
ECG signs of myocardial necrosis.
Statistical Analysis
The data were reported as the mean ⫾ SD and interquartile
range. The Student t test was used for statistical comparison. A p
value of ⬍ 0.05 was considered to be significant. A logistic
regression model, built using a backward stepwise approach, was
carried out to identify the independent variables at hospital
admission that could predict failure (the dependent variable).
Age, the presence of COPD on hospital admission, AMI, heart
and respiratory rate, mean arterial pressure of ⬍ 95 mm Hg,
Pao2, pH, and Paco2 were considered to be independent
variables and were introduced into the model only if they were
associated with the dependent variable in the bivariate analysis at
a permissive significance level (ie, p ⬍ 0.1 [␹2 test]) or if the odds
ratio (OR) was ⬎ 1.5 or ⬍ 0.67. Variables that did not meet at
least one of these conditions were not included in the final
logistic model.
Results
Between January 1999 and December 2000, 58
consecutive patients with ACPE were enrolled in the
study. The underlying diseases were as follows:
ischemic heart disease (34 patients); COPD (16
patients); hypertension (15 patients); diabetes (7
patients); chronic renal failure (8 patients); and
patent ductus (1 patient). Seven patients (12%) had
signs of AMI at the time of hospital admission.
Baseline hemodynamic and respiratory parameters,
the data for which were collected before the onset of
NIPSV, are reported in Table 1. Four patients could
not be treated with NIPSV because of mask intolerance or refusal, five patient progressively worsened
despite receiving NIPSV, and six patients failed the
weaning test. All of these 15 patients were invasively
ventilated and transferred to the ICU. NIPSV was
Clinical Investigations in Critical Care
ward, none of the responder patients received ventilation or were admitted to the ICU.
Logistic regression analysis in 54 patients identified two risk factors for lack of response to NIPSV.
Patients with a mean BP of ⬍ 95 mm Hg at hospital
admission had a 10-fold increased risk of failing the
NIPSV trial (OR, 10.6; 95% confidence interval, 1.8
to 60.8; p ⬍ 0.01). The presence of COPD was also
significantly associated with the need for invasive
ventilation (OR, 9.4; 95% confidence interval, 1.6 to
54.0; p ⬍ 0.05). Twenty-two percent of the patients
died (13 of 58 patients), 26.7% of those (4 of 15
patients) in the failure group and 20.9% of those (9
of 43 patients) in the responder group. Of the 13
patients who died, 3 had been admitted to the
hospital with a diagnosis of AMI. Two of the patients
who died were in the responder group (one died of
ventricular fibrillation on the ward 20 h after undergoing NIPSV, and the second patient died on day
19), and one patient in the failure group died on day
9. Two patients developed AMIs during their hospital stay (1 patient in the failure group on day 4, and
1 of 43 patients in the responder group on day 5).
The latter patient died on the 25th day of the
hospital stay. The mean hospital length of stay did
not differ between the patients in the responder
group and those in the failure group (mean length of
hospital stay, 17 ⫾ 12 days [range, 9.5 to 19.5 days]
vs 19 ⫾ 10 days [range, 9.5 to 28 days], respectively;
p ⫽ 0.4).
Table 1—Demographic Characteristics and Baseline
Clinical Parameters (During Oxygen Therapy) in the
58 Enrolled Patients*
Variables
Values
Age, yr
Male gender, %
Respiratory rate, breaths/min
Arterial blood pH
Pao2, mm Hg
Paco2, mm Hg
Spo2, %
Heart rate, beats/min
Mean arterial BP, mm Hg
74.1 ⫾ 13.0 (69–84)
60.0
36.8 ⫾ 4.2 (35–40)
7.20 ⫾ 0.11 (7.14–7.28)
65.0 ⫾ 34.8 (48–70)
63.7 ⫾ 20.7 (47–76)
80.6 ⫾ 13.7 (75–90)
112.8 ⫾ 24.4 (100–130)
112.6 ⫾ 29.6 (88–136)
*Values given as mean ⫾ SD (interquartile range).
applied with a mean pressure support level of 14 ⫾ 3
cm H2O10 –16 (responder group, 14.1 ⫾ 3.2 cm H2O;
failure group, 14.1 ⫾ 4.1 cm H2O) with a PEEP of
8 ⫾ 2 cm H2O8 –10 (responder group, 8.4 ⫾ 1.8 cm
H2O; failure group, 8.4 ⫾ 1.8 cm H2O). NIPSV
significantly improved hemodynamic and respiratory
parameters in the 43 patients in the responder group
who were discharged from the ED. A positive but
nonsignificant trend was found also in the failure
group (Table 2).
Invasive mechanical ventilation was avoided in
76% of patients in the responder group (16 of 21
patients) and 73% of the patients in the failure group
(27 of 37 patients). Excluding the four patients in
whom NIPSV could not be applied, the mean duration of respiratory support was 118 ⫾ 57 min (range,
105 to 143 min) in the first study period (19 patients)
and 77 ⫾ 22 min (range, 60 to 90 min) in the second
study period (35 patients). In the responder group, 6
patients had AMIs on hospital admission and 37 did
not. Only one patient who was admitted to the
hospital with a diagnosis of AMI was not successfully
treated. The effects of NIPSV were similar in AMI
and non-AMI patients.
Throughout the hospital stay, after referral to the
Discussion
The great majority of patients with ACPE are
initially managed in the ED. When patients do not
respond to conventional medical treatment, ventilator assistance is needed. We tested the hypothesis
that a short NIPSV run in the ED may avoid the use
of invasive ventilation and admittance to the ICU. In
the present study, critically ill patients were selected
Table 2—Effects of NIPSV on Hemodynamic and Respiratory Parameters*
Responder Group (n ⫽ 43)
Failure Group (n ⫽ 11)
Variables
Baseline
End-NIPSV
Baseline
End-NIPSV
Respiratory rate, breaths/min
Arterial blood pH
Pao2, mm Hg
Paco2, mm Hg
Spo2, %
Heart rate, beats/min
Mean arterial BP, mm Hg
36.2 ⫾ 6.0 (35–40)
7.21 ⫾ 0.10 (7.16–7.28)
67.7 ⫾ 39.1 (51–70)
62.3 ⫾ 20.0 (48–75)
82.0 ⫾ 13.7 (79–91)
114.6 ⫾ 24.1 (100–131)
118.6 ⫾ 27.2 (102–138)
24.5 ⫾ 5.7 (20–28)†
7.38 ⫾ 0.10 (7.3–7.4)†
114.4 ⫾ 52.0 (82–119)†
43.7 ⫾ 10.5 (36–47)†
97.5 ⫾ 2.0 (96–99)†
92.3 ⫾ 16.6 (80–104)†
95.1 ⫾ 14.1 (83–106)†
36.1 ⫾ 4.4 (35–39)
7.17 ⫾ 0.10 (7.1–7.2)
55.3 ⫾ 17.6 (44–63)
68.7 ⫾ 23.5 (52–88)
73.9 ⫾ 12.6 (65–79)
106.8 ⫾ 27.2 (87–127)
92.2 ⫾ 27.4 (70–110)‡
31.7 ⫾ 5.8 (28–35)†
7.23 ⫾ 0.10 (7.2–7.3)
66.3 ⫾ 21.3 (59–68)
61.3 ⫾ 21.7 (44–77)
86.7 ⫾ 8.5 (83–92)
107.4 ⫾ 27.0 (85–128)
81.9 ⫾ 18.1 (73–92)
*Values given as mean ⫾ SD (interquartile range).
†p ⬍ 0.05 compared to baseline.
‡p ⬍ 0.05 compared to responder patients at baseline.
CHEST / 123 / 6 / JUNE, 2003
2059
by their need for ventilatory support after undergoing ineffective conventional medical therapy for
ACPE (eg, morphine, oxygen mask, diuretics, and
nitrates) [Table 1]. Patients with severe concomitant
illnesses were excluded. Pneumonia was an exclusion
criterion because in patients with pneumonia NIPSV
already had proven to be a less effective therapy,12,13,16 and the patients probably needed a longer
period of assistance. We did not perform a randomized trial since NIPSV has already proven to be
effective in the treatment of ACPE6,7,11,12,14 –16 and
because our primary end point was the time needed
to treat respiratory failure and to avoid ICU admittance.
The duration of treatment is a critical issue when
treating patients with ACPE outside the ICU. Prolonged ventilatory assistance is impractical in an
environment like the ED, which is frequently understaffed, has limited space, and has a high turnover of
patients. Moreover, NIPSV may dangerously delay,
in some patients, unavoidable tracheal intubation
and invasive mechanical ventilation.7,10,17,18
Despite the fact that most authors have reported a
significant improvement of clinical parameters after
15 to 60 min,6,11–16 NIPSV is usually administered
for a considerable length of time, ranging from 2 to
⬎ 24 h in patients who already have been admitted
to the ICU or are transferred there soon after the
beginning of NIPSV.6,10 –16 As described by other
authors,6,11–16 invasive respiratory support is avoided
in a large percentage of patients, but we have shown
that adequate clinical stability can be obtained in a
much shorter time. A 90-min NIPSV trial applied in
the ED with patients who had ACPE resulted in a
rapid assignment to the best treatment, medical or
invasive support, without inappropriate delay and
use of ED resources. The weaning test identified
patients who, although their condition improved
during NIPSV, did not reach a sufficient clinical
stability to be assigned to pure medical treatment.
Patients in the failure group were invasively treated
and transferred to the ICU, while patients in the
responder group were discharged in a short time
from the ED to the ward. The improvement was
persistent in time, and none of the responder patients needed further ventilatory assistance throughout their hospital stays.
We do not confirm the reported high incidence of
AMI that has been associated with NIPSV.6 During
their hospital stays, only two patients developed new
episodes of AMI, days after undergoing NIPSV and
too late to be attributed to it. Moreover, at variance
with another report,11 six of seven patients with AMI
at baseline were responders. In accordance with the
results of other trials,12,14,16 NIPSV thus may be used
with reasonable safety in patients with AMI. The
2060
overall mortality rate was in the range that has been
reported by other authors (ie, 7 to 25%),6,10 –12,14,16
even if many studies6,10,14 have included patients
before medical treatment was defined to be ineffective, thus enrolling a less critical population.
Moreover, it is reasonable to affirm that deaths
were related to the pathology itself rather than to the
type of respiratory treatment. This finding is supported by the fact that the only death potentially
related to treatment (which occurred during the first
day in a responder patient who had AMI at baseline)
was actually due to a sudden and unexpected malignant arrhythmia while the patient was on the ward.
All the other deaths occurred days after NIPSV was
performed in those who were not candidates for
intensive treatment and probably were the result of
concomitant terminal disease.
Finally, only two baseline conditions, mean arterial
pressure ⬍ 95 mm Hg and a history of COPD,
significantly predicted the failure of NIPSV. The
latter condition could be at least partially explained
by the sum of long-term and short-term increases in
the work of breathing, resulting in an excessive
respiratory workload that could not be rapidly managed by NIPSV alone. However, other concomitant
factors, such as chronic tracheobronchitis, malnutrition, or obesity, cannot be excluded. The absence of
arterial hypertension at baseline is probably consistent with a decreased left ventricular function19 with
decreased cardiac reserves, selecting a group of
patients with more severe conditions. The use of a
NIPSV in ACPE patients with a mean arterial pressure of ⬍ 95 mm Hg at hospital admission cannot
thus be encouraged. In COPD patients with ACPE,
NIPSV may be effective, but the predictable need
for prolonged respiratory assistance suggests caution
in using it in the ED.
ACKNOWLEDGMENTS: We thank Luca Bigatello for discussing our results, and Bruno Simini for his precious advice and
suggestions in preparing and editing the manuscript.
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CHEST / 123 / 6 / JUNE, 2003
2061
Original Contributions
Pressure Support Noninvasive Positive
Pressure Ventilation Treatment of Acute
Cardiogenic Pulmonary Edema
HERBERT NEIL WIGDER, MD, PAUL HOFFMANN, RRT,† DANIEL MAZZOLINI, RRT,†
ARVEY STONE, MD,‡ STEPHEN SCHOLLY, MD,‡ AND JAMES CLARK, MD§
We assessed cardiogenic pulmonary edema (CPE) patient response to
full mask pressure support noninvasive positive pressure ventilation
(NPPV). Adult patients presenting to the emergency department (ED) in
acute respiratory failure who clinically required endotracheal intubation
(ETI) were studied. In addition to routine therapy consisting of oxygen,
nitrates, and diuretics, patients were started on full mask NPPV using a
Puritan Bennett 7200 ventilator delivering pressure support 10 cm H2O,
PEEP 5 cm H2O, Fi02 100%. Pressure support was titrated to achieve tidal
volumes of 5 to 7 mL/kg, and PEEP titrated to achieve oxygen saturation
(SaO2) > 90%. Outcome measures included arterial blood gas (ABG),
Borg dyspnea score, vital signs, and need for ETI. Twenty patients mean
age 74.7 ⴞ 14.3 years were entered on the study. Initial mean values on
Fi02 100% by nonrebreather mask: pH 7.17 ⴞ .13, paCO2 65.5 ⴞ 19.4
mmHg, paO2 73.8 ⴞ 27.3 mm Hg, SaO2 89.7 ⴞ 10.0%, Borg score 8.1 ⴞ
1.4, and respiratory rate (RR) 38 ⴞ 6.3. At 60 minutes of NPPV, improvement was statistically significant: pH 7.28 (difference .11; 95% CI .04-.19),
paCO2 45 (difference 20.5; 95% CI 8-33), Borg score 4.1 (difference 4.0;
95% CI 3-5), and RR 28.2 (difference 9.8; 95% CI 5-14). NPPV duration
ranged from 30 minutes to 36 hours (median 2 hours, 45 minutes).
Eighteen patients (90%) improved allowing cessation of NPPV. Two
patients with concomitant severe chronic obstructive pulmonary disease
(COPD) required ETI. There were no complications of NPPV. NPPV using
full face mask and pressure support provided by a conventional volume
ventilator is an effective treatment for CPE and may help prevent ETI.
(Am J Emerg Med 2001;19:179-181. Copyright © 2001 by W.B. Saunders
Company)
Acute pulmonary edema is a life-threatening emergency
that can require mechanical ventilation to treat. Pressure
From the *Department of Emergency Medicine, Lutheran General
Hospital, Park Ridge, IL, Section of Emergency Medicine, Department of Medicine, University of Chicago, Chicago, IL; †Respiratory
Care Department, Lutheran General Hospital, Park Ridge, IL; ‡Pulmonary Medicine, Lutheran General Hospital, Park Ridge, IL, Department of Medicine, the Chicago Medical School, North Chicago,
IL; §Emergency Medicine Residency Program, University of Chicago, Chicago, IL.
Presented at the American Association for Respiratory Care, December 13, 1999, Las Vegas, NV.
Manuscript received May 1, 2000, returned June 6, 2000, revision
received September 11, 2000, accepted October 10, 2000.
Reprints are not available.
Key Words: NPPV, pressure support ventilation, BiPAP, CPAP,
cardiogenic pulmonary edema.
Copyright © 2001 by W.B. Saunders Company
0735-6757/01/1903-0001$35.00/0
doi:10.1053/ajem.2001.21718
support ventilation is commonly accomplished by endotracheal intubation (ETI). Emergency intubation in acute respiratory failure is an invasive procedure with the potential
for serious complications.
In contrast, NPPV provides ventilation without using an
endotracheal tube. During the last 10 years, increasing attention has focused on using noninvasive ventilatory support to treat patients in acute respiratory failure (ARF).1
This management is as effective as conventional ventilation
in improving gas exchange and avoids the complications of
an invasive intubation with an endotracheal tube.2 Meduri et
al3 reported 158 ARF inpatients treated with face mask noninvasive positive pressure ventilation (NPPV). In this study,
causes of ARF included COPD (chronic obstructive pulmonary disease), status asthmaticus, acute upper airway obstruction, pneumonia and cardiogenic pulmonary edema. In this
series, 5 of 9 cardiogenic pulmonary edema (CPE) patients
in the intensive care unit avoided ETI because of NPPV. No
emergency department (ED) patients were studied.
Rasanen et al4 and Bersten et al5 described mask CPAP
(continuous positive airway pressure) treatment of CPE.
Rusterholtz et al6 successfully treated 8 intensive care unit
CPE patients with NPPV. Sachetti et al7 and Pollack et al.8
studied nasal BiPAP (bilevel positive airway pressure) support for acute respiratory distress (ARD) in the ED and
found it effective treatment of acute pulmonary edema.
Recently, the efficacy of CPAP and nasal BiPAP9,10,11 for
acute pulmonary edema has been questioned. Mask CPAP
is not well tolerated because patients must exhale against
continuous pressure. In addition, mask CPAP does not
provide inspiratory pressure support. Nasal BiPAP also has
disadvantages compared to a conventional volume ventilator. Fi02 is not controllable. Exhaled tidal volumes cannot
be monitored to assess minute ventilation.
Pressure support ventilation is a different mode of ventilation than either CPAP or nasal BiPAP. Pressure support
is a ventilatory mode that augments spontaneous tidal volume. The pressure is terminated when the inspiratory flow
rate drops below a preset value (eg, 25% of the initial
inspiratory flow rate) and is off during exhalation. In contrast, CPAP provides positive pressure throughout both the
inspiratory and expiratory cycles of breathing, and at higher
levels (ie, greater than 5 cm H2O) may be extremely uncomfortable. Although nasal BiPAP provides alternating
179
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 19, Number 3 ■ May 2001
180
pressures for inspiration and expiration, it does not allow
accurate monitoring of expired tidal volumes and Fi02. A
volume ventilator pressure support of 10 cm H2O and 5 cm
H2O end expiratory pressure is equivalent to nasal BiPAP
using settings of 15 cm IPAP and 5 cm EPAP. Using a
volume ventilator, pressure support can be increased if
exhaled tidal volumes and minute ventilation are low. Also,
the volume ventilator can control Fi02 as well as sensitivity
adjustments for leakage within the system.
Despite several advantages, there are few reported cases
of pressure support NPPV treatment for acute cardiogenic
pulmonary edema using full mask and pressure support
provided by a conventional volume ventilator. No studies
have reported use in ED patients. The purpose of this pilot
study was to determine the feasibility of pressure support
NPPV treatment of acute cardiogenic pulmonary edema in
ED patients using a conventional volume ventilator and full
face mask.
MATERIALS AND METHODS
All patients more than 18 years of age who presented with ARF
caused by CPE and clinically appeared to require ETI were candidates for study inclusion. Exclusion criteria included pregnancy,
apnea, and shock. All patients were immediately treated with
routine therapy including FiO2 100% oxygen by nonrebreather
mask, diuretics, and sublingual nitroglycerin tablets 0.4 mg every
5 to10 minutes. The Respiratory Care Department was notified on
the patient’s arrival to bring a Puritan Bennett 7200 ventilator
(Carlsbad, CA) and other appropriate equipment for NPPV to the
ED. NPPV was initiated according to a standard protocol (initial
settings pressure support 10 cm H2O, CPAP 5 cm H2O, FiO2
100%). Pressure support was titrated to achieve tidal volumes of 5
to 7 mL/kg, and PEEP titrated to achieve oxygen saturation
(SaO2) ⬎ 90%.
Outcome measures included ETI, SaO2, arterial blood gas
(ABG), Borg dyspnea score (10 ⫽ severest respiratory distress),
and vital signs. Patients who clinically deteriorated despite NPPV
underwent ETI and ventilation as per standard ED procedures.
Data were collected by the Respiratory Care Department, physicians, and nurses in the ED on a standard data sheet. Data included patient name; age; arrival vital signs, oxygen saturation,
and arterial blood gas; time of treatment with NPPV; duration of
NPPV; repeat measurements of vital signs and oxygen saturation.
TABLE 1.
Statistical analysis was performed using the paired t-test and the
Wilcoxon Matched-Pairs Signed-Ranks Test. Patient confidentiality was protected and individual patient data were never disclosed.
The study was approved by the Institutional Review Board at
Lutheran General Hospital. Patients able to give informed consent
were asked to participate on the study. However, in most cases,
family members provided consent. Consecutive patients who met
criteria were asked to enroll on the study. There were no refusals
to requests for study enrollment.
RESULTS
Twenty patients mean age 74.7 ⫾ 14.3 years were entered on the study. Initial mean values on Fi02 100% by
nonrebreather mask and response to treatment with NPPV
are summarized in Table 1.
NPPV duration ranged from 30 minutes to 36 hours
(median 2 hours, 45 minutes). Mean pressure support was
10 cm H2O and mean PEEP was 5 cm H2O. Eighteen
patients (90%) improved allowing cessation of NPPV. Two
patients with concomitant severe COPD required ETI.
There were no complications of NPPV. No patients showed
electrocardiographic (ECG) evidence of acute myocardial
infarction.
DISCUSSION
ED patients in ARF caused by acute CPE can be successfully treated with full mask pressure support NPPV. This
technique does not have the complications of invasive ETI.
However, just like ETI, ventilatory support using a full face
mask and volume ventilator allows titration of pressure
support to achieve desired tidal volumes.
One reason for this study was our experience with patients not being able to tolerate CPAP or nasal BiPAP. Full
mask NPPV may prove to be more comfortable than mask
CPAP and nasal BiPAP in acute pulmonary edema patients
although this needs to be studied further.
The 2 treatment failures in this study requiring ETI had
concomitant severe COPD. Patient 1 was a 66-year-old
woman with a history of severe COPD and congestive heart
failure (CHF). She presented with a Borg score of 9 (almost
maximal breathing exertion). Initial ABG on 100% oxygen
showed pH 7.12 and paCO2 77. Vital signs were blood
Response to NPPV
pH
paCO2
Borg score
Respiratory rate
Systolic blood pressure
Diastolic blood pressure
Heart rate
*P ⫽ .007 by paired t-test.
†P ⫽ .004 by paired t-test.
‡P ⫽ .002 by Wilcoxon signed ranks test.
§P ⫽ .004 by paired t-test.
#P ⫽ .001 by paired t-test.
㛳P ⫽ .001 by paired t-test.
**P ⫽ .001 by paired t-test.
Initial
60 Minutes
Difference (95% CI)
7.17 ⫾ .13
65.5 ⫾ 19.4 mmHg
8.1 ⫾ 1.4
38 ⫾ 6.3
172 ⫾ 45
97 ⫾ 25
117 ⫾ 21
pH 7.28 ⫾ .09
45.0 ⫾ 16.1 mmHg
4.1 ⫾ 2.3
28.2 ⫾ 8.7
121 ⫾ 24
68 ⫾ 11
97 ⫾ 26
0.11 (.04-.19)*
20.5 (8-33)†
4.0 (3-5)‡
9.8 (4-14)§
51 (31-71)#
29 (19-40)㛳
20 (11-29)**
WIGDER ET AL ■ PRESSURE SUPPORT NPPV TREATMENT OF PULMONARY EDEMA
pressure 120/70, heart rate 130 beats/min, and respiratory
rate 32 breaths/min. Despite intensive medical treatment
and full mask pressure support ventilation, she continued to
deteriorate. After 1 hour of treatment, a clinical decision
was made to endotracheally intubate her. ABG drawn before intubation (but not available at the time of intubation)
showed pH 7.07, paCO2 77, and paO2 145. Patient 2 was a
77-year-old man with a history of COPD and CHF. He
presented with a Borg score of 10 (maximal breathing
exertion). Vital signs were blood pressure 172/89, heart rate
103 beats/min, and respiratory rate 28 breaths/min. Initial
ABG showed pH 7.11, paCO2 81, paO2 42, SaO2 59% on
Fi02 100%. After 40 minutes of intensive medical treatment
including 30 minutes of full mask pressure support ventilation, the patient became unresponsive and bradycardic necessitating ETI.
The effectiveness of NPPV may differ significantly between emergency patients presenting with acute CPE and
those presenting with COPD. Therefore, patient selection
for NPPV may be critical to its success. In our series, the
only 2 treatment failures were patients with concomitant
severe COPD. These results differ from Meduri et al who
intubated 4 of 9 (44%) cardiogenic pulmonary edema patients, but only 9 of 51 (18%) COPD with acute exacerbation patients. However, in Meduri’s series, 11 of 27 (41%)
COPD with pneumonia patients required intubation as did 6
of 12 (50%) COPD with congestive heart failure patients.3
In addition to oxygenation and ventilation, patients can
be treated with medication nebulizers while on NPPV. Although theoretically possible, pneumothorax was not reported as a complication in the study by Meduri et al.
Our study is a pilot study limited by the number of
patients enrolled. However, this series is the largest number
of CPE patients reported using pressure support supplied by
a conventional volume ventilator and full face mask, and the
only such series of ED patients. A larger comparative trial
would provide additional information about the efficacy of
NPPV in ED pulmonary edema patients. Future research is
needed to compare pressure support ventilation against
CPAP and BiPAP for treatment of CPE in ED patients.
181
SUMMARY
Ventilatory support without ETI using full face mask and
volume ventilator is an effective treatment for CPE. Pressure support NPPV in the ED is feasible and may help
prevent ETI.
The authors are indebted to Nancy Cipparone and Mary Dahlman of
the Lutheran General Hospital Research Institute for statistical analysis and to Jane Hynes for manuscript preparation.
REFERENCES
1. Meduri GU: Noninvasive positive-pressure ventilation in patients with acute respiratory failure.Clin Chest Med 1996;17:526-528
2. Antonelli M, Conti G, Rocco M, et al: A comparison of noninvasive positive-pressure ventilation and conventional mechanical
ventilation in patients with acute respiratory failure. N Engl J Med
1998;339:429-435
3. Meduri GU, Turner RE, Abou-Shala N, et al: Noninvasive positive pressure ventilation via face mask, First-line intervention in
patients with acute hypercapnic and hypoxemic respiratory failure.
Chest 1996;109:179-193
4. Rasanen J, Heikklia J, Downs J, et al: Continuous positive
airway pressure by face mask in acute cardiogenic pulmonary
edema. Am J Cardiol 1985;55:296-300
5. Bersten AD, Holt AW, Vedig AE, et al: Treatment of severe
cardiogenic pulmonary edema with continuous positive pressure
delivered by face mask. N Engl J Med 1991;325:1825-1830
6. Rusterholtz T, Kempf J, Berton C, et al: Efficacy of facial mask
pressure support ventilation (FMPSV) during acute cardiogenic pulmonary edema: A descriptive study. Am J Respir Crit Care Med
1995;151:A422 (abstr)
7. Sachetti AD, Harris RH, Paston C , et al: Bi-level positive
airway pressure support system for use in acute congestive heart
failure: Preliminary case series. Acad. Emerg. Med 1995;2:714-718
8. Pollack CV, Torres MT, Alexander L: A feasibility study of the
use of BI-PAP respiratory support in the emergency department.
Ann Emerg Med 1996:27:189-192
9. Keenan SP, Kernerman PD, Cook DJ, et al: Effect of noninvasive positive pressure ventilation on mortality in patients admitted
with acute respiratory failure. A meta-analysis. Crit Care Med 1997;
25:1685-1692
10. Wood KA,Lewis L, Von Hartz B, et al: The use of noninvasive
positive pressure ventilation in the emergency department. Chest
1998; 113:1339-1346
11. Pang D, Keenan SP, Cook DJ, et al: The effect of positive
pressure airway support on mortality and the need for intubation in
cardiogenic pulmonary edema. Chest 1998; 114:1185-1192
Noninvasive pressure support ventilation (NIPSV) with
face mask in patients with acute cardiogenic pulmonary
edema (ACPE)
T. Rusterholtz A1, J. Kempf A1, C. Berton A1, S. Gayol A1, C. Tournoud A1, M. Zaehringer A1, A. Jaeger
A1, P. Sauder A1
A1 Service de Réanimation Médicale et Centre Anti Poisons, Hôpitaux Universitaires de Strasbourg,
Strasbourg, France
Abstract
Objectives: To assess (1) the short-term hemodynamic, respiratory and arterial blood gas effects of NIPSV
in patients with ACPE who were likely to require endotracheal intubation, (2) the initial causes of failure and
(3) the side effects and the difficulties of this technique. Design: Uncontrolled, prospective clinical study.
Setting: Teaching hospital intensive care unit. Patients: 26 consecutive patients with severe ACPE.
Interventions: Noninvasive ventilation via a face mask, using a pressure support mode (20.5 - 4.7 cmH2O),
with an initial fractional inspired oxygen of 93.0 - 16 % and a positive end-expiratory pressure of 3.5 - 2.3
cmH2O. The need to intubate the patients within 48 h was considered as a criterion of failure of the
procedure. Measurements and results: Clinical and biological parameters were measured at 15 and 30
minutes, 1 h and 2 h and at 1 h and 2 h, respectively. There were 5 (21 %) failures and 21 (79 %)
successes. In both the success and the failure groups, clinical and blood gas parameters improved at the
first measure. In the success group, within 15 min of the start of NIPSV, pulse oximetry saturation (SpO2)
had increased from 84 - 12 to 96 - 4 % (p < 0.001), the respiratory rate (RR) had decreased from 36 - 5.3 to
22.4 - 4.9 breaths/min (p < 0.0001) and within 1 h the arterial oxygen tension and pH, respectively, had
increased from 61 - 14 to 270 - 126 mmHg (p < 0.0001) and from 7.25 - 0.11 to 7.34 - 0.07 (p < 0.01) and
the arterial carbon dioxide tension (PaCO2) had decreased from 54.2 - 15 to 43.4 - 6.4 mmHg (p < 0.01).
There were no statistical differences between the success and failure groups for the initial clinical
parameters: SpO2, RR, heart rate, mean arterial pressure. The only differences between the success and
failure groups were in the PaCO2 (54.2 - 15 vs 32 - 2.1 mmHg, p < 0.001) and the creatine kinase (CPK)
(176 - 149 vs 1282 - 2080 IU/l, p < 0.05); this difference in CPK activity was related to the number of patients
who had an acute myocardial infarction (AMI) (4/5 in the failure group vs 2/21 in the success group, p <
0.05). All patients with AMI in the failure group died. Conclusion: Among patients in acute respiratory failure,
those with severe ACPE could benefit from NIPSV if they are hypercapnic, but NIPSV should be avoided in
those with AMI.
Intensive Care Med. 1999 Jan;25(1):21-8.
. . . R&me’s
. . . . . . . . .des
. . . .communications
. . . . . . . . . . . . . . . or-ales
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..----------------------,PNElJMOLOGlE
ENQUETE
MULTICENTRIQUE
SUR L’ASTHME
AIGU
DE
L’ADULTE
AUX URGENCES
: RESULTATS
PRELIMINAIRES.
& Salmeron, & Ellrodt, & Liard, --1_--p.
D. Edkharrat
J.F. Muir F. Neukirch
pour le groupe ASUR (SFUM, SPLF, INSERM U 408).
ASUR cst une enqu&te prospective
de I’asthme aigu de l’adulte aux
ureences. BasCe sur une feuille d’observation
sdcifiaue.
elle conceme
eservices
d’urgences
en France (CHU et CgG) et g &buk? en avril
1997 pour une durkc de un an.
Au cows des 6 premiers mois, 2652 tpisodes ont Bti inclus. L’analyse
prkhminaire
portant sur 956 dossiers retrowe
43 % d’hommes,
Bge
moyen 41 f 18 ans ; 32 % des Patients ont &tC hospitalis&
au tours de
l’annke priddente.
Un traitement de fond Ctait pris dans 70 % des cas
(corticoides
inhales 48 %, cromones
21 %, 02 agomstes
de longue
duke 19 %, thkophyllme
14 %, anticholinergiques
5 o/o).
Avant la prise en charge aux urgences, une intervention
mCdicalc a Bt6
rkaliske dans 42% cas et 7% des patients ont bknt?ficie d’un transport
m&dicalist.
La crise &it de survenue brutale (< 24 h) dans 426 cas
(45 8) et subaiguti (> 24 h) dans 530 cas (55%). Un facteur dkclenchant
a 6te retrow
dans 78% des cas. Le traitement
prkhospitalicr
a
comport6
des I32 agonistes
dans 363 cas (38%) et des corticoides
systkmiques
dans 204 cas (21%). Le DEP B l’arrivke
Btait de 225 f
107 Wmn, la PaC02 de 38.6 f 7,9 mmHg, temolgnant
de la relative
sCvCritC des crises.
L,e traitement instituk aux urgcnces a &e : nkbulisatlon
de 82 agonistes
89 %, d’anticholincrgiques
38 %, corticoTdes
systtmiques
58 %,
thbophylline
0.8 8.
Aprks une p&ode d’observation
d’environ
deux heures, 512 patients
(53 %) ont &k hospitalis&
dent 11 % en Reanimation.
La dur&e
moyenne d’hospitalisatlon
a &e de 6 f. 5 jours.
Ces donnkes soulignent
la friquence
de l’asthme aigu de l’adulte aux
urgences et devraient permettre de mieux adapter la prise en charge et
les mesures de prkvention.
*Travail
realis sous l’tgide de la Soci&t Francophone
des Urgences
MCdicales
et de la Soci&
de Pneumologie
de Langue Frangaise avec
le partenariat des laboratoires
Boehringer Ingelheim France.
EVALUATION
DUN PROGRAMME
D’AMELlCRATlCN
DE LA QUALlTE
DE PRlSE EN CHARGE DES PATIENTS ASTHMATKXJES
ADULTES
AUX URGENCES.
J.P. BAL C. CHOUAlD,
B. HCUSSlZ
J. CAUDRON
sen/ice&
tJrgenBcentreHospitdier-4oavenuede
verdun94ooo
Cl-bteil
D&but6
en 1995
ce programme
a et& d&veloppb
en
plusieurs
Btapes.
L’objectif
de
ce
programme
est
I’amblioration
de
la prise
en
charge
des
patients
asthmatiques
adultes
aux urgences.
A I’issue
d’un audit
initial (AO) un protocole
local a Bt& &4abor&
et valid&
Un
28me
audit
(Al)
6 mois plus tat-d a mesure
I’impact
du
protocole
et fait I’objet
d’une
premiere
mise au point.
Un
38me audit (A2) a BtB realis&
16 mois plus tard.
RBsultats
: Deux types d’items
ont 6% releves
au tours
de
chaque
audit : ceux ayant
trait B la qualit&
de la prise
en
charge
therapeutique
; et ceux qui refletent
la qualitk
du
q
I ’
LA VENTILATION
NON INVASIVE
(WI)
DANS L’ASTHME
AIGU
GRAVE
: UNE NOUVELLE
ATTITUDE
THERAPEUTIQUE
? A
PROPOS DE 2 CAS. F. Thys. J. Roeseler. E. Marion Ph. Mew. A. El
Gariani. E. Dame. P. Matte. L. Jacquet. M.S. Revnaert
Cliniques
Universitaires
Saint-LUG, Urgences, 1200 Bruxelles, Belgique.
L’utilisation de la VNI dans l’asthme aigu est rapport&e par Meduri et ~01.1
dans une Ctude ouverte, non contrbke.
Nous rapportons
2 observations
d’asthme aigu grave dont I’Bat clinique, gazomktrique,
neurologique
et
asucultatoire
s’aggravent
sous traitement
bien conduit
et posent
l’indication d’une intubation et de ventilation artificielle. Cette demikre a
pu hre hit& suite B l’application de la VNI B 2 niveaux de pression (PEP:
4cmH~0,
PIP:lScmH~O)(Ventil+,
Sefam,
Nancy).
Les
rkultats
hCmodynamiques
et gazom&riques
des 2 patients (I/2) sent repris dam le
Dam nos observation,
il est intkessant
de souligner chez ces patients
prksentant
une nette d&gradation clinique et gazom&rique
malgrk un
traitement medical bien conduit, la rapiditd de I’amklioration
sous VNI
(<de 2h). Dans l’bat actuel de notre expkience,
ces observations
favorables apportent un argument supplementaire
pour proposer la VNI
comme traitement
complCmentaire
de l’asthme aigu grave avec les
rkserves qui s’imposent d ce stade d’investiaation.
VENTILATION
F. RENOUX,
J.C. DUCREUX,A.
DES OEDEMES
CANNAMELA
- CHG ROANNE - 42300 ROANNE.
Intrcduction : C&e &de r&respective me& sur 3 am a pour obiectif
d’&aluer d’une part I’efficaciti et de &gager les faeteun init&
de t&me
r&mme i la VNI clans la prise en charge initiile des OAP cardicgkiques.
Rksultats : L&dude a port6 sur 52 patients (ige = 73,4 f 9.0 ans) en
OAP eardiog~ique s&&e (FR = 33,6 f 6,5&n. ; P&O2 = 43,8 i 15,2mmHg
pH = 7,36 + 0,l l), avec VNl (VSPEP 13 fois a VSAIPEP 39 &is) dam I’heure
s&ant k&i&m
La VNI se& d permise une r&up&aticm compkte dans 38
cas (1 lh f 9h), 7 patients sur les 14 khecs ant 6tti intut& dent 5 sent d&&s.
L’analyse statistique des diffkmts
sow groupas (comparaison
de deux
pourcentages par la mkthode cles factoriels, test t de Student-Fisher, Chi 2
con@, &I& de variance) a montrk que d&s la prise en charge, l’hypercapnie
&ait corrklb avec la mortaliti (p<O,OOl). Apr&s la premibre &awe de VNI
(2,3h * 1.9h) la FR, la FC et la TA moyenne (TAm) scat &alement corr&es
avec la mortalitk @<O,OOl).
Fact morttii
N
1 P&02-av
1 FR-ap
1 FC-np
1 TAm-ap
P
R.&m Urg-1998 ; 7 : 118-60
P. BEURET,
SA U - REANMTION
Global
En conclusion
: la mise en place,
selon
une mOthodologie
participative,
d’un protocole
local de traitement
de I’asthme
aux urgences,
amBliore
de fapon durable
la prise en charge
de ces malades.
NON RWASIVE (VNI) EN PHASE INITIALE
AlGUS PULMONAlRJiS (OAP)
52
40/57
co,01
22/27
~O,oo I
92/112
94177
<o,oo 1
CO,001
L&u& de variabiliti avant et ap&s la premike sknce de VNI montre que seule
l’am6lioration de la PC est Ii&z au pronostic @<O,OOl dam le groupe vivant
contre p = 0,5 dans le groupe d&d&). Par ailleurs, la persistance d’une FC
Clevke ou d’une TAm basse satt des facteurs d’khec de VNI @<O,Ol et p<O,OS).
Dam le groupe VNI seule (sue&), contraiau gmupe VNI-IOT (k&c),
on constate une am&oration d&s la fin de la premiere s&we de la FR = 34 * 7
vs 22 f 4hin. (P<O,OOl) ; PaOl = 63 i 24 vs 119 f 4OmmHg @<O,OOl) ; FC =
113 f 25 vs 96 i 16/min. (P<O,OOl) ; TAm = 105 + 24 vs 91 f 19mmHg.
Conclusion : Si la VNI ne semble pas modifier la dur& totale
d’hospitalisation 27 f 45 jours, elle pennet dans 73% des cas d’&iter l’intubation
avec retour i Pitat de santk antkieur. L’absence d’anklioraticn de la FR, FC et
de la Tam et a fortiori l’aggravation de la FC ou de la Tam apris la premike
s&uwe de VNI (&s Ia 2& heure) pourrait faire press&k
la nkessit6
d’intubation et signifier le mauvais pronostic.
Ventilatory and hemodynamic effects of continuous
positive airway pressure in left heart failure
F Lenique, M Habis, F Lofaso, JL Dubois-Rande, A Harf and L Brochard
Physiology Departement, INSERM U296, Henri-Mondor Hospital, Creteil, France.
Abstract
The ventilatory and hemodynamic effects of continuous positive airway pressure (CPAP)
delivered via a face mask (at 0, 5, and 10 cm H2O, and after a return to 0 cm H2O) were
studied in nine patients with acute left heart failure (pulmonary artery occlusion pressure
[PAOP] > or = 18 mm Hg, and cardiac index [CI] < or = 2.8 L/min/m2). CPAP at 10 cm H2O
induced an improvement in lung compliance (60 +/- 10 ml/cm H2O to 87 +/- 20 ml/cm H2O,
p < 0.05) and in lung and airway resistance (5.7 +/- 1.0 cm H2O/L/s to 3.4 +/- 1.0 cm
H2O/L/s, p < 0.05), a reduction in work of breathing (18 +/- 3 J/min to 12 +/- 2 J/min, p <
0.05), and in the pressure-time index of the respiratory muscles (279 +/- 22 cm H2O/s/min to
174 +/- 25 cm H2O/s/min, p < 0.05), without significant changes in breathing pattern. Despite
a significant reduction in the negative swings in intrathoracic pressure (15.2 +/- 1.9 cm H2O
to 10.8 +/- 1.8 cm H2O, p < 0.001), no significant change was observed in CI or stroke
volume during CPAP. However, mean transmural filling pressures decreased significantly
with CPAP, suggesting a better cardiac performance. Neither the level of stroke volume nor of
PAOP, was predictive of changes in CI or in stroke volume. In patients with respiratory
insufficiency caused by congestive heart failure (CHF), CPAP reduces respiratory muscle
effort without altering cardiac output. The slight decrease in mean transmural left and right
atrial pressures suggests an improvement in cardiac performance.
Am. J. Respir. Crit. Care Med., Vol 155, No. 2, 02 1997, 500-505.
Effect of nasal continuous positive airway pressure on
cardiac output and oxygen delivery in patients with
congestive heart failure
DM Baratz, PR Westbrook, PK Shah and Z Mohsenifar
Department of Medicine, Cedars-Sinai Medical Center, University of California, Los Angeles.
Abstract
We studied the acute hemodynamic effects of increasing nasal continuous positive airway pressure (CPAP)
in 13 patients with acute decompensation of congestive heart failure. Heart rate, respiratory rate, pulmonary
capillary wedge pressure, right atrial pressure, systemic blood pressure, and thermodilution cardiac outputs
were measured at baseline, during, and after application of nasal CPAP at increasing pressures of 5, 10,
and 15 cm H2O. Cardiac index, stroke volume, and oxygen delivery were calculated. Based on a significant
change in cardiac output greater than or equal to 400 ml, seven patients were classified as responders,
whereas six patients were considered to be nonresponders. In responders, significant increases were noted
in cardiac index (2.5 +/- 0.7 to 2.9 +/- 0.9 L/min/m2), stroke volume (49 +/- 15 to 57 +/- 16 ml), and oxygen
delivery (10.3 +/- 5.1 to 12.3 +/- 6.0 ml/min/kg) without a change in pulmonary capillary wedge pressure. In
contrast, the nonresponders showed no significant change in any of the hemodynamic parameters.
Improvement in cardiac output could not be predicted by any of the baseline hemodynamic or clinical
variables, nor was it related to random variations since all variables returned to baseline after cessation of
CPAP. Increase in stroke volume without a change in pulmonary capillary wedge pressure (preload)
suggests either improved inotropic function of the left ventricle or reduced left ventricular afterload with
CPAP. Thus, CPAP may offer a new noninvasive adjunct to improving left ventricular function and
augmenting cardiac performance in a subset of patients with congestive heart failure.
Chest, 1992; 102, 1397-1401
Ann Fr Anesth
R&mim
0 Elacvier.
Paris
1999
: IX : 35 l-3
Cas clinique
Traitement d’un aedcme pulmonaire cardioghique
par ventilation en
pression positive continue par l’intermbdiaire
d’une canule CopaT”
C. Avril-Chaize,
Srn~ice
d ‘rrnrsthc;sir-rCa~7i77i~~tion
chi,ur,qiu/e
II. CHRU.
J.P. E&be*,
h6pital
RBSUMB
Le CopaTM ou cuffed oropharyngeal
airway a des indications se situant entre celles du masque facial et celles de
la sonde endotracheale.
Nous I’avons utilise pour la ventilation chez une patiente atteinte d’un cedeme pulmonaire
cardiogenique
grave. I/ a permis une suppleance ventilatoire efficace en pression positive continue, evitant ainsi
I’intubation. Sa facilite de mise en place et I’absence de
stimulation laryngee le rendent interessant pour la prise en
charge ventilatoire de patients en decompensation
cardiaque aigue. II existe deux limites a cette technique : I’absence de protection des voies aeriennes profondes contre
le reflux du contenu gastrique, la contre-indique
dans la
ventilation prolongee, et I’impossibilite de deglutir, incompatible avec un &at de conscience normal. Cette nouvelle
canule pourrait constituer une premiere &ape, avant I’intubation tracheale, pour debuter la reanimation des insuffisances respiratoires aigues, dont I’etiologie laisse supposer une amelioration
rapide. 0 1999 Elsevier, Paris
canule oropharyngbel
/ cedltme pulmonaire
CopaTM /ventilation
mkanique
ABSTRACT
Treatment
of severe cardiogenic
pulmonary
oedema
with continuous
positive airway pressure
via a cuffed
oropharyngeal
airway (Copa’“).
We report the use of a cuffed oropharyngeal
airway (CopaTM), in a patient with an acute respiratory failure from a
cardiogenic
pulmonary oedema, for continuous
positive
pressure ventilation. Considering the ease of use and the
lack of laryngeal stimulation, this device can be considered
HAtel-Dim,
C. hoffey
2. rue de I’Hcitrl-Diru,
35000
Rennes,
Ftmcr
for mechanical ventilation in selected cases with acute cardiac failure. There are two contra-indications:
prolonged
mechanical ventilation, because of the lack of airway protection from gastro-oesophageal
reflux, and normal consciousness, as the patient cannot swallow. This device can
be considered
when starting intensive therapy including
mechanical
ventilation in patients with acute respiratory
failure of foreseen short duration. 0 1999 Elsevier, Paris
cuffed oropharyngeal
ventilation
/ pulmonary
airway / CopaTM
oedema
I mechanical
Le CopaTM (cuffed oropharyngeal airway), mis au
point par Greenberg en 1995 [ 11, se presente comme
une canule de Guedel munie d’un ballonnet gonflable de grand volume (25 a 40 mL) qui assure l’etancheite du systeme dans l’oropharynx. Elle es. munie
d’un raccord standard de 15 mm qui permet le raccordement a un circuit de ventilation
mecanique.
Pour les adultes, quatre tailles, de 8 a 11 cm de longueur, sont actuellement disponibles. Ce nouveau
dispositif a recemment fait son apparition en anesthesie [2]. Ses indications sont cornparables <i celles
du masque larynge. Nous l’avons utilise pour la premiere fois chez une patiente en decompensation cardiaque gauche avec cedeme aigu pulmonaire (OAP),
necessitant quelques heures de ventilation
artificielle.
OBSERVATION
Une femme de 82 ans etait hospitalisee pout’ un bilan d’anevrisme de l’aorte abdominale comprenant
entre autres une scanographie et une arteriographie.
Ses ant&dents
mt!dicaux itaient we miliaire tuberculeuse et une myocardiopathie
ischCmique compliquie, I’annCe prkckdente, d’un infarctus du myocarde ant&o-septo-apical
et, quelques mois plus
tnrd. d’une dCcompensation cardiaque gauche condcutive ?I un arr&t brutal du traitement diurktique. Le
bilan objectivait
une insufflsance r&ale mod&e
(clairance de la crCatinine : 036 mL .min-‘) associCe
in une altkration de la fonction syxtolique du ventricule gauche (fraction d’k.jection du ventricule gauche d&ermide
en &hocardiographie
2 30 o/r). stable
sous un traitement associant diurCtique. inhibiteur de
l’enzyme dc conversion et d&iv& nitrCs.
Au tours de I’artCriographie
est apparu un OAP
&v&e rksistant au traitement par furosCmide (60
puis 80 mg),
saignke
( I SO mL),
dobutamine
(S lLg.kg- ‘.min ‘) et d&ivPs nit& (I puis 2 mg.h- ’ 1.
Deus hew-es apr&s I’arGriographie,
I’ECG ne montrait pas de modification du tracd initial et les enzy11~s cardiaques s’avkraient nor-males. La d&ompensation cardiaque par surcharge osmotique provoquCe
par l’in.jection
de produit de contraste (bolus
de
290 mL de produit
de contraste
hexa-iodChydrosoluble, contenant 320 mg,mL’
d’iode) Ctait
Pvoquie. Des troubles de la conscience (somnoIcnce, absence de rtponse verbale et hypotonie) en
rapport avec une hypercapnie majeure (PaCO, h
95 mmHg pour une PaO, h 74 mmHg) imposaiknt
une assistance ventilatoire.
Un Copa’r” (longiieiir
9 cm) a CtC mis en place. La facilitC de la mancruvre
a per’nis le maintien de la patiente en position assise. Aprks gontlage du ballonnet avec XI mL, d’ail
environ. la ventilation assistke en pression positive
continue a pu s‘effectuer sanb contrainte (pression de
crcte infkrieure il 25 cmH,O) ni fuite, vCritike pal
auscultation cervicale. ni insufflation gastrique v&ifiCe par auscultation Cpigastrique (ventilateur de type
SERVO 900 D1“” en mode de pression assist@e
5 + 20 cmH,O, associk ii une PEP i3 + IO cmH$
et
;i une FIO, = IO0 %I). Initialement
la SpO, &it 5
70 % et la PETCO, h 80 mmHg. La ventilation a
pcrmis une normalisation
des constantes en 4S min
et une baisse de la MO, ii 0,4. L’hypotension
art&
rielle (passage de la pression systolo-diastolique
de
I X)/70 ii 70/N mmHg) contemporaire de la chute de
I’hypercapnie a M corrigke par la dobutamine (IO
(llg.kg ~’.rnin -I). La normalisation
de la PaOz et de
la PaCO, s’est accompagnee de la r&zupiration
d’une conscience normale. lJne heure plus lard, la
malade retirait sa canule. L’amClioration
s’est poursuivie vers la guCrison quasi compl&e en trois heures (PaO, : 90 mmHg pour un apport d’oxygkne
nasal de 3 L,min--’ et PaCO, : 45 mmH::). L’administration de dobutamine a CtC interrompue six heures plus tard. II n’y a pas eu de rCcidive. L’Cchocardiographie,
pratiquCe deux jours plus tard, Ctait
superposable aux pr&zkdentes. La patiente a repris
son traitement habitue1 et a quittC le sewice de cardiologie pour son domicile au cinquikmc jour.
DISCXJSSION
Au tours des OAP graves, I’assistance ventilatoire
est assurCe habituellement
par l’interm&liaire
d’une
intubation endotrachkale. Le masque facial a aussi
M employC & la phase prCcoce de I’OAF’ [ 3 1. L’originalit
de notre observation tient 5 I’utilisation
du
Copa”‘M pour la prise en charge ventilatoire d’une
patiente inconsciente en hypercapnie grave, saris recourir h I’intubation.
Celle-ci impose une mise en
d&zubitus dorsal et I’exposition des cordes vocales,
qui est source de disaturation, de modifications hCmodynamiques, voire de troubles du rythme [ 41. Ces
conskquences nCfastes sent dues & la stimulation laryngke. Elles ne surviennent pas lors de I’insertion
d’un masque laryngk IS]. La tolCrance du CopaFrM.
dans le cas rapportk, a semblk comparablf: B celle du
masque IaryngC. Son utilisation a permis la prise en
charge efficace de la ventilation. tout en respectant
la position assise. saris interruption
des apports
d’oxygkne et saris sti’nulation IaryngCe. (‘es avantages semblent particuli&ement
inGressarts dans un
contexte de dCfaillance cardiaque. L’utilisation
du
Copa.“” est lirnitke par le risque d’inbalation
du
contenu gastrique qui, dt’s qu’il est suspect& fera
prCf&er l’intubation
endotrachCale. P:r ailleurs,
I’impossibilit~
de dkglutition rend son utilisation incompatible avec un &at de conscience normal. En
I-absence de trouble de conscience, l’aille ventilatoire par I’interm~diaire
d‘un masque facial est indiquCe. Initialement
utilisCe en rkanimation
pour la
prise en charge des maladies neuromusc.ulaires, la
ventilation au masque facial a Cti &endue j des atteintes telles que Ies d&ompensations
dc bronchopathies chroniques
obstructives.
des OAP. des
Cchecs d’extubation
ou extubation trop prlcoce [6X]. II en ressort un bCnCfice immCdiat Cvitlent en termes de raccourcissement de la phase aigu@ de la d&
453
(‘iulule Cop’”
compensation
et d’une diminution
du nombre
d’intubations,
surtout en prksence d’une hypercapnie initiale. Le masque facial requiert un niveau de
conscience normal. car il nkessite I’acceptation et
la coopCration du patient.
Le masque laryngt? et le CopaTM sont des solutions
intermkdiaires entre le masque facial et l’intubation
endotrachkale. 11s deviennent particulibrement
ink
resbants dans les dktresses respiratoires ai@% avec
troubles de la conscience rapidement rkversibles, telles clue I’OAP ou I’extubation prCmaturCe 191. Une
autre indication en urgence pourrait @tre la suppl@ance h une intubation difficile. 11spourraient permettre d’attendre dans de meilleures conditions ventilatoires.
une aide technique OLI humaine. Ces
indications
semblent
parfaitement
adaptkes au
copa I M, dont la technique de mise en place s’apparrnte II celle de la canule de Guedel 121, alors que la
mise en place d’un masque laryngt; requiert une certaint expkrience.
CONCLUSION
En situation d’urgence, I’utilisation
du Co~a’~~ pour
le traitement de certaines dktresses respiratoires
aigui;s. en particulier I‘OAP parait intkressante. 11
pourrait. dans certains cas qu’il reste encore g Cvaluw.
constituer un nouveau palier thkapeutique
avant I’intubation.
Comme le masque IaryngC, il s&
duit par sa facilitk de tnise en place et I’absence de
traumatisme en comparaison de I’intubation endotrach6ale. 1-e Copa”‘” pourrait faire partie du matkriel
d’urgence de rkanimation
de premier secours dans
les services de mkdecine, notamment en 1’aJsence
d’une personne en mesure de pratiquer une intubation. 11sne permettent ni aspirations bronchiqdes efficaces, ni protection contre l’inhalation
gastrique.
Leur emploi se limite, aux situations de dktresse respiratoire aigu5 dont I’Cvolution est suppoke rapidement favorable ou en attente d’une intubation endotrachkale, lorsque celle-ci s’avke diffkile.
RtiFkRENCES
I Greenberg RS. Evaluation of the cuffed oropharyngeal airway in
out-patients. Poster-presentation. World Congress of Anaestheaiologists, Sydney 1996.
2 Boufilers E, Maslowski D. Menu H, Guermouche T, Theeten G,
Beague D, et al. Utilisation clinique du CopaTM (cuffed
oronharvngeal airwav). Ann Fr Anesth Reanim 199): ; 17 :
20&c). . L
.
3 Bersten AD, Holt AW, Vedig AE, Skowronski GA, Baggoley CJ.
Treatment of severe cardiogenic pulmonary oedema with
continuous positive airway pressure delivered by face nask. N
Engl J Med 1991 ; 325 : 1825-30.
4 Bruder N, Ortega D, Granthil C. ConsCquences et mcyens de
prkvention des moditications hCmodynamiques Ior! de la
laryngoscopie et de I’intubation endotrachCale. Ann FI Anesth
Rtanim 1992 ; I I : 57-7 I.
5 Hollande J. Riou B. Guerrero M. Landault C. ‘liars P.
Comparaison des effets hCmodynamiques du masque IaryngC et
du tube orotrachCa1. Ann Fr Anesth Reanim 1993 : I2 : 372-5.
6 Brochard L, Mancebo J, Wysocky M, Lofaso E Non- nvasive
ventilation for acute exacerbations of chronic ob!.tructive
pulmonary disease. N Engl 3 Med I995 : 333 : 818-22.
7 Brochard L. Lea modalit& non invasives de ventilation
micanique. Presse Med 1996 ; 25 : 1307.9.
X Abou-Shala N, Meduri U. Non-invasive mechanical \‘e ltilation
in patients with acute respiratory failure. Crit Care Met1 1996 ;
24 : 703-15.
9 Arosio EM, Conci
F. Use of the laryngeal mask airway fol
respiratory distress in the intensive care unit. Anaesthesia 199.5 :
so : 635-h.
Effectiveness of CPAP by mask for pulmonary edema
associated with hypercarbia.
Perel A, Williamson DC, Modell JH.
Abstract
We describe continuous positive airway pressure (CPAP) by mask to reduce
hypercarbia in two patients who had pulmonary edema due to congestive heart failure.
In such patients, beside reducing venous return and filling pressures, CPAP improves
compliance and decreases the work of breathing, thereby improving effective
ventilation. Hence, CPAP may be useful to combat not only hypoxemia but also
hypercarbia that is associated with pulmonary edema.
Intensive Care Med. 1983;9(1):17-9.

Cardiac and respiratory effects of continuous

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