Combination of active compression decompression
cardiopulmonary resuscitation and the inspiratory
impedance threshold device: state of the art
Ralph J. Frascone,a,cDawn Bitzcand Keith Lurieb,d
Purpose of review
Over the past decade, the combination of active compression
decompression (ACD) cardiopulmonary resuscitation (CPR)
and an impedance threshold device (ITD) has been shown to
significantly increase vital organ perfusion pressures and
survival rates in animals and humans. The purpose of this
review article is to summarize the recent advances with this
Building upon animal studies that demonstrated the benefit of
the ITD used with either ACD CPR or standard CPR (S-CPR),
four prospective, randomized clinical trials with ACD/ITD CPR
have been recently completed. One blinded, out-of-hospital
cardiac arrest trial (n = 21 patients) demonstrated that
systemic blood pressures and coronary perfusion pressures
were markedly higher when ACD/ITD CPR was used when
compared directly with ACD CPR alone. The second blinded
trial demonstrated that the combination of ACD/ITD CPR was
effective with both a facemask and an endotracheal tube (n =
15 patients). A third randomized clinical trial (n = 210 patients)
demonstrated that 24-hour survival rates for out-of-hospital
cardiac arrest were more than 65% higher with ACD/ITD CPR
than with S-CPR (P < 0.01). Neurologic function after cardiac
arrest trended higher in patients with witnessed arrest who
received ACD/ITD CPR than in those who received S-CPR
(P < 0.07). In addition, when ACD/ITD CPR was applied later
in the course of treatment, short-term survival rates were
threefold higher in patients receiving ACD/ITD CPR (44%)
than in those receiving S-CPR (14%)(P < 0.05). In that study,
patients with the greatest chance for survival—those with
witnessed cardiac arrest and an initial rhythm of ventricular
fibrillation—had a 23% 24-hour survival rate with S-CPR versus
a 58% 24-hour survival rate with ACD/ITD CPR (P < 0.01). It
should be noted that this trial was performed in a city where an
earlier study found no difference in outcomes between ACD
CPR alone and S-CPR. The fourth clinical trial was a
randomized, double-blinded study of 400 patients with
out-of-hospital cardiac arrest treated by advanced life support
personnel. All patients received ACD CPR: half were treated
with a sham ITD and the other half were treated with an active
ITD. Twenty-four hour survival, the primary endpoint, was 32%
in the active ITD group versus 22% in the sham group (P <
On the basis of the cumulative findings of these studies, it is
concluded that ACD/ITD CPR provides superior vital organ
blood flow and results in significantly higher short-term survival
rates than do ACD CPR alone or S-CPR. Use of the ACD/ITD
CPR technology optimizes perfusion of the heart and brain
during cardiac arrest and results in the highest reported
survival rates of any CPR device technology. Use of this
technology should be encouraged while additional studies are
under way to examine the potential long-term impact of this
active compression decompression, cardiopulmonary
resuscitation, inspiratory impedance threshold device
Curr Opin Crit Care 10:193–201. © 2004 Lippincott Williams & Wilkins.
From theaDepartment of Emergency Medicine, Regions Hospital, St. Paul,
Minnesota, thebDepartment of Emergency Medicine at the University of
Minnesota, St. Paul, Minnesota, thecDepartment of Emergency Medical Services,
Regions Hospital, St. Paul, Minnesota, and thedMinneapolis Medical Research
Foundation at Hennepin County Medical Center, Minneapolis Minnesota, USA
Dr. Lurie is a coinventor of the ACD CPR device and the inspiratory impedance
threshold device and founded a company, Advanced Circulatory Systems Inc., of
Eden Prairie Minnesota, to develop this technology.
Correspondence to Keith Lurie, Department of Emergency Medicine, Hennepin
County Medical Center and the University of Minnesota, 7615 Golden Triangle Dr.,
Suite A, Eden Prairie, MN 55344, USA
Tel: 952 947 9590; fax: 952 942 8336; e-mail: firstname.lastname@example.org
Current Opinion in Critical Care 2004, 10:193–201
active compression decompression
impedance threshold device
standard cardiopulmonary resuscitation
©2004Lippincott Williams & Wilkins
The concept of active compression decompression
(ACD) cardiopulmonary resuscitation (CPR) was in-
spired by a patient who was successfully resuscitated on
several occasions with the use of a common household
plunger to facilitate CPR . This led several investiga-
tors to study the potential benefit of transforming the
chest into an active bellows during CPR [2–6]. To un-
derstand the significance of the chest acting as a bellows,
one capable of forcing blood out of the chest during the
chest compression phase and drawing blood back into
the chest during the chest recoil or decompression phase,
it is first important to understand the mechanisms and
shortcomings of manual closed chest cardiac massage,
often referred to as standard CPR (S-CPR).
The purpose of S-CPR is to pump blood from the chest
to vital organs during the compression phase and to en-
hance the return of blood back into the chest during the
chest wall recoil or decompression phase. Compression
and decompression associated with S-CPR are illustrated
in Figure 1A.
With S-CPR, chest compression results in an elevation of
intrathoracic pressure and in direct compression of the
heart. Both mechanisms result in forward blood flow out
of the chest to perfuse the brain and other vital organs.
However, the effectiveness of S-CPR is largely deter-
mined by the amount of blood returned to the heart.
Blood flow back to the heart is highly dependent on the
degree of chest wall recoil . During the decompression
(or passive relaxation) phase, the chest recoils, causing a
small decrease in intrathoracic pressure (relative to at-
mospheric pressure) [5,6]. This small but important
vacuum results in venous blood return to the right side of
the heart [3,5]. S-CPR by itself is inherently inefficient,
in large part because of the lack of adequate blood return
to the thorax during the chest wall recoil phase. Blood
flow to the vital organs is severely reduced during S-
CPR, even under the best circumstances [2,3,4].
Additionally, in the vast majority of cases, the coronary
perfusion pressures during S-CPR are only marginally
adequate because the pressure gradient between the
aorta, the right atrium, and left ventricle is far from op-
timal [3,7,8]. Myocardial perfusion predominantly occurs
during the decompression phase. The difference be-
tween the diastolic aortic and the right atrial pressures
(coronary perfusion pressure) is thought to be the critical
determinant of CPR efficacy.
The American Heart Association recognized the ineffi-
ciencies of S-CPR in 2000 when they issued an updated
guideline on the performance of CPR . This guideline
reinforces the importance of the chest decompression
phase and emphasizes teaching correct decompression
while performing CPR:
Release the pressure on the chest to allow blood to
flow into the chest and heart. You must release the
pressure completely and allow the chest to return to
its normal position after each compression .
Despite these recommendations, recent studies by Auf-
derheide et al. on patients in Milwaukee, Wisconsin,
have established that even when CPR is performed by
professional rescuers, there is often incomplete chest
wall recoil . Despite training, it is difficult to perform
S-CPR correctly and allow for the chest to recoil fully
after each compression. Incomplete chest wall recoil is a
common error, especially for the overzealous rescuer.
This results in significantly less blood flow back to the
heart and reemphasizes that a device is needed to correct
this widespread problem. Follow-up animal studies have
revealed that the incomplete chest wall recoil observed
in humans results in a decrease in coronary perfusion
pressure, systemic blood pressure, and cerebral perfusion
pressure . One of the benefits of ACD CPR, as we
shall describe, is that proper use of the ACD CPR device
promotes full chest wall recoil and provides guidance to
the user in the performance of CPR.
Active compression decompression CPR increases the
naturally occurring negative intrathoracic pressure by
physically expanding the chest wall and helping it return
to its resting position (Fig. 1B). This can be accom-
plished by a hand-held device (Fig. 2A) or an automated
device (Fig. 2B). During S-CPR, the chest wall’s natural
elasticity will partially recoil from compression. Many
factors can contribute to less than optimal recoil. These
included age, brittle or broken ribs, separated or broken
sternum, barrel-shaped chest, chest concavity, and in-
Figure 1. Phases of cardiopulmonary resuscitation (CPR)
(A) Standard CPR (S-CPR). Chest compression results in an elevation of
intrathoracic pressure and in direct compression of the heart. Both these
mechanisms result in forward blood flow out of the chest. During the
decompression phase, the chest recoils, causing a small decrease in
intrathoracic pressure to return venous blood to the right side of the heart.
Incomplete recoil reduces the vacuum created during chest wall decompression.
(B) Active compression decompression (ACD) CPR uses the same compression
concept as S-CPR but increases the naturally occurring negative intrathoracic
pressure by physically lifting the chest wall and helping it return to its resting
194 Cardiopulmonary resuscitation
complete release of pressure by the performer of CPR.
ACD CPR actively re-expands the chest wall and gen-
erates the negative intrathoracic pressure needed to al-
low passive filling of the heart. By actively re-expanding
the chest wall, ACD CPR resolves many of the problems
encountered with S-CPR. There have been many clini-
cal trials with the ACD CPR device used by itself, as well
as several descriptions of how to use this device [12–26].
Over the past 13 years, this method has been extensively
evaluated in animals and humans [12–26]. Although
ACD CPR does increase vital organ perfusion and
minute ventilation when compared with S-CPR, it has
been difficult to show a consistent benefit from one city
to the next in the evaluation of the clinical benefit of this
technique in patients in cardiac arrest. In St. Paul, Min-
nesota, and Paris, France, the performance of ACD CPR
significantly increased the chances for resuscitation
[21,23]. In Paris, the use of ACD CPR more than
doubled 1-year survival compared with S-CPR .
However, the results with ACD CPR in other cities were
no different from those observed with S-CPR [24–26]. It
has been speculated that these disparities may be the
result of variability in training, a lack of on-scene ad-
vanced life support, and inexperience in the use of the
device by the emergency medical system personnel.
By themselves, both S-CPR and ACD CPR create a
vacuum in the thorax with each chest wall decompres-
sion. However, much of the potential hemodynamic ben-
efit of this vacuum is lost by the influx of inspiratory gas.
The inspiratory impedance threshold device (ITD) was
developed to prevent the influx of respiratory gases dur-
ing the decompression phase of CPR [3,5,13,27–30]. The
ITD harnesses the kinetic energy of chest wall recoil,
thereby augmenting the bellows-like action of the chest
with each compression-decompression cycle.
When the ITD is used during the active decompression
phase of CPR, intrathoracic pressures became markedly
more negative with each decompression. This small,
lightweight device containing pressure-sensitive valves
is designed to selectively impede an influx of inspiratory
gas during chest wall decompression, thereby augment-
ing the amplitude and duration of the vacuum within the
thorax. When used with S-CPR or ACD CPR, the ITD
prevents respiratory gases from entering the lungs during
the decompression phase [3,5,13,27]. The increased in-
trathoracic vacuum generated from using the ITD draws
more venous blood back into the heart, resulting in in-
creased cardiac preload, followed by improved cardiac
output and vital organ perfusion.
The ITD can be used with both a facemask (Fig. 3A)
and an endotracheal tube (Fig. 3B)  The ITD is
inserted into the respiratory circuit, between the endo-
tracheal tube or facemask and the ventilation source (eg
mouth-to-mouth, bag-valve resuscitator, transport venti-
lator). It is designed to prevent inspiratory gas exchange,
except when the rescuer is actively ventilating or the
patient begins to breathe spontaneously. The device al-
lows the rescuer to ventilate the patient without any
resistance and allows for unobstructed patient exhala-
tion. Timing lights on the device prompt the rescuer
when to ventilate. This visual aid works to avoid hyper-
ventilation, given that excessive ventilation rates have
been found to be harmful if not deadly . When CPR
is not being performed or if the patient has successfully
been resuscitated, the ITD should be removed. Sponta-
neous inspiration through the ITD is possible but may
be difficult for a recently resuscitated patient. The crack-
ing pressure, the inspiratory pressure needed to allow for
spontaneous inspiration within the device, can be varied
at the time of manufacturing. Clinical trials to date have
been performed with ITD cracking pressures between
−15 cm and −24 cm H2O. Over the past several years,
with the measure of actual intrathoracic pressures in pa-
Figure 2. Active compression decompression cardiopulmonary
resuscitation (CPR) device variations
(A) Manual active compression decompression CPR device showing the handle,
compression/decompression force gauge, and metronome. The insert shows
how to compress/decompress the chest with elbows locked and wrists rigid.
The device is attached to the sternum. By rocking back and forth, the chest can
be compressed and decompressed. (B) Automated compression
decompression device. The device is pneumatically driven. It is rapidly placed
around the patient and provides continuous compressions with active recoil of
the chest to the full resting position after each compression .
Inspiratory impedance threshold device Frascone et al. 195
tients undergoing CPR, it has become clear that a crack-
ing pressure of −7 cm H2O is adequate for standard CPR
and −15 cm H2O is adequate for ACD CPR . With
lower cracking pressures, normal subjects can breathe
through the ITD .
Since 1995, there have been multiple animal and clinical
investigations related to ACD/ITD CPR [3,5,28,29,33–
44]. The first study established the importance of the
concept . Addition of the ITD in that animal model
demonstrated a doubling of vital organ blood flow com-
pared with ACD CPR alone. The most remarkable find-
ing from this study was the discovery that blood flow to
the brain was greater in the arrested pig treated with
ACD/ITD CPR than in the prearrested pig (Fig. 4).
Compared with S-CPR alone, ACD/ITD CPR resulted
in a 300% increase in blood flow to the brain and a 400%
increase in blood flow to the heart . With S-CPR,
cerebral and cardiac perfusion was doubled by the addi-
tion of the ITD [3,5,38•]. These positive effects quickly
dissipated when the valve was taken out of the respira-
tory circuit. Subsequent animal studies have also dem-
onstrated a significant survival benefit with an associated
markedly improved neurologic function with use of the
ITD during S-CPR [38•].
The first independent, confirmed benefit of the ITD, by
Langhelle et al., demonstrated that the ITD doubled
blood flow to the heart when compared with S-CPR .
There was also a trend toward increased blood flow to
the heart with ACD/ITD CPR. However, no cerebral
blood flow benefit was observed with the ITD in this
study. The study design and/or the way the animal was
prepared may have accounted for the differences. Unlike
earlier and subsequent studies, in the Langhelle et al.
study , cerebral blood flow in the control state was
already 50% of normal. In addition, Langhelle et al. 
attached an automated piston-like device to the chest
wall with small screws and used it to achieve active com-
pression and decompression. This attachment process
may alter the elasticity of the chest and may affect out-
comes. Finally, each pig received multiple interventions,
including S-CPR and ACD CPR, with and without the
ITD. This could have increased the potential for cross-
contamination. Nevertheless, those studies still con-
firmed that the use of the ITD doubles blood flow to the
heart during CPR.
A recent study by Voelckel et al. [37•] demonstrated the
remarkable benefit of ACD/ITD CPR when compared
with S-CPR. Ventricular fibrillation was induced in 10-
kg piglets. To simulate patient “downtime,” no treat-
ment was administered for the first 10 minutes. After 10
minutes, the animals received S-CPR delivered with an
automated device, followed by ACD/ITD CPR, also de-
livered with an automated device. Mean arterial pres-
sure, coronary perfusion pressure, and end-tidal carbon
dioxide levels increased by approximately 30% when
ACD/ITD CPR was used versus S-CPR. By contrast, ce-
rebral and cardiac perfusion doubled with the addition of
ACD/ITD CPR, despite the prolonged time between
arrest and initiation of ACD/ITD CPR. This study also
demonstrates how much the measured coronary perfu-
sion pressures underestimate the actual delivery of blood
flow to vital organs.
In addition to an increase in mean arterial pressures and
cerebral blood flow, the beneficial effects of ACD/ITD
CPR can also be seen on cerebral metabolism. Bahlmann
et al.  reported on the use of ACD/ITD CPR on pigs
in hypothermic cardiac arrest. The group used microdi-
Figure 3. Impedance threshold device (ITD)
(A) ITD on endotracheal tube. (B) ITD on facemask. Lower intrathoracic pressure
in the chest during the decompression phase of cardiopulmonary resuscitation
enhances venous return to the thorax. Each time the chest wall recoils after a
compression, the ITD transiently blocks oxygen from entering the lungs, creating
a small vacuum in the chest, resulting in improved preload.
Figure 4. Porcine model of cardiopulmonary resuscitation
Addition of the impedance threshold device (ITD) demonstrated a doubling of
vital organ blood flow compared with automated compression device (ACD)
CPR alone. Blood flow to the brain was greater in the arrested pig treated with
ACD/ITD CPR than in the prearrested pig [37•].
196 Cardiopulmonary resuscitation
alysis techniques to measure metabolic intermediates,
lactate/pyruvate ratios, and glucose levels. When com-
pared with S-CPR, the use of ACD/ITD CPR resulted
in higher cerebral perfusion pressures and lower pyru-
vate/lactate ratios, indicating better oxygen delivery and
less anaerobic cerebral metabolism. Additionally, mea-
sured cerebral glucose levels were lower in animals
treated with ACD/ITD CPR, a finding consistent with a
more favorable metabolic status. These findings are con-
sistent with those in other animal and clinical trials,
where neurologic outcomes are better with the ITD sec-
ondary to improved cerebral perfusion and metabolism.
Studies by Bahlmann et al.  and Raedler et al.
 also demonstrated another important benefit of
ACD/ITD CPR. They found that the use of this device
combination enhances drug efficacy during CPR. In hy-
pothermic pigs, the effects of exogenous vasopressin
were significantly enhanced with ACD/ITD CPR, as re-
flected by higher coronary and cerebral perfusion pres-
sures and improved cerebral metabolic profiles.
Four randomized clinical trials have been performed
to date to evaluate the effectiveness and safety of
ACD/ITD CPR in humans [30,39••,40••,42••]. The
first study focused on hemodynamics in patients with
out-of-hospital cardiac arrest . All patients received
ACD CPR, the standard of care in France. A total of 10
patients were randomized, in a blinded, prospective trial,
to receive ACD CPR with a sham (nonfunctional) ITD.
Eleven patients were treated with an active (functional)
ITD. In that study, end-tidal carbon dioxide levels rose
more rapidly and reached higher levels with the active
ITD. Systolic and diastolic blood pressures were nearly
normal (109/57 mm Hg) in the active ITD group versus
89/35 in the sham ITD group. In addition, return of
spontaneous circulation occurred more rapidly in the ac-
tive ITD group than in the sham ITD group. On the
basis of these data, the use of ACD/ITD CPR was rec-
ommended as an alternative to S-CPR in the 2000
American Heart Association guidelines (Class IIb recom-
Another interesting recent study showed that the ITD
can work well when applied to a facemask [5,30]. This is
important because it indicates that inspiratory imped-
ance can be added during basic life support airway man-
agement (by first responders and, perhaps, even lay res-
cuers). In other words, the patient does not have to be
endotracheally intubated to achieve benefit from the
ITD. Therefore, inspiratory impedance would not be
limited to the intubated patient receiving advanced life
support. Additionally, this was the first study to measure
intrathoracic pressure in cardiac arrest patients undergo-
ing ACD CPR. To perform this study, Plaisance et al.
[5,30] randomized patients before endotracheal intuba-
tion for either a sham or an active ITD. A facemask and
device (either sham ITD or active ITD) was first used to
ventilate the patient. The same ITD was then used after
endotracheal intubation. Intrathoracic pressure was mea-
sured by use of an air-filled pressure transducer con-
nected to either the facemask or the endotracheal tube.
A pilot study demonstrated no difference between pres-
sures measured at the level of the cricothyroid mem-
brane and those at the facemask. As shown in the rep-
resentative tracing (Fig. 5), addition of the active ITD to
the facemask resulted in an immediate decrease in in-
trathoracic pressure during ACD CPR. In many but not
all patients, there was no discernible difference between
the pressure tracings obtained with the facemask and
those obtained with the endotracheal tube. It is impor-
tant to note that when the facemask was used to venti-
late patients, a two-person technique was used to main-
tain a tight seal between the face and the mask.
Additionally, in some patients, a greater intrathoracic
vacuum was observed when the endotracheal tube was
used. Nonetheless, each time the active ITD was used,
a significant reduction in the decompression phase intra-
thoracic pressure resulted. The active ITD helped both
the facemask and the endotracheal tube to generate an
intrathoracic vacuum during ACD CPR.
These studies demonstrated, for the first time, the de-
gree of negative intrathoracic pressure achieved with
ACD/ITD CPR in humans. The average maximum
negative intrathoracic pressure was −11 mm Hg with the
active ITD versus only −3 mm Hg with the sham ITD.
These results demonstrate how useful the ITD is in
achieving a vacuum effect during CPR. A second im-
portant finding is that it takes as many as 5 compres-
sion/decompression cycles to achieve the maximum
negative intrathoracic pressure. Moreover, each time an
active positive-pressure ventilation was delivered, the
decompression phase intrathoracic vacuum was de-
stroyed and required regeneration. Thus, the less fre-
quent the ventilation rate, the greater the blood flow
back to the heart. A recent study using S-CPR with the
ITD in pigs confirmed this important observation .
This has become an important theme for all types of
CPR: ventilations interrupt coronary perfusion pressure
and should be kept at the minimum required to maintain
ACD/ITD CPR improves survival rates after cardiac ar-
rest. A recent prospective, controlled trial was performed
in Mainz, Germany, in which the two-tiered emergency
response included early defibrillation [39••]. Patients
with out-of-hospital arrest of presumed cardiac cause
were sequentially randomized to ACD/ITD CPR or S-
CPR (the control individuals) by the advanced life sup-
port team after intubation. Patients with an initial heart
rhythm of ventricular fibrillation (42% of the total) who
Inspiratory impedance threshold device Frascone et al. 197
could not be resuscitated by basic life support early de-
fibrillation were enrolled in this clinical trial, as well as
patients with an initial rhythm of asystole or pulseless
electrical activity. Rescuers learned which method of
CPR to use at the start of each work shift. The primary
endpoint was 1-hour survival after a witnessed arrest.
With ACD/ITD CPR (n = 103), return of spontaneous
circulation and 1-hour and 24-hour survival rates were
55%, 51%, and 37% versus 37%, 32%, and 22% for S-CPR
(n = 107) (P = 0.016, 0.006, and 0.033), respectively (Fig. 6).
One-hour and 24-hour survival rates in witnessed arrests
were 55% and 41% with ACD/ITD CPR versus 33% and
23% in control subjects (P = 0.011 and 0.019), respec-
tively [39••]. One-hour and 24-hour survival rates in pa-
tients with a witnessed arrest in ventricular fibrillation
were 68% and 58% after ACD/ITD CPR versus 27% and
23% after S-CPR (P = 0.002 and 0.009), respectively, as
shown in Figure 7. Hospital discharge rates were 18%
after ACD/ITD CPR versus 13% in control participants
(P = 0.41). Overall neurologic function trended higher in
patients receiving ACD/ITD CPR than in control par-
ticipants (P = 0.07), as shown in Figure 8. Importantly,
patients randomized more than 10 minutes after the call
for help to the ACD/ITD CPR group had a greater than
three times higher 1-hour survival rate (44%) than did
control participants (14%) (P = 0.002). These time-
related benefits were observed regardless of presenting
rhythm. Neurologic outcomes in the survivors with de-
lays to treatment with ACD/ITD CPR were similar to
those who were treated with ACD/ITD CPR more rap-
idly. These important clinical data emphasize the impor-
tance of an active compression decompression device
used in combination with an ITD.
Additional support of these findings was provided by
another study recently performed in France [40••]. All
400 patients in that study received ACD CPR. ACD
Figure 5. Example of intratracheal pressures, a surrogate for intrathoracic pressures, in a patient undergoing
automated compression device cardiopulmonary resuscitation (CPR) with the impedance threshold device (ITD)
attached to a facemask vs without
CPR was delivered at 100 compression/decompression cycles/min with a synchronized compression:ventilation ratio of 15:2. (A) Use of sham ITD. (B) Use of active
ITD. Scale: −10 mm Hg to +10 mm Hg. Note the absence of significant decreases in intratracheal pressures with a sham device. With the active ITD, wide fluctuations
in intratracheal pressure are seen with each compression and decompression. After 15 compressions and decompressions, two breaths are delivered, resulting in a
slow rise in intratracheal pressures [5,30].
Figure 6. Outcomes in a comparison of standard (STD) with
active compression decompression/impedance threshold
device (ACD/ITD) cardiopulmonary resuscitation (n = 210) in
Pulse, palpable pulse with CPR; ROSC, return of spontaneous circulation;
Admiss, hospital admission; 1HrS, 1 hour survival; 24HrS, 24 hour survival;
Disch, discharge [39••].
198 Cardiopulmonary resuscitation
CPR has been the method of CPR used by the emer-
gency services in France for nearly a decade. In one arm,
200 patients were treated by advanced life support per-
sonnel with ACD CPR and an active ITD, and the other
200 patients were randomized to the control group and
received treatment with ACD CPR and a sham ITD.
The study was sized and powered from a statistical
standpoint to determine a potential difference in 24-
hour survival rates. As in other studies from France
[21,22,40••], most of the patients had an initial rhythm of
asystole. The group treated with ACD CPR and an ac-
tive ITD had a 24-hour survival rate of 32%, compared
with a 24-hour survival rate of 22% in the control popu-
lation (P < 0.05). Survival rates in both groups were very
low, but differences in neurologic function in the survi-
vors trended in favor of the ACD/ITD CPR group. Only
1/8 survivors treated with the sham device had normal
cerebral function at the time of hospital discharge versus
6/10 in the function ITD group (P < 0.07). The vast
majority of these patients, including the survivors, had an
initial heart rhythm of asystole. Despite having a rhythm
with a very poor prognosis, 32% of the patients lived for
longer than 24 hours after treatment with ACD/ITD
It has been nearly 50 years since the concept of mouth-
to-mouth resuscitation and closed chest cardiac massage
was first described. Only recently have mechanical
means been developed that are capable of achieving
nearly normal blood pressures in patients undergoing
cardiac arrest. While these patients still received low-
dose epinephrine, four recent clinical studies have dem-
onstrated the benefit of ACD/ITD CPR over S-CPR for
patients in cardiac arrest. In patients with an initial heart
rhythm of ventricular fibrillation, the vital importance of
perfusion before and after defibrillation has been dem-
onstrated by both Cobb et al.  and Wik et al. .
Priming the pump increases the chances for successful
conversion of ventricular fibrillation and for resuscitation
of nonventricular fibrillation rhythms. In addition, ani-
mal and human studies demonstrate that in patients with
prolonged cardiac arrest, regardless of the initial heart
rhythm, the use of ACD/ITD CPR has a marked im-
pact on the chances for successful resuscitation. [37•,
39••,42••] From this perspective, the improved perfu-
sion achieved with ACD/ITD CPR fits nicely into the
three phases of CPR paradigm recently described by
Weisfeldt and Becker ; after the first 5 minutes, in-
creased circulation is essential for successful resuscita-
Despite the increased perfusion achieved with
ACD/ITD CPR, most patients still die before hospital
discharge. From this perspective, the use of ACD/ITD
CPR is not a panacea. Much has been learned in recent
years about the importance of postresuscitation care.
Without additional measures to help preserve brain and
cardiac function in the postresuscitation phase, many pa-
tients will still be lost. However, recent studies suggest
that improved perfusion with ACD/ITD CPR, coupled
with hypothermia and other metabolic hibernation strat-
egies, improves measures to preserve vital organ function
after resuscitation [49,50]. This combination promises to
markedly increase the chances for survival in years to
come. A recent study by Nadkarni et al.  suggests that
the combination of ACD/ITD CPR and cooling can re-
sult in increased survival rates and jump-start the cooling
process. This may be important, given the rapidity of
cellular damage and apoptosis after cardiac arrest and
successful resuscitation in the absence of postresuscita-
Figure 7. Outcomes in patients randomized to either standard
(STD) or active compression decompression/impedance
threshold device (ACD/ITD) cardiopulmonary resuscitation
(CPR) with witnessed ventricular fibrillation in Mainz,
Germany (n = 70)
Pulse, palpable pulse with CPR; ROSC, return of spontaneous circulation;
Admiss, hospital admission; 1HrS, 1 hour survival; 24HrS, 24 hour survival;
Disch, discharge [39••].
Figure 8. In patients randomized to treatment with standard
(STD) CPR, neurologic outcomes tended to be worse in
comparison with active compression
decompression/impedance threshold device (ACD/ITD)
treatment in a study from Mainz, Germany
Overall performance category (OPC), overall performance category score. OPC
of 1 = normal neurologic function. OPC of 2 = mild neurologic deficit. OPC
1/2 = patient scored either a 1 or a 2 [39••].
Inspiratory impedance threshold device Frascone et al. 199
tive care that includes some form of metabolic preserva-
The ITD was recently approved as a circulatory en-
hancer device by the United States Food and Drug Ad-
ministration. The ACD CPR device has not yet been
approved. The ITD can be used with any method of
CPR that involves external chest compression. On the
basis of the study from Mainz, Germany, widespread use
of ACD/ITD CPR in patients with a witnessed, out-of-
hospital, ventricular fibrillation cardiac arrest could in-
crease 24-hour survival rates by an additional 100,000
patients out of the 300,000 patients known to die each
year in Europe and North America [39••]. When
coupled with improved postresuscitation care, the poten-
tial impact of widespread use of this technology on the
number one cause of death in adults could be striking
Modern, rigorous, scientific methods have been used to
study ACD/ITD CPR—a scrutiny S-CPR has not under-
gone. This device combination has given researchers
new hope for finally realizing a CPR technique that is
superior to S-CPR. The present data support the wide-
spread use of this new technology. Ongoing clinical trials
will help determine the effect of ACD/ITD CPR use
on hospital discharge rates and neurologic outcomes.
References and recommended reading
Papers of particular interest, published within the annual period of review,
have been highlighted as:
•Of special interest
•• Of outstanding interest
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200 Cardiopulmonary resuscitation
35 Download full-text
Lurie KG, Voelckel W, et al.: Improving S-CPR with an inspiratory impedance
valve in a porcine model of cardiac arrest. Anesth Analg 2001, 93:649–655.
pressure during active compression decompression cardiopulmonary resus-
citation with the inspiratory threshold valve. Anesth Analg 2001, 92:967–
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Lurie KG, Zielinski T, et al.: Use of an inspiratory impedance valve improves
neurologically intact survival in a porcine model of ventricular fibrillation. Cir-
culation 2002, 105:124–129.
Use of the impedance threshold device with standard CPR significantly increased
survival rates and neurologic function in pigs in cardiac arrest compared with those
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24-hour survival rates were 58% with the device combination and only 23% with
standard manual CPR.
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compression decompression CPR in a randomized blinded prospective clinical
trial demonstrated a 45% improvement in 24-hour survival rates for all patients.
Only 1 of 8 survivors in the sham device group had normal neurologic function at
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