Evaluation of LUCAS, a new device for automatic mechanical compression and active decompression resuscitation

Article (PDF Available)inResuscitation 55(3):285-99 · December 2002with231 Reads
DOI: 10.1016/S0300-9572(02)00271-X · Source: PubMed
Abstract
LUCAS is a new gas-driven CPR device providing automatic chest compression and active decompression. In an artificial thorax model, superior pressure and flow were obtained with LUCAS compared with manual CPR. In a randomized study on pigs with induced ventricular fibrillation significantly higher cardiac output, carotid artery blood flow, end-tidal CO(2), intrathoracic decompression-phase aortic- and coronary perfusion pressures were obtained with LUCAS-CPR (83% ROSC) compared to manual CPR (0% ROSC). In normothermic fibrillating pigs, the ROSC rate was 100% after 15 min and 38% after 60 min of LUCAS-CPR (no drug treatment). The ROSC rate increased to 75% if surface cooling to 34 degrees C was applied during the first 30 min of the 1-h resuscitation period. Experience with the first 20 patients has shown that LUCAS is light (6.5 kg), easy to handle, quick to apply (10-20 s), maintains a correct position, and works optimally during transport both on stretchers and in ambulances. In one hospital patient with a witnessed asystole where manual CPR failed, LUCAS-CPR achieved ROSC within 3 min. One year later the patient's mental capacity was fully intact. To conclude, LUCAS-CPR gives significantly better circulation during ventricular fibrillation than manual CPR.
Evaluation of LUCAS, a new device for automatic mechanical
compression and active decompression resuscitation
Stig Steen , Qiuming Liao, Leif Pierre, Audrius Paskevicius, Trygve Sjo
¨
berg
Department of Cardiothoracic Surgery, Heart-Lung Division, University Hospital of Lund, SE-221 85 Lund, Sweden
Received 4 April 2002; received in revised form 29 April 2002; accepted 26 July 2002
Abstract
LUCAS is a new gas-driven CPR device providing automatic chest compression and active decompression. In an artificial thorax
model, superior pressure and flow were obtained with LUCAS compared with manual CPR. In a randomized study on pigs with
induced ventricular fibrillation significantly higher cardiac output, carotid artery blood flow, end-tidal CO
2
, intrathoracic
decompression-phase aortic- and coronary perfusion pressures were obtained with LUCAS-CPR (83% ROSC) compared to manual
CPR (0% ROSC). In normothermic fibrillating pigs, the ROSC rate was 100% after 15 min and 38% after 60 min of LUCAS-CPR
(no drug treatment). The ROSC rate increased to 75% if surface cooling to 34 8C was applied during the first 30 min of the 1-h
resuscitation period. Experience with the first 20 patients has shown that LUCAS is light (6.5 kg), easy to handle, quick to apply
(10
/20 s), maintains a correct position, and works optimally during transport both on stretchers and in ambulances. In one hospital
patient with a witnessed asystole where manual CPR failed, LUCAS-CPR achieved ROSC within 3 min. One year later the patient’s
mental capacity was fully intact. To conclude, LUCAS-CPR gives significantly better circulation during ventricular fibrillation than
manual CPR.
# 2002 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Active compression /decompression; Cardiopulmonary resuscitation (CPR); Coronary perfusion pressure; End-tidal carbon dioxide;
Hypothermia; Return of spontaneous circulation (ROSC)
Resumo
LUCAS e´umnovo aparelho de RCP que funciona com ga´s e que faz compressa
˜
o tora´cica automa´tica e descompressa
˜
o activa.
Num estudo randomizado em porcos com fibrilhac
¸
a
˜
o ventricular induzida foram estudados o de´bito cardı´aco, fluxo sanguı´neo da
arte´ria caro´tida, CO
2
no final da expirac
¸
a
˜
o e presso
˜
es de perfusa
˜
o corona´ria e ao´rtica na fase de descompressa
˜
o intratora´cica , que se
verificou serem significativamente mais elevadas com a RCP com LUCAS (83% ROSC) quando comparado com RCP Manual (0%
ROSC). Em porcos normote´rmicos em fibrilac
¸
a
˜
o a taxa de ROSC foi 100% ao fim de 15 min e 38% ao fim de 60 min de RCP-
LUCAS (sem tratamento farmacolo´gico). A taxa de ROSC aumentou para 75% se fosse aplicado arrefecimento superficial ate´ aos
34 8C nos primeiros 30 min da primeira hora do perı´odo de reanimac
¸
a
˜
o. A experieˆncia com os primeiros 20 doentes mostrou que o
LUCAS e´leve (6.5Kg), fa´cil de manejar, ra´pido de aplicar (10
/20 s), mante´m uma posic
¸
a
˜
o correcta e trabalha de forma o´ptima
durante o transporte em macas ou em ambulaˆncias. Num doente hospitalar com uma assistolia testemunhada em que a RCP
manual falhou a RCP-LUCAS conseguiu ROSC em 3 min. Um ano mais tarde a capacidade intelectual do doente estava intacta.
Para concluir, a RCP-LUCAS da´ uma circulac
¸
a
˜
o significativamente melhor que a RCP manual durante a fibrilac
¸
a
˜
o ventricular.
# 2002 Elsevier Science Ireland Ltd. All rights reserved.
Palavras chave: Compressa
˜
o-descompressa
˜
o activa; Ressuscitac
¸
a
˜
oca´rdio-pulmonar (RCP); Pressa
˜
o de perfusa
˜
o corona´ria; Dio´ xido de carbono tele-
expirato´ rio; Hipotermia; Retorne de circulac
¸
a
˜
o espontaˆnea (ROSC)
Corresponding author. Tel.: /46-46-177200; fax: /46-46-177207
E-mail address: stig.steen@thorax.lu.se (S. Steen).
Resuscitation 55 (2002) 285
/299
www.elsevier.com/locate/resuscitation
0300-9572/02/$ - see front matter # 2002 Elsevier Science Ireland Ltd. All rights reserved.
PII: S 0 3 0 0 - 9 5 7 2 ( 0 2 ) 0 0 2 7 1 - X
Resumen
LUCAS es un nuevo aparato para reanimacio´n cardiopulmonar impulsado por gas que proporciona compresiones tora´cicas y
descompresiones activas automa´ticas. En un modelo de to´rax artificial, se obtuvo presio´n y flujo superiores con LUCAS comparado
con reanimacio´n cardiopulmonar manual. En un estudio randomizado en cerdos con fibrilacio´n ventricular inducida se alcanzaron
valores significativamente mayores de gasto cardı´aco, flujo de arteria coronaria, CO
2
espiratorio, presiones de perfusio´n coronaria y
ao´rtica en fase de descompresio´n con reanimacio´n con LUCAS (83% ROSC) comparado con reanimacio´n manual (0% ROSC). En
cerdos normote´rmicos en fibrilacio´n ventricular, la tasa de retorno a circulacio´n esponta´nea (ROSC) fue de 100% despue´s de 15
minutos y de 38% despue´s de 60 minutos de LUCAS-RCP (sin tratamiento con drogas).La tasa de ROSC a 75% si se aplicaba
enfriamiento superficial a 34 8C en los primeros 30 minutos de el perı´odo de una hora de resucitacio´n. La experiencia con los
primeros 20 pacientes ha mostrado que LUCAS es liviano (6.5 kg), fa´cil de usar, ra´pido para aplicar (10
/20s), mantiene la posicio´n
correcta, y trabaja o´ptimamente durante el transporte, tanto en camillas como en ambulancias. En un paciente de hospital con un
paro presenciado en asistolı´a, sonde la RCP manual fallo´, RCP-LUCAS consiguio´ ROSC en tres minutos. Un an
˜
oma´s tarde la
capacidad mental del paciente estaba intacta. Para concluir, durante la fibrilacio´n ventricular la RCP-LUCAS proporciona una
circulacio´n significativamente mejor que la RCP manual.
# 2002 Elsevier Science Ireland Ltd. All rights reserved.
Palabras clave: Compresio´n/descompresio´n activa; Reanimacio´n cardiopulmonar (RCP); Presio´n de perfusio´ n tisular; Dio´xido de carbono
espiratorio; Hipotermia; Retorno a circulacio´n esponta´nea
1. Introduction
Cardiac arrest, either as asystole or as ventricular
fibrillation (VF), is the most dramatic situation in
medicine. Since Kouwenhoven and coworkers published
their landmark article in 1960 [1], manual closed-chest
compressions (combined with mouth-to-mouth ventila-
tion) has been established as the initial treatment of
choice for circulatory arrest, followed by defibrillation
as soon as the equipment is available, if VF is the cause
of the collapse. With proper training, anyone, anywhere
can initiate cardio-pulmonary resuscitation (CPR).
However, due to fatigue, manual CPR cannot be given
for more than a few minutes before it becomes
ineffective [2], and it cannot be given effectively at all
during transport [3]. Most cardiac arrests occur out-of-
hospital and the survival rates are very poor; in most
published reports the 1-year survival rate is less than 5%.
In a randomized study, Plaisance and coworkers [4]
compared standard manual CPR (n
/377 patients) with
active compression/decompression CPR performed
manually with the CardioPump (AMBU, Copenhagen,
Denmark) (n
/373 patients). The 1-year survival rate
was very poor in both groups, 2 versus 5% (P
/0.03); all
resuscitation efforts with either method were performed
only at the scene of the cardiac arrest, and only if they
were successfully resuscitated at the scene were the
patients transported to hospital. To prevent fatigue,
the rescuers were instructed to alternate after each 3 min
of CPR. The study of Plaisance et al. demonstrates the
need for a mechanical device giving adequate compres-
sions/decompressions continuously until the patient can
be delivered to a hospital with all facilities for the
treatment of heart disease, including direct PTCA and
heart surgery.
Most devices for mechanical chest compression in use
today have operational limitations because they take too
long to apply, they are cumbersome to install and
operate, they are unstable on the chest, heavy, and
expensive to purchase [5]. Therefore, no mechanical
device for chest compression/decompression currently is
used routinely in clinical practice, in spite of the obvious
limitations of manual CPR. Recently, a new device
named LUCAS, has been made commercially available
(Figs. 1 and 2). It is designed to give automatic
mechanical chest compression and active decompres-
sion. It is portable and works during transport both on
stretchers and in ambulances.
The aim of the present investigation was to compare
the efficacy of LUCAS with that of manual compres-
sions on an artificial thorax model allowing exact
analysis of pressure- and flow-curves, and on a pig
model in which relevant physiological variables could be
registered. In an earlier study using the same pig model
we studied the effects of adrenaline (epinephrine) and
noradrenaline (norepinephrine) on end-tidal CO
2
, cor-
onary perfusion pressure and cardiac output during
cardiopulmonary resuscitation [6]. In the present study
we decided to eliminate all drug therapy in order to
elucidate the effects of chest compressions per se. Data
from the first clinical pilot study with LUCAS are also
presented.
2. Material and methods
2.1. The artificial thorax model
A 25 l plastic drum made of polyvinyl chloride (PVC)
was used as an artificial thorax (Fig. 3). A soft plastic
bag (150 ml), simulating a heart, was included in the
S. Steen et al. / Resuscitation 55 (2002) 285 /299286
drum. Pressure (P) was continuously measured in the
bag. By means of a stiff tube penetrating the tight cork
of the drum, the soft bag was connected to an artificial
circulatory system including two artificial heart valves
for flow direction. The plastic drum was filled with 20 l
water and 5 l air, and regained its original shape after
deformation. During compression of the drum manually
or by means of the LUCAS, the soft plastic bag ejected
fluid through the outlet valve (Vo) (Carbomedics aortic
valve, 25 mm Ø). To mimic the Windkessel effect of the
aorta, a side tube with trapped air (C) was included in
the system. Resistance in the flow system was generated
using a tube compressor (R), set to give a systolic
pressure of around 100 mmHg when standard manual
compressions were given by a normal-sized adult male
trained in CPR. (The degree of clamping was adjusted
on the base of pressure measurements before and after
the resistance.) The flow created by drum compression
was measured continuously by a flow probe (F),
(Transonic Systems Inc. HT207, New York, USA).
The filling pressure of the balloon (‘ventricle’) was
adjusted by letting the flow run into an open reservoir
(OR) placed at an appropriate level above the soft bag.
Between the reservoir and the connection to the soft bag
an inlet valve (Vi) (Medtronic Hall, mitral valve, 29 mm
Ø) was inserted. Flow and pressure signals were sampled
on a computer.
2.2. Manual chest compressions in the pig
Manual chest compressions were given by three male
surgeons trained in CPR and with clinical experience of
the procedure. The surgeons were of normal size with a
body weight in the range of 70
/80 kg. Each surgeon
worked in 3-min periods, compressing the lower one
third of the sternum at a target rate of 100 compres-
sions/min. The surgeons were instructed to give the
compressions with the force they would have used on an
Fig. 1. LUCAS is designed to fit on stretchers and to be easy to operate while walking and within ambulances. Defibrillator pads illustrate that
defibrillation may be done under on-going compression /decompression.
S. Steen et al. / Resuscitation 55 (2002) 285
/299 287
adult patient of normal size. The experimental protocols
are depicted in Fig. 4.
2.3. The properties of LUCAS
The LUCAS is a gas-driven device that provides
automatic mechanical compression and active decom-
pression. It consists of a silicon rubber suction cup
similar to that used in the CardioPump and a pneumatic
cylinder mounted on two legs which are connected to a
stiff back plate (Figs. 1 and 2). The cover of the
pneumatics, the legs, and the back plate are made of a
composite material that does not conduct electricity.
The system is powered by oxygen or air from a cylinder,
the gas system in ambulances or the gas outlets in
hospitals. The maximum compression depth is 52 mm
and the maximum compression force is 500 N. The
decompression force is 410 N. A regulator inside
LUCAS ensures that the same force will be obtained if
it is run on air or oxygen. The gas connector fits the
outlets for both oxygen and air and it can be used with
Fig. 2. LUCAS in place on a 23 kg pig. Due to the narrow upper thorax in pigs of this size, the silicon rubber suction cup does not fit snugly to the
chest, and active decompression cannot be adequately tested.
Fig. 3. The artificial thorax model used. P /pressure measurement
within a soft plastic bag. Vo /mechanical outlet valve. R/resistance,
regulated with a tube compressor. C/compliance (Windkessel effect),
regulated by an air-filled side tube. F /flow measured continuously by
a flow probe. OR
/open reservoir for regulation of filling pressure.
Vi/a large inlet valve for rate-unlimited filling of the bag during the
decompression phase.
S. Steen et al. / Resuscitation 55 (2002) 285
/299288
gas sources with pressures ranging from 4 to 7 bar (400/
700 kPa). The default setting for the compression/
decompression frequency is 100 per minute. The height
of the suction cup can be adjusted to fit patients with an
anteroposterior thorax diameter in the range of 17
/26.5
cm. The weight of the device is 6.5 kg and when stowed
in a bag, its dimensions are 32
/64/23 cm. When it is
mounted, the dimensions are 50
/53.8/22.8 cm.
LUCAS is CE-marked and is commercially available
in Europe since December 2001 (Jolife AB, Lund,
Sweden; www.jolife.com).
2.4. Experimental animals
A total of 100 Swedish-bred specific pathogen free
pigs with a mean weight of 22 kg (range 20
/26 kg) were
used. The mean external anteroposterior diameter of the
thorax at the site where the chest compressions were
given, i.e., at the inferior one third of the sternum, was
209
/1 cm (range, 18/23 cm) (Fig. 5).
All the animals received humane care in compliance
with the Guide for the Care and Use of Laboratory
Animals, published by the National Institutes of Health
(NIH publication 85
/23, revised 1985). The Institu-
tional Review Board for animal experimentation at the
University of Lund, Sweden, approved the experimental
protocols. All animal experiments were designed accord-
ing to the Utstein-style guidelines [7].
2.5. Anesthesia and preparation
The pigs had free access to water but were not allowed
to eat on the day of experiment. They were anaesthe-
tized with an induction dose of intramuscular ketamine
(30 ml/kg). Sodium thiopental (5
/8 mg/kg) and atropine
(0.05 mg/kg) were given intravenously before tracheo-
tomy. Anaesthesia and muscle paralysis were main-
tained with a continuous infusion of 30 ml/h of a 10%
glucose solution containing ketamine (16 mg/ml) and
pancuronium (0.6 mg/ml). In study Groups III and IV,
midazolam (0.06 mg/ml) was also added to the infusion.
Macrodex (up to 250 ml) was given to keep the central
venous pressure within a normal range of 3
/8 mmHg on
a PEEP of 8 cm H
2
O.
For monitoring of intrathoracic aortic pressure, a
catheter was introduced via a direct puncture of the left
carotid artery in order to avoid ligation of the artery.
The tip of the catheter was inserted into the thoracic
aorta and in the same way a catheter was inserted into
the right atrium via the left external jugular vein (at
autopsy these positions were confirmed). Separate
catheters were placed inside an artery and a vein for
withdrawal of blood samples. In Group I, a Swan
/Ganz
catheter (7.5 F) was inserted into the pulmonary artery
via the right external jugular vein. An ultrasonic blood
flow probe (3 mm) connected to a flow meter (Transonic
Flowmeter T201D) was placed around the right carotid
artery. A Foley catheter was inserted into the urinary
bladder through a suprapubic cystotomy. The tempera-
ture was measured with a temperature probe placed in
the oesophagus. The animals were kept normothermic
by a heating system in the operation table, if not actively
cooled, as for two thirds of the animals in Group IV.
The mean temperature for the pigs in Groups I
/III at
the end of the experiments was 37.29
/1.0 8C (range,
36.5
/38.4 8C).
2.6. Experimental protocol
For the design of the pig experiments, see Fig. 4.In
Group I 12 animals were randomized to manual or
mechanical chest compressions for 10 min after 90 s of
VF.
In Group II, the LUCAS was started 90 s after start
of VF and ran for 30 min before defibrillation. The
Fig. 4. The design of the pig experiments. The number of pigs with
ROSC (return of spontaneous circulation) is indicated within the
ROSC rectangle. In each case, defibrillation occurred at the end of the
CPR.
S. Steen et al. / Resuscitation 55 (2002) 285
/299 289
intention was to identify potential physiological differ-
ences between ROSC and non-ROSC-pigs during CPR.
In Group III, the animals were randomized into eight
different subgroups with 15, 20, 25, 30, 35, 40, 50 and 60
min of LUCAS-CPR before defibrillation. The aim was
to determine the frequency of ROSC in each group.
In Group IV, the pigs were randomized either to
normothermia or to cooling, the latter divided into two
subgroups: in one VF was induced before cooling
(surface cooling group), and in one after cooling to
32 8C (hypothermia group). The animals were placed
within a strong plastic bag with holes for catheters, flow
probe cable and the silicon rubber suction cup of
LUCAS. In the surface cooling group the plastic bag
was filled with ice cubes directly after induction of VF.
When the oesophageal temperature reached 34 8 C
(after about 30 min, range 28
/33 min), the ice bag
was removed. The temperature continued to fall to
about 32 8C at 60 min, the time at which defibrillation
was attempted. For the ROSC animals, the oesophageal
temperature stabilized at around 31 8C 1 h after ROSC.
In the hypothermia group, cooling was done with the
method described above but VF was induced at 32 8C
and LUCAS-CPR was run for 60 min before defibrilla-
tion, at which time the temperature had stabilized at
around 31 8C.
VF was induced with a 5
/20 mA, 6 Hz and 30 V
alternating current delivered to the epicardial surface via
a needle electrode. Circulatory arrest was confirmed by
a fall in arterial blood pressure and end-tidal CO
2
concentration and an ECG showing VF. Chest com-
pressions were started after an interval of 90 s (Group I
and II) or 30 s (Group III and IV).
Defibrillation was attempted as soon as possible
(within 10 s) after the interruption of chest compressions
with a direct current (DC) countershock of 300 J. In case
of persistant VF, DC countershocks of 360 J were
administered up to 3 times if necessary. If VF or asystole
Fig. 5. Transverse section of a 23 kg pig just distal to processus xiphoideus. The heart ventricles are not compressed directly between the sternum and
the spine during chest compressions due to the central position of the ventricles within the thoracic cavity. The anteroposterior diameter in this pig
was 19.5 cm. Normal ventilated lungs (upper left), atelectatic lungs after disconnection from the ventilator (upper right), lungs extirpated (lower left),
and manual forceful compression without direct compression of the ventricles between sternum and the spine (lower right).
S. Steen et al. / Resuscitation 55 (2002) 285
/299290
persisted after four countershocks (with short periods of
manual chest compression between each shock), resus-
citation was defined as unsuccessful. The pigs with
ROSC were monitored for 2 h, after which they were
euthanized and autopsied. The position of the aortic and
central venous catheters was especially checked, as were
the heart valves, heart septum and ductus arteriosus.
The aortic and pulmonary valve function was investi-
gated by testing for leakage in a vertical position, and
the tricuspid and mitral valves were tested by a quick
injection of saline in a Foley-catheter placed intraven-
tricularly via a stab wound through the ventricular wall.
The autopsies did not show any pathology (special care
was taken when the hearts of the non-survivors were
investigated).
2.7. Haemodynamic measurements
Pressure and blood flow signals were sampled 50
times/s and the mean value for each variable was
recorded every 5 s during the whole experiment, using
a computer supplied with a data acquisition system
(TestPoint, Capital Equipment Corporation, Billerica,
MA). Coronary perfusion pressure was continuously
calculated by the computer as the difference between the
intrathoracic aortic and right atrial pressure during the
decompression phase.
2.8. Blood gas analysis
Blood gases and electrolytes were analyzed directly
after the sample had been obtained using a blood gas
analyzer (ABL 505, Radiometer, Copenhagen). Arterial
and mixed venous O
2
-saturations (SaO
2
,SvO
2
) and total
haemoglobin concentration were analyzed with a multi-
wave-length oximeter (OSM3, Radiometer, Copenha-
gen) using the pig mode. In the hypothermic animals,
the blood gas apparatus was adjusted to measure at the
same temperature as the pig.
2.9. Ventilatory settings and measurements
Pressure-regulated, volume-controlled ventilation
(Servo Ventilator 300, Siemens, Solna, Sweden) was
used to obtain a stable minute volume. Ventilatory
support was continued throughout all the experiments
with a minute volume of 5 l/min at 20 breaths/min and a
PEEP of 8 cm H
2
O in Group I and II, and a minute
volume of 7.5 l/min at 25 breaths/min and a PEEP of 8
cm H
2
O in Group III and IV. An inspired oxygen
concentration (FiO
2
) of 0.21 was used throughout,
except during the periods of chest compressions, when
it was set to 1.0.
The ventilation was not synchronized with the chest
compressions. A prototype infra-red CO
2
analyzer
(Servotek AB, Arlo
¨
v, Sweden) was used, which has a
function similar to that of the Servo 930 CO
2
analyzer,
using an infra-red source and a detector placed astride
the Y-tubing (main stream). The analyzer has a response
time of 5 ms, a low noise level and a full-scale deflection
of 10% CO
2
. It was calibrated to zero with air and also
calibrated with gas containing 5.059
/0.010% CO
2
in air
(Alfax AB, Arlo
¨
v, Sweden). End-tidal CO
2
was mon-
itored continuously and the value was recorded once a
minute on a computer during the course of the experi-
ment.
2.10. Anteroposterior thorax diameter in humans
The anteroposterior thorax diameter of 50 men and
15 women was measured at the level where external
chest compressions should be given. This was done by
placing the subjects on their backs close to a wall,
lowering a stiff plate angled at 908 to the wall and
attached to the wall until it just touch a point between
the middle and lower third of the sternum, and
measuring the distance from the lower edge of the plate
to the floor.
2.11. Clinical pilot study with LUCAS
Permission for a clinical pilot study with LUCAS,
including 20 patients, was given by the Medical Ethics
Committee at the University of Lund. The study was
designed to see if the device was easy and safe to use.
The test was done when standard cardiopulmonary
resuscitation had failed, as a last extra chance to save
the patient’s life. The device used on the first patients in
this pilot study was a prototype with the same pneu-
matic properties as in the later model of LUCAS, but
with an aesthetically less attractive appearance.
2.12. Statistical analysis
All results are expressed as the mean9
/standard error
of the mean (S.E.M.). For statistical analysis the
unpaired Student’s t-test was used.
3. Results
3.1. Manual CPR v s. LUCAS-CPR in the artificial
thorax model
Typical pressure-flow curves for the artificial thorax
model are presented in Fig. 6; in the left panel the
rescuer performs manual CPR as he would have done in
a clinical situation, and in the middle panel his
performance during 5 s of maximal effort is shown. As
seen in the right panel, LUCAS-CPR creates pressure-
flow curves quite different from those seen during
manual CPR, i.e. the area under the curves produced
S. Steen et al. / Resuscitation 55 (2002) 285 /299 291
by LUCAS is greater, with a corresponding increase in
mean pressure and flow. The explosivity of the gas-
driven pneumatics in LUCAS creates an instant increase
and decrease in pressure, with a 50% duty cycle
regarding both time and flow. The high peak pressures
caused by maximal manual CPR cannot be maintained
during the compression phase and therefore can not
compete in efficiency with the LUCAS-CPR, despite
lower peak pressures with the latter.
3.2. Manual CPR vs. LUCAS-CPR in the pig (Group I)
There was no return of spontaneous circulation
(ROSC) with manual CPR, whereas five of six animals
had ROSC with LUCAS-CPR (Fig. 7). The diastolic
and mean arterial pressures were significantly higher
with LUCAS-CPR (Table 1). In Fig. 8 the pressure
curves obtained from the intrathoracic aorta and the
right atrium are superimposed. The areas between the
curves in the decompression phase are greater during
LUCAS-CPR than during manual CPR, indicating a
higher myocardial perfusion pressure during LUCAS-
CPR. The coronary artery perfusion pressure was
around 10 mmHg with manual CPR and around 15
mmHg with LUCAS-CPR (Fig. 9).
The values obtained after 5 min of CPR are presented
in Table 1. The cardiac output, end-tidal CO
2
, right
carotid arterial blood flow and coronary perfusion
pressure were significantly higher with LUCAS-CPR.
There was no significant difference in the blood gas
values (except for a slightly higher PvO
2
value in the
LUCAS-CPR group), which were within normal ranges
in both groups. The five pigs with ROSC in the LUCAS-
CPR group were followed for 2 h before being
euthanized and autopsied. At the end of this observation
period, the arterial pressure, carotid flow and blood
gases were not significantly different from the baseline
values obtained before induction of VF.
3.3. ROSC v s. non-ROSC after 30 min of LUCAS-CPR
(Group II)
There was a 50% ROSC rate in this group of 16
animals. Pressure-flow curves during 30 min of LUCAS-
Fig. 6. Typical pressure-flow curves obtained by external compressions on the artificial thorax model. The left panel shows the data obtained when
the male rescuer (75 kg body weight) did manual compressions with the force he had been trained to use on an adult patient (these values were defined
as 100%). The middle panel shows when the same rescuer performed maximal forceful compressions. The right panel shows LUCAS-compressions.
The gas supply was breathing oxygen from a wall outlet (4 bar).
S. Steen et al. / Resuscitation 55 (2002) 285
/299292
CPR without and with ROSC are shown in Fig. 10,
upper and lower panels, respectively. The coronary
perfusion pressure is shown in Fig. 11 and the end-tidal
CO
2
values in Fig. 12. No significant difference in any
variables measured was seen after 5 and 15 min of
LUCAS-CPR. In Table 2 values after 25 min of
LUCAS-CPR are shown. Coronary perfusion pressure,
end-tidal CO
2
and right carotid arterial flow were
significantly higher in the ROSC group. There was no
significant differences in the blood gases except for
PvCO
2
at 25 min, 5.69/0.4 vs. 7.79/0.7 (P B/0.05) in the
ROSC and non-ROSC pigs, respectively. The corre-
sponding values for SvO
2
at 25 min were 549/6and349/
9% (P/0.093). The animals with ROSC were followed
for 2 h before being euthanized and autopsied. At the
end of this observation period, the arterial pressures,
blood gases and carotid blood flow were not signifi-
cantly different from the baseline values obtained before
the induction of VF.
3.4. ROSC after 15
/60 min of LUCAS-CPR (Group
III)
All animals achieved ROSC after 15 min of LUCAS-
CPR, whereas beyond 15 min there was an increased
rate of animals without ROSC without any obvious
association with CPR time (Fig. 4). The mean coronary
perfusion pressure and the end-tidal CO
2
values of the
last 5 min of the resuscitation period were calculated for
each pig. For all animals with ROSC (n
/27), the mean
coronary perfusion pressure was 159
/5 mmHg, com-
pared with 29
/5 mmHg (P B/0.01) for the non-ROSC
pigs. The corresponding values for end-tidal CO
2
were
2.69
/0.7 and 2.09/1.0% (P B/0.01), respectively. At the
end of the observation period of 2 h, all ROSC pigs had
blood pressure, end-tidal CO
2
, and carotid flow values
that were not significantly different from the values
obtained before the induction of VF.
3.5. LUCAS-CPR in normothermia versus hypothermia
(Group IV)
The results obtained in the Group IV pigs are shown
in Figs. 13
/15 and in Table 3. The coronary perfusion
pressure started to decrease after 20 min of CPR in the
normothermic animals. The end-tidal CO
2
values in the
hypothermic group were stable throughout CPR
whereas a decline over time was seen in the normother-
mic group. In the surface cooling group, the end-tidal
CO
2
value and the oesophagus temperature at 50 min
were the same as in the hypothermic group, reflecting
the reduced metabolism and CO
2
production in these
two groups at this point. The metabolic acidosis (base
excess in Table 3) measured after 50 min of CPR was
more pronounced in the normothermic pigs. The
reactive hyperaemia after ROSC was higher in the
normothermic group (Figs. 13
/15).
3.6. Anteroposterior chest diameter in 65 adult humans
Both the mean and median anteroposterior diameter
was 21 cm (range 17
/26 cm).
3.7. Clinical experience with LUCAS
The pilot study, where LUCAS was used as a last
resort in 20 cases where standard advanced CPR had
failed, documented that LUCAS is easy to apply and
easy to use. In most cases it took less than 20 s to apply.
The staff appreciated the fact that one person could be
used for other purposes during CPR.
In one clinical case the efficacy of LUCAS was
demonstrated. A 55-year-old diabetic man undergoing
peritoneal dialysis due to renal failure suddenly suffered
a witnessed collapse in a nephrology ward. Two
nephrologists started manual chest compressions and
Fig. 7. The pressure- and carotid flow curves in the Group I pigs.
There was no ROSC in the manual Group, 5 of the 6 animals obtained
ROSC with LUCAS-CPR. Data shown as mean9
/S.E.M., n/6(n/5
after defibrillation in lower panel). CAF/carotid arterial blood flow,
SAP, MAP, DAP/systolic, mean and diastolic intrathoracic aortic
pressure. VF
/induction of ventricular fibrillation. Def/defibrilla-
tion.
S. Steen et al. / Resuscitation 55 (2002) 285
/299 293
ventilation with a self-inflating bag, after confirming
that the patient had no palpable pulses and no
spontaneous respiration. The CPR-team (hospital team
consisting of one cardiologist assisted by one specially
trained cardiology nurse and one anaesthesiologist
assisted by one specially trained anaesthesiology nurse)
was called and arrived after 4 min. The ECG showed
asystole. The patient was intubated and the heavily built
male cardiologist in the resuscitation team continued
manual chest compressions. Atropine and adrenaline
were given intravenously. After 9 min of standard CPR
without signs of ROSC, the cardiologist agreed that
LUCAS could be applied to the patient, as a last effort
to save the patient’s life. The assistant nurse, who had
been trained in the use of LUCAS-CPR, quickly applied
the device and immediately after the start of LUCAS,
strong pulses could be palpated. After 3 min of chest
Table 1
Physiological variables in experiments comparing manual CPR with LUCAS-CPR (Group I)
Baseline values Values after 5 min of CPR
Manual CPR LUCAS-CPR P -value Manual CPR LUCAS-CPR P -value
Aortic pressure (mmHg) Mean 68927794ns 33914291 B 0.001
Systolic 90929593ns 77987993ns
Diastolic 56936494ns 17922591 B 0.05
Right atrial pressure (mmHg) Mean 691791ns 23923894 B 0.01
Systolic 9911091ns 60939199 B 0.01
Diastolic 691691ns 791791ns
Pulmonary arterial pressure (mmHg) Mean 18922191ns 31943092ns
Wedge pressure (mmHg) Mean 8911291ns 32952993ns
Coronary perfusion pressure (mmHg) 52935895ns 10921791 B 0.05
Cardiac output (l/min) 2.990.3 3.390.4 ns 0.590.1 0.990.1 B 0.05
(%) 100 100 ns 17 27 B 0.05
End-tidal CO
2
(%) 4.290.3 4.190.1 ns 2.090.2 2.890.1 B 0.05
Carotid arterial blood flow (ml/min) 189924 201919 ns 32955894 B 0.01
(%) 100 100 ns 17 29 B 0.01
Mixed venous blood gas (kPa) PvO
2
7.390.6 8.691 ns 4.890.3 5.290.5 B 0.01
(kPa) PvCO
2
5.690.3 5.190.4 ns 6.190.7 5.790.5 ns
pHv 7.4090.03 7.4390.02 ns 7.2590.06 7.3090.04 ns
(%) SvO
2
80948495ns 43975097ns
Arterial blood gas (kPa) PaO
2
54965793ns 46924895ns
(kPa) PaCO
2
4.490.2 4.190.2 ns 2.690.3 3.890.5 ns
pHa 7.4890.03 7.4990.03 ns 7.5190.05 7.4090.05 ns
(%) SaO
2
10090 10090 ns 100 100 ns
Inspired oxygen fraction 1.0, blood gas apparatus set on the pig mode.
Fig. 8. Typical pressure curves obtained in a 20 kg pig during manual
CPR and during LUCAS-CPR. The area between the curves for
intrathoracic aortic pressure and right atrial pressure gives a picture of
the coronary perfusion pressure. Note the biphasic positive curves and
greater area between the curves during LUCAS-CPR.
Fig. 9. The coronary perfusion pressure obtained during manual CPR
vs. LUCAS-CPR in pigs (Group I). The coarse line shows the mean
value. S.E.M. (thin line) is shown only on one side for the sake of
clarity. n
/6 in both groups.
S. Steen et al. / Resuscitation 55 (2002) 285
/299294
compressions/decompressions with LUCAS, the patient
regained spontaneous circulation. He was transferred to
the intensive care unit and was treated on a ventilator
for 1 week. Blood cultures showed severe sepsis. After
appropriate antibiotic therapy, the patient was weaned
from the ventilator, recovered, and left the hospital. At a
follow-up visit 1 year later, his mental capacity was fully
intact.
Fig. 10. The pressure- and carotid flow curves in pigs with ROSC vs.
pigs without ROSC (Group II). Data shown as mean9
/S.E.M., n /8
in each group. VF/induction of ventricular fibrillation. Def /
defibrillation.
Fig. 11. The coronary perfusion pressure in pigs with ROSC vs. pigs
without ROSC (Group II). Data shown as mean9
/S.E.M., n/8in
each group. S.E.M. is shown only on one side for the sake of clarity.
Fig. 12. End-tidal CO
2
in pigs with ROSC vs. pigs without ROSC
(Group II). Data shown as mean9
/S.E.M., n/8 in each group. P B/
0.05.
Fig. 13. LUCAS-CPR during 1 h of ventricular fibrillation (VF) in
normothermia. Temperature, systolic, mean and diastolic (SAP, MAP,
DAP) intrathoracic aortic pressure, coronary perfusion pressure, and
right carotid arterial blood flow are shown as mean9
/S.E.M. n /8
(n/3 after defibrillation (Def)).
S. Steen et al. / Resuscitation 55 (2002) 285
/299 295
4. Discussion
The animal experiments in this study were performed
and reported according to the Utstein guidelines for
laboratory CPR research [7]. These recommend use of
swine weighing 20
/25 kg. The anteroposterior chest
diameter of pigs this size will be similar to that of
average sized adult humans. Our measurements of 65
adult humans confirmed this. Swine have the advantage
of being uniform in size and shape at similar ages and
weights and there are many similarities in metabolic and
cardiovascular function between swine and humans
Table 2
Physiological variables in ROSC pigs vs. none-ROSC pigs (Group II)
Baseline values Values after 25 min of LUCAS-CPR
ROSC Non-ROSC P -value ROSC Non-ROSC P -value
Aortic pressure (mmHg) Mean 63938098ns 39933192 B 0.05
Systolic 829 929 ns 78 72 ns
Diastolic 589 729 ns 22 14 ns
Coronary perfusion pressure (mmHg) 52936898ns 1894992 B 0.05
End-tidal CO
2
(%) 4.090.1 4.390.2 ns 2.890.1 2.190.3 B 0.05
Right carotid blood flow (ml/min) 130911 148921 ns 47952293 B 0.01
Fig. 14. LUCAS-CPR during 1 h of ventricular fibrillation (VF) with
surface cooling during the first half hour. Temperature, systolic, mean
and diastolic (SAP, MAP, DAP) intrathoracic aortic pressure,
coronary perfusion pressure, and right carotid arterial blood flow are
shown as mean9
/S.E.M. n/8(n/6 after defibrillation (Def)).
Fig. 15. LUCAS-CPR during 1 h of ventricular fibrillation (VF) in
hypothermia. Temperature, systolic, mean and diastolic (SAP, MAP,
DAP) intrathoracic aortic pressure, coronary perfusion pressure, and
right carotid arterial blood flow are shown as mean9
/S.E.M. n /8
(n/6 after defibrillation (Def)).
S. Steen et al. / Resuscitation 55 (2002) 285
/299296
[8,9]. The coronary vascular anatomy is also similar to
that of humans, with the exception of the left azygos
vein, which in the pig enters the coronary sinus rather
than a precaval vein. An important difference is that in
pigs, the ventricles are positioned in the center of the
thoracic cavity, surrounded by lung tissue on all sides
(see Fig. 5). During the compression phase of CPR, the
ventricles of a pig is not compressed by the sternum and
spine, but are compressed indirectly by the pressure
increase inside the chest. This mechanism is known as
‘the thoracic pump theory’, in contrast to ‘the heart
pump theory’, in which it is thought that chest
compression causes a direct compression of the heart
against the spine [5,10,11]. The circulation created by
the chest compressions in our study was probably
caused by a ‘thoracic pump’ rather than a ‘heart
pump’ mechanism.
In the present study the ventilation was kept constant
throughout, with the intention to use end-tidal CO
2
values as an indication of the efficiency of the chest
compressions. Due to the reduced cardiac output during
CPR, the animals were relatively hyperventilated, re-
sulting in respiratory alkalosis that compensated for the
metabolic acidosis that also developed during prolonged
CPR (Table 3). Thus, we think that buffer therapy with
this experimental design would not have added any
benefits for the animals. The use of drugs to increase the
coronary perfusion pressure might have raised the
ROSC, but were excluded in order to be able to judge
the efficacy of chest compressions/decompressions per
se.
In a clinical study comparing manual compression
with manual compression/decompression, the latter
approach significantly improved long-term survival
rates among patients who had cardiac arrest out-of-
hospital [4]. What role did the active decompression play
in our study? The suction cup of LUCAS was too wide
(13.5 cm in diameter) to fit snugly with the precordial
chest in the pigs used. The upper thorax is too narrow
for real vacuum to be created during the compression
phase. This was confirmed by the fact that no suction
mark could be seen after CPR. However, in the pigs
resuscitated for longer than 20 min, the thorax softened
and became more flat. A vacuum was then created, and
after the CPR, a suction mark was seen. In a pilot study
elucidating the efficacy of manual compressions for 30
min using this pig model, the end-tidal CO
2
fell to zero
after about 20 min of manual compressions. At that
time the pig thorax had lost its elastic recoil, and the
anteroposterior diameter had diminished significantly
and no ROSC was obtained. We think that in such a
situation active decompression may be of value, if
thereby an increase in venous return can be accom-
plished. As long as the thorax is intact, with normal
elastic recoil of the chest in each decompression phase,
we think active decompression is of less importance. In
the Group II experiments we observed that after about
15
/20 min with CPR, the non-ROSC animals started to
lose coronary perfusion pressure while the ROSC-pigs
did not (Fig. 11). Paradis et al. measured the coronary
perfusion pressure in 100 patients with cardiac arrest
[12]. In their study 24 patients had ROSC. Initial
coronary perfusion pressure was 1.69
/8.5 mmHg in
patients without ROSC and 13.49
/8.5 mmHg in patients
with ROSC, whereas the maximal coronary pressure
measured was 8.49
/10.0 mmHg in those without ROSC
and 25.69
/7.7 mmHg in those with ROSC. Only patients
with maximal coronary perfusion pressures of 15 mmHg
Table 3
Blood gas values in LUCAS-CPR pigs with normothermia vs. surface cooling during CPR and CPR in hypothermia (Group IV)
Base 10 min CPR 30 min CPR 50 min CPR 10 min after CPR 60 min after CPR 120 min after CPR
End-tidal CO
2
(%)
Normothermia 4.290.2 2.590.2 2.090.3 1.790.5 3.290.8 4.290.1 4.290.1
Surface cooling 4.190.2 2.290.1 2.090.1 1.790.1 2.890.2 2.290.1 2.290.1
Hypothermia 4.390.2 1.790.1 1.990.0 1.790.1 2.490.2 2.590.2 2.590.2
SvO
2
(%)
Normothermia 84933194339830910 67913 75937794
Surface cooling 9193409640933995769381938294
Hypothermia 879538983995319566914 83912 81911
Base excess-arterial
Normothermia 4.390.9 1.191.7 7.592.0 11.292.5 4.192.7 2.190.1 0.790.3
Surface cooling 2.490.9 0.591.2 3.391.4 4.991.2 5.591.9 0.891.2 0.291.9
Hypothermia 3.391.4 0.391.0 3.991.8 6.091.7 7.391.5 4.591.8 5.392.3
pH-arterial
Normothermia 7.5690.02 7.5690.03 7.5090.04 7.4590.03 7.3990.04 7.4590.03 7.4890.03
Surface cooling 7.5190.01 7.5990.02 7.5690.03 7.5590.02 7.4690.02 7.5890.02 7.6190.02
Hypothermia 7.5290.02 7.6890.01 7.5890.03 7.5490.03 7.4590.04 7.4890.06 7.5090.07
All baseline values were obtained at normothermia. All blood gas values were obtained with FiO
2
1.0; the blood gas apparatus was adjusted to
measure at the same temperature as the pig and with the pig mode.
S. Steen et al. / Resuscitation 55 (2002) 285
/299 297
or more had ROSC. These data correspond well with
those obtained on the ROSC and non-ROSC pigs in the
present study, attesting to the relevance of this model.
End-tidal CO
2
levels reflect cardiac output during
CPR. Levine and coworkers monitored end-tidal CO
2
during CPR in 150 consecutive victims of cardiac arrest
out-of-hospital [13]. A 20-min end-tidal CO
2
value of 10
mmHg (1.3 kPa) or less was associated with a lack of
(ROSC) in their study. In the Group I pigs in our study,
manual CPR was able to produce end-tidal CO
2
values
of 2 kPa, but the coronary perfusion pressure in those
pigs was only around 10 mmHg, and no ROSC was
obtained. Thus, in successful CPR, it is not enough to
obtain a critical cardiac output (adequate end-tidal CO
2
values); an adequate coronary perfusion pressure is
equally essential for ROSC.
Early defibrillation is the most important single factor
to influence survival after sudden circulatory arrest, if it
can be accomplished within 4 min, according to a study
published by Cobb and coworkers [14]. In their study,
survival improved if 90 s of external chest compressions
were given prior to defibrillation in the group of patients
where defibrillation could not be given within 4 min of
circulatory arrest. In an experimental study by Sato and
coworkers, they describe the adverse effects of inter-
rupting chest compressions during CPR [15]. In their
model, the coronary perfusion pressure during CPR was
269
/2 mmHg, but 10 s after interruption of CPR, it had
decreased to 69
/3 mmHg, and after 20, 30 and 40 s it
was 49
/2, 49/4and49/4 mmHg, respectively, i.e. close
to zero. If defibrillation was done under ongoing CPR,
the 24 h-survival rate was 80%. If it was delayed by 10 s,
the 24 h survival rate was reduced to 40%, and if it was
delayed by 20 s or more, there were no survivors. With
these results in mind, it is easy to understand why
defibrillation after 4 min of circulatory arrest is not
likely to be successful. After that time, there has been
minimal or no coronary circulation for at least 3 min.
The advice given by Cobb et al. for routine provision of
90 s of CPR prior to a defibrillation seems most logical.
In addition, defibrillation has greater chance of success
if it can be delivered under ongoing CPR, as shown by
Sato et al., i.e. with blood circulation through the heart
muscle tissue [15]. Defibrillation during manual CPR
cannot be done for safety reasons, but it would be one
obvious advantage of mechanical CPR. The exterior of
LUCAS is made of a non-conducting material, and by
using electrode pads on the patient, defibrillations can
be given safely during CPR.
As the Group IV study indicates, surface cooling as
soon as possible after mechanical CPR is initiated may
be of great advantage for several reasons. The coronary
perfusion pressure increased promptly, probably due to
redistribution of the blood volume and increased
systemic vascular resistance. The metabolism will be
reduced by about 6
/7%/8C that the body temperature is
lowered [16,17], with the consequence that less circula-
tion will be needed to ensure an adequate organ
perfusion. Hypothermia will also protect the brain
[18
/20].
Preliminary reports from the clinical pilot study with
LUCAS are promising. It has been easy to handle, it can
be applied to the patient within 10
/20 s, it fits on
stretchers, the suction cup helps to maintain a correct
position and it fits and works well within ambulances.
Defibrillation may be delivered during ongoing chest
compressions. Several prospective randomized studies
within or out-of-hospital are being planned. The most
critical factor for successful CPR out-of-hospital is to
initiate adequate chest compressions and oxygenation as
quickly as possible after cardiac arrest, before the brain
has been irreversibly injured. Traditional manual CPR
will lose none of its importance with the introduction of
mechanical CPR, quite the opposite. Knowing that a
machine is under way to take over the chest compres-
sions should only give the rescuer(s) added strength to
maintain forceful manual CPR until the ambulance
team arrives.
To conclude, gas-driven compressions and active
decompressions with LUCAS give significantly better
circulation during ventricular fibrillation compared to
manual chest compressions.
Acknowledgements
This study was supported by grants from the Uni-
versity Hospital of Lund, the Swedish Heart Lung
Foundation, and the Swedish Medical Research Council
(Project no. K2002-71X-12648-05C).
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    • "Cardiopulmonary resuscitation (CPR) is well known and has been recognised for more than 50 years as a treatment in cases of cardiac arrest [1, 2]. Latest advances in this field have brought to the development of different assisted devices [3][4][5][6]that have shown some efficiency [7] and intended to improve outcome and chances of survival. The Lund University Cardiopulmonary Assist System, 2nd generation (LUCAS™2) device is a fully pneumatic automatic device, equipped with a drag for compression and a suction cup for active decompression (Fig. 1), which needs to be properly placed on the central breast region. "
    [Show abstract] [Hide abstract] ABSTRACT: The aim of our study was to compare traumatic injuries observed after cardiopulmonary resuscitation (CPR) by means of standard (manual) or assisted (mechanical) chest compression by Lund University Cardiopulmonary Assist System, 2nd generation (LUCAS™2) device. A retrospective study was conducted including cases from 2011 to 2013, analysing consecutive autopsy reports in two groups of patients who underwent medicolegal autopsy after unsuccessful CPR. We focused on traumatic injuries from dermal to internal trauma, collecting data according to a standardised protocol. The study group was comprised of 26 cases, while 32 cases were included in the control group. Cardiopulmonary resuscitation performed by LUCAS™2 was longer than manual CPR performed in control cases (study group: mean duration 51.5 min; controls 29.4 min; p = 0.004). Anterior chest lesions (from bruises to abrasions) were described in 18/26 patients in the LUCAS™2 group and in 6/32 of the control group. A mean of 6.6 rib fractures per case was observed in the LUCAS™2 group, but this was only 3.1 in the control group (p = 0.007). Rib fractures were less frequently observed in younger patients. The frequency of sternal factures was similar in both groups. A few trauma injuries to internal organs (mainly cardiac, pulmonary and hepatic bruises), and some petechiae (study 46 %; control 41 %; p = 0.79) were recorded in both groups. LUCAS™2-CPR is associated with more rib fractures than standard CPR. Typical round concentric skin lesions were observed in cases of mechanical reanimation. No life-threatening injuries were reported. Petechiae were common findings.
    Full-text · Article · Jan 2015
    • "The LUCAS™ Chest Compression System (Physio-Control/Jolife AB, Lund, Sweden) has been in clinical use since 2003. Experimental data have shown improved perfusion pressures to the brain and heart, enhanced cerebral blood flow and higher end tidal CO2 as an indirect measure of cardiac output using the LUCAS™ device as compared with the effects of conventional manual CPR [1,2]. The LUCAS™ device has also shown higher end tidal CO2 values in out-of-hospital cardiac arrest (OHCA) victims compared with manual CPR [3]. "
    [Show abstract] [Hide abstract] ABSTRACT: Background The LUCAS™ device delivers mechanical chest compressions that have been shown in experimental studies to improve perfusion pressures to the brain and heart as well as augmenting cerebral blood flow and end tidal CO2, compared with results from standard manual cardiopulmonary resuscitation (CPR). Two randomised pilot studies in out-of-hospital cardiac arrest patients have not shown improved outcome when compared with manual CPR. There remains evidence from small case series that the device can be potentially beneficial compared with manual chest compressions in specific situations. This multicentre study is designed to evaluate the efficacy and safety of mechanical chest compressions with the LUCAS™ device whilst allowing defibrillation during on-going CPR, and comparing the results with those of conventional resuscitation. Methods/design This article describes the design and protocol of the LINC-study which is a randomised controlled multicentre study of 2500 out-of-hospital cardiac arrest patients. The study has been registered at ClinicalTrials.gov (http://clinicaltrials.gov/ct2/show/NCT00609778?term=LINC&rank=1). Results Primary endpoint is four-hour survival after successful restoration of spontaneous circulation. The safety aspect is being evaluated by post mortem examinations in 300 patients that may reflect injuries from CPR. Conclusion This large multicentre study will contribute to the evaluation of mechanical chest compression in CPR and specifically to the efficacy and safety of the LUCAS™ device when used in association with defibrillation during on-going CPR.
    Full-text · Article · Jan 2013
    • "Experimental studies have showed that the use of LUCAS-2 was associated with sustained coronary and cerebral perfusion in an animal model with cardiac arrest [1] [7] So far, only few case reports [8] [9] [10] and small case series [6] [11] [12] have addressed its efficacy and safety in humans with so far encouraging results. "
    [Show abstract] [Hide abstract] ABSTRACT: Cardiac arrest in the catheterization laboratory during percutaneous coronary interventions (PCI) is associated with high mortality, among other things because it may be difficult to perform efficacious cardiopulmonary resuscitation while continuing the coronary intervention. We report on 2 patients who have benefit from ongoing external mechanical chest compression with LUCAS-2 device because of cardiac arrest occurred during non-coronary interventions. Added to the existing data on PCIs performed during cardiac arrest, these first reported cases suggest that the application of the LUCAS-2 device in the cardiac catheterization laboratory may be also expanded to patients undergoing noncoronary interventions.
    Full-text · Article · Sep 2012
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