Simultaneous sterno-thoracic cardiopulmonary resuscitationimproves short-term survival rate in canine cardiac arrests

Sung Oh Hwang a,*, Kang Hyun Lee a, Jin Woong Lee a, Seo Young Lee a,Byung Su Yoo b, Junghan Yoon b, Kyung Hoon Choe b

a Department of Emergency Medicine, Wonju College of Medicine, Yonsei University, 162 Ilsandong, Wonju 220 701, Republic of Koreab Department of Cardiology, Wonju College of Medicine, Yonsei University, 162 Ilsandong, Wonju 220 701, Republic of Korea

Received 2 November 2001; received in revised form 2 December 2001; accepted 11 January 2002

Abstract

We have reported previously that simultaneous sterno-thoracic cardiopulmonary resuscitation (SST-CPR) using a device that

compresses the sternum and constricts the thorax circumferentially during a compression systole that can be achieved using standard

cardiopulmonary resuscitation (STD-CPR). This study was designed to assess whether SST-CPR improves the survival rate of dogs

with cardiac arrest compared with STD-CPR. Twenty-nine mongrel dogs (19�/31 kg) were enrolled in this study. After 4 min of

ventricular fibrillation induced by an AC current, animals were randomized to be resuscitated by either STD-CPR (n�/15) or SST-

CPR (n�/14). Defibrillation was attempted 10 min after the induction of cardiac arrest. Standard advanced cardiac life support was

started if defibrillation was unsuccessful. Aortic blood pressure, coronary perfusion pressure, and end tidal CO2 tension were

measured during CPR and the post-resuscitation period. Survival was determined 12 h after the induction of cardiac arrest. SST-

CPR resulted in a significantly (P B/0.001) higher systolic arterial pressure (919/47 vs 479/24 mmHg), diastolic pressure (439/24 vs

179/10 mmHg), coronary perfusion pressure (359/25 vs 139/9 mmHg), and end tidal CO2 tension (99/4 vs 39/2 mmHg). Two of 15

animals (13%) resuscitated by STD-CPR and seven of 14 animals (50%) resuscitated by SST-CPR survived for 12 h after cardiac

arrest (P B/0.05). In conclusion, SST-CPR improves the short-term survival rate in canine cardiac arrest compared with STD-CPR.

# 2002 Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Cardiopulmonary resuscitation; Cardiac arrest

1. Introduction

The conventional method of supporting the circula-

tion in standard cardiopulmonary resuscitation (STD-

CPR) involves repetitive external chest compression on

the sternum. The mechanism of blood flow has been

debated [1�/4], but there is no dispute that this method

generates only about 15�/25% of the normal cardiac

output [5,6]. Alternative techniques to STD-CPR have

been developed to enhance perfusion during CPR, but

to date few adjuncts have been shown to be superior to

STD-CPR in terms of improving survival. We had

developed a new CPR device, consisting of a piston

and belt, which compresses the sternum and constricts

the thorax. Sterno-thoracic cardiopulmonary resuscita-

tion (SST-CPR) is a new method that performs sternal

compression and thoracic constriction simultaneously in

a cycle (Fig. 1). SST-CPR has shown to be associated

with a higher mean arterial pressure, coronary perfusion

pressure, and end-tidal CO2 tension. This demonstrates

that haemodynamically, it outperforms STD-CPR [7].

This study was designed to assess whether improvements

in haemodynamic effects translated to improved survi-

val in an animal model.

2. Materials and method

The experimental protocol was reviewed and ap-

proved by the Animal Research Committee of the

Wonju College of Medicine, Yonsei University.

* Corresponding author. Tel.: �/82-33-741-1611; fax: �/82-33-742-

3030.

E-mail address: shwang@wonju.yonsei.ac.kr (S.O. Hwang).

Resuscitation 53 (2002) 209�/216

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PII: S 0 3 0 0 - 9 5 7 2 ( 0 2 ) 0 0 0 1 1 - 4

2.1. Experimental preparation

2.1.1. Anaesthesia, artificial ventilation and ECG

monitoring of animals

Thirty adult mongrel dogs weighing 19�/31 kg were

anaesthetized with an intramuscular injection of keta-

mine (20 mg/kg) for induction and intermittent intrave-nous injections of sodium pentobarbital (20�/30 mg/kg)

for maintenance. The depth of anaesthesia was assessed

by the respiration rate, pulse rate and animal movement,

and an additional sodium pentothal was injected as

necessary. Under anaesthesia, the dogs were placed in a

supine position on a table manufactured for the experi-

ment, and restrained at the four extremities. After

tracheal intubation, the dogs were mechanically venti-lated using a volume-cycled respirator (Companion 2800

portable ventilator, Puritan-Bennett Corporation,

USA). End-tidal carbon dioxide was measured using a

rapid response mainstream capnograph (Tidal wave

Novametrix capnography, Novametrix, USA). The tidal

volume was set initially at 12 ml/kg and the ventilation

rate at 20 breaths per minute; ventilator settings were

adjusted to maintain end-tidal carbon dioxide at 35mmHg. After shaving the thorax, limbs, and both

cervical areas, the ECG was monitored via lead II.

2.1.2. Catheterization for haemodynamic monitoring

After achieving surgical anaesthesia, the right internal

jugular vein and right femoral artery were exposed.

Using cutdown technique, an introducer sheath (7.5 Fr,

Arrow international Inc., USA) was placed in the right

femoral artery, and a micromanometer-tipped catheter

(Microtip catheter transducer SPC-350, 5 Fr, 120 cm,

Millar instruments, USA) was advanced into the

thoracic aorta. From a right internal jugular veincutdown, pairs of introducing sheaths (7.5 Fr, Arrow

international Inc., USA) were placed, and a microman-

ometer-tipped catheter (Microtip catheter transducer

SPC-350, 5 Fr, 120 cm, Millar instruments, USA) was

advanced into the right atrium through one of the

sheaths. A balloon tipped pacing electrode (5 Fr, bipolarlead, Arrow international Inc., USA) was introduced to

the right ventricle through one of the other sheaths to

induce ventricular fibrillation. The position of the

pacing electrode on the right ventricle was confirmed

by captured beats on the ECG monitor. A Swan-Ganz

catheter (7 Fr, Swan-Ganz Catheter, Arrow interna-

tional Inc., USA) was introduced through the right

internal jugular vein into the pulmonary artery tomeasure cardiac output. The catheter position was

verified by the presence of typical pressure waves, and

reconfirmed by autopsy at the end of each experiment.

2.2. Experimental procedure

2.2.1. Measurement

Aortic pressure was monitored using a catheter in the

aorta. Dogs were stabilized after catheterization for 10

min, and the baseline data including aortic blood

pressure, right atrial pressure, end tidal CO2 tension,

and cardiac output were measured immediately before

induction of ventricular fibrillation. These variables

were monitored continuously and recorded using acomputerized data acquisition system (MacLab/4S

data acquisition system, ADI instruments, USA) during

the experiment.

The sampling rate of recording was 200 Hz. Cardiac

output was measured in triplicate, and aortic pressure

and right atrial pressure were measured as the mean

value of five consecutive compression�/relaxation cycles.

Coronary perfusion pressure during CPR was calculatedby subtracting the right atrial pressure from the aortic

pressure during diastole from the computerized data

analysis.

Fig. 1. Schematic presentation of simultaneous sternothoracic cardiopulmonary resuscitation. During compression, the strap constricts the thorax

while the piston depresses the sternum.

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216210

2.2.2. Induction of cardiac arrest

Ventricular fibrillation was induced by passing an AC

current of 30�/60 mA through the right ventricular

pacing catheter for 10�/20 s using a supply unitmanufactured by our research team. Ventricular fibrilla-

tion was confirmed by a fibrillation wave on the ECG

monitor, the disappearance of pulsatile aortic pressure,

and an aortic systolic pressure below 10 mmHg.

2.2.3. CPR and assessment of the survival

The animals were randomly assigned to STD- and

SST-CPR. STD-CPR was performed with an automaticmechanical resuscitator (Thumper†, Michigan Instru-

ments, USA) as described in the 1992 Guidelines of the

American Heart Association [8]. Chest compression was

provided on the lower 1/3 of the sternum at a rate of 80

cycles per minute and the force of chest compression was

adjusted to depress the sternum by 30% of its ante-

roposterior diameter. The compression to relaxation

ratio was maintained at 50:50. SST-CPR was performedby placing the piston on the sternum of the animal,

followed by tightening the thorax with a belt, and

compressing the piston of the SST-CPR with an

automatic mechanical resuscitator. The rate, depth,

and duration of the compression of the SST-CPR were

the same as that of the standard CPR. Ventilation was

delivered after every fifth compression by an automatic

mechanical resuscitator, and provided an inspired oxy-gen concentration of 100%. No intervention was applied

for 4 min after the induction of ventricular fibrillation,

and CPR was performed after this period starting with

epinephrine (adrenaline) injection. Epinephrine (adrena-

line) was administered as a 1 mg bolus into the right

atrium at the beginning of the CPR and repeated every 3

min. CPR was performed for 6 min. Ten minutes after

the induction of ventricular fibrillation, electrical defi-brillation was attempted at 2 J/kg, with second and

subsequent attempts at 4 J/kg. If unsuccessful, full

advanced life support, including the administration of

lidocaine, was provided, if animals did not attain a

return of spontaneous circulation (ROSC), after 20 min,

CPR was discontinued. Successfully resuscitated ani-

mals were supported aggressively in an intensive care

setting. Systolic blood pressure was maintained at �/100mmHg with volume administration and/or vasopressors,

which included dopamine or norepinephrine (nor adre-

naline) as indicated. ROSC was defined as an unassisted

aortic pulse with a perfusion rhythm on the ECG

monitor for ]/3 min. Haemodynamic monitoring was

continued for 3 h after the induction of cardiac arrest.

Catheters, except for one in the right atrium, were

removed after the last haemodynamic measurement.Survival was determined at 12 h after initial cardiac

arrest. After the completion of the experiment, eutha-

nasia was performed with an intravenous injection of

KCl. Partial autopsy of the thorax was performed to

verify organ injury caused by each CPR method.

2.3. Data analysis

Differences in aortic blood pressure, right atrial

pressure, coronary perfusion pressure, cardiac output,

and end-tidal CO2 tension generated by STD- and SST-

CPR were evaluated by t -test, and the haemodynamic

parameters of the survivor and non-survivor groups by

Mann�/Whitney U -test. Rates of survival were analyzed

by Fisher’s exact test. A probability of B/0.05 wasconsidered statistically significant.

3. Results

Twenty-nine animals were studied among 30 animals,

excluding one dog that went into cardiac arrest during

preparation. Animals were randomly assigned to eachCPR group; 15 for STD-CPR and 14 for SST-CPR.

Baseline data including body weight, chest circumfer-

ence, and haemodynamic variables before cardiac arrest,

were not significantly different for the two groups

(Table 1).

As shown in Table 2, SST-CPR produced a significant

better haemodynamic effect than STD-CPR during

CPR. Haemodynamic data during the early phase (5.5min after cardiac arrest) of the CPR attempt showed the

efficacy of SST-CPR compared with STD-CPR. The

mean systolic aortic pressure was higher for SST- than

STD-CPR (919/47 vs 479/24 mmHg, P�/0.007), and

the mean diastolic aortic pressure was also higher for

SST- than STD-CPR (439/24 vs 179/10 mmHg, P�/

0.002). Mean diastolic coronary perfusion pressure in

Table 1

Baseline measurements of experimental animals

Variables STD-CPR group

(n�/15)

SST-CPR group

(n�/14)

Body weight (kg) 219/3 239/4

Chest circumference (cm) 599/2 629/5

Heart rate (/min) 2029/28 1889/33

Systolic aortic pressure

(mmHg)

1509/27 1509/27

Diastolic aortic pressure

(mmHg)

1149/22 1149/22

Mean aortic pressure

(mmHg)

1269/23 1249/29

Right atrial pressure

(mmHg)

4.19/1.9 3.99/1.1

Cardiac output (l/min) 4.429/1.15 4.209/1.68

ET CO2 (mmHg) 369/4 359/3

Data are given as mean9/S.D. No statistical difference between two

groups. STD-CPR, standard cardiopulmonary resuscitation; SST-

CPR, simultaneous sternothoracic cardiopulmonary resuscitation;

ETCO2, end tidal carbon dioxide tension.

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216 211

the SST-CPR group was 359/25 mmHg vs 139/9 mmHg

in the STD-CPR group (P�/0.006), and coronary

perfusion pressure higher than 30 mmHg with SST-

CPR appeared to be associated with a greater likelihood

of ROSC. The mean right atrial pressure was 519/33

mmHg for SST-CPR, which was 189/12 mmHg higher

than that of STD-CPR (P�/0.002). The higher right

atrial pressure showed that SST-CPR generated higher

intrathoracic pressure than STD-CPR at the same

compression depth. This finding suggested that the

thoracic constriction of SST-CPR produced a rise in

the intrathoracic pressure. End-tidal CO2 tension, used

to reflect the cardiac output, was 99/4 mmHg for SST-

CPR, which was higher than the 39/2 mmHg achieved

by STD-CPR (P�/0.023). Cardiac output was 0.599/

0.67 mmHg for SST-CPR, and unmeasurable by STD-

CPR. Moreover, SST-CPR was superior to STD-CPR

throughout the resuscitation period. Systolic and dia-

stolic aortic pressure, coronary perfusion pressure, and

end-tidal CO2 tension at the late phase of CPR (8.5 min

after cardiac arrest) were higher for SST- than STD-

CPR. This finding suggests that the haemodynamic

effect of SST-CPR was consistently maintained during

the entire resuscitative period.

Haemodynamic values in the survivors and non-

survivors during CPR are shown in Table 3. For STD-

CPR, aortic pressure, right atrial pressure, coronary

perfusion pressure, and end-tidal CO2 tension, were not

significantly different for survivors and non-survivors.

For SST-CPR, aortic pressure, right atrial pressure, and

coronary perfusion pressure in the survivors were higher

than in the non-survivors during CPR.

Two dogs (13%) with STD-CPR attained ROSC after

defibrillation and survived for 12 h. Seven dogs (50%)

from the SST-CPR group attained ROSC after defi-

brillation and all survived for 12 h (Table 4). The

number of shocks required to produce ROSC was not

different in STD- and SST-CPR groups.

Haemodynamic data for 3 h after ROSC were similar

for STD- and SST-CPR (Table 5). No animal resusci-tated with STD- or SST-CPR required the infusion of

vasopressors to maintain perfusion pressure after

ROSC.

The autopsy undertaken to check for complications of

CPR verified that SST-CPR did not increase the

frequency of complications compared with STD-CPR.

Among the animals that received STD-CPR, two cases

of rib fracture were found, and among animals thatreceived SST-CPR, a case of rib fracture and a case of

lung contusion with minimal haemothorax occurred.

4. Discussion

In this study, we found that SST-CPR were more

effective than STD-CPR in improving the rate of ROSC

and short-term survival in a canine cardiac arrest model.

SST-CPR was also found to have better haemodynamiceffects than STD-CPR. Specifically it enhanced systolic

and diastolic blood pressures, markedly increased cor-

onary perfusion pressure, and produced higher end-tidal

CO2 tension. In particular, SST-CPR produces higher

coronary perfusion pressure compared with STD-CPR,

which is the most decisive index of ROSC in cardiac

arrest patients. Moreover, the high survival rate of

animals with SST-CPR reflects the haemodynamicsuperiority of SST- over STD-CPR.

Survival rate after cardiac arrest is mainly attributed

to the spread of CPR to the layperson, reduced EMS

response time and the introduction of the defibrillator to

the scene and ambulance. Despite its low haemody-

namic efficacy, external chest compression has remained

the best way of generating blood flow in patients with

cardiac arrest since its first trial in 1960s [9]. We believethat there is a need for a new method of generating an

artificial circulation that provides adequate tissue perfu-

sion. The development of such a method could represent

Table 2

Haemodynamics recorded during STD- and SST-CPR

Aortic

systolic

pressure

(mmHg)

Aortic

diastolic

pressure

(mmHg)

Mean

aortic

pressure

(mmHg)

Mean right

atrial

pressure

(mmHg)

Cardiac

output

(l/min)

Coronary

perfusion

pressure

(mmHg)

ETCO2

(mmHg)

5.5 min after cardiac arrest

STD-CPR (n�/15) 479/24 179/10 279/13 189/12 0 139/9 39/2

SST-CPR (n�/14) 919/47 439/24 599/32 519/33 0.599/0.67 359/25 99/4

P value 0.007 0.002 0.003 0.002 �/ 0.006 0.023

8.5 min after cardiac arrest

STD-CPR (n�/15) 549/33 199/13 319/17 209/13 0 159/12 19/2

SST-CPR (n�/14) 959/55 449/24 619/33 409/30 0.149/0.46 269/23 59/12

P value 0.033 0.004 0.008 0.039 �/ 0.011 0.240

Data are given as mean9/S.D. STD-CPR, standard cardiopulmonary resuscitation; SST-CPR, simultaneous sternothoracic cardiopulmonary

resuscitation; ETCO2, end tidal carbon dioxide tension.

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216212

a major turning point in the survival rates after cardiac

arrest.

Since 1980, alternative methods of increased blood

flow have been extensively studied, but these have only

rarely been applied to clinical practice. Two approaches

have been taken to develop new CPR techniques. These

have involved either modification of STD-CPR or the

invention of new devices. Modifications of STD-CPR

have involved simultaneous ventilation compression

CPR (SVC-CPR) [10], interposed abdominal compres-

sion CPR (IAC-CPR) [11], and high frequency CPR

[12]. New CPR devices include: active compression

decompression CPR (ACD-CPR) [13], phased chest

and abdominal compression�/decompression CPR (Life-

stick CPR) [14], vest CPR [15], and use of an inspiratory

impedance valve [16]. We have designed SST-CPR to

exploit both external chest compression, and thoracic

constriction with a strap. SST-CPR is a simple variation

of standard CPR, and is accomplished by the addition

of a thoracic strap that constricts the thorax, while a

piston compresses the sternum. After applying the SST-

CPR device, CPR applied in the same manner as

standard CPR. The mechanism of blood flow by SST-

CPR is designed to apply the cardiac pump and the

thoracic pump simultaneously. SST-CPR is believed to

be haemodynamically superior to STD-CPR, because it

Table 3

Haemodynamics recorded during STD- and SST-CPR in survivors and non-survivors

Aortic

systolic

pressure

(mmHg)

Aortic

diastolic

pressure

(mmHg)

Mean

aortic

pressure

(mmHg)

Mean right

atrial

pressure (mmHg)

Cardiac

output

(l/min)

Coronary

perfusion

pressure

(mmHg)

ETCO2

(mmHg)

5.5 min after cardiac arrest

STD-CPR Survivors (n�/2) 549/16 299/11 379/12 219/8 0 229/11 6.009/0.00

Non-survivors (n�/13) 469/25 159/9 259/13 189/13 0 119/8 2.739/3.93

P value 0.663 0.086 0.255 0.766 �/ 0.134 0.280

SST-CPR Survivor (n�/7) 1219/42 579/25 789/31 559/31 0.719/0.67 499/26 14.79/4.72

Non-survivor (n�/7) 619/32 299/14 399/20 479/37 0.479/0.71 219/14 3.339/5.31

P value 0.019 0.038 0.026 0.703 0.567 0.043 0.003

8.5 min after cardiac arrest

STD-CPR Survivors (n�/2) 599/24 299/13 399/17 229/7 0 219/16 3.009/4.24

Non-survivors (n�/13) 299/13 189/13 299/17 209/14 0 149/11 0

P value 0.830 0.305 0.504 0.821 �/ 0.457 �/

SST-CPR Survivor (n�/7) 1359/52 649/12 889/22 539/39 0.309/0.68 539/14 9.809/16.9

Non-survivor (n�/7) 639/32 279/16 399/21 299/15 0 219/19 0

P value 0.020 0.002 0.005 0.197 0.297 0.014 �/

Data are given as mean9/S.D. STD-CPR, standard cardiopulmonary resuscitation; SST-CPR, simultaneous sternothoracic cardiopulmonary

resuscitation; ETCO2, end tidal carbon dioxide tension.

Table 4

Haemodynamics recorded after ROSC in survivors of STD- and SST-CPR group

Time after ROSC Aortic mean

(mmHg)

Heart rate

(/min)

Cardiac output

(l/min)

PCWP

(mmHg)

Stroke volume

(ml)

SVR

(dyn s/cm5)

Immediate STD-CPR (n�/2) 1549/27 2009/28 2.689/0.62 229/4 149/5 44769/286

SST-CPR (n�/7) 1419/79 1999/24 2.259/1.00 159/8 119/4 54319/3198

P value 0.835 0.949 0.593 0.299 0.484 0.703

1 h STD-CPR (n�/2) 1219/5 1639/45 2.339/0.20 189/11 159/3 40269/196

SST-CPR (n�/7) 1089/40 1599/17 2.189/0.86 159/8 149/6 46789/2989

P value 0.692 0.875 0.828 0.691 0.779 0.779

2 h STD-CPR (n�/2) 1349/8 1599/41 2.349/0.79 99/8 159/1 48029/1979

SST-CPR (n�/7) 1069/20 1659/26 1.459/0.52 139/7 99/3 62549/2060

P value 0.128 0.818 0.131 0.524 0.435 0.435

3 h STD-CPR (n�/2) 1179/4 1599/47 2.959/0.50 129/5 199/3 30839/716

SST-CPR (n�/7) 1069/26 1509/16 1.579/0.82 119/6 109/5 61049/2407

P value 0.609 0.737 0.102 0.960 0.107 0.174

Data are given as mean9/S.D. ROSC, return of spontaneous circulation; STD-CPR, standard cardiopulmonary resuscitation; SST-CPR,

simultaneous sternothoracic cardiopulmonary resuscitation; PCWP, pulmonary capillary wedge pressure; SVR, systemic vascular resistance.

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216 213

maintains the manner of STD-CPR, but additionally

constricts the thorax [7]. As the piston compresses the

sternum, the strap progressively constricts the thorax,

and prevents the thorax from deforming on both sides,

thus maximizing the rise of intrathoracic pressure.

Constriction of the thorax by a strap leads to further

augmentation of the aortic pressure during late phase of

compression systole. Moreover, rapid relaxation of the

strap during the diastolic phase generates a transient

negative intrathoracic pressure. A reduction in in-

trathoracic pressure during the relaxation period en-

hances venous return by decreasing the right atrial

pressure, which may contribute to improve systemic

and coronary blood flow [4].

The primary purpose of CPR is to restore the

circulation, and the ultimate goal of CPR is to improve

survival. Haemodynamically a vital factor to restore a

spontaneous circulation is to generate coronary perfu-

sion pressure during CPR. This new method appears to

improve coronary perfusion pressure and blood flow.

Coronary perfusion pressure needs to be maintained

above 20 mmHg to achieve a ROSC during CPR [17]. In

this study, 10 (71%) of 14 dogs that received SST-CPR

had a coronary perfusion pressure above 20 mmHg and

most of those survived while only two (13%) of 15 dogs

that received STD-CPR showed coronary perfusion

pressure above 20 mmHg. The difference in the cor-

onary perfusion pressures generated by each method

manifested itself as different ROSC and survival rates.

These results suggest that coronary perfusion pressure is

a major determinant for restoring a spontaneous

circulation. Moreover, the higher systolic aortic pressure

generated by SST-CPR also may improve cerebral

perfusion, and should improve neurological outcome

and long-term survival.

The introduction of new CPR device, raises concern

that mechanical trauma may be caused by the device.

Standard CPR may lead to various injuries [18,19], and

CPR devices may also cause injuries to the chest or

abdomen, depending on which part is in compressed.

During ACD-CPR, significantly more sternal and rib

fractures were found compared to STD-CPR [20].

However, phased chest and abdominal compression�/

decompression CPR and ACD-CPR did not increase

incidence of injury to the chest or abdomen even though

active decompression is involved [21]. Notably, SST-

CPR did not increase the incidence of injury to the chest

or rib fracture compared to STD-CPR. However, lung

contusion accompanied by a small haemothorax devel-

oped in one case. In that case, lung contusion was found

at the posterior of the lung. Rapid pulling of the

thoracic strap during compression might have been the

cause of this lung injury. Further investigation is

required to verify the incidence and the cause of this

complication.

This study has some shortcomings. We could not

assess the long-term survival or the neurological status

of the animals, because of research facility limitations.

In view of the fact that a number of patients with a

restored circulation die of organ failure, such as of brain

damage, a higher rate of ROSC might not be always

connected with a higher long-term survival rate. How-

ever, we believe that improvements in haemodynamics

when SST-CPR is used might be expected to reduce the

incidence of brain damage.We could not measure the extent of tissue perfusion

for each method. Cardiac output was measured using a

thermodilution catheter, but because of the poor

circulation, it was impossible to measure cardiac output

during STD-CPR. End tidal CO2 tension was used as an

indicator of blood flow, but it is known that in certain

circumstances end tidal CO2 tension may not reflect the

circulation precisely, for example, due to the effect of

epinephrine (adrenaline) treatment [22]. However, in

this study we believe that end tidal CO2 tension allowed

realistic circulatory volume comparisons, because the

same dosage of epinephrine (adrenaline) was used in

each group, and the laboratory conditions were iden-

tical. However, our result cannot be directly transferred

to humans because the chest configurations of the dog

and human are different. Nevertheless, SST-CPR is

more suitable for humans than animals, because the

human chest is relatively flat, which allows simultaneous

cardiac compression and thoracic constriction to be

easily performed.

Based on our result, we conclude that SST-CPR

improves the short-term survival rate without any

increased incidence of injury in a canine model of

cardiac arrest. Clinical trials are needed to determine

whether SST-CPR causes a similar favourable haemo-

dynamic effect in humans.

Acknowledgements

This study was partly presented at American Heart

Association 72nd Scientific Sessions, New Orleans, LU,

November 1999. This study was supported by a grant of

the RRC Program of MOST and KOSEF, Republic of

Korea.

Table 5

Outcome according to CPR method

STD-CPR (n�/15) SST-CPR (n�/14) P value

ROSC (%) 2 (13) 7 (50) 0.048

Survival (%) 2 (13) 7 (50) 0.048

STD-CPR, standard cardiopulmonary resuscitation; SST-CPR,

simultaneous sternothoracic cardiopulmonary resuscitation; ROSC,

return of spontaneous circulation.

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216214

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Portuguese Abstract and Keywords

O nosso grupo ja tinha relatado que era possıvel fazer reanimacao com compressao esterno-toracica simultanea (SST-CPR) usando

um dispositivo que comprime o esterno e simultaneamente faz constricao toracica circunferencialmente durante a sıstole de

compressao e pode ser aplicado com os algoritmos de reanimacao standards (STD-CPR). Este estudo tem por objectivo comparar a

sobrevida da STD-CPR e SST-CPR em caes em paragem cardıaca. Foram usados 29 caes mongrel, entre 19 e 31 kg. Depois de 4

minutos de FV induzida por corrente AC, randomizaram-se os animais para serem reanimados com o SST (14) ou STD-CPR (15).

Ao fim de 10 minutos de paragem foi feita desfibrilhacao e iniciadas manobras de reanimacao standard se aquela nao teve sucesso.

Durante a reanimacao e no perıodo pos recuperacao da circulacao foram medidos a pressao aortica, a pressao de perfusao

coronaria e o CO2 end tidal . A sobrevivencia foi determinada 12 horas apos a inducao da paragem. A SST-CPR permitiu obter uma

pressao arterial sistolica superior (P B/0.001; 919/47 vs 479/24 mmHg), uma pressao arterial diastolica superior (P B/0.001; 439/24

vs 179/10 mmHg), uma pressao de perfusao coronaria superior (P B/0.001; 359/25 vs 139/9 mmHg) e um CO2 end tidal tambem

mais alto (P B/0.001; 99/4 vs 39/2 mmHg). Dois dos 15 animais (13%) reanimados com STD-CPR e 7 dos 14 (50%) reanimados com

SST-CPR sobreviveram 12 horas (P B/0.05). Em conclusao, a reanimacao com SST-CPR em caes melhora a sobrevivencia a curto

prazo, quando comparado com STD-CPR.

Palavras chave : Reanimacao cardiorespiratoria; Paragem cardıaca

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216 215

Spanish Abstract and Keywords

Previamente hemos reportado que la resucitacion cardiopulmonar cardiotoracica simultanea (SST-CPR) usando un aparato que

comprime el torax y comprime circunferencialmente el torax durante la sistole por compresion puede ser alcanzadausando

reanimacion cardiopulmonar estandar (STD-CPR). Este estudio fue disenado para evaluar si acaso la SST-CPR mejora la tasa de

sobrevida en perros con paro cardiorespiratorio comparado con la STD-CPR. 29 perros mongrel de (19�/31 kg) se incluyeron en este

estudio. Despues de 4 minutos de fibrilacion ventricular inducida por una corriente AC, se randomizaron los animales para ser

resucitados ya sea con STD-CPR (n�/15) o con SST-CPR (n�/14). Se intento la desfibrilacion 10 minutos despues de la induccion

del paro cardıaco. Si la desfibrilacion fracasaba se iniciaba apoyo vital avanzado estandar. Durante la reanimacion cardiopulmonar

y en el perıodo postresucitacion se midieron presion arterial, presion de perfusion coronaria y tension de CO2 espiratorio final. Se

determino sobrevida 12 hrs despues de la induccion del paro cardıaco. La SST-CPR resulto en presion arterial sistolica (919/47,vs

479/24 mmHg), presion diastolica (439/24 vs179/10 mmHg), presion de perfusion coronaria (359/25 vs 139/9 mmHg), tension de

fin de espiracion (99/4 vs 39/2 mmHg) significativamente mas altas (P B/0.001). Dos de 15 animales (13%) resucitados con STD-

CPR y siete de los 14 (50%) resucitados con SST-CPR sobrevivieron por 12 horas despues del paro cardiorespiratorio (P B/0.05) En

conclusiones, SST-CPR mejora la tasa de sobrevida a corto plazo en paro cardiorespiratorio canino comparado con la STD-CPR.

Palabras clave : Reanimacion cardiopulmonar; Paro cardiorespiratorio

S.O. Hwang et al. / Resuscitation 53 (2002) 209�/216216