Article, Emergency Medicine

The effects of 3 different compression methods on intrathoracic pressure in a swine model of ventricular fibrillation

Unlabelled imageAmerican Journal of Emergency Medicine (2013) 31, 100-107

Original Contribution

The effects of 3 different compression methods on intrathoracic pressure in a swine model of ventricular fibrillation

Wei Yuan MM, Shuo Wang MD, Chun-Sheng Li MD?

Beijing Chao-Yang Hospital, Affiliated to Capital Medical University, Beijing, China

Received 8 April 2012; revised 22 May 2012; accepted 15 June 2012

Abstract

Objective: The aim of this study was to provide a realistic comparison of 3 different extracorporeal compression methods during cardiopulmonary resuscitation on intrathoracic pressure (ITP), hemodynamics, and Oxygen metabolism in a swine model of ventricular fibrillation (VF).

Methods: Eight minutes after the development of VF, pigs were subjected to 3 different extracorporeal compression methods: traditional artificial Manual compression, mechanical compression using an AutoPulse apparatus, or manual sucker. Heart rhythm was assessed by electrocardiography after 5 cycles of extracorporeal compression. If VF still occurred, electrical defibrillation was performed. After defibrillation, an additional 5 cycles of extracorporeal compression were performed. Resuscitation was considered to have failed if the above procedure was continued for 30 minutes without return of spontaneous circulation. Hemodynamics and ITP waveforms were monitored continuously. Oxygen metabolism indices were measured, and success rates were compared among the groups.

Results: Manual compression showed advantages over both of the other methods in terms of maximal ITP and fluctuation amplitude, hemodynamic and oxygen dynamic changes, convenience of administration, and duration of treatment. Survival rates and Cerebral performance category scores for the manual compression group were significantly higher than that for the other groups.

Conclusions: Mechanical compression cannot replace traditional artificial manual compression, which remains the preferred method for cardiopulmonary resuscitation.

(C) 2013

Introduction

In cardiopulmonary resuscitation (CPR), increasing intrathoracic pressure (ITP) and pressure changes are significant factors contributing to the improvement of

* Corresponding author. Emergency Department, Beijing, Chao-Yang Hospital, Affiliated to Capital Medical University, Chaoyang Distract, Beijing 100020, China.

E-mail address: [email protected] (C.-S. Li).

perfusion pressure in vital organs, promoting blood circula- tion, and increasing survival rates [1].

Techniques used for extracorporeal compression in out- of-hospital cardiac arrest (OHCA) include artificial manual compression and mechanical compression, and the relative advantages and disadvantages of these 2 methods remain a subject of considerable debate. The 2010 CPR guidelines questioned artificial mechanical setups [2], which are associated with certain advantages, including accurate compression depth, stable compression frequency, and resistance to fatigue as well as several disadvantages, such

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as not performing in real-time, requiring extended prepara- tion time, and introducing pauses in compression. Experi- ments in large animal models [3] have compared artificial apparatuses prepared in advance with manual compression, but this does not apply to real-life situations. Timely and effective extracorporeal compression is the most effective rescue method for OHCA, and the time from cardiac arrest to initiation of compression is a critical factor determining resuscitation outcomes. The aim of this study was to provide a realistic comparison between artificial apparatuses and manual compression for CPR; to do this, we mimicked OHCA in real-time using ventricular fibrillation (VF) for 8 minutes in a large animal model.

Materials and methods

Preparation of experimental animals

Twenty-one Landrace (3-4 months old, 30 +- 1 kg, male and female) were purchased from the Beijing Registered Experimental Animal Center. Before experimentation, pigs were fasted for 12 hours with free access to water. Anesthesia was induced by Intramuscular injection of ketamine (20 mg/ kg), and subsequent ear vein injection of propofol (1.0 mg/kg) according to pervious described [4,5]. The pigs were maintained in a surgical plane of anesthesia by intravenous infusion of pentobarbital (8 mg/kg per hour) and were fixed on an operating table in the supine position. Intubation was performed with an endotracheal tube (6.5F) connected to a ventilator (Drager-Evata IV, Draeger, Germany). After intubation, inspired oxygen concentration, ventilation fre- quency, and tidal volume were 40%, 12 times per minute, and

15 mL/kg, respectively. A respiration monitor (CO2 SMOPlus; Respironics, Cheshire, CT) was used to monitor tidal volume. Electrocardiography was performed using an electrocardiography monitor (HP-M1165; Hewlett-Packard Co, Fullerton, CA). An angiography catheter (7F) was inserted into the left femoral vein for placement of bipolar temporary pacing electrodes into the right ventricle and for injection of iced saline to monitor cardiac output (CO). An arterial catheter (5F, Pulsiocath PV2015L20; Pulsion Med- ical Systems, Munich, Germany) was placed in the descend- ing artery through the left femoral artery, and arterial pressure was monitored using a PiCCO monitor (Pulsion Medical Systems). A Swan-Ganz catheter (7F, Edwards Life Sciences, Irvine, CA) was advanced from the Right internal jugular vein and ftow directed into the pulmonary artery for the measurement of right atrial pressure through a pressure transducer (Biosensors International Corp, Kallang Avenue, Singapore). The animals were randomly divided into 3 groups (n = 7 animals in each group): the A-CPR group, using an AutoPulse apparatus (ZOLL Medical Corp, Chelmsford, MA); the ACD-CPR group, using a manual sucker apparatus (Ambu International, Glostrup, Denmark); and the C-CPR group, using traditional artificial manual hand compression.

Establishment of the model and experimental procedures

Animals were permitted to recover for 45 minutes after surgery. The pacing electrode was then connected to a program-controlled medical stimulator (GY-600A; HuaNan Instrument Co, Ltd, KaiFeng, Henan, China). An esophagus output model (S1S2 300/200 milliseconds) was used to evoke continuous electrical stimulation at a ratio of 8:1 and a step width of 10 milliseconds until occurrence of VF [6]. The confirmation of VF included a rapid decrease in Arterial blood pressure and VF waveforms detected by electrocardiography. Compression apparatuses were placed 8 minutes after the occurrence of VF. In the A-CPR group, the frequency and depth of the compressions were automatically set to 80 per minutes and 20% reduction in the anterior-posterior dimension of the animal’s chest, respectively. The AutoPulse device used in the present study comprised a load-distributing band that was scaled down from the original device designed for human use, allowing an analogous portion of the porcine thorax to be compressed by the band during compression. In the ACD- CPR and C-CPR groups, the frequency was set at 100 times per minute, and the depth was 50 +- 1 mm. Mechanical ventilation was given at a rate of 6 times per minute, with a fraction of inspired oxygen of 100% and tidal volume of 300 mL. Heart rhythm was assessed by electrocardiography after

5 cycles of extracorporeal compression. If VF was still present, electrical defibrillation was performed once at 150 J (biphasic exponential chopped wave). If the first defibrilla- tion was unsuccessful, epinephrine (0.02 mg/kg) was given intravenously, followed by 2 minutes of CPR [7]. After each 2 minutes of CPR, a 10-second pause was interjected to analyze heart rhythm and prepare for another defibrillation attempt. Additional epinephrine, if needed, was given at 3- minute intervals. Heart rhythm was monitored until return of spontaneous circulation (ROSC). Resuscitation was consid- ered to have failed if the above procedure was continued for 30 minutes without ROSC. Return of spontaneous circula- tion criteria included recovery of blood pressure, systolic artery pressure greater than 50 mm Hg, or a mean arterial pressure (MAP) at least 60 mm Hg for more than 10 minutes. After successful resuscitation, the animals underwent a 4- hour intensive care period, during which Ringer solution (20 mL/kg) was administered without any other drugs. The animals were allowed to recover from anesthesia, placed in observation cages, and monitored until 24 hours after resuscitation. During this observation period, the animals had free access to water.

The Quality of chest compressions was monitored using a

HeartStart MRx Monitor/Defibrillator with Q-CPR (Philips Medical Systems, Best, Holland). objective measurements were provided by a compression sensor, which measured the acceleration of the chest during chest compressions. An algorithm in the HeartStart MRx converted this to compres- sion depth. Changes in the thoracic cage were shown as a

characteristic waveform on the screen (Fig. 1), and the compression rate was also displayed. Two horizontal lines drawn in the wave sector indicate the target zone for good compression depth in accordance with American Heart Association guidelines.

Monitoring parameters and methods

ITP waveforms

An incision was performed with a scalpel between right ribs 10th and 11th to cut the skin and superficial muscles. A blunt apparatus was pushed through the chest wall to the Pleural cavity for placement of a large venous catheter, which was connected to a BL-420F Data Acquisition and Analysis System (Taimeng Technology Co, Ltd, Chengdu, Sichuan China) to monitor ITP waveforms.

Hemodynamics

Blood pressure, CO, and heart rate were monitored by a PiCCO monitor. A total of 15-mL iced saline was injected rapidly through a femoral venous catheter to measure CO by the thermodilution method. coronary perfusion pressure was measured as the difference between the middle to late diastolic pressures or CPR decompression time of the aortic and right atrial pressures.

Oxygen metabolism indices

Arterial blood gas was measured to calculate partial pressure of oxygen (PAO2), oxygen delivery (DO2), oxygen consumption (VO2), and Oxygen extraction ratio (ERO2).

Preparation time from VF to compression initiation (8 minutes)

A stopwatch was used to monitor the apparatus preparation time.

24-hour survival rate,”>ROSC time, 24-hour survival rate, and 24-hour cerebral performance category

A stopwatch was used to monitor ROSC times, and the survival time for each pig was recorded. Animals were evaluated at 24 hours after ROSC and awarded a swine

Cerebral Performance Category score. The CPC evaluation used a 5-point scale to assess neurologic function (1, normal: no difficulty with standing, walking, eating, or drinking, and alert and fully responsive to environmental stimuli; 2, mild disability: able to stand but exhibiting an Unsteady gait, drinking but not eating normally, and showing a slower response to environmental stimuli; 3, severe disability: unable to stand or walk without assistance, not drinking or eating, awake but failing to respond normally to noxious stimuli; 4, coma; and 5, brain dead) [8].

Statistical analysis

Data with normal distributions were reported as mean +- SD. Discrete variables, such as ROSC time and survival rate, were compared using Fisher exact test. Continuous variables, including hemodynamics and respiratory parameters, were compared by repeated-measures and multivariate analysis of variance. Significant differences between groups were detected by the Least Significant Difference test. P b .05 was regarded as statistically significant.

Results

Differences in ITP

Baseline ITP measurements ranged from -12 to -16 mm Hg. To account for differences in baseline values, the maximum and minimum ITP values in Table 1 represent absolute differences from baseline values.

Among the 3 resuscitation methods, maximum ITPs were higher in the C-CPR and A-CPR groups than in the ACD- CPR group. No significant difference between the C-CPR and A-CPR groups was observed (P N .05), whereas the differences between the C-CPR and ACD-CPR groups were highly significant (P b .01).

With regard to changes in ITP, A-CPR and C-CPR methods resulted in greater pressure changes than the ACD- CPR method (P b .05), and the change observed in the C-CPR

Fig. 1 Quality control of CPR.

Table 1 Effect of compression method on ITP (mean +- SD)

Group

A-CPR (n = 7)

ACD-CPR (n = 7)

C-CPR (n = 7)

Maximal ITP (mm Hg)

11.71 +- 1.95 a

3.08 +- 0.66 b

17.21 +- 11.01

Minimal ITP (mm Hg)

-(7.08 +- 3.08) a

-(5.29 +- 0.56) b

-(7.14 +- 4.17)

Difference (mm Hg)

18.79 +- 3.60 a

8.37 +- 0.85 b

24.36 +- 14.28

Difference = maximal ITP – minimal ITP.

a P b .05 vs ACD-CPR group.

b P b .01 vs C-CPR group.

group was highly significant (P b .01). Intrathoracic pressure waveforms are shown in Fig. 2A to C.

Changes in ITP during CPR

The CPR process was divided into 4 stages according to ITP changes (Fig. 3): Stage I, after anesthesia, tracheal

intubation was performed for additional ventilation, but the animals were also respiring spontaneously. The waveform showed several pressure increases (mechanical ventilation) separated by deepened negative pressure waveforms (spon- taneous respiration). Stage II, after surgery and VF establishment, the animals showed gasping, with obviously increased breathing amplitude, prolonged expiratory dura- tion, and widened and deepened negative ITP. Stage III,

Fig. 2 Intrathoracic pressure waveforms. A, Intrathoracic pressure waveform in the A-CPR group. B, Intrathoracic pressure waveform in the ACD-CPR group. C, Intrathoracic pressure waveform in the C-CPR group. The ITP waveforms for the different compression methods revealed the following features. The dotted lines represent the baseline ITP. Values above the baseline displayed increasing ITP during compression, whereas values below the baseline displayed the change in ITP during rebound of the thorax. Among the 3 methods, the ITP changes were most obvious in the C-CPR group, with the highest maximum, suggesting that the external force when the thorax was pressed to the deepest position could be completely conducted to the thoracic cavity during C-CPR, thus significantly increasing maximal ITP.

Fig. 3 Intrathoracic pressure waveform changes during CPR. Stage I, After anesthesia, tracheal intubation was performed for additional ventilation, but the animals were also respiring spontaneously. The waveform showed several pressure increases (mechanical ventilation) separated by deepened negative pressure waveforms (spontaneous respiration). Stage II, After surgery and VF establishment, the animals showed gasping, with obviously increased breathing amplitude, prolonged expiratory duration, and widened and deepened negative ITP. Stage III, Representative waveform during compression after electrical defibrillation, displaying deepened and widened negative waveform, which resulted from thorax extension induced by electrical defibrillation, followed by regular ITP change curves induced by compression. stage IV, ROSC with spontaneous respiration and weaning from the respiratory machine, displayed as rapid, small- amplitude ITP change.

representative waveform during compression after electrical defibrillation, displaying deepened and widened negative waveform, which resulted from thorax extension induced by electrical defibrillation, followed by regular ITP change curves induced by compression. Stage IV, ROSC with spontaneous respiration and weaning from the respiratory machine, displayed as rapid, small-amplitude ITP change.

Table 2 Hemodynamic and oxygen dynamic parameters (mean +- SD)

Hemodynamics and oxygen dynamics

No significant differences of all parameters were found among the 3 groups at baseline. All hemodynamic parameters were significantly higher in the C-CPR group than that in both the A-CPR group (P b .05) and the ACD- CPR group (P b .01) during CPR (Table 2). Maximal

A-CPR

(n = 7)

ACD-CPR (n = 7)

C-CPR (n = 7)

mDAP during CPR (mm Hg)

45.8

+- 8.9 a,b

27.3 +- 3.3 c

64.8 +- 25.4

MAP during CPR (mm Hg)

56.7

+- 10.1 a,b

31.7 +- 6.5 c

86.0 +- 33.4

MAP after ROSC (mm Hg)

75.1

+- 7.2

78.5 +- 5.7

81.2 +- 6.4

CPP during CPR (mm Hg)

34.83

+- 8.7 a,b

18.00 +- 4.8 c

58.83 +- 34.5

CO at baseline (L/min)

3.4

+- 0.7

3.8 +- 0.6

3.9 +- 1.2

CO after ROSC (L/min)

0.9

+- 1.1 a,b

2.3 +- 1.4

Tidal volume during CPR (mL)

72.3

+- 2.5 c

54.0 +- 7.1

PAO2 at baseline (mm Hg)

270.2

+- 41.1

222.8 +- 68.9

282.2 +- 54.3

PAO2 after ROSC (mm Hg)

56.5

+- 64.8 c

192.7 +- 101.2

DO2 after ROSC (mL/min)

136.59

+- 151.8 c

340.9 +- 209.8

VO2 after ROSC (mL/min)

8.9

+- 10.8 c

32.8 +- 18.9

ERO2 after ROSC (%)

3.2

+- 3.8 c

8.9 +- 5.9

Abbreviation: mDAP, maximal diastolic artery blood pressure.

a P b .05 vs ACD-CPR group.

b P b .05 vs C-CPR group.

c P b .01 vs C-CPR group.

A-CPR (n = 7)

ACD-CPR (n = 7)

C-CPR (n = 7)

Preparation

162.3 +- 8.4 c,d

7.7 +- 1.5

3.7 +- 0.8

time (s)

Mean ROSC

14.7

N/A

6.0

(min)

ROSC rate

3/7

0/7

5/7

24-h survival

2/7 a,b

0 d

5/7

rate

24-h CPC

4

5

2

ranking

Abbreviation: N/A, not available.

a P b .05 vs ACD-CPR group.

b P b .05 vs C-CPR group.

c P b .01 vs ACD-CPR group.

d P b .01 vs C-CPR group.

diastolic ABP and MAP were higher in the A-CPR group than those in the ACD-CPR group (P b .05).

Table 3 Time to prepare compression, survival rate, and CPC ranking

There was no successful resuscitation in the ACD-CPR group, and therefore, only oxygen dynamics of the A-CPR and C-CPR groups were compared. The tidal volume of compressions was significantly higher in the A-CPR group than that in the C-CPR group (P b .01). For animals with similar baseline PAO2 measurements, PAO2, DO2, VO2, and ERO2 were significantly better in the C-CPR group than those in the A-CPR group after ROSC (P b .01; Table 2).

Preparation time and its relationship with resuscitation outcomes

Apparatus preparation times were significantly longer in the A-CPR group than that in the C-CPR and ACD-CPR groups (P b .01; Table 3). In practice, apparatus preparation times could be longer than 182 seconds, even when prepared by experienced trainees, and in this time frame, some of the VFs changed from coarse fibrillation to fine fibrillation; this could have a significant effect on the entire resuscitation process.

No animals achieved ROSC in the ACD-CPR group, and therefore, only the C-CPR and A-CPR groups were compared. Preparation time was shorter, and the 24-hour survival rate and CPC ranking were higher in the C-CPR group than those in the A-CPR group (P b .05).

Discussion

Since 1960, blood ftow during CPR was thought to be the result of direct compression of the heart between the sternum and spine [9]. However, in the 1980s, researchers began to reinvestigate the mechanisms of blood ftow during CPR. Rudikoff et al [10] argued that blood ftow was caused by

periodic changes in ITP induced by extracorporeal compres- sion and proposed the thoracic pump theory. They verified that changes in ITP were critical for blood ftow during CPR [10]. At present, more people believe that CPR is effective through the combined action of heart pumping and thorax pumping. Based on this theory, many CPR apparatuses have been developed with the aim of replacing manual compres- sion and improving outcomes; however, the use of mechanical apparatuses remains controversial. Therefore, in this study, we compared the effects of manual and mechanical compression for CPR in a realistic animal model. In the evaluation of these different methods, we measured ITP during artificial and mechanical compression. The ITP peak indicates the pressure on the thoracic cavity when the compression reaches the deepest position; the higher the peak, the greater the pressure applied to the heart and the stronger the cardiac ejection. The extent of the change in ITP indicates the change in negative pressure induced by thoracic rebound; the greater the change in ITP, the more obvious the change in negative pressure and the greater the reftux of blood. A previous study found a linear relationship between ITP, CPP, and MAP during extracorporeal compression [11]. Greater changes in ITP during CPR could thus increase CO in OHCA patients [12-14]. The results of the present study indicate that traditional manual compression had advantages

over mechanical compression in all indices of ITP.

The ITP waveforms for the different compression methods revealed that values above the baseline reftected increasing ITP during compression, whereas values below the baseline reftected the change in ITP during rebound of the thorax (Fig. 2). Among the 3 methods, the method applied to the C-CPR group produced the maximum ITP, suggesting that when the thorax was pressed down to the deepest position, this method resulted in higher pressure in the thoracic cavity. This could facilitate the ftow of blood into the peripheral vasculature from arteries in the thoracic cavity; on the other hand, it may also strengthen cardiac blood ejection because the heart is located in the path of compression. Moreover, the ITP change of the C-CPR group was the most obvious of the 3 groups, with a substantial change in pressure that could lead to improved return of blood to the thoracic cavity and filling of the ventricles. Among the 3 mechanical-compression methods, the ITP change generated by the AutoPulse method was closest to traditional manual compression.

Previous studies have shown that ACD-CPR can increase ITP [15], but in this study, ACD-CPR did not improve circulation and did not result in large differences in ITP as we had expected. There are several possible explanations for this. (1) The manual sucker apparatus may have increased the power conduction steps between the administrator and the thoracic wall, buffering the external power and preventing conduction to the thoracic wall, ultimately reducing the peak ITP. (2) In practice, when reaching the deepest position, the administrators have to stop compression and instantly apply an opposing force to effectively expand the thoracic wall and

increase the negative ITP. This is inevitably difficult and easily results in a pause in compressions. (3) Differences in the anatomy of the thoracic cage between animals and humans resulted in ineffective fixation of the manual sucker to the animal thoracic wall, and this necessitated constant adjustment during compression, thus increasing the frequen- cy of pauses in compression. Therefore, to obtain more accurate conclusions, the manual sucker apparatus needs to be modified for Animal experimentation in the future.

Although artificial hand compression had an advantage over the other methods in terms of maximum ITP and differences in ITP, it was also associated with some disadvantages. For example, as shown in Fig. 4, artificial compression inevitably resulted in unstable changes in ITP, although it was performed by multiple trainees in alternation, displaying a gradual decrease in peak pressure during pauses in compression.

In stage II of ITP changes (Fig. 3), after surgery and VF establishment, the animals showed gasping with obviously increased breathing amplitude, prolonged expiratory dura- tion, and widened and deepened negative ITP. A previous study indicated that gasping could increase CO and blood ftow in the cervical arteries through decreased ITP and increased cardiac reftux [16]. The present results indicated that gasping significantly increased negative ITP during CA, tidal volume, and the reftux of venous blood. Gasping during CPR is critical not only to ventilation in resuscitation but also for the production of beneficial Physiologic effects for ROSC [17].

In stage III of ITP changes (Fig. 3), we found that representative waveforms during compression and after electrical defibrillation appeared as deepened and widened negative waveforms. The change in ITP resulted from thorax extension induced by electrical defibrillation, and this was followed by regular ITP curves induced by compression. This feature indicated that even a single attempt at electrical defibrillation at a suitable energy level could restore cardiac rhythm and induce a negative ITP. These changes cannot only increase tidal volume and improve oxygenation during resuscitation but also promote the reftux of venous blood into the atrium, increase heart

Fig. 4 Artificial unstable compression.

filling, and prepare a blood reserve for cardiac ejection produced by subsequent compression. Therefore, electrical defibrillation will restore the heart rhythm and have a positive adjuvant effect during the entire CPR process.

In the present study, the use of PiCCO for real-time monitoring of ABP prevented the need for pauses in compression to observe the effects of the compression method. Comparison of coronary circulation indices sug- gested that manual compression was more effective in improving circulation than mechanical compression, with shorter times for ROSC achievement, higher success rates, and effective increases in the perfusion of important organs. Compression with the manual sucker apparatus failed to produce a stable increase in diastolic pressure, even after extended compression time, resulting in no survival of animals in either group.

Real-time recording with a respiration monitor indicated that the tidal volume in the AutoPulse group was higher than that in the C-CPR group, suggesting that use of the apparatus resulted in less resident air in the lungs, with unfavorable consequences in terms of ITP peak and intrapulmonary Oxygen exchange, further affecting oxygen metabolism during resuscitation and resulting in lower PAO2, DO2, VO2, and ERO2 measurements. This effect was also associated with a lower 24-hour survival rate and CPC ranking.

Because CA usually occurs unexpectedly, we initiated placement of the compression apparatus 8 minutes after VF in the current study, to objectively reftect the real-life relationship between preparation time and resuscitation survival rate. Real-time recordings of preparation times indicated that manual compression administered by trainees (physicians who had worked in the emergency department for at least 5 years) required the shortest preparation time, thus reducing delays in compression. Preparation times for mechanical apparatuses were obviously longer, potentially resulting in fatal delays in CA rescue and significantly decreasing survival rates.

Comparing with manual compression, AutoPulse pro- duces similar ITP but has poor outcomes in terms of hemodynamics and oxygen metabolism, often leading to lower survival rates. This may be explained by long preparation times that extend the duration of VF and reduce the effects of vasoactives, making it difficult to raise arterial pressure in subsequent CPR protocols. On the other hand, the AutoPulse settings, with a frequency of 80 compressions per minute and a 20% reduction in the depth of the compressions cannot be changed, and this may affect the result of the A- CPR group. Although compression using mechanical apparatuses had the advantages of accuracy, stability, and lack of susceptibility to fatigue, mechanical compression could not be administered effectively or in a timely manner, as manual compression could, which significantly affected its usefulness for resuscitation and made mechanical compression an unsuitable replacement for manual com- pression during CPR.

There were a few limitations to the current study. First, in this study, swine were intubated to facilitate a normal respiratory status, which may have improved the compli- ance of the airways. Moreover, because the 2 apparatuses were designed for humans, differences in the anatomy of the thoracic cages of animals and humans may have affected the results. In addition, during CPR in humans, conditions are more complicated than in the experimental setting, and data from animals cannot always be simply extrapolated to human patients.

Conclusions

Compared with mechanical techniques, manual compres- sion during CPR improved ITP, hemodynamics, oxygen metabolism, ROSC rate, 24-hour survival, and CPC ranking. Manual CPR by an experienced person was more timely and convenient, and this remains the basic and most effective rescue method for CA. Our results suggest that manual CPR should not be replaced by compression techniques using mechanical apparatuses.

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