Hemodynamics of active abdominal compression decompression CPR in a rat model of multiple rib fractures with asphyxial cardiac arrest

Abstract

Active abdominal compression-decompression resuscitation (AACD-CPR) has been proposed as an alternative to standard cardiopulmonary resuscitation (STD-CPR) for cases of multiple rib fractures with asphyxial cardiac arrest (CA), yet its underlying hemodynamic effects remain unclear. In this study, thirty-eight rats underwent bilateral rib fracture modeling, with thirty successfully modeled and then randomly assigned to the AACD-CPR, STD-CPR, or sham groups (n = 10 each). After surgical procedures, rats experienced 8 min of asphyxia followed by assigned CPR, or no intervention in the sham group. Hemodynamic and arterial blood gas parameters were measured at multiple time points during and after resuscitation, and rates of return of spontaneous circulation (ROSC) as well as cumulative 240-minute survival were recorded. AACD-CPR resulted in lower right atrial diastolic pressure during resuscitation and less severe acidosis at 30 min post-resuscitation compared to STD-CPR, although other hemodynamic and outcome measures did not differ significantly between the two resuscitation techniques. These findings suggest that AACD-CPR can achieve similar hemodynamic performance and survival outcomes to STD-CPR in a rat model of multiple rib fractures causing asphyxial cardiac arrest, supporting its potential as an alternative when conventional chest compressions are compromised.

Introduction

Multiple rib fractures are a common injury, defined as three or more fractured ribs^1,2, typically resulting from chest trauma or standard cardiopulmonary resuscitation^3,4. Approximately 55% of instances necessitate surgery or ICU admission, with mortality rates varying from 10% to 40%.^{5, 6} Active abdominal compression-decompression resuscitation (AACD-CPR), also known as abdominal lifting and compression CPR, is a novel resuscitation technique based on “abdominal pump” theories, which promotes blood flow during cardiac arrest (CA) by rhythmically compressing and actively decompressing the abdomen, instead of the chest⁵. Many previous studies^7–9 have shown that AACD-CPR could achieve similar or better outcomes than standard cardiopulmonary resuscitation (STD-CPR) for multiple rib fractures with cardiac arrest. However, the hemodynamic mechanism of AACD-CPR during resuscitation is not yet fully understood. Since Hendrickx et al.¹⁰successfully established the asphyxial cardiac arrest rat model in 1984, this model has been widely used in studies related to CA/CPR^11–15. The widespread adoption of the rat model is attributed to the significant similarities in anatomical structures and physiological functions between rats and humans¹⁶. Furthermore, key parameters—including hemodynamics, arterial blood gases, acid-base balance, and metabolic responses during cardiac arrest and the peri-resuscitation period—exhibit data in rats that closely resemble those observed in humans^12,16,17. Although most animal models cannot fully mimic clinical pathophysiological processes¹⁷, animal experiments remain indispensable in preclinical trials due to ethical and humanitarian limitations in human experimentation.The present study was designed to investigate the hemodynamic differences between AACD-CPR and STD-CPR during resuscitation in a rat model of multiple rib fractures complicated by asphyxial cardiac arrest, with the aim of elucidating the possible haemodynamic mechanism by which AACD-CPR achieves similar or improved outcomes.

Materials and methods

The protocol was approved by the Animal Care and Use Committee of the Affiliated Zhengzhou People’s Hospital, Southern Medical University (IACUC202312052). The care and handling of all animals were in accordance with the Guide for the Care and Use of Laboratory Animals¹⁸. The study was reported in accordance with ARRIVE guidelines.

Animal Preparation

Healthy male Sprague-Dawley rats weighing 450–550 g were obtained from Zhuhai BesTest Biotechnology Co., Ltd. (Certificate No. 44822700008524). Animals were housed (3 rats per cage) under standard conditions at 22 °C, 40% humidity, and a 12-hour light-dark cycle, with food and water ad libitum. The animals were fasted but had access to tap water for 12 h before the experiments.

Multiple rib fractures model

The model for multiple rib fractures was established with a slight modification from previous studies^9,19–21. All procedures were carried out under sterile conditions. The rats were anaesthetized with pentobarbital sodium (45 mg/kg intraperitoneally and 10 mg/kg/hour intermittently intravenously during the experiment). Once fully anaesthetized, hair from the neck, chest, upper abdomen and right inguinal area was scraped off. The chest was sterilised, and two longitudinal intermittent incisions were made on both sides of the torso to locate the sixth, seventh and eighth pairs of ribs. Fractures were made approximately 2 cm from the vertebral column using a pair of ophthalmic scissors. After the skin was sutured, the rats were fixed in a supine position on the surgical board. The animals were intubated with a 14-gauge cannula and connected to an end-tidal carbon dioxide detector, then attached to a small animal ventilator (tidal volume: 6 mL/kg, respiratory rate: 60 breaths/minute, positive end-expiratory pressure: 0 cmH2O, FiO₂: 0.21; DW-3000 A Small Animal Ventilator, Zhenghua Biological Apparatus Facilities Co., Ltd. Anhui, China).

The external jugular vein and femoral artery and femoral vein catheterization

The right external jugular vein, femoral artery, and femoral vein were respectively cannulated with a PE-25 catheter for invasive hemodynamics monitoring, arterial blood sampling, and fluid and drug administration, with a slight modification from the previous study²². The right external jugular vein catheterization: The external jugular catheter was marked at 4 cm from the tip. A 1.5 cm incision was made in the right anterior neck area to expose the external jugular vein. The distal end of the right jugular vein was ligated, and the proximal end of the vessel was clamped with a vascular clamp. A small incision was made on the vessel using microdissection scissors near the distal ligature at a 45° angle, cutting approximately ¼ of its cross-sectional area. The PE-25 catheter was carefully inserted into the rat’s right external jugular vein, and the vascular clamp was then released. The catheter was advanced to the 4 cm mark, at which point the tip was positioned in the right atrium. This position was confirmed and adjusted using an ultrasound system for small animals (SonoScape P40 Exp, Sonoscape Medical Corp., Shenzhen, China). The catheter was then secured to the vessel by tightening the proximal ligature. The right femoral artery and vein catheterization: the catheterization of the right femoral artery and vein were similar to that of the right external jugular vein, except that the femoral artery catheter was inserted at the 8 cm mark, with the tip positioned in the descending thoracic aorta, while the femoral vein catheter was inserted at only 1 cm. Hemodynamics parameters and electrocardiogram were continuously monitored by a biological and functional experiment recorder (MedLab-U/4C501, Globalebio Technology Co., Ltd. Beijing, China). All catheters were flushed intermittently with saline containing 2.5 IU/mL of heparin. The rectal core temperature was maintained at 36.5 ± 0.5 °C by a heating lamp. All the rats were allowed to stabilize for 20 min to recover from anesthesia induction and invasive procedures. Baseline hemodynamic parameters were then measured, followed by an arterial blood gas analysis to assess baseline values.

Experimental protocol

Thirty successfully modeled rats were randomly assigned to three groups using a random number table method as follows (Fig. 1A): (i) in the AACD-CPR group (n = 10), the rats underwent 8 min of asphyxia followed by AACD-CPR; (ii) in the STD-CPR group (n = 10), the rats underwent 8 min of asphyxia and STD-CPR; and (iii) in the sham group (n = 10), the rats underwent the same surgical procedure without asphyxia/CPR. The operational procedures for inducing asphyxial cardiac arrest and CPR were conducted with a slight modification from a previous study⁹. After 20 min of surgical stabilization, rats in the AACD-CPR and STD-CPR groups received 0.1 mg/kg vecuronium to prevent respiratory movement. CA was induced by clamping the endotracheal tube and stopping mechanical ventilation, defined as systolic blood pressure (SBP) below 25mmHg with pulseless electrical activity or asystolic rhythm^9,23, typically occurring around 3 min after asphyxia. Resuscitation was started 5 min after the onset of CA. Mechanical ventilation was resumed (tidal volume 8 mL/kg, respiratory rate 80/minute, FiO₂ 1.0, no positive end-expiratory pressure) and AACD-CPR or STD-CPR was performed manually. AACD-CPR was performed with a hand-held suction device (ES-3910, Pincheng Motor Co., Ltd. Shenzhen, China, Fig. 1B) attached to the upper abdomen, actively pushing and pulling at a rate of 200 compressions/minute⁹. Standard chest compressions were performed over the lower-middle sternum at a rate of 200 compressions/minute to a depth of 30% of the ventral-dorsal diameter of the animal’s chest. Intravenous medications (prewarmed to 37 °C) were administered: a bolus of 0.04 mg/kg epinephrine and 50 mg/kg bicarbonate given at 3-minute intervals until return of spontaneous circulation (ROSC). ROSC was defined as an autonomic cardiac rhythm and SBP ≥ 60 mmHg sustained for at least 10 min^23,24. Resuscitation was terminated once spontaneous circulation was achieved or 10 min had elapsed without ROSC. Surviving animals were observed and their hemodynamic and arterial blood gas parameters were monitored for 240 min after resuscitation. Additional anesthesia with pentobarbital sodium (10 mg/kg) was then administered to the surviving rats, which were subsequently rapidly sacrificed by decapitation and subjected to necropsy. All rats that failed to recover were also subjected to necropsy. Necropsy confirmed intra-abdominal injuries resulting from abdominal and precordial compression.

Fig. 1.

The experimental design and outcomes. A, Study protocol. B, The AACD-CPR device used in this study consisted of a silicone sponge rubber suction cup, a suction motor capable of producing 50 kPa suction, and a power adapter plug. C, Kaplan-Meier analysis of cumulative survival at 240 min after resuscitation/operation. AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary resuscitation group; BL, baseline; ACA, asphyxial cardiac arrest; CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation; IC, intensive care; ABGA, arterial blood gas analysis; PR30, PR60, PR120, PR180, PR240: 30, 60, 120, 180, and 240 min after resuscitation. # p < 0.05 versus the Sham group, * p < 0.05 versus the STD-CPR.

Measurements

ECG, AoS (aortic systolic pressure), AoD (aortic diastolic pressure), RaS (right atrial systolic pressure), and RaD (right atrial diastolic pressure) were continuously monitored by a biological and functional experiment recorder (MedLab-U/4C501, Globalebio Technology Co., Ltd. Beijing, China). Coronary perfusion pressure (CPP) was calculated as the difference between time-coincident aortic diastolic pressure and right atrial diastolic pressure. MAP (mean aortic pressure) was calculated by the following equation: MAP = AoD + 1/3 (AoS - AoD). EtCO₂ (End-tidal CO₂) was continuously monitored with a small animal capnograph (RM-C1, Lifes Biological Laboratory Equipment Co., Ltd., Wuxi, China) connected between the rat’s tracheal intubation tube and the small animal ventilator. Myocardial function and CBF (carotid blood flow) were measured by ultrasound (SonoScape P40 Exp, Sonoscape Medical Corp., Shenzhen, China) using a 12.5-MHz transducer at baseline, at 5 min of CPR, and 30, 60, 120, 180, and 240 min after ROSC. CO (cardiac output) and EF (ejection fraction) were used to estimate myocardial contractility. CI (cardiac index) was calculated by the following equation༚CI = CO/body weight. Arterial blood samples to be analyzed for blood gas (Blood gas analyzer cobas b123, Alit Life Sciences, Shanghai, China) were drawn at baseline, and 30, 120, and 240 min after ROSC.

Statistical analysis

The sample size was calculated using G*Power 3.1.9.7 software. The “ANOVA: Repeated measures, within-between interaction” option from the F-test family was selected, and the “A priori: Compute required sample size—given α, power, and effect size” option was used for the power analysis. The analysis was performed with a significance level of 5%, statistical power of 80%, and an effect size of 0.25. With three groups in the study, the minimum required sample size was determined to be 30 rats (10 per group) in order to detect statistically significant differences between the groups. Variables are presented as mean ± SD or frequencies (%). Kaplan-Meier analysis and log-rank tests were used for survival analysis. The Chi-square test was used to analyze categorical variables. Independent samples t-test was utilized to compare differences between two groups, and one-way ANOVA followed by Bonferroni’s or Dunnett’s T3 post hoc test for multiple groups, with a P value of < 0.05 deemed statistically significant. Statistical analyses were performed with SPSS software (version 26.0, IBM, Chicago, IL). Graphs were generated using GraphPad Prism 9.5.1 (GraphPad Software. Inc, La Jolla, CA) and Scienceslides 2016 (VisiScience. Inc, Chapel Hill, NC).

Results

Baseline characteristics

A total of 38 rats were utilized in the study, with 30 rats successfully establishing a model of multiple rib fractures and undergoing vessel catheterization, while 8 rats died due to modeling failure. There were no significant differences in body weight, rectal temperature, baseline hemodynamics, and baseline arterial blood gas measurements among the three groups (all P > 0.05).

Resuscitation outcomes

No significant difference was observed in the rate of ROSC between the AACD-CPR and STD-CPR groups (50% vs. 60%, P > 0.05, Table 1). The survival rates at 60, 120, 180, and 240 min post-ROSC did not show any significant variation between the AACD-CPR and STD-CPR groups (all P > 0.05, Table 1). The log-rank analysis of the 240-minute survival curves, as depicted in the survival curve (Fig. 1C), indicated no significant distinction between the AACD-CPR and STD-CPR groups (P > 0.05). There were no notable variations in the asphyxial time to CA between the two groups, nor in the survival time of rats that experienced ROSC (both P > 0.05, Table 1). Despite the shorter duration of CPR observed in the AACD-CPR group rats in comparison to the STD-CPR group (87.6 ± 26.3 vs. 105.3 ± 24.4), the observed difference was not statistically significant (P > 0.05, Table 1).

Table 1.

Survival Rate, Asphyxial Time to CA, CPR Duration and Survival Time between AACD-CPR and STD-CPR Groups.

Variable	AACD (n = 10)	STD (n = 10)	P value
Survival rate
ROSC	5 (50.0%)	6 (60.0%)	1.000
PR 60	5 (50.0%)	6 (60.0%)	1.000
PR 120	4 (40.0%)	5 (50.0%)	1.000
PR 180	4 (40.0%)	5 (50.0%)	1.000
PR 240	4 (40.0%)	5 (50.0%)	1.000
Asphyxial time to CA (second)	230.4 ± 33.9	233.2 ± 25.3	0.836
CPR duration in rats with ROSC (second)	87.6 ± 26.3	105.3 ± 24.4	0.277
Survival time in rats with ROSC (minute)	214.0 ± 58.2	212.0 ± 68.6	0.961

AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary.

Resuscitation group; ROSC, return of spontaneous circulation; PR, post resuscitation; PR60, PR120, PR180, PR240: 60, 120, 180, and 240 min after resuscitation; CA, cardiac arrest; CPR, cardiopulmonary resuscitation.

Resuscitation and post-resuscitation hemodynamics

The hemodynamic parameters of the three groups change at different time points during the experiment, as shown in Figs. 2, 3, 4 and 5. The right atrial diastolic pressure (RaD) was consistently lower in the AACD-CPR group than in the STD-CPR group at 1, 3, and 5 min during resuscitation (Fig. 3). There were no significant differences (all P > 0.05, Figs. 2, 3, 4 and 5) in mean arterial pressure (MAP), aortic systolic pressure (AoS), aortic diastolic pressure (AoD), right atrial systolic pressure (RaS), coronary perfusion pressure (CPP), end-tidal carbon dioxide (EtCO₂), cardiac output (CO), cardiac index (CI), ejection fraction (EF), and carotid blood flow (CBF) between the AACD-CPR and STD-CPR groups at different time points during resuscitation. Similarly, no significant differences (all P > 0.05) were observed in MAP, AoS, AoD, RaS, RaD, CPP, EtCO₂, CO, CI, EF, and CBF at each time point within 240 min post-resuscitation when comparing the AACD-CPR and STD-CPR groups (Figs. 2, 3, 4 and 5). The sham group showed no changes throughout the experiment (Figs. 2, 3, 4 and 5).

Fig. 2.

Comparison of mean arterial pressure (MAP), aortic systolic pressure (AoS), and aortic diastolic pressure (AoD) among three groups. A, Changes in MAP. B, Changes in AoS. C, Changes in AoD. * p < 0.05 versus the STD-CPR. AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary resuscitation group; BL, baseline; ACA, asphyxial cardiac arrest; CPR, cardiopulmonary resuscitation; CPR1, CPR3, CPR5, CPR7, CPR9: refer to the first, third, fifth, seventh, and ninth minutes of cardiopulmonary resuscitation, respectively; PR30, PR60, PR120, PR180, PR240: 30, 60, 120, 180, and 240 min after ROSC. * p < 0.05 versus the STD-CPR.

Fig. 3.

Comparison of right atrial systolic pressure (RaS), right atrial diastolic pressure (RaD), coronary perfusion pressure (CPP) among three groups. A, Changes in RaS. B, Changes in RaD. C, Changes in CPP. AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary resuscitation group; BL, baseline; ACA, asphyxial cardiac arrest; CPR, cardiopulmonary resuscitation; CPR1, CPR3, CPR5, CPR7, CPR9: refer to the first, third, fifth, seventh, and ninth minutes of cardiopulmonary resuscitation, respectively; PR30, PR60, PR120, PR180, PR240: 30, 60, 120, 180, and 240 min after ROSC. * p < 0.05 versus the STD-CPR.

Fig. 4.

Comparison of cardiac output (CO), changes in cardiac index (CI), left carotid blood flow (CBF) among three groups. A, Changes in CO. B, Changes in CI. C, Changes in CBF. AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary resuscitation group; BL, baseline; ACA, asphyxial cardiac arrest; CPR, cardiopulmonary resuscitation; CPR5, refer to the fifth minutes of cardiopulmonary resuscitation; PR30, PR60, PR120, PR180, PR240: 30, 60, 120, 180, and 240 min after ROSC. * p < 0.05 versus the STD-CPR. * p < 0.05 versus the STD-CPR.

Fig. 5.

Comparison of heart rate (HR), ejection fraction (EF), end-tidal carbon dioxide (EtCO₂) among three groups. A, Changes in HR. B, Changes in EF. C, Changes in EtCO₂. * p < 0.05 versus the STD-CPR. AACD, active abdominal compression decompression CPR group; STD, standard cardiopulmonary resuscitation group; BL, baseline; ACA, asphyxial cardiac arrest; CPR, cardiopulmonary resuscitation; CPR1, CPR3, CPR5, CPR7, CPR9: refer to the first, third, fifth, seventh, and ninth minutes of cardiopulmonary resuscitation, respectively; PR30, PR60, PR120, PR180, PR240: 30, 60, 120, 180, and 240 min after ROSC. * p < 0.05 versus the STD-CPR.

Blood gas parameters

The arterial blood gas parameters of the three groups before and after resuscitation are detailed in Table 2. The AACD-CPR group had higher pH, BE, and HCO₃ and lower lactate levels at 30 min after ROSC compared to the STD-CPR group. Other parameters such as rectal temperature, PaO₂, PaCO₂, glucose, potassium, sodium, and hemoglobin levels did not show significant differences between the AACD-CPR and STD-CPR groups at any observation time points during the experiment (all P > 0.05). No changes in arterial blood gas parameters were observed in the sham group during the experiment.

Table 2.

Comparison of arterial blood gas analysis values before and after resuscitation among three groups.

Variable	Group	Baseline	PR30 *	PR120 *	PR240 *
Rectal temperature,℃	AACD	36.7 ± 0.4 (n = 10)	36.5 ± 0.2 (n = 5)	36.7 ± 0.2 (n = 4)	36.8 ± 0.3 (n = 4)
	STD	36.7 ± 0.4 (n = 10)	36.7 ± 0.2 (n = 6)	36.9 ± 0.2 (n = 5)	36.8 ± 0.2 (n = 5)
	SHAM	36.8 ± 0.2 (n = 10)	36.7 ± 0.3 (n = 10)	36.7 ± 0.2 (n = 10)	36.8 ± 0.2 (n = 10)
PH	AACD	7.40 ± 0.03 (n = 10)	7.30 ± 0.08 a, d (n = 5)	7.37 ± 0.04 (n = 4)	7.38 ± 0.05 (n = 4)
	STD	7.42 ± 0.03 (n = 10)	7.19 ± 0.07 a, k (n = 6)	7.35 ± 0.04 (n = 5)	7.38 ± 0.04 (n = 5)
	SHAM	7.40 ± 0.04 (n = 10)	7.39 ± 0.04 d, k (n = 10)	7.39 ± 0.04 (n = 10)	7.39 ± 0.04 (n = 10)
PaO2, mmHg	AACD	99.5 ± 10.5 (n = 10)	217.7 ± 64.8 (n = 5)	260.7 ± 63.9 (n = 4)	311.5 ± 68.8 (n = 4)
	STD	98.8 ± 12.0 (n = 10)	206.2 ± 77.0 (n = 6)	252.2 ± 80.2 (n = 5)	281.5 ± 71.4 (n = 5)
	SHAM	101.2 ± 11.4 (n = 10)	224.4 ± 70.7 (n = 10)	280.0 ± 49.5 (n = 10)	308.3 ± 52.3 (n = 10)
PaCO2, mmHg	AACD	41.1 ± 3.2 (n = 10)	57.8 ± 11.0 g (n = 5)	39.5 ± 3.9 (n = 4)	38.1 ± 2.0 (n = 4)
	STD	39.6 ± 3.2 (n = 10)	60.1 ± 7.6 k (n = 6)	41.8 ± 4.1 (n = 5)	39.0 ± 3.8 (n = 5)
	SHAM	39.8 ± 3.2 (n = 10)	39.2 ± 3.3 g, k (n = 10)	38.5 ± 3.0 (n = 10)	37.4 ± 3.1 (n = 10)
BE, mmol/L	AACD	0.6 ± 1.8 (n = 10)	−10.6 ± 1.6 c, k (n = 5)	−1.7 ± 1.3 (n = 4)	−1.0 ± 1.5 (n = 4)
	STD	1.3 ± 1.6 (n = 10)	−14.4 ± 1.9 c, g (n = 6)	−1.9 ± 1.8 (n = 5)	−1.6 ± 1.8 (n = 5)
	SHAM	−0.2 ± 1.6 (n = 10)	−0.7 ± 1.4 g, k (n = 10)	−0.8 ± 1.4 (n = 10)	−1.0 ± 1.4 (n = 10)
Glucose, mmol/L	AACD	10.5 ± 2.3 (n = 10)	8.2 ± 3.3 (n = 5)	8.6 ± 1.8 (n = 4)	7.6 ± 1.3 (n = 4)
	STD	11.5 ± 2.0 (n = 10)	7.8 ± 3.1 (n = 6)	9.0 ± 2.5 (n = 5)	7.8 ± 1.7 (n = 5)
	SHAM	12.1 ± 2.4 (n = 10)	10.5 ± 2.8 (n = 10)	10.2 ± 2.6(n = 10)	8.2 ± 1.6 (n = 10)
K+, mmol/L	AACD	4.0 ± 0.3 (n = 10)	4.7 ± 0.6 d (n = 5)	4.4 ± 0.4 (n = 4)	4.0 ± 0.5 (n = 4)
	STD	3.9 ± 0.4 (n = 10)	4.6 ± 0.5 h (n = 6)	4.3 ± 0.5 (n = 5)	4.1 ± 0.7 (n = 5)
	SHAM	4.0 ± 0.3 (n = 10)	4.0 ± 0.3 d, h (n = 10)	4.0 ± 0.3 (n = 10)	3.9 ± 0.2 (n = 10)
Na+, mmol/L	AACD	139.4 ± 3.3 (n = 10)	138.9 ± 2.8 (n = 5)	137.6 ± 2.8 (n = 4)	137.1 ± 3.9 (n = 4)
	STD	140.3 ± 3.0 (n = 10)	137.0 ± 3.0 (n = 6)	136.4 ± 3.1 (n = 5)	136.5 ± 2.0 (n = 5)
	SHAM	140.0 ± 2.7 (n = 10)	140.3 ± 3.3 (n = 10)	139.7 ± 3.1 (n = 10)	140.2 ± 3.4(n = 10)
Hb, g/L	AACD	140.1 ± 10.4(n = 10)	139.5 ± 9.8 (n = 5)	139.2 ± 9.5 (n = 4)	136.3 ± 8.7 (n = 4)
	STD	144.9 ± 9.0 (n = 10)	143.4 ± 9.4 (n = 6)	141.5 ± 10.7 (n = 5)	138.7 ± 10.1(n = 5)
	SHAM	143.0 ± 9.2 (n = 10)	141.9 ± 9.3 (n = 10)	140.6 ± 9.6 (n = 10)	139.3 ± 8.5(n = 10)
Hct, %	AACD	41.4 ± 2.5 (n = 10)	44.4 ± 3.5 (n = 5)	42.4 ± 2.9 (n = 4)	40.2 ± 3.2 (n = 4)
	STD	43.8 ± 3.4 (n = 10)	46.4 ± 4.8 (n = 6)	43.8 ± 4.0 (n = 5)	42.0 ± 3.7 (n = 5)
	SHAM	43.6 ± 3.0 (n = 10)	43.0 ± 2.9 (n = 10)	42.0 ± 2.9 (n = 10)	40.9 ± 2.6 (n = 10)
HCO3−, mmol/L	AACD	27.3 ± 2.7 (n = 10)	18.1 ± 2.8 a, g (n = 5)	24.4 ± 3.1 d (n = 4)	28.5 ± 2.3 (n = 4)
	STD	27.9 ± 2.2 (n = 10)	14.0 ± 2.6 a, k (n = 6)	21.8 ± 2.7 j (n = 5)	27.2 ± 1.8 (n = 5)
	SHAM	28.5 ± 2.8 (n = 10)	28.9 ± 1.9 g, k (n = 10)	28.3 ± 2.1 d, j (n = 10)	29.1 ± 1.7 (n = 10)
Lactate, mmol/L	AACD	1.0 ± 0.5 (n = 10)	5.3 ± 0.7 c, g (n = 5)	2.9 ± 0.8 g (n = 4)	1.7 ± 0.5 (n = 4)
	STD	0.9 ± 0.4 (n = 10)	7.1 ± 1.2 c, k (n = 6)	3.3 ± 0.6 k (n = 5)	1.8 ± 0.6 h (n = 5)
	SHAM	1.0 ± 0.4 (n = 10)	1.1 ± 0.4 g, k (n = 10)	1.1 ± 0.4 g, k (n = 10)	1.0 ± 0.4 h (n = 10)

* Arterial blood gas data after cardiopulmonary resuscitation are data from ROSC rats at different time points after resuscitation; PR30, PR120, PR240: 30, 120, and 240 min after resuscitation; BE, base excess; AACD vs. STD: a = p < 0.05; b = p < 0.01; c = p < 0.005; AACD vs. sham: d = p < 0.05; e = p < 0.01; f = p < 0.005; g = p < 0.001; STD vs. sham: h = p < 0.05; i = p < 0.01; j = p < 0.005; k = p < 0.001. Analysis of variance with the Bonferroni/Dunnett’s T3 post hoc correction.

Complications of resuscitation

Necropsy revealed no gross damage to the liver, spleen, lungs, heart, or other visceral organs in 30 rats in this experiment.

Discussion

In this study, we compared hemodynamic and arterial blood gas parameters between AACD-CPR and STD-CPR during resuscitation and up to 240 min after resuscitation in a rat model of multiple rib fractures with asphyxial cardiac arrest. Compared with the STD-CPR group, the AACD-CPR group had lower right atrial diastolic pressure at 1, 3, and 5 min during resuscitation and milder acidosis at 30 min after ROSC. Except for the above improvements, no significant differences in other hemodynamic and arterial blood gas parameters were observed between the AACD-CPR and STD-CPR groups throughout the experiment. There was no significant improvement in the rates of ROSC and 240-minute survival in the AACD-CPR group, and no significant variance in the concomitant injury of resuscitation between the AACD-CPR and STD-CPR groups.

For nearly half a century, since Kouwenhoven and Safar et al²⁵. pioneered the theory of closed chest cardiopulmonary resuscitation in 1960, the cornerstone of traditional CPR has consisted primarily of two components: chest compressions and artificial ventilation²⁶. It is commonly believed that STD-CPR, based on chest compressions, primarily operates through the “thoracic pump” and “cardiac pump theory” mechanism^17–30. However, the effectiveness of chest compressions is a critical factor in the success of CPR, regardless of the underlying theory³⁰. During chest compressions, the pressure in the chest cavity rises by pressing on the lower sternum, creating a pressure gradient between the inside and outside of the thoracic cavity, which helps move blood from the inner to the outer chest vessels. When the compression is released, the thoracic pressure drops, creating a difference in venous pressure and helping blood flow from the peripheral veins back to the heart. However, in cases of cardiac arrest with multiple rib fractures, the closed negative pressure in the thoracic cavity is disrupted, which leads to increased thoracic cavity pressure, reduced chest compliance, and limit chest recoil or the “suction” effect⁹. Consequently, the pressure gradient of blood vessels inside and outside the thoracic cavity is challenging to establish, and STD-CPR based on chest compression may not effectively establish circulating blood volume and fulfill its resuscitation role^8,9. AACD-CPR is a novel CPR technique based on the “abdominal pump” theories⁷. It involves using a handheld suction device attached to the upper abdomen to create periodic intra-abdominal pressure fluctuations or an artificial “abdominal pump” through a continuous cycle of actively pulling upward and pressing downward. When the abdomen is pulled upward, the diaphragm moves downward, expanding the thoracic and abdominal cavities and increasing their negative pressure, which promotes blood return to the abdominal and thoracic cavity. When the abdomen is pushed down, the pressure in the abdominal cavity increases, compressing the diaphragm, which reduces the volume of the thoracic cavity and increases the pressure in the thoracic cavity, facilitating blood flow from the internal thoracic vessels to the external thoracic vessels. In addition, active pulling of the abdomen increases the negative pressure in the thoracic cavity, causing the lungs to expand and air to enter the alveoli to complete the inhalation movement. As the abdomen is pressed, the negative pressure in the thoracic cavity decreases and the lungs are compressed and retracted to expel gas from the alveoli and complete the expiration movement⁷. AACD-CPR can perform synchronous artificial respiration and cardiopulmonary resuscitation without interrupting circulation⁷. Because AACD-CPR achieves effective circulatory blood flow by pushing and pulling on the abdomen instead of the chest, theoretically, the use of the AACD-CPR technique in cases with multiple rib fractures combined with cardiac arrest may lead to a better outcome.

Most of the current literature supports AACD-CPR for achieving comparable or superior outcomes to STD-CPR^7–9,31. Li et al⁸. used AACD-CPR to resuscitate 35 adult patients with chest trauma and found higher ROSC rates compared to STD-CPR. Wang et al³¹. conducted a systematic review of the published literature and found that AACD-CPR increased ROSC rates and decreased neurological injury. However, because these studies are nonrandomized controlled studies or the included studies are nonrandomized controlled studies, the quality of the research and the level of evidence for conclusions are lower. Zhang et al.⁷conducted a prospective, randomized, controlled clinical trial of 84 patients with cardiac arrest but no chest trauma using AACD-CPR and STD-CPR and found no significant difference in ROSC rates between the two CPR methods. In this single-blind, randomized, controlled animal study, we found that the use of AACD-CPR and STD-CPR to resuscitate rats with multiple rib fractures and cardiac arrest resulted in comparable ROSC and 240-minute survival rates, similar to Zhang’s study⁷. Most hemodynamic parameters of the two CPR techniques during and after resuscitation showed no significant differences in this experiment. Hemodynamics further confirmed the similar outcomes of both CPR techniques.

Our study found that right atrial diastolic pressure was consistently lower at 1, 3, and 5 min during AACD-CPR resuscitation. This decrease may be due to the significant negative pressure generated by AACD-CPR in the thoracic cavity during resuscitation. Lower right atrial diastolic pressure during resuscitation could potentially improve CPP and overall tissue perfusion^31–34.> In our study, we found that the mean CPP during resuscitation was higher in the AACD-CPR group, with a shorter mean time to ROSC. However, these improvements did not reach statistical significance, possibly because the reduction in RAD produced by the original experimental rat device was not substantial enough to affect CPP in this experiment. If a better and more efficient AACD-CPR modified rat device becomes available in the future, the improvement in CPP will be greater and there may be statistical differences. Nevertheless, the time to restore circulation was shortened, which to some extent reduced the severity of ischemia and hypoxia in the rats. In addition, the piston effect of the diaphragm in the thoracic and abdominal cavities directly facilitated some ventilation during resuscitation. These factors probably contributed to the milder acidosis observed in the AACD group 30 min after ROSC.

This study has several limitations: First, due to limitations in laboratory equipment, there was no continuous monitoring of cardiac output and common carotid artery blood flow during resuscitation, resulting in inadequate data collection. Second, the study was conducted with a limited sample size of rodents with multiple rib fractures and asphyxiation-induced cardiac arrest. Therefore, it is uncertain whether these findings can be extrapolated to humans or to cardiac arrests from other causes. Finally, it would have been optimal to use a mechanical approach to control both force and displacement during CPR. However, due to the limitations of the experimental apparatus, the trained observer method was used to monitor and control the depth and rate of chest and abdominal compressions. The lack of specific feedback from the device makes it difficult to accurately assess the similarity of manual compressions in each rat. This issue could potentially affect the experimental results, similar to many previous rat cardiac arrest studies that relied on manual chest or abdominal compressions^35–38.

Conclusions

Our study demonstrated that AACD-CPR achieved comparable rates of ROSC and 240-minute survival compared to the STD-CPR group in a rat model of multiple rib fractures with asphyxial cardiac arrest. Furthermore, both resuscitation approaches demonstrated comparable hemodynamics throughout the experiment, with the exception of the AACD-CPR group exhibiting lower right atrial diastolic pressure at 1, 3, and 5 min during resuscitation and milder acidosis at 30 min after ROSC. The AACD-CPR technique may be a promising alternative for multiple rib fracture cases complicated by asphyxia-induced cardiac arrest.

Author contributions

S. Z: Conceptualization, Methodology. Z.D: Data curation, Writing- Original draft preparation. Z.D, H.W, L.H, J. L, and X. W: Visualization, Investigation. Z.D and S.Z: Supervision. Z.D: Software, Validation.: Z.D: Writing- Reviewing and Editing.

Funding

This work was supported by Henan Province Natural Science Fund Project (232300420059).

Data availability

The datasets used and/or analyzed in the current study are available from the corresponding author upon reasonable request.

Declarations

Competing interests

The authors declare no competing interests.

Ethics approval and consent to participate

This study was approved by the Animal Care and Use Committee of the Affiliated Zhengzhou People’s Hospital, Southern Medical University (Zhenzhou, China) (IACUC202312052).