Elsevier

Resuscitation

Volume 64, Issue 3, March 2005, Pages 363-372
Resuscitation

Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest

https://doi.org/10.1016/j.resuscitation.2004.10.009Get rights and content

Abstract

Introduction:

Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival.

Hypothesis:

Incomplete chest wall recoil during the decompression phase of standard CPR increases intrathoracic pressure and right atrial pressure, impedes venous return, decreases compression-induced aortic pressures and results in a decrease of mean arterial pressure, coronary and cerebral perfusion pressure.

Methods:

Nine pigs in ventricular fibrillation (VF) for 6 min, were treated with an automated compression/decompression device with a compression rate of 100 min−1, a depth of 25% of the anterior–posterior diameter, and a compression to ventilation ratio of 15:2 with 100% decompression (standard CPR) for 3 min. Compression was then reduced to 75% of complete decompression for 1 min of CPR and then restored for another 1 min of CPR to 100% full decompression. Coronary perfusion pressure (CPP) was calculated as the diastolic (aortic (Ao)–right atrial (RA) pressure). Cerebral perfusion pressure (CerPP) was calculated multiple ways: (1) the positive area (in mmHg s) between aortic pressure and intracranial pressure (ICP) waveforms, (2) the coincident difference in systolic and diastolic aortic and intracranial pressures (mmHg), and (3) CerPP = MAP  ICP. ANOVA was used for statistical analysis and all values were expressed as mean ± S.E.M. The power of the study for an alpha level of significance set at 0.05 was >0.90.

Results:

With CPR performed with 100%–75%–100% of complete chest wall recoil, respectively, the CPP was 23.3 ± 1.9, 15.1 ± 1.6, 16.6 ± 1.9, p = 0.003; CerPP was: (1) area: 313.8 ± 104, 89.2 ± 39, 170.5 ± 42.9, p = 0.03, (2) systolic aortic minus intracranial pressure difference: 22.8 ± 3.6, 16.5 ± 4, 23.7 ± 4.5, p = n.s., and diastolic pressure difference: 5.7 ± 3, −2.4 ± 2.4, 3.2 ± 2.5, p = 0.04 and (3) mean: 14.3 ± 3, 7 ± 2.9, 12.4 ± 2.9, p = 0.03, diastolic aortic pressure was 28.1 ± 2.5, 20.7 ± 1.9, 20.9 ± 2.1, p = 0.0125; ICP during decompression was 22.8 ± 1.7, 23 ± 1.5, 19.7 ± 1.7, p = n.s. and mean ICP was 37.1 ± 2.3, 35.5 ± 2.2, 35.2 ± 2.4, p = n.s.; RA diastolic pressure 4.8 ± 1.3, 5.6 ± 1.2, 4.3 ± 1.2 p = 0.1; MAP was 52 ± 2.9, 43.3 ± 3, 48.3 ± 2.9, p = 0.04; decompression endotracheal pressure, −0.7 ± 0.1, −0.3 ± 0.1, −0.75 ± 0.1, p = 0.045.

Conclusions:

Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures.

Introduction

International CPR guidelines recommend that during CPR the chest wall should be compressed 100 times per minute and that the chest wall should be allowed to fully recoil after each chest compression [1], [2]. However, it is well documented that when a rescuer performs 100 compressions per minute, fatigue often occurs rapidly and consequently frequent changes in personnel are required to sustain the rate [1], [2]. Fatigue may have a greater effect on the decompression phase of CPR since the upward force needed to fully oppose gravity may result in significant energy consumption by the rescuer [3]. The person performing CPR has to lift his/her upper body weight 100 times per minute to allow for full chest wall recoil. If that is not done, then the result is incomplete decompression, smaller chest wall compression depth and increased residual intra-thoracic pressure during decompression, reflecting part of the rescuer's body weight that is transferred through the arms to the patients’ chest wall.

While complete chest wall decompression is recommended in the International guidelines, it has certainly not been emphasized. Little is known about the degree of negative intrathoracic pressure generated by the natural recoil of the human chest wall. Generating negative intrathoracic pressure during the decompression phase of CPR may optimize hemodynamics by drawing venous blood back to the heart, providing cardiac preload prior to the next chest compression phase [4], [5]. Endotracheal pressures (ETP) were recently measured using a tracheal manometer as a surrogate of intrathoracic pressures in patients suffering from out of hospital cardiac arrest [6]. The endotracheal pressure tracing revealed two critical errors that were commonplace among the trained professional rescuers. First, patients received excessive ventilation rates. This is the subject of a separate report that demonstrated that excessive ventilation rates during cardiac arrest were both common and dangerous [6]. Hyperventilation resulted in hypotension and decreased survival rates in a subsequent study in pigs [6] as it elevated intrathoracic pressure with little or no opportunity for generating negative intrathoracic pressure, thereby decreasing venous return. The second important finding, described in the companion paper in this edition of Resuscitation by Aufderheide et al. was that professional rescuers were observed to maintain a continuous pressure on the chest wall during the decompression phase of CPR at sometime during resuscitative efforts in 6 (46%) of 13 consecutive cases, preventing full chest wall recoil. Incomplete chest wall recoil results in a residual positive intrathoracic pressure during the decompression phase of CPR. The current report is focused on the potentially harmful effects of incomplete chest wall recoil on hemodynamics and cerebral perfusion pressure in a porcine model of cardiac arrest.

Despite the importance of the decompression phase of CPR, little is known about the physiological effects of incomplete chest wall decompression. We hypothesized that incomplete chest wall recoil will cause an increase in residual intrathoracic pressure, will hinder venous return and in combination with the smaller increase in systemic arterial pressures during compression (due to the smaller distance of the compression stroke) will result in increased diastolic right atrial pressures, decreased aortic pressure, coronary and cerebral perfusion pressure.

Section snippets

Materials and methods

The study was approved by the Institutional Review Board of the Minneapolis Medical Research Foundation at the Hennepin County Medical Center. The animals received care in compliance with the 1996 Guide for the Care and Use of Laboratory Animals by the National Research Council in a facility that was accredited by the American Association for Accreditation of Laboratory Animal Care. Anesthesia was used in all surgical interventions to avoid any unnecessary suffering. Experiments were performed

Preparatory phase

The preparatory aspects of this study have been previously described [4]. In brief, each animal received 7 ml (100 mg/ml) of intramuscular ketamine HCl (Ketaset®, Fort Dodge Animal Health, Fort Dodge, IA) for initial sedation. Propofol anesthesia (PropoFlo®, Abbott Laboratories, North Chicago, IL) (2.3 mg/kg), was initially delivered as an intravenous (i.v.) bolus via the lateral ear vein. While spontaneously breathing, but sedated, the pigs were intubated with a 7.5 French tracheal tube.

Experimental protocol

There was minimal blood loss following surgical preparation of the animals. Once the surgical preparations were completed, and the oxygen saturation was >92% and ETCO2 stable between 36 and 40 mmHg for >5 min, ventricular fibrillation (VF) was induced by delivering direct electrical current via a temporary pacing wire positioned in the right ventricle. Then the volume-controlled ventilator was disconnected from the tracheal tube and the dose of propofol was reduced to 100 μg/kg/min. After 6 min of

Results

A total of nine pigs were entered in the study. With 75% of chest wall recoil, the average amount of residual chest compression at the end of decompression phase was 1.2 cm. All nine pigs survived at least 15 min after returning to a perfusing rhythm.

With incomplete chest wall recoil there were significant increases in decompression endotracheal pressure, right atrial pressure and significant decreases in SBP, DBP, MAP, CPP and CerPP (Table 1, Fig. 1, Fig. 2, Fig. 3). When compared with 100%

Discussion

The results of this study demonstrate the critical importance of full expansion of the chest during the decompression phase of CPR. Incomplete decompression had a detrimental effect on coronary perfusion pressure and cerebral perfusion pressure. To our knowledge, the negative hemodynamic effects of incomplete chest wall recoil during CPR have not been previously reported. The effect of incomplete chest wall recoil on the calculated cerebral perfusion pressure was particularly profound during

Conclusion

This study demonstrated, for the first time, that incomplete decompression has significant deleterious effects on coronary perfusion pressure and cerebral perfusion pressure. The residual positive intrathoracic pressure during the decompression phase, in combination with the decreased compression distance, were associated with higher diastolic right atrial pressure, decreased aortic pressure, calculated coronary and cerebral perfusion pressures and overall undermined the efficiency of CPR.

Conflict of interest statement

There are no conflicts of interest to disclose that would inappropriately influence or bias this work.

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