Decompression Phase Of Cardiopulmonary Resuscitation Research Articles

Supraglottic airway devices variably develop negative intrathoracic pressures: A prospective cross-over study of cardiopulmonary resuscitation in human cadavers

Aim of the studyNegative intrathoracic pressure (ITP) during the decompression phase of cardiopulmonary resuscitation (CPR) is essential to refill the heart, increase cardiac output, maintain cerebral and coronary perfusion pressures, and improve survival. In order to generate negative ITP, an airway seal is necessary. We tested the hypothesis that some supraglottic airway (SGA) devices do not seal the airway as well the standard endotracheal tube (ETT). MethodsAirway pressures (AP) were measured as a surrogate for ITP in seven recently deceased human cadavers of varying body habitus. Conventional manual, automated, and active compression-decompression CPR were performed with and without an impedance threshold device (ITD) in supine and Head Up positions. Positive pressure ventilation was delivered by an ETT and 5 SGA devices tested in a randomized order in this prospective cross-over designed study. The primary outcome was comparisons of decompression AP between all groups. ResultsAn ITD was required to generate significantly lower negative ITP during the decompression phase of all methods of CPR. SGAs varied in their ability to support negative ITP. ConclusionIn a human cadaver model, the ability to generate negative intrathoracic pressures varied with different SGAs and an ITD regardless of the body position or CPR method. Differences in SGAs devices should be strongly considered when trying to optimize cardiac arrest outcomes, as some SGAs do not consistently develop a seal or negative intrathoracic pressure with multiple different CPR methods and devices.

COMPARISON OF AMIODARONE AND LIDOCAINE IN A PROLONGED VENTRICULAR FIBRILLATION CANINE MODEL

COMPARISON OF AMIODARONE AND LIDOCAINE IN A PROLONGED VENTRICULAR FIBRILLATION CANINE MODEL

Improved cerebral perfusion pressures and 24-hr neurological survival in a porcine model of cardiac arrest with active compression-decompression cardiopulmonary resuscitation and augmentation of negative intrathoracic pressure*

Generation of negative intrathoracic pressure during the decompression phase of cardiopulmonary resuscitation enhances the refilling of the heart. We tested the hypothesis that when compared with closed-chest manual compressions at 80 chest compressions per min, treatment with active compression-decompression cardiopulmonary resuscitation at 80 chest compressions/min combined with augmentation of negative intrathoracic pressure would lower intracranial pressure and increase cerebral perfusion, thereby improving neurologically intact survival rates following prolonged untreated cardiac arrest. Prospective, randomized animal study. Animal laboratory facilities. A total of 26 female farm pigs in two different protocols (n = 17 and n = 9). Seventeen pigs were subjected to 8.5 mins of untreated ventricular fibrillation and prospectively randomized to cardiopulmonary resuscitation at 80 chest compressions/min or active compression-decompression cardiopulmonary resuscitation at 80 chest compressions/min plus an impedance threshold device. Coronary perfusion pressures (29.5 ± 2.7 mm Hg vs. 22.4 ± 1.6 mm Hg, p = .03), carotid blood flow (44.0 ± 12.2 vs. 30.9 ± 10.4, p = .03), and 24-hr neurological survival (88% vs. 22%, p = .015) were higher with active compression-decompression cardiopulmonary resuscitation + an impedance threshold device. Cerebral perfusion pressures, measured in nine additional pigs, were improved with active compression-decompression cardiopulmonary resuscitation + an impedance threshold device (21.9 ± 1.2 mm Hg vs. 8.9 ± 0.8 mm Hg, p < .0001). With active compression-decompression cardiopulmonary resuscitation + impedance threshold device, mean diastolic intracranial pressure during decompression was lower (12.2 ± 0.2 mm Hg vs. 16.6 ± 1.2 mm Hg, p = .02) and the downward slope of the decompression phase intracranial pressure curve was steeper (-60.3 ± 12.9 mm Hg vs. -46.7 ± 11.1 mm Hg/sec, p < .001). Active compression-decompression cardiopulmonary resuscitation + an impedance threshold device increased cerebral perfusion pressures and lowered diastolic intracranial pressure and intracranial pressure rate during the decompression phase. These mechanisms may underlie the observed increase in cerebral perfusion pressure, carotid blood flow, and survival rates with favorable neurologic outcomes in this pig model of cardiac arrest.

Abstract 39: Intrathoracic Pressure Regulation During and After Cardiopulmonary Resuscitation: A Feasibility Study

Objective: Reduction of intrathoracic pressures to -10 cm H2O during the decompression phase of cardiopulmonary resuscitation (CPR) increases cardiac preload, lowers intracranial pressures, and increases circulation and survival rates in pigs undergoing standard CPR. In this proof of concept study, we tested the hypothesis that augmentation of negative intrathoracic pressure during standard (S) CPR with intrathoracic pressure regulation (IPR) providing continuous negative intrathoracic pressure of -10 cm H2O between positive pressure ventilations will improve circulation, using end tidal (ET) CO2 as a non-invasive surrogate of organ perfusion, in patients receiving S-CPR. Methods: In this first clinical evaluation of IPR (CirQLatorTM, Advanced Circulatory Systems Inc, Roseville, MN) paramedic supervisors in Toledo OH performed CPR, applied IPR in 12 adult patients, and measured ETCO2, blood pressure and O2 saturation upon return of spontaneous circulation (ROSC) rates. IPR was continued after ROSC to help maintain perfusion. Values are expressed as mean ± SEM and statistical significance was determined by a paired Student's t-test. ETCO2 and blood pressure are expressed in mmHg. Results: IPR was used together with S-CPR to treat cardiac arrest in 12 patients: mean age 64 ± 3; 4 were male and the initial recorded rhythms were ventricular fibrillation (n=2), pulseless electrical activity (n=3), and asystole (n=7). Time from the initial 911 call to IPR application was 16±1 min. Initial ETCO2 when IPR was applied was 21± 3. Maximum ETCO2 during CPR was 44 ± 4, (p &lt; 0.001 compared with initial ETCO2). There was ROSC in 9/12 patients: 3 patients with asystole did not have ROSC. Time from IPR application to ROSC was 16 ± 3 minutes. Systolic/diastolic blood pressures immediately after ROSC were 126 ±13/72 ± 8. O2 saturation at ROSC was 96 ± 1%. IPR was used in 8/9 patients post ROSC for 8 ± 3 min. There were no observed adverse events. Conclusion: Clinical application of IPR during CPR increased ETCO2 values and resulted in ROSC in 9/12 patients, providing first clinical proof-of-concept that this new non-invasive technology increases circulation during CPR. Based upon these positive data, further study of IPR in patients in cardiac arrest is warranted.

Use of the impedance threshold device in cardiopulmonary resuscitation.

Although approximately one million sudden cardiac deaths occur yearly in the US and Europe, cardiac arrest (CA) remains a clinical condition still characterized by a poor prognosis. In an effort to improve the cardiopulmonary resuscitation (CPR) technique, the 2005 American Heart Association (AHA) Guidelines for CPR gave the impedance threshold device (ITD) a Class IIa recommendation. The AHA recommendation means that there is strong evidence to demonstrate that ITD enhances circulation, improves hemodynamics and increases the likelihood of resuscitation in patients in CA. During standard CPR, venous blood return to the heart relies on the natural elastic recoil of the chest which creates a transient decrease in intrathoracic pressure. The ITD further decreases intrathoracic pressure by preventing respiratory gases from entering the lungs during the decompression phase of CPR. Thus, although ITD is placed into the respiratory circuit it works as a circulatory enhancer device that provides its therapeutic benefit with each chest decompression. The ease of use of this device, its ability to be incorporated into a mask and other airway devices, the absence of device-related adverse effects and few requirements in additional training, suggest that ITD may be a favorable new device for improving CPR efficiency. Since the literature is short of studies with clinically meaningful outcomes such as neurological outcome and long term survival, further evidence is still needed.

Improved Cardiopulmonary Resucitation Device

Cardio-pulmonary resuscitation (CPR) plays an important role in the outcome of sudden cardiac arrest, where survival rates continue to be very low, about 5%. CPR has evolved significantly from the days when it was standard practice to flap the arms of victimes, or roll their bodies back and forth over a wooden barrel. Today, many people know the standard technique of giving chest compressions. Others may know about enhancement devices (e.g., ResQPOD) that use a basic mechanics concept of creating negative thoracic pressure during the decompression phase of CPR. This is done by adding inflow resistance to the patient's airway, such that a vacuum is created at each chest decompression. The vacuum pulls blood into the thorax, in effect “priming the pump” with more blood, which is then ejected in the next compression phase. We present an enhancement to the above proven concept of airway restriction during CPR by further adding total airway occlusion to the inflow and outflow of air at appropriate times, by use of a CPR enhancement device (CED). With a face mask and electronic airway valve, maximal vacuum and positive pressures are created in the thorax to enhance blood circulation during cardiac arrest. A CPR cycle is proposed with five phases including two for free air exchange, without the need to interrupt compressions, and adhering to AHA guidelines of 100 compressions per minute. To test the CED, a human cardiopulmonary model is described that allows blood pressure changes to be measured with the various forms of CPR, new and conventional. Preliminary data from testing both CED and standard CPR on the thorax model were found in terms of mean, systolic and diastolic pressure. T-tests evaluated statistical significance. During normal CPR, average systolic pressure was found to be 35.3±0.6 mmHg. When the CED was applied, the average systolic pressure was found to be 62.9±4.5 mmHg (p=0.0002). Average diastolic pressure for normal CPR was found to be 30.4±0.4 mmHg while that of the CED was observed to be 28.6±1.2 mmHg (p=0.095,NS). The MAP calculated from standard CPR resulted in an average of 32.0±0.4 mmHg, while that using the CED was 40±2.1 mmHg, (p=0.002). Based on this preliminary testing and data analysis, the CED shows a significant improvement in systolic and mean arterial pressure in comparison to standard CPR. This supports the CED five phase method that provides positive pressure and vacuum in the cardiopulmonary system during resuscitation. Future work will compare the CED to other CPR enhancement devices.

Critical Thinking in Anesthesia

Critical Thinking in Anesthesia

From laboratory science to six emergency medical services systems: New understanding of the physiology of cardiopulmonary resuscitation increases survival rates after cardiac arrest.

The purpose of this study is to: 1) describe a newly mechanism of blood flow to the brain during cardiopulmonary resuscitation using the impedance threshold device in a piglet model of cardiac arrest, and 2) describe the survival benefits in humans of applying all of the highly recommended changes in the 2005 guidelines related to increasing circulation during cardiopulmonary resuscitation, including use of the impedance threshold device, from six emergency medical services systems in the United States. Animal studies prospective trial with each piglet serving as its own control. Historical controls were used for the human studies. Piglets and patients with out-of-hospital cardiac arrest. Piglets (10-12 kg) were treated with an active (n = 9) or sham (n = 9) impedance threshold device after 6 mins of ventricular fibrillation. Humans were treated with cardiopulmonary resuscitation per the American Heart Association 2005 guidelines and the impedance threshold device. The primary endpoint in the piglet study was carotid blood flow which increased from 59 mL/min without an impedance threshold device to 91 mL/min (p = 0.017) with impedance threshold device use. Airway pressures during the chest recoil phase decreased from -0.46 mm Hg to -2.59 mm Hg (p = 0.0006) with the active impedance threshold device. Intracranial pressure decreased more rapidly and to a greater degree during the decompression phase of cardiopulmonary resuscitation with the active impedance threshold device. Humans: Conglomerate quality assurance data were analyzed from six emergency medical services systems in the United States serving a population of approximately 3 million people. There were 920 patients treated for cardiac arrest after implementation of the 2005 American Heart Association guidelines, including impedance threshold device use, and 1750 patients in the control group during the year before implementation. Demographics were similar between the two groups. Survival to hospital discharge was 9.3% in the control group versus 13.6% in the intervention group. The odds ratio, 95% confidence interval, and p value were 1.54 (1.19-1.99) and p = 0.0008, respectively. This survival advantage was conferred to patients with a presenting cardiac arrest rhythm of ventricular fibrillation (28.5% vs. 18.0%, p = 0.0008). Use of the impedance threshold device in piglets increased carotid blood flow and coronary and cerebral perfusion pressures and reduced intracranial pressure during the decompression phase of cardiopulmonary resuscitation at a faster rate than controls, resulting in a longer duration of time when intracranial pressures are at their nadir. Patients in six emergency medical services systems treated with the impedance threshold device together with the renewed emphasis on more compressions, fewer ventilations, and complete chest wall recoil had a nearly 50% increase in survival rates after out-of-hospital cardiac arrest compared with historical controls.

The impedance threshold valve for adult cardiopulmonary resuscitation: a review of the literature

Heart-lung interaction is an important parameter in the understanding of blood-flow induction during cardiopulmonary resuscitation. The impedance threshold valve is a device which has been created to increase venous return by occluding the airway during the decompression phase of cardiopulmonary resuscitation. This review analyzes the available literature focusing on the rationale of this device. Animal and human studies suggest that the impedance threshold valve increases cardiopulmonary circulation by taking advantage of the kinetic energy of the movement of the chest wall during standard cardiopulmonary resuscitation or active chest-wall decompression. When used in conjunction with active compression/decompression cardiopulmonary resuscitation during clinical evaluation, addition of the impedance valve resulted in sustained systolic and diastolic pressures as well as improvement of vital-organ blood flow. Recent studies have also found an increase in short-term survival rates. It seems clear, from both animal and human data, that enhancement of preload by a decrease in the intrathoracic pressures in the decompression phase improves overall cardiopulmonary resuscitation efficacy. By this means, the impedance threshold valve may be beneficial in patients in asystole or shock-refractory ventricular fibrillation. The potential long-term benefits of this new valve remain under investigation.

Use of an inspiratory impedance threshold device on a facemask and endotracheal tube to reduce intrathoracic pressures during the decompression phase of active compression–decompression cardiopulmonary resuscitation

Use of an inspiratory impedance threshold device (ITD) significantly increases coronary perfusion pressures and survival in patients ventilated with an endotracheal tube (ETT) during active compression-decompression cardiopulmonary resuscitation. We tested the hypothesis that the ITD could lower intratracheal pressures when attached to either a facemask or ETT. An active and sham ITD were randomly applied first to a facemask and then to an ETT during active compression-decompression cardiopulmonary resuscitation in 13 out-of-hospital cardiac arrest patients in a randomized, double-blinded, prospective clinical trial. The compression-to-bag-valve ventilation ratio was 15:2. Airway pressures (surrogate for intrathoracic pressure) were measured with a pressure transducer. A sham and an active ITD were used for 1 min each in a randomized order, first on a facemask and then on an ETT. Statistical analyses were made using Friedman's and Wilcoxon's rank-sum tests. For the primary end point, mean +/- sd maximum negative intrathoracic pressures (mm Hg) during the decompression phase of cardiopulmonary resuscitation were -1.0 +/- 0.73 mm Hg with a sham vs. -4.6 +/- 3.7 mm Hg with an active ITD on the facemask (p = .003) and -1.3 +/- 1.3 mm Hg with a sham ITD vs. -7.3 +/- 4.5 mm Hg with an active ITD on an ETT (p = .0009). Decompression phase airway pressures with the facemask and ETT were not statistically different. Use of an active ITD attached to a facemask or an ETT resulted in a significantly lower negative intratracheal pressure during the decompression phase of active compression-decompression cardiopulmonary resuscitation when compared with controls. Airway pressures with an ITD on either a facemask or ETT were similar. The ITD-facemask combination was practical and enables rapid deployment of this life-saving technology.

Incomplete chest wall decompression: a clinical evaluation of CPR performance by EMS personnel and assessment of alternative manual chest compression–decompression techniques

Background: Complete chest wall recoil improves hemodynamics during cardiopulmonary resuscitation (CPR) by generating relatively negative intrathoracic pressure and thus draws venous blood back to the heart, providing cardiac preload prior to the next chest compression phase. Objective: Phase I was an observational case series to evaluate the quality of chest wall recoil during CPR performed by emergency medical services (EMS) personnel on patients with an out-of-hospital cardiac arrest. Phase II was designed to assess the quality of CPR delivered by EMS personnel using an electronic test manikin. The goal was to determine if a change in CPR technique or hand position would improve complete chest wall recoil, while maintaining adequate duty cycle, compression depth, and correct hand position placement. Standard manual CPR and three alternative manual CPR approaches were assessed. Methods and results: Phase I—The clinical observational study was performed by an independent observer noting incomplete chest wall decompression and correlating that observation with electronically measured airway pressures during CPR in adult patients with out-of-hospital cardiac arrest. Rescuers were observed to maintain some residual and continuous pressure on the chest wall during the decompression phase of CPR, preventing full chest wall recoil, at some time during resuscitative efforts in 6 (46%) of 13 consecutive adults (average ± S.D. age 63 ± 5.8 years). Airway pressures were consistently positive during the decompression phase (>0 mmHg) during those observations. Phase II: This randomized prospective trial was performed on an electronic test manikin. Thirty EMS providers (14 EMT-Basics, 5 EMT-Intermediates, and 11 EMT-Paramedics), with an average age ± S.D. of 32 ± 8 years and 6.5 ± 4.2 years of EMS experience, performed 3 min of CPR on a Laerdal Skill Reporter™ CPR manikin using the Standard Hand Position followed by 3 min of CPR (in random order) using three alternative CPR techniques: (1) Two-Finger Fulcrum Technique—lifting the heel of the hand slightly but completely off the chest during the decompression phase of CPR using the thumb and little finger as a fulcrum; (2) Five-Finger Fulcrum Technique—lifting the heel of the hand slightly but completely off the chest during the decompression phase of CPR using all five fingers as a fulcrum; and (3) Hands-Off Technique—lifting the heel and all fingers of the hand slightly but completely off the chest during the decompression phase of CPR. These EMS personnel did not know the purpose of the studies prior to or during this investigation. Adequate compression depth was poor for all hand positions tested and ranged only from 29.9 to 48.5% of all compressions. When compared with the Standard Hand Position, the Hands-Off Technique decreased mean compression duty cycle from 46.9 ± 6.4% to 33.3 ± 4.6%, ( P < 0.0001) but achieved the highest rate of complete chest wall recoil (95.0% versus 16.3%, P < 0.0001) and was 129 times more likely to provide complete chest wall recoil (OR: 129.0; CI: 43.4–382.0). There were no significant differences in accuracy of hand placement, depth of compression, or reported increase in fatigue or discomfort with its use compared with the Standard Hand Position. Conclusions: Incomplete chest wall decompression was observed at some time during resuscitative efforts in 6 (46%) of 13 consecutive adult out-of-hospital cardiac arrests. The Hands-Off Technique decreased compression duty cycle but was 129 times more likely to provide complete chest wall recoil (OR: 129.0; CI: 43.4–382.0) compared to the Standard Hand Position without differences in accuracy of hand placement, depth of compression, or reported increase in fatigue or discomfort with its use. All forms of manual CPR tested (including the Standard Hand Position) in professional EMS rescuers using a recording manikin produced an inadequate depth of compression more than half the time. These data support development and testing of more effective means to deliver manual as well as mechanical CPR.

Augmentation of ventricular preload during treatment of cardiovascular collapse and cardiac arrest.

Despite aggressive measures for the treatment of cardiovascular collapse and cardiac arrest, the hypotension associated with these malignant processes usually leads to profound vital-organ ischemia and death. A fundamental therapeutic challenge of such life-threatening processes is the restoration of adequate blood flow to the heart and the brain. However, to maintain adequate forward blood flow out of the heart, venous blood return must be drawn back into the heart. With the exception of administration of exogenous fluid replacement, there are limited ways to enhance blood flow back to the heart during prolonged hypotension. This article describes the potential value of a new impedance threshold valve for the treatment of cardiac arrest and hypotension. The valve was designed to create a vacuum within the thorax during the decompression phase of cardiopulmonary resuscitation or during inhalation. By transiently blocking inspiratory gas exchange during the decompression phase of cardiopulmonary resuscitation, after phrenic nerve-stimulated gasping, or during spontaneous ventilation, the impedance-valve concept may have clinical value in the treatment of patients in cardiac arrest, hemorrhagic shock, and cardiovascular collapse secondary to a number of life-threatening clinical processes.

Recent advances in active compression-decompression cardiopulmonary resuscitation

In an attempt to improve upon the currently poor outcomes for patients in cardiac arrest, new methods and devices have been developed to enhance the efficiency and efficacy of standard cardiopulmonary resuscitation (CPR). One new approach, active compression-decompression (ACD) CPR was developed to lower the intrathoracic pressure during the decompression phase of CPR, thereby enhancing venous blood return to the thorax. Over the past decade the ACD CPR device has been extensively evaluated in animals and humans. ACD CPR is the only new approach for improving CPR efficacy with a mechanical device that has achieved clinical relevance. More recently, an inspiratory impedance threshold valve (ITV™) has been developed that causes a further reduction in intrathoracic pressures, augmenting the efficiency of both standard and ACD CPR. Consequently, ACD CPR and the impedance valve were recently recommended by the American Heart Association. Clinical trials are underway to determine the long-term, potential value of these new technologies.

Recent advances in mechanical cardiopulmonary resuscitation devices

Over the past 40 years since standard closed-chest cardiopulmonary resuscitation was first described, several mechanical devices have been developed to increase vital organ perfusion in patients in cardiac arrest. The newer approaches aim to increase forward blood flow by increasing intrathoracic pressures and by direct cardiac compression during the “compression phase.” Equally important is the enhancement of venous return during the decompression phase of cardiopulmonary resuscitation. New approaches designed to increase venous return to the thorax during cardiopulmonary resuscitation include innovations that decrease “decompression phase” intrathoracic pressure and those that alternate abdominal compression with chest wall compression. The potential clinical value of these newer mechanical approaches is reviewed. In addition, some devices in the development stage are described.