Active Compression-decompression Cardiopulmonary Resuscitation Research Articles

Enhanced perfusion during advanced life support improves survival with favorable neurologic function in a porcine model of refractory cardiac arrest.

To improve the likelihood for survival with favorable neurologic function after cardiac arrest, we assessed a new advanced life support approach using active compression-decompression cardiopulmonary resuscitation plus an intrathoracic pressure regulator. Prospective animal investigation. Animal laboratory. Female farm pigs (n = 25) (39 ± 3 kg). Protocol A: After 12 minutes of untreated ventricular fibrillation, 18 pigs were randomized to group A-3 minutes of basic life support with standard cardiopulmonary resuscitation, defibrillation, and if needed 2 minutes of advanced life support with standard cardiopulmonary resuscitation; group B-3 minutes of basic life support with standard cardiopulmonary resuscitation, defibrillation, and if needed 2 minutes of advanced life support with active compression-decompression plus intrathoracic pressure regulator; and group C-3 minutes of basic life support with active compression-decompression cardiopulmonary resuscitation plus an impedance threshold device, defibrillation, and if needed 2 minutes of advanced life support with active compression-decompression plus intrathoracic pressure regulator. Advanced life support always included IV epinephrine (0.05 μg/kg). The primary endpoint was the 24-hour Cerebral Performance Category score. Protocol B: Myocardial and cerebral blood flow were measured in seven pigs before ventricular fibrillation and then following 6 minutes of untreated ventricular fibrillation during sequential 5 minutes treatments with active compression-decompression plus impedance threshold device, active compression-decompression plus intrathoracic pressure regulator, and active compression-decompression plus intrathoracic pressure regulator plus epinephrine. Protocol A: One of six pigs survived for 24 hours in group A versus six of six in groups B and C (p = 0.002) and Cerebral Performance Category scores were 4.7 ± 0.8, 1.7 ± 0.8, and 1.0 ± 0, respectively (p = 0.001). Protocol B: Brain blood flow was significantly higher with active compression-decompression plus intrathoracic pressure regulator compared with active compression-decompression plus impedance threshold device (0.39 ± 0.23 vs 0.27 ± 0.14 mL/min/g; p = 0.03), whereas differences in myocardial perfusion were not statistically significant (0.65 ± 0.81 vs 0.42 ± 0.36 mL/min/g; p = 0.23). Brain and myocardial blood flow with active compression-decompression plus intrathoracic pressure regulator plus epinephrine were significantly increased versus active compression-decompression plus impedance threshold device (0.40 ± 0.22 and 0.84 ± 0.60 mL/min/g; p = 0.02 for both). Advanced life support with active compression-decompression plus intrathoracic pressure regulator significantly improved cerebral perfusion and 24-hour survival with favorable neurologic function. These findings support further evaluation of this new advanced life support methodology in humans.

Advances in clinical studies of cardiopulmonary resuscitation.

The survival rate of patients after cardiac arrest (CA) remains lower since 2010 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) was published. In clinical trials, the methods and techniques for CPR have been overly described. This article gives an overview of the progress in methods and techniques for CPR in the past years. Original articles about cardiac arrest and CPR from MEDLINE (PubMed) and relevant journals were searched, and most of them were clinical randomized controlled trials (RCTs). Forty-two articles on methods and techniques of CPR were reviewed, including chest compression and conventional CPR, chest compression depth and speed, defibrillation strategies and priority, mechanical and manual chest compression, advanced airway management, impedance threshold device (ITD) and active compression-decompression (ACD) CPR, epinephrine use, and therapeutic hypothermia. The results of studies and related issues described in the international guidelines had been testified. Although large multicenter studies on CPR are still difficult to carry out, progress has been made in the past 4 years in the methods and techniques of CPR. The results of this review provide evidences for updating the 2015 international guidelines.

How do outcomes after active chest compression-decompression cardiopulmonary resuscitation (CPR) compare with those after standard compression CPR?

How do outcomes after active chest compression-decompression cardiopulmonary resuscitation (CPR) compare with those after standard compression CPR?

Abstract 249: Sodium Nitroprusside Combined with Intrathoracic Pressure Regulation Increases Neurologically Favorable 24-Hour Survival in a Porcine Model of Prolonged Ventricular Fibrillation

Introduction: Use of epinephrine and standard (S) CPR has not been shown to improve neurologically-sound survival after cardiac arrest. Treatment with the potent vasodilator sodium nitroprusside (SNP) improves neurologically intact survival rates in animals when combined with abdominal compression, active compression decompression (ACD) CPR, and an impedance threshold device (ITD). We recently observed that SNP combined with ACD-CPR and a new intrathoracic pressure regulator (IPR), which provides continuous negative intrathoracic pressure after each positive pressure ventilation, increases blood flow to the heart and brain in the absence of epinephrine or abdominal compression. We hypothesized that this combination of SNP plus ACD CPR plus IPR (S-A-I) would improve 24h survival with favorable neurologic function compared with S-CPR. Method: After 12 minutes of untreated ventricular fibrillation (VF), 14 pigs received 3 minutes of S-CPR and were then randomized to a) a bolus of epinephrine (0.05mcg/kg), 2 more minutes of S-CPR and up to 3 defibrillation shocks or b) S-A-I and up to 3 shocks 2 minutes later. All resuscitated animals received therapeutic hypothermia for 4 hours. The primary endpoint was favorable neurologic outcome 24h after resuscitation defined by a Cerebral Performance Category score ≤ 2 (CPC with 1 for no deficit and 5 as dead or unable to resuscitate) as determined by a blinded veterinarian. Hemodynamic parameters and left ventricular ejection fraction were recorded. Data are presented as mean±SEM. Results: At 24 hours, 0/7 pigs in the S-CPR group vs. 5/7 pigs in S-A-I had favorable outcome (p=0.02). One pig survived 24 hours in the S-CPR group with a CPC of 4 vs. 5 in the S-A-I group with a CPC of 1.4±0.2. Carotid blood flow and ETCO2 were higher with S-A-I_vs. S-CPR and epinephrine (127±32 vs. 22±4 ml/min, p=0.005, and 46±5 vs. 22±3 mmHg, respectively, p=0.001). Conclusion: After prolonged VF in pigs, treatment with the combination of ACD CPR, an intrathoracic pressure regulator and SNP, in the absence of epinephrine, significantly increased carotid flow, ETCO2 levels, and neurologically-favorable 24 hour survival rates compared with S-CPR and epinephrine. This novel and promising approach should be considered for a Phase 1 human trial.

Abstract 103: Rib and Sternum Fractures After Cardiopulmonary Resuscitation: An Autopsy Study

Introduction: Chest compression during cardiopulmonary resuscitation (CPR) is associated with skeletal chest injury. The aim of this study was to investigate the incidence of rib and sternum fractures after mechanical active compression-decompression CPR (aCPR) and standard manual CPR (mCPR). Method: This prospective study was conducted from January 1 2005 through December 31 2013. We included adult patients (age ≥18 years) who did not survive after CPR and were referred for clinical autopsy. The patients had been treated with either the aCPR device Lund University Cardiac Arrest System (LUCAS) or mCPR only. Patient and CPR data was drawn from autopsy referral documents or the patient medical records. Out of many referred cases, inclusion required examination by one of two pathologists with experience of CPR-related injuries. Autopsy was performed with special attention given to skeletal chest injuries and a standardized written protocol was used. Results: In the period 2005-2013 we included 362 cases treated with aCPR and 52 cases treated with mCPR. Sternum fracture was found in 291/362 cases (80 %) in the aCPR group and in 20/52 cases (38 %; p<0.001) in the mCPR group. Rib fracture was found in 349/362 cases (96 %) in the aCPR group and in 40/52 cases (77 %; p<0.001) in the mCPR group. Fracture on ≥ three ribs was present in 334/362 cases (92 %) in the aCPR group and in 36/52 cases (69 %; p<0.001) in the mCPR group. In the majority of cases there were multiple bilateral rib fractures, with a median of 10 fractures per case (interquartile range 7 to 13 fractures) in the aCPR group and 7 fractures per case (interquartile range 1 to 9.75 fractures; p<0.001) in the mCPR group. There was no fracture in 6/362 cases (1.7 %) in the aCPR group and in 10/52 cases (19 %; p<0.001) in the mCPR group. Conclusion: The incidence of rib and sternum fracture was significantly higher after aCPR than after mCPR, sternum fractures being twice as common and rib fractures being markedly more numerous after aCPR. These findings should be considered in the light of emerging survival data.

Bundled postconditioning therapies improve hemodynamics and neurologic recovery after 17 min of untreated cardiac arrest

ObjectiveIschemic postconditioning (stutter CPR) and sevoflurane have been shown to mitigate the effects of reperfusion injury in cardiac tissue after 15min of ventricular fibrillation (VF) cardiac arrest. Poloxamer 188 (P188) has also proven beneficial to neuronal and cardiac tissue during reperfusion injury in human and animal models. We hypothesized that the use of stutter CPR, sevoflurane, and P188 combined with standard advanced life support would improve post-resuscitation cardiac and neurologic function after prolonged VF arrest. MethodsFollowing 17min of untreated VF, 20 pigs were randomized to Control treatment with active compression/decompression (ACD) CPR and impedance threshold device (ITD) (n=8) or Bundle therapy with stutter ACD CPR+ITD+sevoflurane+P188 (n=12). Epinephrine and post-resuscitation hypothermia were given in both groups per standard protocol. Animals that achieved return of spontaneous circulation (ROSC) were evaluated with echocardiography, biomarkers, and a blinded neurologic assessment with a cerebral performance category score. ResultsBundle therapy improved hemodynamics during resuscitation, reduced need for epinephrine and repeated defibrillation, reduced biomarkers of cardiac injury and end-organ dysfunction, and increased left ventricular ejection fraction compared to Controls. Bundle therapy also improved rates of ROSC (100% vs. 50%), freedom from major adverse events (50% vs. 0% at 48h), and neurologic function (42% with mild or no neurologic deficit and 17% achieving normal function at 48h). ConclusionsBundle therapy with a combination of stutter ACD CPR, ITD, sevoflurane, and P188 improved cardiac and neurologic function after 17min of untreated cardiac arrest in pigs.All studies were performed with approval from the Institutional Animal Care Committee of the Minneapolis Medical Research Foundation (protocol #12-11).

ABSTRACT 117

Background and aims: Neurological outcome following cardiopulmonary arrest in children is poor and depends upon the quality and technique of CPR delivered. Active compression-decompression CPR (ACD-CPR) has been shown to result in improved hemodynamic outcomes, but neurological outcome has not yet been evaluated. We have developed a novel adhesive glove device (AGD) that allows us to achieve active compression-decompression CPR in neonate and pediatric piglet models of cardiac arrest. Aims: We hypothesized that ACD-CPR delivered by the adhesive glove device (AGD-CPR) results in better brain perfusion as compared to S-CPR and, thus, resulting in improved neurological outcome. Methods: Prospective, randomized, controlled survival animal study. Ten anesthetized & ventilated piglets of either sex (~12Kg) were randomized after 8 minutes of untreated VF to receive either Standard CPR (S-CPR) or AGD-CPR for 5 minutes. Neurologic outcome were determined using an already established multiple neurological deficit score by a veterinary neurologist at baseline and 24 hours after CPR. Data (mean±SD) were analyzed using Wilcoxon Mann-Whitney test; p-value ≤0.05 was considered significant. Results: AGD-CPR group exhibited better neurological outcome as compared to S-CPR group. Furthermore, four animals on the S-CPR group were blind, while all animals on the AGD-CPR group were visual.Table 1: Neurological outcome scoresConclusions: ACD-CPR delivered by our novel adhesive glove device (AGD-CPR) results in better neurological outcome in a swine model of cardiac arrest.

Active chest compression-decompression for cardiopulmonary resuscitation.

Active compression-decompression cardiopulmonary resuscitation (ACDR CPR) uses a hand-held suction device, applied mid-sternum, to compress the chest then actively decompress the chest after each compression. Randomised controlled trials testing this device have shown discordant results. To determine the effect of active chest compression-decompression CPR compared to standard chest compression CPR on mortality and neurological function in adults with cardiac arrest treated either in-hospital or out-of-hospital. We updated the searches of CENTRAL in The Cochrane Library (Issue 12 of 12, 2012), MEDLINE (OVID, 1946 to January week 1 2013), and EMBASE (OVID, 1980 to week 1 2013) on 14 January 2013. We checked the reference list of retrieved articles, contacted experts in the field, and searched ClinicalTrials.gov. All randomised or quasi-randomised studies comparing active compression-decompression with standard manual chest compression in adults with a cardiac arrest who received cardiopulmonary resuscitation by a trained medical or paramedical team. We independently extracted data on an intention-to-treat basis. When needed, we contacted the authors of the primary studies. If appropriate, we cumulated studies and pooled relative risk (RR) estimates. We predefined subgroup analyses according to setting (out-of-hospital or in-hospital) and attending team composition (with physician or paramedic only). In this update, 27 new related publications were found, but they did not all fulfil inclusion criteria or concerned participants already reported in previous publications. In the end, we included 10 trials in this review: Eight were in out-of-hospital settings; one was set in-hospital only; and one had both in-hospital and out-of-hospital components. Allocation concealment was adequate in four studies. The two in-hospital studies were different in quality and size (773 and 53 participants). Both found no differences between ACDR CPR and STR in any outcome.Out-of-hospital trials cumulated 4162 participants. There were no differences between ACDR CPR and STR for mortality either immediately (RR 0.98, 95% confidence interval (CI) 0.94 to 1.03) or at hospital discharge (RR 0.99, 95% CI 0.98 to 1.01). The pooled RR of neurological impairment of any severity was 1.71 (95% CI 0.90 to 3.25), with a non-significant trend to more frequent severe neurological damage in survivors of ACDR CPR (RR 3.11, 95% CI 0.98 to 9.83). However, assessment of neurological outcome was limited, and few participants had neurological damage.There was no difference between ACDR CPR and STR with regard to complications such as rib or sternal fractures, pneumothorax, or haemothorax (RR 1.09, 95% CI 0.86 to 1.38). Skin trauma and ecchymosis were more frequent with ACDR CPR. Active chest compression-decompression in people with cardiac arrest is not associated with any clear benefit.

Use of impedance threshold device in conjunction with our novel adhesive glove device for ACD-CPR does not result in additional chest decompression

ObjectiveTo evaluate the hemodynamic effects of using an adhesive glove device (AGD) to perform active compression–decompression CPR (AGD-CPR) in conjunction with an impedance threshold device (ITD) in a pediatric cardiac arrest model. DesignControlled, randomized animal study. MethodsIn this study, 18 piglets were anesthetized, ventilated, and continuously monitored. After 3min of untreated ventricular fibrillation, animals were randomized (6/group) to receive either standard CPR (S-CPR), active compression–decompression CPR via adhesive glove device (AGD-CPR) or AGD-CPR along with an ITD (AGD-CPR+ITD) for 2min at 100–120compressions/min. AGD is delivered using a fingerless leather glove with a Velcro patch on the palmer aspect and the counter Velcro patch adhered to the pig's chest. Data (mean±SD) were analyzed using one-way ANOVA with pair wise multiple comparisons to assess differences between groups. p-Value≤0.05 was considered significant. ResultsBoth AGD-CPR and AGD-CPR+ITD groups produced lower intrathoracic pressure (IttP, mmHg) during decompression phase (−13.4±6.7, p=0.01 and −11.9±6.5, p=0.01, respectively) in comparison to S-CPR (−0.3±4.2). Carotid blood flow (CBF, % of baseline mL/min) was higher in AGD-CPR and AGD-CPR+ITD (respectively 64.3±47.3%, p=0.03 and 67.5±33.1%, p=0.04) as compared with S-CPR (29.1±12.5%). Coronary perfusion pressure (CPP, mmHg) was higher in AGD-CPR and AGD-CPR+ITD (respectively 19.7±4.6, p=0.04 and 25.6±12.1, p=0.02) when compared to S-CPR (9.6±9.1). There was no statistically significant difference between AGD-CPR and AGD-CPR+ITD groups with reference to intra-thoracic pressure, carotid blood flow and coronary perfusion pressure. ConclusionActive compression decompression delivered by this simple and inexpensive adhesive glove device resulted in improved cerebral blood flow and coronary perfusion pressure. There was no statistically significant added effect of ITD use along with AGD-CPR on the decompression of the chest.

Treatment of non-traumatic out-of-hospital cardiac arrest with active compression decompression cardiopulmonary resuscitation plus an impedance threshold device

BackgroundA recent out-of-hospital cardiac arrest (OHCA) clinical trial showed improved survival to hospital discharge (HD) with favorable neurologic function for patients with cardiac arrest of cardiac origin treated with active compression decompression cardiopulmonary resuscitation (CPR) plus an impedance threshold device (ACD+ICD) versus standard (S) CPR. The current analysis examined whether treatment with ACD+ITD is more effective than standard (S-CPR) for all cardiac arrests of non-traumatic origin, regardless of the etiology. MethodsThis is a secondary analysis of data from a randomized, prospective, multicenter, intention-to-treat, OHCA clinical trial. Adults with presumed non-traumatic cardiac arrest were enrolled and followed for one year post arrest. The primary endpoint was survival to hospital discharge (HD) with favorable neurologic function (Modified Rankin Scale score≤3). ResultsBetween October 2005 and July 2009, 2738 patients were enrolled (S-CPR=1335; ACD+ITD=1403). Survival to HD with favorable neurologic function was greater with ACD+ITD compared with S-CPR: 7.9% versus 5.7%, (OR 1.42, 95% CI 1.04, 1.95, p=0.027). One-year survival was also greater: 7.9% versus 5.7%, (OR 1.43, 95% CI 1.04, 1.96, p=0.026). Nearly all survivors in both groups had returned to their baseline neurological function by one year. Major adverse event rates were similar between groups. ConclusionsTreatment of out-of-hospital non-traumatic cardiac arrest patients with ACD+ITD resulted in a significant increase in survival to hospital discharge with favorable neurological function when compared with S-CPR. A significant increase survival rates was observed up to one year after arrest in subjects treated with ACD+ITD, regardless of the etiology of the cardiac arrest.

Active compression-decompression cardiopulmonary resuscitation (CPR) versus standard CPR for cardiac arrest patients: a meta-analysis.

Active compression-decompression cardiopulmonary resuscitation (ACDCPR) has been popular in the treatment of patients with cardiac arrest (CA). However, the effect of ACD-CPR versus conventional standard CPR (S-CRP) is contriversial. This study was to analyze the efficacy and safety of ACD-CPR versus S-CRP in treating CA patients. Randomized or quasi-randomized controlled trials published from January 1990 to March 2011 were searched with the phrase "active compression-decompression cardiopulmonary resuscitation and cardiac arrest" in PubMed, EmBASE, and China Biomedical Document Databases. The Cochrane Library was searched for papers of meta-analysis. Restoration of spontaneous circulation (ROSC) rate, survival rate to hospital admission, survival rate at 24 hours, and survival rate to hospital discharge were considered primary outcomes, and complications after CPR were viewed as secondary outcomes. Included studies were critically appraised and estimates of effects were calculated according to the model of fixed or random effects. Inconsistency across the studies was evaluated using the I2 statistic method. Sensitivity analysis was made to determine statistical heterogeneity. Thirteen studies met the criteria for this meta-analysis. The studies included 396 adult CA patients treated by ACD-CPR and 391 patients by S-CRP. Totally 234 CA patients were found out hospitals, while the other 333 CA patients were in hospitals. Two studies were evaluated with high-quality methodology and the rest 11 studies were of poor quality. ROSC rate, survival rate at 24 hours and survival rate to hospital discharge with favorable neurological function indicated that ACD-CPR is superior to S-CRP, with relative risk (RR) values of 1.39 (95% CI 0.99-1.97), 1.94 (95% CI 1.45-2.59) and 2.80 (95% CI 1.60-5.24). No significant differences were found in survival rate to hospital admission and survival rate to hospital discharge for ACD-CPR versus S-CRP with RR values of 1.06 (95% CI 0.76-1.60) and 1.00 (95% CI 0.73-1.38). Quality controlled studies confirmed the superiority of ACD-CPR to S-CRP in terms of ROSC rate and survival rate at 24 hours. Compared with S-CRP, ACD-CPR could not improve survival rate to hospital admission or survival rate to hospital discharge.

Abstract 78: Modified Rankin Score at Hospital Discharge Is Predictive of 1-Year Neurological Function in Survivors After Cardiac Arrest

Background: A randomized multicenter clinical trial compared standard CPR (S-CPR) with active compression decompression CPR plus an inspiratory impedance threshold device (ACD+ITD) in patients with non-traumatic, out-of- hospital cardiac arrest (OHCA) from a presumed cardiac cause. Survival to hospital discharge (HD) with favorable neurologic function, defined as a modified Rankin Score (MRS) ≤3, and one year survival were greater in the ACD+ITD group. We evaluated the concordance of the primary endpoint, HD with MRS ≤3, with multiple secondary neurologic endpoints assessed at one year. Methods: A total of 813 patients were enrolled in the S-CPR group and 842 in the ACD+ITD group. MRS at HD, and Cerebral Performance Category (CPC), Overall Performance Category (OPC), Health Utilities Index (HUI) and Cognitive Abilities Screening Instrument (CASI) assessments were based on responses from consented survivors and known deaths at one year. Neurologic assessments were administered by research staff blinded to the CPR treatment. Survival data were available for 98% of subjects. Fisher’s Exact Test, Pearson Chi-Square test, Mann-Whitney U test, and t-test for Equality of Means were used, as applicable, for comparisons. All statistical tests were 2-sided and p-values < 0.05 were regarded as significant. Results: The MRS (≤3 vs. >3) neurological assessment at HD was highly predictive of whether or not a patient would be alive with favorable neurological function in both study groups, assessed using the CPC score (<3 vs. ≥3) at one year (98.0% observed agreement, kappa = 0.800, p < 0.001). Similar concordance was also shown with overall survival, OPC, HUI, CASI. Table shows data for MRS and CPC comparisons. Conclusion: Neurological status at the time of HD, as measured by MRS, is highly predictive of long-term neurological function at one year. This is the first time that the MRS at the time of HD has demonstrated the ability to predict long-term outcomes for patients with OHCA.

Abstract 196: Does Health Status Influence the Willingness to Provide Informed Consent? Results from a Cardiac Arrest Trial Conducted Under Waiver of Informed Consent

Background Federal regulation 21 § CFR 50.24 allows an initial waiver of informed consent (IC) for treatment of certain medical emergencies but requires the consent process be initiated at the earliest feasible opportunity. In a recent out-of-hospital cardiac arrest (OHCA) trial conducted under 21 § CFR 50.24, data from public records were collected which shed light on whether the willingness to provide subsequent IC was associated with study outcomes. We hypothesized that IC was less likely to be obtained in subjects with significantly compromised health status. Methods A post-hoc analysis was conducted using data from a NIH-funded randomized, controlled OHCA clinical trial comparing active compression decompression CPR plus an impedance threshold device (ACD+ITD) with standard CPR. The primary endpoint was survival to hospital discharge (HD) with favorable neurologic function [Modified Rankin Scale (MRS) score <3]. The status of the consent process was tabulated for all subjects who survived to hospital admission. Unadjusted Fisher’s exact test and associated odds ratios were used to compare the MRS at HD by IC status. Results Among a total study population of 1655 subjects, 457 survivors were admitted to the hospital, and 440 had known HD status (see table). Survival with a MRS≤3 was significantly higher in subjects where IC was given: 35.0% vs 4.1%, p < 0.001. Sixteen of the 17 cases with missing MRS outcomes were in the IC denied group. Even if all were considered to have favorable outcomes, the resulting rate (21.1%) was less than that seen among subjects with IC given (p = 0.015). Conclusion Subjects who denied IC were significantly less likely to have favorable outcome. These findings suggest that some resuscitation trials may unknowingly under-represent those subjects with the worst prognoses in a target study population despite pre-specified inclusion and exclusion criteria, due to the unwillingness or inability of the subjects or their families to provide IC.

Abstract 296: Determinants of Incidence of Ventricular Fibrillation as First Recorded Rhythm During Out-of-Hospital Cardiac Arrest and Association with Long-Term Neurological Outcomes: Observations from a Large Randomized Clinical Study

Background: We sought to identify the factors that were associated with higher incidence of VF and survival with good neurological function in the ResQ Trial patients that compared standard cardiopulmonary resuscitation (S-CPR) versus active compression decompression CPR with an inspiratory impedance threshold device (ACD+ITD) in patients with out of hospital cardiac arrest (OHCA). Methods: A retrospective analysis of a randomized multicenter clinical study of 1655 patients with OHCA. 88.3% (106/120) of the patients discharged with good neurological function [Modified Rankin Score (MRS)≤3] had a first recorded rhythm of ventricular fibrillation/pulseless ventricular tachycardia (VF). The first rhythm was recorded in 99.4% (1645/1655) of the cases about 9.5 minutes after 911 call, on average 3 minutes after the arrival of EMS on the scene and after CPR was performed for at least 2 minutes. Results: A total of 32.8% of the patients had VF as presenting rhythm and 42.8% received bystander CPR. Presence of bystander CPR was associated with a higher VF incidence only in the S-CPR group (40.8% versus 23.1% with no bystander, p=0.001) but survival was 7.6% versus 4.6% p=0.09. Presence or absence of bystander CPR let to similar VF incidence and survival in the ACD+ITD group 36.1% versus 33.9% and 9.0% versus 8.9% respectively, p>0.2. After propensity adjustment for witnessed arrest, age <67, gender, public location, bystander CPR lost significance. In the absence of bystander CPR, ACD+ITD significantly increased the incidence of first recorded VF compared to S-CPR from 106/459 (23.1%) to 164/484 (33.9%) [OR 1.71, 95% CI (1.27, 2.30), p<0.001], and in patients with VF, return of spontaneous circulation increased from 65/459 (14.2%) to 104/484 (21.5%) [OR 1.66, 95% CI (1.16, 2.37), p=0.004], leading to an overall doubling of survival with MRS≤3 from 21/455 (4.6%) to 43/482 (8.9%) [OR 2.02, 95% CI (1.15, 3.65), p=0.009]. After propensity adjustment ACD+ITD remained a significant predictor of an MRS≤3, (p= 0.02). Conclusions: VF was the most important predictor of survival with MRS≤3. In the absence of bystander CPR, ACD+ITD increased VF incidence as the first recorded rhythm and doubled survival to hospital discharge with MRS≤3 compared to S-CPR.

ONE-SHOCK VERSUS CONTINUOUS DEFIBRILLATION IN AN 8-MIN VENTRICULAR FIBRILLATION CANINE MODEL OF CARDIAC ARREST

ObjectivesTo investigate the resuscitation effect of a one-shock defibrillation protocol versus conventional continuous defibrillation with treatment variation imposed by active compression-decompression CPR (ACD CPR) or standard CPR (STD CPR).Methods and...

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.

Advanced life support and mechanical ventilation

Artificial ventilation is one of the best known resuscitation procedures. It is generally accepted that there must be oxygen delivery to vital organs during cardiac arrest and resuscitation in order to prevent irreversible damage, but there is an increasing number of ventilation concepts for resuscitation. Traditional and alternative methods of ventilation are reviewed. The need for positive-pressure ventilation during resuscitation as an essential gold standard might be overestimated at least in the first minutes of cardiopulmonary resuscitation (CPR). The co-founders of the concept of cardiocerebral resuscitation could show positive effects of a sole passive oxygenation at the beginning of advanced life support (ALS). Research was published on continuous positive airway pressure (CPAP) ventilation as well as on CPAP plus pressure support ventilation. In addition to positive-pressure ventilation, the use of an impedance threshold device, partly in addition with active compression-decompression CPR, was investigated in both experimental and clinical settings. None of these methods alone could be proven to improve the outcome of cardiac arrest. The role of high oxygen concentration during CPR also remains unclear. Positive-pressure ventilation with pure oxygen remains, in clinical practice, the gold standard in ALS. Further research should focus on the role of passive oxygenation during early ALS. The concentration of oxygen needed during resuscitation has to be defined and alternative ventilation patterns, regarding the impact of CPR, should be investigated.

Controlled pauses at the initiation of sodium nitroprusside-enhanced cardiopulmonary resuscitation facilitate neurological and cardiac recovery after 15 mins of untreated ventricular fibrillation

A multipronged approach to improve vital organ perfusion during cardiopulmonary resuscitation that includes sodium nitroprusside, active compression-decompression cardiopulmonary resuscitation, an impedance threshold device, and abdominal pressure (sodium nitroprusside-enhanced cardiopulmonary resuscitation) has been recently shown to increase coronary and cerebral perfusion pressures and higher rates of return of spontaneous circulation vs. standard cardiopulmonary resuscitation. To further reduce reperfusion injury during sodium nitroprusside-enhanced cardiopulmonary resuscitation, we investigated the addition of adenosine and four 20-sec controlled pauses spread throughout the first 3 mins of sodium nitroprusside-enhanced cardiopulmonary resuscitation. The primary study end point was 24-hr survival with favorable neurologic function after 15 mins of untreated ventricular fibrillation. Randomized, prospective, blinded animal investigation. Preclinical animal laboratory. Thirty-two female pigs (four groups of eight) 32±2 kg. After 15 mins of untreated ventricular fibrillation, isoflurane-anesthetized pigs received 5 mins of either standard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine. After 4 mins of cardiopulmonary resuscitation, all animals received epinephrine (0.5 mg) and a defibrillation shock 1 min later. Sodium nitroprusside-enhanced cardiopulmonary resuscitation-treated animals received sodium nitroprusside (2 mg) after 1 min of cardiopulmonary resuscitation and 1 mg after 3 mins of cardiopulmonary resuscitation. After 1 min of sodium nitroprusside-enhanced cardiopulmonary resuscitation, adenosine (24 mg) was administered in two groups. A veterinarian blinded to the treatment assigned a cerebral performance category score of 1-5 (normal, slightly disabled, severely disabled but conscious, vegetative state, or dead, respectively) 24 hrs after return of spontaneous circulation. Sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine, and controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine resulted in a significantly higher 24-hr survival rate compared to standard cardiopulmonary resuscitation (7 of 8, 8 of 8, and 8 of 8 vs. 2 of 8, respectively p<.05). The mean cerebral performance category scores for standard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine were 4.6±0.7, 3±1.3, 2.5±0.9, and 1.5±0.9, respectively (p<.01 for controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+adenosine compared to all other groups). Reducing reperfusion injury and maximizing circulation during cardiopulmonary resuscitation significantly improved functional neurologic recovery after 15 mins of untreated ventricular fibrillation. These results suggest that brain resuscitation after prolonged cardiac arrest is possible with novel, noninvasive approaches focused on reversing the mechanisms of tissue injury.

Potential negative effects of epinephrine on carotid blood flow and ETCO2 during active compression–decompression CPR utilizing an impedance threshold device

ObjectivesThis study examines the effects of IV epinephrine administration on carotid blood flow (CBF) and end tidal CO2 (ETCO2) production in a swine model of active compression–decompression CPR with an impedance threshold device (ACD-CPR+ITD). MethodsSix female swine (32±1kg) were anesthetized, intubated and ventilated. Intracranial, thoracic aorta and right atrial pressures were measured via indwelling catheters. CBF was recorded. ETCO2, SpO2 and EKG were monitored. V-fib was induced and went untreated for 6min. Three minutes each of standard CPR (STD), STD-CPR+impedance threshold device (ITD) and active compression–decompression (ACD)-CPR+ITD were performed. At minute 9 of the resuscitation, 40μg/kg of IV Epinephrine was administered and ACD-CPR+ITD was continued for 1min. Statistical analysis was performed with a paired t-test. p values of <0.05 were considered statistically significant and all values are reported in mmHg unless otherwise noted. ResultsAortic pressure, cerebral and coronary perfusion pressures increased from STD<STD+ITD<ACD-CPR+ITD (p<0.001). Epinepherine administered during ACD-CPR+ITD signficantly increased mean aortic pressure (29±5 vs 42±12, p=0.01), cerebral perfusion pressure (12±5 vs 22±10, p=0.01), and coronary perfusion pressure (8±7 vs 17±4, p=0.02); however, mean CBF and ETCO2 decreased (respectively 29±15 vs 14±7.0ml/min, p=0.03; 20±7 vs 18±6, p=0.04). ConclusionsIn this model, administration of epinepherine during ACD-CPR+ITD signficantly increased markers of macrocirculation, while significantly decreasing carotid blood flow and ETCO2. This calls into question the ability of calculated perfusion pressures to accurately reflect oxygen delivery to end organs. The administration of epinepherine during ACD-CPR+ITD does not improve cerebral tissue perfusion.

Use of the impedance threshold device improves survival rate and neurological outcome in a swine model of asphyxial cardiac arrest*

To assess whether intermittent impedance of inspiratory gas exchange improves hemodynamic parameters, 48-hr survival, and neurologic outcome in a swine model of asphyxial cardiac arrest treated with active compression-decompression cardiopulmonary resuscitation. Prospective, randomized, double-blind study. Laboratory investigation. Thirty healthy Landrace/Large-White piglets of both sexes, aged 10 to 15 wks, whose average weight was 19 ± 2 kg. At approximately 7 mins following endotracheal tube clamping, ventricular fibrillation was induced and remained untreated for another 8 mins. Before initiation of cardiopulmonary resuscitation, animals were randomly assigned to either receive active compression-decompression cardiopulmonary resuscitation plus a sham impedance threshold device (control group, n = 15), or active compression-decompression cardiopulmonary resuscitation plus an active impedance threshold device (experimental group, n = 15). Electrical defibrillation was attempted every 2 mins until return of spontaneous circulation or asystole. Return of spontaneous circulation was observed in six (40%) animals treated with the sham valve and 14 (93.3%) animals treated with the active valve (p = .005, odds ratio 21.0, 95% confidence interval 2.16-204.6). Neuron-specific enolase and S-100 levels increased in the ensuing 4 hrs post resuscitation in both groups, but they were significantly elevated in animals treated with the sham valve (p < .01). At 48 hrs, neurologic alertness score was significantly better in animals treated with the active valve (79.1 ± 18.7 vs. 50 ± 10, p < .05) and was strongly negatively correlated with 1- and 4-hr postresuscitation neuron-specific enolase (r = -.86, p < .001 and r = -.87, p < .001, respectively) and S-100 (r = -.77, p < .001 and r = -0.8, p = .001) values. In this model of asphyxial cardiac arrest, intermittent airway occlusion with the impedance threshold device during the decompression phase of active compression-decompression cardiopulmonary resuscitation significantly improved hemodynamic parameters, 24- and 48-hr survival, and neurologic outcome evaluated both with clinical and biochemical parameters (neuron-specific enolase, S-100).