Evaluation of LUCAS, a new device for automatic mechanical compression and decompression resuscitation

Lund University, Lund, Skåne, Sweden
Resuscitation (Impact Factor: 4.17). 12/2002; 55(3):285-99. DOI: 10.1016/S0300-9572(02)00271-X
Source: PubMed


LUCAS is a new gas-driven CPR device providing automatic chest compression and active decompression. In an artificial thorax model, superior pressure and flow were obtained with LUCAS compared with manual CPR. In a randomized study on pigs with induced ventricular fibrillation significantly higher cardiac output, carotid artery blood flow, end-tidal CO(2), intrathoracic decompression-phase aortic- and coronary perfusion pressures were obtained with LUCAS-CPR (83% ROSC) compared to manual CPR (0% ROSC). In normothermic fibrillating pigs, the ROSC rate was 100% after 15 min and 38% after 60 min of LUCAS-CPR (no drug treatment). The ROSC rate increased to 75% if surface cooling to 34 degrees C was applied during the first 30 min of the 1-h resuscitation period. Experience with the first 20 patients has shown that LUCAS is light (6.5 kg), easy to handle, quick to apply (10-20 s), maintains a correct position, and works optimally during transport both on stretchers and in ambulances. In one hospital patient with a witnessed asystole where manual CPR failed, LUCAS-CPR achieved ROSC within 3 min. One year later the patient's mental capacity was fully intact. To conclude, LUCAS-CPR gives significantly better circulation during ventricular fibrillation than manual CPR.

Download full-text


Available from: Trygve Sjöberg,
  • Source
    • "The LUCAS™ Chest Compression System (Physio-Control/Jolife AB, Lund, Sweden) has been in clinical use since 2003. Experimental data have shown improved perfusion pressures to the brain and heart, enhanced cerebral blood flow and higher end tidal CO2 as an indirect measure of cardiac output using the LUCAS™ device as compared with the effects of conventional manual CPR [1,2]. The LUCAS™ device has also shown higher end tidal CO2 values in out-of-hospital cardiac arrest (OHCA) victims compared with manual CPR [3]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background The LUCAS™ device delivers mechanical chest compressions that have been shown in experimental studies to improve perfusion pressures to the brain and heart as well as augmenting cerebral blood flow and end tidal CO2, compared with results from standard manual cardiopulmonary resuscitation (CPR). Two randomised pilot studies in out-of-hospital cardiac arrest patients have not shown improved outcome when compared with manual CPR. There remains evidence from small case series that the device can be potentially beneficial compared with manual chest compressions in specific situations. This multicentre study is designed to evaluate the efficacy and safety of mechanical chest compressions with the LUCAS™ device whilst allowing defibrillation during on-going CPR, and comparing the results with those of conventional resuscitation. Methods/design This article describes the design and protocol of the LINC-study which is a randomised controlled multicentre study of 2500 out-of-hospital cardiac arrest patients. The study has been registered at ClinicalTrials.gov (http://clinicaltrials.gov/ct2/show/NCT00609778?term=LINC&rank=1). Results Primary endpoint is four-hour survival after successful restoration of spontaneous circulation. The safety aspect is being evaluated by post mortem examinations in 300 patients that may reflect injuries from CPR. Conclusion This large multicentre study will contribute to the evaluation of mechanical chest compression in CPR and specifically to the efficacy and safety of the LUCAS™ device when used in association with defibrillation during on-going CPR.
    Scandinavian Journal of Trauma Resuscitation and Emergency Medicine 01/2013; 21(1):5. DOI:10.1186/1757-7241-21-5 · 2.03 Impact Factor
  • Source
    • "Experimental studies have showed that the use of LUCAS-2 was associated with sustained coronary and cerebral perfusion in an animal model with cardiac arrest [1] [7] So far, only few case reports [8] [9] [10] and small case series [6] [11] [12] have addressed its efficacy and safety in humans with so far encouraging results. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cardiac arrest in the catheterization laboratory during percutaneous coronary interventions (PCI) is associated with high mortality, among other things because it may be difficult to perform efficacious cardiopulmonary resuscitation while continuing the coronary intervention. We report on 2 patients who have benefit from ongoing external mechanical chest compression with LUCAS-2 device because of cardiac arrest occurred during non-coronary interventions. Added to the existing data on PCIs performed during cardiac arrest, these first reported cases suggest that the application of the LUCAS-2 device in the cardiac catheterization laboratory may be also expanded to patients undergoing noncoronary interventions.
    The American journal of emergency medicine 09/2012; 31(2). DOI:10.1016/j.ajem.2012.07.022 · 1.27 Impact Factor
  • Source
    • "Cardiac arrest (CA) due to ventricular fibrillation (VF) has frequently been used in animal cardiopulmonary resuscitation (CPR) models for measuring CPP, which is done by calculating the pressure gradient between the aorta and the right atrium during the end of the decompression phase [4-6]. Studies in animals and in humans have demonstrated a positive correlation between CPP and return of spontaneous circulation (ROSC) [5-9], however, little is known about the relationship between CPP and directly measured intracoronary blood flow velocity during mechanical CCs or manual CCs. Measurements of intracoronary blood flow is performed with a Doppler flow wire and the method has previously been used to measure coronary blood flow before and after percutaneous coronary intervention (PCI) in patients with stable circulation [10-12] or when correlating other modalities for measuring coronary blood flow [13,14]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Mechanical chest compressions (CCs) have been shown capable of maintaining circulation in humans suffering cardiac arrest for extensive periods of time. Reports have documented a visually normalized coronary blood flow during angiography in such cases (TIMI III flow), but it has never been actually measured. Only indirect measurements of the coronary circulation during cardiac arrest with on-going mechanical CCs have been performed previously through measurement of the coronary perfusion pressure (CPP). In this study our aim was to correlate average peak coronary flow velocity (APV) to CPP during mechanical CCs. In a closed chest porcine model, cardiac arrest was established through electrically induced ventricular fibrillation (VF) in eleven pigs. After one minute, mechanical chest compressions were initiated and then maintained for 10 minutes upon which the pigs were defibrillated. Measurements of coronary blood flow in the left anterior descending artery were made at baseline and during VF with a catheter based Doppler flow fire measuring APV. Furthermore measurements of central (thoracic) venous and arterial pressures were also made in order to calculate the theoretical CPP. Average peak coronary flow velocity was significantly higher compared to baseline during mechanical chests compressions and this was observed during the entire period of mechanical chest compressions (12 - 39% above baseline). The APV slowly declined during the 10 min period of mechanical chest compressions, but was still higher than baseline at the end of mechanical chest compressions. CPP was simultaneously maintained at > 20 mmHg during the 10 minute episode of cardiac arrest. Our study showed good correlation between CPP and APV which was highly significant, during cardiac arrest with on-going mechanical CCs in a closed chest porcine model. In addition APV was even higher during mechanical CCs compared to baseline. Mechanical CCs can, at minimum, re-establish coronary blood flow in non-diseased coronary arteries during cardiac arrest.
    BMC Cardiovascular Disorders 12/2011; 11(1):73. DOI:10.1186/1471-2261-11-73 · 1.88 Impact Factor
Show more