Clinical paperDoes compression-only cardiopulmonary resuscitation generate adequate passive ventilation during cardiac arrest?☆
Introduction
The aim of cardiopulmonary resuscitation (CPR) is to deliver oxygen to vital organs until a spontaneous circulation can be achieved. The earlier that CPR is started, the better the outcome1, 2, 3, 4, 5, 6, 7, 8 and bystander CPR is strongly predictive of long term survival.9, 10 Adequate tissue oxygen delivery depends on both adequate cardiac output and adequate oxygen content in the circulating arterial blood. The process of bystander CPR results in two mutually conflicting processes in achieving this goal. External chest compression generates forward blood flow but does so at the expense of interruptions in rescue breaths. Blood flowing through the pulmonary vasculature is therefore limited in the oxygen content it is able to accumulate. Conversely, the delivery of rescue breaths to oxygenate alveolar gas necessitates a pause in external chest compression. This pause in chest compression results in a rapid decrease in forward blood flow and reduced oxygen delivery to vital organs. CPR therefore results in a cyclical ventilation:perfusion (V:Q) mismatch where V:Q > 1 during rescue breaths and V:Q < 1 during external chest compressions.
There is increasing evidence that interruptions to external chest compression are disastrous to outcome from cardiac arrest and that chest compressions are, at least initially, of greater priority than regular ventilation. Even short interruptions in compressions lead to a fall in vital organ perfusion,11, 12 which is associated with a decreased rate of return of spontaneous circulation (ROSC),12 reduced defibrillation success,13, 14 myocardial stunning14 and worse outcome in an animal model.15 Additionally, the benefits of rescue breaths during bystander CPR have been questioned16 since ventilation may occur during compression-only CPR through active and passive mechanisms. After a non-hypoxic cardiac arrest, patients usually continue to breath actively for some short period, before the respiratory centre in the brain ceases to function because of hypoxia. The breathing pattern is abnormal and manifests as gasping. Gasping respirations have been observed in animal and human studies. In animal studies, significant tidal volumes have been documented and are associated with an increased chance of successful resuscitation.17, 18, 19, 20 In pigs, agonal respiration occurs during the first 2 min following induction of ventricular fibrillation. This declines over time, to 42% at 3 min and 17% at 7 min. Many animals had supranormal tidal volumes and near normal minute ventilation.20 Similar results have been observed in rodents.17 Human studies have also documented that agonal ventilation is common in the early stage of cardiac arrest, occurring in as many as 40% patients suffering an out-of-hospital cardiac arrest.19 In humans, the airway tends to be at least partially obstructed during external chest compression, which may explain why, contrary to animal findings, gasping alone is inadequate to maintain oxygenation.7, 19
Once external chest compression has commenced, ventilation may occur passively through chest recoil resulting from external chest compression, which generates a negative intrathoracic pressure and entrains air through an open airway. Several animal studies have recently demonstrated the ability of chest compressions to generate varying degrees of tidal volumes and gas exchange, generally being more effective with an airway adjunct used to maintain a patent airway.21, 22, 23 Although the results of these animal studies suggest that passive ventilation may be effective in humans, the anatomical differences between animal and human thoracic cages may limit the translation of these results between species.
This study aims to investigate passive tidal volumes generated during optimal external chest compression (using a mechanical device to provide chest compressions) in the presence of an unobstructed airway (intubated) during cardiac arrest in humans.
Section snippets
Methods
Ethics approval was obtained from the North and Mid Hampshire Local Research Ethics Committee. The study was conducted in the Emergency Department of a UK District General Hospital. Adult patients (aged > 18 years) suffering cardiac arrest in or out-of-hospital who were treated in the Emergency Department at North Hampshire Hospital, Basingstoke, were eligible for inclusion in the study.
Resuscitation attempts were made according to the European Resuscitation Council 2000 guidelines that were in
Results
We hoped to recruit a total of 30 patients over a 12-month period. For logistical reasons beyond our control, only 17 patients were recruited over this period. Data was collected from all 17 patients (11 male). Median age was 66.1 years (range 47–82 years). Median estimated weight was 80 kg (range 60–120 kg). Sixteen cases were considered to be primarily cardiac in aetiology; one was secondary to an electrocution. None of the patients survived. Patient demographics and time intervals from
Discussion
Passive ventilation occurring as a result of compression-only CPR in humans appears to be ineffective in generating tidal volumes adequate for gas exchange. In all patients, passive tidal volumes were significantly less than the patient's estimated deadspace. Additionally, CO2 minute volume, an estimate of actual gas exchange, was approximately 10% of the normal range. We are unaware of any other study that has measured end-tidal CO2 during measurement of passive ventilation. EtCO2 is a measure
Conflict of interest
TT is Critical Care Products Specialist for Respironics Inc., from whom the ventilation measuring equipment was purchased. CD and JO have no conflict of interest.
Acknowledgements
We thank the Resuscitation Council (UK) for support of this study through a Research Fellowship. We also thank Hampshire Ambulance Service NHS Trust and North Hampshire Hospitals NHS Trust for support of this study.
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A Spanish translated version of the summary of this article appears as Appendix in the final online version at 10.1016/j.resuscitation.2007.04.002.