Chest Compression Only Cardiopulmonary Resuscitation for Primary Cardiac Arrest
Cardiovascular disease continues to be the leading cause of death in most industrialized nations of the world. Unfortunately, the first sign of cardiovascular disease often is the last, because the first sign is frequently sudden cardiac arrest.
Despite Standards in 1974, Standards and Guidelines in 1980, Guidelines in 1986, and Updates of Guidelines in 1992, 2000, and 2005, the survival rate of patients with out-of-hospital cardiac arrest (OHCA) in the United States averaged 7.6% and was unchanged from 1978 to 2008. Likewise, survival of patients with OHCA secondary to ventricular fibrillation (VF), those dramatically more likely to survive, also was unchanged for >2 decades, averaging 17.7%.
A major reason for these previously low rates of survival was the lack of bystander cardiopulmonary resuscitation (CPR) because of the decades-old requirement of mouth-to-mouth ventilation as the first step. Most bystanders, including medical personnel, would call but then await the arrival of emergency medical services personnel. Such OHCA patients rarely survived.
Our University of Arizona Sarver Heart Center Resuscitation Research Group found in animal models of ventricular fibrillation (VF) arrest that survival was better with continuous chest compressions than with no CPR until defibrillation at 10 minutes. As a result, since the early 1990s, we have recommended chest compression only CPR (CO-CPR) as the initial therapy for witnessed primary cardiac arrest, defined as, “An unexpected, seen or heard, collapse of a person who is not responsive and is not breathing normally.”
Not breathing normally is important, because the majority of subjects with primary VF arrest gasp for the first few minutes. The recognition of gasping as a sign of a recent primary cardiac arrest must be emphasized. Gasping has been reported in 55% of witnessed arrests by Clark and associates.1 We reported that 39% of patients with OHCA in Arizona who were gasping survived in comparison with only 9% of patients who were not gasping.
Between 1993 and 2002 we published several studies, each showing no difference in survival of animals with VF-induced cardiac arrest receiving CO-CPR in comparison with those receiving the then guidelines CPR that recommended beginning and interrupting each set of 15 chest compressions with 2 mouth-to-mouth ventilations, interrupting each set of chest compressions by only 4-second time spans. Thus, we have long recommended CO-CPR for patients with primary cardiac arrest.
A landmark observation was published in 2000 by researchers from England and our colleague Karl B. Kern, MD, on their analysis of videos of recently CPR-certified lay individuals, showing that they interrupted chest compressions for an average of 16 seconds to deliver the guidelines recommended “two quick breaths.”2 Accordingly, we then compared survival in our resuscitation research laboratory between VF-arrested swine treated with CO-CPR or with realistic bystander CPR where each set of chest compressions was interrupted a realistic16 seconds for ventilations. Survival was 80% with CO-CPR and 13% with CPR that included 16-second interruptions for ventilations.
A major concern of opponents of CO-CPR for primary cardiac arrest was, and evidently still is, that the lack of assisted ventilation results in low blood arterial oxygenation. In an experiment of VF arrest, arterial blood gasses were measured at baseline, twice during CO-CPR and passive oxygenation, and twice during assisted ventilation. In sinus rhythm, the arterial blood gas was 85 mm Hg (97% saturation), and fell to 70 mm Hg (93% saturation) after 9.5 minutes of untreated VF. The lack of a significant decrease in saturation was because the blood remaining in the arterial system following primary cardiac arrest was not circulating and therefore was still adequately saturated. However, after the initiation of CO-CPR, the arterial blood saturation decreased to 44 mm Hg (61% saturation) after 14 minutes, and then to 31 mm Hg (34% saturation) 16 minutes after primary cardiac arrest (Figure). Is an arterial saturation of 34% harmful? Insights into this question may be found in published research of individuals climbing Mount Everest. In such a report, 1 individual had an arterial saturation of 34%, showing that saturations as low as 34% for long periods of time are compatible with life in humans.3
The results of our extensive efforts to advocate and teach CO-CPR as part of cardiocerebral resuscitation for patients with primary cardiac arrest in the state of Arizona were published in 2010.4,5 The percentage of lay CPR providers who performed CO-CPR was 20% in 2006, ≈45% in 2007 and 2008, and ≈75% during 2008 and 2009. In all patients with OHCA, the survival rate was 7.8% in those receiving guidelines CPR and 13.3% for those who received CO-CPR. In the subset of patients with a witnessed cardiac arrest and a shockable rhythm, the survival rate was 17.7% in those receiving guidelines CPR and 34% in those patients receiving CO-CPR. Notably, the guidelines CPR survival rate of all patients with OHCA or those with a witnessed OHCA and a shockable rhythm was the same as that previously reported in the United States between 1978 and 2008, as described above.
The American Heart Association’s 2015 CPR guidelines for bystanders may still not be optimal because they continue to recommend the same approach (chest compressions interrupted for mouth-to-mouth ventilation) for 2 entirely different etiologies of cardiac arrest: primary cardiac arrest, including those from VF where the arterial blood is usually well saturated at the time of the arrest, and secondary cardiac arrest from respiratory failure, where severe arterial desaturation is the major cause of the arrest.
It must also be emphasized that CO-CPR is not and was never recommended for respiratory arrests.
This article is a brief summary from the Hans Dahll Award; an invited lecture presented December 9, 2015, at the Citizens Emergency Cardiac Care National Meeting, San Diego, CA. The dedication and collaboration of the other members of the University of Arizona College of Medicine Resuscitation Research Group is gratefully acknowledged. The Hans Dahll Award, designated for a single individual, was therefore accepted on behalf of the University of Arizona Sarver Heart Center Resuscitation Group, which initially included my colleagues Dr Bob Berg, Dr Ben Bobrow, Lani Clark, Dr Karl B. Kern, Ron Hilwig, DVM, Dr Charles Otto, and Dr Mathias Zuercher.
The opinions in this article are not necessarily those of the editors or of the American Heart Association.
Circulation is available at http://circ.ahajournals.org.
- © 2016 American Heart Association, Inc.
- Bobrow BJ,
- Zuercher M,
- Ewy GA,
- Clark L,
- Chikani V,
- Donahue D,
- Sanders AB,
- Hilwig RW,
- Berg RA,
- Kern KB
- Ewy GA