I recently received a question from a reader regarding a recent blog post I had done on compressions. In that article I discussed the science behind why allowing full recoil is important for adequate coronary perfusion. One can assume that the reasoning behind the 2015 AHA Guidelines cap of 120 on compressions, has something to do with allowing an adequate amount of time for recoil (diastole). The question that was proposed, was my thoughts on a prospective single center observational study done in September of 2016. This study included 222 patients in cardiac arrest who received manual chest compressions while in a hospital. The results were a mean chest compression rate of 139 + or - 15. Overall 53% achieved ROSC. This study concluded by saying that “In this sample of adult IHCA patients, a chest compression rate of 121-140 compressions / min had the highest ratio of ROSC." At a first glance this seems very intriguing. However once I began to scrutinize this study, I noticed some concerns. Here is my analysis of this study. 1. My first thought was that in this multivariable logistic regression they used ROSC as an outcome rather than CPC scores. If we want to utilize ROSC as an endpoint, we need more epi! 2. The study says that the compressors did not know why they were being observed, did not use a metronome, and were rotated every two minutes. Chest compressions were measured with defibrillation electrodes, which recorded change in thoracic impedance. This technique does not allow recording of chest compression depth and recoil. I also am curious if they rotated compressors every two minutes, how they were able to blindly maintain consistent rates above 120 amongst multiple providers. 3. The participant inclusion criteria used was (1) Age > 18 years, (2) cardiac arrest, defined as a documented absence of pulse and CPR initiated, and (3) cardiac arrest witnessed in hospital. We know that witnessed cardiac arrest with immediate CPR obviously increases the likelihood of ROSC and improved CPC. It was also mentioned that "a high proportion of these participants were already intubated. I wonder what the results would be for this in OOH arrest. 4. The latter part of this study mentions a high proportion of participants received a CPC of 5 (death), resulting in not enough power to find a statistically significant difference in neurological outcome. In my blog and podcast regarding the science of compressions I refer to three contributing factors to an adequate coronary perfusion pressure (CPP). You need to have an adequate amount of aortic reserve pressure at the site of the coronary ostia during diastole, you need an adequate amount of recoil to allow a bellow effect and draw blood into the coronary arteries, and you need an end ventricular pressure low enough to not compromised coronary flow. An aspect I didn’t mention in this article is factors that contribute to adequate cerebral flow. In the Thoracic Pump Theory it is believed that the recoiling state of the decompressed chest creates a negative pressure which draws blood back into the heart. This negative pressure helps reduce ICP by optimizing cerebral drainage and reducing the flow resistance within the brain. One can assume that increased compressions per minute allows less time in diastole. This could possibly explain the low CPC score for this study. The Study From The ERC. https://www.ncbi.nlm.nih.gov/m/pubmed/27666168/