
I've been taking cardiopulmonary resuscitation (CPR) classes periodically since medical school many years ago. For me, one of the hardest part of these classes has been keeping track of the ever-changing Official Ratio™ of chest compressions to breaths. Is it 5:1? 15:2? That's one reason why the following recent study in the Journal of the American Medical Association (JAMA) caught my eye:
Bobrow, B.J. (2008). Minimally Interrupted Cardiac Resuscitation by Emergency Medical Services for Out-of-Hospital Cardiac Arrest. JAMA, 299(10), 1158-1165.
This study compared standard advanced life support with a new protocol known as minimally interrupted cardiac resuscitation (MICR). The results:
patients treated with MICR were at least 3 times more likely to survive their cardiac arrest than patients treated with the standard life support protocol.
Just what is MICR and why should it make such a difference?
The main idea behind MICR is that the "C" in CPR is a whole lot more important than the "P" part. Unlike the mixture of chest compressions and assisted breaths given in standard CPR, the MICR protocol starts off with 200 uninterrupted chest compressions. Electrical defibrillation was not performed until after these initial 200 chest compressions. Why do it this way? As the authors state:
During resuscitation efforts, the forward blood flow produced by chest compressions is so marginal that any interruption of chest compressions is extremely deleterious, especially for favorable neurological outcomes. Excessive interruptions of chest compressions by prehospital personnel are common. Therefore, MICR emphasizes uninterrupted chest compressions.
In other words: CPR is a very poor substitute for an actual heart. Interrupting chest compression downgrades this "poor" to "
piss poor".

But what's the benefit of not ventilating a patient? How does a patient get any oxygen if one omits the "pulmonary" part of CPR?
...positive pressure ventilations during cardiac arrest may be harmful because they increase intrathoracic pressure, thereby decreasing venous return and subsequent myocardial and cerebral blood flow. Probably due to the excitement and stress of resuscitation efforts, excessive ventilations by both physicians and EMS personnel are common.
Immediately after a sudden VF cardiac arrest, aortic oxygen and carbon dioxide concentrations do not vary from the prearrest state because there is no blood flow and oxygen consumption is minimal. Therefore, when chest compressions are initiated, the blood flowing from the aorta to the coronary and cerebral circulations provides adequate oxygenation at an acceptable pH. At that time, myocardial oxygen delivery is limited more by blood flow than oxygen content. Adequate oxygenation and ventilation can continue without rescue breathing because the lungs serve as a reservoir of oxygen that allows adequate oxygen exchange with the limited pulmonary blood flow during cardiopulmonary resuscitation...
In addition, substantial ventilation occurs from chest compression–induced gas exchange (ie, small volumes exhaled with each compression and inhaled with chest recoil) and spontaneous gasping by the patient in cardiac arrest during cardiopulmonary resuscitation.
Is it time to change the way we do CPR? Maybe. Maybe not.
This
is a nicely designed prospective study with a large sample size (n = 883), and published in an English-language major medical journal. I commend the authors for this excellent work and am impressed by their results. However, this JAMA article has a major flaw: the CPR protocols used were not randomized. Lack of randomization can allow all sorts of bias to creep into a study. For example, the effects seen in this study could even represent an example of the
Hawthorne effect. I don't think I can improve on the authors' own conclusion:
These results need to be confirmed in a randomized trial.
I agree. If a randomized controlled trial corroborates the findings in this study, I expect to see a lot of changes in official CPR protocols. For an excellent further commentary on this study, please see
this JAMA editorial.

At this point, you might be wondering: "How can CPR possibly matter to a radiologist?"
If so, 5 points for
Gryffindor for raising that question. But just 5.
A fair number of radiology procedures involve injecting some
contrast agent (lay term = "dye") into a patient. Cardiac arrythmias are an uncommon but known complication of these agents. Thus, these studies are only performed when a radiologist is around to monitor the exam and treat any adverse reactions, including cardiac arrest.
I haven't had to do CPR on a patient since I entered radiology. However, a friend had a cardiac arrest before my eyes at a dance last year. Fortunately, CPR and a nearby automatic external defibrillator (AED) were enough for me, my spouse and several other pals to restart my friend's heart, which is still beating strong at local dances 15 months later.

I guess you could say this event made CPR really,
really relevant to me -- relevant not only as a physician, but also as a precocious geezer and potential CPR customer myself. These days I travel to local dances with a personal AED just in case cardiac lightning strikes again in my vicinity. If it does, I'm also going to pay a lot more attention to my chest compressions, and keep them as uninterrupted as possible.