WDWDWWD: Chest Compressions

Today we're rolling out the first in a series of posts looking at Why Do We Do What We Do (WDWDWWD). Today we're taking a trip back in time to figure out why we do chest compressions during cardiac arrest.

“Push Hard & Push Fast.” Anyone who has ever taken a CPR class has heard the phrase, and pumped up and down on a patient’s chest while humming “Stayin’ Alive” to keep to the beat. But do you know exactly why we’re doing compressions? The 2010 American Heart Association guidelines tell us to place patients in cardiac arrest on a firm surface, overlap our hands and place them over the lower half of the breastbone, and compress at a rate of at least 100 beats per minute, achieving at least 2 inches in anterior-posterior depth with each compression, and allowing for complete recoil with each beat.

The first documented successful utilization of closed-chest cardiac compressions was performed in 1891 by a German surgeon, Dr. Friedrich Maass. Back then, pulseless arrest was thought to be related to ventilations because nearly every documented case occurred in the operating room. Therefore, compressions were timed with ventilations and usually performed at a rate of 30-40 beats/min. In 1981, Maass was performing a cleft-lip repair on a 9 year old boy. The child was difficult to sedate and received multiple doses of the anesthetic of the time, chloroform. Apparently the patient received a bit too much of the sedative and he lost his pulse. In line with the teaching of the time, Maass performed compressions at a rate of 30-40bpm for 30 minutes. Then, as they were about to declare the patient dead, Maass “went to direct compression of the heart  region and, in [his] excitement, [he] worked very fast and vigorously” and after 30 more minutes, a carotid pulse was palpable. Unfortunately, word didn’t travel quickly in the late 19th century, and Maass’ discovery did not become common knowledge. The topic would only be picked up 67 years later.

In 1960, a surgeon from Johns Hopkins, Dr. Kouwenhoven one again described closed-chest compressions in the setting of 20 patients who became pulseless in the OR. In his original paper, he includes the following diagram:

Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac compressions. JAMA 1960 Jul 9;173:1064-7.

Look familiar? His technique is pretty much unchanged from what we use today.

So now we know that compressions work, the next question to ask is, ‘Why?’. In 1990 a team of EM physicians from Henry Ford Hospital posited that the answer was coronary perfusion pressure (CPP). CPP is the difference between end diastolic aortic pressure and right atrial pressure. If you think about it, the inflow of your heart is the vena cavae dumping into your right atrium, and the outflow is the aorta, by subtracting your inflow from your outflow you get the coronary perfusion pressure. The perfusion pressure can also be thought of as a surrogate to coronary blood flow.

The team from Henry Ford measured the CPP  during compressions in 100 patients who experienced nontraumatic out of hospital cardiac arrest. About a quarter of those patients achieved ROSC and the authors compared the CPPs in those who did and did not. Using a c-index, they found that the maximal achieved CPP almost perfectly predicted whether a patient would achieve ROSC. In fact, no one with a maximal CPP below 15mmHg achieved ROSC. This data was in line with earlier studies performed in dog models. Eventually it became generally agreed upon that the goal CPP during compressions lies between 30-40mmHg.

Because measuring CPP directly is quite invasive, researchers took to investigating easier methods of monitoring compression adequacy. In 1985, Sanders et al showed that a linear relationship existed between end tidal CO2 (ETCO2) and coronary perfusion pressure. 30mmHg CPP corresponded to 10mmHg ETCO2 - a number you will find in the guidelines to this day. Weil et al showed that ETCO2 is associated with cardiac output, also an easy to measure parameter. You can read more about ETCO2 here.

So how do we achieve good cardiac output? The answer lies in applying adequate force at an adequate rate. Many studies done on animals models, such as dogs, and in humans found a linear relationship existed between depth of sternal displacement and cardiac output. A more recent study published in 2012 showed that increased depth of compression was related to increased probability of return of spontaneous circulation and advocated for a depth of over 38mm (1.5in).

In 1984, Maier et al also showed that by increasing compression rate, increases in mean arterial pressure and cardiac output could also be achieved. This study also showed that coronary flow occurred mostly during diastole, emphasizing the importance of allowing for chest recoil and full diastole to occur. There may be a limit to how fast we want to compress, however. A recent study showed that compression rates over 125 were actually associated with adverse outcomes.

Studies have also shown that it is incredibly important to minimize gaps in compressions. As they say, a picture is worth a thousand words, so I will let this figure from Cunningham et al (2012) do the talking.

Cunningham et al. Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation. Am J Emerg Med. 2012 Oct;30(8):1630-8. doi: 10.1016/j.ajem.2012.02.015. Epub 2012 May 23.

You can see from the image, that each time a break was taken in compressions, perfusion pressure dropped. It takes time to work up to adequate perfusion pressure, and the longer breaks take, the less time the patient will spend at the correct pressure.

This is why it is vitally important to minimize interruptions in compressions as much as possible. If you are participating in a code, try to anticipate what will be needed next. If you think the residents or attendings will want to do an echo during the pause, make sure the ultrasound is ready and the probe is gel’d up. If you are checking the pulse, keep your fingers in position while compressions are happening so you dont have to fumble around trying to find the right spot during the pulse check. Finally, if you are doing compressions, you may be asked to ‘call the shock’. That way you can compress right up until the shock is delivered and start back up again after. (Though I would encourage you discuss this with the person who is running the code way before the patient even shows up to avoid any confusion).

So there we have it. Compressions are performed many times everyday in many different settings. They’re our first line of defense when a patient loses their pulse, and often something that you as a medical student will be called on to do! Hopefully by understanding why each parameter of compressions is important, we can ensure that we’re providing adequate compressions when needed. So go out there, and remember to push hard and push fast.