Adult Cardiac Arrest Algorithm – Asystole/PEA Video

 

Transcript:
Hi. I’m Mark for ACLS Certification Institute. In today’s video, we’re going to review another arrest algorithm with the focus on asystole and PEA. Let’s take a look at our arrest algorithm. Of course, it starts with establishing unresponsiveness, getting some help coming, activating the EMS or calling the cod if you’re in the hospital, making sure they have an airway, bagging them, assessing the rhythm. Then we’re going to see is this a shockable rhythm or not. If it’s not a shockable rhythm, is the patient in asystole or PEA. Now, I know what you’re thinking. When we’re talking about asystole and PEA, you’re probably thinking this “R.I.P.” and you wouldn’t be wrong. Asystole and PEA carry with them horrible outcomes, dismal prognoses. Usually these are end-of-life- rhythms—PEA and asystole—so don’t get your hopes up, but what we’re looking for is should this occur suddenly, is there a reversible cause, is something we can do to fix this immediately.

Starting with asystole, the name asystole has nothing to do with a rhythm. It doesn’t describe the electrical activity. ‘Systole’ is actually Greek for contractions and ‘-a’ the prefix means without, so ‘asystole’ means ‘without contraction.’ On the monitor, it’ll appear like this: a flatline. There is no electrical activity in the heart, thus no contractions, no cardiac output—dead guy. According to the AHA guidelines, we’re going to start chest compressions immediately. Should this asystole occur in a younger person, start chest compressions immediately. We need to find a cause. We need to be looking for why did this patient become asystolic. The guidelines recommend epinephrine be administered 1 mg every 3 to 5 minutes. Reassess the patient while you’re trying to find a cause.

p>Next, PEA (pulseless electrical activity). PEA used to be called EMD back in the day, which stood for electrical mechanical disassociation. What we have in PEA is any organized rhythm that’s not generating a palpable pulse. I’ll go on further to say it’s a rhythm that should have a pulse. For example, let’s look at this rhythm right here. What does that look like to you? The same thing it looks like to me: a normal sinus rhythm. Except in this case, the patient has no pulse, no appreciable pulse with this rhythm. They should, but they don’t. That’s what makes it PEA. PEA is not a rhythm. It’s a state. It’s a condition.

There are three rhythms that can’t be PEA:

• V-fib
• V-tach
• Asystole

Why? Because we wouldn’t expect a pulse with these rhythms. PEA is an organized electrical activity where we expect to see a pulse but we don’t have one. Looking at our algorithm, the treatment, again, is epinephrine and continuous chest compressions. We need to focus on what is the cause of this, why does this patient have a pulseless electrical activity state. The two leading causes of PEA in the adult population are hypovolemia and hypoxia. Address the airway. If you’re going to be bagging them with chest compressions, consider an advanced airway early. Because they’re not generating a pulse, peripheral IV vascular access may be difficult to obtain. Don’t waste any time. Go straight to IO infusion. It’s fast, reliable, and you can put a lot of fluid in through an IO, so do not hesitate. Gain IO access on this patient. Tank them up. Get some fluid in them. See if that’s a reversible cause. They estimate that it takes a pressure between 40 and 60 systolic to actually generate a peripheral pulse. In PEA (pulseless electrical activity), they may still have contractions, they may still be moving blood forward, but we just can’t feel it. Maybe a quick Doppler. Listen for heart tones to see are we generating heart tones. What creates heart tones? Valves opening and closing. What causes those valves to open and close? Pressure changes within the chambers of the heart. The papillary muscles and the chordae tendineae do nothing to open and close the valves. All they do is keep the valve from going too far. If you’re hearing heart tones, that means that valves are opening and closing. More, you have pressure within the chambers of the heart that is causing those valves to open and close and make that sound. Again, consider hypovolemia and tank your patient up if appropriate

When we go back and we look at the algorithm for PEA and asystole, we can see that there’s not a whole lot going on. We have chest compressions and we have epinephrine, and we’re doing those so we can buy some time to figure out what’s going on. When it comes to asystole and PEA, you have to very quickly become this guy: “Hello, I’m with the Medical Detection Unit. I’m here investigating the possible causes of this PEA or asystole.” Like any good medical detective, when it comes to PEA, we need to look for clues. A great place to start is by looking at the cardiac rhythm. If the rhythm is narrow-complex and tachycardic, that tells us a couple of things, a couple of clues. It’s narrow-complex, which means the electrical activity is taking a fairly normal pathway. The heart’s doing okay, but it’s tachycardic. It’s fast and it’s compensating, usually for a volume loss. If you have a narrow-complex tachycardic PEA rhythm, be thinking hypovolemia and fluids may be the answer, as opposed to a wide, slow PEA. This is usually a dying heart, hypoxic and dying, not good. They’re great clues to start with to determine what is the cause of this PEA. Remember, the goal in a pulseless electrical activity is to find the underlying cause. We have a list of our usual suspects. Who are they? The H’s and T’s. That’s who we need to question, interrogate, and see if one of these characters is responsible for this pulseless electrical activity. Find it, identify it, and fix it quickly.

I’m Mark for ACLS Certification Institute. Thank you for watching. I will see you in our next video.

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