Pulseless Electrical Activity (PEA)

00:01 All right, we’re gonna switch gears a little bit now and talk about pulseless electrical activity.

00:07 And this is one of my favorite rhythms to think about because it’s physiologically much more complex and interesting than V-fib and V-tach and there’s a broad differential that you’ll gonna learn about.

00:18 So what is PEA? PEA again, stands for Pulseless Electrical Activity.

00:24 And what that means is that there’s organized electrical conduction on the monitor.

00:29 Normal looking QRS complexes with P waves and T waves and all the things you expect from a cardiac rhythm.

00:36 However, there is clinically no pulse.

00:40 So normal looking activity on the monitor but no pulse when you actually palpate the neck.

00:48 What is the single most important intervention for PEA? It’s a little bit of a trick question.

00:53 The most important intervention is to figure out what caused it and fix that.

00:57 So unlike V-fib and V-tach where we do the same thing for everybody across the board regardless of the cause.

01:03 In the case of PEA, we’re only gonna be able to make our patient better if we can figure out the cause and treat it.

01:10 Now of course, we’re gonna provide support and care in the meantime but ultimately, our goal is gonna be to make a diagnosis.

01:18 There’s two major mechanisms of PEA that I’d like you to be aware of.

01:23 One is the empty heart and the other is EMD or Electromechanical Dissociation.

01:29 We’re gonna compare and contrast these a little bit.

01:33 So in the case of an empty heart, the heart is conducting normally.

01:36 There’s nothing wrong with the heart’s conduction system.

01:39 You know, if I were to get shot right now in the aorta and all of my blood volume were to pour out on the floor, there’s nothing wrong with my heart, it’s gonna conduct perfectly normally.

01:50 In the case of electromechanical dissociation the heart is also conducting normally.

01:55 Electrical activity in the heart is preserved.

01:58 However, when the heart is empty, again, if I got shot in the aorta and all of my blood's on the floor, there’s nothing wrong with my heart itself.

02:08 So at least in the short term, it’s gonna keep contracting just as hard and fast as it can to try to profuse my body.

02:15 So contraction occurs and it’s normal.

02:18 However, that contraction ultimately is ineffective, right? Because no matter how hard the heart squeezes if there’s nothing inside of it, if my blood is on the floor and not inside the heart, the hearts not gonna fill, it’s not gonna send blood out to the body.

02:32 By contrast, in electromechanical dissociation, there are normal cardiac action potentials that yield the pretty spikes that we see on the cardiac monitor.

02:43 However, these action potentials do not yield cardiac contraction.

02:48 So the heart's conduction is normal but the contraction is either absent or so impaired that it doesn’t produce a pulse.

02:59 Ultimately, empty heart PEA is caused either by hypovolemia as I mentioned with the example of all my blood volume being on the floor, or can be caused by some kind of an obstructive process that prevents the heart from filling.

03:13 So examples of those are things like cardiac tamponade.

03:16 You’ve got a big collection of blood around the heart.

03:18 It physically compresses the heart.

03:20 The heart can’t fill normally, so it can’t send blood out to the body normally.

03:25 Same with tension pneumothorax, right? You have a huge high pressure air collection in the chest, it’s gonna mechanically squish the heart and prevent normal filling.

03:33 These are all empty heart forms of PEA.

03:37 By contrast, electromechanical dissociation is gonna be caused by systemic derangements in the body.

03:44 So these are gonna be things that affect energy metabolism such that the heart is able to produce the energy to maintain normal conduction but it’s not able to maintain the energy to enable mechanical contraction.

03:58 And as you can imagine, contraction requires a lot more metabolic energy than conduction.

04:04 So it’s gonna be the thing to go in the setting of severe derangements of metabolism in the body.

04:12 So what’s your differential diagnosis of PEA? There’s a common mnemonic that’s used which is the H’s and the T’s.

04:18 And I’m gonna tell you a secret, I don’t love this because it doesn’t force you to think about it physiologically but a lot of students find it useful so we'll go through them.

04:26 Hypovolemia.

04:27 Like we already mentioned, if you don’t have any blood volume, your heart's gonna be empty.

04:31 Your heart's not gonna have a good output.

04:34 Hypoxia.

04:36 Well, how do we make energy in the body? We make it out of oxygen and glucose.

04:40 So if you’re hypoxic, your aerobic metabolism is gonna be ineffective and you’re not gonna be able to produce a normal amount of energy to drive cardiac contraction.

04:49 So it’s potentially a cause of PEA.

04:53 Acidosis or hydrogen ion, 'cause you know, we had to make it start with an H.

04:57 In that kind of a situation, you know, there’s a different optima for every process in the body.

05:03 There’s PH optimum, temperature optimum, and physiologic processes just don’t work right when you have extreme derangements of those optima.

05:13 So in the case of profound acidosis, the heart actually can’t squeeze normally.

05:18 So even though conduction is intact the cardiac contraction is not.

05:25 Hyper or hypokalemia, it has to be pretty profound, but severe derangements of potassium can actually precipitate PEA.

05:34 Hypothermia, like I mentioned, for the same reason as acidosis.

05:37 If the body is really, really cold the heart's not gonna be able to contract normally.

05:42 We talked about tension pneumothorax, as a cause of empty heart PEA and the same for tamponade.

05:48 There’s a number of toxins that can potentially produce PEA by uncoupling energy metabolism from normal cardiac contraction.

06:00 Massive MIs can cause such profound reduction in cardiac squeeze that you can’t actually clinically detect a pulse.

06:08 And massive PEs can cause such severe obstruction of normal pulmonary blood flow that they basically cause empty heart PEA the same way any other obstructive cause would.

06:18 So with PEA, it’s even more important than with other types of cardiac arrest to understand the underlying cause and to identify what’s going on.

06:27 So you wanna get as much information as you can about the circumstances that led up to the arrest.

06:33 What was the patient doing when it happened? Did the patient have any symptoms beforehand? Did they suddenly clutch their chest and complain of pain or were they grasping for breath? Did they turn blue? Did they attempt suicide? Was there some type of trauma? All of these things will help you narrow the differential for PEA and treat the patient accordingly.

06:54 For physical exam, it’s especially important if you don’t have a good history, which in many cases of cardiac arrest you won’t.

07:01 But if the patient has any signs of physical trauma when you look at them, maybe you’re gonna think about more hemorrhage as a potential cause of PEA or tension pneumothorax.

07:09 If the patient's pregnant that should make you think about pulmonary embolism.

07:13 If they have a dialysis catheter hanging out of the chest, that’s gonna make you think about hyperkalemia, etc.

07:20 So physical findings can potentially give you clues that will help narrow your differential and prioritize your treatments so that you can help the patient with PEA.

07:30 Another nice adjunct we have nowadays is bedside ultrasound.

07:34 So ultrasound is a great extension of physical exam.

07:37 It allows us to look inside the body in ways that we couldn’t before and identify in real time, is there a pericardial effusion present or signs of tamponade? Is there evidence of a pneumothorax which is seen by absence of lungs sliding on ultrasound? Is there an abnormal cardiac ejection fraction, maybe the heart's just barely beating.

07:58 Maybe the IVCs really distended suggesting the patient is volume overloaded.

08:02 Or maybe it’s really collapsible and tiny suggesting that they're dehydrated.

08:08 So ultrasound is especially good for cardiac tamponade and pericardial effusion.

08:13 This is an example of a cardiac ultrasound where you can see some of the chamber’s labeled.

08:18 But most importantly, you see a large pericardial effusion which is outlined here on the screen.

08:23 And that’s big enough that you would certainly want to perform a pericardial synthesis and get rid of that to see if that helps the heart beat more effectively and improves your cardiac output.

08:36 There's also the inferior vena cava which is a great overall indicator of your patient’s volume status.

08:42 So like I mentioned before, patients who are really volume depleted either from dehydration maybe from a diarrhoeal illness, or hemorrhage, blood loss.

08:51 These patients will have very, very skinny, collapsible inferior vena cavas.

08:57 So if your vena cava's tiny or if collapses down to nothing when you breath in deeply.

09:03 That suggests the patient in need of volume.

09:06 Whereas you IVC is normal in caliber and it doesn’t collapse down to nothing or maybe it’s even distended, that suggests that you’re euvolemic or potentially even volume overloaded.

09:17 So these can help kind of guide your thinking a little bit about the patient and particularly for patients who have evidence of intervascular volume depletion, by giving them fluids or blood, you can potentially reverse their PEA.

09:32 I didn’t have an image to show you here but I’ll also just mention, ultrasound is very commonly used to evaluate for tension pneumothoraces.

09:40 There’s a number of test that you can do that'll help you quickly identify that at the bedside without moving the patient.