The phrase you will hear most often in your nursing school career isn’t, “This is on the test” or “Choose the members for your group project” or even “Get comfy for six hours of lecture.” Nope…the most common phrase (and probably the most important one) is “What are you going to do about it?” It’s also the most common thought running through your head once you’re out there doing your thang as an RN! Here’s what I mean by that…
Got a low SpO2 level? Great. Know what caused it? Super! But, what are you going to do about it? Patient in a-fib? Got it. Know what this does to cardiac output? Fantastic! But, what are you going to do about it? As RNs, we don’t just sit around at the nursing station charting our assessments (though it can feel like it!). When we spot an abnormal assessment finding or something goes haywire with our patient…(all together now) WE DO SOMETHING ABOUT IT!!!!
In this post we’ll talk about the most common arrhythmias you’ll see in the clinical setting and what you are going to do about it. And since I don’t have these images in my own library (yet), I’ll link to outside sources so you can at least see what they look like. Let’s roll, rockstars!
Problems with the ol’ ticker can originate in the atria or the ventricles. Typically, atrial problems aren’t as serious as ventricular problems, so we’ll start there. Baby steps, y’all! And by the way, does anyone else have serious trouble spelling “arrhythmia?” It never looks right to me! Ok, onward we go!
Sinus Tachycardia: Probably the most basic of arrhythmias that you’ll see is sinus tach. This is a regular rhythm that originates at the sinus node and is above 100bpm. You go into sinus tach all the time….when exercising, maybe right before a skills check-off and possibly even when you’ve had too much caffeine! Your patients will be in sinus tach for a variety of reasons…dehydration, anemia, fever and pain are some common ones. Here’s what it looks like!
So, what are you going to do about it? Basically, you’ll address the underlying problem (so, a little detective work is in order!). If they’re dehydrated…give ’em fluids! If they’re anemic, do they need blood? If they’ve got a fever…give ’em a Tylenol or institute cooling measures. If they’ve got pain, give ’em something to relieve pain and try some pain-relieving measures such as re-positioning, distraction and whatnot.
Note that because tachycardia does increase oxygen demands on the heart, you’ll want to give your patient some oxygen. If they’re out of bed, get ’em back in bed or at least have them sit down…we don’t want to tax their heart more than necessary.
There are other tachycardias that are definitely more serious and we’ll get to those later on. The key here is that this is SINUS tachycardia…you KNOW it originates in the sinus node because why??? Because of the presence of P waves. If you can’t see the P waves, we got other issues and we’ll talk about that later on 🙂 Note that even sinus tach can cause symptoms if your patient is already compromised. In that case, we’ll get more aggressive with treatment (similar to what we’d do in SVT).
Sinus Tachycardia in a nutshell: Put on some oxygen, get ’em in bed, and address the underlying cause!
Sinus Bradycardia: Here’s another of the common arrhythmias, AKA Sinus Brady. This is a regular rhythm that originates in the sinus node (helloooooo P waves!) and is below 60bpm. Is it super scary? Usually not. I was in sinus brady this morning as my resting heart rate is typically in the 50s. And no, it’s not because I’m in fabulous shape…I just sleep really really good! But yes, you will see sinus brady in endurance athletes all the time…sometimes you’ll see it caused by medication overdoses (typically those that block the AV node) and it occurs with vaso-vagal stimulation as well. Think of your patient who is trying like the dickens to have a bowel movement. They’re sitting there on the commode bearing down like a champ and BAM! Sinus brady…that’s a vagal response! This explains why we use a vagal maneuver to treat some tachycardias (more on this in a bit!)
What to do about sinus brady? If it’s asymptomatic then you’re just going to note it and monitor it. If the patient is symptomatic (low BP or altered LOC), then you’re going to get that heart rate up and get it up pronto! The most common way is to give Atropine 0.5mg IV and watch it do it’s magic. If the patient is severely compromised, then you go to electricity and perform percutaneous pacing. It’s painful so give ’em Versed if you can! In the super sick patients we can also give dopamine or epi IV…that’s an automatic ticket to the ICU…do not pass go!
Note that certain meds can cause bradycardia…if you suspect your brady is due to something like an overdose of digoxin or too many beta-blockers, talk to the doc about getting an antidote on board asap.
QUIZ TIME! What’s the antidote for digoxin? How about beta blockers? Answers at the bottom!
Symptomatic Sinus Bradycardia in a nutshell: Atropine or pacing. If severe, dopamine and/or epinephrine IV. Consider reversing certain meds.
Sinus Arrhythmia: This one is really interesting and actually somewhat common. You will most likely see it in younger folks and is considered a normal finding in children and some adults. It involves a slight variation in the rhythm and typically occurs in tandem with the respiratory cycle…the heart rate goes up on inspiration and slows down with expiration. So, obviously, it’s an irregular rhythm that originates at the sinus node (P waves for everyone!). And since it’s benign we’re not going to do anything about it…except maybe print a strip and show it to your friends…it’s kinda cool.
Sinus Arrhythmia in a nutshell: Note it and move on.
Premature Atrial Contractions (PACs): These guys occur when there’s an irritable little group of atrial cells that fire off prematurely, causing a contraction that comes earlier than it should have. When you look at your P-waves, you’ll notice that the P-wave associated with your PAC will look different from the others. That’s because it’s not firing in the exact same way as the others. Neat, huh? Occasionally, very early P waves will be hidden in the T-wave, so look for T-waves that look a little funky…the reason it looks a little funky is because there’s a P in there, hiding out.
So who gets PACs? People with heart failure, anxiety, pulmonary disease, MI, caffeine, nicotine and alcohol. You’ve probably felt them on yourself from time to time. I got them a lot in nursing school when I was running on coffee and adrenaline (take better care of yourself than I did…please!).
What are you going to do about your patient’s PACs? Typically you won’t do anything except note it in the chart. Be sure to identify the underlying rhythm, as PACs are not a rhythm in and of themselves. So, you’ll say something like NSR with PACs. Though they are more or less harmless, they can give you hints about atrial irritability…so keep an eye on them since they can, on occasion, lead to more serious arrhythmias.
PACs in a nutshell: Usually no big deal, keep an eye out and move on.
Atrial Flutter: Happily, atrial flutter is typically super easy to spot. It basically will look like a saw-tooth pattern on your ECG. Common causes include heart failure, thyrotoxicosis, ischemia, MI and rheumatic heart disease. The rhythm can be regular or irregular, depending on how the ventricles respond to the rapidly firing atria…but for the most part you’ll see it as a regular rhythm. Each little saw-tooth is actually indicative of the atria impulses, but since they’re not really P-waves, they have their own name…they’re called Flutter Waves or F-waves.
Your ventricular rate will vary, and depends on how well the AV node does its job. Your atrial rate is going to be super fast, around 250-350bpm, though typically around 300bpm. Woah! What’s that going to do to your patient?
What are you going to do about atrial flutter? The first thing to Sherlock on this is to find out if it’s new onset or not. If it’s new onset (less than 48 hours), we can get them out of it lickity-split using meds or electricity in the form of synchronized cardioversion. But if it’s been hanging around a while, we typically avoid that…why? Like a-fib, there’s a huge risk for blood clots…that atria isn’t filling or emptying adequately, so there’s some residual blood just kicking around in there getting all clotty. If we kick the heart out of this abnormal rhythm and into a super-efficient regular rhythm, the atrium is going to empty completely, send that clot to the ventricles and out the ventricles to where? You guessed it…huge risk for ischemic stroke folks…no bueno! So, if you’re going to be converting these folks that have been in A-flutter for more than 48 hours, they need to start on anticoagulants asap!
What else are we going to do? Let’s say your ventricular rate is super fast…we want to get that down, right? So, controlling ventricular rate is key in A-flutter. This will typically be your beta-blockers and calcium channel blockers (I most often saw diltiazem used). Here’s a great article that goes into more detail…including information about ablation therapy. So cool!
Atrial Flutter in a nutshell: control the ventricular rate, cardiovert, use anticoagulants as needed.
Atrial Fibrillation: You’ll see A-Fib probably ten times as often as you’ll see A-Flutter. It’s caused by chaotic cells in the atria that make them quiver instead of contract. The rhythm is irregularly irregular, and this is THE hallmark sign of A-Fib. You won’t be able to measure the atrial rate, because there are no P-waves, and your ventricular rate can often be really fast. When it’s above 100bpm, we call this “A-Fib uncontrolled” meaning the ventricular rate is not controlled adequately by the AV node. It can be caused by lots of things such as coronary artery disease, heart failure, MI, pulmonary disease and ischemia. I’ve even heard of it being brought on by an alcohol binge! See note above about taking care of yourself 🙂
QUIZ TIME! What will happen to cardiac output? What else are you going to be concerned about? Answers at the end of this post (no peeking!)
So, what are you going to do about Atrial Fibrillation? If it’s new onset, we can get them out of it pretty quickly using electricity (synchronized cardioversion) or amiodarone. Typically the biggest thing you want to deal with in A-Fib is keeping the ventricular rate below 100 while also decreasing the risk of throwing a clot.
Recall that the atrium is quivering…it’s not doing a darn thing that’s useful and the blood that’s in there is just getting swooshed around like in a washing machine. Just like in A-Flutter, that blood is going to get super clotty if we don’t do something about it. Anticoagulants to the rescue! In fact, your chronic A-Fib patient will need to be on anticoagulants forever and ever and ever…unless, for some reason, they convert back to a normal rhythm! Not sure how much this happens, though!
To control the ventricular rate we’ll throw some beta-blockers or calcium channel blockers at it. At the hospital where I work we give amiodarone to new-onset folks in hopes it will slow the rate AND knock them back into a sinus rhythm.
Atrial Fibrillation in a nutshell: Control the rate, try to convert them back to a sinus rhythm, give anticoagulants.
Supraventricular Tachycardia: Remember when we talked about Sinus Tachycardia and mentioned the presence of P-Waves? The P-Waves are what tell us the rhythm is originating from the sinus node. But what if the rate is super fast and you can’t see the P-Waves? As long as the QRS is narrow, then we know it originates in the atrium…but without seeing P-Waves we don’t really know where. So, we call it a Supraventricular Tachycardia…meaning it starts “supra” to the ventricle and that’s all we know about it. This is a regular rhythm and you’ll typically see rates above 150bpm. Here’s a great example!
SVT is kinda unpredictable, but some common causes include heart failure, pericarditis, pneumonia and even smoking/alcohol/cocaine.
What are you going to do about SVT? The very first thing you’re going to do is quickly assess if your patient is stable or unstable. If they are experiencing hemodynamic compromise (low blood pressure, decreased LOC, chest pain) then you’re going to treat mucho more aggressively than if he’s just saying, “I feel a fluttering in my chest.” Get oxygen on everyone, get ’em back to bed and try a vagal maneuver if your patient can participate. Happily, vagal maneuvers work a lot of the time in asymptomatic cases…yay!
If your patient is super sick, you’re going to need to shock them out of this rhythm using either electricity or a medication called adenosine. If you’re using electricity, again this will be a synchronized cardioversion…but you’ll want to try adenosine first if you can. Adenosine “resets” the sinus node by STOPPING THE HEART for about 7 seconds. Trust me, this is the longest 7 seconds of your life. Your patient will be in ASYSTOLE for all of those 7 seconds…and you will be soooo tempted to glue your eyes to the monitor. Watch your patient…reassure him and remain super calm (calmness is contagious!) You’ll know he’s back in NSR when the beeps pick up on the monitor again.
I remember the first time I gave adenosine…I had floated to telemetry that day and had a patient in unstable SVT. I called one of my ICU buddies to come down and we got the crash cart in the room, hooked him up to the monitor and tried like heck to act like we do this every day…super calm, smiling, reassuring him the whole time. Afterward he told me if felt like getting kicked in the chest…poor guy had a rough day that day.
QUIZ TIME: What is the difference between cardioversion and synchronized cardioversion? Answers at the bottom.
SVT in a nutshell: Vagal maneuver, adenosine, synchronized cardioversion.
For a quick refresher on heart blocks, check out this post…I’ll wait right here. For some reason, spotting these arrhythmias always gives me a bit of a thrill. Heart blocks can be subtle on the monitor, so spotting one means you’ve been paying attention. Good job!
First Degree Heart Block: The main dealio with this guy is that the PR interval is consistently prolonged. Your rhythm will be regular and your rate can be fast, regular or slow. It’s not considered dangerous because the impulses ARE getting through after all…but be aware that it can progress to a higher degree of block. It’s commonly caused by drugs that affect the AV node, inferior MI, coronary disease and rheumatic heart disease. It looks like this!
What to do about First Degree Block? Monitor and pat yourself on the back for noticing it. If your patient is symptomatic, remove any AV-blocking drugs and consider a pacemaker for those at super high risk for progressing on to a deadlier block.
First Degree Block in a nutshell: Monitor, consider stopping certain meds, consider pacemaker.
Second Degree Heart Block Type 1: This is where I get cranky…the Second Degree blocks go by too many names and it makes me scowl. This one also goes by the name “Wenckebach” or “Mobitz I” Seriously…three names for one disorder!!! Personally I think this Wenckebach character and this Mobitz fella should just duke it out cage-match style and the winner shall reign supreme. Arrrgh! Ok, rant over.Personally I think this Wenckebach character and this Mobitz fella should just duke it out… Click To Tweet
Wenckebach is caused by the same types of things that cause a First Degree block as well as mitral valve prolapse. In this block, the PR interval gets progressively longer and then there’s a dropped QRS. So, your atrial rhythm will be regular but your ventricular rhythm will be irregular. It’s usually not symptomatic, unless those dropped ventricular beats put them into a bradycardia with decreased cardiac output. Check out this fabulous music video about Wenckebach.
What are you going to do about Wenckebach AKA Mobitz I AKA Second Degree Heart Block Type 1? If your patient is asymptomatic…monitor it closely as it can progress to a more dangerous block! If they are having symptoms including low blood pressure, chest pain, syncope or dizziness then you’re going to need to treat more aggressively. This could be atropine (to bring the rate up) or pacing to also keep the rate up…note that the symptoms associated with Wenckebach are typically due to the bradycardia that could occur…fix the rate and symptoms improve!
If your patient is sicky-sick or his block causes prolonged pauses, then he’ll probably get a pacemaker placed. With ANY patient having chest pain, please put them on oxygen. Thank you.
Wenckebach in a nutshell: Monitor if asymptomatic. If sick, give atropine and/or pace.
Second Degree Heart Block Type 2: This guy also has an alias…it’s Mobitz II. As you may have guessed, this one is more serious than Mobitz I/Wenckebach/Second Degree Type 1…that’s because a second degree block of this type is more typically associated with bradycardia and can easily become a Third Degree Block and, trust me, you don’t want to go there.
In this block, ventricular beats are dropped but the occurrence is totally random. There’s just no rhyme or reason to it….and that’s what’s so disconcerting. If you have more than a few in a row…guess what just happened? Your heart rate dropped WAY low and now your patient is having symptoms. Not good at all. Your P waves will march along just fine and dandy, so your atrial rate is regular…but since some QRS will be dropped, the ventricular rate is irregular.
Whatcha gonna do about Mobitz II? Most likely, your patient will not be feeling great, so this isn’t a “watch and wait” kind of scenario. No siree. If your patient is on any AV-blocking meds, I’d consider stopping those ASAP. Get those pacer pads on the patient (try to do this without totally freaking them out) and make sure a cardiologist is enroute. They may need transcutaneous pacing to keep their rate up and they’ve just bought themselves a permanent pacer, which hopefully gets placed before they go into complete heart block (coming up next).
Mobitz II in a nutshell: If symptomatic…pacing, pacing, pacing. If asymptomatic…assume they’ll be showing symptoms soon or perhaps going into a higher block. Be ready!
Third Degree Heart Block: This one has another name and that’s Complete Heart Block…and it is exactly what it sounds like. Super duper bad. It can occur with MI, conduction system disease, open-heart surgery, congenital heart disease, digoxin toxicity and AV-blocking meds. In this block the atria and the ventricles are not chatting with each other at all. The atria are contracting all on their own and the ventricles aren’t getting any conduction at all through that AV node…it is “completely blocked.” Does that mean the ventricles are just taking a siesta? Nope…they’re plugging along minding their own beeswax. The rhythms are regular, just disjointed from one another, kinda like this.
What to do about Third Degree Block? Most likely your patient is bradycardic and symptomatic. Even if they are not, you’re still going to get those pacing pads on them and pace if necessary. They are at high risk for sudden cardiac death. If that doesn’t make you nervous, then maybe you shouldn’t be a nurse…just sayin’. Definitely stop any AV-blocking meds and get a cardiologist on the team. This guy is likely going to need a permanent pacemaker.
Third Degree Block in a nutshell: Probably needs pacing, be super vigilant and ready for a code!
If you’ve hung in with me this far, we’re on the home stretch! In this section we’ll cover the arrhythmias that originate in the ventricles. Ready?
Premature Ventricular Contractions (PVCs): Just like PACs, PVCs are early beats that occur within a rhythm. The difference is that they originate in the ventricle so you’ll see no P-Wave and a wide QRS. If your patient is having multiple PVCs, take a gander at the QRS complexes. If they’re all the same, then they’re all originating from the same spot in the ventricle…if they’re different, then they are originating from multiple spots.
In healthy folks, PVCs aren’t typically dangerous. They occur here and there due to things like electrolyte imbalance (K and Mg), stimulants, hyypoxia and increased catecholamine levels. In sicker patients, they can also occur due to MI, ischemia, acidosis, heart failure and digoxin toxicity. If your patient has a central line, notice if the PVCs occur more frequently in certain positions. Pull out that morning’s chest x-ray and see if the tip of the catheter is too deep…it can irritate the ventricle making it irritable!
What are you going to do about PVCs? If your patient is asymptomatic and the PVCs are sporadic, you probably won’t do much except replace electrolytes as needed, run a strip and note it in the chart. If they’re occurring frequently or the patient is having symptoms, you’ll correct electrolyte imbalances, look for drug toxicity (such as digoxin), may give amiodarone in some cases. Again…even if I haven’t said it in every section….if your patient has symptoms then give oxygen please!
PVCs in a nutshell: Usually not a big deal. Correct K, Mg, Ca; reverse toxic agents; pull back on central lines; possibly amiodarone.
Ventricular Tachycardia: V-Tach is pretty common, but mainly as “runs of V-Tach” meaning the patient had a few ventricular beats in a row and then went back to doing business as usual. Full-on V-Tach is a code type situation. Note that V-Tach can have a pulse or it can be pulseless. We’ll talk about V-Tach WITH a pulse right here…and deal with the scary stuff further down. Here’s what sustained V-Tach looks like…pretty obvious, huh?
Your rate in V-Tach will typically be above 100bpm, with wide and funky-looking QRS complexes that occur regularly. It is caused by the same things that cause PVCs, but the treatment is going to be more aggressive in many cases.
QUIZ TIME! Will vagal maneuvers work on V-Tach? Why or why not?
What to do about V-Tach? If your patient is having “runs of V-Tach” they may be completely asymptomatic. You might hear them say they feel a “fluttering” in their chest during the run, but often times I’d go into the patient’s room and ask them how they feel and they’d say, “fine.” Now, if the V-Tach persists, that’s another story. It is typically not tolerated well and you can quickly find yourself in a code situation. If your patient is having runs of V-Tach or is in full-on sustained V-Tach you’ll want to correct electrolytes, get them on some oxygen and probably give amiodarone. Stay vigilant as they can quickly deteriorate into a pulseless V-Tach (more on this further down)!
V-Tach in a nutshell: Correct electrolytes, amiodarone, be ready for a code just in case.
Torsades de Pointes: This is a very particular type of polymorphic V-Tach that occurs with QT prolongation. If you don’t know what that is yet…don’t worry about it….you’ll cover that in your advanced MS course. The short version is that your QRS impulses will revolve around the isolectric line, creating a very characteristic tracing on the ECG that looks like this…very distinctive, no? Notice how they’re all different? This means they’re originating from different parts of the ventricle. Patients in Torsades can deteriorate to V-Fib quickly, so I guess your next question is…
What are you going to do about Torsades de Pointes? Treatment is typically magnesium replacement, which will inhibit calcium and, in turn, inhibit the early active depolarization that precipitates Torsades. You’ll also want to STOP any drugs that prolong the QT interval and may need to correct other electrolytes as well. If your patient is sick as heck, then transcutaneous pacing may be used. This isn’t a very common rhythm, but it’s so distinctive and easy to recognize, I thought I’d include it.
Torsades in a nutshell: Twisting QRS, give mag.
Idioventricular Rhythm: If all other pacemaker sites in the heart fail, you’ll have an idioventricular rhythm at a rate of 20-40bpm. What do you think this is going to do to cardiac output? If you said, “nothing good,” then you’re right. This is usually the sign of a dying heart…I see it most often in patients who are on comfort care and for whom we are allowing a natural death. The QRS will widen progressively until asystole occurs.
The QRS will be wide, and the rhythm will probably be regular initially and then progress to more irregularity as it continues. Note that the idioventricular rhythm can be “accelerated” giving the patient a normal-ish cardiac output and fewer symptoms. This is called AIVR for short and is often self-limiting with no treatment necessary. AIVR can be caused by drug toxicity, ischemia and structural heart problems…fix the underlying cause and you probably fix the AIVR. Whew! It is also a common “reperfusion” rhythm…meaning that once the heart has been reperfused thanks to to cardiac intervention, they can have AIVR for a period of time.
What are you doing about this idioventricular rhythm? If you’re not at an end-of-life/comfort care scenario, then idioventricular rhythm can be treated with a pacemaker as it usually doesn’t respond to drug treatment. Accelerated idioventricular rhythm or AIVR probably will be self-limiting and not require much beyond a very watchful eye.
Idioventricular rhythm in a nutshell: Pacemaker or allow natural death.
The Pulseless Rhythms
Let’s face it…some rhythms just don’t generate a pulse. These are Pulseless V-Tach, Ventricular Fibrillation, Asystole and PEA.
Pulseless V-Tach: The tricky thing about pulseless V-Tach is that on the monitor it will LOOK just like good ol’ V-Tach…so the first thing you’re going to do when you hop into that room is LOOK AT YOUR PATIENT. Are they dead or are they alive? In pulseless V-Tach (as in all pulseless states, your patient will look pretty darn bad.) Another quick clue with pulseless V-Tach is that your BP and O2 sat will also tank….but always always look at your patient!
What to do about Pulseless V-Tach? Check for a pulse and when you don’t find it, hit that code button and start CPR. Follow your ACLS algorithm which includes the exact same treatment as V-Fib (below)…compressions, electricity, epinephrine and amiodarone. Keep at it and do those compressions hard and fast. If they’re on a vent, take ’em off and bag ’em. Vents are set with pressure limits so that they don’t overcome the pressure in the chest causing barotrauma…compressions drastically increase intrathoracic pressure, so the vent thinks the lung pressures are too high and WILL NOT deliver a breath! Take ’em off the vent and do it manually!
Pulseless V-Tach in a nutshell: ACLS is your friend. Compressions, electricity, epi, amiodarone.
Ventricular Fibrillation: This is bad. This is very bad. I remember with extreme clarity my first patient that went into V-Fib. He’d had a biiiiig surgery and was super super sick. I was running my tush off all night hanging FFP, titrating multiple pressors, dealing with the vent. It was intense. THANK THE NURSING GODS that I had friends in the room when this guy coded. He started to cough a little bit against the ET and then BAM…right into V-Fib. It was awful. We ran that code like champs, got pulses back, but it was too late for him. Sad story.
In V-Fib, the ventricles are basically just quivering. They are not contracting, not ejecting blood and not creating a pulse. This is ALWAYS a pulseless rhythm and will either be fine or course. It can be caused by all sorts of things such as hypoxia, ischemia, extreme electrolyte imbalance, acidosis, and end stage cardiac disease. In the case of my fella, he was super acidotic and his K level was also high. Bad combo.
What are you going to do about V-Fib? Follow your ACLS algorithm! Start compressions STAT. If your patient is on a vent, have the very next person in the room take him off and bag him…if he’s not on a vent, get the BVM and go to town. Get the crash cart in there and shock him. Resume compressions immediately, give epi and amiodarone and continue on your ACLS algorithm.
V-Fib in a nutshell: Hit the code button and start compressions…your team will get there fast!
Asystole: This is your classic “flat-line” that you see on the ECG with that annoying beep that always accompanies it on TV. If you’re watching a silly show like Grey’s Anatomy, they’ll rush into the room and shock the patient. Is that how you treat asystole? Nothing gets me yelling at the television more than incorrect medical procedures and practices!
In asystole, the heart is doing nothing, no electrical activity, no contractions, nada. This person has essentially deceased (or will as soon as the brain runs out of oxygen). Asystole is rarely reversed, but that doesn’t stop us from trying.
What to do about asystole? If you see a flat line on your monitor, get into the room STAT and look at your patient. With any luck, they’ve just removed their leads to take a selfie…but if they are in asystole they’re going to look like it. Press that code button and get on the chest. Hard and fast is the name of the game. Epi will be your drug of choice for this one. Will you shock the patient? Of course not. Asystole is not a shockable rhythm and I just wish all TV producers knew that. Sigh.
Asystole in a nutshell: Hit the code button, get on the chest and stay strong until your team arrives.
Pulseless Electrical Activity (PEA): This one can be tricky because it looks just like a regular rhythm on the monitor! The problem is, the electrical impulses are not being captured and not resulting in any kind of mechanical activity. Let’s say you’re out at the nurses’ station and you suddenly see your O2 and Arterial BP tank…though it looks like your patient is in NSR, get in there! With any luck, they’ve taken off their pulse oximetry probe and pulled their art line (well, pulling an art line isn’t great, but compared to PEA it’s a piece of cake). Check your patient and check for a pulse!
What will you do if you spot PEA? The ACLS algorithm is exactly the same as asystole…hit that code button, start compressions, give epi and hope for the best. PEA is a rhythm you’ll often see after asystole….while it looks like you “got ’em back,” you actually haven’t. Sad stuff.
PEA in a nutshell: ACLS all the way. Code button, compressions, epi.
Well, that was a doozy! Did it help? Do you have other questions? Let me know in the comments below! Now to those quiz answers!
Sinus Brady question: The antidote for digoxin is Digibind. The antidote for beta blockers is glucagon.
A -Fib question: You’ve lost “atrial kick” so cardiac output will drop by about 20-25%. You’re also going to be super concerned about clot formation from the blood just sloshing around in that quivering atrium.
SVT question: Synchronized cardioversion uses a low-voltage that is synced with the cardiac cycle so that it lands on the R-wave…if it were to land on the T-wave, this could lead to V-Fib, which you have learned is Very Bad. Unsynchronized cardioversion delivers a high-powered shock as soon as the button is pushed…it’s not synced to the patient because there’s nothing to sync to…no R wave, no T wave, no danger for R-on-T phenomenon. This is what you use when you’re shocking V-Fib or pulseless V-Tach.
V-Tach question: Vagal maneuvers affect the sinus node, and since V-Tach doesn’t have anything to do with the sinus node, vagal maneuvers rarely help.
Hope you all had as much fun as I did going over all these arrhythmias! Leave your questions, ideas, thoughts, comments, inspiration and joy in the comments below!