Welcome to the Rapid Response RN Podcast, helping you keep your finger on the
pulse of your patient's condition. With real life stories from the front lines of
nursing, this podcast can help you sharpen your assessment skills, improve
your ability to recognize the signs and symptoms of your patient's decline, be
inspired to speak up and advocate and know how to jump into action to promote
the best outcome for your patients. Hey everybody, I'm your host Sara Lorenzini, a
rapid response nurse and educator who loves telling stories to teach critical
thinking. On today's episode, we're going to talk about an arrhythmia that is very
near and dear to my heart, all pun intended. Today we're talking about
supraventricular tachycardia, which I have treated hundreds of times in my
patients, but dealt with even more times than that personally. Yep, you heard me
right, I have or had SVT. About five years ago, I finally agreed to get an
ablation and thank God I haven't had any episodes since then. We will talk more
about my personal experience later and this exciting rapid response call, but
first, a little announcement. I have started an Instagram account for the
podcast. So much of what we talk about really needs a visual to go alongside it,
so after many, many requests, I finally gave in and just made one. My plan is to
supplement the podcast with videos and shareable educational resources to
support you and your professional development as a nurse. I will also post
every time a new episode drops, so you don't have to keep checking back on your
podcast app. So if you would like to stay updated and have access to all these
visual aids, come follow me at the rapid response RN on Instagram. Now, let's dive
into this rapid response call. So I arrived at the patient's bedside and
find a 40-ish-year-old male who's awake and alert and, aside from the scared
look in his eyes, he looks pretty darn stable. I'm going to call him Vince for
this episode, but that was not his name. No hippo violations on this podcast. So
Vince's skin is pink, warm, dry, he's able to converse with us, he's just a
little tequipnik like in the 30s. The nurse tells me that Telly just called her
and said his heart rate is 200. 200? I'm thinking, this guy, wow, he's compensated
pretty well. But I walk over, I feel his radio pulse, and it just felt like a
vibrating thread. I could never have counted that. So I throw him on the
defibrillator, not to shock him, just to get a quick look at the rhythm for
myself, and sure enough, 200 beats per minute. He's becoming visibly more
distressed by the minute, probably a combination of his heart racing out of
his chest and the growing number of people in the room, and the various
interdisciplinary team members who are arriving to, you know, help him, and the
fact that I just attached him to a defibrillator. Like, all those things
might be a little anxiety inducing. So I held his hand, I made him look at me and
not the monitor or the 10 people in the room, and I said, Vince, your heart is
just racing, and I know what that feels like. I actually have the same thing,
and sometimes it can be a little scary, but it is treatable.
I've got you, we're going to fix this. I proceeded to try and talk him through
some vagal maneuvers as I was placing a new IV in his
anti-cubital. We tried bearing down, coughing, blowing
through a syringe, nothing worked. By that time, the physician had arrived and
ordered some adenosine. I said, okay, Vince, I'm going to be giving
you a medication called adenosine. It helps fix the electrical part of your
heart, and when I give it, you may feel a little pressure in your chest or
lightheadedness. That's actually to be expected, and that's
kind of how you know it's working. I've given it hundreds of times to other
patients, and it either works or doesn't, but I've never seen it harm anyone.
So I'm going to be right here next to you the whole time.
Side note, notice that I didn't say, I'm going to give you a drug to stop your
heart. Well, that may be a true statement about
adenosine and what it does to the body. Nobody will respond well to that
warning. Instead, I use words like slow down or
fix the fast rhythm, or if you really got to say it,
reboot the electrical system of your heart. But don't say stop.
Please don't tell your patient that you're going to stop their heart.
Not helpful. Maybe not. So I drew up the first
six milligrams of adenosine and attached it to the stopcock with a tenomal
flush ready to power flush it in. With the physician,
respiratory therapist, and a crash card at the bedside,
I hit the print button on the defibrillator. I slammed the adenosine
followed by the flush, and I've got events. We all stared at the monitor as
our speakers tightened in anticipation of the worst-case scenario,
while we watched his fast rhythm slow to a nice five seconds of
asystole. And then it sped right back up again to 200.
From the printed strip, we confirmed that it wasn't a fib or another rhythm that
might need a different treatment. This was definitely SVT.
No P-waves, regular, and so so fast. At this point, Vince was really freaking out.
I mean, we gave the drug. He felt all the scariness of his
heart stopping, and it didn't work. So now what?
The doctor ordered a repeat of 12 milligrams, which I had already drawn up
because, in my experience, six doesn't usually work.
As of today, ACLS still recommends starting with six milligrams as the
first dose, and if unsuccessful, repeating the adenosine with a double dose
for round two. So I explained to Vince that we need to do the same thing
again with double the dose. He's trying to look a little paler,
so I sacked with his blood pressure one more time before I administered the 12
milligrams of adenosine. It was 92 or 50.
Okay, so the doc says let's just do it. I slammed the second dose and deja vu.
His heart slows to a systole, and then races right back up to 200 beats a
minute. Poor guy. I mean, adenosine
sucks, but it's worth it if it works. It just
didn't. I expected him to be like full-blown freakout at this point,
but he wasn't. In fact, now he's starting to get a little
clammy and drowsy, so I sacked with his blood pressure again, and it was
70 over 40. I said doc, we got a cardiovert. I don't have
enough blood pressure for sedation. He's crashing.
Fortunately, the D-fib pads were already on him, so I flipped the defibrillator
into secreted cardioversion mode. At this point,
Vince isn't responding to me at all, but I still said to him,
"Vince, I'm so sorry. This is gonna hurt, but it's gonna save your life, my friend."
and I said all right guys let's go ahead and charge the defibrillator to 120 joules we're
going to cardiovert. All right everyone clear? I scanned the room to make sure no one was touching
the patient. Shocking? Shock delivered. The energy jolts through his body and his chest came up off
the bed. We all looked at the monitor. Normal sinus rhythm heart rate of 95. We recycled a blood
pressure. His blood pressure is improving. He starts waking up and ever in the room you can just
feel took a big sigh of relief. We fixed him for now. But now the question is why did he go
into SVT in the first place? Because we're gonna have to address that too. So let me just summarize
what happened because it all happened so very fast and then we'll discuss the pathophysiology of
SVT and its treatment. So Vince's heart started racing at 200 beats per minute. Initially he
was compensating pretty well by breathing a little faster but he was still perfusing all of his
organs, awake and alert, talking to us with a stable blood pressure. So we tried the least
invasive intervention first. Vagal maneuvers. All of them. But to no avail. Then pharmacological
interventions. We gave adenosine 6 milligrams followed by 12 milligrams which also did not convert
him. There are other pharmaceutical options but when he became unresponsive and hypotensive
there was no time for more drugs. He needed to be cardioverted. So we delivered a synchronized shock
and he converted back into sinus rhythm. Yay! Now let's discuss SVT. Honestly we've made it
a little confusing for folks new to nursing because SVT is an abbreviation for supraventricular
tachycardia. So supraventricular or above the ventricles and tachycardia or heart rate greater
than 100 beats per minute. But there are a lot of rhythms that originate above the ventricles
that are fast that would fall into that category. Like sinus tachycardia is a supraventricular
tachycardia, atrial fibrillation and atrial flutter are supraventricular and now hang on for
the acronym overload SNRT AVRT AVNRT MAT and the list goes on and on are all forms of supraventricular
tachycardia. Generally speaking you know rhythm is supraventricular or originating above the
ventricles when the QRS complex is narrow. So all tachycardias with a narrow complex should
be called SVT but for some reason in practice you might find nurses and physicians grouping
SVTs into three categories. Not because there's actually three categories but because the treatment
often falls under about three category options. So the first is sinus tachycardia which has a P-way
proceeding every QRS. This means the sinoatrial node or the pacemaker of the heart is starting
to beat like it's supposed to. The SA node is supposed to be in charge. It will respond to
stimuli like pain or anxiety or dehydration. So for sinus tachycardia it's important to treat the
source be it pain medication or anxiety medication or IV fluids or whatever's causing the tachycardia.
Then the second category would be like an atrial fibrillation which is an apparent pathway or
multiple inherent pathways that are trying to run the show and sending out electrical impulses from
throughout the atrium. So the atrium just end up fibrillating hence the name and the ventricles
are just randomly responding to some of the signals but thank god not all of them. The telltale sign
of AFib is being irregularly irregular with absent P-waves since the SA node is being completely
overrun by the misbehaving parts of the atrium. They're sending out all their own electrical
impulses so no P-waves just a lot of artifact looking squiggles between the QRS complexes
and the complexes are irregular without any pattern to them because they aren't in alignment
with the atrium. AFib is treated with diltizum or amiodarone or metropolol and then there's SVT
which is also a narrow complex tachycardia. It looks pretty regular that you cannot clearly
discern P-waves because it's so fast they just get hidden in the other complexes. So
they are all SVTs but then we call one of them the regular one without P-waves with
sudden onset and a rate above 150 we call that one SVT. How confusing right? I mean really SVT
is an umbrella term that for some reason people use to describe a specific type of SVT. It would
be like if we chose to call the femur leg bone and not its specific name even though there are
four leg bones and they all look very different and they work different and we call the other leg
bones by their specific name like patella, fibula, tibia but we just thought the femur should be
called leg bone because it falls into the leg bone category. Well SVT is an SVT but there are actually
several rhythms that could be occurring when we say they've got SVT and I recognize that an audio
platform is not the ideal modality for describing something you identify visually. So I would
highly recommend pulling up some photos and different types of SVT to help you differentiate.
The blog life in the fast lane I would highly recommend it really breaks down very well
with great visuals. All this stuff we're talking about today with diagrams so if you wanted to
pull them up I highly recommend it. So now that we know we are talking about a narrow complex
tachycardia that is regular and doesn't have p waves rather than saying it's an AVRT or an AVNRT
or any other acronym I'll just be referring to all of these non-AFib non-A flutter non-sinus
tachycardia tachycardias as SVT. So SVT usually is said non-set like the patient's rhythm was normal
and now without warning it just flips into tachycardia. Usually sinus tachycardia is more
of a gradual onset and it's associated with some sort of stimulus like increasing pain or stress
or dehydration and like I said if it's a physiological response to a stressor then fix the stressor,
treat the pain, give the anti-anxiety med, bowl of some fluids, don't jump straight to a cardiac
rate limiting drug because that could make things worse. But SVT seemingly comes with that warning
and is almost like just flipping a switch. SVT can be an indicator that something else is up
but it can also be pretty benign. The kind of SVT that I had just randomly occurs to some young
healthy people I would be just chilling in a chair and the next thing you know boom
my heart starts racing at 220 beats a minute. I did find that being dehydrated and having caffeine
would most definitely send me into an episode of SVT so I had to learn how to survive on nightshift
without caffeine and somehow stay hydrated. Then when I got pregnant it got really bad
happening a few times a month. Then my second pregnancy was like every single week by the
time I hit my 30s even when I wasn't pregnant I started having an episode a few times a week
and I just got really good at bearing down to convert out but a couple times I stayed in it
for over an hour and I just couldn't convert. I was really close to getting a denicine like
in the ER, IV in place, a denicine drawn up like that kind of close but I had seen my patients
reactions to denicine and I did not want to see what it felt like so literally one time my blood
pressure was 80 over 40 and I was still refusing it. I tried one last time to bear down and cough
while simultaneously massaging my carotid and I finally converted thank goodness but by that time
I had had enough and I finally gave in and got an ablation. I wish I would have done it sooner.
It has absolutely improved my quality of life. Imagine trying to take care of a patient when
all of a sudden you can feel your heart just start racing and your neck feels like it's
vibrating out of your chest then your vision starts to get a little blurry and you have to
play it cool because from the outside no one can tell what you're experiencing. They cannot
tell that you just flipped into SVT so you don't want to alarm your patient. Several times I just
said excuse me I'll be right back and I would step in the hallway drop into a squat, bear down,
convert then stand back up wait for my vision to correct and then go right back to caring for the
patient. It sucked I'm glad those days are over. So that's a great lead into our next segment let's
talk about vagal maneuvers. Why in the world would taking a big poop convert someone out of an
arrhythmia? Well the vagus nerve basically runs down the scent of your body with branches that
wrap through your mouth your ears your neck your heart your lungs your digestive organs. The vagus
nerve stimulates the parasympathetic nervous system. Remember the sympathetic nervous system
is the fight or flight hormones that get you all jacked up and ready for action but the parasympathetic
activation is the balance that allows you to rest and digest. So the vagus nerve when stimulated
helps slow the heart rate and drop the blood pressure opposite of sympathetic stimulation.
That is why when things stimulate the vagus nerve it helps to convert SVT back to a slower rhythm.
Actions that stimulate the vagus nerve include coughing, bearing down like like you're trying
to have a bowel movement or push a baby out, cold ice to the face either by dunking the patient's
face in a bucket of water or placing bags of ice on their face for like the startled diving reflex.
The most common thing that I've seen work is called the valve salvo maneuver and that's where
you have the patient blow as hard as they can for a good 15 to 30 seconds into a pinch straw or get
them a surrender and instruct them to try to blow out the plunger from the other side. This induces
a temporary slowing of the heart rate that hopefully gives the essay note a chance to get
herself together and take control again of the conduction pathway.
These are some things that you can direct your patient to do while you're getting ready for
the next step. So you can be getting the IV in place, you can get the crash cart close by,
get the patient on the monitor, draw up your medications. I've definitely seen it work. In
fact, it worked 100% of the time for me personally, eventually, but according to a study called the
revert trial, the valve salvo maneuver alone is only effective 5 to 20% of the time.
There's also something called the modified valve salvo maneuver. So y'all, I have never heard of
this till now. I literally just learned about it while researching for this podcast. I googled
effectiveness of valve salvo maneuver when converting to SVT and I found it. So let me
share with you what I learned about the modified valve salvo maneuver. So you have to have your
patient sitting upright, just like the regular valve salvo maneuver, they blow through a syringe
for 15 seconds, then you quickly lay their head flat and perform a passive leg raise.
So to pull this off effectively, you really need three people. One to coach the patient and the
blowing through the syringe part, one at the head of the bed to drop it into position, and one person
to grab hold of both legs and lift them in the air. Sounds crazy, right? But here's the crazy part.
It works way better than the valve salvo maneuver that I've been doing to help patients for years.
When you add in the fun, drop you flat and hoist your feet in the air part, the success of the
modified valve salvo maneuver is more like 43% in converting SVT back to sinus rhythm. And it's way
safer and more comfortable for the patient than our other options. So thanks, Applebowlm, at all,
for looking into this one for us. I can't wait to try it on my next SVT rapid response call.
The final non pharmacological non electrical option for treating SVT is carotid sinus massage.
This is another way to stimulate the vagus nerve. But don't go rubbing down the patient's neck.
There are definitely risk involved in doing that. So carotid sinus massage should be performed by
the provider. Alright, so if all of our attempts to calm things down with vagal stimulation fail,
and they often do, the next option is drugs. It's very debatable as to the best drug for SVT.
The one that I see physicians want to try first is adenosine. Adenosine briefly stops all conduction
through the AB node. Like no conduction means no heart squeezing, which means no pulse, which looks
like a brief period of a systole on the monitor. But it is really brief. The half life of adenosine
is about five to 10 seconds. So it may stop the heart and freak everyone out in the room,
but it's just for a few seconds. In order to make it actually reach the heart in time to be
effective, you need to give it in a large bore IV in the AC or higher. I use a stopcock so I can
rapidly push the adenosine and then flip the stopcock to quickly chase it with the power
flush of saline. But imagine what the patient must feel when you do that. It's described in
textbooks as quote "unimpending sense of doom" quote, which means they feel like they're going to die.
Most patients have told me it hurt in their chest or they felt like the wind was being knocked out of
them. I've never had a patient say that wasn't so bad. They all hate it. The first dose is six
milligrams and if that doesn't work, then you have to do it again with double the dose at 12
milligrams. If that doesn't work, it's time to consider other options. So since we know how
terrible adenosine feels, there are other drug options that are just as recommended in the
literature but not nearly as exciting as adenosine. You could give calcium channel blockers,
usually verapamil, five to 10 milligrams slow IV push, or you can give a beta blocker like
metropilol, which is dosed about five milligrams, also administered at a very slow IV push rate.
Both verapamil and metropilol doses can be repeated if the first one doesn't work.
But they don't work as fast as adenosine, so they take about five to ten minutes to convert
the patients for them. Just take a seat and be patient. Both of these rate limiting drugs
also affect blood pressure. Therefore, it's important to take the blood pressure before
administration and retake it after the dose to make sure it doesn't drop the patient's blood
pressure too much. One little caveat for a drug administration for SVT. There are a few variations
of SVT for which nodal blockers like adenosine, calcium channel blockers, beta blockers,
would be completely contraindicated. The most common of these pre-excitation rhythms is called
Wolff-Parkinson-White syndrome. Wolff-Parkinson-White syndrome, or WPW, has a very distinct morphology.
It has a shortened PR interval and a delta wave from the pre-excitation of the ventricles
through the accessory pathway that they have. Giving nodal blocking agents would actually
worsen things for the patient and could throw them into VFib, which is much worse than SVT.
So for patients with WPW, they can safely get procanomide or obviously synchronized cardio
version. In summary, get a good history, look closely at the shape of those chorus complexes.
WPW is a very rare abnormality, but that's why we only push adenosine with the defibrillator pads
hooked up to the patient. Because if by chance the patient did have WPW, we didn't know it,
and our adenosine administration throws them into VFib, we can defib immediately without delay.
So we've talked about the safest option for all patients, big ole maneuvers.
If those don't work, our first line therapy is medication. But if a patient exhibits hemodynamic
instability, meaning their blood pressure is dropping, the level of consciousness is waning,
their pale or diaphoretic or become unresponsive, it's time to skip the meds and move on to electricity.
Remember, the patients with a pulse, we don't defibrillate them, we synchronize cardiovert.
Synchronized cardioversion is where the machine senses the R waves and waits to deliver a shock
on an R wave because accidental firing on a T wave could throw the patient into ventricular
fibrillation. Again, much worse than SVT. The joules used for synchronized cardioversion
honestly depends on the make and model of your defibrillator and physician preference.
Some physicians I work with just jump straight to 200 joules to promote first shock success.
But 120 joules to the trick prevents. So why did vent start out stable and then become unstable?
Well, initially, he was compensating with an increased respiratory rate,
and that was able to meet the increased oxygen demands that the racing heart was putting on his
lungs. But increased heart rate can only increase cardiac output to a point. Eventually, the heart
is just squeezing so fast for so long, cardiac output is going to drop. Think about how fast 200
squeezes per minute is. That's 3.33 squeezes per second. So there just isn't enough time for the
heart to fully fill with blood in diastole before it's fired to squeeze again. So each squeeze
just becomes a smaller and smaller amount. With time, stroke volume drops, so cardiac output drops,
and blood pressure drops, and that's why trying medications to convert an unstable patient is
a bad idea because all those drugs you would give are going to drop blood pressure. Yes,
synchronized cardioversion is risky, but when you weigh out the risk versus the benefits,
the risk of not doing anything is greater than the risk of synchronized cardioversion.
And luckily, it worked. It converted events back to a normal rate. So when, before I wrap up,
I want to let you know that I made a little SVT treatment options cheat sheet and posted on
Instagram. So if you ever need to refer back to any of this stuff in this podcast,
you should be able to easily find it on my Instagram page. And now to summarize. SVT is just
an umbrella term for fast rhythms that originate above the ventrules. But for some reason, the ones
with sudden onset with regular QRS complexes and hidden P waves, we call SVT. So what's the first
thing you should do when you discover your patients in SVT? Like, let's say telly calls you
and says your patient's heart rate is 180 per minute. I would say the first step is to determine
if they're stable or unstable. Like, how is their color? Are they diaphoretic? Are they awake and
talking to you or drowsy or unresponsive? What is their blood pressure? And once you eyeball the
patient, just call a rapid response. If you determine the patient is unstable, we're going
to be jumping straight to synchronized cardioversion. But if they're compensating for now,
let's go least invasive to most invasive. Start by walking your patient through some
easy vagal maneuvers. And heck, try out the modified Valsava with a few buddies. Evidently,
it works 43% of the time. Your patient may think you're crazy, but they'll thank you if it works
and you convert them back to sinus rhythm. If all of your vagus nerve stimulation attempts don't
do the trick, it's time to choose a medication. Hopefully, while you're coaching your patient
through the vagal maneuvers, you are also securing a large bore IV, getting the defibrillator,
applying oxygen, drawing up the drugs. Identity needs to be pushed fast. And it works fast.
And it wears off fast. Thank God. Every other drug we discussed, calcium channel blockers,
beta blockers, purcane of mine are all pushed slow and take time to take effect. So,
don't give up if the patient doesn't convert immediately. And if drugs don't work, you can
always do synchronized cardioversion. If the patient is stable, you'd want to sedate them first.
But if they're decompensating, skip the sedation and jump straight to electricity.
Shocking SVT or any rhythm with a pulse always needs to be in synchronized cardioversion mode.
The final thing I want you to take away from Vince's story is that when we are dealing with an
emergency and your patient's crashing, remember that they are a human and not a machine we're
trying to fix. It's easy to get caught up in all the tasks that need to be completed that we forget
to explain things to the patient and family. There's still time for the power of human touch.
You don't have to talk like you're on a battlefield. Staying calm is important
for you so you can be able to think clearly and for the patient to see that you've got things
under control. For you, this is just another day at the office, but for your patient,
they'll remember this day, these moments for the rest of their life. So keep them informed,
involve them in the process, provide comfort and support. To paraphrase Maya Angelou,
they may forget your name and everything you did, but they will never forget how you made them feel.
Well, that's it for today's episode. If you liked this podcast, I'd love to hear from you.
You can shoot me an email with questions or comments and it would mean so much if you could
take a moment to write a review on iTunes as this helps more listeners find this podcast.
Thanks for listening and I hope you learned something that will save a life.
Remember, nursing is a team sport, so trust your intuition and don't give up advocating
until you are confident you've done what's right by your patient.
You've been listening to the Rapid Response RN podcast. The views and opinions expressed on this
show are that of Sarah Lorenzini and hers alone. They are not intended as medical advice and should
not take the place of your institution's policies or procedures. Evidence-based practice is ever
changing and your patient's care should reflect the current best practice. If you want to get in
contact with Sarah, you can find her at
[email protected] or on the Rapid Response
RN Podcast Facebook page as well as the podcast website rapidresponsern.com
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