You're in the bay. Once you get over to the bed,
we'll give you the story. Everything's going
to happen super fast. Welcome to the emergency
room. Alright guys, so this right here is going
to be over dysrhythmia arrhythmias I don't know
the difference between a dysrhythmia or an arrhythmia
If there is a difference, please, you know, let
me know or You know it for me. It doesn't really
matter. You know, I use the terms interchangeably
But what I will say is I do not know What arrhythmia
is they're going to go over in this particular
episode because I haven't listened to it yet
but Um, we can just kind of do like a little
overview real quick. Um, so your easy ones are
going to be v fib just look like a bunch of squiggles
on the EKG paper or on the lead strip. And then
you have fine v fib, um, fine v fib. If you're
taking like an AHA course, it will literally
look like a systole, but they'll have a little
bit of like a little wave in there. you know,
and they're going to be like, oh, that's coarse.
That's fine. VFib. And you're like, it's asystole,
you know, but they're going to call it, you know,
fine VFib. And for the AHA is concerned, asystole
is quite literally a flat line. But in an emergency
situation, fine VFib and asystole are going to
look the same. But you have VFib, which is like
I said, it's going to be just that squiggle line
on the EKG paper. then you have fine v fib it's
just going to be smaller squiggles on the on
the um ekg paper and then you have your v tac
which is just going to look like big tombstones
or the mcdonald sign over and over again and
then you have torsades which you will get you
know that really really big v tac And then it
shrinks down into small VTAC or V fib and then
it shoots back out VTAC again and then V fib
and then VTAC. At least that's the way it looks
on the EKG paper. Again, I'm not a cardiologist
by any means, so I don't know what the hell is
actually happening in torsades. All I know is
that you're going to try to slow that shit down
with some mag and then hope for the best with
your other ACLS drugs. And then you will have
your a fib your a fib with RVR now the big thing
with a fib with RVR is that you're gonna have
a fib and then in a run of RVR you're gonna have
a very rapid, you know QRS complex, you know
that are really really close together and then
you'll get your rhythm back, you know of your
a fib, which is that irregular regular, you know,
kind of pattern. And then your RVR again will
be like a really short squished together QRS
complex next to each other, maybe three, four
or five of them. And then it shoots back out
to your normal rhythm. And then you have a flutter.
Now, not too long ago in the ER, I heard the
term a flutter with RVR. I don't know if that's
a thing. But if it is then you're going to be
looking for the same thing you're going to be
looking for your sawtooth pattern in between
your QRS complexes and then I'm assuming your
QRS complexes are going to squish together and
you got you're going to get like four or five
six beats and then it'll shoot back out to your
normal rhythm and then shoot back down in and
to those really tight QRS complexes and then
I guess shoot back out to like the regular irregular
rhythm and then that's your a flutter and You
have your NSR Which is your normal sinus? And
then you have Brady and then you have your tacky
it did I don't know if they're going to get into
heart blocks in this particular Episode but the
easiest way to tell a heart block is your heart
blocks are going to be predicated by your P wave
and everything with heart blocks is going to
be P P wave related. So your first degree heart
block, you're going to be having your P wave,
which is going to be a little bit further away
from your QRS complex than you would like it
to be. I can't remember the exact numbers because
I don't have an EKG ruler in front of me or the
criteria, but your P wave will be completely,
you know, kind of move back a little bit. And
that right there will be your first degree. Your
second degree type one, if I'm not mistaken,
is your Mobitz one. If I'm not mistaken, I should
probably look this up before I give you guys
the wrong. Information, let me pause real quick.
Okay, just checked it. So Mo bits one is your
winking Bach your winky Bach Arrhythmia right
heart block and so it is the Arrhythmia that
has that little Rhyme to it wider wider wider
drop then you have a winky Bach Again, you're
looking at your P wave All these heart blocks
my little piece of advice to you guys don't over
complicate this shit It's literally your P wave
for these heart blocks So with type one or with
your first degree heart block your P wave is
sitting a little bit further back from the QRS
complex Right in your mo bits one your heart
your second degree heart block type one is your
P wave will be normal and then it will get further
away from the from the QRS complex and then further
away from the complex again. And then you'll
have a drop beat and then your P wave will show
back up right next to your QRS complex and then
start getting wider and wider out from the QRS
complex before another beat drops. Okay, that's
your type one for Mobitz. And then your type
two is your P wave will stay the same, whether
it's further or closer to your QRS complex is
irrelevant. But it will be it'll be stationary.
And then on your EKG paper, you'll just have
a drop beat just out of nowhere. Right. And then
you'll get your beat back. And then the P wave
will be right where it needs to be. OK. And then
your third degree heart block is going to be
your P wave is doing its own, its own damn thing.
Right. So the atria are just doing their own
thing. They're not synchronized with their ventricles
at all. So they're contracting without any coordination
with the ventricles. Right. And so your P wave
will be where it's supposed to be. It'll be like
in this random ass spot. between your T wave
and your QRS complex or hell, it could be hidden
in the T wave. And what it will look like is
that you'll have this little notch up or this
little spike in your T wave and then you'll have
your QRS complex or hell your your P wave could
be hidden in the QRS complex, which is very difficult
to kind of see. On the EKG paper, you might get
lucky and see like a notch, you know, in your.
What is your our wave? You might get a little
higher of a notch than everywhere else, you know,
but or it might look like like a bundle branch
block. So you might get like a little cat ear
looking thing or maybe even a W in your. What
is that? QRS, I guess your Q your Q wave Whichever
one is the bottom one that comes down. Damn it.
It comes down Right. You might get a W with that,
right? And so you might get fortunate enough
to get that Right, but typically your P wave
is going to be doing its own fucking thing, right?
And it's not going to follow any sort of logic.
It's just going to be doing its own thing, you
know And so that's how you know that you're in
a third degree heart block, which is your more
serious heart block. I will say the rarest ones
that I've seen is a type one, your winky Bach,
right? Where it just gets wider and wider and
then drops, right? I've only seen it once in
clinical practice. And me and the hospitalist
were like, what is a type one? And we were all
excited. and the patient had no idea what the
hell we were talking about because it's so uncommon
to find um but so with your heart blocks don't
over complicate the shit it is all going to be
determined on your p -wave okay again your p
-wave is going to determine what type of heart
block you have all right So don't be looking
at your QRS complex. Don't be looking at your
fucking T wave. Everything about heart blocks
is going to be in your P wave as in Papa your
P wave. Okay. And then, um, again, I don't know
if they're going to be getting into these, but
you have your bundle branch blocks. So again,
I don't know, like lead one, two, three, your
V one V two. V3, you know, in your AVR, I think
it's SVR. Like, I don't know where you're going
to find these at. Like, I know that, you know,
nurse practitioners and stuff like that, I can
look in your PAs and your MDs will look at the
strip and they'll like compare Lee wanted to
to like AVR or something like that. But for our
intensive purposes for our in school is your
left and right bundle branch blocks. If I'm not
mistaken. I believe. Let me check before I give
you guys wrong information. So with your left
bundle branch block, your EKG paper might show
like a little Batman looking thing where your
QRS complex looks like either a cat or a Batman,
where there's like two peaks, you know, at the
top of the QRS complex. I'd have like two peaks
or. your QRS complex on the part that goes down
will look like a W. Okay. And then on your right
bundle branch block, like when you're getting
ready to repolarize, go for the ventricles to
repolarize to get your T wave, that little space
at the end of the QRS complex before you get
to the T wave will look like a U. like it'll
dip down and make like a U or you might even
get an inverted T wave right and then um they
might go over you know potassium your peak T
waves just remember as the more and more potassium
the body has it'll start really throwing off
the the heart's ability to regulate itself and
so you can get these massive peak T waves to
the point to where The car is complex completely
fades away as the potassium gets higher to where
the potassium gets so high. That the only thing
you're going to look at is a t -wave and at that
point you're just going to be running into the
attack if they sneeze right so. It doesn't take
much for them to get thrown into the attack if
they have that much potassium so you're going
to be looking at like insulin. with dextrose
your di and then you're going to be looking at
calcium um especially in high potassium you're
going to be giving calcium and gluconate um the
way i describe it to my patients who have high
potassium is that calcium is going to go in and
kind of hug the heart you know because the heart's
kind of having like this anxiety attack right
now so calcium will go in and kind of give the
heart a hug and keep it stable and keep it from
throwing itself into this wonky ass arrhythmia,
right? So it goes in and it hugs the heart. And
then you have, you have KXL8, right? So you can
shit it out. And then a new one is going to be
Albuterol. So there you give a lot of Albuterol,
which also helps the shift. So it's called a
shifting protocol in the ER. We call it a shifting
protocol. So you're looking at D50. Might give
an amp or two a d50 and it started insulin drip
to get the potassium back into the cells And
then you're going to be giving calcium gluconate.
You're going to be giving KX light or low calma
whichever one that you have on hand and then
If they're really really bad off, they might
get hemodialysis emergent dialysis to pull that
extra potassium out And then you have your arrhythmias
with calcium and stuff like that. Okay. But the
big ones are going to be like potassium. And
we went over VTAC, VFib. We went over the bundle
branch blocks. And then we went over your heart
blocks. And then we went over your atrial dysrhythmias
with Aflutter and Afib and then your Afib with
RVR and Afib or Aflutter with RVR, which is something
new to me. So outside of that, man, I think that's
it. All right. This is going to be the episode
over dysrhythmias. I just wanted to make sure
that we covered those because I don't know what
they're going to touch on in this episode, but
I want to make sure that especially for the heart
blocks that you guys don't get tripped up with
the heart blocks again. Broken record. You're
looking at your fucking P wave. All right. Your
P wave will determine what type of heart block
you are in. If your P wave is sitting a little
bit further from the QRS complex. You're in a
you're in a hard block type. You're in a hard
block one first degree hard block. And then if
your P wave starts marching away from your QRS
complex and then you get a drop beat, that's
going to be a Winky Bot or Mobitz type one second
degree hard block Mobitz type one. And then if
your key if your P wave is stationary. a then
you get a random drop beat that's going to be
a second degree heart block mobits type two and
then if your P wave is just all over the damn
place you know your atria are just contracting
whatever the fuck they feel like it then you're
going to be in a third degree heart block okay
so again your heart blocks are going to be determined
by the P wave This is coming from nursing school.
This is not a cardiologist telling you this,
but for your intensive testing purposes. Okay.
Your heart blocks are going to be determined
by your P wave. Now, if you want to be a cardiologist
and you want to say, well, your V1 and your V2
and your AVR, you know, leads need to look like
this and all that. Well, then you do that, man.
But in the ER and for nursing on our end when
just looking at the shit your P wave determines
what type of heart block you have All right,
and then yeah, that's it. All right guys Enjoy
the episode. Okay, I'm back like a bad habit.
Um, I want to go over PVC's and then by Jiminy
and try Jiminy Again, I do not know what arrhythmias
this episode will go over because I haven't listened
to it yet. But your PVCs are your preventricular
contractions. So you will have like a normal
QRS complex. Right. And then just out of nowhere,
you'll get this really bizarre looking kind of
beat looking thing. And it's just where the ventricles
just kind of contracted a little too early. So
what I've come to learn is the ventricles are
extremely sensitive. And so if the ventricles
start reading that they're not getting enough
oxygen, then they'll start to freak out and then
they'll start throwing PVCs like all over the
damn place, right? So for a good chunk, I'm not
going to give a percentage, but I will say if
your patient doesn't have a cardiac history and
you're in the ER, wherever the hell you're at,
if they don't have a cardiac history, then if
you see PVCs, they're probably just sitting in
a weird position and you might want to just set
them up, pull them up, put some oxygen on them,
something. to get them to get oxygenated, even
though their pulse ox is probably reading 90
or something like that. Just slap some O2 on
them at two liters and then see if that kind
of resolves their weird looking PVCs. Because
again, the ventricles are extremely sensitive.
We had a patient that had a shot that the I guess
the terminating portion of it dipped a little
too low into the heart. And I guess it started
You know, rubbing the ventricles as it was contracting.
And so they would throw a little weird PVC is
whenever she would sit in like a weird position.
And she said it was normal and she can feel it.
So she sits in certain positions that way. It
doesn't do that. But we'll go into by Jiminy.
And let me check before I give you guys wrong
information. OK. So by Jiminy will be a normal
QRS. complex and then you'll have a P you have
a PVC and it'll be one for one so you'll have
a QRS and then you have a PVC then you have a
QRS then you have a PVC you have a QRS and then
you have a PVC there right there is going to
be by Jiminy okay and then you have try Jiminy
which is a two for one special so you'll get
two QRS complexes and then you'll get one PVC
so QRS QRS PVC QRS, QRS, PVC, QRS, QRS, PVC.
That will be trigeminy. Okay, so you'll just
have your normal PVCs. And then you will have
your by Jiminy, which will be one for one. So
QRS, PVC, and then you'll have your trigeminy,
which will be QRS QRS PVC so a two -for -one
special with try Jiminy so basically every second
beat will be by Jiminy and then every third beat
will be try Jiminy okay and now I think I am
done when you look at a healthy city from above
at night it's it's like a perfect network of
light Everything is synchronized. Traffic lights
change precisely when they need to. Power routes
to the neighborhoods pulling the most current.
And, you know, the whole grid just hums. Right.
Yeah, it's totally balanced. Exactly. But if
a main substation blows or like a rogue signal
scrambles the system, the entire city goes dark
in an instant. And that sudden darkness, you
know, that catastrophic failure of the grid is
exactly what we're looking at today. But inside
the human chest. Because we aren't just here
to memorize squiggly lines on an ECG paper. Today,
we are taking a really dense clinical text on
electrocardiographic monitoring and aggressively
applying an intensivist filter for this deep
dive. Yeah, we really are. If you are an ICU
nurse standing at the bedside, your job isn't
to react to the darkness. Your job is to anticipate
the deterioration before the grid goes down.
Exactly. I mean, critical care is about evaluating
failing physiology in real time. You are constantly
running this loop. Like, what is the mechanical
problem? How is the physiology failing? What
is the immediate threat to the patient's life?
Right. And then what is my intervention? Thought
on. And finally, the reassessment. So today,
we are analyzing the highest yield, most dangerous
cardiac dysrhythmias. We're breaking down exactly
what will kill your patient first and the priority
actions you have to take to stop it. We've got
to start with the absolute worst case scenarios,
like when the heart's grid just experiences a
massive explosive system failure. We're talking
about ventricular tachycardia, or VT, and ventricular
fibrillation, VF. These are the lethal threats.
I mean, to give you the 80 -20 breakdown, VT
occurs when an ectopic focus, like a rogue cell
in the ventricles, just completely hijacks the
electrical system. It takes over. Yeah, it becomes
the new pacemaker, firing at a massive rate,
usually between 150 to 200. beats per minute,
and then VF is the progression of that chaos.
So it gets worse. Oh, much worse. Instead of
one rogue cell, you have multiple ectopic foci
firing all at once. The ventricles aren't even
pumping anymore. They're just kind of quivering
like a bag of worms. So mechanically, like at
the bedside, How does that actually translate
to the patient's physiology? I mean, if the heart
is beating at 250 beats a minute, isn't it just
pumping a ton of blood? That's a super common
misconception actually, but it's the exact opposite.
At that extreme rate, your diastolic filling
time is functionally zero. Oh, wow. Right. The
heart is beating so fast that it never has a
fraction of a second to relax and fill with blood.
So if you have no filling time, your stroke volume
basically plummets to zero. And if your stroke
volume is zero, your cardiac output is zero.
Which means cardiopulmonary arrest, like zero
oxygen delivery to the tissues. The brain and
organs are actively dying. Precisely. The moment
cardiac output drops to zero, you see this rapid
clinical deterioration. Your patient becomes
totally unresponsive, pulseless, and apneic.
And what are we seeing on the monitor? On the
ECG, VT looks like wide, distorted QRS complexes,
so greater than 0 .12 seconds, marching out rapidly
with absolutely no visible P waves. VF, on the
other hand, just looks like chaotic, irregular
waveforms of varying amplitude. There is no structure
to it at all. OK, but how do we spot the spark
before the explosion? The source material talks
a lot about this trigger called the R -on -T
phenomenon. It sounds like something hitting
at the exact wrong microsecond. It is. T wave
as the relative refractory period of ventricular
repolarization. The reset phase. Exactly. The
heart cells are resetting. And during that specific
phase, they are incredibly unstable and highly
excitable. If a premature ventricular contraction
of PVC happens to fire and land perfectly on
the peak of that T wave. It's like slamming a
car into reverse while you're speeding 80 miles
an hour down the highway. Just completely shred
the engine. That is exactly what happens electrically.
That single mistimed PVC throws the entire ventricular
conduction system into lethal VT or VF. So if
I'm at the bedside and I see this wide bizarre
complex on the monitor My instinct is to immediately
grab the defibrillator and shock them. Right.
Stop right there. That instinct is like the number
one trap that novice nurses fall into on exams
and at the bedside. Wait, really? Yes. You always
treat the patient, not the monitor. Your absolute
first priority nursing action is to check the
patient's responsiveness and check for a central
pulse. But if the monitor shows VT, wouldn't
they automatically be pulseless? Not always.
A patient can have stable ventricular tachycardia.
They might be sitting up talking to you with
a palpable pulse, even though the monitor shows
VT. Oh. Yeah. And if you take the defibrillator
and deliver an unsynchronized shock to a stable
patient with a pulse, you could actually cause
the RNT phenomenon we just talked about, and
literally push them right into lethal ventricular
fibrillation. Wow. OK, so that completely changed
the ADPIE protocol. If they are stable and talking,
we're looking at synchronized cardioversion.
or IV antirevimix. But if I check that pulse
and there's nothing, like they're unresponsive
and apneic, then what's the escalation? Then
you escalate instantly. Call the code. Next,
you start high quality CPR to mechanically force
blood to the brain. Then you perform rapid defibrillation
within two minutes. And defibrillation is just
a massive wave of electricity, like 360 joules
for monophasic monitors or 120 to 200 for biphasic.
But what is that electricity actually doing?
Are we restarting the heart? We aren't restarting
it, no. We are momentarily stopping it. Stopping
it. Yeah. The shock depolarizes the entire myocardium
all at once. It wipes the slate clean. It stops
all those chaotic ectopic foci in their tracks
with the hope that the sinus node, the natural
pacemaker, can wake up, reboot, and regain control
of the grid. So while we are doing CPR and shocking,
what are the primary meds we are pushing to fix
the underlying physiology? We use epinephrine
first. It's a potent alpha adrenergic agonist.
So a vasopril. Exactly. We aren't giving it to
stimulate the heart. We are giving it to clamp
down the peripheral blood vessels, skyrocketing
the systemic vascular resistance so that whatever
little blood we are moving with CPR gets shunted
directly to the central circulation, you know,
the heart and the brain. That makes total sense.
And the source material mentions amiodarone as
well. Yes, Amidron is our primary anti -arrhythmic
here. It's a class 3 potassium channel blocker.
And what's the mechanism there? It works by delaying
repolarization and prolonging the action potential.
Essentially, it calms down that highly irritable
ventricular tissue, making it harder for those
rogue ectopic cells to fire again once we shock
the patient out of the rhythm. OK, so if I'm
synthesizing this into a core -intensivist framework,
and if you only remember five things about this,
one, the core pathophysiology is the ventricles
going rogue, destroying filling time and cardiac
output. Two, the key assessment finding is an
unresponsive, pulseless apneic patient. Three,
the most dangerous complication is sudden cardiac
death. Four, priority nursing action is immediate
CPR and rapid defibrillation. And five, the most
important treatment is shocking the heart to
reset the SA node. You nailed it. So for the
one -sentence clinical picture, it's a totally
unresponsive patient with a chaotic or wide complex
rhythm on the monitor. Got it. And if you see
wide, bizarre QRS complexes and no pulse, think
pulseless VT or VF and do immediate CPR and defibrillation.
Perfect. So that's what happens when the ventricles
basically explode. But let's shift to a completely
different kind of grid failure. What happens
when the main power lines just get entirely severed?
Ah, you're talking about complete heart block
or third degree AV block. If VT is an electrical
explosion, this is a silent choke. The text describes
this as complete AV dissociation. So the top
of the heart and the bottom of the heart are
entirely divorced from one another. Completely
divorced, it's usually triggered by severe ischemic
heart disease like an acute MI or drug toxicity
from beta blockers or digoxin. So the physiology
changes how? Well, the SA node up in the atria
is firing perfectly fine, generating normal P
waves at 60 to 100 beats per minute. But the
AV node, which is the gateway to the ventricles,
becomes a brick wall. absolutely no electrical
impulses get through. Wait, if no impulses get
through, how does the patient not just instantly
flatline and die? Because the heart has backup
generators. When the ventricles realize they
aren't getting the signal, an escape pacemaker
somewhere in the ventricular tissue wakes up
and takes over. Oh, that's a clever compensation.
It is, but here is the decompensation problem.
The further down the conduction system you go,
the slower the inherent rate. That ventricular
escapism only fires at 20 to 60 beats per minute.
20 to 60. So we're looking at profound bradycardia.
The cardiac output must be tanking. Exactly.
The patient is bradycardic, hypotensive, and
severely hypoperfusing. Early on, they might
just complain of extreme fatigue, but you know
they are actively deteriorating if their mentation
drops, their MAP plummets, or they experience
syncope. On the ECG, how do we distinguish this
from other blocks? I mean, I know there are second
degree blocks where beats get dropped. Pattern
recognition is key here. In second degree type
one, or Benkebock, the PR interval gets progressively
longer until a beat drops. Longer, longer, longer
drop. Right. In type two, the PR interval is
constant, but you randomly drop QRS complexes.
But in third degree, there is zero relationship.
The P waves march out at their own regular rate.
The QRS complexes march out at their own much
slower regular rate. The PR intervals are completely
chaotic because the atria and ventricles are
total divorced. All right, so I've identified
it on the monitor and the patient is like gray,
confused, and their blood pressure is crashing.
What is the priority nursing action? I know atropine
is the standard ACLS drug for symptomatic bradycardia.
Do we just push atropine to speed up the heart?
No, and this is a massive exam trap and a crucial
bedside pearl. Think about the pathophysiology.
Atropine works by blocking vagal stimulation,
which speeds up the SA node in the atria. But
in third degree block, the pathway is physically
severed at the AV node. Oh, so if you push atropine,
you are just making the top of the heartbeat
faster. but that signal is still hitting a brick
wall. Exactly. It's like standing on one side
of a canyon where the bridge is out and screaming
at a stopped train on the other side to move.
It does absolutely nothing for the ventricles.
Atropine is useless here. So we have to pace
them mechanically instead. Right. First priority.
Apply transcutaneous pacemaker pads, TCP, to
the anterior and posterior chest. Next, you set
the pacing rate and the voltage on the external
generator. Your goal is to achieve ventricular
capture. Capture meaning the electricity from
the pads is actually successfully triggering
the heart muscle to squeeze. Yes. On the monitor,
you will see a sharp pacemaker spike immediately
followed by a wide QRS complex. And mechanically,
you must confirm capture by feeling for a corresponding
mechanical pulse. But wait, transcutaneous pacing
means we are shooting enough external electrical
current through the skin, fat, and skeletal muscle
of the chest wall to force the heart to beat.
That has to be brutally painful for the patient.
Oh, it is agonizing. The current causes the chest
muscles to twitch forcefully with every single
beat. So an independent and vital nursing action,
assuming the patient is conscious and has an
airway, is providing immediate analgesia and
sedation. And TCP is just a temporary bridge,
right? Yes, exactly. While you are pacing them
externally, you might hang a dopamine or epinephrine
drip to temporarily support the blood pressure.
But the definitive treatment, the THIDA -N in
your priority list, is preparing the patient
for the insertion of a temporary transvenous
or a permanent pacemaker. Okay, pulling this
all together for the five things to remember.
One, core pathophysiology is complete failure
of AV conduction, so atria and ventricles beat
independently. Two, key assessment is profound
bradycardia with signs of hypoperfusion, like
shock or syncope. Three, most dangerous complication
is periods of a systole and cardiovascular collapse.
Thought on. Four, priority nursing action is
initiating transcutaneous pacing. And five, the
most important treatment is permanent pacemaker
insertion. Perfect. So the one sentence clinical
picture here. A patient with profound symptomatic
bradycardia where the ECG shows regular P waves
and regular QRS complexes that march out completely
independently of one another. And the rule of
thumb. If you see totally dissociated P waves
and QRS complexes with hypotension, think complete
heart block and do transcutaneous pacing immediately.
That is exactly how an intensivist approaches
it. Now we've covered the bottom of the hard
going rogue and the connections being severed.
Let's move above the ventricles to our final
topic, the REIT race. We are looking at atrial
fibrillation and paroxysmal superventricular
tachycardia, or PSVT. Right, these are superventricular,
meaning the chaotic electrical activity originates
above the bundle of his. But if the problem is
in the top of the heart, why is it so dangerous
for the whole system? It all comes back to how
the atrial behavior impacts the ventricles and
ultimately cardiac output. Let's look at PSVT
first. This is usually caused by a reentrant
loop like a short circuit that traps the electrical
signal in a continuous rapid circle. And what's
the rate? It causes abrupt extreme heart rates
of 150 to 220 beats per minute. Ah, so we are
back to the diastolic filling problem. Even though
the signal originates in the atria, a rate of
200 beats a minute drastically cuts into the
ventricular relaxation time. Stroke volume drops,
causing profound hypotension and ischemia. Exactly.
But atrial fibrillation presents a different
mechanical problem. In AFib, there are ectopic
foci all over the atria firing chaotically, usually
between 350 to 600 times a minute. 600. How do
the ventricles not just match that rate and literally
explode? Thankfully, the AV node acts as a gatekeeper.
It won't let all 600 impulses through. But because
the atria are firing so chaotically, they aren't
actually contracting. They are just quivering.
So they lose their squeeze. Right. When you lose
that synchronized atrial contraction, you lose
what we call the atrial kick, that final coordinated
squeeze of blood down into the ventricles right
before they pump. And how much does that actually
matter for the patient's perfusion? Losing the
atrial kick drops your overall cardiac output
by 20 to 30 percent. Wow. Yeah, if your patient
already has a compromised heart, that sudden
drop in perfusion can throw them right into heart
failure. So on the monitor, what's the distinguishing
pattern between the two? Well, PSVT is a regular,
rapid, narrow, complex tachycardia. It's so fast
that the P wave is usually buried inside the
preceding T wave. And AFib. AFib is classically
described as an irregularly irregularly irregularly
irregularly irregularly irregularly irregularly
irregularly irregularly irregular rhythm. The
QRS complexes are narrow, but the distance between
them is completely random. And there are no distinct
P waves at all, just a chaotic, fibrillatory
baseline. OK, let's talk interventions, because
I know they differ drastically. Start with AFib.
If the AV node is letting too many beats through,
say, a ventricular rate of 130, our priority
is rate control, right? We need to slow down
that AV node conduction. Yes. We use medications
like Diltiazem, which is a calcium channel blocker,
or Metaprolol, a beta blocker. But AFib has...
a unique massive complication that you must assess
for before you try to convert them back to a
normal sinus rhythm. The plot risk. Because the
atria are just quivering, the blood isn't being
efficiently inked in. It gets stagnant, especially
in that small anatomical pouch called the left
atrial appendage. Exactly. Blood stasis leads
to thrombi. If a patient has been in AFib for
more than 48 hours, you have to assume they have
a clot in their heart. If you just shock them,
or give them a rhythm converting drug, and the
atria suddenly give a strong, effective squeeze,
you'll dislodge the clot, pump it right up the
carotids, and cause a massive, embolic stroke.
Precisely. So the nursing priority completely
changes. If it's been over 48 hours, they require
anticoagulation like warfarin or illiquis for
three to four weeks before you can safely attempt
cardioversion. Wow, three to four weeks. Yeah.
The only exception is if you do a transesophageal
echocardiogram right then and there to definitively
prove there is no clot. That is a brilliant safety
check to keep in mind. Okay, what about PSVT?
The patient's heart is suddenly racing at 180
beats a minute. They are feeling palpitations,
chest pressure, and dyspnea. For PSVT, our actions
are ranked. First, assuming they are stable,
we try vagal maneuvers. We ask the patient to
bear down as if they're having a bowel movement,
the Valsalva maneuver. And that just stimulates
the vagus nerve to naturally slow the AV node.
deep into adenosine, and honestly, the mechanism
sounds terrifying. It's described as a hard reboot
for the heart. It absolutely is, and it can be
terrifying for the patient. Adenosine briefly
blocks conduction through the AV node entirely.
When you push it, it effectively causes a brief
period of complete assistal. So they just flatline?
Yeah. The patient will flatline on the monitor
for a few seconds before the SA node hopefully
reasserts itself and takes over in a normal rhythm.
You are intentionally flatlining them. So the
independent nursing action here has to be massive
patient education. You have to warn them that
they're going to feel a sudden, intense wave
of chest pressure and a feeling of impending
doom. Yes, you must explain that it will feel
terrible, but it will pass in seconds. And from
a pharmacological standpoint, adenosine has a
half -life of less than 10 seconds. So you have
to push it fast. Extremely fast. If you push
it slowly, the blood enzymes will chew it up
before it ever reaches the heart. So it's a rapid
IV push. One to two seconds, ideally through
a stopcock on a line as close to the heart as
possible, followed instantly by a rapid 20 -milliliter
saline flush. elevate the arm to get it central.
Exactly. But what if the adenosine fails, or
what if the PSVT patient is hemodynamically unstable
from the start like crashing blood pressure,
altered mental status? Then we don't mess around
with meds. We go straight to synchronized cardioversion.
We are delivering a shock to convert the rhythm.
But here is where we circle all the way back
to the very beginning of our discussion. If you
are doing a synchronized cardioversion, you must
visually confirm that the sync button on the
defibrillator is engaged. Why? Oh, because if
the sync button is on, the machine reads the
patient's ECG and times the delivery of the electrical
shock to fall precisely on the R wave of the
QRS complex. And if you forget to hit the sync
button... Then it's just a blind defibrillation
shock. And if that blind shock randomly lands
on the T wave, that's the R on T phenomenon.
You'll send the patient straight from PSVT into
lethal ventricular fibrillation. Exactly. A simple
missed button can kill your patient instantly.
That is why understanding the underlying electrophysiology
is critical. So synthesizing this supraventricular
section into the five things to remember. One,
corpathal is extreme atrial rates, destroying
diastolic filling time in PSVT or causing blood
stasis in AFib. Right. Two, key assessment is
an irregular irregular rhythm for AFib, or an
abrupt extreme cacocardia for PSVT. Three, most
dangerous complication is embolic stroke for
AFib or severe hypotension for PSVT. Exactly.
Four, priority nursing action is to control the
ventricular rate and assess for hemodynamic instability.
And five, most important treatment is adenosine
for PSVT, rate controlling drugs, and anticoagulation
for AFib. Perfect, so the one -sentence clinical
picture for PSVT. A patient experiencing palpitations
and dyspnea with a regular heart rate of 180
beats per minute. And the rule. If you see a
sudden, regular, narrow, complex tachycardia
at 180, think PSVT and do vagal maneuvers or
push adenosine. And for AFib, if you see an irregularly
irregular rhythm with no P waves, think AFib
and prioritize rate control and stroke prevention.
That encapsulates the entire intensivist mindset
we've been talking about. You aren't just reacting
to alarms, you're evaluating the failing physiology
at a cellular and mechanical level. You understand
why losing atrial kit compromises perfusion,
why a severed AV node makes atropine useless,
and why a mistimed shock causes sudden death.
You are anticipating the bottlenecks in the grid
before the lights go out. It changes entirely
how you look at the patient. But as we wrap up,
there's a fascinating detail in the source material
about the future of this grid management. We
talked earlier about pacing patients with third
degree block and the eventual need for a permanent
transvenous pacemaker. But those wires, those
leads, come with massive complications. They
do, yeah. Transvenous leads run directly through
the blood vessels into the heart. Over time,
those wires can fracture, the insulation can
break down, or they can become highways for severe
systemic infections like endocarditis. But the
text mentions a future where we eliminate the
wires completely. Leadless. Battery -free pacemakers.
Yes. The engineering is incredible. We are looking
at a future where a tiny receiver, like a seed,
is placed directly into the cardiac chamber tissue.
There are no batteries or wires inside the heart.
So how does it work? An external transmitter
beams ultrasound energy right through the patient's
chest tissue. That little seed captures the acoustic
energy and converts it into the electrical pacing
pulse that stimulates the muscle. Beaming sound
waves to power a heart. That is just mind blowing.
It raises some profound clinical questions for
you to mull over. I mean, if we completely remove
intravenous leads from the equation, how will
that alter the landscape of ICU complications?
How will it redefine cardiac resynchronization
therapy for our most vulnerable in infection
-prone, heart failure patients. behind every
intervention, every medication mechanism, and
every subtle change in the vital trends. Because
anticipating the deterioration is exactly how
you save a life. Though the next time you look
up at that monitor, don't just see jagged white
lines. Look for the flow of energy. Look for
the failing physiology. Be the one who understands
exactly how to keep the city's lights on when
the grid starts to fail. Thanks for joining us
on this deep dive.