Anytime, you have unstable V-tach,
you need to cardiovert your patient.
So you're gonna perform synchronized cardio version
and get them out of V-tach
If they're stable,
you might choose to manage them medically.
And medical management of V-tach
is gonna be antiarrhythmic drugs.
The most commonly used one
is probably amiodarone at least in the US,
although procainamide is a very safe and effective drug,
and sotalol can also be used.
Now, the reason that we used these antiarrhythmics
is that they are non-selective.
So they don't just act on the AV node
like your beta blockers and your calcium channel blockers do,
they act on the entire myocardium and decrease automaticity
sort of decrease the willingness of the heart
to generate an action potential.
So they're gonna work
on rhythms that are originating
outside of the normal conduction system.
Basically, they are gonna work on ventricular rhythms.
Now, if you have a patient who has regular,
monomorphic ventricular tachycardia,
you might think,
hey, maybe this is actually a supraventricular rhythm,
and you can consider adenosine.
It’s the one AV nodal blocking agent
that's reasonable to attempt in wide complex rhythms
because it is so short acting,
its unlikely to cause any major problems
like a beta blocker or a calcium channel blocker would.
But really, the main stay of treatment for V-tach
is gonna be cardioversion for unstable patients
and antiarrhythmic medication,
specifically amiodarone or procainamide
for patients who are stable.
All right, so we covered our wide complex rhythms,
again, wide complex rhythm,
we're gonna treat it like ventricular tachycardia
and we're gonna be safe.
Now, we're gonna move on to narrow complex rhythms.
So narrow complexes suggests
a supraventricular origin of the rhythm.
All narrow complex rhythms must by definition
originate above the AV node
because they are using those fast conduction pathways
in the His-Purkinje System.
There are several different loci
from which narrow complex dysrhythmias can originate.
So there's of course,
the sinoatrial node which is where sinus tachycardia comes from.
There's atrial rhythms
like atrial fibrillation,
atrial flutter, multi focal atrial tachycardia, etc.
And then there are ectopic foci of pace making
which are gonna be your supraventricular tachycardias.
Once you've identified
that you have a narrow complex tachydysrhythmia,
like we said before,
your next question is if it is regular or irregular.
So were gonna start off talking about the irregular rhythms.
So our two irregular rhythms are atrial fibrillation
and atrial flutter.
In atrial fibrillation,
what's happening is electricity is wheezing around the atria
in a completely uncontrolled way,
so the conduction in the atria is random,
and impulses are sent down the through AV node
from the atria in random intervals.
So basically, anytime the node is not refractory,
an impulse might be sent to it
and would then be conducted to the ventricles.
This produces the classic irregularly
irregular rhythm of atrial fibrillation.
The electrical conduction in the atria is random,
the transmission of impulses to the AV node is random,
and that produces a rhythm that has no regularity whatsoever
in terms of the RR interval.
Atrial flutter by contrast is a little bit more organized,
when the atria flutter,
they typically conduct at a regular rate
of 300 atrial beats per minute.
what is usually a regular ventricular response rate.
Now the ventricles typically cannot
conduct at 300 beats per minute.
So the most common ventricular rate we see
in atrial flutter is gonna be 150.
So two to one conduction every other atrial beat
gets conducted to the ventricles
so the atrial rate is 300,
the ventricular rate is 150.
However, you can get an irregular rhythm with atrial flutter
because you can get sometimes get variable conduction
through the AV node.
So let's talk about how you diagnose atrial fibrillation,
so like we said before
the QRS complexes are narrow,
so they are less than a 120 milliseconds long.
The rate or the RR interval is irregularly irregular.
So I've denoted the RR interval
for several of the beats on this rhythm strip
and you can see that 1 is 7, 1 is 15, 1 is 10,
1 is 8, 1 is 10.
There's no predictability to it,
they're just randomly fluctuating
in terms of how frequently the QRS' are coming along.
There's also a randomly fluctuating baseline.
So you can see,
there's that waviness in the baseline
that represents the fibrillatory action of the atria
and there are no organized P-waves.
So you're not seeing regular,
organized atrial activity,
you're just seeing this random fluctuation on the baseline.
Now by contrast,
atrial flutter looks a little bit different.
So in atrial flutter,
you have this sawtooth atrial waves
and I've sort of outlined those for you in green
but you can see they go up and down
almost like the teeth of a crosscut saw.
Like we said before,
the most common atrial rate in atrial flutter
is gonna be 300 beats per minute
and I've marked all of the atrial waves with arrows
so that you can see where they are.
The ventricles can't conduct at 300 beats per minute
so every other atrial beat is conducted to the ventricles
producing a QRS rate of 150
and you can see the QRS complexes noted again on this rhythm strip.
This produces a two to one atrial ventricular conduction rate.
So I've highlighted each set of two atrial waves
with the one corresponding ventricular wave
and you can see you've got two atrial waves,
one ventricular wave,
two atrial waves,
one ventricular wave,
so this is a two to one atrial-ventricular conduction ratio.
Now, that's not always what we see,
you can see flutter with slower ventricular response rates,
so in this particular ECG,
we're seeing a four to one conduction ratio.
So for every four atrial waves,
we have a QRS complex
but you can also see three to one, five to one,
and variable conduction rates
that produce an irregular QRS interval.
So how do we manage atrial fibrillation
and atrial flutter?
First and foremost,
if your patient is unstable,
you cardiovert them,
'cause that’s what we do for every single unstable tachyarrhythmia.
But assuming they’re stable,
we’re gonna be using AV nodal blockers
to try to decrease the ventricular response rate.
So the goal is not to get the patient
out of atrial fibrillation or flutter.
The goal is to slow down the heart rate
by decreasing the ventricular response rate.
So you block the AV node,
you make it more difficult for impulses
from the atria to pass through into the ventricles
and you slow down the ventricular rate.
Again, calcium channel blockers or beta blockers
are the main save of treatment for this.
Amiodarone can also be used
and is appropriate in some circumstances.
It has AV nodal blocking effects
as well as global anti dysrhythmic effects.
I do wanna mention
that A-fib is commonly associated
with underlying non-cardiac pathology.
So for example,
patients with sepsis,
patients with inter abdominal catastrophes,
patients with pulmonary emboli,
they will often present in atrial fibrillation.
And if A-fib is a complication
of some other underlying disease process,
it’s usually safest to focus your treatment
on that underlying disease process
rather than focusing on rate control
or slowing down the atrial fibrillation.
There’s actually some studies that show worst outcomes
when we treat A-fib aggressively,
particularly in patients with sepsis
as oppose to when we just leave it alone
and focus on the sepsis.
So if you think that your A-fib
is related to some underlying disease process,
you might consider withholding specific rate control agents.
But if the patient's coming in
with this as their primary complaint
then of course you're gonna wanna treat it.
so the other thing that we wanna think about with atrial fibrillation
Not every patient with A-fib needs to be anti-coagulated,
but there are some indications for anti-coagulation
that you wanna think about.
So any patient with a prosthetic valve
is always gonna be anti-coagulated.
Honestly, whether they are or aren’t an A-fib.
A patient with a prior history of stroke or TIA
should definitely be anti-coagulated
if they are an A-fib.
And then there's a scoring called the CHA2DS2,
and I've put it here on the slide,
I’m not gonna go through it
in any kind of detail.
But I want you to be aware
that there is this scoring system
that helps us assess the risk of stroke
related to atrial fibrillation
and if your patient has a CHADS2 score of greater than two,
you wanna think about anti-coagulating them
assuming that there aren’t any counter indications.