Now on this ECG, take a look at this. Twist,
twist, twist, narrow point; twist, twist, twist,
narrow point. What is the other name for this?
It is called polymorphic ventricular tachycardia.
Allow the name to speak to you. Polymorphic,
various changes in shape of whom? The ventricular
representation of your ECG is your QRS complex.
The most common type of polymorphic ventricular
tachycardia that you will be responsible for
is this one, it's called torsade de pointes. Now with torsade
de pointes, what preceded this? What is the
predisposing factor? Well the QT, which is
all ventricular activity. Let me give you some important
points. Pay attention. QT, all ventricular
activity. Let's do QRS complex first. What
does that mean to you? Ventricular depolarization.
What does that mean to you? The ventricles
are going to contract. Which action potentional
are you bringing into play here? 01234, or
403, which one please? 01234, do that for me.
It will make your life heck of a lot easier
clinically. Please do that for me. With that
QRS complex and let us say that you want to
block it for whatever reason, you want to
block it. What kind of drug might you be thinking?
I want you to block that depolarization. A phase
0 blocker. What is that phase 0 in 01234
with mechanical top actual potential? Good.
It is a voltage-gated sodium channel. What
if you gave too much of that voltage-gated
sodium channel class I type of antiarrhythmic?
If you gave too much, then what may then
happen? Prolong the QT. Let me give you another one.
Tell me about that T wave. I told you QT is what
you are paying attention to. Tell me what
T wave represents. Ventricular repolarization.
Let us talk about that actual potential again.
01234, which phase of actual potential 01234
represents the T wave and ventricular depolarization?
It is phase 3, isn't it? Think about that. Of course,
it is. Repolarization, potassium efflux. I
want you to block the potassium channel, a
class III drug. Drug such as amiodarone, what
may then happen? You prolong the T, means you
prolong the QT. What do you know about 1 and 3?
What do you know about class I and class III
antiarrhythmics? Are you seeing as to how
beautifully we are able to walk through the
physio, the disease, and the management.
Adverse effects. Class I and class III may
then cause long QT syndrome that you already
know. Now you are putting it together and
you're predisposed to this sucker, which is
your torsade de pointes. Or you are born with
this genetically and one you definitely want
to you is romano-ward. Why did I say romano like that? It
is because I need you to know the Romano has
no deafness. Romano-ward is congenital long
QT syndrome. Couldn't help it, born with it,
but there's no deafness where you have another
one where Lange-Nielsen is involved.
That is also congenital long QT syndrome and
that is involved with deafness. There is a
lot more going on here than meets the eye
and you know that. You can't just look at this and be
like, "That must be torsade de pointes, that was
such a simple question." No such thing. There
is history behind this and we walked through
some important ones. Let us continue.
With torsade de pointes associations, now be
careful here, I want you to do something with me for
magnesium. Who is this patient? Third trimester, female, pregnant.
She goes to the
bathroom and she is urinating quite a bit.
Her weight gain is not in proportion to her
gestational age, which actually means she has
accelerated weight gain here. Her blood pressure
is 160/90. She has hemolytic anemia and you
know well maybe she seems little jaundiced. There
is going to be an increase in liver function
test, your transaminases, and the platelet
count 50,000. For all these together, tell
me what is going on and what are you worried
about and why am I bringing this up here?
Because I am referring to pre-eclampsia. Pre-eclampsia,
what happen? A pregnant lady, third trimester and she was urinating.
When she urinates quite
a bit because there is protein loss. In addition
because of protein loss, I told you there
was weight gain accelerated, greater than what
was expected for gestational age because of
edema. I said there was blood pressure 160/90,
what is definition of hypertension? 140/90.
And I told you there was hemolytic anemia, elevated
liver transaminases and there was low platelet. HELLP
syndrome. That is worse case for pre-eclampsia.
Is it not? Yes, it is. So, tell me next step
of management. Magnesium, why? Because if
you don't give magnesium, there is every possibility
that pre-eclampsia may go into eeclampsia,
so what was in this patient or what is being
introduced to the patient that goes into eeclampsia?
Seizures. So my point is this. Magnesium,
if you are deficient of it may result in seizures.
Hypomagnesemia, you are rendered well predisposed
to torsades de pointes. So I need you to think
if you want in layman’s terms seizures of
the heart and the seizures of the brain. Amd
point is, you give magnesium or you are looking
for a patient perhaps that has hypomagnesemia.
Aren't you worried about seizures in such
patients? Are you worried about torsade de
pointes in such patients? Of course, you are.
Put things together, do not memorize things
one at a time. Try to parellel your organ systems
and if you can do it effectively, that is
why I am here. Use me.
Bradycardia. What is happening? You are slowing
down your heart rate. The more that you slow
your heart rate, you are predisposed to what?
Twisting. Also what about that QT? We already
talked about drugs. Let us take a look at
few of them. We have antidepressants, phenothiazines.
Quinidine, a sodium channel blocker. Procainamide,
sodium channel blocker. Disopyramide, sodium
channel blocker. Why am I bringing these up?
Because I just told you, class I, by blocking
the sodium channel, you might be doing what?
Creating a long QT scenario. Floroquinolone
antibiotics and antifungals. Here is some
ABCs, antibiotics, antifungal, antipsychotics,
antidepressants, at least, know some of those
and antiarrhythmics. You actually have ABCD.
Obvious I don't know my alphabet, but you
do the alphabet and you'll walk through anti,
anti-A arrhythmia, B biotics,
C well you might want to pronounce it being
psychotic if that helps, D is going to be
depressants. Anyhow work with C there a little
bit. Can you do that for me? Thank you, appreciate it
greatly. Let us move on.
Ventricular tachy. We have torsade de pointes.
What happens, worse case scenario? Look
at this. Decreased cardiac output, syncope
and is scary. The ventricle is not working
properly may lead into v.fib. You don't want
this at all. Right, this is no joke. You try
to control this ASAP. Worried about cardiac
arrest and death. Next well corrected with
electrolyte imbalance, which one? Which electrolyte
are you focusing upon most importantly again?
Magnesium, good. So if you are hypomagnesemic,
think of seizures. Next setting of hemodynamic
instability, what is your next step of management?
Good. Electrical cardioversion. What does hemodynamic
instability mean to you? The stress, dizziness,
syncope, low blood pressure. Isoproteranol
or dobutamine, what about these? Well, these
could be used to maintain a tachy, utilized,
so just may be. Just keep that in mind.
A nonselective beta agonist, isoproteranol.
Or dobutamine is selective beta-1 agonist.
Now we are going to worse case scenario. Tried
everything you could, maybe wasn’t effective enough
and your patient still goes into v.fib. Very
very obscure type of QRS complexes. This is
not ventricular tachycardia. Your patient
is very much at risk for stand still. Torsade
de pointes, patient unconscious, result
in sudden cardiac death. So this is no joke.