And yes, we do paralyze patients! Modern
muscle relaxants are rapid in onset,
predictable in recovery sequence, and have
minimal cardiovascular effects. But they produce
no amnesia, and no analgesia. And one
of the great errors that occurs in anesthesia,
is to think that a muscle relaxant is an anesthetic.
They're used primarily in surgical procedures
where muscle relaxant is necessary for adequate
surgical access. This is most commonly abdominal
surgery, thoracic surgery and surgery
on heavily muscled areas, such as the thigh.
They're also used so the anesthetist or other physician
can secure the airway with minimal trauma to
the patient. It paralyzes the muscles
of the airway, allowing the vocal
cords to remain open, and makes it easier
to place an endotracheal tube.
It's often used when patients who require prolonged
ventilation in the operating room, or in
the intensive care unit. They prevent
movement. They prevent breathing.
They prevent escape, the patients can't get away.
But they do NOT produce analgesia.
And probably even more importantly,
they do NOT produce amnesia.
Do not produce sleep
or unconsciousness directly.
So they are not anesthetics, they are adjuncts
to anesthesia, and their used
in the absence of drugs that cause amnesia
or drugs that produce analgesia, is very
bad practice. One of the nice things about muscle relaxants
is that, amongst all the drugs used by anesthesiologists,
they're about the only drugs we actually know
exactly how they work. They either cause
depolarization of muscle fibers in what
is referred to as an irreversible action,
this is the depolarizing muscle relaxant
succinylcholine, or they competitively
block depolarization of muscle fibers
by competing with normal neuro-transmitters,
non-depolarizing muscle relaxants,
and the newest of all of these is Rocuronium. So,
depolarizing muscle relaxants actually
pass across the neuromuscular junction
to the muscle end-plate and cause
depolarization of the muscle. In other words,
they act as if they were a normal neuro-transmitter
and cause normal contraction of the muscle. However,
this contraction is brief,
and we refer to it as fibrillations,
when we can see the twitching of the muscles,
and it's irreversible. The drug just sits
there and doesn't allow the muscle to repolarize,
which is the normal sequence, in normally functioning
muscles. Now, that's not to say that it stays
forever. It tends to get diluted over time
in normal body fluids. And there is a substance
in most people, called Pseudocholinesterase,
which will break down Succinylcholine and get rid
of it in a really quite rapid fashion.
However, we'll talk briefly about this
in another lecture where
people do not have Pseudocholinesterase.
The more commonly used drugs now
are non-depolarizing muscle relaxants. So they don't cause
the fasciculations that you get with Succinylcholine.
And what happens with them is,
they pass across the neuromuscular junction,
they attach themselves to the neuromuscular
end-plate, and they
sit there for a period of time. But they are
in competition with Acetylcholine, which
is the normal neuro-transmitter. Anything
that tends to increase the concentration
of Acetylcholine, will reduce the effect
of the muscle relaxant. Anything that tends
to reduce the effectiveness, or the presence
of Acetylcholine, will increase the effectiveness
of the muscle relaxant. And this
is kind of a diagram of how these
drugs work. They change the polarization
of the neuromuscular sarcolemma,
the surface of the muscle, so that there's
a movement of sodium and potassium
in opposite directions, and there's
a change in polarity, which results in an action
potential. Acetylcholine does this by opening up
channels that allow depolarization
of the muscle fiber.
Non-depolarizing muscle relaxants block
the effect of Acetylcholine by competing
for those same receptors. And Succinylcholine
causes depolarization, but it doesn't
allow repolarization. And without
the cycles continuing, depolarization
and repolarization, no further contractions
can occur. So Succinylcholine,