Let's talk about the cardiac depressants like
the calcium channel blockers.
I'm going to use two prototypical calcium channel blockers,
one from each class and explain how they work
First, there is verapamil, which is a
non-dihydropyridine calcium channel blocker.
And there is nifedipine, which is a
dihydropyridine calcium channel blocker.
Now, the nifedipine will block L-type calcium channels.
In the case of nifedipine, it causes vasodilation peripherally.
And the case of verapamil, it causes vasodilation peripherally
as well as cardiac suppression in the way that the heart is beating.
So, there is less inotropy and less chronotropy.
Now, side effects of these particular agents are constipation,
pretibial edema, nausea, flushing and dizziness.
Toxicity includes AV block. So, you can have
sinus node depression, AV block,
and this is usually from verapamil which
has the most activity at the heart.
Other cardiac depressants can be beta blockers.
So, you talk about propranolol as the prototypical drug.
And I've already mentioned beta blockers
multiple times in previous lectures.
Beta blockers reduce heart rate, cardiac force and blood
pressure, and it's used in prevention only of angina.
It is not for treating acute angina attacks. Remember that
vasospastic forms of angina do not respond well to beta blockers.
What beta blockers do is just reduce the oxygen demand
that the heart is asking for.
Let's talk about metabolic rate modifiers.
These are relatively new agents.
They are partial fatty acid oxidase inhibitors,
or pFOX inhibitors.
This increase the efficiency of oxygen utilization
by the myocardium.
It shifts the energy production
from fatty acids to glucose.
It may also have an effect on slow sodium channels
in the heart, we are not entirely sure,
but we do see a reduced heart rate, reduced contractile
force, and we think, and in some studies it had shown
that we have less intracellular calcium,
which is why we think it may work on calcium channels.