Anti Angina

Medications

Mechanism
of Action

Useful For

Nitrates
(Nitroglyceri
n)

Gets
converted to
NO within
the cell by
mitochondri
al aldehyde
dehydrogen
ase (MAD).
Increases
cGMP* &
causes
relaxation.

Stable
anginaDecreases
wall
tension
decreases
O2
demand.

= Mainstay
for
immediate
relief
(sublingual
to skip first
pass
metabolism)

Sildenafil,
Vardenafil,
Tadalafil
The fils

Ca Channel
Blockers
Dihydropyra
dine
Nifedipine
Dilitiazem
Verapamil
*All have
different
binding sites

Beta
Blockers
Esmolol =
short acting

PDE 5
(causes
breakdown
of cGMP)
Inhibitor

All act on L
type calcium
channels.
DHP at
clinical
doses has
NO cardiac
effect unlike
the others.
Diltiazem
increases
exercise
tolerance
and delays
onset of
stable
angina!
Antagonize
beta effects
of
catecholami
nes on
heart,

Variant
Angina
(relaxes
SMC)
Unstable
Angina
(decreases
O2 demand
and spasm)
Pulmonary
hypertensi
on, erectile
dysfunction
, Builds up
endogenou
s nitrate
levels
Stable
Angina and
hypertensi
on
*Variant
Angina
*Unstable
Angina
*Since they
relax
coronary
vascular
smooth
muscles
Before M
B1
selective
After M
B1 = B2

Why?
1) Venous dilation
(at clinical range)
Increased Venous
capacitance.
REDUCTION of
ventricular
preload.
2) Improves cardiac
blood flow by
reduction of
vascular spasm.

Excretio
n&Meta
bolism
Excrete
d by
kidney.

Side
Effects
Headaches
, Reflex
tachycardi
a (due to
drop in b.p

sympathet
ic
activation,
Orthostatic
hypotensio
n=
syncope.
Tolerance
from
continuous
exposure
Contraindi
cated with
alpha
blocker
and
nitrates.

Especially
nifedipine/amlodipine
slow decrease in TPR
slow drop in blood
pressure minimizing
potential reflex
tachycardia.
*Overall decrease in O2
demand.
Non DHP blockers:
Decrease contractility
and heart rate.
Decrease O2 demand.

Atenolol if there is
liver damage.
Propranolol, metoprolol
all eliminated by liver.
DO NOT USE

vessels and
bronchi.

Carvedilol
& labetalol
are mixed
alpha and
beta
blockers.

PROPRANOLOL in
patients with asthma
(B2 antagonist will
vasoconstrict) or
diabetes.

Intracellular actions of cGMP =

- K channel activation and hyperpolarization
- INCREASE Ca2+ sequestration
- Decrease in Ca2+ sensitivity.
Smooth muscle relaxation.
Beta 2 Receptor mediates vasodilation. Blocking it would cause and increase in TPR
and constriction.
Selective does not block other receptors (just all betas)
Specific does NOT antagonize cardiac stimulation and vasodilation elicited by agents
other than Beta blockers.