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Flashcards in calcium channel blockers Deck (35):
1

types of angina

1) “Classic”, “Stable”, or “EffortInduced”
• 2) “Unstable”
• 3) “Variant”, “Rest”, “Vasospastic”, or
“Prinzmetal”
• 4) “Acute Coronary Syndrome”
• 5) “Mixed

2

Classic Angina

Most common form of angina
• Caused by a fixed coronary artery
obstruction (generally atheromatous)Classic Angina
• The pattern of pain remains stable.
“It always starts to hurt
on the 3rd or 4th fairway

3

Classic Angina
• Pain is relieved by

rest or NTG

4

UNSTABLE ANGINA

Pain at rest or with increasing frequency,
duration, severity, or as the result of less
exertion.
• Pain not relieved by NTG or prolonged
(>20 minutes) rest.

5

Prinzmetal Angina

Pain is episodic and unrelated to exertion.
• Although patient might have
atherosclerosis, angina is the result of
arteriospasm and unrelated to exertion or
rest. Treated with NTG or
Calcium Channel Blockers

6

Acute Coronary Syndrome

• Atheromatous plaque ruptures
• Inflammatory cells and mediators are
activated
• “Lipid Pool” forms
• Thrombus forms and propagates
• Vasoconstriction occurs
Vascular occlusion occurs
• Cardiac muscle sickens and dies
• Characteristic MI “biomarkers”
are released

7

Characteristic MI “biomarkers

MYOGLOBIN, CKMB, TRPONIN 1, CK

8

Mixed Angina

Patients have angina during exertion
and at rest.• Caused by a fixed obstruction combined
with vasospasm &/or endothelial
disruptions

9

Two Angina Rx Strategies

1) Increase O₂ delivery
• 2) Decrease O₂ demand

10

The heart is already an 0₂ “sucker” and
extracts

75% of oxygen delivered to it
at rest.

11

• Arterial blood pressure determines how
much

myocardial wall stress is necessary
to overcome that resistance and pump
blood. So…arterial (overwhelmingly arteriolar)
tone determines SVR ~~systolic wall
stress.

12

Venous (capacitance) tone determines

how much blood can be “stored” in the
venous blood delivery system before it’s
returned to the heart. So venous tone determines
~~diastolic wall stress

13

Organic Nitrates and Nitrites

Cause rapid decrease in my0₂cardial demand and
prompt relief of stable,unstable, and variant
angina.

14

Organic Nitrates and Nitrites all work

similarly and differ in their onset
and duration of action.

15

most commonly used
nitrate/nitrite and one you will become
most comfy with.

NTG

16

Organic Nitrates and Nitrites
Side Effects

*Cyanide toxicity and Nipride (discussed earlier)
*Reflex tachycardia ( INCREASE myo₂cardial demand and
decrease coronary perfusion via diastolic filling)
* Reflex positive inotropy ( increase myo₂cardial
demand) *High sustained doses can cause
methemoglobinemia (huh?) particularly
in peds +/- Tylenol exposure.

17

methemoglobinemia

blood with an oxidized heme group. chocolate brown pee

18

what to do when you see methemoglobinemia

#1) Tell the physician
#2) Prepare to give methylene blue at
1-2 mg/kg (up to 50 mg) IV over 3-5
minutes
#3)…and ascorbic acid
#4) …and lots of pure O₂

19

If the patient doesn’t respond to
these therapies for methemoglobinemia

they may be
deficient in the enzyme glucose-6-
phosphate dehydrogenase (G6PD)

20

G6PD-deficient patients who don’t
respond to methylene blue and
ascorbic acid require

1) Exchange transfusions take all blood out and put back in
2) Hyperbaric oxygen

21

dont give organic nitrates and nitrites with vasodilators

kill patient by hypovolemia

22

sodium channel blockers

Emerging class of drugs.
• Effect the transmembrane sodium/calcium
exchange. Less calcium enters the
cardiomyocyte to relieve the cardiac
workload.

23

ranolazine

ranexa. Sodium channel blocker. Also works by shifting cardiac
metabolism from fatty acids
…to carbs
Which require less O₂ to
metabolize

24

Cardiac ischemia decreases

he
transmembrane potential, increases the Ca⁺⁺ flow
into cells which activates ATP-consuming
systems which causes a positive feedback loop
contributing to even more profound ischemia. makes it easy to depolarize

25

calcium channel blockers work by

Smooth muscle is dependent on an inflow of Ca⁺⁺
to maintain ‘tone”…
-As those Ca⁺⁺ channels are “blocked”, those inner
circular and outer longitudinal vascular smooth
muscles relax.

26

Perhaps because there’s more sm. muscle in
arterioles than venules

Arteries are much more
affected by Ca⁺⁺ channel
blockade.
…so arterial dilate, SVR drops, and arterial
pressure falls.

27

calcium channel blockers effect on body

Consequently these agents
decrease afterload (which decrease myO₂cardial
consumption)
*And dilate coronary arteries (which increase
myO₂cardial delivery)

28

ca channel blocker can worsen HF by

negative inotrope

29

Calcium Channel Blockers
You only need to know three:

Verapamil (Calan, Isoptin)
2) Diltiazem (Cardizem)
3) Nifedipine (Procardia)
*They are differentiated by their ability to affect
the myocardium vs. vascular smooth muscle.

30

Nifedipine

procardia. A dihydropyridine derivative
(there are many “…ipines”)
-Almost exclusively a vasodilator with little
dromotropic or chronotropic effect.
*D.O.C. for variant angina (why?) caused by constriction
*Causes reflex tachycardia (why?

31

Verapamil

calan,isoptin. A diphenalkylamine derivative
-Strong negative dromotropic,
chronotropic, and inotropic effects.
-Weak vasodilatory effects.*Dramatically decreases impulse
conduction through the SA & AV nodes
which are rich in calcium pumps.
*D.O.C. for many supraventricular
tachyarrhythmias, such as SVT. because it slows down conduction times

32

Diltiazem

cardizem. Utilized extensively to prevent radial
artery spasm during harvest and postoperatively
to maintain patency.

33

beta blockers

Act as negative chronotropes and inotropes
to myO₂cardial consumption.
*Which adrenergic receptors are most related
to the heart???!!

34


*D.O.C. for exercise-induced angina

beta blockers

35

β-Blockers and Ca⁺⁺ Channel
Blockers are commonly
administered with

nitrates.