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pharmocology > calcium channel blockers > Flashcards

calcium channel blockers Flashcards

1
Q

types of angina

A

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

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2
Q

Classic Angina

A 
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
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3
Q

Classic Angina

• Pain is relieved by

A

rest or NTG

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4
Q

UNSTABLE ANGINA

A

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.

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5
Q

Prinzmetal Angina

A

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

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6
Q

Acute Coronary Syndrome

A 
• 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
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7
Q

Characteristic MI “biomarkers

A

MYOGLOBIN, CKMB, TRPONIN 1, CK

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8
Q

Mixed Angina

A

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

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9
Q

Two Angina Rx Strategies

A

1) Increase O₂ delivery

• 2) Decrease O₂ demand

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10
Q

The heart is already an 0₂ “sucker” and

extracts

A

75% of oxygen delivered to it

at rest.

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11
Q

• Arterial blood pressure determines how

much

A 
myocardial wall stress is necessary
to overcome that resistance and pump
blood. So…arterial (overwhelmingly arteriolar)
tone determines SVR ~~systolic wall
stress.
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12
Q

Venous (capacitance) tone determines

A

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

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13
Q

Organic Nitrates and Nitrites

A

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

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14
Q

Organic Nitrates and Nitrites all work

A

similarly and differ in their onset

and duration of action.

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15
Q

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

A

NTG

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16
Q

Organic Nitrates and Nitrites

Side Effects

A

*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
Q

methemoglobinemia

A

blood with an oxidized heme group. chocolate brown pee

18
Q

what to do when you see methemoglobinemia

A 
#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
Q

If the patient doesn’t respond to

these therapies for methemoglobinemia

A 
they may be
deficient in the enzyme glucose-6-
phosphate dehydrogenase (G6PD)
20
Q

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

A

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

2) Hyperbaric oxygen

21
Q

dont give organic nitrates and nitrites with vasodilators

A

kill patient by hypovolemia

22
Q

sodium channel blockers

A 
Emerging class of drugs.
• Effect the transmembrane sodium/calcium
exchange. Less calcium enters the
cardiomyocyte to relieve the cardiac
workload.
23
Q

ranolazine

A 
ranexa. Sodium channel blocker. Also works by shifting cardiac
metabolism from fatty acids
…to carbs
 Which require less O₂ to
 metabolize
24
Q

Cardiac ischemia decreases

A

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
Q

calcium channel blockers work by

A

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
Q

Perhaps because there’s more sm. muscle in

arterioles than venules

A 
Arteries are much more
affected by Ca⁺⁺ channel
blockade.
…so arterial dilate, SVR drops, and arterial
pressure falls.
27
Q

calcium channel blockers effect on body

A

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

28
Q

ca channel blocker can worsen HF by

A

negative inotrope

29
Q

Calcium Channel Blockers

You only need to know three:

A

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

30
Q

Nifedipine

A

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
Q

Verapamil

A

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
Q

Diltiazem

A

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

33
Q

beta blockers

A

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

34
Q

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

A

beta blockers

35
Q

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

A

nitrates.

pharmocology (20 decks)

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