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
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.