Topic 9 CaChannelBlockers Flashcards

(59 cards)

1
Q

Most common form of angina

A

Classic Angina

The pattern of pain remains stable

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2
Q

Classic Angina caused by

A

Caused by a fixed coronary artery
obstruction (generally atheromatous)
The pattern of pain remains stable

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3
Q

Classic Angina pain relieved by what?

A

Pain is relieved by rest or nitroglycerin

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4
Q

What is Unstable Angina?

A

Pain at rest or with increasing frequency, duration, severity, or as the result of less exertion

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5
Q

Unstable angina pain not relieved by what?

A

Pain not relieved by NTG or prolonged

(>20 minutes) rest

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6
Q

Prinzmetal Angina pain?

A
  • Pain is episodic and unrelated to exertion

- Angina is the result of arteriospasm and unrelated to exertion or rest

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7
Q

Prinzmetal Angina is treated with?

A

Treated with NTG or Calcium Channel Blockers

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8
Q

Acute Coronary Syndrome

A

Atheromatous plaque ruptures
Inflammatory cells and mediators are activated
Vasoconstriction occurs

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9
Q

Acute Coronary Syndrome form what?

A

Lipid Pool
Thrombus forms and propagates
Vasoconstriction occurs

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10
Q

Acute Coronary Syndrome what biomarkers are released?

A

Characteristic MI “biomarkers” are released

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11
Q

What happens with Acute Coronary Syndrom

A

Vascular occlusion occurs

Cardiac muscle sickens and dies

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12
Q

Mixed Angina is caused by what?

A

Caused by a fixed obstruction combined

with vasospasm &/or endothelial disruptions

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13
Q

What is Mixed Angina ?

A

Patients have angina during exertion and at rest

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14
Q

Rx strategies for Angina

A

1) Increase O₂ delivery

2) Decrease O₂ demand

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15
Q

Heart extracts what % of oxygen that is delivered to them

A

extracts ~75% of oxygen delivered to it

at rest

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16
Q

What determines how much myocardial wall stress is necessary to overcome that resistance and pump blood ?

A

Arterial blood pressure

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17
Q

arterial (overwhelmingly arteriolar) tone determines what?

A

determines SVR ~~ systolic wall stress

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18
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

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19
Q

What determines how much blood can be “stored” in the venous blood delivery system before it’s returned to the heart

A

Venous (capacitance) tone

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20
Q

venous tone determines

A

diastolic wall stress

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21
Q

Diastolic wall stress is determined by what?

A

Venous tone

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22
Q

Organic Nitrates and Nitrites cause what? relief what?

A

Cause rapid decrease in my0 ₂cardial demand and prompt relief of stable, unstable, and variant angina

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23
Q

Nitroglycerin

A

Nitrobid

Organic Nitrates and Nitrites

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24
Q

Nitroprusside

A

Nipride

Organic Nitrates and Nitrites

25
Isosorbide mononitrate
Imdur Organic Nitrates and Nitrites
26
Isosorbide dinitrate
Isordil Organic Nitrates and Nitrites
27
the most commonly used nitrate/nitrite
Nitroglycerin
28
Organic Nitrates and Nitrites side affects
Cyanide toxicity and Nipride (discussed earlier) * Reflex tachycardia (Increase myo₂cardial demand and decrease coronary perfusion via diastolic filling) * Reflex positive inotropy (increase myo₂cardial demand)
29
High sustained doses of Organic Nitrates and Nitrites can cause what?
High sustained doses can cause methemoglobinemia particularly in peds +/-Tylenol exposure
30
chocolate brown blood, blood with an oxidized heme group
“methemoglobinemia”
31
If your patient has Methemoglobinemia what are the 4 steps you take?
``` #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 ```
32
If a patient with Methemoglobinemia does not respond to initial typical therapy (the 4 steps) what is prob going on?
They are deficient in glucose-6-phosphate dehydrogenase (G6PD)
33
G6PD-deficient patients who don’t respond to methylene blue and ascorbic acid require what two things?
1) Exchange transfusions | 2) Hyperbaric oxygen
34
Sodium Channel Blockers effect what?
Effect the transmembrane sodium/calcium exchange. | Less calcium enters the cardiomyocyte to relieve the cardiac workload
35
Ranolazine
Ranexa Sodium Channel Blocker
36
Ranexa
Ranolazine Sodium Channel Blocker
37
Ranolazine (Ranexa) works by shifting what?
Also works by shifting cardiac metabolism from fatty acids...to carbs Which require less O₂ to metabolize
38
Cardiac ischemia does what?
Cardiac ischemia decreases the 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
39
Ca Channel Blockers do what?
Block the calcium cardiac transmembrane current is critical in myocardial contraction 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
40
Ca Channel Blockers affects what vasculature much more?
Arteries are much more affected by Ca⁺⁺ channel blockade...so arterial dilate, SVR drops, and arterial pressure falls
41
Ca channel blockers do what to afterload and myocardial consumption
Consequently these agents DECREASE afterload (which DECREASE myO₂cardial consumption) And dilate coronary arteries (which INCREASE myO₂cardial delivery)
42
Ca Channel Blockers do what heart failure?
They also have the potential to worsen heart | failure
43
Verapamil
Calan, Isoptin Ca Channel Blockers
44
Diltiazem
(Cardizem) Ca Channel Blockers
45
Nifedipine
(Procardia) Ca Channel Blockers
46
Nifedipine (Procardia) is a derivative of what?
dihydropyridine derivative
47
Nifedipine (Procardia) has what effects?
Almost exclusively a vasodilator with little dromotropic or chronotropic effect. *D.O.C. for variant angina
48
Nifedipine (Procardia) causes what HR side affect?
Causes reflex tachycardia
49
Verapamil (calan, Isoptin) is a derivative of what?
A diphenalkylamine derivative
50
Verapamil (calan, Isoptin) causes what effects?
Strong negative dromotropic, chronotropic, and inotropic effects. -Weak vasodilatory effects
51
Verapamil (calan, Isoptin) does what with impulse conduction?
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
52
Diltiazem (Cardizem) is classified as what?
Classified as a benzothiazepine
53
Diltiazem (Cardizem) has what effects?
mix of vasodilatory and cardiac effects
54
Diltiazem (Cardizem) has what effects compared to verapamil? (Chonotripic, SVR, Tachycardia)
Less negative chronotropic and dromotropic than verapamil, less decrease SVR and reflex tachycardia than nifedipine
55
What drug is utilized extensively to prevent radial artery spasm during harvest and post-operatively to maintain patency
Diltiazem (Cardizem) (Ca Channel Blocker)
56
β- Blockers, chonotropic/inotropic effects?
Act as negative chronotropes and inotropes to DECREASE myO₂cardial consumption
57
β- Blockers are the D.O.C. for what?
D.O.C. for exercise-induced angina
58
Verapamil (calan, Isoptin) is the DOC for what?
many supraventricular tachyarrhythmias, such as SVT
59
β-Blockers and Ca⁺⁺ Channel Blockers are commonly administered with what?
nitrates