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Pharmacology > Pharm 9- Ca Channel Blockers > Flashcards

Pharm 9- Ca Channel Blockers Flashcards

1
Q

4 Categories of Antianginal Drugs

A
  1. Organic Nitrates
  2. Sodium Channel Blockers
  3. Calcium Channel Blockers
  4. B Blockers
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2
Q

Types of Angina

A
  1. “Classic,” “Stable,” “Effort-induced”
  2. “Unstable”
  3. “Variant,” “Rest,” “Vasospastic,” “Prinzmetal”
  4. Acute Coronary Syndrome
  5. Mixed
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3
Q

Classic Angina

A

Most common form of angina
Caused by a fixed coronary artery obstruction (generally atheromatous)
Stable pain pattern
Relived by rest or Nitro

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4
Q

Relationship between % blockage and degree of debilitaiton

A

Not a great relationship; ex. sometimes even a 30% blockage can be very debilitating

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5
Q

How does classic angina present in women?

A

Does not always present as pain

Exhaustion, nausea, diaphoresis

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6
Q

Unstable Angina

A

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

Pain not relieved by NTG or prolonged rest (>20 minutes)

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7
Q

Prinzmetal Angina

A

Pain is episodic and unrelated to exertion
May have atherosclerosis, but angina is the result of arteriospasm and unrelated to exertion or rest
Tx: NTG; calcium channel blockers

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8
Q

Acute Coronary Syndrome

A

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

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9
Q

Mixed Angina

A

Patients have angina during exertion and at rest

Cause: Fixed obstruction combined w. vasospasm and or endothelial disruptions

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10
Q

Two Angina Rx Strategies

A
  1. Increase O2 Delivery

2. Decrease O2 Demand

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11
Q

What are the determinants of myocardial oxygen consumption?

A
  1. Wall stress (intraventricular pressure, ventricular radius/vol, wall thickness)
  2. Heart Rate
  3. Contractility
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12
Q

What percent O2 does the heart extract at rest?

A

75% of oxygen delivered to it; O2 “sucker”

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13
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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14
Q

What determines SVR?

A

Arterial (overwhelmingly arteriolar) tone determines SVR ~ systolic wall stress.

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15
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 determines this.

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16
Q

What does venous tone determine?

A

Diastolic wall stress

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17
Q

What do organic nitrates and nitrites do?

A

Cause RAPID decrease in myocardial demand and prompt relief of stable, unstable, and variant angina.

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18
Q

% Obstructions vs. Angina

A

50% Obstruction: Potential angina
99% Obstruction: Resting angina
70% obstruction: Exercise induced angina
30% obstruction: no angina

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19
Q

What are the 4 organic nitrates and nitrites?

A

Nitroglycerine (Nitrobid)
Nitroprusside (Nipride)
Isosorbide mononitrate (Imdur)
Isosorbide dinitrate (Isordil)

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20
Q

How do nitrates result in vascular smooth muscle relaxation?

A

Increase nitrates
Increase nitric oxide
Increase cGMP
Increase dephosphorylation of myosin light chain

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21
Q

What is the most common nitrate/nitrite?

A

NTG

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22
Q

What are the side effects of organic nitrates and nitrites?

A

Cyanide toxicity and Nipride
Reflex tachycardia (increase myocardial demand and decrease coronary perfusion via diastolic filling)
Reflex positive inotropy (increase myocardial demand)

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23
Q

What can a high sustained dose of organic nitrates and nitrites cause?

A

Methemoglobinemia; particularly in peds +/- Tylenol exposure

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24
Q

Methemoglobinemia

A

Blood turns chocolate brown, blood disorder in which an abnormal amount of methemoglobin – a form of hemoglobin – is produced; blood with an oxidized heme group

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25
Q

What do you do if you have methemoglobinemia on bypass?

A
  1. Tell physician
  2. Prepare to give methylene blue at 1-2 mg/kg (up to 50 mg) IV over 3-5 minutes
  3. Absorbic acid
  4. Lots of pure o2
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26
Q

What does it mean if a methemoglobinemia patient does not response to the standard therapies?

A

May be deficient in the enzyme glucose-6-phosphase dehydrogenase (G6PD)

27
Q

If a methemoglobinemia patient is deficient in G6PD, how do you treat them?

A
  1. Exchange transfusions

2. Hyperbaric oxygen

28
Q

Exchange Transfusion

A

Exchange transfusion is a potentially life-saving procedure that is done to counteract the effects of serious jaundice or changes in the blood due to diseases such as sickle cell anemia. The procedure involves slowly removing the patient’s blood and replacing it with fresh donor blood or plasma.

29
Q

Hyperbaric Oxygen

A

Hyperbaric oxygen therapy (HBOT) is breathing 100% oxygen while under increased atmospheric pressure; Hemoglobin is saturated, but the blood can be hyperoxygenated by dissolving oxygen within the plasma

30
Q

You should never give direct vasodilators in patients with…

A

Hypovolemia

31
Q

How do sodium channel blockers work?

A

Effect the transmembrane sodium/calcium exchange; less calcium enters the cardiomyocyte to relieve the cardiac workload

32
Q

What is an example of a sodium channel blocker?

A

Ranolazine (Ranexa)

33
Q

How else does Ranexa work?

A

Shifting cardiac metabolism from fatty acids to carbs; which require less O2 to metabolize

34
Q

How does cardiac ischemia affect the transmembrane potential? What does this result in?

A 
Decreases transmembrane potential
Increases Ca++ flow into cells
Activates ATP-consuming systems
Positive feedback loop
More profound ischemia
35
Q

What does smooth muscle depend on to maintain tone?

A

Inflow of Ca ++; as Ca++ channels are blocked the inner circular and outer longitudinal vascular smooth muscles relax

36
Q

Which has more smooth muscle? Arterioles or venules?

A

Arterioles have more smooth muscle.

37
Q

Which is more affected by Ca++ channel blockade (arterioles or venules)?

A

Arterioles (more smooth muscle); arterioles dilate, SVR drops, arterial pressure drops

38
Q

How do calcium channel blockers work?

A

Decrease inflow of calcium; decreased afterload which decreases myocardial consumption

Dilates coronary arteries (increases myocardial delivery)

39
Q

How do calcium channel blockers worsen heart failure?

A

Negative inotrope

40
Q

Name 3 calcium channel blockers.

A
  1. Verapamil (Calan, Isoptin)
  2. Diltiazem (Cardizem)
  3. Nifedipine (Procardia)
41
Q

How are the three calcium channel blockers differentiated?

A

By their ability to affect the myocardium vs. vascular smooth muscle.

42
Q

What is Nifedipine (Procardia) derived from?

A

Dihydropyridine derivative

43
Q

Nifedipine (Procardia)

A

Vasodilator
(Little dromotropic or chronotropic effect)
Reflex tachycardia

44
Q

What is the drug of choice for variant angina and why?

A

Nifedipine (Procardia); vasodilator but no dromotropic or chronotropic effect so it wont increase the workload of the heart

45
Q

Verapamil (Calan, Isoptin) is derived from what?

A

Diphenalkylamine derivative

46
Q

Verapamil (Calan, Isoptin)

A

Strong negative dromotropic, chronotropic, and inotropic effects. Weak vasodilatory effects.

47
Q

Dromotropic

A

speed of impulse conduction through the SA and AV nodes, which are rich in calcium pumps

48
Q

What is the drug of choice for SVTs? Why?

A

Verapamil; negative dromotropic/ chronotropic effects so it slow the conduction speed and therefore slows down the tachycardia

49
Q

Diltiazem (Cardizem)

A

Benzothiazepine; mix of vasdilatory and cardiac effects, “middle of the road drug”

Less negative chronotropic and dromotropic than verapamil, less decrease in SVR and reflex tachycardia than nifedipine (procardia)

50
Q

What is Diltiazem used EXTENSIVELY for?

A

Prevent radial artery spasm during harvest and post-operatively to maintain patency

51
Q

What is the drug of choice for exercise-induced angina?

A

Beta Blockers

52
Q

What are beta blockers?

A

Act as negative chronotropes and inotropes to decrease myocardial consumption.

53
Q

Which adrenergic receptors are most related to the heart?

54
Q

What are the treatments for long term vs short term angina?

A

Long term- beta blockers

short term- nitrates

55
Q

What are commonly administered with nitrates?

A

Beta Blockers and Ca++ channel blockers

56
Q

What drugs are used to treat angina without concomitant disease?

A

Long-acting nitrate
Beta blockers
Ca++ Channel Blockers

57
Q

What drugs are used to treat angina + recent MI?

A

Long-acting nitrate

Beta blockers

58
Q

What drugs are used to treat angina + asthma/COPD?

A

Long acting nitrate

Ca ++ channel blockers

59
Q

What drugs are used to treat angina + hypertension?

A

Long-acting nitrate (less effective)
Beta blockers
Ca++ channel blockers

60
Q

What drugs are used to treat angina + diabetes?

A

Long acting nitrates

Ca ++ channel blockers

61
Q

What drugs are used to treat angina + chronic renal disease?

A 
Long acting nitrate
Beta Blockers (less effective)
Ca++ channel blockers
62
Q

Nitrates Alone have what effects on the heart?

A 
HR: Reflex Increase
Arterial Pressure: Decrease
End-diastolic volume: Decrease
Contractility: Reflex increase
Ejection time: Decrease
63
Q

Beta Blockers or Calcium Channel Blockers have what effects on the heart?

A 
HR: Decrease
Arterial pressure: Decrease
End-diastolic volume: Increase
Contractility: Decrease
Ejection time: Increase
64
Q

Combine Nitrates with B-Blockes or Ca++ Blockers have what effects on the heart?

A 
HR: Decrease
Arterial Pressure: Decrease
End-diastolic volume: None or decrease
Contractility: None
Ejection time: None

Pharmacology (23 decks)

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