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Cardiovascular > Vasodilators in Angina > Flashcards

Vasodilators in Angina Flashcards

1
Q

Damage to _____ can alter the ability of coronary vasculature to dilate

A

endothelium

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2
Q

True or False: Beta blockers are typically considered first line defense against angina if they are tolerated by the patient

A

True

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3
Q

Are B-adrenergic blockers used for angina treatment?

A

For stable angina, YES. They decrease O2 demand through decreasing HR and contractility and they lower BP.

For variant angina (vasospastic), no. B-adrenergic blockers do not vasodilate so they don’t do anything for variant angina.

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4
Q

Does norepinephrine vasodilate or vasoconstrict?

A

Vasoconstrict. It acts on the A1 receptors

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5
Q

Management of angina is centered around what?

A

Increasing O2 supply and/or reducing O2 demand.

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6
Q

Which side effects are associated with amlodipine?

A. Bradycardia
B. Cough
C. Edema
D. QT prolongation
E. Hypotension
F. Flushing
A

Edema, hypotension, flushing.

Amlodipine is a pure vasodilator so you consider the side effects that are peripheral.

It wouldn’t cause Bradycardia or QT prolongation. Cough is side effect of ACE inhibitors, not -dipines.

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7
Q

How do ACE inhibitors vasodilate?

A

They increase bradykinin which triggers eNOS (endothelial nitric oxide synthase) to create nitric oxide which causes smooth muscle relaxation/vasodilation through cGMP.

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8
Q

How are CCBs metabolized and what should be kept in mind?

A

Metabolized by cytochrome P450. Effects may fluctuate if administered with inhibitors or inducers.

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9
Q

Does epinephrine vasodilate or vasoconstrict?

A

Vasodilate. It acts on the B2 receptors

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10
Q

All calcium channel blockers are vaso_____.

A

vasodilators

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11
Q

What is the most common calcium channel blocker?

A

Amlodipine

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12
Q

Nitrates are the drug of choice for ______ _______ of angina.

A

acute exacerbation

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13
Q

What is the main purpose of Beta Blockers in treatment of Angina?

A

Decreasing myocardial O2 demand

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14
Q

How can verapamil cause constipation?

A

L-type channels in intestinal muscles causes relaxation of intestines and stops propulsion.

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15
Q

Coronary blood flow is decreased by increased _______

A

Left ventricular end diastolic pressure (preload)

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16
Q

Name 5 calcium channel blockers

A
  1. amlodipine
  2. verapamil
  3. diltiazem
  4. nifedipine
  5. felodipine
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17
Q

Of verapamil, diltiazem, and the dihydropyridines, which have the major adverse effect of hypotension?

A

They all do. They all vasodilate

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18
Q

What do you do if a patient whose angina was previously well controlled with once-daily isosorbide mononitrate states that he recently has been taking it twice a day to control angina symptoms that are occurring more frequently during early morning hours?

A

You should advise the patient not to take twice a day because that depletes the nitrosothiol groups necessary for NO formation (tachyphylaxis/tolerance). You should also recommend that he take the once-daily administration in the evening because some patients have worse symptoms in the morning so shifting the regimen time can help.

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19
Q

What are 4 contraindications for B blockers?

A
  1. Severe bradycardia
  2. Asthma (relative - via B2 block)
  3. Peripheral vascular disorders (relative - via B2 block)
  4. Abrupt withdrawal -> precipitates SNS overactivity
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20
Q

Prophylactic treatment for chronic angina is typically done with beta blockers. When would you use nitrates?

A

When beta-blockers are contraindicated in a particular patient or poorly tolerated, or they can be used in addition to beta blockers if angina persists with beta-blocker usage.

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21
Q

Is B1 selectivity in metoprolol and atenolol absolute or dose-dependent?

A

Dose-dependent

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22
Q

Do B2 receptors dilate or constrict?

A

dilate

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23
Q

What is a potential adverse reaction for ranolazine? (to do with conduction)

A

Can prolong the QT interval (through inhibition of HERG channel - IKr) in dose-dependent manner (higher doses)

Torsades de pointes has not been observed but use cautiously with QT-prolonging drugs

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24
Q

How do you treat stable angina?

A

Beta blockers, nitrates, calcium channel blockers

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25
Q

When are CCBs used in angina? (3 things)

A
  1. used for vasospastic angina
  2. long-acting agents are commended for stable angina if beta-blockers are contraindicated or poorly tolerated
  3. can be added to beta-blockers if angina persists
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26
Q

Broadly speaking, how do you increase O2 supply and reduce O2 demand?

A

Increasing O2 supply is done surgically (CABG/PTCA) or secondarily with vasodilator drugs. Decreasing myocardial O2 demand is achieved pharmacologically with vasodilators and negative inotropic and chronotropic agents.

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27
Q

Name the vasodilator that is a sustained release preparation that is used chronically PO.

A

Isosorbide mononitrate

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28
Q

Nitrates result in reduction of what two things?

A
  1. Reduced Left Ventricular End Diastolic Pressure (leads to decreased wall tension => decreased myocardial O2 demand)
  2. Reduced systemic vascular resistance
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29
Q

How do you increase regional flow distribution to increase myocardial oxygen supply?

A

Nitrates, CCBs, B-blockers

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30
Q

How do you decrease preload => decrease ventricular volume and pressure => decrease myocardial wall tension => lower myocardial oxygen demand?

A

Nitrates

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31
Q

What is something to consider with continuous exposure of nitrates?

A

Tachyphylaxis (tolerance). This happens because of depletion of nitrosothiol groups necessary for NO formation. Nitrate free interval of 6-14 hours is recommended (typically during sleep)

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32
Q

Of Verapamil, diltiazem, and the dihydropyridines, which has the most major adverse effects?

A

Verapamil (hypotension, bradycardia, avblock, CHF, and constipation)

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33
Q

Which CCB is most likely to cause constipation?

A

Verapamil

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34
Q

For drug administration, wtf does Dr. French mean with SL and TS?

A

SL = sublingual, TS = translingual spray

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35
Q

Which b-blocker is a1, b1, and b2 (vasodilating)?

A

Labetalol, carvedilol

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36
Q

What is the mechanism for nitrates and PDE 5 inhibitor DDI?

A

Sildenafil, tadalafil, and vardenafil are erectile dysfunction drugs that are PDE inhibitors. They prevent the breakdown of cGMP so that vasodilation persist for the erection. Nitrates create excess NO which also increases cGMP which causes even more vasodilation causing a dangerous drop in BP resulting in syncope or worse.

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37
Q

What are 5 adverse reactions of ranolazine?

A
  1. bradycardia
  2. hypotension
  3. palpitations
  4. edema
  5. QT interval prolongation (possible)
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38
Q

Nitrates dilate primarily on the ____ side.

A

Primarily venous side. But not exclusively… it’s dose dependent

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39
Q

Of Verapamil, diltiazem, and the dihydropyridines, which have the major adverse effect of Constipation?

A

Verapamil

40
Q

Dihydropyridines (nifedipine) have ____ ratio of vascular dilation to cardiac effects.

A

Greater

41
Q

What are 6 minor toxicities for CCBs?

A

Flushing, edema, dizziness, nausea, constipation, gingival hyperplasia

42
Q

Afterload is controlled through what level of vasculature?

A

Arterioles. Afterload goes up if you have to pump against more resistance.

43
Q

What is the difference between B-receptor blockers?

A

Relative affinities for B1, B2, and a1 receptors

44
Q

If your patient has been prescribed a sustained-release oral nitrate preparation for prophylaxis of angina (e.g. isosorbide mononitrate), you should be most alert for what side effect?

A

Postural hypotension. If you change position, the baroreceptors tell norepinephrine to go vasoconstrict but the oral nitrate is out there vasodilating so there is an increase of time that it takes for the vessels to react.

45
Q

Of Verapamil, diltiazem, and the dihydropyridines, which have the major adverse effect of CHF?

A

Verapamil only. This is because verapamil has greater negative inotropic effect and AV node suppression than diltiazem.

46
Q

True or False: Oral bioavailability for CCBs is predictable.

A

FALSE. Oral bioavailability varies widely (10-90%). In clinic, you typically have no idea what bioavailability to expect when giving oral CCBs but you just give whatever dosage was determined in clinical trails to give adequate levels.

47
Q

In treating angina, which beta blockers are preferred?

A

Cardioselective agents (metoprolol or atenolol)

48
Q

What are 4 adverse reactions for vasodilators?

A
  1. Throbbing headache
  2. Orthostatic hypotension
  3. Reflex tachycardia
  4. Facial flushing
49
Q

Name 3 endothelial dependent vasodilators that trigger the creation of nitric oxide

A
  1. ACh
  2. Histamine
  3. Bradykinin
50
Q

Nitrates can cause reflex tachycardia. What can you do to block this side effect?

A

Beta blockers

51
Q

Preload is controlled through what level of vasculature?

A

Venules. Venoconstriction brings blood back to heart (higher preload). Venodilation brings less blood back to the heart (lower preload).

52
Q

If drugs are applied sublingually, does it bypass first pass effect?

A

Yes, anything but oral and some rectal administration bypasses liver for first pass.

53
Q

Which b-blocker is B1 selective (cardioselective)?

A

Metoprolol, atenolol

54
Q

Which of the following anti-anginas agents can lower blood pressure?

A. Nifedipine
B. Sublingual nitroglycerin
C. Oral nitrates (e.g. isosorbide, dinitrate)
D. Metoprolol
E. Verapamil
F. Diltiazem
A

All of the above

BP = CO x Systemic Vascular Resistance

55
Q

Which drugs are pure vasodilators? (two categories)

A

nitrates and -dipines

56
Q

For acute angina, what administration route would you use for nitrates?

A

SL, TS

57
Q

What are the primary and secondary effects of nitrates?

A

Primary: decreased wall tension => decreased myocardial O2 demand
Secondary: improves perfusion of ischemic myocardium

58
Q

How do you increase coronary blood flow to increase myocardial oxygen supply?

A

Nitrates and CCBs

59
Q

What is the mechanism of action of nitrates?

A

Nitrates are converted into nitric oxide which activates guanylate cyclase to convert GTP into cGMP. cGMP leads to relaxation of smooth muscle (vasodilation)

60
Q

How do you treat variant angina?

A

Calcium channel blockers, nitrates

61
Q

Name a vasodilator that can be taken IV/SL to bypass first pass effect.

A

Nitroglycerin

62
Q

True or false: Verapamil and diltiazem each have their distinct sites on cardiac nodal tissue and cardiac muscle

A

true

63
Q

What is typical angina?

A

Angina that derives from the formation of atherosclerotic plaques

64
Q

For anti-ischemic therapies, which drugs are given acutely to prevent cardiac events? Which are given chronically?

A

Nitrates are given acutely, all others are given chronically

65
Q

What should you avoid (pharmacokinetically) for dihydropyridines (-dipines)?

A

Rapid onset. Rapid onset may rapidly lower BP which can cause reflex tachycardia which exacerbates the angina and causes increased risk for MI

66
Q

Coronary blood flow is inversely proportional to coronary vascular _______.

A

resistance

67
Q

The LQT3 mutant Na+ channels can result in long QT because of incomplete inactivation of Na+ channels. What does this do to O2 demand?

A

Persistent late Na+ current can lead to intracellular Na+ overload which in turn leads to reversal of the Na+-Ca++ exchanger and subsequent intracellular Ca++ overload. Ca++ overload can result in an increased diastolic tension which increases O2 demand causing risk for anemia.

68
Q

What is the most common beta blocker?

A

Metoprolol

69
Q

All of the following drugs can be useful for managing stable angina in a patient with CAD EXCEPT:

A. Amlodipine
B. Metoprolol
C. Immediate-release nifedipine
D. Isosorbide dinitrate
E. Atenolol
A

Immediate-release nifedipine. Immediate release or rapid onset dilators or Ca channel blockers can cause problems with wide swings in hemodynamics. These trigger baroreceptors to react and cause reflex tachycardia.

70
Q

Coronary blood flow only happens during ____ (shortened by ______)

A

Diastole, tachycardia

71
Q

How do you decrease heart rate to lower myocardial oxygen demand?

A

B-blocker and some CCBs

72
Q

What are 4 major adverse reactions of CCBs?

A

Cardiac depression (more risk with verapamil or diltiazem because these act directly on the cardiac L-type channels)

  1. Cardiac arrest
  2. Bradycardia
  3. AV block
  4. Congestive heart failure
73
Q

Which of the following anti-anginal drugs does NOT act as a vasodilator and should not be used in the treatment of vasospastic angina?

A. Diltiazem
B. Nifedipine
C. Nitroglycerin
D. Oral nitrates (e.g. isosorbide dinitrate)
E. Metoprolol
F. Verapamil
A

Metoprolol. Metoprolol decreases O2 demand but doesn’t vasodilate.

74
Q

What is a DDI for nitrates?

A

Erectile dysfunction drugs (including viagra). Avoid the use of nitroglycerin if it is suspected or known that the patient has taken sildenafil or vardenafil within the previous 24 hours or tadalafil within 48.

Nitrates may cause severe hypotension refractory to vasopressor agents.

75
Q

What is the suffix for calcium channel blockers that are pure vasodilators?

A

-dipine

76
Q

For pharmacokinets, the route that you give a drug influences _____ and _____.

A

onset, duration

77
Q

How do you decrease cardiac contractility to lower myocardial oxygen demand?

A

B-blocker and some CCBs

78
Q

Do calcium channel blockers vasodilate or vasoconstrict?

A

Vasodilate

79
Q

Of Verapamil, diltiazem, and the dihydropyridines, which have the major adverse effect of Bradycardia?

A

Verapamil and diltiazem because they work on the L-type receptors on the heart

80
Q

What is variant angina?

A

Angina caused by vasospasm

81
Q

Drugs that relax vascular smooth muscle can produce a reflex tachycardia that can increase myocardial O2 consumption and exacerbate symptoms in anginal patients. Which of these anti-anginal agents are most likely to cause reflex tachycardia?

A. Diltiazem
B. Metoprolol
C. Nifedipine
D. Nitroglycerin
E. Verapamil
A

C and D. Nifedipine, nitroglycerin

82
Q

For prophylactic treatment for chronic angina, what administration route would you use for nitrates?

A

Long-acting oral, topical, or transdermal preparations.

83
Q

B-blockers are used to lower heart rate to lower the myocardial O2 demand. However, they can also increase LV volume. How?

A

B-blockers will block the B2 receptors on smooth muscle which inhibits the dilation ability of vasculature. This can cause LV volume to go up because more blood is brought back to the heart (lack of vasculature dilation)

84
Q

What is the difference between metoprolol tartrate and metoprolol succinate?

A

Metoprolol succinate is Slow acting and Sustained. You can remember this because Succinate.

85
Q

How do you treat unstable angina?

A

Antithrombotics, beta blockers, nitrates calcium channel blockers

86
Q

What is the first-line therapy for stable angina patients unless use is contraindicated?

A

Beta blockers

87
Q

How do you decrease afterload => decrease ventricular volume and pressure => decrease myocardial wall tension => lower myocardial oxygen demand?

A

Calcium channel blockers

88
Q

What drug is given to counter persistent late Na current from LQT3 mutants?

A

Ranolazine. Ranolazine blocks to stubborn Na current.

89
Q

True or false: Ranolazine increases exercise capacity

A

True. Has been abused by athletes.

90
Q

Ca channels dilate primarily on the ____ side.

A

Primarily arterial side. But not exclusively… it’s dose dependent.

91
Q

When do you use ranolazine for angina treatment?

A

It is used as an add-on to standard anti-anginal therapy. It reduces symptoms of chronic stable angina and increases exercise capacity. It can be used as a substitute for beta blockers if they are not tolerated or are contraindicated.

92
Q

Why do Nitrates increase heart rate?

A

Vasodilation lowers BP. Baroreceptors react increasing HR. (reflex tachycardia)

93
Q

Many CCBs have major adverse effects in common. However, Verapamil has a few that are unique to it. What are these adverse effects unique to Verapamil?

A

AV block, CHF, constipation

All effects: Hypotension, Bradycardia, AV blocks, CHF, Constipation

94
Q

Which B-Blocker is nonselective (B1 and B2)?

A

Propranolol

95
Q

Nitrates increase heart rate indirectly because causing vasodilation to lower BP triggers baroreceptors which increase the HR to compensate (reflex tachycardia). Verapamil and diltiazem also decrease BP, but why don’t verapamil and diltiazem increase heart rate?

A

They block directly at L-type calcium channels at the AV node. (Class 4 anti arrhythmic)

96
Q

What is tachyphylaxis?

A

Medical term for building tolerance with exposure

97
Q

Name 3 nitrate vasodilators

A
  1. Isosorbide mononitrate
  2. Nitroglycerin
  3. Isosorbide dinitrate

Cardiovascular (22 decks)

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