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D&T3 Cardiology > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

Describe the general mechanism of vasodilators (in regards to arterial and venous)?

A

Arteriodilation –> Decreased TPR –> Decreased BP

Venodilation –> Decreased CO –> Decreased BP

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2
Q

What is the normal physiological response to decreased BP?

A
  1. Increase Sympathetic Activity –> Increased CO and PR –> Increased BP
  2. Increase Renin –> AII –> Increased Aldo –> Increased Na+ and H2O –> Increased Blood Volume –> Increased BP
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3
Q

Angiotensin II stimulated what?

A

Aldosterone and NE

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4
Q

What are the classes of Vasodilators?

A
  1. Ca Channel Blockers
  2. K Channel Openers
  3. Guanyly Cyclase Activators
  4. Phosphodiesterase Inhibitors
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5
Q

What are the Ca Channel Blocker drugs?

A
  1. Dihydropyridines
    • Amlodipine
    • Other drugs ending in pine
  2. Non-Dihydropyridines
    • Verapamil
    • Diltiazem
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6
Q

What is the MOA of Ca Channel Blockers?

A

Decrease Ca++ Influx through L-Type Ca++ Channels

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7
Q

What are the vascular and cardiac effects of Ca Channel Blockers?

A
  1. Arteriodilation –> Decreased TPR –> Decreased BP
  2. Inhibition of Phase 2 of AP in Cardiac Muscle Cells (Decreased Ca++ available for contraction in the heart musculature)
  3. Inhibition of Phase 0 of AP in SA and AV nodes (results in slower HR due to SA and decreased conduction due to AV block)
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8
Q

What is the order of effectiveness of the Ca Channel Blockers in terms of CARDIAC effects?

A

Verapamil > Diltiazem > DHPs (Amlodipine)

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9
Q

Which Ca Channel Blocker has the most potent vascular effect?

A

Amlodipines (And other DHPs)

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10
Q

Describe the metabolism of Ca Channel Blockers?

A

Hepatic Metabolism

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11
Q

Describe the pharmacokinetics of Ca Channel Blockers

A
  1. Effective orally

2. qd (1/day) or bid dosing

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12
Q

What are the therapeutic uses of Ca Channel Blockers?

A
  1. Angina
  2. Supraventricular Tachyarrhythmias
  3. HTN
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13
Q

How do Ca Channels work to treat Angina?

A
  1. Increase Coronary Blood Flow
  2. Decrease Myocardial Oxygen Consumption
    - Decrease Afterload
    - Decrease CO (Verapamil and Diltiazem)
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14
Q

How do Ca Channels work to treat Supraventricular Tachyarrhythmias?

A
  1. Decrease AV Nodal Conduction (Verapamil) and control rate in A flutter and fib
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15
Q

How do Ca Channel Blockers work to treat HTN?

A
  1. Decrease TPR
  2. Decrease CO (Verapamil and Diltiazem)
    * *The decrease in BP only results in mild increase in HR b/c these drugs have effects on the heart
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16
Q

What are common adverse effects of Ca Channel Blockers?

A
  1. Hypotension (worse with DHPs)
  2. CHF
  3. AV Block (Not with DHPs)
  4. Edema (Worse with DHPs)
  5. Headaches
  6. Constipation (Verapamil only)
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17
Q

What are the contraindications and precautions of Ca Channel Blockers?

A
  1. Avoid Short Acting Agents
  2. Severe Hepatic Dysfxn
  3. LV Dysfxn (Verapamil and Diltiazem)
  4. Hypotension
  5. AV Block (Verapamil and Diltiazem)
  6. Sick Sinus Syndrome (Verapamil and Diltiazem)
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18
Q

With which drugs do Ca Channel Blockers have interactions?

A
  1. CYP3A4 Inhibitors
  2. B Blockers (Verapamil and Diltiazem)
  3. Digoxin (Verapamil)
  4. Antiarrhythmic Drugs
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19
Q

Which drug is a K Channel opener?

A

Minoxidil

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20
Q

What is the MOA of Minoxidil?

A

Increase K+ efflux from vascular smooth muscle –> hyper polarization –> relaxation –> Decreased TPR

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21
Q

What are the effects of K Channel Openers?

A
  1. Potent Arterial Vasodilation –> Decreased TPR

* *Severe compensatory responses (Increases HR, CO and Fluid Retention)

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22
Q

What is Minoxidil used for?

A

Treatment of refractory/malignant HTN

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23
Q

What are the side effects of Minoxidil?

A
  1. Fluid Retention (treat w/ loop)
  2. Tachy (give B-blocker)
  3. Hypertrichosis
  4. Pericardial Effusion/ Cardiac Tamponade
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24
Q

What is the MOA of Guanylyl Cyclase Activators?

A

Activation of Guanylyl Cyclase –> Increased cGMP –> Vasodilation

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25
Q

What are the 3 Classes of Guanylyl Cyclase Activators?

A
  1. Nitroprusside
  2. Organic Nitrates
  3. Hydralazine
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26
Q

What are the effects of Nitroprusside?

A
  1. Arteriodilation (decreased TPR)
  2. Venodilation (decreased CO)
  3. Increase HR (due to reflex from decreasing BP)
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27
Q

Describe the kinetics of Nitroprusside

A

Unstable, with a t1/2 of minutes; IV only

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28
Q

What are the Therapeutic Uses of Nitroprusside?

A
  1. Hypertensive Emergencies
  2. Acute CHF
  3. MI
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29
Q

What is the side effect of chronic Nitroprusside?

A

Thiocyanate/Cyanide Toxicity

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30
Q

How is Cyanide from the breakdown of Nitroprusside converted to the less toxic Thiocyanate?

A

Rhodanase enzyme couples the cyanide with Thiosulfate

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31
Q

What are the symptoms of Thiocyanate Toxicity?

A
  1. Weakness
  2. Nausea
  3. Disorientation
  4. Delerium
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32
Q

What are the symptoms of Cyanide toxicity?

A
  1. Anoxia
  2. Hypoxia
  3. Convulsions
  4. Respiratory Arrest
33
Q

Which Guanylyl Cyclase inhibiting drugs are classified as Organic Nitrates?

A
  1. Nitroglycerin

2. Isosorbide Dinitrate (longer acting)

34
Q

What are the effects of Organic Nitrates?

A

Venodilation&raquo_space;> Arteriodilation

35
Q

What effect is seen with low doses of Organic Nitrates?

A
  1. Venodilation (decreased LVEDV –> decreased SV –> decreased CO)
  2. Reflex causes increased HR and TPR
  3. Mild effect on BP
36
Q

What effects are seen with high doses of Organic Nitrates?

A
  1. Venodilation
  2. Arteriodilation
  3. Increased HR (reflex)
    * *Decreased CO, TPR and BP; Increased HR
37
Q

Where are Organic Nitrates metabolized?

A

Liver; via glutathione-organic nitrate reductase

38
Q

Which drugs have extensive first pass elimination and must be given sublingually, transdermally or via IV?

A

Organic Nitrates

39
Q

What are the therapeutic uses of Organic Nitrates?

A
  1. Angina
  2. CHF ** (use with Hydralizine)
  3. Acute MI
40
Q

What are the adverse effects of Organic Nitrates?

A
  1. Excessive Hypotension (HA, tachy, orthostatic hypotension and angina)
  2. Tolerance
41
Q

Poorly perfused coronary vessels result in what condition?

A

Angina

42
Q

What is the therapeutic use of NO?

A

Hypoxic respiratory failure in neonates with pulmonary hypertension

43
Q

What are the adverse effects of NO?

A
  1. Pulmonary Edema (due to NO2 formation)

2. Hypoxemia upon sudden withdrawal

44
Q

What is the effect of Hydralazine?

A
  1. Arterial Dilation –> decreased TPR and BP; Increased HR
45
Q

How is Hydralazine administered?

A

Orally

46
Q

What is the therapeutic use of Hydralazine?

A
  1. CHF **(good if used with ISDN)

2. Hypertension

47
Q

What are the side effects of Hyrdralazine?

A
  1. Fluid Retention
  2. Tachy
  3. +ANA –> Lupus like syndrome
48
Q

Describe the features of the Lupus Like Syndrome caused by Hydralazine

A
  1. Seen in slow acetylators
  2. No renal involvement
  3. Reversible
  4. Occurs at HIGH doses
49
Q

What is Fenoldopam?

A

A rapid acting IV D1-Receptor Agonist that causes peripheral vasodilation

50
Q

What is the therapeutic use of Fenoldopam?

A

Hypertensive Emergencies

51
Q

What are the adverse effects of Fenoldopam?

A
  1. Hypersensitivity
  2. Tachy
  3. Hypotension
52
Q

What are the PDE Inhibitor Drugs?

A
  1. Sildenafil
  2. Tadalafil
  3. Vardenafil
53
Q

What is the MOA of Sildenafil, Tadalafil and Vardenafil?

A

Inhibit PDE Type 5 –> increased effect of NO –> Increased cGMP –> relaxed muscle in corpus cavernous –> erection and –> relaxed muscle in the lower UT –> urination

54
Q

What is the therapeutic use of the PDE inhibitors?

A
  1. Tx of ED

2. Tx of BPH (Tadalafil)

55
Q

Describe the kinetics of the PDE Inhibitors

A
  1. Given orally

2. Hepatic Metabolism

56
Q

What are the side effects of PDE Inhibitors?

A
  1. Hypotension
    - Contraindications:
  2. Use of Organic Nitrates
  3. Use of alpha-blockers
  4. CYP3A4 interacting drugs
57
Q

What are the effects of Angiotensin II?

A
  1. Vasoconstriction
  2. Increased Aldosterone Secretion –> Na retention
  3. Vascular remodeling
58
Q

The net effect of the RAA system is what?

A

Increasing TPR and BP

59
Q

In addition to converting Angiotensin I –> II, what is the converting enzyme involved in?

A

The breakdown of Bradykinin into inactive products

**More Bradykinin –> Increased PG synthesis –> Cough

60
Q

Dry Cough is associated with what medication?

A

ACE Inhibitors

61
Q

What is the MOA of ACE Inhibitors?

A

Inhibit ACE –> decreased Angiotensin II formation –> decreased Aldo, vasoconstriction, NE, and cardiac remodeling; Increased Bradykinin and PGs

62
Q

What is the net effect of ACE Inhibitors?

A
  1. Decreased TPR
  2. Decreased Na+ and Fluid Retention
  3. Decreased BP
  4. Slightly elevated HR
63
Q

What are the ACE Inhibitor Drugs?

A
  1. Enalapril
  2. Lisinopril
  3. “pril” drugs
64
Q

Which class of drugs are predominantly prodrugs? What are the exceptions?

A

ACE Inhibitors

-Exception- Lisinopril and Captopril

65
Q

Which ACE Inhibitor is metabolized in the liver prior to renal excretion?

A

Fosinopril

66
Q

What are the Therapeutic Uses of ACE Inhibitors?

A
  1. HTN
  2. CHF
  3. Post MI
  4. Diabetic Nephropathy
67
Q

What are the side effects of ACE Inhibitors?

A
  1. Fetopathic Potential
  2. Cough
  3. Hyperkalemia
  4. Renal Failure
  5. Hypotension
  6. Hypersensitivity
68
Q

What are the contraindications and precautions of using ACE Inhibitors?

A
  1. Pregnancy
  2. Bilateraly Renal Artery Stenosis
  3. Hyperkalemia
  4. Hypersensitivity
69
Q

ACE Inhibitors are contraindicated in hyperkalemia, so which conditions would not permit ACE Inhibitor use?

A
  1. Renal Disease
  2. Use of K+ Sparing Diuretics
  3. K+ Supplementation
70
Q

What are the Angiotensin II “AT” Receptor Antagonists?

A
  1. Losartan
  2. Valsartan
  3. “Sartan Drugs”
71
Q

What is the MOA of AT Receptor Antagonists?

A

MOA- competitive antagonism at AT1 Receptors

–> decreased Aldo, vasoconstriction, NE and remodeling

72
Q

What are the net effects of AT Receptor Antagonists?

A
  1. Decreased TPR
  2. Decreased Na+ and Fluid Retention
  3. Decreased BP
73
Q

What are the therapeutic uses of AT Receptor Antagonists?

A
  1. HTN
  2. CHF
  3. Post MI
  4. Diabetes
74
Q

What are the adverse effects of AT receptor Antagonists?

A
  1. Fetopathic Potential
  2. Hyperkalemia
  3. Hypotension
  4. Hypersensitivity
75
Q

What are the contraindications to use of AT Receptor Antagonists?

A
  1. Pregnancy
  2. Renal Artery Stenosis
  3. K+ Diuretics
  4. K+ Supplements
  5. Hypersensitivity
76
Q

What drug is an inhibitor of Renin?

A

Aliskiren

77
Q

What is the use of Aliskiren?

A

HTN

78
Q

What are the general uses of vasodilators and RAA System Inhibitors?

A
  1. HTN
  2. Angina and Ischemia
  3. CHF

D&T3 Cardiology (7 decks)

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