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Pharmacology > Antianginal Agents and Vasodilators > Flashcards

Antianginal Agents and Vasodilators Flashcards

1
Q

What are the major determinants of myocardial oxygen supply

A

coronary blood flow

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2
Q

Direct factors that influence coronary blood flow and ultimately myocardial oxygenation include

A

Directly related to perfusion pressure (aortic pressure)

  1. Blood flows only during diastole (shortened by
    tachycardia)
  2. Blood flow also decreased by increased LVEDP
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3
Q

coronary blood flow and ultimately myocardial oxygenation are inversely proportionate to ___, which is determined by:

A

coronary vascular resistance

  1. Vascular control by metabolites (autoregulation) is
    most important
    - Damage to endothelium can alter ability of
    vasculature to dilate
  2. Neural and humoral control (autonomic activity) of vascular tone has only small effect
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4
Q

coronary blood flow can be increased with what types of meds?

A
  1. nitrates
  2. CCBs
  3. BBs improve regional flow distribution by improving flow to ischemic subendocardial tissue
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5
Q

Major determinants of myocardial oxygen consumption

A
  1. contractile state (myocardial contractility)
  2. HR
  3. myocardial wall tension and stress
    - Preload (venules) - LV volume
    - Afterload (arterioles) - SBP
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6
Q 
Drugs that relax vascular smooth muscle can produce a reflex tachycardia that can increase myocardial oxygen consumption and exacerbate symptoms in anginal patients. Which of the following anti-anginal agents are most likely to cause reflex tachycardia? A.  Diltiazem 
B.  Metoprolol 
C.  Nifedipine 
D.  Nitroglycerin
E.  Verapamil
A

C.  Nifedipine– also really lowers systolic pressure/afterload
D.  Nitroglycerin– also really lowers LV volume/preload

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7
Q

What meds can you use to decrease HR and cardiac contractility in order to decrease O2 demand?

A

BB

some CCBs

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8
Q

how can you decrease preload or afterload inorder to decrease myocardial wall tension and ultimately decrease myocardial O2 demand?

A

decrease preload w/ nitrates

decrease afterload w/ CCBs (Nifedipine)

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9
Q

Angina is most often due to

A

atherosclerotic obstruction of large coronary vessels that result in decreased blood supply

*imbalance between O2 requirement of heart and oxygen supplied to it by coronary vessels

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10
Q

In variant angina, there are no overt plaques but intense vasospasms. Vasocontriction causes supply ____.
Therefore treatment is aimed at ___

A

decrease

preventing vasospasm

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11
Q

in unstable angina, there is plaque rupture, platelet aggregation, thrombus formation, unopposed vasoconstriction. Thrombus forms and supply ___. Therefore treatment is aimed at ___

A

decreases

reducing thrombosis, decreasing demand which increases supply

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12
Q

In stable angina, the lumen is narrowed by plaque and there is inappropriate vasoconstriction. This results in demand ___. Therefore treatment is aimed at __

A

increase

decreasing demand, which increases supply

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13
Q

What meds are used to treat stable angina?

A

BBs
nitrates
CCBs

*decrease demand= increase supply

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14
Q

What meds are used to treat unstable angina?

A
  • anti-platelet agent
  • anti-coagulant
  • BB
  • nitrates
  • CCBs

*reduce thrombosis, decrease demand= increase supply

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15
Q

What meds are used to treat variant angina?

A

(vasodilators)
Nitrates
CCBs*

*prevent vasospasm AND increase O2 supply

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16
Q

Primary prevention of angina includes

A
  1. RF modification and amelioration:
    - tx HTN
    - stop smoking
    - initiate HMG-CoA reductase inhibitors (statin) to tx dyslipidemia
    - glycemic control in DM
  2. Anti-platelet therapy
    - ASA (low dose)
    - if GI bleed on low dose ASA, then add PPI
    - If allergy to ASA, then clopidogrel
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17
Q

The goal of pharmacotherapy in the treatment of angina is to:

A

restore the balance between O2 demand and O2 supply by increasing supply or reducing demand

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18
Q

One can improve coronary blood flow (MBF) primary intervention ____ or pharmacologically with ___

A

primary: CABG or PCI

Pharmacologically: vasodilators

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19
Q

Reduction of myocardial oxygen requirement (MVO2) is achieved pharmacologically with the use of what drugs?

A
  • vasodilators (nitrates or CCBs)

- negative inotropic and chronotropic agents

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20
Q

What is the chronic pharmacological therapy for stable angina?

A

Reducing oxygen demand with:

  • nitrates,
  • CCBs
  • β-blockers
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21
Q

Imbalance occurs as O2 supply decrease due to reversible coronary artery vasospasm (associated w/ atheromas), commonly at rest

A

Variant angia

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22
Q

What is acute pharmacotherapy for ACS/unstable angina?

A
  1. antiplatelet-anticoagulant, surgery, fibrinolytics for CLOT– use ASA, heparin, PGIIB-IIIA inhibitors, PTCA/CABG
  2. use BB for arrhythmias
  3. tx pain w/ NTG, morphine
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23
Q

What meds do you use for post MI therapy?

A
  1. ACEIs
  2. Statin
  3. BB
  4. ASA
  5. Clopidogrel (if post stent)
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24
Q

Examples of Nitrate Vasodilators

A
  1. Isosorbide Mononitrate (Ismo®) - PO
  2. Nitroglycerin (Nitrostat®) – IV / SL / TD
  3. Isosorbide dinitrate (Isordil®) - PO
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25
Q

name 5 CCBs

A
  1. verapamil (Isoptin)
  2. diltiazem (Cardizem, Cardia XT)
  3. nifedipine (Procardia)
  4. Felodipine ER (Plendil)
  5. Amlodipine (Norvasc)
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26
Q

describe the mechanism of nitrates

A

Nitrate turns into NO in/at vascular SmM–> activates Gcyclase–> increases GTP to cGMP–> relaxes smooth muscle (vasodilates)

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27
Q

describe the mechanism of CCBs

A

Blocks Ca2+ entryin L-type Ca2+ channels so it cannot bind calmodulin–> does NOT activate MLCK–> decrease myosin-PO4—> increase relaxation/dilation

*vascular SmM is most sensitive (arterioles>veins)

28
Q

What are the primary and secondary effects of nitrates

A

results in reduction in LVEDP (PCWP) and systemic vascular resistance

Primary: decrease wall tension –> decreased
myocardial O2 demand

Secondary: improves perfusion of ischemic myocardium

29
Q

best route of nitro for rapid achievement of therapeutic levels is ____

A

sublingual

  • rapid pain relif in 45sec-5 min
  • can repeat 3x every 5 min
30
Q

describe the PK of nitrates

A
  1. poor oral F (high first pass effect therefore needs higher dose)
  2. half life: 2-8 min (rapid denitration in liver)
31
Q

describe the transdermal administration of nitro

A

once daily dosing initially effective for 24 hrs

32
Q

what nitrate product has the longest and shortest duration of action

A

Longest: transdermal patch (over 8 hrs)

Shortest: IV (3-5 min)

33
Q

What is the onset and duration of isosorbide mononitrate

A

onset: 30-60 min
duration: 6-8 hrs
* given 20mg PO BID

34
Q

What is first line nitro therapy for acute angina

A

sublingual tablet or translingual spray

35
Q

What nitro preparations and meds are used for prophylaxis chronic angina (2nd line therapy)

A

long-acting oral, topical, transdermal (long term utility is limited by potential for tolerance development)

can be added to BB if initial treatment not successful or used as monotherapy if BB are contraindicated or caise side effects

36
Q

how can nitrates be used for variant angina

A

long-acting oral, topical, transdermal are second line to CBBs (effective, less desirable due to tolerance development)

*drug of choice to abort or shorten episode- given sublingually

37
Q

uses of nitrates

A
  1. acute angina
  2. prophylaxis for chronic angina
  3. variant angina
  4. control of BP in perioperative HTN
  5. in CHF associated w/ acute MI (IV nitro “unloads” damaged heart)
38
Q

adverse reactions of nitrates

A
  1. Throbbing headache (30-60%)
  2. Orthostatic hypotension (over than 10-15 mm drop in BP)
  3. Reflex tachycardia
  4. Facial flushing
    - -direct extension of therapeutic vasodilation
  5. tachyphylaxis w/ continuous exposure (tolerance)
39
Q

how can one prevent tachyphylaxis that can occur w/ continuous exposure to nitrates?

A

Nitrate free interval of 6-14 hours each day is recommended

40
Q

What are drug-drug interactions with nitrates?

A
  • Phosphodiesterase inhibitors
  • do not use if sildenafil or vardenafil within the previous 24 hours or tadalafil within 48 hours.

*Nitrates may cause severe hypotension refractory to vasopressor agents

41
Q

describe how different CCBs have selectivity for vascular vs Heart Ca2+ channesl

A

Dihydropyridines (nifedipine): greater ratio of vascular (relaxation) effects

Verapamil and diltiazem: prominent effects at cardiac nodal tissue (phase 0 at SA and AV node– suppression of SA/AV node) and on cardiac muscle (phase 2– suppression of contractility)

42
Q

rate the CCBs (verapamil, diltiazem, dihydropyridine) in order from most to least effect for:

  • vasodilation
  • negative inotropic effect
  • suppress AV node conduction
A
  • vasodilation: Dihydropyridine, diltiazem, verapamil
  • negative inotropic effect: verapamil, diltiazem, dihydropyridine (0 to +)
  • suppress AV node conduction: verapamil, diltiazem, dihydropyridine (0)
43
Q

Major adverse side effects of verapamil

A
  1. hypotension
  2. bradycardia, AV block*
  3. CHF*
  4. constipation***
44
Q

Major adverse side effects of Diltiazem

A
  1. hypotension
  2. peripheral edema
    - -due to vasodilation
  3. bradycardia
45
Q

Major adverse side effects of dihydropyridines (amlodipine, nifedipine)

A
  1. hypotension
  2. HA, flushing
  3. peripheral edema

*all due to vasodilation

46
Q

Short-acting dihydroyridines often have what effect?

A

rapidly lower BP –> reflex
activation of the SNS –> tachycardia, exacerbation ofangina and increased risk for MI

AVOID USE!!

47
Q

____ formulations of dihydropyridines–> fewer symptomatic side effects - reduced likelihood of angina if medication is suddenly withdrawn

A

Longer acting dihydropyridines and extended-release

48
Q

describe the oral bioavailability of CCBs

A
  • varies widely
  • extensively protein bound
  • metabolized by cP450–> plasma levels fluctuate if administered with inhibitors or inducers
49
Q

Uses of CCBs

A
  1. angina
  2. prophylaxis for chronic stable angina: long agents recommended if BB are contraindicated or poorly tolerated)
  3. variant angina (1st line over nitrates)
  4. arrhythmias
  5. HTN
  6. subarachnoid hemorrhage
  7. inhibition of premature labor
50
Q

how do CCBs help with angina

A

results in long-lasting decrease in SVR–> decrease in myocardial O2 requirement and coronary arterial tone (aiding in spasm-induced angina)

51
Q

Adverse reactions of CCBs

A
  1. cardiac depression (more w/ verapamil or diltiazem)– cardiac arrest, brady, AV block, CHF
  2. flushing
  3. edema
  4. dizziness (esp. -dipine class)
  5. nausea
  6. constipation (more common w/ verapamil)
  7. Gingival hyperplasia possible
52
Q

List the nonselective BB, cardioselective BB, and vasodilating BB

A

Nonselective (B1 and B2): propranolol

B1 selective (cardioselective): metoprolol, atenolol
*NOT absolute B1 selectivity- dose dependent

A1, B1, B2 (vasodilating)- labetalol, carvedilol

53
Q

Describe the mechanism of action of beta blockers in angina

A
  1. Useful in stable angina due to hemodynamic effects that decrease O2
    requirements (during rest and exercise)
  2.   Decreased HR, BP, and contractility
    2.  Can block reflex tachycardia associated with use of nitrate
    vasodilators in chronic stable angina

**NOT vasodilators, thus no role in variant (vasospastic) angina

54
Q

NOT vasodilators, thus no role in variant (vasospastic) angina

A

beta blockers

55
Q

Can block reflex tachycardia associated with use of nitrate

vasodilators in chronic stable angina

A

beta blockers

56
Q

Uses of beta blockers in angina

A
  1. prophylaxis for chronic stable angina– 1st line therapy (cardioselective preferred ie. metop. atenol.)

**Not for variant angina as it may increase tendency for vasospasm due to unopposed (by block of B2 vasodilation) A1 vasoconstriction

57
Q

What is the only antianginal angent proven to prevent infarction and improve survival in MI patients

A

beta blockers

58
Q

What are contraindications for beta 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
59
Q

describe the mechanism of action of Ranolazine

A
  1. In ischemia, 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
  2. Ca++ overload can result in both mechanical dysfunction (increased diastolic tension) and further imbalance between O2 demand and supply
  3. Ranolazine inhibits this late Na+ current
60
Q

Ranolazine inhibits the late Na+ current and prevents

A

intracellular Ca2+ overload which can lead to:

  • ischemia and
  • hypertrophy
  • mechanical dysfunction (increased diastolic tension)
61
Q

describe the PK of Ranolazine

A
  1. high variability in absorption
  2. hepatic elimination
  3. administer 2x daily
62
Q

Adverse reactions of Ranolazine

A
  1. prolong QT interval
  2. bradycardia
  3. hypotension
  4. palpitations
  5. edema

*minimal hemodynamic effects relative to other anginal agents

63
Q

Use of ranolazine for angina

A
  1. chronic stable angina add-on to standard anti-anginal therapy– reduces sx and increases exercise capacity
  2. can substitute for BB if no tolerated or contraindicated

*No effect on HR or BP

64
Q

What anti-anginal nitrate agents requires a
drug free interval each day to lessen the development
of tolerance to its antianginal actions?

A

oral nitrates (isosorbide dinitrate)

65
Q

Primary target is relaxation of venous capacitance vessels leading to a reduction in preload and a reduction in myocardial oxygen demand. The action to dilate coronary artery vessels, resulting in an increase in myocardial oxygen supply, plays a greater role in variant angina.

66
Q

Primarily reduces vasoconstriction in both coronary and noncoronary vessels, increasing coronary blood flow and reducing cardiac afterload (all classes).

Pharmacology (31 decks)

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