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RC Test 3 > B4.050 Treatment of Angina > Flashcards

B4.050 Treatment of Angina Flashcards

1
Q

etiology of CAD

A

mainly due to obstruction of coronaries by atheromatous plaques

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2
Q

leading cause of death in US

A

heart disease
both women and men
CAD is principle type of heart disease

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3
Q

three major risk factors of CAD

A

high BP
high LDL cholesterol
smoking
49% of americans have one of the three at least

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4
Q

other risk factors of CAD

A 
diabetes
overweight/ obesity
poor diet
physical inactivity
excessive alcohol use
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5
Q

what is angina pectoris

A

primary symptom of heart disease, refers to chest pain resulting from myocardial ischemia

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6
Q

characterize angina pectoris

A

chest pain when amount of blood delivered to heart by coronary arteries cannot supply enough O2 to satisfy myocardial requirement
oxygen need exceeds oxygen supply

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7
Q

for immediate relief of angina

A

organic nitrates (nitroglycerin)

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8
Q

for prophylaxis for angina

A

CCBs and B blockers

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9
Q

describe pain associated with angina

A

severe chest pain described as: strangling, constricting, suffocating, crushing, heavy, or squeezing
chest discomfort may be vague (esp in women) and accompanied by numbing, nausea, sweating, SOB
usually retrosternal; often radiating down left arm though may involve both arms
typically relieved within minutes by rest or w nitro

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10
Q

2 types of angina

A

classic/ atherosclerotic

variant/ angiospastic / prinzmetals

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11
Q

etiology of classic angina

A

atheromatous obstruction of large coronaries

especially present w exercise

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12
Q

treatment of classic angina

A

if uncontrolled by drugs, may require coronary bypass or angioplasty

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13
Q

etiology of variant angina

A

spasm or constriction of in atherosclerotic coronary vessels

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14
Q

treatment of variant angina

A

relieved by nitrates or CCBs

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15
Q

what determines oxygen demand of myocardium

A

cardiac workload:

  1. contractility (major determinant)
  2. HR
  3. wall stress (IV pressure, ventricular volume, wall thickness)
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16
Q

what drugs help with myocardial ischemia?

A

drugs that reduce cardiac size, rate, or force and therefore reduce cardiac oxygen demand
CCBs, B-blockers

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17
Q

what is the main energy source in the heart and why is it significant

A

fatty acid oxidation

required more oxygen than glycolysis

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18
Q

mechanism of trimetazidine

A

shift myocardial metabolism towards greater use of glucose
has potential to reduce O2 demand without affecting hemodynamics
called pFOX inhibitors: partially inhibit fatty acid oxidation

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19
Q

what determines O2 supply

A

O2 delivery

extraction (better when blood speed is slower moving through vessels)

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20
Q

how might additional O2 be supplied to the myocardium

A

ONLY by increasing O2 delivery through coronary blood flow

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21
Q

what are the determinants of O2 delivery through coronary blood flow

A

directly related to perfusion pressure and duration of diastole
inversely proportional to coronary vascular resistance, determined by: metabolic products, autonomic activity, various drugs
damage to endothelium of coronary vessels increases vascular resistance

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22
Q

what are some mechanical interventions that can increase O2 supply

A

stent
angioplasty
coronary bypass surgery

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23
Q

how do CCBs impact vascular tone

A

decrease intracellular Ca2+

Ca2+ needed in pathway to myosin/actin contraction

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24
Q

why does increasing cAMP relax vascular smooth muscle

A

cAMP phosphorylates MLCK which prevents it from phosphorylating myosin light chains allowing them to contract

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25
Q

what drugs increase cAMP

A

B2 agonists

not used in angina

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26
Q

what is the mechanism of action of nicorandil

A

K+ channel opener

prevents depolarization

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27
Q

how does increasing cGMP relax vascular smooth muscle?

A

cGMP dephosphorylates myosin light chains preventing them from relaxing

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28
Q

how does NO work to relax muscle?

A

activator of soluble guanylyl cyclase

guanylyl cyclase is involved in converting GTP to cGMP

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29
Q

how does sildenafil work

A

inhibits PDE5, which normally breaks down cGMP

if you inhibit the breakdown, you have more free cGMP, thus more relaxation

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30
Q

how do organic nitrates, CCBs, and B blockers decrease myocardial O2 demand?

A

decrease

  • HR
  • ventricular volume
  • BP
  • contractility
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31
Q

what is 4th drug group used in angina?

A

recently approved

ranolazine

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32
Q

mechanism of action of ranolazine

A

reduces intracellular calcium concentration and thus reduces contractility and work

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33
Q

mechanism of action of allopurinol

A

inhibits xanthine oxidase (which contributes to oxidative stress and endothelial dysfunction)
high doses prolong exercise time in patients w angina

34
Q

direct bradycardic agent

A

ivabradine

35
Q

mechanism of action of ivabradine

A

inhibit hyperpolarization activated sodium channel in the SA node

36
Q

rho-kinase inhibitor

A

fasudil

37
Q

mechanism of action of fasudil

A

reduce coronary vasospasm in experimental animals

38
Q

where do nitrates primarily work and why

A

venous side

this is where enzymes are primarily found

39
Q

why does sodium nitroprusside act on both veins and arteries

A

doesn’t require enzymes to work

40
Q

what can endogenously release NO

A

endothelial cells

41
Q

what is the mechanism of action of NO

A

activate guanylyl cyclase
GC can then convert GTP to cGMP
CGMP dephosphorylates myosin light chains
relaxation

42
Q

2 types of nitrates

A

short acting 3-60 min

long acting 2-10 hours

43
Q

routes of administration of short acting nitrates

A

inhalant

sublingual

44
Q

routes of administration of long acting nitrates

A 
oral
ointment
buccal
transdermal
chewable
45
Q

4 primary nitrates

A 
amyl nitrite (short only)
nitroglycerin (short or long)
isosorbide dinitrate (short or long)
isosobide mononitrate (long only)
46
Q

other effects of NO

A

erection via relaxation of corpora cavernosa
increased cGMP in platelets decreases aggregation
nitrite ion reaction with hemoglobin can cause methemoglobinemia

47
Q

3 primary mechanisms by which nitrate therapy is beneficial

A
  1. pronounced dilation of large veins to reduce preload, myocardial O2 demand, and cardiac work
  2. redistribution of regional coronary blood flow from normal to ischemic areas due to preferential dilation of large epicardial arteries
  3. mild arteriolar dilation to reduce afterload and myocardial O2 demand
48
Q

harmful effects of nitrates

A

reflex tachycardia and contractility

  • increased myocardial O2 demand
  • reduced perfusion due to shortened diastole
49
Q

how to prevent harmful effects of nitrates

A

add B-blocker of CCB to nitrate administration

50
Q

issue with oral nitrates

A

rapidly metabolized by hepatic reductase

fast acting drugs bypass the liver

51
Q

fastest acting nitrate preparations

A

inhaled amyl nitrite

IV sodium nitroprusside

52
Q

sublingual nitroglycerin pharmacokinetics

A 
used for immediate angina relief
rapid action (onset 1-3 min), short (duration 10-30 min), but not suitable for maintenance or chronic therapy
53
Q

how do you minimize tolerance from nitrates?

A

during chronic treatment use lowest effective dose with nitrate free intervals of 10-12 hrs daily

54
Q

acute nitrate toxicity

A

strong vasodilation resulting in orthostatic hypotension, tachycardia, and throbbing headaches

55
Q

“Monday disease”

A

manufacturers that are chronically exposed to high nitrate levels become tolerant
after a weekend away from nitrates, get headache and dizziness on Mondays bc tolerance diminishes

56
Q

2 important cardio actions of intracellular calcium

A

triggers contraction in myocardium and vascular smooth muscle
required for pacemaker activity of SA node and for conduction through AV node

57
Q

how are Ca2+ channels regulated in heart and vascular smooth muscle

A

opened by stimulation of B receptors to enhance calcium entry
closed by CCBs to inhibit calcium entry

58
Q

which muscles are most sensitive to CCBs

A

vascular smooth muscles, bronchiolar, GI, and uterine

arterioles more sensitive than veins

59
Q

how is CCB tissue selectivity established

A

L-type Ca channel has 3 different binding sites (1A, 1B, 1C)
1A = vascular
1B = combo
1C = myocardial

60
Q

what happens on the molecular level with a CCB binds to a calcium channel?

A

pores close on calcium channel

decrease of transmembrane Ca currents

61
Q

major cardiac effects of CCBs

A

decreased contractility
decreased SA node impulse generation
decreased AV node conduction

62
Q

discuss differences in tissue selectivity and how they impact HR

A

nifedipine (dihydropyridines) strongest vasodilator, verapamil strongest cardiac effects, diltiazem in between
HR increased by nifedipine bc of reflex tachy after vasodilation, HR decreased by verapamil due to SA and AV depression

63
Q

beneficial effects of dihydropyridines

A

coronary vasodilation > increased myocardial O2 supply

vasodilation of systemic arteries > decreased afterload

64
Q

harmful effect of dihydropyridines

A

increased risk of MI
pronounced hypotension > reflex tachy > increased cardiac workload
short acting CCB should be avoided in patients with HTN

65
Q

beneficial effects of verapamil/diltiazem

A

reduced SA automaticity and AV conduction

decreased myocardial contractility and bradycardia > reduced cardiac workload

66
Q

harmful effect of verapamil and diltiazem

A

the potential for serious cardiac depression that could result in
-cardiac arrest
-AV block
-CHF
don’t use in pts with ventricular dysfunction of SA-AV node disturbances

67
Q

other CCB effects

A

inhibition of insulin secretion
interference with platelet aggregation
flushing, edema, dizziness, nausea, constipation

68
Q

how do verapamil and diltiazem enhance digoxin toxicity

A

reduce digoxin renal clearance to increase plasma digoxin

69
Q

B blockers used in angina

A

atenolol
metoprolol
sometimes propranolol, nadolol

70
Q

when are B blockers especially useful

A

management of angina associated with effort

reduce myocardial O2 requirements at rest and during exercise

71
Q

which is better for angina, B blockers or CCBs?

A

B blockers produce better outcomes and symptomatic treatment

72
Q

what have B blockers been shown to do in patents with heart disease

A

reduce mortality in patients with MI

improve survival and prevent stroke in hypertensive pts

73
Q

beneficial effects of B blockers in angina

A

decreased sympathetic activity > decreased contractility, HR, and vasoconstriction > decreased cardiac workload > decreased O2 demand
direct vasodilation by some B blockers
bradycardia prolongs diastole and increases perfusion time

74
Q

harmful effect of B blockers

A

may induce or worsen CHF whenever sympathetic activity is critical to support cardiac performance

75
Q

goals of effective antianginal therapy

A

increase exercise tolerance

decrease frequency and duration or myocardial ischemia

76
Q

which drugs are more effective for variant angina

A

nitrates and CCBs

B-blockers do not dilate spastic coronary blood vessels

77
Q

angina therapy for hypertensive patient

A

monotherapy w slow release CCB or B blocker

78
Q

angina therapy for normotensive patient

A

long acting nitrates

79
Q

most effective drug combos

A 
B blocker + CCB
2 CCBs (vera and nife)
80
Q

how can harmful effects of CCBs or B blockers be avoided?

A

combined treatment w nitrates

RC Test 3 (22 decks)

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