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CV > 093014 ischemic heart disease pharmacology > Flashcards

093014 ischemic heart disease pharmacology Flashcards

1
Q

how much of oxygen is extracted from bllod traveling through coronary circulation?

A

75%, so to increase oxygen supply you won’t get much from increasing the amount extracted of oxygen

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2
Q

myocardial oxygen supply depends on

A

oxygen content of blood

coronary blood flow (increased demand for oxygen is met by increased coronary flow)

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3
Q

coronary blood flow depends on

A

diastolic perfusion pressure

coronary vascular resistance (in small arterioles)

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4
Q

intrinsic regulation of coronary vascular resistance is accomplished through?

A

LOCAL METABOLITES (adenosine, lactate, etc coming from muscle working hard.

endothelial factors

neural innervation

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5
Q

why does perfusion of coronary arteries increase during diastole?

A

during systole-contraction compresses the coronary arteries

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6
Q

sympathetic intrinsic regulation of coronary vasculture resistance

A

alpha1 receptors-CONSTRICTION
beta 2 receptors-minor dilation

however, sympathetic nervous system is overriden by metabolic (adnosine, lactate, pH) factors regulating vascular resistance and blood flow

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7
Q

the subencodardial plexus is really dependent on what phase of heart contraction?

A

diastole

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8
Q

what factors determine oxygen demand of the myocardium?

A

wall stress (P * r/2h) –h is for wall thickness
contractililty
heart rate

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9
Q

wall stress

A

tangential force acting on the myofibers tending to pull them apart

energy is used to oppose this force

approximated by Laplace’s law

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10
Q

coronary flow reserve

A

the maximal increase in blood flow achievable above normal resting flow

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11
Q

why is subendocardium susceptible to ischemia with a limiting stenosis particularly in the case of exertion?

A

reduced perfusion pressure

elevated LV end diastolic pressure with exertion impedes subendocardial flow

increased HR decreases time during diastole (when the subendocardium receives blood flow)

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12
Q

ECG changes with subendocardial ischemia

A

ST segment depression

T wave inversion

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13
Q

variant angina

A

no overt plaques

intense vasospasm

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14
Q

syndrome X

A

patients with typical signs of angina (related to exertion) who have no evidence of significant atherosclerotic stenoses…likely to due inappropriate constriction of blood vessels

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15
Q

ECG patterns for chronic stable angina

A

during ischemia, ST segment depression and T wave inversion

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16
Q

what can you do to detect chronic stable angina?

A

stress testing:
with exercise
or
with pharamcological agents (dobutamine-increases myocardial oxygen demand. adnosine-causes coronary vasodilation)

17
Q

coronary angiography

A

lesions visualized radiographically after injecting a radiopaque contrast media into artery

18
Q

general principles of anti-angina therapy

A

decrease O2 demand

increase O2 supply

19
Q

medical therapy of stable angina

A

acute episodes (goal is fast relief of discomfort)-stop exercise. fast-acting nitrates (nitroglycerin as sublingual tablet or spray)

prevention (goal is to reduce frequency of angina by decreasing cardiac workload and by increasing myocardial perfusion): 
3 classes of drugs used for prevention-
long acting nitrates
beta adrenergic receptor blockers
calcium channel blockers

prevention of acute cardiac events:
antiplatelet therapy
lipid regulating therapy

revascularization (in some cases)

20
Q

nitrates MOA (for use in angina)

A

in smooth musc, free nitrate is converted to nitric oxide. NO activates guanylyl cyclase, increasing cGMP. cGMP activates cGMP-dependent protein kinase (PKG). PKG phoshphorylates various targets leading to decreased calcium and dephosphorylation of myosin

general vasodilator but much greater effect on venous blood vessels (decreases preload)

is also a coronary dilator–mostly beneficial for vasospasm cases

21
Q

nitroglycerin bioavailability

A

low due to extensive first pass metabolism in liver

22
Q

tolerance of nitrates

A

complete tolerance can develop if used continually for more than few hours (but also reverses rapidly 24 hours of stopping drug)

therefore, should use smallest effective dose and schedule nitrate-free periods (on-off therapy) of at least 8 hours to prevent tolerance

23
Q

side effects of nitrates

A

headache
hypotension
reflex tachycardia
flushing

24
Q

beta adrenergic receptor blockers MOA (for angina)

A

reduce oxygen demand by decreasing force of ventricular contraction and heart rate. decreases BP (afterload)

can increase time in diastole to increase coronary perfusion to increase a bit oxygen supply to ischemic areas

decrease in cardiac output can lead to increase in preload that increases wall tension

both non-selective (propranolol, timolol) and beta1 selective antagonists (metoprolol, atenolol) are effective

not effective for angina due exclusively to vasospasm

25
Q

contraindications of beta blockers

A

used cautiously or avoided in pts with obstructive airway disease

not used in pts with acutely decompensated heart failure

pts with marked bradycardia or certain heart blocks

pts with insulin treated diabetes

26
Q

side effects of beta blockers

A

fatigue, sexual dysfxn

27
Q

calcium channel blockers MOA

A

antagonize voltage gated L-type calcium channels

28
Q

dihydropyridines MOA

A

potent vasodilators (preferentially dilate arteries)-so decreases afterload and vasodilates coronary arteries

potent for relief of vasospasm

29
Q

ex of dihydropyridines

A

nifedipine

amlodipine

30
Q

non-dihydropyridines MOA

A

vasodilators but less potent than dihydropyridines (dilate peripheral and coronary arteries)

relieve ischemia primarily by decreasing HR and contractility

31
Q

examples of non-dihydropyridines

A

verapamil,diltiazem

32
Q

side effects of calcium channel blockers

A 
headache, flushing
decrease contractility
bradycardia
edema
constipation
33
Q

ranolazine

A

decreases frequency of anginal episodes and increases exercise capacity

believed to inhibit late sodium current in cardiac myocytes

34
Q

medical therapy to prevent acute cardiac events

A

antiplatelet therapy

lipid regulating therapy

35
Q

revascularization by can done by

A

PCI-angioplasty

coronary artery bypass graft surgery

CV (34 decks)

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