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Cardio > Anti-Ischemic Medications > Flashcards

Anti-Ischemic Medications Flashcards

1
Q

what affects myocardial O2 supply?

A 
carrying capacity (hemoglobin content and pulmonary O2 supply)
coronary flood flow volume
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2
Q

What modulates coronary blood flow volume?

A

coronary artery perfusion pressure, compressive forces on coronary artery and intrinsic coronary artery resistance

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3
Q

what is the coronary blood flow volume at its max?

A

ventricular diastole

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4
Q

what is the key mediator of coronary blood flow?

A

NO messenger system at R2

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5
Q

what are some key features of NO?

A

potent arteriolar and venodilator
produced by the endothelium from L-arginine thru activation of eNOS.
diffuses across endothelium and triggers vascular smooth muscle cell relaxation (converts GTP to cGMP) via enzyme guanylate cyclase which decreases Ca2+ concentration

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6
Q

what causes increase in demand?

A

increased HR, contractility and wall stress

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7
Q

what effects myocardial O2 consumption?

A

HR and SBP

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8
Q

how do beta blockers work to treat myocardial ishcemia?

A

B1 adrenergic receptors normally activate Gs –> increased cAMP –> activate L-type Ca2+ channels –> Ca2+ induced Ca2+ channel release from SR –> increased contractility and O2 consumption
Blocking this prevents O2 consumption

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9
Q

Laplace law

A

wall stress = (LVP X LV radius)/2h

h = myocardial wall thickness

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10
Q

what are the different categories of anti-ischemic medications?

A

nitrates
beta-adrenergic receptor antagonists
Ca2+ channel antagonists

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11
Q

where are B1 receptors located?

A

SA node, AV node, His-Purkinge, myocardium, JG apparatus, adipocytes

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12
Q

What does stimulation of B1 receptors do?

A

increased contractility and O2 consumption

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13
Q

Where are B2 receptors located?

A

peripheral and coronary vasculature, bronchi, peripheral muscle, uterine muscle

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14
Q

what does stimulation of B2 receptors do?

A

dilation of peripheral vasculature and relaxation of pulmonary bronchioles

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15
Q

what does antagonism of B2 receptors do?

A

claudication in patients with peripheral vascular disease, coronary vasospasm in patients with vasospastic angina and bronchospasm in patients with reactive airway disease (asthma)

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16
Q

where are alpha receptors located?

A

peripheral circulation

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17
Q

what does stimulation of alpha receptors do?

A

vasoconstriction

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18
Q

what does blocking alpha receptors do?

A

vasodilation and decreased afterload

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19
Q

what are some properties of beta blockers?

A

cardioselectivity –> block beta1 specifically, unless high dose
intrinsic sympathomimetic activity - weak beta agonist that block affects from more potent endogenous catecholamines
alpha adrenoreceptor blocking activity

20
Q

what is the usefulness of the alphaadrenoreceptor blocking activity of alpha receptors?

A

prevents unopposed receptor stimulation, treats hypertension, and increases survival in LV systolic dysfunction

21
Q

what are the adverse effects of nitrates?

A 
Headache and flushing
Hypotension
Hypoxemia
Contraindicated with sildenafil
Methemoglobinemia
22
Q

what is nebivol?

A 
3rd gen beta block (D isomer)
NO donor (L isomer)
cardioselective
23
Q

lipophillic drugs characteristics

A

metabolized by the liver with short t1/2 and crosses BBB

24
Q

hydrophillic drug characteristics

A

metabolized by the kidney with long t1/2 and does not cross BBB

25
Q

what are the adverse effects of beta blockers?

A 
CNS effects 
Conduction abnormalities
CHF
Peripheral vascular disease
Exacerbation of insulin associated hypoglycemia
26
Q

What is the mechanism of action of nitrates?

A

mitochondrial aldehyde dehydrogenase converts nitrates to NO (sulfhydryl group)

27
Q

What are the effects of low dose nitrates?

A

low dose - venodilation, decreased preload, myocardial wall tension, myocardial O2 demand

28
Q

what are the effects of high dose nitrates?

A

arterial vasodilation, which increases blood supply by recruiting collaterals

29
Q

what are contraindications for nitrates?

A

PDE inhibitors because it can lead to hypotension

30
Q

What is the metabolism of nitrates?

A

hepatic

31
Q

what are the categories of calcium channel antagonists?

A

dihydropyridines
benzothiazepines
phenylalkylamine

32
Q

what are adverse effects of calcium channel antagonists?

A 
Hypotension
Exacerbation of CHF
Conduction abnormalities
Edema
Gastrointestinal
Gingival hyperplasia
Increase in cardiovascular mortality?
33
Q

what are dihydropyridines?

A

they are potent vasodilators with little effect on SA node function but may cause reflex tachy cardia
the second generation are more vasoselective

34
Q

How do beta blockers with intrinsic sympathomimetic activity drugs compare to those without ISA?

A

less bradycardia and negative inotropic effect at rest, attenuates exercise induced increases in HR and myocardial contractility
may increase mortality in patients with CAD, therefore not first line

35
Q

how do non-dihydropyridines compare to dihydropyridines?

A

more potent effect on sinus and AV nodal calcium channel recovery –> more pronounced negative chronotropic and dromotropic effects on cardiac conduction system –> symptomatic sinus bradycardia and AV nodal blockade

36
Q

what are benzothiazepines?

A

diatiazem
effect sinus and AV node CA2+ channel recovery –> decreased chronotropic and dromotropic effects –> symptomatic sinus bradycardia + AV blockade
can use with beta blocker and monitor HR and PR interval

37
Q

Phenylalkylamine

A

more potent effects on sinus and AV node Ca2+ channel recovery –> more decreased chronotropic and dromotropic effects
DO NOT use with beta blocker –> increased risk of heart block
monitor HR and PR interval

38
Q

how are calcium channel antagonists metabolized?

A

hepatically except for diltiazem which is hepatically metabolized and renally excreted

39
Q

what drugs increase the bioavailability of Ca2+ channel antagonists?

A

cimetidine (H2 blocker) phenytoin, carbamezapine

40
Q

what drug interaction does diltiazem have?

A

with verapamil it increases bioavailability of cyclosporine

41
Q

what drug interaction does verapamil have?

A

increases serum digoxin and with diltiazem it increases bioavailability of cyclosporine

42
Q

what is ranolazine?

A

its an anti-ischemic drug that may shift metabolism in ischemic myocyte from energy inefficient fatty acid oxidation to glucose metabolism to decrease myocardial O2 demand

decrease myocardial oxygen demand thru prevention of intracellular Ca overload and improvement in diastolic relaxation and wall tension.

43
Q

adverse effects of ranolazine

A

QT prolongation and torsades de pointes

44
Q

what is the metabolism of ranolazine?

A

CYP3A (liver)

45
Q

what are some recommendations of ranolazine use?

A

Contraindicated in pts with liver disease.
Do not use with strong CYP3a inhibitors.
Modify dose with moderate CYP3a inhibitors.
Modify dose with CKD.
Can increase serum digoxin levels.

46
Q

what is the first line drug for myocardial ischemia?

A

beta blockers without ISA

Cardio (6 decks)

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