Antianginals Flashcards

1
Q

T/F During the cardiac cycle, the major blood flow to the heart itself occurs during diastole.

A

TRUE

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2
Q

What are the 2 major determinates of coronary blood flow?

A

(1) Oxygen demand

(2) Oxygen supply

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3
Q

What are the 3 components associated with Oxygen demand?

A

(1) Heart Rate
(2) Contractility
(3) Preload, Afterload

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4
Q

What are the 4 components of Oxygen supply?

A

(1) Coronary patency
(2) Diastolic BP
(3) Blood O2 capacity
(4) Collateral circulation

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5
Q

T/F When there is an increase in O2 demand, there is sufficient O2 supply in the body to meet it.

A

FALSE; The demand outweighs the supply (O2 demand > O2 supply)

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6
Q

What are the 3 types of Angina Pectoris?

A

(1) Typical (stable)
(2) Varient (Prinzmetals)
(3) Atypical (unstable)

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7
Q

What happens during stable angina pectoris?

A

(1) Fixed atherosclerotic narrowing- fixed, stable buildup in the artery
(2) Heavy substernal discomfort
(3) Nitroglycerin

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8
Q

What happens during varient angina pectoris?

A

(1) Coronary vasospasm

(2) Discomfort at rest

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9
Q

what happens during unstable angina pectoris?

A

(1) Atherosclerotic plaque rupture, thrombosis

(2) Discomfort with stress or rest

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10
Q

What are the 3 Nitrates?

A

(1) Nitroglycerin
(2) Isosorbide mono
(3) Isosorbide dinitrate

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11
Q

What do nitrates do?

A

Smooth muscle dilator (veins > arterioles)

(1) Selective venodilator: decrease venous return (preload)= decreased ED pressure, volume= decreased tension and decrease O2 demand
(2) Small decrease in PR: decreases afterload= decreased O2 demand
(3) Coronary dilation: increase total blood flow and increase O2 supply

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12
Q

What dose do you give when giving nitrates? Why?

A

A small to moderate dose; it will become a selective venodilator if you use low doses and if you use a high dose you will significantly decrease the PR which will stimulate a reflex tachycardia (which will increase O2 demand)

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13
Q

Is coronary dilation transitory? What does that mean?

A

Yes; it means that the coronary dilation only lasts for a minute or two and then slowly goes back to how it was previously before the drug was administered.

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14
Q

What is the major antianginal effect of nitrates?

A

The decrease in venous return (i.e. the decrease of preload to the heart)

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15
Q

What is Nitroglycerin’s mechanism of action?

A

It is a nitric oxide donor that stimulates more production of NO that in turn leads to relaxation in the smooth muscle cell.

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16
Q

When are nitrates used?

A

Acute stable

and variant angina

17
Q

How is NG taken? What is it for?

A

(1) Sublingual- stopping an acute attack
(2) Ointments (prophylaxis)
(3) Transdermal- (prophylaxis) reduce frequency and severity of attacks

18
Q

Why can’t NG be taken orally?

A

It has 100% first-pass metabolism

19
Q

How is Isosorb mono-dinitrate taken? What is it for?

A

Orally; for prophylaxis: reduces frequency and severity of attacks

20
Q

What are the limitations of nitrates?

A

(1) They will produce a tolerance: chronic exposure will lead to loss of effectiveness- need a 8-12 hr free period every 24 hours to combat this
(2) headache, hypotension, tachycardia (with high doses)

21
Q

What are the beta blockers?

A

Propranolol, Metoprolol

22
Q

What do beta blockers do?

A

(1) Reduces cardiac sympathetic effects: decrease HR, contractility, which decreases O2 demand

23
Q

When are beta blockers used?

A

Prophylaxis which decreases the severity and frequency of stable angina

24
Q

Why are beta blockers not used for variant angina?

A

because they are not very active against it; in variant angina you have coronary vasospasm and if you use a non-selective beta blocker you are going to block the dilating receptors which can potentially make the angina worse

25
Q

What do beta blockers do when taken post MI?

A

reduces mortality; you have increased sympathetic drive to the heart post MI leading to an increased risk of ventricular arrhythmias. The beta blocker will reduce the propensity of getting another MI.

26
Q

What are the adverse effects of beta blockers?

A

(1) cardiac suppression
(2) Rebound effect: if you give a beta blocker chronically and then take them off, you have to lower the dose little by little for the beta receptors will go back to normal (receptors are increased with chronic use)

27
Q

What are the precautions of beta blockers?

A

(1) Asthma
(2) Diabetes
(3) Heart failure
(4) Peripheral vascular disease

28
Q

What are the calcium channel blockers?

A

Verapamil, Diltiazem, Nifedipine

29
Q

What do calcium channel blockers do?

A
  • Blocks Ca entry into cells (L-type Ca channels)
    (1) Smooth muscle: N>V>D: decreases afterload which decreases O2 demand; decreases coronary resistance which increases O2 supply
    (2) Cardiac muscle: V>D»N (little effect);
    • V,D: decrease HR, contractility, and decrease O2 demand
    • N: reflex tachycardia
30
Q

Why does Nifedipine produce a reflex tachycardia?

A

it does not effect Ca channels in the heart, just the smooth muscle so that if you vasodilate too much you’re going to have a baroreceptor sympathetic reflex tachycardia.

31
Q

What are the uses of Ca channel blockers?

A

Mostly for variant angina, also for stable anging (used as prophylaxis)

32
Q

What are the limitations of Ca channel blockers?

A
  • V/D: hypotension, bradycardia, decrease CO

- N: hypotension, tachycardia

33
Q

What are the antiangina combinations?

A

(1) Nitrates and beta blocker
- decrease O2 demand and blunts reflex tachycardia
(2) Nitrates and Ca-blocker (V/D)
- V/D: decrease O2 demand and increase O2 supply
(3) Beta blocker and Ca blocker (N)
- N: blunts reflex tachycardia

34
Q

Why would you be in caution to combine nitrates and Nifedipine? Beta blocker and V/D?

A

(1) because you can get hypotension which will lead to a reflex tachycardia (neither drug work in the heart)
(2) because if you put 2 drugs that will blunt reflex tachycardia you have potential for enhanced cardiac suppression (both the drugs work in the heart)