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Flashcards in Antianginals Deck (45):

3 triggers for angina

1. Physical exertion
2. Mechanical stress
3. Increased contractility, pulse rate and BP


What is angina?

Pain when the heart becomes anoxic (oxygen deprived)


When does anginal pain occur most often?

- At nighttime - midnight to 8 am.
Clusters of chest pain for months followed by weeks with no symptoms


What things might be a trigger for angina?

- Stress
- Cold
- Hyperventilation


Describe Typical (exertional) angina

- Coronary arteries not able to transport enough oxygen to meet myocardium demand
- Oxygen imbalance causes ischemia
- Stress, exertion, eating, etc. (block flow of blood)
**If demand exceeds available oxygen, then necrosis occurs = myocardial infarction


Describe the amount of alpha and beta receptors in a normal coronary artery

When they are normal, mainly beta 2 receptors are present.


Epinephrine acts on what receptor and has what effect?

- Acts on both beta 2 and beta 1.
- On beta 2, it causes vasodilation ( improves bloodflow to heart)
- On beta 1, it increases demand of the heart


Individuals with variant angina have what type of receptors in their coronary arteries?

They have more alpha 1 receptors than beta 2 receptors = vasoconstriction


What is the effect of having more alpha 1 receptors in coronary arteries than beta 2 receptors?

- Epinephrine usually increases heart rate and cardiac output but with the amount of alpha 1 receptors, also vasoconstricts the coronary arteries, reducing amount of blood delivered to heart.
- Results in lack of oxygenation due to vasospasm


EKG diagnosis of variant angina consists of what?

Elevated S-T segment which is not present in normal angina


What general categories of drugs may be used in treatment of unstable angina?

1. Nitrates
2. Beta blockers
3. Calcium channel blockers
4. Antiplatelet drugs
5. Antithrombin therapy


Nitrites and Nitrates cause what?

- Relaxation of all smooth muscle
- Results in arterial and venous vasodilation
- Drugs work on endothelial cells that produce nitric oxide


What is the biochemical process behind the action of nitrites and nitrates

Nitric Oxide activates guanylyl cyclase which converts GTP to cGMP, which then causes dephosphorylation of light chain myosin (2nd messenger system)


4 general effects caused by nitrites and nitrates

1. Produce vasodilation
2. Decrease venous return to the heart (decrease preload)
3. Decreased work
4. Decrease O2 demand


Side effects of Nitrites and Nitrates

1. Vasodilation = intense and fast = causes headache
2. Weakness, dizziness
3. Flush
4. Postural hypotension and syncope = accentuated by alcohol
5. Reflex sympathetic activity - tachycardia and increased peripheral resistance
a. Beta blockers are used to keep tachycardia under control
6. Rash
7. Nitrates oxidize hemoglobin to methemoglobin
8. Large doses of nitrites/nitrates for long-term use decreases oxygen-carrying capabilities


What might be the problem arising from nitrates being able to oxidize hemoglobin to methemolgobin?

Blood no longer carries oxygen well! Bad for someone who is experiencing angina


Route of administration for nitrites and nitrates

1. Sublingual
2. Topical
3. Oral
4. Transdermal


Describe the onset, duration, and purpose for amyl nitrate

1. Onset


Purpose of Nitroglycerin:

Rescue drug = in office emergency kit


How is nitroglycerin administered and what is its onset?

- Administered sublingually and absorbs through mucosa
Onset: 1-3 minutes


If needed to give in case of emergency, what is the sequence of administration

Pill or metered dose spray sublingually = wait 5 minutes; re-administer up to 3 doses, then 911


Why is nitroglycerin stored in a small brown vial?

It is photosensitive


T or F, Nitroglycerin is only offered as a very rapid onset short term situational drug.

False, there is also a transdermal patch that has a longer duration (up to 12 hours). Used as part of a long-term therapy


Name the long-acting nitrates

1. Isosorbide dinitrate
2. Isosorbide mononitrate


Isosorbide dinitrate onset and duration of action

- Onset = 2-10 minutes
- Sublingual tablet = 1-2 hour duration
- Oral tablet = 4-6 hours


Isosorbide mononitrate onset and duration of tablet

- Onset = 30-60 minutes
- Oral tablet = half life of 4 hours


Indications for Beta Blockers:

Indicated for all acute coronary syndromes


General mode of action for Beta blockers

- Decrease workload of the heart by decreasing cardiac output (afterload) and arterial pressure, which decreases venous return, decreases preload and decreases oxygen demand
**Decreased oxygen demand decreases angina


T or F, Beta blockers do not cause vasodilation



Patients with what medical history will ALWAYS be taking beta blockers? Why?

- Patients with history of myocardial infarction
- They have been shown to decrease mortality after MI
Also, increase chance of surviving second heart attack


5 side effects of beta blockers

1. Bradycardia
2. Contraindicated in some forms of congestive heart failure
3. Contraindicated for variant angina
4. Bronchial constriction/Asthma attacks


T or F, Beta blockers are contraindicated for variant angina and typical angina

False, contraindicated for variant but ok for typical


Why are beta blockers contraindicated for variant angina?

Patient does not have enough beta receptors in coronary arteries, then if block, vasospasm = more angina


Nonselective beta blockers are contraindicated in what patients?



Cardioselevtive beta blockers are preferred for what patients?

- Insulin-dependent diabetics
- Asthmatics


Beta blockers are often combined with what anti-hypertensive drug?

Diuretic to prevent sodium retention


Cardioselective effects of beta blockers are achieved at what level of dosage?

- Low doses
Lost at high doses


Oral care considerations with beta blockers

1. Non-selective beta blockers enhance the pressor response to epinephrine: hypertension and reflex bradycardia
2. OK to use epinephrine with cardioselective agents
3. NSAIDS may reduce effects of beta blockers when used for >3 weeks
4. No precautions needed with short term NSAID use


T or F, Calcium channel blockers have a positive inotropic effect

False, Negative inotropic effect


Biochemical action of calcium channel blockers

Block Ca+ entry into the myocardial cell = less Ca+ inside of the cell maintains troponin's inhibitory effects by decreasing contraction of the heart


Why use a calcium channel blocker in an antianginal scenario?

- Because the heart does not speed up, no pain from angina.
- Some of these drugs cause smooth muscle relaxation of coronary arteries = vasodilation.
- Decreases contraction of the heart


Which calcium channel blockers decrease force of contraction of myocardium:

1. Verapamil
2. Diltiazem


Which calcium channel blockers vasodilate coronary arteries to improve myocardial oxygenation



Which calcium channel blockers vasodilate peripheral arteries and veins, decreasing afterload and preload, which reduces the work of the heart?

1. Nifedipine
2. Nicardipine


Oral care considerations with antianginals?

1. Limit extend of procedures per visit
2. Limit epinephrine in local anesthesis to 2 cartidges
3. Consider local anesthetics without vasoconstrictor
4. Remember gingival hyperplasia with some calcium channel blockers