Anti Anginal Drugs

Front 1

Lots of pts after having an angioplasty do or do not still experience persistent ischemia?

Back 1

DO

Front 2

ANgina pectoris

Back 2

due to imbalance between oxygen supply of heart and oxygen demand. leads to ischemia -- which causes pain
- characterized by sudden severe substernal chest pain

Front 3

Acute coronary syndrome in which there is decreased blood supply to the heart can cause
1.
2.
3.

Back 3

1. Angina pectoris
2. MI
3. Sudden death due to fatal arrhythmias

Front 4

Angina pectoris has what type of time course in terms of pain?

Back 4

- STABLE-- Brief sub-sternal pain
- Self-limiting with cessation of precipitating event
- Precipitated by exercise, stress, eating, sex, etc
- May occur at rest or while asleep

Front 5

Unstable angina means

Back 5

pain pattern doesnt occur just b/c of exertion, pattern will change -- MI PENDING!

Front 6

Vasospastic angina aka

Back 6

Printzmetal angina- due to vasospasm, can be drug induced (cocaine) or thyamine deficiency

Front 7

Name the factors determing myocardial O2 demand.
1.
2.
3.
In general how do anti anginals work?

Back 7

1. ventricular stress determined by preload- venous return (vasodilation decreases venous return)
2. heart rate
3. contractility- if you reduce periperal arteriolar resistance will reduce level of contractility necessary

Front 8

Can O2 supply to the heart i.e. blood O2 carrying capacity, CO, SVR, coronary resistance, be affected to a great deal?

Back 8

NO O2 supply to the heart cannot be changed a lot (except through decreasing HR which would increase diastolic time)

Front 9

Are ace inhibitors commonly used to treat angina?

Back 9

No

Front 10

What surgical tx is used for angina?

Back 10

- Percutaneous transluminal angioplasty/ balloon angioplasty/stent.
- CABG- coronary arteyr bypass graft

Front 11

Lots of pts after having an angioplasty do or do not still experience persistent ischemia?

Back 11

DO

Front 12

ANgina pectoris

Back 12

due to imbalance between oxygen supply of heart and oxygen demand. leads to ischemia -- which causes pain
- characterized by sudden severe substernal chest pain

Front 13

Acute coronary syndrome in which there is decreased blood supply to the heart can cause
1.
2.
3.

Back 13

1. Angina pectoris
2. MI
3. Sudden death due to fatal arrhythmias

Front 14

Angina pectoris has what type of time course in terms of pain?

Back 14

- STABLE-- Brief sub-sternal pain
- Self-limiting with cessation of precipitating event
- Precipitated by exercise, stress, eating, sex, etc
- May occur at rest or while asleep

Front 15

Unstable angina means

Back 15

pain pattern doesnt occur just b/c of exertion, pattern will change -- MI PENDING!

Front 16

Which nitrates are used in acute unstable angina (acute MI)? Which nitrates are used preventatively?

Back 16

-Acute: NItroglycerin tablets
- Preventative:
- Erythrityl tetranitrate
- pentaerythritol tetranitrate
- isosorbide dintrate
- isosorbine mononitrate

Front 17

Nitroglycerin is given sublingually and not usually PO b/c?
- Is nitroglycerin a Tx or does it provide just symptomatic releif?

Back 17

there is large first pass effect, so given in other forms to prevent liver access to the med
- Nitroglycerin provides syjmptomatic relief

Front 18

NTG - MOA, PK

Back 18

MOA: Vasodilation mainly of the VEINS over the arteries thus is preload reducer . When denitrated by glutathione S transferase in smooth muscle cells, free nitrite ion is released, then NO activates guanylate cyclase, increasing cyclic GMP. Increased cGMP in sarcoplasmic reticulum leading to relaxation. Prove NO independant of endothelial state-- good even if endothelial injury is severe.
PK: Should not be given orally and has half life of 1.5 minutes. B/c NTG is dependant on sulhydrl containing intermediary, once these sulfahydryl groups are depleted will lead to tolerance. Thus must have 10-12 hr NITRATE FREE period. Transdermal patches are most effective prophylaxis but must be removed for 10-12 hrs). Arteriolar dilation ONLY occurs if NO is given IV otherwise only venous return is seen (i.e. reduced preload)

Front 19

Isosorbide dintrate and isosorbide mononitrate-PK, USE

Back 19

- thse are different from NTG b/c are resistant to hepatic metabolism (first pass).
Use: acute relief of angina, prophylaxis if expecting angina (before you do lawn work), can be used prophylactically long term

Front 20

Nitrates- Tox, CI

Back 20

CI: should not be used with PDE5 inhibitors-- erectile dysfunction meds-- must be nitrate free for 24 hrs before use of these meds
Tox: headache, tachyphylaxis (minimized if remove night time dose)

Front 21

Beta blocker- MOA, Use

Back 21

MOA; beta adrenergic blocker
Use: used prophylactically to prevent angina. Beta blockers are also used to tx htn, cardiac arrhythmias, in pts with essential tremor and to suppress symptoms of hyperthyroidism

Front 22

Which beta blockers are non selective?

Back 22

- carvedilol, propranolol, timolol, nadolol, labetalol, pindolol

Front 23

Which beta blockers are selective for beta 1 receptors?

Back 23

metoprolol, atenalol, acebutolol, betacolol, bisoprolol, and esmolol

Front 24

Beta blockers- MOA, CI

Back 24

MOA: beta adrenoreceptors increase cAMP, beta blockers compete with epi and NE to reduce beta effects.
- decrease HR, resulting in decrease myocardial oxygen demand and increased O2 delivery to the heart, decrease myocardial contractility helping to conserve energy and decrease demand.
CI: if pt has pre-existing vasospasm, b/c beta blocking will lead to unopposed alpha action-- may lead to more vasoconstriction
- obstructive airway disease- relative CI
- heart block
- pts with peripheral vascular diseas
- Raynauds diseae
- diabetes- relative CI-- b/c symptoms of hypoglycemia can be masked- may also decrease insulin
- ABRUPT discontinuation should be avoided b/c will lead to rebound increase in frequency and severity of angina- must titrate pt down from beta blockers

Front 25

Beta blocker- HR goal
Do beta blockers just provide symptomatic relief or do they improve the survival rates?

Back 25

- Hr goal-- KEY PT - adjust dose to reduce resting HR to 55-60 bpm
- also increase in HR should not exceed 75% of HR response associated with onset of ischemia-i.e. if with exercise start experiencing pain at 100 bpm, must adjust beta blocker so that with exercise HR stays at 75 bpm
- beta blockers improve survival rate of pts with recent MI, prevent stroke and CHF in pts with htn

Front 26

Beta blockers- Tox

Back 26

- Cns side effects- when beta blockers are lipophillic- dizzy, fatigue, depression, lethargy, drowsiness, unusual dreams
- impotence, wheezing, dyspnea

Front 27

Propranolol- PK

Back 27

- is non selective, different metabolisms, dose titration very important

Front 28

Atenolol/metoprolol-PK

Back 28

- cardioselective, replaced propranolol. Less frequent dosing and narrower range of dosing
- atenolol- kidney excretion
- metoprolol- inactivated by hepatic metabolism

Front 29

Calcium channel blockers- Use

Back 29

Use: prophylaxis of angina, and prevent second MI. Also used for
- htn,
- SVT
- Raynauds
- prevents cerebral vasospasm following SAH

Front 30

CCBs- MOA

Back 30

- inhibits passage of calcium ions through voltage gated L type calcium channels in cell membranes of heart and vascular smooth muscle. Calcium channels open more slowly than Na channels. Contribute to plateau phase of cardiac AP

Front 31

Nifedipine- PK, Tox, Class

Back 31

- dihyrdropyridines (CCB-also includes amlodopine, and nicardipine)
- PK: short acting, do not change conduction of heart
- Tox: hypotension, dizziness, flushing, nausea, and edema

Front 32

Verapamil- Class, Pk, Tox

Back 32

Class: Phenyalkylamines (CCB)
PK: short and long
Tox: hypotension, Myocardial depression, heart failure, constipation, edema, and bradycardia
- change conduction of heart along with diltiazem, dihydropyridines do not change conduction of heart

Front 33

Diltiazem- Class, PK

Back 33

Class: benxothiazepines (CCB)
PK: short or long
Tox: hypotension, dizziness, flushing, bradycardia, and edema
- change conduction along with verapamil, but dihydropyridines do not change conduction

Front 34

CCBs- effects

Back 34

- relax coronary vascular smooth muscle, useful for coronary vasospasm.
- also can do arteriolar dilatation and decrease afterload
- decrease myocardial contractility
- verapamil and diltiazem decrease cardiac contractility - lack reflex tachycardia-- useful for pts with unstable coronary artery disease
- good for pts with pulmonary problems

Front 35

CCBs- CI, Tox

Back 35

CI: heart failure
- verapamil and diltiazem cannot be given to pts with heart block or bradycardia
Tox: flushing, headache (b/c of vasodilation), ankle swelling, verapamil causes constipation

Front 36

CCBs- Drug Intxns

Back 36

- beta blockers- pharmacodynamic interaction)
- verapamil has significant pharmacokinetic interxn with digoxin increasing its plasma concentration. Check plasma digoxin levels after a week.

Front 37

Aspirin- MOA

Back 37

MOA: inhibits COX-- anti inflammatory and stops platelet aggregation
- improves survival rate in pts w/ AMI and reduces MI risk in pts with stable and unstable angina
- also helps pts with TIA and reduces stroke risk
- decreases risk of thromboembolism in pts with atrial fib and following valve replacement

Front 38

What meds should be give w/ STABLE angina?

Back 38

- want prophylactic tx-
- HTN- monotherapy with CCBs OR beta blocker
- normotensive- monotherapy w/ long acting nitrates
- combo therapy is better
- beta blocker w/ dihydropyridine CCB
- 2 CCBs
- long acting nitrate w/ beta blocker OR CCB
- CABG or angioplasty also possible therapy

Front 39

What meds for UNSTABLE angina?

Back 39

- verapamil more effective than propranolol
- adding nifedipine to beta blocker and nitrate therapy also helpful
- asprin
- IV heparin or thrombolytic agents

Front 40

What meds for vasospastic angina?

Back 40

- nitrates and CCBs most more effective than beta blocker therapy
- all CCbs have sim efficacy
- Beta blocker may worsen
- surgical revascularization and angioplasty NOT indicated