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CV II Exam 3 > Anti-anginal agents > Flashcards

Anti-anginal agents Flashcards

1
Q

Chronic coronary artery disease medications

A 
Aspirin
B blockers
Nitrates
CCBs
ACEIs
Ranolazine
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2
Q

Acute coronary syndrome medications

A

Aspirin
B blockers
Nitrates

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3
Q

If patient has unstable angina or NSTMI add medications

A 
Heparin
Gp IIa-IIIb antagonist
ADP receptor antagonist
or
Bivalirudin
ADP receptor antagonist
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4
Q

If patient has STMI with thrombolysis add medications

A

Thrombolytic agent
Heparin
ADP receptor antagonist

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5
Q

If patient has STMI with angioplasty add medications

A 
Heparin
Gp IIa-IIIb antagonist
ADP receptor antagonist
or
Bivalirudin
ADP receptor antagonist
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6
Q

Post MI medications

A

Statin
ACEI
Aldosterone receptor antagonist

Continue aspirin and ADP receptor antagonist

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7
Q

Angina pectoris

A

Primary symptom of ischemic heart disease

Temporary and reversible imbalance between myocardial O2 supply and demand

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8
Q

Usual underlying cause of angina

A

CAD

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9
Q

Increase demand on heart seen with

A

Increase HR, ventricular contraction and wall tension

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10
Q

Decrease O2 supply seen with

A

Decrease coronary blood flow, and O2 carrying capacity of blood (or both)

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11
Q

How does angina feel to patient?

A

Heavy pressing substernal discomfort

Often radiating to left shoulder, flexor aspect of left arm, jaw, or epigastrium

Women, elderly, and diabetes most likely to have atypical symptoms

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12
Q

Typical angina

A

Usually fixed atherosclerotic narrowing of an epicardial coronary artery on which exertion or emotional stress superimposes an increase in myocardial O2 demand

Angina induced by exercise, relieved by rest and/or nitro and lasts no longer than 15 min with 5 - 15 episodes per week

ST segment depression

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13
Q

Atypical angina

A

Angina at rest
Also called Variant, Vasospastic, or Prinzmetal’s
Focal or diffuse coronary vasospasm episodically reduces coronary flow
Transient ST segment elevation during angina

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14
Q

Unstable angina

A

Rupture of an atherosclerotic plaque, with consequent platelet adhesion and aggregation leading to decrease coronary blood flow

Abrupt decreases in blood flow due to thrombus or embolus signals impending MI

If symptoms not relieved by 3 NTG tablets within 15 minutes should call 911 or get to nearest ED immediately

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15
Q

Pathophysiology of angina

A

O2 supply available to the heart is significantly lowered
O2 demands of exertional situations can no longer be met
Autoregulatory mechanisms usually fail to mitigate this imbalance

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16
Q

Agents decreasing O2 demand

A

B blockers and some CCBs (HR and contractility)

Nitrates and CCBs (Preload and afterload)

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17
Q

Agents increasing O2 supply

A

Vasodilators (especially CCBs)

Also statins and antithrombins

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18
Q

Therapeutic approach to angina

A

Increase oxygen supply

Decrease oxygen demand

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19
Q

Increasing oxygen supply difficult with

A

Atherosclerotic plaque

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20
Q

Exertion angina therapeutic approach

A

Decrease work on heart

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21
Q

Unstable angina therapeutic approach

A

Decrease work and increase blood flow

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22
Q

Prinzmetal’s angina therapeutic approach

A

Relax the vasculature

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23
Q

Treatment of typical angina

A

Decrease demand by decreasing HR, contractility and wall tension

Initial therapy:
B blocker and aspirin
B blocker and aspirin and long-acting nitrate

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24
Q

When to use clopidogrel for typical angina

A

When aspirin is contraindicated

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25
When to use ACEIs for typical angina
Diabetes or left ventricular dysfunction
26
When to use CCB DHPs or long-acting nitrates for typical angina
When initial therapy with B blocker is contraindicated, not successful, or leads to unacceptable side effects
27
Treatment of unstable angina
Unstable angina can lead to MI **MONA Add B blocker unless contraindicated If B blocker contraindicated use verapamil or diltiazem if no LV dysfunction Increase blood flow - antiplatelet agent (aspirin) Add heparin to decrease thrombus Percutaneous coronary interventions - Angioplasty and stents Coronary bypass grafts (cabbage) Thrombolytics (Alteplase, Reteplase, Tenecteplase, Streptokinase)
28
Organic nitrate mechanism
Prodrugs that are sources of nitric oxide -> vasodilation Increase NO -> increase cGMP -> increase removal of PO4 from Myosin -> relaxation
29
Pharmacodynamics of organic nitrates
Decrease both preload and afterload Relax vascular smooth muscle (V>A) Decrease venous return, preload, **O2 demand, afterload Directly dilate coronary arteries, especially subendocardial regions compressed during systole Transient increase in oxygen supply Prevent coronary vasospasm
30
How should NTG be administered
Sublingual Miss first pass effect Needs to be converted to NO first
31
Nitroglycerin (NTG)
Nitro | Several routes of administration
32
Isosorbide dinitrate
Long acting
33
Isosorbide-5-mononitrate
Long acting
34
Adverse effects of nitrates
Headaches, facial flush, dizziness Orthostatic hypotension - alcohol worsens
35
Tolerance of NTG
Effectiveness diminishes significantly with continued use Limitation to therapy Loss of capacity to convert to NO?
36
Drug holidays
Can alleviate effects of tolerance
37
Contraindications of nitrates
Acute MI - right ventricular infarction | Patients on erectile dysfunction drugs - potentially dangerous fall in BP
38
Increased intracellular contraction in SM
Ca++ -> calmodulin ->MLCK -> add PO4 to myosin -> contraction
39
CCB and SM contraction
Block increase in calcium Bind L-type calcium channels Block contraction = dilation (mostly arterioles)
40
CCBs with prominent cardiac effects
Non-DHPs | Verapamil and Diltizem
41
CCBs with prominent arteriolar vasodilation effects
DHPs | Nifedipine, Amlodipine, Felodipine, Isradapine, Nicardipine, Nisoldipine, Nimodipine
42
PD of CCB in angina
Relax arteriolar SM Decrease afterload -> decrease O2 demand Dilation of coronary arteries = increase O2 supply
43
CCB and cardiac cells
Calcium binding to troponin allows for contraction Calcium involved in conduction through slow channels CCBs have negative ionotropic effect but reflex tachycardia from decreased BP negates effects
44
CCB and SA/AV Nodes
Depolarization is through Ca channels All CCBs block channels but only non-DHPs effect recovery and frequency Non-DHPs decrease rate of SA firing and decrease AV nodal conduction
45
Supraventricular tachycardias
Treat with Non-DHP CCBs
46
CCB and hemodynamic effects
Decrease coronary vascular resistance and increase coronary blood flow
47
DHP CCB hemodynamic effects
More potent vasodilators Decrease arterial pressure, reflex increase HR and contractility, CO increase, ventricular function improved, peripheral blood flow improved, venous tone unchanged
48
Non-DHP CCB hemodynamic effects
Verapamil - reflex tachycardia due to arterial dilation is blunted by direct negative inotropic effect Diltiazim - less negative HR
49
PK of CCBs
Good oral absorption but high 1st pass effect Amlodipine, felodipine, isradipine slowly absorbed, with long half life Verapamil sometimes used IV
50
Adverse effects of CCBs
**Constipation (Verapamil) Peripheral edema, coughing, wheezing, pulmonary edema Excessive vasodilation - dizziness, hypotension, headache, flushing, nausea Coronary steal with angina
51
Contraindications of CCBs
Use with B blocker - potential AV block | Should not be used in patients with ventricular dysfunction, SA or AV nodal conduction defects and systolic BP < 90 mmHg
52
B blockers in anginal therapy
Major - decrease HR Minor - decrease contractility (decrease work and O2 demand) Long term - decrease peripheral resistance
53
Ideal B blockers for anginal therapy
Atenolol, Metoprolol
54
Cheap B blockers for anginal therapy
Propranolol
55
B blockers in chronic stable angina
Monotherapy for mild to moderate angina of effort Combination therapy with long acting nitrate or DHP CCB Always after MI
56
What angina cannot be treated with B blocker?
Vasospasm - Prinzmetal's
57
Limitations to using B blocker for chronic stable angina
Bradyarrhythmias or AV block Compensated congestive heart failure Asthmatics and diabetics use with extreme caution
58
Antiplatelet agent for angina
Aspirin Decrease mortality in patients with unstable angina - reduce MI and death Inhibit platelet aggregation that would lead to MI
59
Sufficient dose of aspirin
85-325 mg per day
60
Aspirin mechanism
Blocks production of prostaglandins Irreversibly inhibits cyclooxygenase Platelets have no nuclei and cannot produce new cyclooxygenase
61
Clopidogrel
Plavix Blocks ADP receptor binding mediated activation of GPIIa/IIIb complex Irreversible, long-term inhibition of platelet aggregation Useful for unstable angina, prophylaxis and treatment of TIA and completed stroke Treatment for stent placement
62
Drugs used during angioplasty
Abciximab - Monoclonal antibody against glycoprotein IIb/IIIa receptor Tirofiban and eptifibatide inhibit ligand binding to IIb/IIIa receptor Treatment of unstable angina when angioplasty or atherectomy planned within 24 hrs
63
Acute prophylaxis and treatment of single anginal attacks
NTG | Onset: 1-3 min, duration: 20-30 min
64
Maintenance therapy of chronic stable angina
B blockers, CCBs, or long duration nitrates | or combination
65
Vasospastic angina
CCBs or nitrates

CV II Exam 3 (13 decks)

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