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CV II Exam III > Anti-Anginal Agents (Martin) > Flashcards

Anti-Anginal Agents (Martin) Flashcards

1
Q

nitroglycerin

A

nitrate

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2
Q

isosorbide dinitrate

A

nitrate

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3
Q

verapamil

A

CCB

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4
Q

Diltiazem

A

CCB

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5
Q

Nifedipine

A

DHP CCB

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6
Q

Amlodipine

A

DHP CCB

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7
Q

Felodipine

A

DHP CCB

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8
Q

Aspirin

A

Anti-platelet

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9
Q

Clopidogrel

A

Anti-platelet

ADP receptor blocker on platelets

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10
Q

Dipyridamole

A

Antiplatelet

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11
Q

nicardipine

A

CCB- DHP

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12
Q

UFH

A

unfractionated heparin- anticoagulant

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13
Q

LMWH

A

anticoagulant

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14
Q

what are the 3 drug groups traditionally used in the treatment of angina

A

oraganic nitrates
ccb
b-blockers

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15
Q

what is angina pectoris?

A

Angina is the primary symptom of ischemic heart disease
temporary and reversible imbalance between myocardial O2 supply and demand

increase demand - from increase HR, increase ventricular contraction, and increase ventricular wall tension
decrease supply – from decreased coronary blood flow, O2 carrying capacity of blood, or both
coronary artery disease (CAD) usually the underlying cause

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16
Q

what is the sensation of angina

what patients have atypical symptoms of angina

A

Heavy pressing substernal discomfort (rarely called pain)= pressure
Often radiating to left shoulder, flexor aspect of left arm, jaw, or epigastrium
Significant minority of patients describe a different location or character
Women, elderly, and diabetes most likely to have atypical symptoms

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17
Q

what is typical angina

A

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

Hx = angina induced by exercise, relieved by rest and/or nitroglycerin (NTG)- acute acting vasodilator

lasts no longer than 15 min, 5 - 15 episodes/wk

ST segment depression

18
Q

what is atypical angina

A

angina at rest

Variant, vasospastic, prinzmetal’s

focal or diffuse coronary vasospasm episodically reduces coronary flow

transient ST segment elevation during angina

19
Q

what is unstable angina

A

Rupture of an atherosclerotic plaque, with consequent platelet adhesion and aggregation  coronary blood flow
Abrupt decreases in blood flow due to thrombus or embolus signals impending myocardia infarction (MI)
If symptoms not relieved by 3 NTG tablets within 15 minutes should call 911 or get to nearest ED immediately

20
Q

Typical angina therapeutic objectives?

A

decrease O2 demand - decrease HR, decrease contractility or wall tension

B-blocker + aspirin (use clopidogrel if aspirin is contraindicated)

B-blocker + aspirin + long -acting nitrate

nitrate (usually NTG sublingual) For acute attacks

ACE inhibitor in patients with diabetes or left ventricular dysfunction

Long-acting calcium channel blocker (DHPs) or long-acting nitrates for reducing symptoms when initial therapy with b blocker is contraindicated, not successful, or leads to unacceptable side effects.

21
Q

which agents decrease the O2 DEMAND of the heart…

A

b-blockers
ccb’s

organic nitrates - modify preload and afterload

22
Q

what agents increase O2 supply?

A

vasodilators (Ca entry blockers)

23
Q

therapeutics in unstable angina?

A

MONA***

1st
morphine- relieve pain and anxiety
O2
nitroglycerin- coronary vasodilator
Aspirin

+ beta blocker OR CCB non-DHP if beta blocker is contraindicated (decrease O2 demand of the heart)

increase blood flow (aspirin) + heparin to decrease thrombus

percutaneous coronary interventions (PCI)
–> angioplasty, placement of stents, require a cath lab

Coronary bypass graft

thrombolytics (alteplase, reteplase, tenecteplase, streptokinase)

24
Q

what are organic nitrates

what is their MOA

A

prodrugs that are sources of NO

nitroglycerin is an organic nitrate

MOA
decrease preload and afterload
relax vascular smooth m.
Mainly relaxation of large veins decrease¯ venous return decrased ¯ preload decrease ¯ O2 demand (major effect)

smaller ¯ in afterload

Directly dilate coronary arteries, especially subendocardial regions compressed during systole

­ increase in oxygen supply (transient), effective in prevention of coronary vasospasm

MECHANISM
In healthy subjects, NO dilates coronary arteries
In exertional angina, direct infusion of NTG into heart does not relieve angina, but sublingual NTG does.*** (not an effect on myocardium per se and must be converted to NO)

25
Q

what is the mechanism of NTG at the molecular level

A

Nitrate (NTG) is converted to NO

NO activates guanylyl cyclase to activate guanylyl cyclase

active GC converts GTP to cGMP (normally phosphodiesterase inactivates cGMP)

cGMP leads to dephosphorylation of myosin LC and relaxation of smooth muscle

26
Q

isosorbide dinitrate

A

long acting nitrate vasodilator

sublingual Q2-3 hr, oral, sustained release tablet Q12 hr

27
Q

what are the adverse effects of nitrates?

A

headaches (can be severe), facial flush, dizziness (Monday disease)

orthostatic hypotension (alcohol worsens this)

***Can develop tolearance - effectiveness diminishes with continued use!

drug holidays can alleviate the tolerance (8 hr drug free period per day)

28
Q

what are the contraindications for Nitrates

A

In acute MI - avoid if right ventricular infarction b/c higher right sided filling pressures are needed

patients on erectile dysfunction drugs ***
these drugs also are phosphodiesterase inhibitors which elevated cGMP, and synergistic effects with NO can lead to potentially dangerous fall in BP
-Sildenafil (Viagra)
Tadalafil (Cialis)
Vardenafil (Levitra)

29
Q

CCB’s mechanism of action…. in angina

A

normally Ca2+ activates Calmodulin –> which activates myosin light chain kinase –> leading to phosphorylation of Myosin Light chain and contraction….

all these drugs bind to L-type calcium channels at different sites and block Ca2+ entry through these channels

this leads to relaxation of arteriolar smooth muscle –> decreased afterload and decreased O2 demand

also these increase O2 supply due to dilation of coronaries

30
Q

CCB’s mechanism on smooth muscle

A

Voltage-sensitive (L-type) Ca++ channels mediate entry of Ca++ into smooth muscle, cardiac myocytes, SA & AV nodal cells in response to electrical stimulation

Ca++ triggers contraction of vascular smooth muscle

CCBs block channel and produce relaxation of arterioles***, little effect on veins

Mostly decrease afterload***, little effect on preload

31
Q

CCB’s mechanism of action of cardiac cells

A

In myocytes, Na+ entry through “fast” channels is the primary carrier of current in the depolarization event, but Ca++ entry through slow channels is an additional component

Ca++ entry may also induce Ca++ release from SR

Ca++ binds to troponin- relieves inhibition of troponin on contractile apparatus – allows actin-myosin contraction

CCBs block Ca++ entry, cause negative inotropic effect –but concurrent decrease in vascular resistance causes decrease BP and baroreceptor reflex (reflex tachy) which negates negative inotropic effect

32
Q

what are the MOA’s of DHP CCB’s and nonDHP CCB’s on the SA and AV nodes ….

A

Depolarization is largely through L-type Ca++ current

DHPs block channel but do not effect recovery of channel & are not “frequency (use) dependent”

Verapamil & diltiazem block channel, delay recovery of channel, & are frequency dependent

Therefore, verapamil & diltiazem decrease the rate of SA node depolarization + slow AV nodal conduction

These properties makes them useful for treatment of supraventricular tachyarrhythmias

33
Q

what are the hemodynamic effects of CCB’s

I.e. effects coronary vascular resistance and coronary blood flow?

A

All ccb’s decrease coronary vascular resistance and increase coronary blood flow

DHP’s are more potent arterolar vasodilators than the non-DHP’s

DHPs decrease arterial P, slight reflex increase HR & contractility, CO increase, ventricular function improved, peripheral blood flow improved, venous tone unchanged

verapamil–> reflex tachy due to arterial dilation is blunted by direct negative inotropic effects

34
Q

Contraindications of CCB’s

A

non-DHP’s are contraindicated in a patient taking a beta blocker*** b/c of the potential for AV block

non-DHP’s should not be used in patients with ventricular dysfunction, SA or AV nodal conduction defects and systolic BP <90

35
Q

what are signs of toxicity of CCB’s

A

Excessive vasodilation – dizziness, hypotension, headache, flushing, nausea

Constipation*** (esp., verapamil), peripheral edema, coughing, wheezing, pulmonary edema

“Coronary steal” worsens angina

It is caused when there is narrowing of the coronary arteries and a coronary vasodilator[2] is used - “stealing” blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.

36
Q

aspirin

A

blocks production of prostaglandins –> irreversibly inhibits Cyclooxygenase

decreases mortality in patients with unstable angina, reducing incidence of MI and death

decrease incidence of MI in chronic stable angina due to inhibition of platelet aggregation

once per day 85-325 mg tablet

37
Q

Clopidogrel

A

Selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex
Irreversible, long-term inhibition of platelet aggregation
Useful for unstable angina, prophylaxis and treatment of TIA and completed stroke
Standard practice to treat for patients undergoing stent placement

38
Q

therapeutic guidelines for acute prophylaxis and treatment of single anginal attack

A

nitroglycerin

onset 1-3 min. 20-30 min duration

39
Q

therapeutic guideline for maintanence therapy of chronic stable angin

A

b-blockers, CCB’s or long duration nitrates or combination

40
Q

therapeutic guidelines for vasospastic angina….

A

Ca channel blockers or nitrates

CV II Exam III (14 decks)

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