Vasodilators in Angina

Question 1

Major determinant of myocardial O2 supply is

Answer 1

Coronary Blood flow- blood flow during diastole is decreased during tachycardia (also decreased by increased LVEDP)

Question 2

Myocardial O2 supply is inversely proportional to

Answer 2

coronary vascular resistance- damage to endothelium can alter ability of vasculature to dilate. Vascular control by metabolites (autoregulation) is most important.

Question 3

Determinants for myocardial oxygen demand

Answer 3

1) Contractile state
2) Heart rate
3) LV pressure and ventricular volume

Question 4

Drug that increase coronary blood flow

Answer 4

Nitrates and CCBs

Question 5

Preload decreased by

Answer 5

Nitrates

Question 6

Afterload decreased by

Answer 6

CCBs

Question 7

-dipines properties (SA-AV Node(HR), Cardiac Muscle contractility and afterload)

Answer 7

CCBs. Inc, none to dec, dec

Question 8

Diltiazem (SA-AV Node(HR), Cardiac Muscle contractility and afterload)

Answer 8

CCB. Dec, none to dec, dec

Question 9

Verapamil (SA-AV Node(HR), Cardiac Muscle contractility and afterload)

Answer 9

CCB. Dec, Dec, Dec

Question 10

Drugs that decrease demand

Answer 10

Beta-blockers
Nitrates
Calcium Channel Blockers

Question 11

Drugs that reduce thrombosis

Answer 11

Antiplatelet Agents - Anticoagulants

Beta-blockers – Nitrates – CCBs

Question 12

Drugs that prevent vasospasm

Answer 12

Nitrates

Calcium Channel Blockers

Question 13

Variant (Prinzmetal) Angina

Answer 13

Caused by coronary vasospasm with or without atheromatous plaque. Occurs commonly at rest.

Question 14

Variant Chronic Pharmacotherapy

Answer 14

Reversing or preventing vasospasm and increasing supply with vasodilators (nitrates or Ca++ channel blockers)ion

Question 15

Nitrate Pathway

Answer 15

Nitrates to NO to inc cGMP to Vasodilation

Question 16

Nitroprusside

Answer 16

converts to NO and affects venules and aterioles (causing decreased BP)

Question 17

Increased cGMP results in

Answer 17

reduction of LVEDP and systemic vascular resistance

Question 18

Transdermal (ointment or patch), Sublingual/lingual and IV all bypass

Answer 18

First pass effect! (much higher doses for oral)

Question 19

Nitrate Adverse Rxns

Answer 19

Throbbing headache
Orthostatic hypotension
Reflex Tachycardia
Facial Flushing
(due to vasodilation)
Tachyphylaxis (tolerance- need nitrate free interval of 6-14 hours)

Question 20

Dihydropyridines effects (nifedipine)

Answer 20

greater ratio of vascular (dilation) to cardiac (rate-conduction-contractility) effects

Question 21

Verapamil and Diltiazem (effects)

Answer 21

prominent effects at cardiac nodal tissue (phase 0 at SA and AV node) and on cardiac muscle (phase 2)

Question 22

Rapid onset -dipines may rapidly lower…?

Answer 22

BP! causes reflex activation of the SNS which leads to tachycardia, exacerbation of angina and increased risk for MI

Question 23

CCB Properties

Answer 23

1) Variable Oral bioavailability
2) Extensively protein bound
3) Metabolized by cytochrome P450

Question 24

CCB Use in Angina

Answer 24

Long-lasting decrease in peripheral vascular resistance

Reduced heart O2 requirement

Reduced coronary arterial tone (aid in vasospastic angina)

Question 25

CCB other uses

Answer 25

Arrhythmias Hypertension Subarachnoid hemorrhage Inhibition of Premature labor

Question 26

Verapamil/diltiazem vs Dihydropyridines

Answer 26

Dyhydropyridines greatly increase vasodilation while not having Negative inotropic effect and suppressing AV node conduction

Question 27

CCB Adverse Rxns (verapamil/diltiazem more)

Answer 27

Cardiac arrest Bradycardia AV block Congestive heart failure)

Question 28

B-Blocker Uses in Angina

Answer 28

Decreased O2 demand Can block reflex tachycardia from use of nitrates NOT vasodilators -> no use in variant angina

Question 29

B-Blocker Use

Answer 29

Angina patients with concomitant hypertension or arrhythmias responsive to β-blockers

Question 30

B-Blocker Contraindications

Answer 30

Asthma Peripheral vascular disorders Abrupt withdrawal  precipitates SNS overactivity

Question 31

Failure of Late Na+ Current Inactivation causes

Answer 31

Ischemia! Decreased O2 supply and increased demand. Caused by increased extravascular compression and diastolic wall tension.

Question 32

What drug blocks Failure of Late Na+ Current Inactivation?

Answer 32

Ranolazine. Administered bid.

Question 33

Ranolazine Adverse Rxns

Answer 33

Can Prolong QT interval Cardiovascular effects (~ 5%): bradycardia, hypotension, palpitations, edema

Question 34

Ranolazine Use

Answer 34

Add-on to standard anti-anginal therapy Reduces symptoms of chronic stable angina and increases exercise capacity Can substitute for beta-blockers if not tolerated or contraindicated