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34 Cards in this Set

  • Front
  • Back
What kind of angina do you get with chronic coronary artery disease?
stable angina
Acute Coronary Syndromes
1. Unstable Angina
2. Non-Q wave (non-ST elevation): MI
3. Q Wave (ST elevation): MI
Risk Factors for Coronary Artery Disease
Age
Genetic predisposition
Hypertension
Cigarrete smoke
Diabetes Mellitus
Dyslipidemia
Chlamydia infection ?

Risk factors are additive
Stable angina
lumen narrowed by plaque
inappropriate vasoconstriction
Unstable Angina
plaque ruptured
platelet aggregation
thrombus formation
unoppossed vasoconstriction
Variant Angina
no overt plaque
intense vasospasm
When do you start seeing symptoms when an artery is occluded?
anything between 40% and 80% occlusion angina while exercisiing

occlusion greater than 80% symptoms at rest
What are the determinants of Myocardial Ischaemia
imbalance of supply and demand of oxygen
Drugs used for Angina Pectoris
1. Nitrates
2. B-blockers
3. Calcium Channel Blockers

others not covered in this lecture: antiplatelet agents, antilipid drugs)

Combination: nitrate + B-blocker: vasodilator and reflex tachycardia inhibition
Myocardial Ischemia during Exercise and effect of Nitrates:
1. Very Effective: takes 2 minutes
2. Does not do much at rest
3. Stress test: oxygen demand greater than supply: give nitrate
Nitrates
Nitroglycerine (glyceryl trinitrate)
Isosorbide Dinitrate
Isosorbide Mononitrate
Nitrates PD
relaxation of all smooth muscle, including vascular smooth muscle

1. prompt relaxation of venous tone
-enhancement of venous capacitance
-reduction of cardiac preload

2. gradual decrease in arteriolar resistance: decrease afterlaod and deccrease peripheral resistance:

leads to decrease in myocardial oxygen demand

use spray: bucally absorbed
Nitrates PK
Nitroglycerine:sublingual, buccal, transdermal, i.v.

NOT P.O.: high first pass metabolism
Nitrates USE
Acute attacks of angina pectoris

Anticipated Attacks

Prolonged preventive therapy (ISMN, ISDN: long acting)

Paroxysmal nocturnal dyspnea in CHF

As spasmolytic in colic pain (biliary, renal, intestinal)
Nitrate Tolerance
1. need to use glutathione system---> used up

2. Nitrates: will not be able to use if glutathione is all used up
Sodium Nitroprusside
strongest vasodilator

does not need any activation

limitelss

not dependent on glutathione
Factors that induce Nitrate Tolerance
continous or prolonged nitrate exposure
Large doses
frequent dosing
Prevent Tolerance
intermittent dosing
small doses
infrequent dosing
provide nitrate-free interval
Typical Nitrate Regimen
NTG patch, remove patch for 10-12 h/day

ISMN (t1/2= 4-5 hrs) two daily doses 7 hours apart

glutathine system recharges in between dosages: nitrous free interval
ISDN vs. ISMN
pg. 5 go over it.
Sodium Nitroprusside
Ferrocyanide Compound

direct NO-donator---> very effective, immediate acting vasodilator

i.v. infusion, t1/2<3 min, protect from light, converted to cyanide and thiocyanide
Sodium Nitroprusside
1. in ICU and emergency setting may be used in certain hypertensive emergencies
2. controlled hypotension during surgery
3. Special forms of severest cardiac failure: Grade IV or when waiting for transplant
Sodium Nitroprusside: AE and Precautions
Extreme Caution:
borderline systolic blood pressure
myocardial ischemia in absence heart failure
hepatic or renal insufficiency

AE: severe nausea, vomiting headache, other CNS disturbances

TOX: cyanide intoxication

may be used for some hours only, then discontinue
Coronary Steal Syndrome
Hydralazine
Dypyridamole

caused when there is narrowing of the coronary arteries and an arteriolar vasodilator 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. Dilating the other arterioles causes blood to be shunted away from the coronary vessels
Calcium Channel Blockers
Verapamil
Diltiazem
Nifedipine (and dihydropyridines)

PK: p.o., iv highly bound by serum proteins, hepatic metabolism, renal excretion

PD: block L-type calcium channels
-cardiodepressant effects
-arteriolar vasodilation
Calcium Channel Blockers AE
dihydropyridines (due to excessive vasodilation)
dizziness, headache, flushing, digital dyasthesia, nausea, peripheral edema

constipation, reflex tachycardia
verapamil, diltiazem bradycardia, slow SA and AV conduction
Some substances increase digoxin plasma levels
Verapamil Indications
Angina
Hypertension
Arrhythmia
Nifedipine and other Dihydropyridines
angina
hypertension

NOT FOR ARRHYTHMIA
Diltiazem
Angina
Hypertension
Arrhythmia
B-blocker in Angina Pectoris
Propanolol
Atenolol
Metoprolol

reduce the severityand frequency in exertional angina, somewhat effective in unstable angina

negative inotropic, negative chrontropic, reduced systolic blood pressure during exercise

Net Effect= reduced myocardial O2 demand
When do you use B-blockers in Angina Pectoris?
cardioprotective in post MI-patients, given early, continued for 2-3 yrs (b1-selective blocker)

Ineffective in vasospastic angina, may worsen condition

B-blockers has somewhat vasoconstriction properties: worsen symptoms
Beta Blocker vs. Ca-channel Blocker
Type of Angina
Exertional: B-blocker

Vasospastic: Ca channel blocker
Beta Blocker vs. Ca-channel Blocker
Concomitant Disease
COPD, Asthma: Ca Channel Blocker

Ventricular Arryhtmia: B-blocker
Beta Blocker vs. Ca-channel Blocker
Age of Patient
< 40: B-blocker

>60: Ca-channel blocker