drus classification and treatment

1. Angina pectoris
Presented by :-
V. RAVI KISHORE

2. Definition :-
It is defined as the chest pain towards left arm
shoulder due to less supply of O2 (or) more demand
of O2.
 Due to imbalance between myocardium oxygen
requirement and oxygen supply.
 Types of angina pectoris
a) Stable angina
b) Variant angina
c) Unstable angina

3. Stable angina
 Typical, classic,
Common angina
 Most common
angina
 Occurs during
emotional stress,
heavy exercise,
 Esily predictable
 Treating more
rest,nitroglycern
 Also due to
atherosclerosis
Variant angina
 Prize metal
angina
 Occurs in rest
also
 Due to Spasm of
coronary artery
Unstble angina
 Uncommon or
atypicaltype
 Occurs in
exercise and
also during rest
 Prolanged
angina may
lead to
Miocardial
infraction
 Unpredictable

4. Risk factors :
 Age
 Sex
 Obesity
 Smoking
 Diabetes
 Hypertension
 Renal dysfunction
Age :-
For men >55 yrs and >65 for women

5. Classification of ANTI ANGINAL DRUGS
 The drugs used to treat angina are called Anti
Anginal Drugs
1) NITRATES :-
a) Short acting
--nitroglycerin (or)
--glyceryltri nitrate
b) Long acting
-- isosorbide mononitrate
-- isosorbide dinitrate

6. 2) Ca +2 channel blockers :-
--felodipine
--nifedipine
--amlodipine
--diltiazem
--verapamil
3) BETA blockers :-
--propanolol
--esmolol
--sotalol
--metaprolol
--atenolol

7. 4) K+ channel opener :-
--nicorandil
5) Vasodilators :-
--hydralazine
--minoxidil
6) Miscellaneous :-
--aspirin
--dipyridamole

8. PATHOPHYSIOLOGY
 Myocardial ischemia develops when coronary blood
flow becomes inadequate to meet myocardial O2
demand.
 This is because myocardial cell switch from aerobic to
anaerobic metabolism with a progressive impairment of
metabolic , mechanical and electrical functions.
 Studies have shown that adenosine may be the main
chemical mediator of anginal pain . During ischemia
ATP is degraded to adenosine, which after diffusion to
the extra cellular space, cause anginal pain .

9. Goals of treatment :-
 All the treatment for people with coronary
artery disease have the same goal.
 To decrease the elivated symptoms
 To reduce mortality due to CAD progression

10. DRUG THERAPHY :-
 Currently there are 3 main types of drugs used
a) Nitrates
b) Beta blockers
c) Ca+2 channel blockers
 Nitrates and Ca+2 channel blockers may be
added if needed.
1) NITRATES:- It improves blood flow by relaxing
& dialating veins and arteries.
Ex:- Nitroglycerin & Isosorbide mononitrate
SIDE EFFECTS :-
 Headace, light headedness, flushing, and increase in
heart rate

11. Mechanism of action

12. BETA BLOCKERS
 They reduces the heart rate, BP, & force of
contraction and amount of oxygen the heart
requires to pump blood.
Ex :- Atenolol, Proponolol, Esmolol,Nadolol
Sides effects :-
1)Cardiac effect :- Worsen heart failure,
Bradycardia.
2)Non-cardiac effect :- constriction of airway,
circulatory problems , Impotance , Hallucination,
Insomnia & Fatigue.

13. Mechanism of action
Resistance

14. Ca+2 channel blockers
 They dilate arteries & lower blood pressure.
Which decreases the force of contractions.
 They also dilate veins, reduces the amount of
blood returning to the heart which reduces the
work load of the heart.
Ex :- Amlodipine, Nifedipine, Felodipine.

15. Mechanism of action

16. Combination therapy
 Nitarates + beta blockers --- in stable angina .
 Ca+2 channel blockers + beta blockers –in
stable angina when the above combination has
failed.
 Ca+2 channels + nitrates :- in unstable angina.
 All 3 together :- when the combination of 2 drugs
has filed where
a) Nitrates :- decreased Preload
b) Ca+2 channel blockers :- decreased
afterload.
c) Beta blockers :-decreased heart rate &
myocardial contraction.

17. Other measures in managing CAD
 Anticoagulents
Ex :- 1) Aspirin :- it help to prevent blood clooting.
Keeping the narrowed artaries open and lowering
the risk of a heart attack.
 Treat high BP.