These slides contain detailed description of antianginal drugs including : Introduction, Definition of Angina, Types of Angina, Classification of antianginal drugs - nitrates, beta adrenergic blockers, calcium channel blockers, potassium channel openers, ( with their classification, pharmacological action, mechanism of action, available forms, therapeutic uses, pharmacokinetics, adverse effects, and contraindications ) Nursing responsibility, Summary.

1. PRESENTATION
ON
ANTI-ANGINAL
DRUGS
By Priyanshi

2. INTRODUCTION
An antianginal is a drug used in the
treatment of angina pectoris, a symptom
of ischaemic heart disease. So, medicinal
agents used for relieving or preventing
pathological conditions associated
with coronary insufficiency and the related
ischemic heart diseases are referred to as
antianginal drugs.

3. DEFINITION : ANGINA
► Angina pectoris is a syndrome characterized by
sudden severe pressing substernal chest pain or
heaviness radiating to the neck, jaw, back and arms.
It is often associated with diaphoresis, tachypnoea
and nausea.
► Primary cause is due to imbalance between
myocardial oxygen demand and oxygen supplied by
coronary vessels.
– This imbalance may be due to:
1. A decrease in myocardial oxygen delivery.
2. An increase in myocardial oxygen demand.

4. Determinant of myocardial
oxygen delivery
► Coronary blood flow
Determined by : Perfusion pressure
Duration of diastole
Coronary vascular resistance
► Arteriovenous oxygen difference

5. Determinant of myocardial
oxygen demand
► Wall stress
Determined by : Intraventricular pressure
Ventricular volume
Wall thickness
► Heart rate
► Contractility

6. TYPES OF ANGINA
►There are three types of
angina:
1. STABLE ANGINA
(CLASSICAL ANGINA)
2. UNSTABLE ANGINA
3. VARIANT ANGINA
(PRINZMETAL’S ANGINA)

7. STABLE ANGINA
In this type of angina attacks predictably
provoked by exercise, emotion, eating or
coitus and subside when the increased
energy demand is withdrawn. By reducing
the cardiac work, usually leads to complete
relief of the pain. It constitutes about 90%
of angina cases.

8. UNSTABLE ANGINA
It is characterized by increased frequency
and severity of attacks that result from a
combination of atherosclerosis plaques,
platelet aggregation at fractured plaques,
and vasospasm.

9. VARIANT ANGINA
In this type of angina attacks occur at rest
or during sleep and are unpredictable. It is
responsible for less than 10% of angina
cases.

10. CLASSIFICATION OF
ANTIANGINAL AGENTS
NITRATES
► Short acting (10 minutes) : Glyceryl trinitrate (GTN
and Nitroglycerin)
► Long acting (1 hour) : Isosorbide dinitrate
Isosorbide mononitrate
Erythrityl tetranitrate
Pentaerythritol tetranitrate
BETA–ADRENERGIC BLOCKERS
► Propranolol
► Metoprolol
► Atenolol

11. CALCIUM CHANNEL BLOCKERS
► Phenylalkylamine : Verapamil
► Benzodiazepin : Diltiazem
► Dihydropyridines : Nifedipine
Felodipine
Amlodipine
Nitrendipine
Nimodipine
POTASSIUM CHANNEL OPENERS
► Nicorandil

12. OTHERS
► Dipyridamole
► Trimetazidine
► Ranolazine
► Ivabradine
► Oxyfedrine

13. CLINICAL CLASSIFICATION
• TO ABORT OR TERMINATE ANGINAL
ATTACK :
Nitroglycerin (sublingually), Isosorbide dinitrate
(sublingually)
• FOR CHRONIC PROPHYLAXIS :
Nitrates, Beta–blockers, Calcium channel blockers,
Potassium channel openers and other drugs

14. TREATMENT OF ANGINA PECTORIS

15. NITRATES

16. CLASSIFICATION OF
NITRATES
Rapidly acting nitrates
► Used to terminate acute attack of angina
► E.g.- Nitroglycerin and Amyl nitrate
► Usually administered sublingually
Long acting nitrates
► Used to prevent an attack of angina
► E.g.- Erythrityl tetranitrate, Isosorbide dinitrate,
Pentaerythritol tetranitrate
► Administered orally or topically

17. PHARMACOLOGICAL
ACTIONS
PRELOAD
REDUCTION
REDISTRIBU
TION OF
CORONARY
FLOW
EFFECTS ON
SMOOTH
MUSCLES
AFTERLOAD
REDUCTION

18. PRELOAD REDUCTION
Nitroglycerin relaxes vascular smooth muscle and dilates
both arterial and venous vessels
I
Dilation of veins is more predominant than dilation of
arteries, resulting in peripheral pooling of blood and
decreased venous return
I
Decreased preload

19. AFTERLOAD REDUCTION
Nitrates also produce some arteriolar
dilation
I
Decrease peripheral resistance
I
Reduction of afterload

20. REDISTRIBUTION OF
CORONARY FLOW
Dilation of coronary arteries
I
Increase blood supply to the myocardium

21. EFFECTS ON SMOOTH
MUSCLES
►Relax the bronchi, biliary tracts and
esophagus muscles.
►Also dilates cutaneous vessels and
meningeal vessels.

22. MECHANISM OF ACTION

23. AVAILABLE FORMS
►Sublingual tablets
►Topical ointment
►Transdermal patches
►Translingual spray
►Transmucosal tablets
►Intravenous ( IV )

24. PREPARATION DOSE ROUTE
DURATION OF
ACTION
TABLETS
1, 2, 3 mg
0.5 mg Sublingual 1 – 3 min/30 min
OINTMENT 2% Skin 30 min/12 hrs
TRANSDERMAL
PATCHES
one patch for 14
to 16 hr per day
Skin Max. 24 hrs
SPRAY 0.4 – 0.8 mg Sublingual 2 min/60 min
CAPSULE 5 – 15 mg Oral 20 min/4 – 8 hrs
INJECTION
5 mg/ml
5 – 20 microgram/
min
Intravenous 2 min/5 min

25. THERAPEUTIC USES
► Angina pectoris
► Myocardial infarction
► Congestive cardiac failure
► Biliary colic
► Cyanide poisoning
► Esophageal spasm
► Acute coronary syndrome

26. PHARMACOKINETICS
► Organic nitrates are lipid soluble, well
absorbed from buccal mucosa, intestines and
skin.
► Ingested orally, all except Isosorbide
mononitrate undergo extensive and variable
first pass metabolism in liver.
► They are rapidly denigrated by a glutathione
reductase and a mitochondrial aldehyde
dehydrogenase.

27. COMPARISON OF PHARMACOKINETIC OF
PROPERTIES OF NITRATES

28. ADVERSE EFFECTS
► Throbbing headache
► Flushing of the face
► Dizziness
► Postural hypotension
► Tachycardia
► Palpitation
► Weakness
► Methemoglobinemia

29. CONTRAINDICATIONS
►Renal ischemia
►Severe anaemia
►Cerebral haemorrhage
►Acute myocardial infarction
►Patients receiving antihypertensive
agents

30. BETA–BLOCKERS

31. HEMODYNAMIC EFFECTS
►Decrease heart rate.
►Reduced blood pressure and cardiac
contractility without appreciable
decrease in cardiac output.

32. MECHANISM OF ACTION
Decrease coronary supply
I
Decrease the heart rate by blocking beta receptor
I
Decrease the work of heart
I
Decrease oxygen consumption
I
Increase redistribution of blood

33. THERAPEUTIC USES
►Decreased frequency and severity of
attacks.
►Increased exercise tolerance.
►Lowers sudden cardiac death.
►Routinely used in unstable angina with
myocardial infarction.
►Avoid abrupt withdrawal.

34. ADVERSE EFFECTS
►Hypotension
►Depression
►Bradycardia
►Heart block
►Congestive heart failure

35. CONTRAINDICATIONS
►Congestive heart failure
►Complete heart block
►Pulmonary edema
►Cardiogenic shock
►Asthma

36. CALCIUM
CHANNEL
BLOCKERS

37. HEMODYNAMIC EFFECTS
►Decrease heart rate.
►Reduced blood pressure and cardiac
contractility without appreciable
decrease in cardiac output.

38. MECHANISM OF ACTION
Coronary artery dilation
I
Decrease coronary bed resistance
(Relieved coronary vasospasm)
I
Increase coronary blood flow
I
Increase oxygen supply

39. MECHANISM OF ACTION
Reduction on peripheral resistance
(Secondary to dilatation of aorta)
I
Decrease blood pressure
I
Decrease afterload
I
Decrease workload
I
Decrease oxygen consumption

40. THERAPEUTIC USES
► Improve oxygen delivery to ischemic
myocardium
► Vasodilate coronary arteries
► Particularly useful in treating vasospastic angina
► Reduce myocardial oxygen consumption
► Decrease afterload
► Non–dihydropyridines also lower heart rate and decrease
contractility

41. VERAPAMIL
► It dilates arterioles and decreases total peripheral
resistance.
► It shows AV conduction directly and decreases heart
rate, contractility, blood pressure and oxygen
demand.
► It also has some alpha adrenergic blocking activity.
► Verapamil has greater negative inotropic effects than
amlodipine, but it is a weaker vasodilator.
► Verapamil should not be given with beta-blockers,
digoxin, cardiac depressants like quinidine and
disopyramide.

42. DILTIAZEM
► Diltiazem also shows AV conduction, decreases the
rate of firing of the sinus node pacemaker, and is
also a coronary artery vasodilator.
► Diltiazem can relieve coronary artery spasm and is
particularly useful in patients with variant angina.
► It is somewhat less potent vasodilator than
nifedipine and verapamil, and has modest direct
negative inotropic action, but direct depression of
SA node and AV conduction are equivalent to
verapamil.

43. NIFEDIPINE
► Nifedipine is the prototype DHP with a rapid onset
and short duration of action. It causes arteriolar
dilatation and decreases total peripheral resistance.
► Nifedipine is usually administered as an extended
release oral formulation.
► It causes direct depressant action on heart in higher
dose.
AMLODIPINE
► It is an oral dihydropyridine, functions mainly as an
arteriolar vasodilator.

44. LACIDIPINE
► It is a highly vasoselective newer DHP.
NITRENDIPINE
► It a calcium channel blocker with additional action of
vasodilatation action. Vasodilation action is due to
release NO form the endothelium and inhibit cAMP
phosphodiesterase.
NIMODIPINE
► It is short acting DHP which penetrates blood brain
barrier very efficiently due to high lipid solubility.

45. PHARMACOKINETICS
DRUGS
ONSET OF
ACTION
PEAK OF
ACTION
HALF LIFE
NIFEDIPINE 20 minutes 1 hour 3-4 hours
VERAPAMIL 1-2 hours 5 hours 8-10 hours
DILTIAZEM 15 minutes 30 minutes 3-4 hours
NICARDIPINE 20 minutes 45 minutes 2-4 hours
FELODIPINE 2-5 hours 6-7 hours 11-16 hours

46. ADVERSE EFFECTS
►Nausea
►Vomiting
►Dizziness
►Flushing of the face
►Tachycardia (due to hypotension)
►Edema

47. CONTRAINDICATIONS
►Cardiogenic shock
►Recent myocardial infarction
►Heart failure
►Atrioventricular block

48. POTASSIUM
CHANNEL
OPENERS

49. MECHANISM OF ACTION

50. NICORANDIL
► Antianginal action of nicorandil is medically through
ATP sensitive K+ channels therapy hyperpolarizing
vascular smooth muscle.
► Nicorandil is well absorbed orally, nearly completely
metabolized in liver and is excreted in urine.
Administered i.v. during angioplasty for acute MI, it
is believed to improve outcome.
► ADR : Flushing, palpitation, weakness, headache,
dizziness, nausea and vomiting.
► DOSE : 5–10 mg tablets, 2 mg /vial

51. OTHER
ANTIANGINAL
DRUGS

52. DIPYRIDAMOLE
► It inhibits platelet aggregation.
► It is a powerful coronary dilator.
TRIMETAZIDINE
► It acts by non hemodynamic mechanisms.
► The mechanism of action of trimetazidine is
uncertain, but it may improve cellular tolerance to
ischaemia by inhibiting mitochondrial long chain 3–
ketoacyl–Coa thiolase.
RANOLAZINE
► This novel antianginal drug primarily acts by
inhibiting a late Na+ current in the myocardium.

53. OXYPHEDRINE
► It improves myocardial metabolism.
IVABRADINE
► This ‘pure’ heart rate lowering antianginal drug has
been introduced recently as an alternative to beta–
blockers.
► It blocks cardiac pacemaker cell ‘f’ channels.

54. COMBINATION DRUG
THERAPY
NITRATES + BETA–BLOCKERS
►The additive efficiency is primarily a result of
one drug blocking the adverse effect of other
agent on net myocardial oxygen consumption.
►Beta–Blockers — blocks the reflex tachycardia
associated with nitrates.
►Nitrates — attenuate the increase in the left
ventricular and diastolic volume associated with
beta–blockers by increasing venous
capacitance.

55. CALCIUM CHANNEL BLOCKERS +
BETA–BLOCKERS
►It is useful in the treatment of exertional
angina that is not controlled adequately with
nitrates and beta–blockers.
►Beta–blockers — attenuate reflex tachycardia
produced by nifedipine.
►These two drugs produce decrease blood
pressure.

56. CALCIUM CHANNEL BLOCKERS +
NITRATES
► It is useful in severe vasospastic or
exertional angina (particularly in patient with
exertional angina with congestive heart
failure and sick sinus syndrome).
► Nitrates reduce preload and afterload.
► Calcium channel reduces the afterload.
► Net effect is on reduction of oxygen demand.

57. TRIPLE DRUG THERAPY
NITRATES + CALCIUM CHANNEL
BLOCKERS + BETA–BLOCKERS
► It is useful in patients with exertional angina
not controlled by the administration of other
types of anti anginal agents.
► Nifedipine — decrease after load.
► Nitrates — decrease preload.
► Beta–blockers — decrease heart rate and
myocardial contractility.

58. NURSING
RESPONSIBILITY
Nursing Intervention
Client Teaching

59. NURSING INTERVENTION
►History collection.
►Assess the duration, time started and
character of pain.
►Monitor vital signs.
►Assist in various diagnostic tests like ECG,
Echo and other blood investigation.
►Nitrates should be kept away from flame.
►Store nitrates in original container.
►An analgesic can be given to treat headache.

60. Intravenous
►Do not mix NTG with other drugs.
►Do not use PVC tubings for IV administration
because it absorb the nitrates .
►Use glass bottles and tubings.
►It is given by infusion pump.

61. Ointment/transdermal patch
► Remove transdermal patches before
defibrillation to prevent burns.
► Rotate ointment and transdermal patches sites.
► Remove ointment and previous patch before
applying new ointment or patch.
► Do not trim transdermal patch or alter dose.
► Do not rub or massage the area after
application of ointment.

62. ► Apply to the chest, upper arm, or upper thigh to
promote absorption and increase onset of
systemic action.
► Do not get ointment on hands as it can cause
headache.
► Wash hands after application.
► Apply to a non hairy sites, avoid application to
skin folds or irritated sites.
Sublingual tablets
► Place under the skin.

63. Transmucosal tablets
► The nurse should place one tablet between lip
and gum above incisors or between cheek and
gum to promote slow dissolving and extended
absorption.
Spray
► Do not shake while administering.
► Hold vertically and spray under the tongue.
► Advice do not swallow immediately.

64. CLIENT TEACHING
► NTG lose potency if exposed to light, moisture
or heat.
► Avoid alcohol, hot bath as they cause
vasodilation and lead to hypotension.
► Teach about adverse effects.
► Encourage client to discontinue tobacco which
causes vasoconstriction.
► Encourage to eat high fiber rich diet.

65. ► Do not eat food or smoke until tablets dissolve.
► Instruct client not to chew sublingual tablets,
place under the tongue.
► In acute anginal attacks, teach client to lie
down and take NTG tablets as soon as possible
( upto 3 tablets in every 5 minutes ).
► If no relief go for emergency services.

66. SUMMARY
► Anti anginal drugs may relieve attacks of acute
myocardial ischaemia by increasing
myocardial oxygen supply or by decreasing
myocardial oxygen demand.
► Three groups of pharmacological agents have
been shown to be effective in reducing the
frequency, severity, or both of primary or
secondary angina.
► These agents include the nitrates,
adrenoceptor antagonists, and calcium entry
blockers.

67. THANK YOU