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1. Anti Anginal Drugs
By: Muhammad Aurangzeb
Lecturer-INS/KMU

2. Objectives
By the completion of this section the learners will be
able to:
• Discuss the main classes of drugs that are used for
treating AP.
• Discuss the nursing responsibility of each class of
drugs.
• Calculate the drug dosage accurately while
administering oral and parenteral medications.

3. Angina pectoris (AP)
• Angina pectoris – chest pain due to imbalance
between the oxygen requirement of the heart and
oxygen supplied to it via the coronary vessels.

4. Definition of terms
• Angina Pectoris – is the principal symptoms of
patient with ischemic heart disease.
• Manifested by sudden, severe, pressing
• substernal pain that often radiates to the left
shoulder and along the flexor surface of the left arm.
• Usually precipitated by exercise, excitement or a
heavy meal.

5. Cont…
• Myocardial ischemia which produces angina results
from imbalances in myocardial oxygen supply &
demand relationship such as decreased oxygen
supply and/or increased oxygen demand.
Etiology
• Decrease oxygen supply
• Increase demand for oxygen

6. Types of angina
• Atherosclerotic angina (classic angina [common form]):
Attacks are predictably provoked (stable angina) by
exercise, emotion, eating and subside when the increased
energy demand is withdrawn. Rest, by reducing cardiac work,
usually leads to complete relief of the pain within 15 min.
Atherosclerotic angina constitutes about 90% of angina
cases.
• Secondary to advanced atherosclerosis of the coronary
vessels
• Associated with ST-segment depression on ECG

7. Types of angina
• Vasospastic angina (rest angina,
variant angina, or Prinzmetal’s
angina [uncommon form]):
• Attacks occur at rest or during
sleep.
• Vasospastic angina is responsible
for less than 10% of angina cases.
• Associated with ST-segment
elevation on ECG
• Secondary to vasospasm of the
coronary Vessels
Coronary artery calibre changes
in classical and variant angina

8. Types of Angina
• Unstable angina (crescendo angina, also known as
acute coronary syndrome): It is characterized by
increased frequency and severity of attacks that
result from a combination of atherosclerotic
plaques, platelet aggregation at fractured plaques,
and vasospasm.
• the duration of manifestation is longer than the first
two and has the manifestation of Myocardial
infarction
Reference: Drugs Used in the Treatment of Angina Pectoris. In: Trevor AJ, Katzung BG, Kruidering-Hall M. eds.
Katzung & Trevor's Pharmacology: Examination & Board Review, 11e New York, NY: McGraw-Hill; 2015.

9. Treatment of Angina Pectoris
• Drugs used in angina exploit two main strategies:
– reduction of oxygen demand
– increase of oxygen delivery to the myocardium

10. Classification of antianginal drugs
• Nitrates
– Short acting: Glyceryl trinitrate (GTN, Nitroglycerine)
– Long acting: Isosorbide dinitrate (short acting by
sublingual route), Isosorbide, mononitrate,
• β Blockers: Propranolol, Metoprolol, Atenolol and
others.
• Calcium channel blockers
– Phenyl alkylamine: Verapamil
– Benzothiazepine: Diltiazem
– Dihydropyridines: Nifedipine,, Amlodipine, Nitrendipine,
Nimodipine,

11. Classification of antianginal drugs
• Clinical classification
• Used to abort or terminate attack: GTN (angisid), Isosorbide
dinitrate (sublingually).
• Used for chronic prophylaxis: All other drugs.

12. Antianginal drugs
• I. Agents which ↓ O2 demand & ↑ O2 Supply
– A. Nitrates
– B. Calcium channel blockers
• II. Agents which ↓ O2 demand
– Beta blockers

13. Nitrates/ Organic Nitrates
• Preload reduction: Peripheral pooling of blood → decreased
venous return (preload reduction).
• Afterload reduction: Nitrates also produce some arteriolar
dilatation → slightly decrease total peripheral resistance
or afterload on heart.
• Redistribution of coronary flow: In the arterial tree, nitrates
preferentially relax bigger conducting (angiographically visible)
coronary arteries than arterioles or resistance vessels.

14. Nitrates/ Organic Nitrates
Mechanism of action:
• The organic nitrate agents are prodrugs that are sources of
NO. NO activates the soluble isoform of guanyl cyclase,
thereby increasing intracellular levels of cGMP. In turn,
cGMP promotes the dephosphorylation of the myosin
light chain and the reduction of cytosolic Ca2+ and leads to
the relaxation of smooth muscle cells in a broad range of
tissues.
References: Eschenhagen T. Treatment of Ischemic Heart Disease. In: Brunton LL, Hilal-Dandan R, Knollmann
BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 13e New York, NY: McGraw-Hill

15. Nitrates
Coronary artery dilatation
Decrease coronary bed resistance
(Relieved coronary vasospasm)
Increase coronary blood
flow
Increase oxygen supply

16. Nitrates
Reduction on peripheral resistance
(Secondary to dilatation of aorta)
Decrease blood
pressure
Decrease after load
Decrease workload
Decrease oxygen consumption

17. Nitrates
Reduced venous return
(Due to dilatation of the veins)
Decrease left ventricular
volume
Decrease preload
Decrease workload
Decrease oxygen consumption

18. Effects
1. Coronary artery dilatation
2. Reduction of peripheral arterial
resistance – decrease after load
3. Reduce venous return –
decrease preload

19. Pharmacokinetics of Nitrates/ Organic
Nitrates
• 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 denitrated by a glutathione reductase and a
mitochondrial aldehyde dehydrogenase.

20. Uses of Nitrates/ Organic Nitrates
• Angina pectoris: GTN produces relief within 3 min in 75%
patients, the rest may require another dose or take longer
(up to 9 min).
• Acute coronary syndromes: Nitrates are useful by decreasing
preload as well as by increasing coronary flow.
• Myocardial infarction (MI): GTN is frequently used during
evolving MI with the aim of relieving chest pain and
limiting the area of necrosis by favorably altering O2
balance in the marginal partially ischemic zone.

21. Adverse effects Nitrates/ Organic
Nitrates
• Headache is the most common adverse effect of nitrates. High
doses of nitrates can also cause postural hypotension, facial
flushing, and tachycardia.
• Phosphodiesterase type 5 inhibitors such as sildenafil
potentiate the action of the nitrates. To prevent the
dangerous hypotension that may occur, this combination is
contraindicated.

22. β Blockers
• The β-adrenergic blockers decrease the oxygen demands of
the myocardium by blocking β1 receptors, resulting in
decreased heart rate, contractility, cardiac output, and
blood pressure.
• All β blockers are nearly equally effective in decreasing
frequency and severity of attacks and in increasing
exercise tolerance in classical angina, but cardioselective
agents (atenolol, metoprolol) are preferred over
nonselective β1 + β2 blockers (e.g. propranolol).

23. Hemodynamics Effects
Decrease heart rate
Reduced blood pressure and cardiac
contractility without appreciable
decrease in cardiac output
B-Blockers

24. B-Blockers
Decrease heart rate & Contractility
Increase duration of diastole
Decrease workload
Increase coronary blood flow
Increase oxygen supply
Decrease O2 consumption

25. Calcium channel blockers
– Phenyl alkylamine: Verapamil
– Benzothiazepine: Diltiazem
– Dihydropyridines: Nifedipine, Felodipine,
Amlodipine, Nitrendipine, Nimodipine, Lacidipine,
Lercanidipine, Benidipine

26. Calcium channel blockers
Pharmacological actions:
• Smooth muscle: The CCBs cause relaxation by decreasing
intracellular availability of Ca2+. The dihydropyridines (DHPs) e.g.
amlodipine have the most marked smooth muscle relaxant
and vasodilator action; verapamil is somewhat weaker
followed by diltiazem.

27. Calcium channel blockers
Pharmacological actions:
• Heart: calcium channel blockers protect the tissue by
inhibiting the entrance of calcium into cardiac and smooth
muscle cells of the coronary and systemic arterial beds
and decreases smooth muscle tone and vascular resistance,
afterload.

28. Ca - Channel Blockers
Effects
2. Coronary artery dilatation
3. Reduction on peripheral arterial
resistance – decrease after load

29. Ca Channel Blockers
Coronary artery dilatation
Decrease coronary bed resistance
(Relieved coronary vasospasm)
Increase coronary blood
flow
Increase oxygen supply

30. Ca channel Blockers
Reduction on peripheral resistance
(Secondary to dilatation of aorta)
Decrease blood
pressure
Decrease after load
Decrease workload
Decrease oxygen consumption

31. Calcium channel blockers
• Phenyl alkylamine: Verapamil:
• It dilates arterioles and decreases total peripheral resistance.
• It slows atrioventricular (AV) conduction directly and
decreases heart rate, contractility, blood pressure, and
oxygen demand.
• It also has some α adrenergic blocking activity.
• Verapamil has greater negative inotropic effects than
amlodipine, but it is a weaker vasodilator.
• Verapamil should not be given with β blockers, digoxin,
cardiac depressants like quinidine and disopyramide.

32. Calcium channel blockers
• Benzothiazepine: Diltiazem:
• Diltiazem also slows 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 A-V
conduction are equivalent to verapamil.

33. Calcium channel blockers
• Dihydropyridine (DHP) calcium channel blockers: 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.

34. Adverse effects of CCBs
• Frequent side effects are palpitation, flushing, ankle
edema, hypotension, headache, drowsiness and
nausea. Nifedipine has paradoxically increased the frequency
of angina in some patients.

35. Uses Calcium channel blockers
• Calcium channel blockers can be safely given to
patients with peripheral vascular disease in whom β
blockers are contraindicated.
• CCB are used for the treatment of
– angina pectoris
– hypertension
– cardiac arrhythmias

36. References
• Karch, A. M., & Karch. (2011). Focus on nursing pharmacology.
Wolters Kluwer Health/Lippincott Williams & Wilkins. [Link]
• Katzung, B. G. (2017). Basic and clinical pharmacology.
McGraw-Hill Education.
• Lehne, R. A., Moore, L. A., Crosby, L. J., & Hamilton, D. B.
(2004). Pharmacology for nursing care.
• Smeltzer, S. C., & Bare, B. G. (1992). Brunner & Suddarth’s
textbook of medical-surgical nursing. Philadelphia: JB
Lippincott