Angina pectoris is characterized by chest pain or heaviness due to atherosclerosis in the coronary arteries. There are different types including classic angina brought on by exertion, unstable angina with unpredictable symptoms at rest, and Prinzmetal angina due to coronary artery spasm. Treatment involves vasodilators like nitrates, calcium channel blockers, beta blockers, and other drugs to increase blood flow and decrease workload on the heart. Nursing care focuses on medication administration and monitoring for side effects, providing comfort measures, educating on risk factor reduction, and evaluating treatment effectiveness.

1. Mu

4. ANGINA PECTORIS
• It is characterized by sudden
sever pressing chest pain or
heaviness radiating to the neck,
back, and arms.
• Primarily due to the
development of fatty tumors
(atheromas) in the lumen of
blood vessels in a process called
atherosclerosis.

5. TYPES OF ANGINA
NORMAL
CLASSIC
ANGINA
UNSTABLE
ANGINA
PRINZMETAL
ANGINA
MOST
COMMON

6. ANGINA PECTORIS
CLASSIC ANGINA
• Lasts for several
seconds
• Symptoms appear
on exertion, rest
• Symptoms relief
on rest
• Predictable
UNSTABLE ANGINA
• Recurrent attack
of angina
• Symptoms may
even appear at
rest
• May not relief on
rest
• Unpredictable
PRINZMETAL
ANGINA
• Uncommon
pattern occurs at
rest and due to
coronary artery
spasm.
• Responds
promptly to
vasodilators, such
as nitroglycerin
and CCBs.

8. DRUGS USED IN ANGINA PECTORIS
Vasodilators Cardiac depressants Other drugs
Nitrates & Nitrites Calcium blockers Beta blockers
Metabolism
modifiers
• amyl nitrate
• isosorbide mononitrate
• isosorbide dinitrate
• nitroglycerin
• amlodipine
• diltiazem
• nicardipine
• nifedipine
• verapamil
• acebutolol
• esmolol
• metoprolol
• nadolol
• propranolol
• timolol
• Piperazine acetamides
(ranolazine)
• Non-Nitrate Vasodilators
(dipyridamide)

10. MECHANISM OF ACTION
Relax smooth
muscles
Afterload
reduction
Redistribution of
coronary flow
Preload
reduction

11. RELAXATION OF SMOOTH
MUSCLES
Relaxes the bronchi,
biliary tracts & esophagus
muscles
Dilates cutaneous vessels
& meningeal vessels

12. REDISTRIBUTION OF CORONARY
FLOW
Dilatation of coronary
arteries
Increase blood supply to
the myocardium

13. PRELOAD REDUCTION
Relaxes vascular smooth muscle
Dilation of veins
Peripheral pooling of blood and decreased
venous return
Lower oxygen demand by decreasing the
workload of the heart.

14. AFTERLOAD REDUCTION
Produce arteriolar dilatation
Decrease peripheral resistance
Lower oxygen demand by decreasing the
workload of the heart.

15. INDICATIONS
Drop in systemic blood pressure Increasing blood flow to healthy
arteries and veins

16. DOSAGE
Preparation Dose Route
Duration of
action
Brand name
Tablet 0.5mg Sublingual 1-3min/ 30min Angised
Spray 0.4-0.8mg Sublingual 2min/ 60min Nitrolingual
Capsule 5-15mg Oral 20min/ 4-8hr Angispan-tr
Transdermal patch
(5-10mg)
One patch for 14-
16hr per day
Skin Max. 24hr Nitroderm-tts
Injection 5mg/ml 5-20mcg/min Intravenous 2min/5min Nitroject
Ointment 2% Skin 30min/12hr Nitrol

17. CONTRAINDICATIONS
• Allergy to nitrate
• Head trauma
• Cerebral hemorrhage
• Pregnancy and lactation
• Hepatic and renal disease
• Severe anemia

18. ADVERSE EFFECTS
Headache Dizziness Flushing Nausea &
Vomiting
Orthostatic
Hypotension
Reflex
Tachycardia

19. NURSING MANAGEMENT
• Instruct patient not to
swallow sublingual
preparations to ensure
therapeutic effects.
• Take three tablets with a 5-
minute interval, for a total of
doses. If the pain does not
subside, seek medical help.
• Ask for presence of burning
sensation to ensure drug
potency.
• Protect drug from sunlight to
maintain drug potency.
• Take drug with water and
don’t crush.

20. NURSING MANAGEMENT
• Rotate injection sites and
provide skin care as
appropriate to prevent skin
abrasion and breakdown.
• Avoid abrupt stop of long-
term therapy.
• Provide comfort measures:
small frequent meals,
appropriate room
temperature and light, noise
reduction, ambulation
assistance, reorientation and
skin care.

22. ISOSORBIDE DINITRATE & ISOSORBIDE
MONONITRATE
• Slower onset and a longer duration of action
Taken orally.
tablets
Sustained- release capsules
Mononitrate:
20-40mg orally
Dinitrate:
5-10mg sublingually or
orally

24. CALCIUM CHANNEL BLOCKER
Most Potent Least Potent

25. THERAPEUTIC ACTION
Drop in systemic blood pressure Increasing blood flow to healthy
arteries and veins

26. Ca++ CHANNEL BLOCKERS
Block the entry of Ca++ ions into the
smooth & cardiac muscles
Decrease intracellular Ca++
Vasodilation
Smooth muscles relaxation
Increased
preload
Decreased
afterload

27. DOSAGE
Route Onset Peak Duration
Oral 30-60mins 2-3h 2-4h
SR, ER 30-60mins 6-11h Varies
IV Immediate 2-3mins varies

28. CONTRAINDICATIONS
• Allergy to drugs.
• Heart block and sick sinus syndrome
• Renal and hepatic dysfunctions
• Heart failure

29. ADVERSE EFFECT
• CNS • GI
Hepatotoxicity of the
drug

30. ADVERSE EFFECT
• CV • EENT

31. NURSING MANAGEMENT
• Monitor blood pressure and
heart rate and rhythm to
detect possible development
of adverse effects.
• Provide comfort measures for
the patient to tolerate side
effects.
• Educate client on measures to
avoid angina attacks such as
diet changes, rest period and
etc.)
• Emphasize to the client the
importance of strict adherence
to drug therapy to ensure
maximum therapeutic effects.

33. BETA BLOCKER

34. BETA BLOCKERS
Decrease blood pressure, contractility and heart
rate by blocking beta-receptors
Decrease the work of the heart
Decrease oxygen consumption
Increase redistribution of blood

35. DOSAGE
Route Onset Peak Duration
Oral 15mins 90mins 15-19H
IV Immediate 6-90mins 15-19H

36. CONTRAINDICATIONS
• Bradycardia, heart block and cardiogenic shock
• Pregnancy and lactation
• Diabetes, COPD, Thyrotoxicosis and Peripheral
vascular diseases

37. ADVERSE EFFECT
• CNS • GI

38. ADVERSE EFFECT
• CV • RESPIRATORY

39. NURSING MANAGEMENT
• Give drug as ordered
following safe and
appropriate administration to
ensure therapeutic effects.
• Provide comfort measures:
ambulation assistance, raised
siderails, appropriate room
light and temperature and
rest periods.
• Monitor cardiopulmonary
status closely to detect
possible alterations in vital
signs.
• Educate client about the need
to not abruptly stop therapy.

40. EVALUATION
• Monitor patient response to
the therapy.
• Monitor for presence of
mentioned adverse effects.
• Monitor effectiveness of
comfort measures.
• Monitor for compliance to
drug therapy regimen.
• Monitor laboratory tests.

44. • It is used synonymously with
coronary occlusion and heart
attack. Yet MI is the most
preferred term that can result in
myocardial death.
• In an MI, an area of the
myocardium is permanently
destroyed because plaque
rupture and thrombus formation
result in complete occlusion of
the artery.
MYOCARDIAL INFARCTION (MI)

45. CLINICAL MANIFESTATIONS

46. • Tachycardia and tachypnea:
to compensate for the
decreased oxygen supply, the
heart rate and respiratory rate
speed up.
• Fever: occurs at the onset of
MI, but at a low-grade
temperature.
CLINICAL MANIFESTATIONS
• Shortness of breath: because of
increased oxygen demand and a
decrease in the supply of
oxygen.
• Indigestion: as a result of the
stimulation of the sympathetic
nervous system
• Coolness in extremities,
perspiration, anxiety and
restlessness.

47. • Tachycardia and tachypnea:
to compensate for the
decreased oxygen supply, the
heart rate and respiratory rate
speed up.
• Fever: occurs at the onset of
MI, but at a low-grade
temperature.
CLINICAL MANIFESTATIONS
• Shortness of breath: because
of increased oxygen demand
and a decrease in the supply
of oxygen.
• Indigestion: as a result of the
stimulation of the
sympathetic nervous system

48. PREVENTION
A healthy lifestyle could help prevent the development of MI.

49. PHARMACOLOGIC THERAPY

50. PHARMACOLOGIC THERAPY
Analgesic drugs reduce pain and anxiety, also effects
as vasodilator and decreases the workload of the heart.
To provide and improve oxygenation of ischemic myocardial
tissue; given via nasal cannula at 2-4L/min.
First-line of treatment; causes vasodilation and
increases blood flow to the myocardium.
Prevents the formation of thromboxane which causes
platelet to aggregate and arteries to constrict.

51. PHARMACOLOGIC THERAPY
Too dissolve the thrombus in a coronary artery,
allowing blood flow again, minimizing the size of the
infarction
Prevent clots from becoming larger and block coronary
arteries.
To avoid intense straining that may trigger
arrhythmias or another cardiac arrest
To limit the size of infarction and give rest to the
patient. Valium is usually given.

52. NURSING MANAGEMENT
• Administer oxygen along
with medication therapy to
assist with relief of
symptoms.
• Encourage bed rest with the
back rest elevated to help
decrease chest discomfort and
dyspnea.
• Encourage changing of
positions frequently to help
keep fluid from pooling in the
bases of the lungs.
• Check skin temperature and
peripheral pulses frequently
to monitor tissue perfusion.

53. NURSING
MANAGEMENT
• Provide information in an
honest and supportive
manner.
• Monitor the patient closely for
changes in cardiac rate and
rhythm, heart sounds, blood
pressure, chest pain,
respiratory status, urinary
output and lab. Values.
• Check if:
a. Absence of pain or s/sx.
b. Myocardial damage is
prevented.
c. Absence of respiratory
dysfunction.
d. Adequate tissue perfusion.
e. Anxiety is reduced.
EVALUATION

54. DISCHARGE and HOME CARE
GUIDELINES
• Education. Teach patient
about heart-healthy living.
• Home care. Give emphasis
on the scheduling and
keeping-up with the follow-
up appointments.
• Follow-up monitoring.
Remind patient about follow-
up monitoring including
periodic lab testing and
ECGs.
• Adherence. Monitor patient’s
adherence to dietary
restrictions and prescribed
medications.