ANGINA PECTORIS

BY
AJU-NOR IORAFAGA.
BAYERO UNIVERSITY KANO
PRESENTED AT ACCIDENT AND EMERGENCY NURSING,
SCHOOL OF POST BASIC NURSING STUDIES,
NATIONAL ORTHOPAEDIC HOSPITAL,
DALA-KANO.
APRIL, 2024.
CONTENT
INTRODUCTION
DEFINITION
TYPES
CAUSES/RISK FACTORS
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS
DIAGGNOSIS
MANAGEMENT
PREVENTION
CONCLUSION
INTRODUCTION
• Angina pectoris is the common Cardiovascular syndrome
usually characterized by episodes of paroxysms of pain or
discomfort in the anterior chest.
• The pain is mainly retrosternal.
• It may radiate to neck, shoulder and left upper limb.
• Differentiated from other chest pain by location, duration,
character and relation to exercise.
 DEFINITION

• It is a chest pain, discomfort, or

tightness resulting from a transient and
reversible myocardial ischaemia
• It is a sudden, excruciating, tightening
and squeezing pain felt at retrosternal
area of the chest, caused by imbalance
between myocardial oxygen supply and
oxygen demand.
 TYPES
1. STABLE ANGINA.

• This is predictable and consistent

chest pain that occurs on exertion
and is relieved by rest and/or nitro-
glycerine.
• It is usually lasts less than 15
minutes.
• It is commonly seen in elderly
people 50 years and above.
2. UNSTABLE ANGINA
• Unstable angina does not follow a regular pattern.
• It can occur when at rest and is considered less common and more
serious because rest does not relieve it, and may not respond to
usual angina medications .
• It can last for 15 minutes or more
• This version can signal a future heart attack within a short time –
hours or weeks.
3. VARIANT ANGINA.
• Variant (Prinz metal’s) angina is rare and can occur at rest, usually
due to abnormal narrowing or coronary artery vasospasm.
• Pain usually occurs at rest and awakens the patient from sleep.
• It is commonly seen in people between 30 to 40 years.
4. REFRACTORY ANGINA. [READING ASSIGNMENT]
5. SILENT ISCHAEMIA ANGINA. [READING ASSIGNMENT]
 CAUSES/RISK FACTORS
Non- modifiable risk
Modifiable risk factors factors
• Physical exertion • Gender (affects men more than
• Exposure to cold female)

• Eating a heavy meal. • Age (40 and above)

• Tobacco use. • Family history.
• Diabetes. • Race. ( higher in Non-Hispanic
whites & blacks, followed by Asian)
• Obesity.
• Physical exertion. This can precipitate an attack by increasing
myocardial oxygen demand.
• Eating a heavy meal. A heavy meal increases the blood flow to the
mesenteric area for digestion, thereby reducing the blood supply
available to the heart muscle; in a severely compromised heart,
shunting of the blood for digestion can be sufficient to induce anginal
pain.
• Tobacco use. Chewing tobacco, smoking and long-term exposure to
second-hand smoke damage the interior walls of arteries including
arteries to your heart allowing deposits of cholesterol to collect and
block blood flow.
• Diabetes. Diabetes increases the risk of coronary artery disease, which
leads to angina and heart attacks by speeding up atherosclerosis.
• Obesity. Obesity raises the risk of angina and heart disease
because it’s associated with high blood cholesterol levels, high
blood pressure and diabetes. Also, your heart has to work
harder to supply blood to the excess tissue.
• Exposure to cold. This can cause vasoconstriction and
elevated blood pressure, with increased oxygen demand.
 PATHOPHYSIOLOGY
• The pathophysiology involves a
mismatch between myocardial
oxygen supply and demand.
• This can occur due to coronary artery
spasm, atherosclerosis etc. which
leads to narrowing of coronary
arteries, reducing blood flow.
• Ischemia, resulting from decreased
blood flow.
• Anaerobic respiration with lactic acid
accumulation leading to the
characteristic chest pain of angina.
CLINICAL MANIFESTATIONS
• Chest pain. The pain is often felt deep in the chest behind the sternum
and may radiate to the neck, jaw, left arms and shoulders.
• Shortness of breath. An increase in oxygen demand could cause
shortness of breath.
• Syncope.
• Numbness: A feeling of weakness in the neck, shoulder arms, wrist and
hand.
• Pallor. Inadequate blood supply to peripheral tissues causes pallor.
• Weakness.
• Nausea.
• Sweating
 ASSESSMENT AND DIAGNOSTIC FINDINGS

• Details medical history: Involving predisposing factors,

onset, aggravating factors and relieves.
• Stress electrocardiogram: It measures the heart's electrical activity
while the patient exercises on treadmill or stationary bike. It helps assess
how well the heart response to stress and can detect abnormalities. If
patient experiences chest pain, shortness of breath during the exercise is
indication of angina.
• Cardiac enzymes (Aspartate Aminotransferase, Creatine
Phosphokinase, Creatine Kinase etc) elevation indicates myocardial
damage.
• Blood test: Partial pressure of carbon dioxide (Pco2), potassium, and
myocardial lactate; may be elevated during the anginal attack (all play a
role in myocardial ischemia and may perpetuate it).
• Echocardiogram: May reveal abnormal valvular action as the cause of
chest pain.
• Electrocardiogram: Often normal when a patient at rest or
when pain-free; depression of the ST segment or T wave
inversion signifies ischemia. Dysrhythmias and heart block may
also be present. Significant Q waves are consistent with a prior
MI
• Serum lipids (total lipids, lipoprotein electrophoresis, and
isoenzymes cholesterols, triglycerides; phospholipids): May be
elevated (CAD risk factor).
 MANAGEMENT

The objectives of the management of angina are to decrease the

oxygen demand of the myocardium and increase the oxygen supply.
Pharmacologic Therapy
• Nitroglycerine gives long-term and short-term reduction of
myocardial oxygen consumption through selective vasodilation
within three (3) minutes.
• Beta-blockers reduces myocardial oxygen consumption by
blocking beta-adrenergic stimulation of the heart. They Block
sympathetic impulses to the heart. E.g. Atenolol, Propranolol
• Calcium channel blockers have negative inotropic effects by
decreasing the force of cardiac muscles contraction. Decrease
sinoatrial node automaticity. E.g. Nifedipine
• Antiplatelet medications prevent platelet aggregation, and
anticoagulants prevent thrombus formation. E.g. Aspirin
Nursing management
• Oxygen therapy is usually initiated at the onset of chest pain in an
attempt to increase the amount of oxygen delivered to the myocardium
and reduce pain.
Lifestyle changes recommended to treat angina pectoris include:
• Stopping smoking
• Controlling weight
• Regularly checking cholesterol levels
• Resting and slowing down during stress
• Avoiding large meals
• Learning how to handle or avoid stress
• Eating fruits, vegetables, whole grains, low-fat or no-fat
dairy products, and lean meat and fish
 COMPLICATIONS
• Myocardial infarction. Myocardial infarction is the end result of angina
pectoris if left untreated.
• Cardiac arrest. The heart pumps more and more blood to compensate
the decreased oxygen supply, and the cardiac muscle would ultimately
fail leading to cardiac arrest.
• Cardiogenic shock. MI also predisposes the patient to cardiogenic
shock.
 PREVENTIONS
• Stopping smoking
• Weight controlling
• Regularly cholesterol levels checking
• Adequate resting
• Avoiding large meals
• Learning how to handle or avoid stress
• Eating healthy diet.
 CONCLUSION

• Angina pectoris is recurring chest pain, discomfort, resulting

from imbalance between myocardial oxygen supply and oxygen
demand.
• The is generally described as sudden, excruciating, tightening
and squeezing pain felt at retrosternal area of the chest.
• The management objective is to decrease the oxygen demand of
the myocardium and to increase the oxygen supply.
 REFERENCES

• Basavanthappa BT. Medical Surgical Nursing; second edition Volume 2

• Brunner and Suddarth. Medical Surgical Nursing; twelfth edition Volume 1
• VanPutte, Rogan & Russo. Seeley’s Anatomy and Physiology; tenth edition
 Practice Quiz

1. The pain of angina pectoris is 2. The nurse advises a patient that

produced primarily by: sublingual nitroglycerin should alleviate
angina pain within:
A. Vasoconstriction.
A. 3 to 4 minutes.
B. Movement of thromboemboli.
B. 10 to 15 minutes.
C. Myocardial ischemia.
C. 30 minutes.
D. The presence of atheroma.
D. 60 minutes.
3. The scientific rationale supporting the 4. Calcium channel blockers act by:
administration of beta-blockers is the drug’s
A. Decreasing SA node automaticity.
ability to:
B. Increasing AV node conduction.
A. Block sympathetic impulses to the heart.
C. Increasing the heart rate.
B. Elevate blood pressure.
D. Creating a positive inotropic effect.
C. Increase myocardial contractility.

D. Induce bradycardia.
 1. Answer: C. Myocardial ischemia.
5. All of the following are
type of angina except for: Ischemia causes lactic acid production that triggers the pain.

A. Stable angina. 2. Answer: A. 3 to 4 minutes.

B. Unstable angina. Nitroglycerin given sublingually alleviates angina pain within 3

minutes.
C. Refractory angina.
3. Answer: A. Block sympathetic impulses to the heart.
D. Direct angina.
Beta-blockers reduces myocardial oxygen consumption by blocking
beta-adrenergic stimulation of the heart.

4. Answer: A. Decreasing SA node automaticity.

Calcium channel blockers decrease sinoatrial node automaticity.

5. Answer: D. Direct angina.

Direct angina is not a type of angina.