Angina Pectoris

DEFINITION A disease marked by brief sudden attacks of chest pain or discomfort caused by deficient
oxygenation of the heart muscles usually due to impaired blood flow to the heart.

TYPES:

 Stable Angina

Induced by effort, relieved by rest. Good prognosis.

 Unstable Angina

Angina of increasing frequency or severity; occurs on minimal exertion or at rest; associated with ↑↑risk of MI.

 Variant Angina Pectoris

Angina due to coronary artery spasm, which can occur even in normal coronary arteries. The pain usually occurs
during rest and resolves rapidly with short-acting nitrates (eg gtn spray). ecg during pain shows st segment elevation.

Risks and triggers:

Smoking increases risk but hypertension and hypercholesterolaemia do not. Probable triggers include cocaine,
amphetamine, marijuana, low magnesium, and artery instrumentation (eg during angiography).

 Nocturnal Angina Pectoris

RISK FACTORS:

MODIFIABLE RISK FACTORS:

 Tobacco use
 High blood cholesterol or triglyceride levels
 Lack of exercise
 Obesity
 Stress
NONMODIFIABLE RISK FACTORS:

 Family history of heart disease

 Older age
 Diabetes
 High blood pressure

CAUSES

Development of atherosclerosis; coronary artery disease is thought to begin with damage or injury to the inner
layer of a coronary artery, sometimes as early as childhood.

The damage may be caused by various factors, including: Smoking, High blood pressure, High cholesterol,
Diabetes or insulin resistance, Sedentary lifestyle

PATHOPHYSIOLOGY:
SYMPTOMS:

CARDIOVASCULAR- Angina pectoris- it is sensation of chest pain, pressure or squeezing

often due to insufficient blood flow to the heart muscle as a result of obstruction.

Ischemia: Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen that
is needed for cellular activities.

Low cardiac output- Chest pain –chest pain occurs suddenly, severe immobilizing chest pain that
not relieved by rest, position change and medications.

Decrease pulse rate.

BP may be elevated because of sympathetic stimulation or decreased BP because of decreased

contractility, development of cardiogenic shock.

Myocardial infarction- when the blood flow decreases or stop to apart of the heart, causing
damage to the heart muscle.

Diaphoresis –excessive sweating

ECG changes – ST segment and T wave changes, also show tachycardia, bradcardia, or
Dysarrithmias

RESPIRATORY-Shortness of breath.  Pulmonary edema  Chest heaviness  Dyspnea-

difficulty of breathing  Fatigue

Genitourinary-Decreased Urinary Output May Indicate Cardiogenic Shock.

Gastrointestinal- Nausea And Vomiting

Skin- Cool, Clammy ,Diaphoretic , And Pale Appearance On Skin

DIAGNPOSTIC EVALUATION
Physical Examination

History collection

Stress test

Chest X-ray

Electrocardiogram (ECG)

Echocardiogram

Cardiac catheterization (angiogram)

COMPLICATIONS: Heart attack  Heart failure  Abnormal heart rhythm (arrhythmia)

PREVENTION:

Quitting smoking

Monitoring and controlling other health conditions, such as high blood pressure, high cholesterol and diabetes

Eating a healthy diet and maintaining a healthy weight

Increasing physical activity. Aim for 150 minutes of moderate activity each week. Plus, it's recommended that
person get 10 minutes of strength training twice a week and to stretch three times a week for 5 to 10 minutes
each time.

Reducing your stress level

Limit alcohol consumption to two drinks or fewer a day for men, and one drink a day or less for women.

Get an annual flu shot to avoid heart complications from the virus
MEDICAL MANAGEMENT:

Address exacerbating factors:

Anaemia, tachycardia (eg fast AF), thyrotoxicosis.

Secondary prevention of cardiovascular disease:

 • Stop smoking; exercise; dietary advice; optimize hypertension and diabetes control.
 • 75mg aspirin daily if not contraindicated.
 • Address hyperlipidaemia.
 • Consider ACE inhibitors, eg if diabetic.

PRN symptom relief:

Glyceryl trinitrate (GTN) spray or sublingual tabs. Advise the patient to repeat the dose if the pain has not gone after
5min and to call an ambulance if the pain is still present 5min after the second dose. SE: headaches, BP↓.

Anti-anginal medication:

First line: β-blocker and/or calcium channel blocker (do not combine β-blockers with non-dihydropyridine calcium
antagonists). If these fail to control symptoms or are not tolerated, trial other agents.

 β-blockers: eg atenolol 50mg BD or bisoprolol 5–10mg OD.

 Calcium antagonists: amlodipine—start at 5mg OD; diltiazem—dose depends on formulation.
 Long-acting nitrates: eg isosorbide mononitrate—starting regimen depends on formulation.
Alternatives: GTN skin patches. SEs: headaches, ↓BP.
 Ivabradine: Reduces heart rate with minimal impact on BP. Patient must be in sinus rhythm. Start with
5mg BD (2.5mg in elderly). (Acts by selectively and specifically inhibiting the cardiac
pacemaker current)
 Ranolazine: inhibits late Na+ current. Start at 375mg BD. Caution if heart failure, elderly, weight <60kg or
prolonged QT interval.
 Nicorandil: A K+ -channel activator. Start with 5–10mg BD. CI: acute pulmonary oedema, severe
hypotension, hypovolemia LV failure. (Nicorandil is an anti-angina medication that has the dual
properties of a nitrate and ATP-sensitive K+ channel agonist.[6] In humans, the nitrate action
of nicorandil dilates the large coronary arteries at low plasma concentrations. [6] At high
plasma concentrations nicorandil reduces coronary vascular resistance, which is associated
with increased ATP-sensitive K+ channel (KATP) opening)