ANGINA PECTORIS
A heavy meal increases the
- Angina pectoris is a clinical syndrome usually
characterized by episodes or paroxysms of pain or
pressure in the anterior chest.
- The cause is insufficient coronary blood flow,
resulting in a decreased oxygen supply when
there is increased myocardial demand for oxygen
in response to physical exertion or emotional
stress.
CLASSIFICATIONS
1. Stable angina. There is predictable and consistent
pain that occurs on exertion and is relieved by
rest and/or nitroglycerin.
2. Unstable angina. The symptoms increase in
frequency and severity and may not be relieved
with rest or nitroglycerin.
3. Intractable or refractory angina. There is severe
incapacitating chest pain.
4. Variant angina. There is pain at rest, with
reversible ST-segment elevation and thought to
be caused by coronary artery vasospasm.
5. Silent ischemia. There is objective evidence of
ischemia but patient reports no pain.
PATHOPHYSIOLOGY
Angina is usually caused by atherosclerotic disease.
- Almost invariably, angina is associated with a
significant obstruction of at least one major
coronary artery.
- Oxygen demands not met. Normally, the
myocardium extracts a large amount of oxygen
from the coronary circulation to meet its
continuous demands.
- Increased demand. When there is an increase in
demand, flow through the coronary arteries
needs to be increased.
- Ischemia. When there is blockage in a coronary
artery, flow cannot be increased, and ischemia
results which may lead to necrosis or myocardial
infarction.
CAUSES
Several factors are associated with angina.
- Physical exertion. This can precipitate an attack
by increasing myocardial oxygen demand.
- Exposure to cold. This can cause vasoconstriction
and elevated blood pressure, with increased
oxygen demand.
- Eating a heavy meal.
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.
- Stress. Stress causes the release of
catecholamines, which increased blood pressure,
heart rate, and myocardial workload.
CLINICAL MANIFESTATIONS
The severity of symptoms of angina is based on the
magnitude of the precipitating activity and its effect
on activities of daily living.
- Chest pain. The pain is often felt deep in the chest
behind the sternum and may radiate to the neck,
jaw, and shoulders.
- Numbness. A feeling of weakness or numbness in
the arms, wrists and hands.
- Shortness of breath. An increase in oxygen
demand could cause shortness of breath.
- Pallor. Inadequate blood supply to peripheral
tissues cause pallor.
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.
ASSESSMENT AND DIAGNOSTIC FINDINGS
The diagnosis of angina pectoris is determined
through:
- ECG: Often normal when 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.
- 24-hour ECG monitoring (Holter): Done to see
whether pain episodes correlate with or change
during exercise or activity. ST depression without
pain is highly indicative of ischemia.
- Exercise or pharmacological stress
electrocardiography: Provides more diagnostic
information, such as duration and level of activity
 attained before onset of angina. A markedly
positive test is indicative of severe CAD. Note:
Studies have shown stress echo studies to be
more accurate in some groups than exercise
stress testing alone.
- Cardiac enzymes (AST, CPK, CK and CK-MB; LDH
and isoenzymes LD1, LD2): Usually within normal
limits (WNL); elevation indicates myocardial
damage.
- Chest x-ray: Usually normal; however, infiltrates
may be present, reflecting cardiac
decompensation or pulmonary complications.
- pCO2, potassium, and myocardial lactate: May
be elevated during anginal attack (all play a role in
myocardial ischemia and may perpetuate it).
- Serum lipids (total lipids, lipoprotein
electrophoresis, and isoenzymes cholesterols
[HDL, LDL, VLDL]; triglycerides; phospholipids):
May be elevated (CAD risk factor).
- Echocardiogram: May reveal abnormal valvular
action as cause of chest pain.
- Nuclear imaging studies (rest or stress scan):
Thallium-201: Ischemic regions appear as areas of
decreased thallium uptake.
- MUGA: Evaluates specific and general ventricle
performance, regional wall motion, and ejection
fraction.
- Cardiac catheterization with angiography:
Definitive test for CAD in patients with known
ischemic disease with angina or incapacitating
chest pain, in patients with cholesterolemia and
familial heart disease who are experiencing chest
pain, and in patients with abnormal resting ECGs.
Abnormal results are present in valvular disease,
altered contractility, ventricular failure, and
circulatory abnormalities. Note: Ten percent of
patients with unstable angina have normal-
appearing coronary arteries.
- Ergonovine (Ergotrate) injection: On occasion,
may be used for patients who have angina at rest
to demonstrate hyperspastic coronary vessels.
(Patients with resting angina usually experience
chest pain, ST elevation, or depression and/or
pronounced rise in left ventricular end-diastolic
pressure [LVEDP], fall in systemic systolic
pressure, and/or high-grade coronary artery
narrowing. Some patients may also have severe
ventricular dysrhythmias.)
MEDICAL MANAGEMENT
The objectives of the medical management of angina
are to increase the oxygen demand of the
myocardium and to increase the oxygen supply.
- Oxygen therapy. 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.
NURSING MANAGEMENT
- Treating angina. The nurse should instruct the
patient to stop all activities and sit or rest in bed
in a semi-Fowler’s position when they experience
angina, and administer nitroglycerin sublingually.
- Reducing anxiety. Exploring implications that the
diagnosis has for the patient and providing
information about the illness, its treatment, and
methods of preventing its progression are
important nursing interventions.
- Preventing pain. The nurse reviews the
assessment findings, identifies the level of activity
that causes the patient’s pain, and plans the
patient’s activities accordingly.
- Decreasing oxygen demand. Balancing activity
and rest is an important aspect of the educational
plan for the patient and family.
MYOCARDIAL INFARCTION
- Myocardial infarction (MI), is used synonymously
with coronary occlusion and heart attack, yet MI
is the most preferred term as myocardial ischemia
causes acute coronary syndrome (ACS) that can
result in myocardial death.
- In an MI, an area of the myocardium is
permanently destroyed because plaque rupture
and subsequent thrombus formation result in
complete occlusion of the artery.
- The spectrum of ACS includes unstable angina,
non-ST-segment elevation MI, and ST-segment
elevation MI.
PATHOPHYSIOLOGY
- Unstable angina. There is reduced blood flow in a
coronary artery, often due to rupture of an
atherosclerotic plaque, but the artery is not
completely occluded.
- Development of infarction. As the cells are
deprived of oxygen, ischemia develops, cellular
 injury occurs, and lack of oxygen leads to
infarction or death of the cells.
CAUSES
- Vasospasm. This is the sudden constriction or
narrowing of the coronary artery.
- Decreased oxygen supply. The decrease in oxygen
supply occurs from acute blood loss, anemia, or
low blood pressure.
- Increased demand for oxygen. A rapid heart rate,
thyrotoxicosis, or ingestion of cocaine causes an
increase in the demand for oxygen.
CLINICAL MANIFESTATIONS
- Chest pain. This is the cardinal symptom of MI.
Persistent and crushing substernal pain that may
radiate to the left arm, jaw, neck, or shoulder
blades. Pain is usually described as heavy,
squeezing, or crushing and may persist for 12
hours or more.
- Shortness of breath. Because of increased oxygen
demand and a decrease in the supply of oxygen,
shortness of breath occurs.
- Indigestion. Indigestion is present as a result of
the stimulation of the sympathetic nervous
system.
- Tachycardia and tachypnea. To compensate for
the decreased oxygen supply, the heart rate and
respiratory rate speed up.
- Catecholamine responses. The patient may
experience such as coolness in extremities,
perspiration, anxiety, and restlessness.
- Fever. Unusually occurs at the onset of MI, but a
low-grade temperature elevation may develop
during the next few days.
PREVENTION
- Exercise. Exercising at least thrice a week could
help lower cholesterol levels that cause
vasoconstriction of the blood vessels.
- Balanced diet. Fruits, vegetables, meat and fish
should be incorporated in the patient’s daily diet
to ensure that he or she gets the right amount of
nutrients he or she needs.
- Smoking cessation. Nicotine causes
vasoconstriction which can increase the pressure
of the blood and result in MI.
ASSESSMENT AND DIAGNOSTIC FINDINGS
- Patient history. The patient history includes the
description of the presenting symptoms, the
history of previous cardiac and other illnesses,
and the family history of heart diseases.
- ECG. ST elevation signifying ischemia; peaked
upright or inverted T wave indicating injury;
development of Q waves signifying prolonged
ischemia or necrosis.
- Cardiac enzymes and isoenzymes. CPK-MB
(isoenzyme in cardiac muscle): Elevates within 4–
8 hr, peaks in 12–20 hr, returns to normal in 48–
72 hr.
- LDH. Elevates within 8–24 hr, peaks within 72–
144 hr, and may take as long as 14 days to return
to normal. An LDH1 greater than LDH2 (flipped
ratio) helps confirm/diagnose MI if not detected
in acute phase.
- Troponins. Troponin I (cTnI) and troponin T
(cTnT): Levels are elevated at 4–6 hr, peak at 14–
18 hr, and return to baseline over 6–7 days. These
enzymes have increased specificity for necrosis
and are therefore useful in diagnosing
postoperative MI when MB-CPK may be elevated
related to skeletal trauma.
- Myoglobin. A heme protein of small molecular
weight that is more rapidly released from
damaged muscle tissue with elevation within 2 hr
after an acute MI, and peak levels occurring in 3–
15 hr.
- Electrolytes. Imbalances of sodium and potassium
can alter conduction and compromise
contractility.
- WBC. Leukocytosis (10,000–20,000) usually
appears on the second day after MI because of
the inflammatory process.
- ESR. Rises on second or third day after MI,
indicating inflammatory response.
- Chemistry profiles. May be abnormal, depending
on acute/chronic abnormal organ
function/perfusion.
- ABGs/pulse oximetry. May indicate hypoxia or
acute/chronic lung disease processes.
- Lipids (total lipids, HDL, LDL, VLDL, total
cholesterol, triglycerides, phospholipids).
Elevations may reflect arteriosclerosis as a cause
for coronary narrowing or spasm.
- Chest x-ray. May be normal or show an enlarged
cardiac shadow suggestive of HF or ventricular
aneurysm.
- Two-dimensional echocardiogram. May be done
to determine dimensions of chambers,
septal/ventricular wall motion, ejection fraction
(blood flow), and valve configuration/function.
- Nuclear imaging studies: Persantine or Thallium.
Evaluates myocardial blood flow and status of
myocardial cells, e.g., location/extent of
acute/previous MI.
- Cardiac blood imaging/MUGA. Evaluates specific
and general ventricular performance, regional
wall motion, and ejection fraction.
- Technetium. Accumulates in ischemic cells,
outlining necrotic area(s).
- Coronary angiography. Visualizes
narrowing/occlusion of coronary arteries and is
usually done in conjunction with measurements
of chamber pressures and assessment of left
ventricular function (ejection fraction). Procedure
is not usually done in acute phase of MI unless
angioplasty or emergency heart surgery is
imminent.
- Digital subtraction angiography (DSA). Technique
used to visualize status of arterial bypass grafts
and to detect peripheral artery disease.
- Magnetic resonance imaging (MRI). Allows
visualization of blood flow, cardiac chambers or
intraventricular septum, valves, vascular lesions,
plaque formations, areas of necrosis/infarction,
and blood clots.
- Exercise stress test. Determines cardiovascular
response to activity (often done in conjunction
with thallium imaging in the recovery phase).
IMMEDIATE TREATMENT FOR MI
MONA TASS
- M: Morphine
o Analgesic drugs such as morphine are to
reduce pain and anxiety, also has other
beneficial effects as a vasodilator and
decreases the workload of the heart by
reducing preload and afterload.
- O: Oxygen
o To provide and improve oxygenation of
ischemic myocardial tissue; enforced together
with bedrest to help reduce myocardial
oxygen consumption. Given via nasal cannula
at 2 to 4 L/min.
- N: Nitroglycerine
o First-line of treatment for angina pectoris and
acute MI; causes vasodilation and increases
blood flow to the myocardium.
- A: Aspirin
o Aspirin prevents the formation of
thromboxane A2 which causes platelets to
aggregate and arteries to constrict. The earlier
the patient receives ASA after symptom
onset, the greater the potential benefit.
- T: Thrombolytics
o To dissolve the thrombus in a coronary artery,
allowing blood to flow through again,
minimizing the size of the infarction and
preserving ventricular function; given in some
patients with MI.
- A: Anticoagulants
o Given to prevent clots from becoming larger
and block coronary arteries. They are usually
given with other anticlotting medicines to
help prevent or reduce heart muscle damage.
- S: Stool Softeners
o Given to avoid intense straining that may
trigger arrhythmias or another cardiac arrest.
- S: Sedatives
o In order to limit the size of infarction and give
rest to the patient. Valium or an equivalent is
usually given.
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.
- 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,
changes in skin color, and laboratory values.