NURSING MANAGEMENT FOR PATIENTS WITH CARDIOVASCULAR

DISORDERS
MAIN SYMPTOMS AND SIGNS OF HEART DISEASES
Chest pain/discomfort, dyspnoea, palpitations, cyanosis, dizziness and syncope, edema,
cough, hemoptysis, fatigue and tiredness, pulse changes, urination during day,
urination during night (nocturia)
1) Chest Pain or Discomfort history: is very important although a cardinal
manifestation of heart disease, also originates from non-cardiac intrathoracic
structures aorta, pulmonary artery, bronchopulmonary tree, pleura, mediastinum,
oesophagus and diaphragm tissues of the neck and thoracic wall skin, thoracic
muscles, cervicodorsal spine. Chest Pain points to note in the history location
radiation character aggravating factors relieving factors time relationships duration,
frequency and pattern of occurrence setting in which it occurs associated factors
2) Breathlessness (dyspnea): abnormally uncomfortable awareness of breathing
regarded as abnormal only when it occurs at rest or at level of physical activity not
expected to cause it associated with diseases of heart lungs chest wall respiratory
muscles also associated with anxiety. Exertional dyspnea comes on during exertion
and subsides with rest commonly due to heart failure or lung disease. Orthopnea
breathlessness on lying flat A symptom of left ventricular failure due to
redistribution of fluid from the lower extremities to the lung. Paroxysmal Nocturnal
dyspnea a variant of orthopnea patient awakes from sleep severely breathless
persistent cough, may have white frothy sputum a manifestation of left ventricular
failure.

3) Oedema/ Peripheral Oedema a feature of chronic heart failure due to excessive salt
and water retention in patients found in the ankles, legs, thighs and lower abdomen
and over the sacrum associated with other features of heart failure. Causes of
peripheral oedema: Cardiac failure, Chronic venous insufficiency, nephrotic
syndrome, liver disease,drugs retaining sodium.
4) Palpitations: is rapid beating of the heart caused by disorders of cardiac rhythm and
rate history in palpitation beginning, rapid heart rate with regular or irregular rhythm.
Palpitations can be associated with drug use such as tobacco, coffee, tea, alcohol
epinephrine, aminophylline, associated with anxiety state

5) Syncope: is sudden temporary loss of consciousness associated with loss of postural

tone with spontaneous recovery not requiring electrical or chemical cardioversion due
to sudden vasodilation or sudden fall in cardiac output.

6) Cough: is a sudden, usually involuntary, expulsion of air from the lungs with a
characteristic and easily recognizable sound. The nature of the sputum is often
helpful pink frothy sputum - pulmonary oedema, clear white mucoid sputum –
viral infection or longstanding bronchial irritation thick, yellowish sputum –
infection, rusty sputum – pneumococcal pneumonia, blood streaked sputum –
tuberculosis, lung cancer or pulmonary infarction
7) Fatigue common in patients with impaired cardiovascular function consequent to a
reduced cardiac output associated with muscular weakness may be caused by drugs
e.g. β -blockers may also result for excessive blood pressure reduction in patients
with hypertension or heart failure caused by excessive diuresis or diuretic induced
hypokalaemia

8) Other symptoms: Nocturia common in early heart failure, Anorexia, Abdominal

fullness, right upper quadrant abdominal discomfort, weight loss.
.

MODIFIABLE FACTORS & SOME RISK FACTORS OF CARDIOVASCULAR

DISORDER
Cardiovascular disorder can be avoided or altered, potentially slowing the disease process or
even reversing it. Risk Factors of cardiac disease include:
 Elevated serum lipid levels
 Hypertension
 Cigarette smoking
 Diabetes mellitus
 Sedentary lifestyle
 Stress
 Obesity
 Excessive intake of saturated fats, carbohydrates, andsalt.

Nonmodifiable Risk Factors

Non modifiable factors increase a person’s risk of cardiovascular disease:

 Age
  Male gender
 Family history
 Race
Susceptibility to cardiovascular disease increases with age; disease before age 40 is unusual.
However, the age-disease correlation may simply reflect the longer duration of exposure too
their risk factors. Women are less susceptible than men to heart disease until after
menopause; then they become as susceptible as men. It is proposed that estrogen has a
protective effect to the heart.

A positive family history also increases a person’s chances of developing premature

cardiovascular disease. Although it affects all races, blacks are most susceptible to
cardiovascular disease.

HEART FAILURE

Heart failure, also known as congestive heart failure, is recognized as a clinical syndrome
characterized by signs and symptoms of fluid overload or of inadequate tissue perfusion.

 Heart failure is the inability of the heart to pump sufficient blood to meet the needs
of the tissues for oxygen and nutrients.
 The term heart failure indicates myocardial disease in which there is a problem with
contraction of the heart (systolic dysfunction) or filling of the heart (diastolic
dysfunction) that may or may not cause pulmonary or systemic congestion.
 Heart failure is most often a progressive, life-long condition that is managed with
lifestyle changes and medications to prevent episodes of acute decompensated heart
failure.
Classification

Heart failure is classified into two types: left-sided heart failure and right-sided heart failure.
Left-Sided Heart Failure

 Left-sided heart failure or left ventricular failure have different manifestations with
right-sided heart failure.
 Pulmonary congestion occurs when the left ventricle cannot effectively pump blood
out of the ventricle into the aorta and the systemic circulation.
 Pulmonary venous blood volume and pressure increase, forcing fluid from the
pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary
interstitial edema and impaired gas exchange.
Right-Sided Heart Failure

 When the right ventricle fails, congestion in the peripheral tissues and the viscera
predominates.
 The right side of the heart cannot eject blood and cannot accommodate all the blood
that normally returns to it from the venous circulation.
 Increased venous pressure leads to JVD and increased capillary hydrostatic pressure
throughout the venous system.
The American College of Cardiology and American Heart Association have
classifications of heart failure.

Stage A. Patients at high risk for developing left ventricular dysfunction but without
structural heart disease or symptoms of heart failure. No limitation of physical activity

Stage B. Patients with left ventricular dysfunction or structural heart disease that has not
developed symptoms of heart failure. Slight limitation

Stage C. Patients with left ventricular dysfunction or structural heart disease with current or
prior symptoms of heart failure. Marked limitation
Stage D. Patients with refractory end-stage heart failure requiring specialized interventions.
Inability to carry on any physical activity without discomfort

Pathophysiology

Heart failure results from a variety of cardiovascular conditions, including

chronic hypertension, coronary artery disease, and valvular disease.
  As HF develops, the body activates neurohormonal compensatory mechanisms.
 Systolic HF results in decreased blood volume being ejected from the ventricle.
 The sympathetic nervous system is then stimulated to
release epinephrine and norepinephrine.
 Decrease in renal perfusion causes renin release, and then promotes the formation
of angiotensin I.
 Angiotensin I is converted to angiotensin II by ACE which constricts the blood
vessels and stimulates aldosterone release that causes sodium and fluid retention.
 There is a reduction in the contractility of the muscle fibers of the heart as the
workload increases.
 Compensation. The heart compensates for the increased workload by increasing the
thickness of the heart muscle.
Incidences

Heart failure can affect both women and men, although the mortality is higher among
women.

 There are also racial differences; at all ages death rates are higher in African
American than in non-Hispanic whites.
 Heart failure is primarily a disease of older adults, affecting 6% to 10% of those older
than 65.
 It is also the leading cause of hospitalization in older people.
Causes

Systemic diseases are usually one of the most common causes of heart failure.

 Coronary artery disease. Atherosclerosis of the coronary arteries is the primary

cause of HF, and coronary artery disease is found in more than 60% of the patients
with HF.
 Ischemia. Ischemia deprives heart cells of oxygen and leads to acidosis from the
accumulation of lactic acid.
 Cardiomyopathy. HF due to cardiomyopathy is usually chronic and progressive.
  Systemic or pulmonary hypertension. Increase in afterload results from
hypertension, which increases the workload of the heart and leads to hypertrophy of
myocardial muscle fibers.
 Valvular heart disease. Blood has increasing difficulty moving forward, increasing
pressure within the heart and increasing cardiac workload.
Clinical Manifestation

LEFT SIDED HEART FAILURE

 DYSPNEA: may be precipitated by minimal to moderate activity, also occurs during

rest.
 ORTHOPNEA: dyspnea that develop in recumbent position, and is relieved with the
elevation of the head of pillow.
 COUGH: Cough is initially dry and nonproductive. Large volume of frothy sputum,
which is sometimes pink, may be produced usually indicating severe pulmonary
congestion.
 HEMOPTYSIS: Pink or blood stained mucus could be produced.
 ADVENTITIOUS BREATH SOUND: May be heard in varous areas of the lungs,
as failure worsen pulmonary congestion increases and crackles may be auscultated
throughout the lung field.
 PULMONARY CONGESTION: Sustained high pressure in the pulmonary veins
eventually forces the fluid from the blood into the surrounding aveoli which transfer
oxygen to the bloodstream.

Left-sided HF

 Dyspnea or shortness of breath may be precipitated by minimal to moderate activity.

 Cough. The cough associated with left ventricular failure is
initially dry and nonproductive.
 Pulmonary crackles. Bibasilar crackles are detected earlier and as it worsens,
crackles can be auscultated across all lung fields.
 Low oxygen saturation levels. Oxygen saturation may decrease because of increased
pulmonary pressures.
RIGHT- SIDED HEART FAILURE
 ANOREXIA and NAUSEA: Results from the venous engorgement and venous
stasis within the abdominal organs.
 WEIGHT GAIN: Due to retention of fluid
 HEPATOMEGALY: Results from the venous engorgement of the liver increased
pressure may interfere with the liver’s ability to function.
 EDEMA (BIPEDAL): fluid retention
 ASCITES: accumulation of fluid in the peritoneal cavity. Increased pressure within
the portal vessels forces fluid into the abdominal cavity.
 DISTENDED JUGULAR NECK VEIN: increased venous pressure leads to
distended neck vein.
Right-sided HF

 Enlargement of the liver result from venous engorgement of the liver.

 Accumulation of fluid in the peritoneal cavity may increase pressure on
the stomach and intestines and cause gastrointestinal distress.
 Loss of appetite results from venous engorgement and venous stasis within the
abdominal organs.

Prevention

Prevention of heart failure mainly lies in lifestyle management.

 Healthy diet. Avoiding intake of fatty and salty foods greatly improves the
cardiovascular health of an individual.
 Engaging in cardiovascular exercises thrice a week could keep the cardiovascular
system up and running smoothly.
 Smoking cessation. Nicotine causes vasoconstriction that increases the pressure
along the vessels.
Complications

Many potential problems associated with HF therapy relate to the use of diuretics.

 Hypokalemia. Excessive and repeated dieresis can lead to hypokalemia.

  Hyperkalemia. Hyperkalemia may occur with the use of ACE inhibitors, or
spironolactone.
 Prolonged diuretic therapy might lead to hyponatremia and result
in disorientation, fatigue, apprehension, weakness, and muscle cramps.
 Dehydration and hypotension. Volume depletion from excessive fluid loss may lead
to dehydration and hypotension.

Assessment and Diagnostic Findings

HF may go undetected until the patient presents with signs and symptoms of pulmonary and
peripheral edema.

 ECG: May show hypertrophy, axis deviation, ischemia, and damage patterns.
Dysrhythmias and ST-T segment abnormalities may be present.
 Chest x-ray: May show enlarged cardiac shadow or abnormal contour indicating
ventricular aneurysm.
 Sonograms (echocardiography, Doppler, and transesophageal echocardiography):
May reveal chamber dimensions, valvular function/structure, and ventricular dilation
and dysfunction.
 Heart scan (MUGA): Measures cardiac volume, ejection fraction, and wall motion.
 Exercise or pharmacological stress myocardial perfusion: Determines presence of
myocardial ischemia and wall motion abnormalities.
 PET scan: Sensitive test for evaluating myocardial ischemia and viability.
 Cardiac catheterization: Assesses pressures, differentiates right- versus left-sided
heart failure, and evaluates coronary artery patency.
 Liver enzymes: Elevated in liver congestion/failure.
 Digoxin and other cardiac drug levels: Determines therapeutic range.
 Bleeding and clotting times: Identifies clotting risks and therapeutic range.
 Electrolytes: May be altered due to fluid shifts, renal function, or diuretic therapy.
 Pulse oximetry: Measures oxygen saturation, especially in conjunction with COPD or
chronic HF.
 Arterial blood gases (ABGs): Reflects respiratory and acid-base status.
 BUN/creatinine: Evaluates renal perfusion and function.
  Serum albumin/transferrin: Indicates protein intake and liver function.
 Complete blood count (CBC): Assesses for anemia, polycythemia, and dilutional
changes.
 ESR: Evaluates acute inflammatory reaction.
 Thyroid studies: Determines thyroid activity as a potential precipitator of HF.

MEDICAL MANAGEMENT:

 ACE Inhibitors. ACE inhibitors slow the progression of HF, improve exercise
tolerance, decrease the number of hospitalizations for HF, and
promote vasodilation and diuresis by decreasing afterload and preload.
 Angiotensin II Receptor Blockers. ARBs block the conversion of angiotensin I at
the angiotensin II receptor and cause decreased blood pressure, decreased systemic
vascular resistance, and improved cardiac output.
 Beta Blockers. Beta blockers reduce the adverse effects from the constant
stimulation of the sympathetic nervous system.
 Diuretics. Diuretics are prescribed to remove excess extracellular fluid by
increasing the rate of urine produced in patients with signs and symptoms of fluid
overload.

 Calcium Channel Blockers. CCBs cause vasodilation, reducing systemic vascular

resistance but contraindicated in patients with systolic HF.
Nutritional Therapy

 Sodium restriction. A low sodium diet of 2 to 3g/day reduces fluid retention and the
symptoms of peripheral and pulmonary congestion, and decrease the amount of
circulating blood volume, which decreases myocardial work.
 Patient compliance. Patient compliance is important because dietary indiscretions
may result in severe exacerbations of HF requiring hospitalizations.
Additional Therapy

 Supplemental Oxygen. The need for supplemental oxygen is based on the degree of
pulmonary congestion and resulting hypoxia.
  Cardiac Resynchronization Therapy. CRT involves the use of a
biventricular pacemaker to treat electrical conduction defects.
 Ultrafiltration. Ultrafiltration is an alternative intervention for patients with severe
fluid overload.
 Cardiac Transplant. For some patients with end-stage heart failure, cardiac
transplant is the only option for long term survival.

Nursing Management

1) Administer prescribed medications, diuretics, digitalis, anticoagulants,

vasodilators.

2) Check intake and output.

3) Weigh daily.

4) Provide a low- sodium diet.

5) Auscultate lung sounds.

6) Determine degree of JVD.

7) Assess dependent edema.

8) Monitor vital signs.

9) Administer oxygen as prescribed.

10) Psychological support

MYOCARDIAL INFARCTION

. Myocardial infarction is the necrosis of an area of cardiac tissue as a result of obstruction of

blood flow through a coronary artery or one of its branches

. The myocardial tissue dies as a result of the occlusion

. Signs/Symptoms:

. 1. Chest pain, substernally with radiation to arm, neck, jaw, or back; and unrelieved by rest
or nitrates.

. 2. Diaphoresis and cool, clammy, pale skin.

. 3. Nausea and vomiting.

. 4. Dyspnea.

. 5. Palpitations or syncope.

. 6. Restlessness and anxiety.

. 7. Tachycardia or bradycardia.

Pathophysiology

 In each case of MI, a profound imbalance exists between myocardial oxygen supply
and demand. 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

The causes of MI primarily stems from the vascular system.

 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
Some of the patients have prodromal symptoms or a previous diagnosis of CAD, but about
half report no previous symptoms.

 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

A healthy lifestyle could help prevent the development of MI.

 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

The diagnosis of MI is generally based on the presenting symptoms.

 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).

NURSING MANAGEMENT

 . Provide quiet, calm environment

 . Keep client on bedrest for 24-48 hours

 . Give medications as ordered –analgesics, O2, Nitroglycerin

 . Elevate head of bed

 . Watch for any more chest pain

 . Maintain IV line

 . Monitor for signs of CHF, cardiogenic shock, and pulmonary edema

 . Evaluate signs of MI

 . Skin color, and temperature

 . Monitor vitals
 . Observe EKG for dysrhythmias

 . Monitor fluid volume levels

 . Check labs

Home care Teaching

 . Teach about medications

 . Include follow-up with physician

 . May need to teach about CAD

 . Teach modification of risk factors –weight, diet, smoking, exercise, etc.

 Notify of any chest pain

Problem and nursing care for patients with myocardial infarction (nursing care
in the CCU)

Problem-1 -Chest pain

-Assess chest pain

-Obtain a 12 Leads ECG recording

-Give analgesic and nitrates order

-Oxygen therapy

-Cardiac monitor

-Provide physical and emotional rest

 . Problem-2- Risk for decreased cardiac output

-Assess for signs and symptoms of decreased cardiac output hourly and report to the
physician following hypotension ,tachycardia, fatigue ,reduced urine output ,cool
moist ,cyanotic extremities
 -Promote rest

-Administered O2 and nitrates as ordered

-Monitor heart rhythm

 . Problem-3- Respiratory difficulties

-Assess the patient every 4 hours for chest discomfort

Administered O2 -Liquid diet for24 hours as prescribed

. Teach adhere to the diet and activity prescription

 . Problem-4- Anxiety and fear of death

-Allow patient to express Anxiety and fear

-Use of flexible visiting hours allows the presence of supportive family

-Administer communication by answering questions

-Administer Sedative and anti anxiety medication as ordered

Encouraged active participation in hospital cardiac rehabilitation program

MEDICAL MANAGEMENT;

 Oxygen
 Aspirin
 Nitroglycerine
 Morphine
 Thrombolytics
 Stool softener
 Sedatives
Nursing Priorities

1. Relieve pain, anxiety.

2. Reduce myocardial workload.
3. Prevent/detect and assist in treatment of life-threatening dysrhythmias or
complications.
4. Promote cardiac health, self-care.
Nursing Interventions

Nursing interventions should be anchored on the goals in the nursing care plan.

 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.

ANGINA

Angina pectoris is chest pain, caused by myocardial ischemia is not a separate disease, but
rather a symptom of coronary artery disease (CAD). It is caused by a blockage or spasm of a
coronary artery, leading to a diminished myocardial blood supply. The lack of oxygen causes
myocardial ischemia, which is felt as chest discomfort, pressure, or pain. Angina may occur
anywhere in the chest, neck, arms, or back, but the most commonly described location is pain
or pressure behind the sternum. The pain often radiates to the left arm but can also radiate
down both arms and to the back, shoulder, jaw, or neck. Angina is a clinical syndrome
usually characterized by episodes of 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.

Types of Angina

Angina can be classified into three different phases: stable, unstable, and variant.

 Stable angina is chest pain that occurs predictably on exertion. This type of angina is
associated with stable plaque build-up in the coronary arteries.
 Variant or Prinzmetal’s angina is a less common form of angina. It is characterized
by episodes of chest pain that occur at rest. Unlike stable and unstable angina, variant
angina is caused by coronary artery vasospasms, which can cause an increase in
myocardial oxygen demand and a transient ST-segment elevation.
 Unstable angina is pain that occurs more often and in unpredictable patterns. It can
occur while the client is at rest, as well as with minimal exertion, and often causes the
client to limit their activity.
Pathophysiology

Angina is usually caused by atherosclerotic disease.

 Almost invariably, angina is associated with 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.
 Schematic Diagram for Angina Pectoris via Scribd.
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. 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.
 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.

Gerontologic Considerations

Here’s what you need to know when caring for geriatric patients with angina pectoris:

 The elderly person with angina may not exhibit the typical pain profile because of the
diminished responses of neurotransmitters that occur with aging.
 Often, the presenting symptom in the elderly is dyspnea.
 Sometimes, there are no symptoms (“silent” CAD), making recognition and diagnosis
a clinical challenge.
 Elderly patients should be encouraged to recognize their chest pain–like symptom
(eg, weakness) as an indication that they should rest or take prescribed medications.
Complications

Here are the common complications for patients with angina pectoris.
  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 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.
 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 the 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 the 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 the 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 hyper spastic 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.
 Nitroglycerin 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.
 Calcium channel blockers have negative inotropic effects.
 Antiplatelet medications prevent platelet aggregation,
and anticoagulants prevent thrombus formation.
NURSING MANAGEMENT
1. Perform pain assessment: Identify precipitating events, if any, as well as
frequency, duration, intensity, and location of the pain.
2. Assess and document the client’s response to medication.
3. Monitor vital signs every five (5) minutes during the initial anginal attack.
4. Auscultate heart sounds. Monitor heart rate and rhythm.
5. Elevate the head of the bed if the client is short of breath or during nitrates
administration.

Discharge and Home Care Guidelines

The goals of education are to reduce the frequency and severity of anginal attacks, to delay
the progress of the underlying disease if possible, and to prevent complications.

 Reduce anginal attacks. Activities should be planned to minimize the occurrence of

angina episodes.
 Follow-up monitoring. The patient may need reminders about follow-up monitoring,
including periodic blood laboratory testing and ECGs.
 Compliance to therapeutic regimen. The home care nurse may monitor the patient’s
compliance to dietary restrictions and to prescribed antianginal medications.

HYPERTENSION

Hypertension is one of the most common lifestyle diseases to date. It affects people from all
walks of life.

 Hypertension is defined as a systolic blood pressure greater than 140 mmHg and
a diastolic pressure of more than 90 mmHg.
 This is based on the average of two or more accurate blood pressure
measurements during two or more consultations with the healthcare provider.

Classification of Hypertension
  Normal. The normal range for blood pressure is between, less than 120 mmHg and
less than 80 mmHg.
 Elevated. Elevated stage starts from 120 mmHg to 129 mmHg for systolic blood
pressure and less than 80 mmHg for diastolic pressure.
 Stage 1 hypertension. Stage 1 starts when the patient has a systolic pressure of 130
to 139 mmHg and a diastolic pressure of 80 to 89 mmHg.
 Stage 2 hypertension. Stage 2 starts when the systolic pressure is already more than
or equal than 140 mmHg and the diastolic is more than or equal than 90 mmHg.
 Hypertensive Crisis: Systolic is greater than 180mmHg and diastolic is greater than
120mmHg.

Pathophysiology

In a normal circulation, pressure is transferred from the heart muscle to the blood each time
the heart contracts and then pressure is exerted by the blood as it flows through the blood
vessels.

The pathophysiology of hypertension follows.

 Hypertension is a multifactorial
 When there is excess sodium intake, renal sodium retention occurs, which increases
fluid volume resulting in increased preload and increase in contractility.
 Obesity is also a factor in hypertension because hyperinsulinemia develops and
structural hypertrophy results leading to increased peripheral vascular resistance.
 Genetic alteration also plays a role in the development of hypertension because
when there is cell membrane alteration, functional constriction may follow and also
results in increased peripheral vascular resistance.

Causes

Hypertension has a lot of causes just like how fever has many causes. The factors that are
implicated as causes of hypertension are:

 Increased sympathetic nervous system activity. Sympathetic nervous system

activity increases because there is dysfunction in the autonomic nervous system.
  Increase renal reabsorption. There is an increase reabsorption of sodium, chloride,
and water which is related to a genetic variation in the pathways by which the
kidneys handle sodium.
 Increased RAAS activity. The renin-angiotensin-aldosterone system increases its
activity leading to the expansion of extracellular fluid volume and increased
systemic vascular resistance.
 Decreased vasodilation of the arterioles. The vascular
endothelium is damaged because of the decrease in the vasodilation of the arterioles.
Clinical Manifestations

Many people who have hypertension are asymptomatic at first. Physical examination may
reveal no abnormalities except for an elevated blood pressure, so one must be prepared to
recognize hypertension at its earliest.

 Headache. The red blood cells carrying oxygen is having a hard time reaching the
brain because of constricted vessels, causing headache.
 Dizziness occurs due to the low concentration of oxygen that reaches the brain.
 Chest pain. Chest pain occurs also due to decreased oxygen levels.
 Blurred vision. Blurred vision may occur later on because of too much constriction
in the blood vessels of the eye that red blood cells carrying oxygen cannot pass
through.
Prevention

Prevention of hypertension mainly relies on a healthy lifestyle and self-discipline.

 Weight reduction. Maintenance of normal body weight can help prevent

hypertension.
 Adopt DASH. DASH or the Dietary Approaches to Stop Hypertension includes
consummation of a diet rich in fruits, vegetable, and low-fat dairy.
 Dietary sodium retention. Sodium contributes to an elevated blood pressure, so
reducing the dietary intake to no more than 2.4 g sodium per day can be really
helpful.
 Physical activity. Engage in regular aerobic physical activity for 30 minutes thrice
every week.
  Moderation of alcohol consumption. Limit alcohol consumption to no more than 2
drinks per day in men and one drink for women and people who are lighter in
weight.
Complications

If hypertension is left untreated, it could progress to complications of the different body

organs.

 Heart failure. With increased blood pressure, the heart pumps blood faster than
normal until the heart muscle goes weak from too much exertion.
 Myocardial infarction. Decreased oxygen due to constriction of blood vessels may
lead to MI.
 Impaired vision. Ineffective peripheral perfusion affects the eye, causing problems
in vision because of decreased oxygen.
 Renal failure. Blood carrying oxygen and nutrients could not reach the renal system
because of the constricted blood vessels.
Assessment and Diagnostic Findings

Assessment of the patient with hypertension must be detailed and thorough. There are also
diagnostic tests that can be performed to establish the diagnosis of hypertension.

Assessment

 Assess the patient’s health history

 Perform physical examination as appropriate.
 The retinas are examined to assess possible organ damage.
 Laboratory tests are also taken to check target organ damage.
Diagnostic Tests

 Urinalysis is performed to check the concentration of sodium in the urine though the
specific gravity.
 Blood chemistry (e.g. analysis of sodium, potassium, creatinine, fasting glucose, and
total and high density lipoprotein cholesterol levels). These tests are done to
determine the level of sodium and fat in the body.
 12-lead ECG. ECG needs to be performed to rule presence of cardiovascular
damage.
 Echocardiography. Echocardiography assesses the presence of left ventricular
hypertrophy.
 Creatinine clearance. Creatinine clearance is performed to check for the level of
BUN and creatinine that can determine if there is renal damage or not.
 Renin level. Renin level should be assessed to determine how RAAS is coping.
 Hemoglobin/hematocrit: Not diagnostic but assesses relationship of cells to fluid
volume (viscosity) and may indicate risk factors such as hypercoagulability, anemia.
 Blood urea nitrogen (BUN)/creatinine: Provides information about renal
perfusion/function.
 Glucose: Hyperglycemia (diabetes mellitus is a precipitator of hypertension) may
result from elevated catecholamine levels (increases hypertension).
 Serum potassium: Hypokalemia may indicate the presence of primary aldosteronism
(cause) or be a side effect of diuretic therapy.
 Serum calcium: Imbalance may contribute to hypertension.
 Lipid panel (total lipids, high-density lipoprotein [HDL], low-density lipoprotein
[LDL], cholesterol, triglycerides, phospholipids): Elevated level may indicate
predisposition for/presence of atheromatous plaques.
 Thyroid studies: Hyperthyroidism may lead or contribute to vasoconstriction and
hypertension.
 Serum/urine aldosterone level: May be done to assess for primary aldosteronism
(cause).
 Urinalysis: May show blood, protein, or white blood cells; or glucose suggests renal
dysfunction and/or presence of diabetes.
 Creatinine clearance: May be reduced, reflecting renal damage.
 Urine vanillylmandelic acid (VMA) (catecholamine metabolite): Elevation may
indicate presence of pheochromocytoma (cause); 24-hour urine VMA may be done
for assessment of pheochromocytoma if hypertension is intermittent.
 Uric acid: Hyperuricemia has been implicated as a risk factor for the development of
hypertension.
 Renin: Elevated in renovascular and malignant hypertension, salt-wasting disorders.
 Urine steroids: Elevation may indicate hyperadrenalism, pheochromocytoma,
pituitary dysfunction, Cushing’s syndrome.
  Intravenous pyelogram (IVP): May identify cause of secondary hypertension, e.g.,
renal parenchymal disease, renal/ureteral calculi.
 Kidney and renography nuclear scan: Evaluates renal status (TOD).
 Excretory urography: May reveal renal atrophy, indicating chronic renal disease.
 Chest x-ray: May demonstrate obstructing calcification in valve areas; deposits in
and/or notching of aorta; cardiac enlargement.
 Computed tomography (CT) scan: Assesses for cerebral tumor, CVA, or
encephalopathy or to rule out pheochromocytoma.
 Electrocardiogram (ECG): May demonstrate enlarged heart, strain patterns,
conduction disturbances. Note: Broad, notched P wave is one of the earliest signs of
hypertensive heart disease.

Nursing Priorities

1. Maintain/enhance cardiovascular functioning.

2. Prevent complications.
3. Provide information about disease process/prognosis and treatment regimen.
4. Support active patient control of condition.
Nursing Interventions

The objective of nursing care focuses on lowering and controlling the blood pressure without
adverse effects and without undue cost.

 Encourage the patient to consult a dietitian to help develop a plan for improving
nutrient intake or for weight loss.
 Encourage restriction of sodium and fat
 Emphasize increase intake of fruits and vegetables.
 Implement regular physical activity.
 Advise patient to limit alcohol consumption and avoidance of tobacco.
 Assist the patient to develop and adhere to an appropriate exercise regimen.

Discharge and Home Care Guidelines

Following discharge, the nurse should promote self-care and independence of the patient.
  The nurse can help the patient achieve blood pressure control
through education about managing blood pressure.
 Assist the patient in setting goal blood pressures.
 Provide assistance with social support.
 Encourage the involvement of family members in the education program to support
the patient’s efforts to control hypertension.
 Provide written information about expected effects and side effects.
 Encourage and teach patients to measure their blood pressures at home.
 Emphasize strict compliance of follow-up check up.

MEDICAL MANAGEMENT

 The medications used for treating hypertension decrease peripheral

resistance, blood volume, or the strength and rate of myocardial contraction.
 For uncomplicated hypertension, the initial medications recommended
are diuretics and beta blockers.
 Only low doses are given, but if blood pressure still exceeds 140/90 mmHg, the dose
is increased gradually.
 Thiazide diuretics decrease blood volume, renal blood flow, and cardiac output.
 ARBs are competitive inhibitors of aldosterone binding.
 Beta blockers block the sympathetic nervous system to produce a slower heart
rate and a lower blood pressure.
 ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II and
lowers peripheral resistance.

Stage 1 Hypertension

 Thiazide diuretic is recommended for most and angiotensin-converting enzyme-

1, aldosterone receptor blocker, beta blocker, or calcium channel blocker is
considered.

Stage 2 Hypertension
 Two-drug combination is followed, usually including thiazide diuretic and
angiotensin-converting enzyme-1, or beta-blocker, or calcium channel blocker.