What is Pneumonia?

Respiratory diseases are rampant today because it is easier spread in

crowded areas. Pneumonia is one of the most common respiratory problems
and it affects all stages of life.
● Pneumonia is an inflammation of the lung parenchyma caused by

various microorganisms, including bacteria, mycobacteria, fungi, and

viruses.
● Pneumonitis is a more general term that describes the inflammatory

process in the lung tissue that may predispose and place the patient at
risk for microbial invasion.
Classification
Pneumonia is classified into four: community-acquired pneumonia (CAP)
and hospital-acquired pneumonia (HAP), pneumonia in the
immunocompromised host, and aspiration pneumonia.
Community-Acquired Pneumonia
● CAP occurs either in the community setting or within the first 48 hours
after hospitalization.
● The causative agents for CAP that needs hospitalization
include streptococcus pneumoniae, H. influenza, Legionella,
and Pseudomonas aeruginosa.
● Only in 50% of the cases does the specific etiologic agent become
identified.
● Streptococcus pneumoniae is the most common cause of CAP in
people younger than 60 years of age.
● Viruses are the most common cause of pneumonia in infants and
children.
Hospital-Acquired Pneumonia
● HAP is also called nosocomial pneumonia and is defined as the onset of
pneumonia symptoms more than 48 hours after admission in patients
with no evidence of infection at the time of admission.
● HAP is the most lethal nosocomial infection and the leading cause
of death in patients with such infections.
● Common microorganisms that are responsible for HAP
include Enterobacter species, Escherichia coli, influenza, Klebsiella
species, Proteus, Serratia marcescens, S. aureus, and S. pneumonia.
● The usual presentation of HAP is a new pulmonary infiltrate on chest x-
ray combined with evidence of infection.
Pneumonia in the Immunocompromised Host
● Pneumonia in immunocompromised hosts includes Pneumocystis
pneumonia, fungal pneumonias and Mycobacterium tuberculosis.
● Patients who are immunocompromised commonly develop pneumonia
from organisms of low virulence.
● Pneumonia in immunocompromised hosts may be caused by the
organisms also observe in HAP and CAP.
Aspiration Pneumonia
● Aspiration pneumonia refers to the pulmonary consequences resulting
from entry of endogenous or exogenous substances into the lower
airway.
● The most common form of aspiration pneumonia is a bacterial infection
from aspiration of bacteria that normally reside in the upper airways.
 ● Aspiration pneumonia may occur in the community or hospital setting.
● Common pathogens are S. pneumonia, [Link], and S. aureus.
Pathophysiology
Having an idea about the disease process helps the patient understand the
treatment regimen and its importance, increasing patient compliance.
● Pneumonia arises from normal flora present in patients

whose resistance has been altered or from aspiration of flora present in

the oropharynx.
● An inflammatory reaction may occur in the alveoli,

producing exudates that interfere with the diffusion of oxygen and

carbon dioxide.
● White blood cells also migrate into the alveoli and fill the normally air-

filled spaces.
● Due to secretions and mucosal edema, there are areas of the lung that

are not adequately ventilated and cause partial occlusion of the alveoli
or bronchi.
● Hypoventilation may follow, causing ventilation-perfusion mismatch.
● Venous blood entering the pulmonary circulation passes through the

under ventilated areas and travels to the left side of the heart
deoxygenated.
● The mixing of oxygenated and poorly oxygenated blood can result

to arterial hypoxemia.
Epidemiology
Pneumonia has affected a lot of people, especially those who have a weak
immune system. Learning statistics on pneumonia could give you an idea
about how many has fallen victim to this respiratory disease.
● Pneumonia and influenza account for nearly 60,000 deaths annually.
● Pneumonia also ranks as the eighth leading cause of death in the

United States.
● It is estimated that more than 915, 000 episodes of CAP occur in adults

65 years old and above in the United States.

● HAP accounts for 15% of hospital-acquired infections and is the leading

cause of death in patients with such infections.

● The estimated incidence of HAP 4 to 7 episodes per 1000

hospitalizations.
Causes
Each type of pneumonia is caused by different and several factors.
Community-Acquired Pneumonia
● Streptococcus pneumoniae. This is the leading cause of CAP in

people younger than 60 years of age without comorbidity and in those 60

years and older with comorbidity.
● Haemophilus influenzae. This causes a type of CAP that frequently

affects elderly people and those with comorbid illnesses.

● Mycoplasma pneumoniae.

Hospital-Acquired Pneumonia
● Staphylococcus aureus. Staphylococcus pneumonia occurs through

inhalation of the organism.

● Impaired host defenses. When the defenses of the body are down,

several pathogens may invade the body.

● Comorbid conditions. There are several conditions that lower the

immune system, causing bacteria to pool in the lungs and eventually

result in pneumonia.
● Supine positioning. When the patient stays in a
 ●

prolonged supine position, fluid in the lungs pools down and stays
stagnant, making it a breeding place for bacteria.
● Prolonged hospitalization. The risk for hospital infections or nosocomial
infections increases the longer the patient stays in the hospital.
Clinical Manifestations
Pneumonia varies in its signs and symptoms depending on its type but it is
not impossible to diagnose a specific pneumonia through its clinical
manifestations.

● Rapidly rising fever. Since there is inflammation of the lung

parenchyma, fever develops as part of the signs of an infection.
● Pleuritic chest pain. Deep breathing and coughing aggravate the pain in
the chest.
● Rapid and bounding pulse. A rapid heartbeat occurs because the body
compensates for the low concentration of oxygen in the body.
● Tachypnea. There is fast breathing because the body tries to
compensate for the low oxygen concentration in the body.
● Purulent sputum. The sputum becomes purulent because of the
infection in the lung parenchyma which produced sputum-filled with pus.
Prevention
It is better to prevent the occurrence of pneumonia instead of treating the
disease itself. Here are several ways that can help prevent pneumonia.
● Pneumococcal vaccine. This vaccine can prevent pneumonia in healthy

patients with an efficiency of 65% to 85%.

● Staff education. To help prevent HAP, the CDC (2004) encouraged staff

education and involvement in infection prevention.

● Infection and microbiologic surveillance. It is important to carefully

observe the infection so that there could be an appropriate application of

prevention techniques.
● Modifying host risk for infection. The infection should never be allowed

to descend on any host, so the risk must be decreased before it can

 ●

affect one.
Complications
Pneumonia has several complications if left untreated or the interventions are
inappropriate. These are the following complications that may develop in
patients with pneumonia.
● Shock and respiratory failure. These complications are encountered

chiefly in patients who have received no specific treatment and

inadequate or delayed treatment.
● Pleural effusion. In pleural effusion, the fluid is sent to the laboratory

for analysis, and there are three stages: uncomplicated, complicated, and
thoracic empyema.
Assessment and Diagnostic Findings
Assessment and diagnosis of pneumonia must be accurate since there are a
lot of respiratory problems that have similar manifestations. The following are
assessments and diagnostic tests that could determine pneumonia.
● History taking. The diagnosis of pneumonia is made through history

taking, particularly a recent respiratory tract infection.

● Physical examination. Mainly, the number of breaths per minute and

breath sounds is assessed during physical examination.

● Chest x-ray. Identifies structural distribution (e.g., lobar, bronchial); may

also reveal multiple abscesses/infiltrates, empyema (staphylococcus);

scattered or localized infiltration (bacterial); or diffuse/extensive nodular
infiltrates (more often viral). In mycoplasmal pneumonia, chest x-ray may
be clear.
● Fiberoptic bronchoscopy. May be both diagnostic (qualitative cultures)

and therapeutic (re-expansion of lung segment).

● ABGs/pulse oximetry. Abnormalities may be present, depending on

extent of lung involvement and underlying lung disease.

● Gram stain/cultures. Sputum collection; needle aspiration of empyema,

pleural, and transtracheal or transthoracic fluids; lung biopsies and blood

cultures may be done to recover causative organism. More than one type
of organism may be present; common bacteria include Diplococcus
pneumoniae, Staphylococcus aureus, a-hemolytic streptococcus,
Haemophilus influenzae; cytomegalovirus (CMV). Note: Sputum cultures
may not identify all offending organisms. Blood cultures may show
transient bacteremia.
● CBC. Leukocytosis usually present, although a low white blood cell

(WBC) count may be present in viral infection, immunosuppressed

conditions such as AIDS, and overwhelming bacterial pneumonia.
Erythrocyte sedimentation rate (ESR) is elevated.
● Serologic studies, e.g., viral or Legionella titers, cold

agglutinins. Assist in differential diagnosis of specific organism.

● Pulmonary function studies. Volumes may be decreased

(congestion and alveolar collapse); airway pressure may be increased

and compliance decreased. Shunting is present (hypoxemia).
● Electrolytes. Sodium and chloride levels may be low.
● Bilirubin. May be increased.
● Percutaneous aspiration/open biopsy of lung tissues. May reveal

typical intranuclear and cytoplasmic inclusions (CMV), characteristic

giant cells (rubeola).
Medical Management
The management of pneumonia centers is a step-by-step process that
zeroes on the treatment of the infection through identification of the
causative agent.
● Blood culture. Blood culture is performed for identification of the causal

pathogen and prompt administration of antibiotics in patients in whom

CAP is strongly suspected.
● Administration of macrolides. Macrolides are recommended for people

with drug-resistant S. pneumoniae.

● Hydration is an important part of the regimen

because fever and tachypnea may result in insensible fluid losses.

● Administration of antipyretics. Antipyretics are used to treat fever and

headache.
● Administration of antitussives. Antitussives are used for treatment of

the associated cough.

● Bed rest. Complete rest is prescribed until signs of infection are

diminished.
● Oxygen administration. Oxygen can be given if hypoxemia develops.
● Pulse oximetry. Pulse oximetry is used to determine the need for oxygen

and to evaluate the effectiveness of the therapy.

● Aggressive respiratory measures. Other measures include

administration of high concentrations of oxygen, endotracheal intubation,

and mechanical ventilation.
Nursing Management
Nurses are expected to perform both dependent and independent functions
for the patient to aid him or her towards the restoration of their well-being.
Nursing Assessment
Nursing assessment is critical in detecting pneumonia. Here are some tips for
your nursing assessment for pneumonia.
● Assess respiratory symptoms. Symptoms of fever, chills, or night

sweats in a patient should be reported immediately to the nurse as these

can be signs of bacterial pneumonia.
● Assess clinical manifestations. Respiratory assessment should further

identify clinical manifestations such as pleuritic pain,

bradycardia, tachypnea, and fatigue, use of accessory muscles for
breathing, coughing, and purulent sputum.
● Physical assessment. Assess the changes in temperature and pulse;

amount, odor, and color of secretions; frequency and severity of cough;

degree of tachypnea or shortness of breath; and changes in the chest x-
ray findings.
● Assessment in elderly patients. Assess elderly patients for altered

mental status, dehydration, unusual behavior, excessive fatigue, and

concomitant heart failure.
Diagnosis
Through the data collected during assessment, the following nursing
diagnoses are made:
● Ineffective airway clearance related to copious

tracheobronchial secretions.
● Activity intolerance related to impaired respiratory function.
● Risk for deficient fluid volume related to fever and a rapid respiratory

rate.
Nursing Care Planning & Goals
Planning is essential to establish the interventions that are appropriate for
the patient’s condition.
● Improve airway patency.
● Rest to conserve energy.
 ● Maintenance of proper fluid volume.
● Maintenance of adequate nutrition.
● Understanding of treatment protocol and preventive measures.
● Absence of complications.
Nursing Priorities
. Maintain/improve respiratory function.
. Prevent complications.
. Support recuperative process.
. Provide information about disease process, prognosis, and treatment.
Nursing Interventions
These nursing interventions, if implemented appropriately, would result in the
achievement of the goals of the management of pneumonia.
To improve airway patency:
● Removal of secretions. Secretions should be removed because retained

secretions interfere with gas exchange and may slow recovery.

● Adequate hydration of 2 to 3 liters per day thins and loosens pulmonary

secretions.
● Humidification may loosen secretions and improve ventilation.
● Coughing exercises. An effective, directed cough can also improve

airway patency.
● Chest physiotherapy. Chest physiotherapy is important because it

loosens and mobilizes secretions.

To promote rest and conserve energy:
● Encourage avoidance of overexertion and possible exacerbation of

symptoms.
● Semi-Fowler’s position. The patient should assume a comfortable

position to promote rest and breathing and should change positions

frequently to enhance secretion clearance and pulmonary ventilation and
perfusion.
To promote fluid intake:
● Fluid intake. Increase in fluid intake to at least 2L per day to replace

insensible fluid losses.

To maintain nutrition:
● Fluids with electrolytes. This may help provide fluid, calories, and

electrolytes.
● Nutrition-enriched beverages. Nutritionally enhanced drinks and shakes

can also help restore proper nutrition.

To promote patient’s knowledge:
● Instruct patient and family about the cause of pneumonia, management

of symptoms, signs, and symptoms, and the need for follow-up.

● Instruct patient about the factors that may have contributed to the

development of the disease.

Evaluation
Expected patient outcomes include the following:
● Demonstrates improved airway patency.
● Rests and conserves energy by limiting activities and remaining in bed

while symptomatic and then slowly increasing activities.

● Maintains adequate hydration.
● Consumes adequate dietary intake.
● States explanation for management strategies.
● Complies with management strategies.
● Exhibits no complications.
● Complies with treatment protocol and prevention strategies.
Discharge and Home Care Guidelines
Patient education is crucial regardless of the setting because self-care is
essential in achieving a patient’s well-being.
● Oral antibiotics. Teach the patient about the proper administration,

potential side effects, and symptoms to report.

● Breathing exercises. Teach the patient breathing exercises to promote

secretion clearance and volume expansion.

● Follow-up check up. Strict compliance to follow-up checkups is

important to check the latest chest x-ray result or physical examination

findings.
● Smoking cessation. Smoking should be stopped because it inhibits

tracheobronchial ciliary action and irritates the mucous cells of the

bronchi.
Documentation Guidelines
Documentation of data must be accurate and up-to-date to avoid
unnecessary legal situations that might occur.
● Document breath sounds, presence and character of secretions, use of

accessory muscles for breathing.

● Document character of cough and sputum.
● Document respiratory rate, pulse oximetry/O2 saturation, and vital signs.
● Document plan of care and who is involved in planning.
● Document client’s response to interventions, teaching, and actions

performed.
● Document if there is use of respiratory devices or airway adjuncts.
● Document response to medications administered.
● Document modifications to plan of care.

What is Chronic Obstructive Pulmonary Disease?

Nurses care for patients with COPD across the spectrum of care, from
outpatient to home care to emergency department, critical care, and hospice
settings.
● Chronic Obstructive Pulmonary Disease (COPD) is a condition of

chronic dyspnea with expiratory airflow limitation that does not

significantly fluctuate.
● Chronic Obstructive Pulmonary Disease has been defined by The Global

Initiative for Chronic Obstructive Lung Disease as

“a preventable and treatable disease with some significant
extrapulmonary effects that may contribute to the severity in individual
patients.”
● This updated definition is a broad description of COPD and its signs and

symptoms.
Classification
There are two classifications of COPD: chronic bronchitis and emphysema.
These two types of COPD can be sometimes confusing because there are
patients who have overlapping signs and symptoms of these two distinct
disease processes.
Chronic Bronchitis
● Chronic bronchitis is a disease of the airways and is defined as the
presence of cough and sputum production for at least 3 months in
each of 2 consecutive years.
● Chronic bronchitis is also termed as “blue bloaters”.
● Pollutants or allergens irritate the airways and leads to the production of
sputum by the mucus-secreting glands and goblet cells.
● A wide range of viral, bacterial, and mycoplasmal infections can produce
acute episodes of bronchitis.
Emphysema
● Pulmonary Emphysema is a pathologic term that describes an abnormal
distention of airspaces beyond the terminal bronchioles and destruction
of the walls of the alveoli.
● People with emphysema are also called “pink puffers”.
● There is impaired carbon dioxide and oxygen exchange, and the
exchange results from the destruction of the walls of overdistended
alveoli.
● There are two main types of emphysema: panlobular and centrilobular.
○ In panlobular, there is destruction of the respiratory bronchiole,

alveolar duct, and alveolus.

○ All spaces in the lobule are enlarged.
○ In centrilobular, pathologic changes occur mainly in the center of

the secondary lobule.

Pathophysiology
In COPD, the airflow limitation is both progressive and associated with an
abnormal inflammatory response of the lungs to noxious gases or particles.
 ● An inflammatory response occurs throughout the proximal and peripheral
airways, lung parenchyma, and pulmonary vasculature.
● Due to the chronic inflammation, changes and narrowing occur in the
airways.
● There is an increase in the number of goblet cells and enlarged
submucosal glands leading to hypersecretion of mucus.
● Scar formation. This can cause scar formation in the long term and
narrowing of the airway lumen.
● Wall destruction. Alveolar wall destruction leads to loss of alveolar
attachments and a decrease in elastic recoil.
● The chronic inflammatory process affects the pulmonary vasculature and
causes thickening of the vessel lining and hypertrophy of smooth muscle.
Epidemiology
Mortality for COPD has been increasing ever since while other diseases have
decreasing mortalities.
● COPD is the fourth leading cause of death in the United States.
 ● COPD also account for the death of 125, 000 Americans every year.
● Mortality from COPD among women has increased, and in 2005, more
women than men died of COPD.
● Approximately 12 million Americans live with a diagnosis of COPD.
● An additional 2 million may have COPD but remain undiagnosed.
● The annual cost of COPD is approximately $42.6 billion with overall
healthcare expenditures of $26.7 billion.
Causes
Causes of COPD includes environmental factors and host factors. These
includes:
● Smoking depresses the activity of scavenger cells and affects the

respiratory tract’s ciliary cleansing mechanism.

● Occupational exposure. Prolonged and intense exposure to

occupational dust and chemicals, indoor air pollution, and outdoor air
pollution all contribute to the development of COPD.
● Genetic abnormalities. The well-documented genetic risk factor is a

deficiency of alpha1- antitrypsin, an enzyme inhibitor that protects the

lung parenchyma from injury.
Clinical Manifestations
The natural history of COPD is variable but is a generally progressive
disease.
● Chronic cough. Chronic cough is one of the primary symptoms of

COPD.
● Sputum production. There is a hyperstimulation of the goblet cells and

the mucus-secreting gland leading to overproduction of sputum.

● Dyspnea on exertion. Dyspnea is usually progressive, persistent, and

worsens with exercise.

● Dyspnea at rest. As COPD progress, dyspnea at rest may occur.
● Weight loss. Dyspnea interferes with eating and the work of breathing is

energy depleting.
● Barrel chest. In patients with emphysema, barrel chest thorax

configuration results from a more fixed position of the ribs in the

inspiratory position and from loss of elasticity.
Prevention
Prevention of COPD is never impossible. Discipline and consistency are the
keys to achieving freedom from chronic pulmonary diseases.
● Smoking cessation. This is the single most cost-effective intervention

to reduce the risk of developing COPD and to stop its progression.

● Healthcare providers should promote cessation by explaining the risks of

smoking and personalizing the “at-risk” message to the patient.

Complications
There are two major life-threatening complications of COPD: respiratory
insufficiency and failure.
● Respiratory failure. The acuity and the onset of respiratory failure

depend on baseline pulmonary function, pulse oximetry or

arterial blood gas values, comorbid conditions, and the severity of other
complications of COPD.
● Respiratory insufficiency. This can be acute or chronic, and may

necessitate ventilator support until other acute complications can be

treated.
Assessment and Diagnostic Findings
Diagnosis and assessment of COPD must be done carefully since the three
main symptoms are common among chronic pulmonary disorders.
● Health history. The nurse should obtain a thorough health history from
patients with known or potential COPD.
● Pulmonary function studies. Pulmonary function studies are used to
help confirm the diagnosis of COPD, determine disease severity, and
monitor disease progression.
● Spirometry. Spirometry is used to evaluate airway obstruction, which is
determined by the ratio of FEV1 to forced vital capacity.
● ABG. Arterial blood gas measurement is used to assess
baseline oxygenation and gas exchange and is especially important in
advanced COPD.
● Chest x-ray. A chest x-ray may be obtained to exclude alternative
diagnoses.
● CT scan. Computed tomography chest scan may help in the differential
diagnosis.
● Screening for alpha1-antitrypsin deficiency. Screening can be
performed for patients younger than 45 years old and for those with a
strong family history of COPD.
● Chest x-ray: May reveal hyperinflation of lungs, flattened diaphragm,
increased retrosternal air space, decreased vascular markings/bullae
(emphysema), increased bronchovascular markings (bronchitis), normal
findings during periods of remission (asthma).
● Pulmonary function tests: Done to determine cause of dyspnea,
whether functional abnormality is obstructive or restrictive, to estimate
degree of dysfunction and to evaluate effects of therapy,
e.g., bronchodilators. Exercise pulmonary function studies may also be
done to evaluate activity tolerance in those with known pulmonary
impairment/progression of disease.
● The forced expiratory volume over 1 second (FEV1): Reduced FEV1 not
only is the standard way of assessing the clinical course and degree of
reversibility in response to therapy, but also is an important predictor of
prognosis.
● Total lung capacity (TLC), functional residual capacity (FRC), and residual
volume (RV): May be increased, indicating air-trapping. In obstructive
lung disease, the RV will make up the greater portion of the TLC.
● Arterial blood gases (ABGs): Determines degree and severity of
disease process, e.g., most often Pao2is decreased, and Paco2 is normal
or increased in chronic bronchitis and emphysema, but is often
decreased in asthma; pH normal or acidotic, mild respiratory alkalosis
secondary to hyperventilation (moderate emphysema or asthma).
● DL CO test: Assesses diffusion in lungs. Carbon monoxide is used to
measure gas diffusion across the alveocapillary membrane. Because
carbon monoxide combines with hemoglobin 200 times more easily
than oxygen, it easily affects the alveoli and small airways where gas
exchange occurs. Emphysema is the only obstructive disease that causes
diffusion dysfunction.
● Bronchogram: Can show cylindrical dilation of bronchi on inspiration;
bronchial collapse on forced expiration (emphysema); enlarged mucous
ducts (bronchitis).
● Lung scan: Perfusion/ventilation studies may be done to differentiate
between the various pulmonary diseases. COPD is characterized by a
mismatch of perfusion and ventilation (i.e., areas of abnormal ventilation
in area of perfusion defect).
● Complete blood count (CBC) and differential: Increased hemoglobin
 ●

(advanced emphysema), increased eosinophils (asthma).

● Blood chemistry: alpha1-antitrypsin is measured to verify deficiency and
diagnosis of primary emphysema.
● Sputum culture: Determines presence of infection, identifies pathogen.
● Cytologic examination: Rules out underlying malignancy or allergic
disorder.
● Electrocardiogram (ECG): Right axis deviation, peaked P waves (severe
asthma); atrial dysrhythmias (bronchitis), tall, peaked P waves in leads II,
III, AVF (bronchitis, emphysema); vertical QRS axis (emphysema).
● Exercise ECG, stress test: Helps in assessing degree of pulmonary
dysfunction, evaluating effectiveness of bronchodilator therapy, planning/
evaluating exercise program.
Medical Management
Healthcare providers perform medical management by considering
the assessment data first and matching the appropriate intervention to the
existing manifestation.
Pharmacologic Therapy
● Bronchodilators. Bronchodilators relieve bronchospasm by altering the
smooth muscle tone and reduce airway obstruction by allowing
increased oxygen distribution throughout the lungs and improving
alveolar ventilation.
● Corticosteroids. A short trial course of oral corticosteroids may be
prescribed for patients to determine whether pulmonary function
improves and symptoms decrease.
● Other medications. Other pharmacologic treatments that may be used
in COPD include alpha1-antitrypsin augmentation
therapy, antibiotic agents, mucolytic agents, antitussive
agents, vasodilators, and narcotics.
Management of Exacerbations
● Optimization of bronchodilator medications is first-line therapy and
involves identifying the best medications or combinations of medications
taken on a regular schedule for a specific patient.
● Hospitalization. Indications for hospitalization for acute exacerbation of
COPD include severe dyspnea that does not respond to initial
therapy, confusion or lethargy, respiratory muscle fatigue, paradoxical
chest wall movement, and peripheral edema.
● Oxygen therapy. Upon arrival of the patient in the emergency room,
supplemental oxygen therapy is administered and rapid assessment is
performed to determine if the exacerbation is life-threatening.
● Antibiotics. Antibiotics have been shown to be of some benefit to
patients with increased dyspnea, increased sputum production, and
increased sputum purulence.
Surgical Management
Patients with COPD also have options for surgery to improve their condition.
● Bullectomy. Bullectomy is a surgical option for select patients

with bullous emphysema and can help reduce dyspnea and improve
lung function.
● Lung Volume Reduction Surgery. Lung volume reduction surgery is

a palliative surgery in patients with homogenous disease or disease that

is focused in one area and not widespread throughout the lungs.
● Lung Transplantation. Lung transplantation is a viable option for

definitive surgical treatment of end-stage emphysema.

Nursing Management
Management of patients with COPD should be incorporated with teaching
and improving the respiratory status of the patient. Learn about the nursing
care management of patients with Chronic Obstructive Pulmonary Disease
using the nursing process in this guide.

Nursing Assessment
Assessment of the respiratory system should be done rapidly yet accurately.
● Assess patient’s exposure to risk factors.
● Assess the patient’s past and present medical history.
● Assess the signs and symptoms of COPD and their severity.
● Assess the patient’s knowledge of the disease.
● Assess the patient’s vital signs.
● Assess breath sounds and pattern.

Diagnosis
Diagnosis of COPD would mainly depend on the assessment data gathered
by the healthcare team members.
● Impaired gas exchange due to chronic inhalation of toxins.
● Ineffective airway clearance related to bronchoconstriction, increased

mucus production, ineffective cough, and other complications.

● Ineffective breathing pattern related to shortness of breath, mucus,

bronchoconstriction, and airway irritants.

● Self-care deficit related to fatigue.
● Activity intolerance related to hypoxemia and ineffective breathing

patterns.
Planning & Goals
Goals to achieve in patients with COPD include:
● Improvement in gas exchange.
● Achievement of airway clearance.
● Improvement in breathing pattern.
● Independence in self-care activities.
● Improvement in activity intolerance.
● Ventilation/oxygenation adequate to meet self-care needs.
● Nutritional intake meeting caloric needs.
● Infection treated/prevented.
● Disease process/prognosis and therapeutic regimen understood.
● Plan in place to meet needs after discharge.

Nursing Priorities
. Maintain airway patency.
. Assist with measures to facilitate gas exchange.
. Enhance nutritional intake.
. Prevent complications, slow progression of condition.
. Provide information about disease process/prognosis and treatment
regimen.
Nursing Interventions
Patient and family teaching is an important nursing intervention to enhance
self-management in patients with any chronic pulmonary disorder.
To achieve airway clearance:
● The nurse must appropriately administer bronchodilators and

corticosteroids and become alert for potential side effects.

● Direct or controlled coughing. The nurse instructs the patient in direct

or controlled coughing, which is more effective and

reduces fatigue associated with undirected forceful coughing.
To improve breathing pattern:
 ● Inspiratory muscle training. This may help improve the breathing
pattern.
● Diaphragmatic breathing. Diaphragmatic breathing reduces respiratory

rate, increases alveolar ventilation, and sometimes helps expel as much

air as possible during expiration.
● Pursed lip breathing. Pursed lip breathing helps slow expiration,

prevents collapse of small airways, and control the rate and depth of
respiration.
To improve activity intolerance:
● Manage daily activities. Daily activities must be paced throughout the

day and support devices can be also used to decrease energy

expenditure.
● Exercise training. Exercise training can help strengthen muscles of the

upper and lower extremities and improve exercise tolerance and

endurance.
● Walking aids. Use of walking aids may be recommended to improve

activity levels and ambulation.

To monitor and manage potential complications:
● Monitor cognitive changes. The nurse should monitor for cognitive

changes such as personality and behavior changes and memory

impairment.
● Monitor pulse oximetry values. Pulse oximetry values are used to

assess the patient’s need for oxygen and administer supplemental

oxygen as prescribed.
● Prevent infection. The nurse should encourage the patient to be

immunized against influenza and S. pneumonia because the patient

is prone to respiratory infection.
Evaluation
During evaluation, the effectiveness of the care plan would be measured if
goals were achieved in the end and the patient:
● Identifies the hazards of cigarette smoking.
● Identifies resources for smoking cessation.
● Enrolls in smoking cessation program.
● Minimizes or eliminates exposures.
● Verbalizes the need for fluids.
● Is free of infection.
● Practices breathing techniques.
● Performs activities with less shortness of breath.

Discharge and Home Care Guidelines

It is important for the nurse to assess the knowledge of patient and family
members about self-care and the therapeutic regimen.
● Setting goals. If the COPD is mild, the objectives of the treatment are to

increase exercise tolerance and prevent further loss of pulmonary

function, while if COPD is severe, these objectives are to preserve
current pulmonary function and relieve symptoms as much as possible.
● Temperature control. The nurse should instruct the patient to avoid

extremes of heat and cold because heat increases the temperature and
thereby raising oxygen requirements and high altitudes
increase hypoxemia.
● Activity moderation. The patient should adapt a lifestyle of moderate

activity and should avoid emotional disturbances and stressful situations

that might trigger a coughing episode.
● Breathing retraining. The home care nurse must provide the education
 ●

and breathing retraining necessary to optimize the patient’s functional

status.
Documentation Guidelines
Documentation is an essential part of the patient’s chart because the
interventions and medications given and done are reflected on this part.
● Document assessment findings including respiratory rate, character of

breath sounds; frequency, amount and appearance

of secretions laboratory findings and mentation level.
● Document conditions that interfere with oxygen supply.
● Document plan of care and specific interventions.
● Document liters of supplemental oxygen.
● Document client’s responses to treatment, teaching, and actions

performed.
● Document teaching plan.
● Document modifications to plan of care.
● Document attainment or progress towards goals.

What is 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.
● Stage B. Patients with left ventricular dysfunction or structural heart
disease that has not developed symptoms of heart failure.
● Stage C. Patients with left ventricular dysfunction or structural heart
disease with current or prior symptoms of heart failure.
● Stage D. Patients with refractory end-stage heart failure requiring
specialized interventions.
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.

Statistics
Just like coronary artery disease, the incidence of HF increases with age.
● More than 5 million people in the United States have HF.
● There are 550, 000 cases of HF diagnosed each year according to the

American Heart Association.

● HF is most common among people older than 75 years of age.
● HF is now considered epidemic in the United States.
● HF is the most common reason for hospitalization of people older than 65

years of age.
● It is also the second most common reason for visits to the physician’s

office.
● The estimated economic burden caused by HF is more than $33

billion annually in direct and indirect costs and is still expected to

increase.
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 Manifestations
The clinical manifestations produced y the different types of HF are similar
and therefore do not assist in differentiating the types of HF. The signs and
symptoms can be related to the ventricle affected.
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 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,

ARBs, 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
The overall goals of management of HF are to relieve patient symptoms, to
improve functional status and quality of life, and to extend survival.
Pharmacologic Therapy
● 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
Despite advances in the treatment of HF, morbidity and mortality remains
high. Nurses have a major impact on outcomes for patients with HF.

What is 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
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.
● Schematic Diagram of Myocardial Infarction via Scribd
Statistics and Epidemiology
“Time is muscle”; this is the reflection of the urgency of appropriate
treatments to improve patient outcome.
● Each year in the United States, nearly 1 million people have acute MIs.
● One fourth of the people with the disease die of MI.
● Half of the people who die with acute MI never reach the hospital.

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).
Medical Management
The goals of medical management are to minimize myocardial damage,
preserve myocardial function, and prevent complications.
 Mnemonics for Myocardial Infarction
Pharmacologic Therapy
● Morphine administered in IV boluses is used for MI to
reduce pain and anxiety.
● ACE Inhibitors. ACE inhibitors prevent the conversion of angiotensin I to
angiotensin II to decrease blood pressure and for the kidneys to
secrete sodium and fluid, decreasing the oxygen demand of the heart.
● Thrombolytics. Thrombolytics dissolve the thrombus in the coronary
artery,allowing blood to flow through the coronary artery again,
minimizing the size of the infarction and preserving ventricular function.
Emergent Percutaneous Coronary Intervention
● The procedure is used to open the occluded coronary artery and promote
reperfusion to the area that has been deprived of oxygen.
● PCI may also be indicated in patients with unstable angina and NSTEMI
 ●

for patients who are at high risk due to persistent ischemia.

Nursing Management
The nursing management involved in MI is critical and systematic, and
efficiency is needed to implement the care for a patient with MI.
Nursing Assessment
One of the most important aspects of care of the patient with MI is
the assessment.
● Assess for chest pain not relieved by rest or medications.
● Monitor vital signs, especially the blood pressure and pulse rate.
● Assess for presence of shortness of breath, dyspnea, tachypnea, and

crackles.
● Assess for nausea and vomiting.
● Assess for decreased urinary output.
● Assess for the history of illnesses.
● Perform a precise and complete physical assessment to detect

complications and changes in the patient’s status.

● Assess IV sites frequently.

Diagnosis
Based on the clinical manifestations, history, and diagnostic assessment
data, major nursing diagnoses may include.
● Ineffective cardiac tissue perfusion related to reduced coronary blood

flow.
● Risk for ineffective peripheral tissue perfusion related to decreased

cardiac output from left ventricular dysfunction.

● Deficient knowledge related to post-MI self-care.

Planning & Goals

To establish a plan of care, the focus should be on the following:
● Relief of pain or ischemic signs and symptoms.
● Prevention of myocardial damage.
● Absence of respiratory dysfunction.
● Maintenance or attainment of adequate tissue perfusion.
● Reduced anxiety.
● Absence or early detection of complications.
● Chest pain absent/controlled.
● Heart rate/rhythm sufficient to sustain adequate cardiac output/tissue

perfusion.
● Achievement of activity level sufficient for basic self-care.
● Anxiety reduced/managed.
● Disease process, treatment plan, and prognosis understood.
● Plan in place to meet needs after discharge.

Nursing Priorities
. Relieve pain, anxiety.
. Reduce myocardial workload.
. Prevent/detect and assist in treatment of life-threatening dysrhythmias or
complications.
. 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.
Evaluation
After the implementation of the interventions within the time specified,
the nurse should check if:
● There is an absence of pain or ischemic signs and symptoms.
● Myocardial damage is prevented.
● Absence of respiratory dysfunction.
● Adequate tissue perfusion maintained.
● Anxiety is reduced.

Discharge and Home Care Guidelines

The most effective way to increase the probability that the patient will
implement a self-care regimen after discharge is to identify the patient’s
priorities.
● Education. This is one of the priorities that the nurse must teach the

patient about heart-healthy living.

● Home care. The home care nurse assists the patient with scheduling and

keeping up with the follow-up appointments and with adhering to the

prescribed cardiac rehabilitation management.
● Follow-up monitoring. The patient may need reminders about follow-up

monitoring including periodic laboratory testing and ECGs, as well as

general health screening.
● Adherence. The nurse should also monitor the patient’s adherence to

dietary restrictions and prescribed medications.

Documentation Guidelines
To ensure that every action documented is an action done, documentation
must be secured. The following should be documented:
● Individual findings.
● Vital signs, cardiac rhythm, presence of dysrhythmias.
● Plan of care and those involved in planning.
● Teaching plan.
● Response to interventions, teaching, and actions performed.
● Attainment or progress towards desired outcomes.
● Modifications to plan of care.