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EMPHYSEMA
ANATOMY OF EMPHYSEMA




 Emphysema is a lung disease involving damage to the air sacs
  (alveoli).There is progressive destruction of alveoli and the surrounding
  tissue that supports the alveoli. With more advanced disease, large air cysts
  develop where normal lung tissue used to be. Air is trapped in the lungs due
  to lack of supportive tissue which decreases oxygenation.
DEFINITION

Emphysema is a long-term, progressive disease of the
 lung(s) and occurs when the alveolar walls are
 destroyed along with the capillary blood vessels that
 run within them. This lessens the total area within the
 lung where blood and air can come together, limiting the
 potential for oxygen and carbon dioxide transfer.
In early emphysema, there is associated inflammation of
 the small airways or bronchioles that limits the amount
 of air that can flow to the alveoli. In more severe
 emphysema, there is also loss of elasticity in the alveolar
 walls that have not been destroyed. When the patient
 breathes out, the alveoli and small airways collapse. This
 makes it hard for air to get out of the lungs and makes it
 even harder for new air to enter.
ETIOLOGY

The main cause of emphysema is smoking, which
 activates inflammatory cells in the lung. This
 inflammation causes; 1) swelling within the bronchioles,
 and 2) activation of enzymes called proteases which
 attack and destroy lung tissue (the alveolar wall
 structures).
There is a genetic predisposition to emphysema. The
 relatively rare condition known as alpha 1-antitrypsin
 deficiency is the genetic deficiency of a chemical that
 protects the lung from damage by proteases.
Emphysema is also a component of aging. As the lungs
 get older, the elastic properties decrease, and the
 tensions that develop can result in small areas of
 emphysema.
PATHOPHYSIOLOGY

Emphysema is characterized by abnormal
 permanent enlargement of the airspaces distal to the
 terminal bronchioles, accompanied by destruction of
 their walls without obvious fibrosis.
There are 4 types of emphysema:
 - centriacinar
 - panacinar
 - distal acinar
 - irregular
1) Centriacinar emphysema
  - The central parts of acini, formed by
  respiratory bronchioles are affected while distal
  alveoli are spared.
  - In severe centracinar emphysema, distal acinus
  also become involved.
  - This emphysema is consequence of cigarette
  smoking in people who do not have congenital
  deficiency of alfa-one antitrypsin.
2) Panacinar emphysema
  - Acini are uniformly enlarged from the level of
  respiratory bronchiole to the terminal blind alveoli
  - More commonly occur in lower lung zone.
  - Occurs in people with alpha-one antitrypsin
  deficiency.
3) Distal acinar emphysema
  - Proximal portion of acinus is normal but the
  distal part is primarily involved.
  - The emphysema is more striking adjacent to the
  pleura, along the lobular connective tissue septa,
  and at margins of lobules.
  - the characteristic findings are the presence of
  multiple, continuous, enlarged airspace that range
  in diameter from less than 0.5mm to more than
  2.0cm, sometimes forming cystlike structure called
  bullae.
IRREGULAR EMPHYSEMA

4) Irregular emphysema
  - acinus is irregularly involved
PATHOGENESIS

Protease-antiprotease imbalance favors emphysema.
Patient with genetic deficiency of antiprotease alpha-
 one antitrypsin have tendency to develop pulmonary
 emphysema and is compounded by smoking.
Alpha-one antitrypsin is normally present in serum,
 tissue fluids and macrophage which is major
 inhibitor of protease ( elastase ) secreted by
 neutrophils during inflammation.
Most people develop symptomatic emphysema
 which occurs at an earlier age and with greater
 severity if individuals smoke.
The following sequence is postulated:
1. Neutrophils which is source of elastase normally
   sequestered in peripheral capillaries, including
   those in lung, and few gain access to alveolar space.
2. Any stimulus that increase either the number of
   leucocytes in the lung wil increase elastase and
   increase proteolytic activity.
3. With low level of serum alpha-one antitrypsin,
   elastic tissue destruction is unchecked and
   emphysema results.
This imbalance also help explains the effect of
 cigarette smoking in development of emphysema,
 particularly centriacinar form in subjects with
 normal amount of alpha-one antitrypsin.
This is because in smokers, neutrophils and
 macrophages accumulate in alveoli nicotine
 stimulate reactive oxygen species to attract and
 activate more neutrophils elastase
 increasealveoli destruction emphysema
SIGNS AND SYMPTOMS

A person with emphysema will have shortness of
 breath -- during physical activity and when the
 condition is more advanced, also during rest.
Patients may eventually need supplemental oxygen
 and may have to rely on mechanical respiratory
 devices.
Other symptoms of emphysema include chronic
 cough, frequent respiratory infections, reduced
 appetite, weight loss and fatigue.

RISK FACTOR

Smoking
Genetic deficiency of alpha-one antitrypsin
Age
INVESTIGATION

 Oximetry
 Oxygenated blood is a brighter red and becomes purpler in
 color when oxygen is removed. The oximeter is a device
 usually placed on a finger and detects the pulse of blood. A
 light is transmitted through the tissue, and the amount of
 the brighter red color is determined, enabling a measure of
 oxygen saturation, a measure of hemoglobin oxygen
 content. This value is usually greater than 90%.
Radiology
A plain chest x-ray may show lungs that have
 become too inflated and too lucent, signs that lung
 tissue destruction has occurred.
Pulmonary Function Tests
A variety of lung functions can be measured and
 may include how much air the lungs can hold and
 empty with each breath, the degree of airflow
 obstruction, the available surface for exchange of
 carbon dioxide and oxygen, the amount of trapped
 gases, and how elastic the lungs are with
 inspiration and expiration.
Blood Tests
A complete blood cell count (CBC) may be
 performed to check for an increase in the number
 of red blood cells. In response to lower blood
 oxygen concentrations, the body manufactures
 more red blood cells to try to deliver as much
 oxygen as possible to cells.
An arterial blood gas ( ABGs ) test will measure the
 amount of oxygen and carbon dioxide in the blood
TREATMENT

Bronchodilators
Bronchodilators are used to relax the smooth
 muscles that surround the bronchioles and allow the
 breathing tubes to dilate and allow more air flow.
 These medications can be inhaled using nebulizer
 machine These medications can either be short or
 long acting.
The bronchodilators include the albuterol agents
 (Ventolin HFA, Proventil HFA, and Pro Air) and the
 anticholinergic agent, ipratropium bromide
 (Atrovent).
- Tablets and Extended-Release Tablet : Relief of
 bronchospasm in adults and children 6 years and
 older with reversible obstructive airway disease.
ADMINISTRATION

Aerosol and inhalation powder are indicated for children
 4 years and older, solution for inhalation for children 2
 years and older.
Nebulization ( facemask or mouth piece ). Use
 compressed air or oxygen with gas flow of 6-10 L/min ,
 single treatment last for 5 to 15 minutes.
Children maintained on the tablets or syrup may be
 switched to extended-release tablet. ( eg. One 4mg
 extended-release tablet q 12 hrs is comparable to one
 2mg tablet q 6 hrs. )
Take extended-released tablet whole with aid of liquids:
 do not chew or crush. The outer coating of extended-
 release tablet will be excreted out in feces.
ACTION KINECTIC

Stimulates beta-2 receptors of bronchi, leading to
 bronchodilation. Causes less tachycardia and is
 longer-acting.
DOSAGE

Inhalation aerosol
Bronchodilation
Adults and children over 4 years of age :
180 ( 2 inhalation ) q 4-6 hrs.
Maintainence : 180 mcg ( 2 inhalation ) 4 times
per day.
Prophylaxis of exercise-induced
  bronchospasm
Adults and children over 4 years of age:
180 mcg ( 2 inhalation ) 15 min before exercise
Inhalation solution
Bronchodilation
Adult and children over 12 years of age:
2.5 mg 3-4 times per day by nebulization ( dilute
0.5 mL of the 0.5% solution with 2.5mL sterile
NNS and deliver over 5-15 min )
Children 2-12 years of age :
2.5mg 3-4 times per day by nebulization.
Syrup
Bronchodilation
Adults and children over 14 years of age,
  usual
Initial:
- 2-4 mg ( 5-10 mL ) 3-4 times per day, up to
maximum of 8mg 4 times per day.
Children over 6-12 years initial:
- 0.1 mg/kg 3 times per day, not to exceed 2mg
3 times per day
Tablets
Bronchodilation
Adults and children over 12 years of age,
  initial:
- 2 or 4 mg 3-4 times per day, then increase dose
  needed up to maximum of 8 mg 4 times per day, as
  tolerated.
Children 6-12 years of age, usual, initial :
- 2 mg 3-4 times per day, then if necessary increase
  the dose in the stepwise fashion to a maximum if
  24 mg/day in divided dose.
SIDE EFFECTS

 Most common
- headache, palpitations/ tachycardia, tremor, bronchospasm.
 GIT
- diarrhea, dry mouth, appetite loss, epigastric pain
 CNS
- excitement, nervousness, tension, tremor, dizziness, weakness,
  drowsiness, restlessness, headache, insomnia, ,malaise, fatique,
  lightheadedness, aggressive behavior.
 Respiratory
- Cough, wheezing, dyspnea, bronchospasm, dry throat, throat
  irritation, bronchitis
 CVS
- Palpitations, tachycardia, BP changes, hypertension, tight chest,
  chest pain.
IPRATROPIUM BROMIDE

USES
- Treatment of COPD ( including bronchospasm ) in
  those who are on regular aerosol bronchodilators
  theraphy and who inquire a second bronchodilators
Action kinetics :
- Ipratropium is an antocholinergic drug that acts to
  inhibit the effect of acetylcholine following vagal
  berve stimulation. This result in bronchodilation
  which is primarilly a local, site- specific effect.
DOSAGE

Aerosol
COPD
- 2 inhalations q 6 hours not to exceed 12
  inhalations/24 hr
 Inhalation solution
COPD
- One 3-ml vial given 4 times per day via nebulization
  with up to 2 additional 3mL doses daily, if needed.
SIDE EFFECT

Most common:
- Bronchitis, URTI, headache, pain, dyspnea,
  coughing, nausea, pharyngitis, sinusitis.
Antibiotics
Since patients with emphysema are at risk for
 infections like pneumonia, antibiotics may be
 prescribed when the usually clear sputum changes
 color, or when the patient presents with systemic
 signs of an infection (fever, chills, weakness).
Oxygen
As the disease progresses, patients may require
 supplemental oxygen to be able to function. Often it
 begins with nighttime use, then with exercise, and as
 the disease worsens, the need to use oxygen during
 the day for routine activities increases.
COMPLICATION

 People with emphysema have a higher mortality than those
  with normal lung function. Causes of death include
  respiratory failure, lung infections such as pneumonia and
  influenza, and other diseases related to smoking. These
  include cancer, heart disease, and stroke. Eventually, severe
  shortness of breath will limit the person's normal daily
  activities.
 Emphysema patients are at increased risk of contracting
  recurrent respiratory infections and lung cancer, and are at
  high risk for respiratory and coronary failure. Enlargement
  and strain on the right side of the heart. (Emphysema makes
  the heart work harder to keep the lungs supplied with blood
  because of damage to the lungs' circulatory system and other
  tissue damage.)
NURSING INTERVENTIONS

1.   Nursing diagnosis
     - Difficulty in breathing in related to compressed lung.
     Objective
     - Ensure that patient can breath better during the time of
     admission in ward.
     Intervention
     - Position patient in Semi-Fowler’s position so that patient’s lung
     can expand better as abdominal pressure decrease and patient can
     breath better and more comfortable.
     - Assess patients appearance whether there is any blueish as this
     indicate that patient is not receiving adequate oxygen into the
     body.
     - Assess the patients vital sign 4 hourly especially SPO2, breathing
     pattern, respiratory rate to detect whether patient is receiving
     enough oxygen into the body.
- Auscultate lungs and document significant
change in breath sound to indicate any
abnormality in lung such as presence of mucus so
that early intervention can be carry out.
- Monitor’s ABGs of patient so that PaCO2 and
PaO2 in body of patient so that any abnormality
is detected.
-Give oxygen supply to patient such as nasal
prong so that patient can receive more oxygen
and cells in body can get enough oxygen.
- Give patient bronchodilater so that airway is
open and can breath more easily.
2) Nursing diagnosis
  - Weight loss in related to loss of appetite
  Objective
  - Ensure that patient’s body weight is maintain during times in ward.
  Nursing intervention
  - Assess body weight of patient once a week to indicate any changes in
  weight so that further interventions can be carry out.
  - Give patient’s favourite food so that patient have appetite to eat.
  - Encourage patient’s family member to bring food from house so that
  patient has more appetite to eat.
  - Encourage patient to eat more frequent and less amount at the same time.
  - Make sure that environment is clean when feeding patient.
  - Encourage family member to bring utensils from home so that patient can
  eat comfortably.
  - Encourage patient’s family member to encourage patient to eat more
  because encourages from family members is most effective.
  - Explain the purpose of eating food so that patient can recover faster as food
  contains protein and vitamins that needed for better recovery.
HEALTH EDUCATION

Encourage patient to reduce smoking so that
 nicotine will not further damage the alveoli and
 reduce severity of emphysema.
Encourage patient to perform deep breathing so that
 lung exercise is perform and lung can recover faster.
Encourage patient’s family member to buy SMI for
 patient so that patient can perform lung exercise.

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Emphysema

  • 2. ANATOMY OF EMPHYSEMA  Emphysema is a lung disease involving damage to the air sacs (alveoli).There is progressive destruction of alveoli and the surrounding tissue that supports the alveoli. With more advanced disease, large air cysts develop where normal lung tissue used to be. Air is trapped in the lungs due to lack of supportive tissue which decreases oxygenation.
  • 3. DEFINITION Emphysema is a long-term, progressive disease of the lung(s) and occurs when the alveolar walls are destroyed along with the capillary blood vessels that run within them. This lessens the total area within the lung where blood and air can come together, limiting the potential for oxygen and carbon dioxide transfer. In early emphysema, there is associated inflammation of the small airways or bronchioles that limits the amount of air that can flow to the alveoli. In more severe emphysema, there is also loss of elasticity in the alveolar walls that have not been destroyed. When the patient breathes out, the alveoli and small airways collapse. This makes it hard for air to get out of the lungs and makes it even harder for new air to enter.
  • 4. ETIOLOGY The main cause of emphysema is smoking, which activates inflammatory cells in the lung. This inflammation causes; 1) swelling within the bronchioles, and 2) activation of enzymes called proteases which attack and destroy lung tissue (the alveolar wall structures). There is a genetic predisposition to emphysema. The relatively rare condition known as alpha 1-antitrypsin deficiency is the genetic deficiency of a chemical that protects the lung from damage by proteases. Emphysema is also a component of aging. As the lungs get older, the elastic properties decrease, and the tensions that develop can result in small areas of emphysema.
  • 5. PATHOPHYSIOLOGY Emphysema is characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis. There are 4 types of emphysema: - centriacinar - panacinar - distal acinar - irregular
  • 6. 1) Centriacinar emphysema - The central parts of acini, formed by respiratory bronchioles are affected while distal alveoli are spared. - In severe centracinar emphysema, distal acinus also become involved. - This emphysema is consequence of cigarette smoking in people who do not have congenital deficiency of alfa-one antitrypsin.
  • 7.
  • 8. 2) Panacinar emphysema - Acini are uniformly enlarged from the level of respiratory bronchiole to the terminal blind alveoli - More commonly occur in lower lung zone. - Occurs in people with alpha-one antitrypsin deficiency.
  • 9.
  • 10. 3) Distal acinar emphysema - Proximal portion of acinus is normal but the distal part is primarily involved. - The emphysema is more striking adjacent to the pleura, along the lobular connective tissue septa, and at margins of lobules. - the characteristic findings are the presence of multiple, continuous, enlarged airspace that range in diameter from less than 0.5mm to more than 2.0cm, sometimes forming cystlike structure called bullae.
  • 11.
  • 12. IRREGULAR EMPHYSEMA 4) Irregular emphysema - acinus is irregularly involved
  • 13. PATHOGENESIS Protease-antiprotease imbalance favors emphysema. Patient with genetic deficiency of antiprotease alpha- one antitrypsin have tendency to develop pulmonary emphysema and is compounded by smoking. Alpha-one antitrypsin is normally present in serum, tissue fluids and macrophage which is major inhibitor of protease ( elastase ) secreted by neutrophils during inflammation. Most people develop symptomatic emphysema which occurs at an earlier age and with greater severity if individuals smoke.
  • 14. The following sequence is postulated: 1. Neutrophils which is source of elastase normally sequestered in peripheral capillaries, including those in lung, and few gain access to alveolar space. 2. Any stimulus that increase either the number of leucocytes in the lung wil increase elastase and increase proteolytic activity. 3. With low level of serum alpha-one antitrypsin, elastic tissue destruction is unchecked and emphysema results.
  • 15. This imbalance also help explains the effect of cigarette smoking in development of emphysema, particularly centriacinar form in subjects with normal amount of alpha-one antitrypsin. This is because in smokers, neutrophils and macrophages accumulate in alveoli nicotine stimulate reactive oxygen species to attract and activate more neutrophils elastase increasealveoli destruction emphysema
  • 16.
  • 17. SIGNS AND SYMPTOMS A person with emphysema will have shortness of breath -- during physical activity and when the condition is more advanced, also during rest. Patients may eventually need supplemental oxygen and may have to rely on mechanical respiratory devices. Other symptoms of emphysema include chronic cough, frequent respiratory infections, reduced appetite, weight loss and fatigue. 
  • 18. RISK FACTOR Smoking Genetic deficiency of alpha-one antitrypsin Age
  • 19. INVESTIGATION  Oximetry  Oxygenated blood is a brighter red and becomes purpler in color when oxygen is removed. The oximeter is a device usually placed on a finger and detects the pulse of blood. A light is transmitted through the tissue, and the amount of the brighter red color is determined, enabling a measure of oxygen saturation, a measure of hemoglobin oxygen content. This value is usually greater than 90%.
  • 20.
  • 21. Radiology A plain chest x-ray may show lungs that have become too inflated and too lucent, signs that lung tissue destruction has occurred. Pulmonary Function Tests A variety of lung functions can be measured and may include how much air the lungs can hold and empty with each breath, the degree of airflow obstruction, the available surface for exchange of carbon dioxide and oxygen, the amount of trapped gases, and how elastic the lungs are with inspiration and expiration.
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  • 23. Blood Tests A complete blood cell count (CBC) may be performed to check for an increase in the number of red blood cells. In response to lower blood oxygen concentrations, the body manufactures more red blood cells to try to deliver as much oxygen as possible to cells. An arterial blood gas ( ABGs ) test will measure the amount of oxygen and carbon dioxide in the blood
  • 24. TREATMENT Bronchodilators Bronchodilators are used to relax the smooth muscles that surround the bronchioles and allow the breathing tubes to dilate and allow more air flow. These medications can be inhaled using nebulizer machine These medications can either be short or long acting. The bronchodilators include the albuterol agents (Ventolin HFA, Proventil HFA, and Pro Air) and the anticholinergic agent, ipratropium bromide (Atrovent).
  • 25.
  • 26. - Tablets and Extended-Release Tablet : Relief of bronchospasm in adults and children 6 years and older with reversible obstructive airway disease.
  • 27. ADMINISTRATION Aerosol and inhalation powder are indicated for children 4 years and older, solution for inhalation for children 2 years and older. Nebulization ( facemask or mouth piece ). Use compressed air or oxygen with gas flow of 6-10 L/min , single treatment last for 5 to 15 minutes. Children maintained on the tablets or syrup may be switched to extended-release tablet. ( eg. One 4mg extended-release tablet q 12 hrs is comparable to one 2mg tablet q 6 hrs. ) Take extended-released tablet whole with aid of liquids: do not chew or crush. The outer coating of extended- release tablet will be excreted out in feces.
  • 28. ACTION KINECTIC Stimulates beta-2 receptors of bronchi, leading to bronchodilation. Causes less tachycardia and is longer-acting.
  • 29. DOSAGE Inhalation aerosol Bronchodilation Adults and children over 4 years of age : 180 ( 2 inhalation ) q 4-6 hrs. Maintainence : 180 mcg ( 2 inhalation ) 4 times per day. Prophylaxis of exercise-induced bronchospasm Adults and children over 4 years of age: 180 mcg ( 2 inhalation ) 15 min before exercise
  • 30. Inhalation solution Bronchodilation Adult and children over 12 years of age: 2.5 mg 3-4 times per day by nebulization ( dilute 0.5 mL of the 0.5% solution with 2.5mL sterile NNS and deliver over 5-15 min ) Children 2-12 years of age : 2.5mg 3-4 times per day by nebulization.
  • 31. Syrup Bronchodilation Adults and children over 14 years of age, usual Initial: - 2-4 mg ( 5-10 mL ) 3-4 times per day, up to maximum of 8mg 4 times per day. Children over 6-12 years initial: - 0.1 mg/kg 3 times per day, not to exceed 2mg 3 times per day
  • 32. Tablets Bronchodilation Adults and children over 12 years of age, initial: - 2 or 4 mg 3-4 times per day, then increase dose needed up to maximum of 8 mg 4 times per day, as tolerated. Children 6-12 years of age, usual, initial : - 2 mg 3-4 times per day, then if necessary increase the dose in the stepwise fashion to a maximum if 24 mg/day in divided dose.
  • 33. SIDE EFFECTS  Most common - headache, palpitations/ tachycardia, tremor, bronchospasm.  GIT - diarrhea, dry mouth, appetite loss, epigastric pain  CNS - excitement, nervousness, tension, tremor, dizziness, weakness, drowsiness, restlessness, headache, insomnia, ,malaise, fatique, lightheadedness, aggressive behavior.  Respiratory - Cough, wheezing, dyspnea, bronchospasm, dry throat, throat irritation, bronchitis  CVS - Palpitations, tachycardia, BP changes, hypertension, tight chest, chest pain.
  • 34. IPRATROPIUM BROMIDE USES - Treatment of COPD ( including bronchospasm ) in those who are on regular aerosol bronchodilators theraphy and who inquire a second bronchodilators Action kinetics : - Ipratropium is an antocholinergic drug that acts to inhibit the effect of acetylcholine following vagal berve stimulation. This result in bronchodilation which is primarilly a local, site- specific effect.
  • 35. DOSAGE Aerosol COPD - 2 inhalations q 6 hours not to exceed 12 inhalations/24 hr  Inhalation solution COPD - One 3-ml vial given 4 times per day via nebulization with up to 2 additional 3mL doses daily, if needed.
  • 36. SIDE EFFECT Most common: - Bronchitis, URTI, headache, pain, dyspnea, coughing, nausea, pharyngitis, sinusitis.
  • 37. Antibiotics Since patients with emphysema are at risk for infections like pneumonia, antibiotics may be prescribed when the usually clear sputum changes color, or when the patient presents with systemic signs of an infection (fever, chills, weakness).
  • 38. Oxygen As the disease progresses, patients may require supplemental oxygen to be able to function. Often it begins with nighttime use, then with exercise, and as the disease worsens, the need to use oxygen during the day for routine activities increases.
  • 39. COMPLICATION  People with emphysema have a higher mortality than those with normal lung function. Causes of death include respiratory failure, lung infections such as pneumonia and influenza, and other diseases related to smoking. These include cancer, heart disease, and stroke. Eventually, severe shortness of breath will limit the person's normal daily activities.  Emphysema patients are at increased risk of contracting recurrent respiratory infections and lung cancer, and are at high risk for respiratory and coronary failure. Enlargement and strain on the right side of the heart. (Emphysema makes the heart work harder to keep the lungs supplied with blood because of damage to the lungs' circulatory system and other tissue damage.)
  • 40. NURSING INTERVENTIONS 1. Nursing diagnosis - Difficulty in breathing in related to compressed lung. Objective - Ensure that patient can breath better during the time of admission in ward. Intervention - Position patient in Semi-Fowler’s position so that patient’s lung can expand better as abdominal pressure decrease and patient can breath better and more comfortable. - Assess patients appearance whether there is any blueish as this indicate that patient is not receiving adequate oxygen into the body. - Assess the patients vital sign 4 hourly especially SPO2, breathing pattern, respiratory rate to detect whether patient is receiving enough oxygen into the body.
  • 41. - Auscultate lungs and document significant change in breath sound to indicate any abnormality in lung such as presence of mucus so that early intervention can be carry out. - Monitor’s ABGs of patient so that PaCO2 and PaO2 in body of patient so that any abnormality is detected. -Give oxygen supply to patient such as nasal prong so that patient can receive more oxygen and cells in body can get enough oxygen. - Give patient bronchodilater so that airway is open and can breath more easily.
  • 42. 2) Nursing diagnosis - Weight loss in related to loss of appetite Objective - Ensure that patient’s body weight is maintain during times in ward. Nursing intervention - Assess body weight of patient once a week to indicate any changes in weight so that further interventions can be carry out. - Give patient’s favourite food so that patient have appetite to eat. - Encourage patient’s family member to bring food from house so that patient has more appetite to eat. - Encourage patient to eat more frequent and less amount at the same time. - Make sure that environment is clean when feeding patient. - Encourage family member to bring utensils from home so that patient can eat comfortably. - Encourage patient’s family member to encourage patient to eat more because encourages from family members is most effective. - Explain the purpose of eating food so that patient can recover faster as food contains protein and vitamins that needed for better recovery.
  • 43. HEALTH EDUCATION Encourage patient to reduce smoking so that nicotine will not further damage the alveoli and reduce severity of emphysema. Encourage patient to perform deep breathing so that lung exercise is perform and lung can recover faster. Encourage patient’s family member to buy SMI for patient so that patient can perform lung exercise.