Chapter (34)-new-Medical Nutrition Therapy for Pulmonary Diseases

1. Chapter (34)
Medical Nutrition Therapy for Pulmonary Disease
Prepared by: Dr. Fadwa Ghazi
Hammouh
1

2. • During fetal life, from birth to maturity, and
throughout adulthood, the pulmonary
system is intertwined with nutrition.
• Optimal nutrition permits the proper growth
and development of the respiratory organs,
supporting structures of the skeleton and
muscles, and related nervous, circulatory,
and immunologic systems.
2

3. • A well-functioning pulmonary system enables the
body to obtain the oxygen needed to meet its
cellular demands for energy from macronutrients
and to remove metabolic byproducts.
• Overall, a person’s nutritional well-being and
proper metabolism of nutrients are essential for
the formation, development, growth, maturity,
and protection of healthy lungs and associated
processes throughout life.
3

4. THE PULMONARY SYSTEM
• The respiratory structures include the
nose, pharynx, larynx, trachea, bronchi,
bronchioles, alveolar ducts, and alveoli.
• Supporting structures include the skeleton
and the muscles (e.g., the intercostal,
abdominal, and diaphragm muscles).
• Within a month after conception,
pulmonary structures are recognizable.
4

5. • The pulmonary system grows and matures
during gestation and childhood, and no
new alveoli are produced after
approximately age 20 years.
• As aging occurs, there is a loss of lung
capillaries and the lungs lose elasticity.
5

6. 6

7. • The lungs enable the body to obtain the
oxygen needed to meet its cellular
metabolic demands and to remove the
carbon dioxide (CO2) produced.
• Healthy nerves, blood, and lymph are
needed to supply oxygen and nutrients to
all tissues.
7

8. • The lungs also filter, warm, and humidify
inspired air.
• The respiratory center is the name for
structures involved in the generation of
rhythmic respiratory movements and
reflexes, and is located in the medulla and
pons.
8

9. 9

10. • The electrical impulses generated by the
respiratory center are carried by the
phrenic nerves to the diaphragm and other
respiratory muscles.
• Contraction of diaphragm and other
muscles increases the intrathoracic
volume, which creates negative
intrathoracic pressure and allows air to be
sucked in.
10

11. • The air traverses through upper and lower
airways and reaches alveoli.
• The alveoli are surrounded by capillaries
where gas exchange takes place.
• The large pulmonary blood vessels and the
conducting airways are located in a well
defined connective tissue compartment —
the pleural cavity.
11

12. • The lungs are an important part of the body’s
immune defense system, because inspired
air is laden with particles and
microorganisms.
• Mucus keeps the airways moist and traps the
particles and microorganisms from inspired
air.
• The airways have 12 types of epithelial cells,
and most cells that line the trachea, bronchi,
and bronchioles have cilia.
12

13. • The cilia are “hair-like” structures that
move the superficial liquid lining layer from
deep within the lungs, toward the pharynx
to enter the gastrointestinal tract, thereby
playing an important role as a lung defense
mechanism by clearing bacteria and other
foreign bodies.
• Each time a person swallows, the particle-
and microorganism- containing mucus
passes into the digestive tract.
13

14. • When bacteria inhaled by the patient are
not cleared effectively, the patient is prone
to develop recurrent chest infections that
may eventually lead to bronchiectasis.
14

15. • The epithelial surface of the alveoli
contains macrophages. By the process of
phagocytosis, these alveolar macrophages
engulf inhaled inert materials and
microorganisms and digest them.
15

16. • The alveolar cells also secrete surfactant,
a compound synthesized from proteins and
phospholipids that maintains the stability of
pulmonary tissue by reducing the surface
tension of fluids that coat the lung.
16

17. • The lungs have several metabolic
functions. For example, they help regulate
the body’s acid-base balance.
• The body’s pH is maintained partially by
the proper balance of CO2 and O2.
17

18. • The lungs also synthesize arachidonic acid
that ultimately may be converted to
prostaglandins or leukotrienes. These
appear to play a role in bronchoconstriction
seen in asthma.
18

19. • The lungs convert angiotension I to
angiotensin II by the angiotension-
converting enzyme (ACE) found mainly in
the numerous capillary beds of the lungs.
Angiotensin II increases blood pressure.
19

20. • Because of the ultrastructure and the fact
that they receive the total cardiac output,
lungs are well suited to function as a
chemical filter.
• They protect the systemic circulation from
exposure to high levels of circulating
vasoactive substances.
20

21. • Although serotonin, 5-hydroxytryptamine (5
HT), and norepinephrine are totally or
partially eliminated or inactivated in the
pulmonary circulation, epinephrine and
histamines pass through the lungs
unchanged.
21

22. Effect of Malnutrition on the Pulmonary System
• The relationship between malnutrition and
respiratory disease has long been
recognized.
• Malnutrition adversely affects lung
structure, elasticity, and function;
respiratory muscle mass, strength, and
endurance; lung immune defense
mechanisms; and control of breathing.
22

23. • For example, protein and iron deficiencies
result in low hemoglobin levels that
diminish the oxygen- carrying capacity of
the blood.
• Low levels of calcium, magnesium,
phosphorus, and potassium compromise
respiratory muscle function at the cellular
level.
23

24. • Hypoalbuminemia, as measured by serum
albumen, contributes to the development of
pulmonary edema by decreasing colloid
osmotic pressure, allowing body fluids to
move into the interstitial space.
• Decreased levels of surfactant contribute
to the collapse of alveoli, thereby
increasing the work of breathing.
24

25. • The supporting connective tissue of the
lungs is composed of collagen, which
requires ascorbic acid for its synthesis.
• Normal airway mucus is a substance
consisting of water, glycoproteins, and
electrolytes, and thus requires adequate
nutritional intake.
25

26. Effect of Pulmonary Disease on Nutritional Status
• Pulmonary disease substantially increases
energy requirements. This factor explains
the rationale for including body composition
and weight parameters in nutrition
assessment.
• Weight loss from inadequate energy intake
is significantly correlated with a poor
prognosis in persons with pulmonary
diseases.
26

27. • Malnutrition leading to impaired immunity
places any patient at high risk for
developing respiratory infections.
• Malnourished patients with pulmonary
disease who are hospitalized are likely to
have lengthy stays and are susceptible to
increased morbidity and mortality.
27

28. • The complications of pulmonary diseases
or their treatments can make adequate
food intake and digestion difficult.
• Absorption and metabolism of most
nutrients are affected.
28

29. • As pulmonary disease progresses, several
conditions may interfere with food intake
and overall nutrition status.
• For example, abnormal production of
sputum, vomiting, tachypnea (rapid
breathing), hemoptysis, thoracic pain, nasal
polyps, anemia, depression, and altered
taste secondary to medications are often
present.
29

30. 30

31. Medical Management
• Pulmonary system disorders may be
categorized as primary, such as
tuberculosis (TB), bronchial asthma, and
cancer of the lung; or secondary when
associated with cardiovascular disease,
obesity, human immunodeficiency virus
(HIV) infection, sickle cell disease, or
scoliosis. Conditions also may be acute or
chronic.
31

32. • Examples of acute conditions include
aspiration pneumonia, airway obstruction
from foods such as peanuts, and allergic
anaphylaxis from consumption of shellfish.
• Examples of chronic conditions include
cystic fibrosis (CF) and chronic obstructive
pulmonary disease (COPD).
32

33. • The assessment of pulmonary status
generally starts with physical examination
using percussion and auscultation.
• These bedside techniques provide important
information on the patient’s breathing.
• Numerous diagnostic and monitoring tests
such as imaging procedures, arterial blood
gas determinations, sputum cultures, and
biopsies also can be employed.
33

34. • Signs and symptoms of pulmonary disease
include cough, dyspnea (shortness of
breath), fatigue, early satiety, anorexia, and
weight loss.
34

35. • Pulmonary function tests are used to
diagnose or monitor the status of lung
disease; they are designed to measure the
ability of the respiratory system to
exchange oxygen and CO2.
35

36. • Pulse oximetry is one such test. A small
device called a pulse oximeter, which uses
light waves to measure the oxygen
saturation of arterial blood, is placed on the
end of the finger.
• Normal for a young, healthy person is 95%
to 99%.
36

37. 37

38. • Spirometry is another common pulmonary
function test.
• This involves breathing into a spirometer
that gives information on lung volume and
the rate at which air can be inhaled and
exhaled.
38

39. 39

40. CHRONIC PULMONARY DISEASE
ASTHMA
• Asthma is a chronic disorder that affects
the airways and is characterized by
bronchial hyper-reactivity, reversible airflow
obstruction, and airway remodeling.
40

41. • Asthmatic symptoms include periodic
episodes of chest tightness,
breathlessness, and wheezing.
• Asthma has become more prevalent and
has been increasing at the rate of 25% to
75% every decade since 1960 in
westernized countries.
41

42. Pathophysiology
• Asthma is the result of a complex
interaction between environmental
exposures and genetics.
• When people are genetically susceptible,
environmental factors exacerbate airway
hyper-responsiveness, airway
inflammation, and atopy (tendency to
develop allergic reaction) that eventually
leads to asthma.
42

43. • Environmental factors that are linked to the
development of asthma include indoor
allergies (dust mites, animal allergies) and
outdoor allergies (pollen and fungi).
43

44. • Increased risk of asthma development also
has been linked to air pollution, tobacco
smoke exposure, small size at birth,
respiratory infection, and lower
socioeconomic status.
44

45. • Clinicians identify three key areas when
diagnosing asthma:
1. Airflow obstruction that is at least partially
reversible
2. Airflow obstruction that recurs
3. Exclusion of other diagnoses
45

46. • Symptoms such as wheezing, coughing,
shortness of breath, and chest tightness
occur in most patients, and symptoms that
worsen at night is a common feature.
46

47. • Although allergic asthma or “extrinsic
asthma” is due to chronic allergic
inflammation of the airways, “intrinsic
asthma” is triggered by nonallergic factors
such as exercise, certain chemicals, and
extreme emotions.
47

48. • A life-threatening situation with markedly narrow
airways, known as status asthmaticus, can result
when asthma has not been treated properly.
• Corticosteroid therapy is often prescribed, but
chronic use may place the individual at risk for
osteopenia (precursor to osteoporosis), bone
fractures, or steroid-induced hyperglycemia.
• Some evidence supports the effectiveness of
sublingual immunotherapy in the treatment of
asthma and rhinitis, but more studies are needed
on optimal dosages.
48

49. Medical Management
• The essential components of asthma
therapy are routine monitoring of
symptoms and lung function, patient
education, control of environmental
triggers, and pharmacotherapy.
• Pharmacologic treatment must be tailored
to the individual patient and is used in a
stepwise manner.
49

50. • The medications and the regime chosen
depend on the severity of the asthma,
which can be classified as an acute attack,
intermittent, mild persistent, moderate
persistent, or severe persistent. Quick
relief and long-term controller medications
are used as therapy for asthma.
50

51. • Although quick-relief medications include
short-acting beta agonists (bronchodilators)
and steroid pills, long-term controller
medications include inhaled long-acting
beta agonists and leukotriene modifiers.
• Inhaled corticosteroids are the cornerstone
of pharmacologic management with
persistent asthma.
51

52. • Some younger patients with refractory
asthma need maintenance doses of
systemic steroids.
• Because steroids change bone metabolism
and the development of osteoporosis,
these children benefit from increased
calcium intake.
52

53. 53

54. • Two newer therapies are anti-IgE (anti-
immunoglobulin E) therapy and bronchial
thermoplasty, which are used in selected cases
of severe asthma.
• Immunomodulator therapies with anti-IL-5 (anti-
interleukin-5) antibodies, anti-IL-4 alpha subunit
antibodies, human necrosis factor TNF-alpha
(tumor necrosis factor-alpha) inhibitors, and the
use of macrolide antibiotics for their
antiinflammatory actions are some of the
experimental approaches.
54

55. • Antibiotics for exacerbation of asthma are
not recommended by current clinical
practice guidelines, because respiratory
infection triggering asthma attacks are
more often viral rather than bacterial.
55

56. Medical Nutrition Therapy
• When treating asthma, the dietitian
nutritionist addresses the dietary triggers,
corrects energy and nutrient deficiencies
and excesses in the diet, educates the
patient on a personalized diet that provides
optimal levels of nutrients, monitors growth
in children, and watches for food-drug
interactions.
56

57. • Modulation of antioxidant intake with
nutritional supplementation has a beneficial
effect on the severity and progression of
asthma.
• Although a slight inverse association was
seen between a low vitamin E intake and
wheezing symptoms, no association was
found between vitamin E and asthma.
57

58. • Further studies are required to understand
the mechanism of vitamin E on the
inflammation of the immune system.
• Low blood carotenoid levels also have
been linked with asthma.
58

59. • A diet rich in antioxidants and
monounsaturated fats seems to have a
protective effect on childhood asthma by
counteracting oxidative stress.
• Studies have also associated asthma with
reduced selenium status.
59

60. • In the childhood asthma prevention study
omega-3 polyunsaturated fatty acid (PUFA)
fish oil was supplemented throughout
childhood and wheezing was reduced.
• This effect did not continue into later
childhood. Supplementation of vitamin C
and zinc also have been reported to
improve asthma symptoms and lung
function.
60

61. • In one study an insufficient serum level of
less than 30 ng/dL of vitamin D was
associated with an increase in asthma
exacerbation in the form of ER visits and
hospitalizations.
• In another, high doses of vitamin D
supplementation were not shown to have
any protective effect.
61

62. • A higher than desirable BMI during
childhood is associated with a significant
increase in the development of asthma.
• Institution of diets that help with weight loss
in asthmatic obese children seem to show
improvements with the control of asthma,
static lung function, and improved quality of
life.
62

63. • Gastroesophageal reflux disease (GERD) and
food allergens are the two most common dietary
triggers for asthma. GERD is highly prevalent in
asthmatic patients.
• A critical component of medical nutrition therapy
for asthmatic patients is a diet free of known
irritants such as spicy foods, caffeine,
chocolate, and acidic foods Limiting the intake
of high fat foods and portion control can prevent
gastric secretions, which exacerbate GERD.
63

64. • Food allergens and food additives are
other potential dietary triggers for asthma.
• An immunoglobulin E-mediated reaction to
a food protein can lead to
bronchoconstriction.
• Completely avoiding the allergenic food
protein is the only dietary treatment
currently available for food allergies.
64

65. • Some sulfites, such as potassium
metasulfite and sodium sulfide, used in the
processing of foods, have been found to be
a trigger for asthmatics.
• Some asthma patients need maintenance
oral steroids, and these patients are prone
to develop drug-nutrient interaction
problems.
65

66. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
• COPD is now the third most common cause of
death in the world and is predicted to be the fifth
most common cause of disability by 2020.
• Smoke from cigarettes is a major risk factor,
along with that from biomass fuel used for
cooking and heating in rural areas of developing
countries.
• Occupational smoke or dust, air pollution, and
genetic factors are also factors in the
development of COPD.
66

67. 67

68. • Patients with COPD suffer from decreased
food intake and malnutrition that causes
respiratory muscle weakness, increased
disability, increased susceptibility to
infections, and hormonal alterations.
68

69. Pathophysiology
• COPD is a term that encompasses chronic
bronchitis (a long-term condition of COPD
in which inflamed bronchi lead to mucus,
cough and difficulty breathing) and
emphysema (a form of long-term lung
disease characterized by the destruction of
lung parenchyma with lack of elastic recoil).
• These conditions may coexist in varying
degrees and are generally not reversible.
69

70. • Patients with primary emphysema suffer
from greater dyspnea and cachexia.
• On the other hand patients with bronchitis
have hypoxia, hypercapnia (increased
amount of carbon dioxide), and
complications such as pulmonary
hypertension and right heart failure.
70

71. 71

72. • Alpha-1 antitrypsin deficiency is present in
1% to 2% of COPD patients and is likely
underrecognized.
• COPD exacerbations can be caused by
Haemophilus influenzae, Moraxella
catarrhalis, S. pneumonia, rhinovirus,
coronavirus, and to a lesser degree,
organisms such as P. aeruginosa, S.
aureus, Mycoplasma spp., and Chlamydia
pneumoniae.
72

73. • Allergies, smoking, congestive heart failure,
pulmonary embolism, pneumonia, and systemic
infections are the reason for 20% to 40% of
COPD exacerbations.
• Although cigarette smoking is considered a
major risk factor for developing COPD, only
about 20% of smokers develop the disease.
• Osteoporosis in COPD patients not only
predisposes patients to painful vertebral
fractures but also affects lung function by
altering the configuration of the chest wall.
73

74. • Frequent acute exacerbations in COPD patients
increase the severity of chronic system inflammation.
• This leads to bone loss by inhibiting bone
metabolism. Lack of sun exposure and physical
activity with COPD leads to a lack of 25-hydroxy
vitamin D (25-OHD), which regulates bone
metabolism by promoting the absorption of calcium.
• Factors that influence the prognosis of COPD are
the severity of disease, genetic predisposition,
nutritional status, environmental exposures, and
acute exacerbations.
74

75. Medical Management
• In general, COPD therapies have a limited effect
compared with therapies in asthma. No disease-
modifying medications exist that can change the
progression of airway obstruction in COPD.
• Inhaled bronchodilators remain the mainstay of
treatment for COPD patients. Usually these are
given by metered dose inhalers (MDI), but for
severe dyspnea, may be administered in a
nebulized form.
75

76. • Anticholinergic medications such as
ipratropium bromide or Spiriva (tiotropium
bromide), a long-acting anticholinergic
agent with specificity for muscarinic
receptors, can be added to the treatment.
Theophylline continues to be used in some
cases.
76

77. • Inhaled steroids and a trial of oral steroids
may be required for some patients.
• Antibiotics often are prescribed when an
exacerbation is considered to be due to
bacterial infection.
77

78. • Pulmonary hypertension is a risk factor that shortens life
expectancy and is common in advanced COPD.
• The first step in treating pulmonary hypertension in
patients with COPD is appropriate management of their
obstructive lung disease as mentioned earlier.
• The exact indication for pulmonary hypertension specific
therapies in COPD patients is unclear.
• Current recommendations state that pulmonary
hypertension specific therapies should be considered
when pulmonary hypertension is persistent despite
optimization of COPD management and when pulmonary
hypertension is out of proportion to the degree of air flow
obstruction.
78

79. • Patients who are hypoxemic need supplemental oxygen.
Pulmonary rehabilitation may be helpful in advanced
COPD.
• Patients with severe COPD may suffer respiratory failure
related to complications such as pneumothorax,
pneumonia, and congestive heart failure, or due to
uncontrolled administration of high-dose oxygen or
narcotic sedatives.
• The patients in respiratory failure need mechanical
ventilation. In addition to facing major physical
impairment and chronic dyspnea, COPD patients are at
an increased risk of developing depression that should be
identified and treated.
79

80. 80

81. Medical Nutrition Therapy
• Malnutrition is a common problem
associated with COPD, with prevalence
rates of 30% to 60% due to the extra
energy required by the work of breathing
and frequent and recurrent respiratory
infections.
• Breathing with normal lungs expends 36 to
72 kcal/day; it increases 10-fold in patients
with COPD.
81

82. • Infection with fever increases metabolic rate even
further.
• An independent predictor of increased mortality in
COPD patients is low body weight. Weight loss in
advanced COPD is considered an independent risk
factor for mortality, whereas weight gain reverses
the negative effect of decreased body weight.
• Low body weight is due to poor nutritional intake,
an increased metabolic rate, or both. Inadequate
food intake and poor appetite are the primary
targets for intervention in patients with COPD.
82

83. • These two issues mean COPD patients struggle
to meet their nutritional needs. Depletion of
protein and vital minerals such as calcium,
magnesium, potassium, and phosphorus
contribute to respiratory muscle function
impairment.
• In severe malnutrition inadequate electrolyte
repletion during aggressive nutrition repletion can
lead to severe metabolic consequences related
to refeeding syndrome.
83

84. • There are two main goals in managing the
hypermetabolism seen in stable COPD:
1) the prevention of weight loss, and
2) the prevention of the loss of lean body
mass (LBM).
84

85. • These goals can be achieved by ensuring the
following:
• Small frequent meals that are nutritionally dense
• The patient eats the main meal when energy level is
at its highest
• Adequate calories, protein, vitamins, and minerals to
maintain a desirable weight - a BMI of 20 to 24 kg/m2
• Availability of foods that require less preparation and
can be heated easily in a microwave oven
• Limitation of alcohol to fewer than 2 drinks/day (30 g
alcohol)
• A period of rest before mealtimes
85

86. • People with COPD suffer a poor prognosis
when they have malnutrition that predisposes
them to infections.
• The ability to produce lung surfactant,
exercise tolerance, and respiratory muscle
force are reduced in the presence of
infection.
• Weight loss leads to an increased load on the
respiratory muscles, contributing to the onset
of acute respiratory failure.
86

87. • Many factors affect nutritional status during
the progression of COPD.
• Although body weight and BMI should be
followed because they are easily obtained
markers of nutritional status in patients,
they can underestimate the extent of
nutritional impairment.
87

88. • Current evidence suggests that a prudent
diet pattern helps in protecting smokers
against malnutrition.
• A combination of nutritional counseling and
nicotine replacement seems to optimize
success.
88

89. • Studies have shown an inverse relationship
between dietary iron and calcium intake
and COPD risk.
• Iron deficiency anemia is seen in 10% to
30% of patients with COPD. It has been
seen that correcting the anemia and iron
deficiency by either blood transfusions or
intravenous iron therapy improves dyspnea
in COPD patients.
89

90. • COPD patients are also at higher risk of
developing osteoporosis resulting from
steroid usage, smoking, and vitamin D
depletion.
• Maintaining adequate levels of vitamin D
(25-OHD) is a health-promoting strategy
for COPD patients.
90

91. • The primary goals of nutrition care for
patients with COPD are to facilitate
nutritional well-being, maintain an
appropriate ratio of lean body mass to
adipose tissue, correct fluid imbalance,
manage drug-nutrient interactions, and
prevent osteoporosis.
• Nutritional depletion may be evidenced
clinically by low body weight for height and
decreased grip strength.
91

92. • Calculation of BMI may be insufficient to
detect changes in fat and muscle mass.
• Instead, determination of body composition
helps to differentiate lean muscle mass
from adipose tissue and overhydration
from dehydration.
92

93. • In patients with cor pulmonale (increased
blood pressure which leads to enlargement and
failure of the right ventricle of the heart) and the
resultant fluid retention, weight maintenance, or
gain from fluid may camouflage actual wasting
of lean body mass.
• Thus for patients retaining fluids, careful
interpretation of anthropometric measurements,
biochemical indicators, and functional
measures of nutrition status is Necessary.
93

94. • A combination of nutritional supplements
and anabolic steroids can increase muscle
mass and reverse any negative effects of
weight loss.
• Exercise tolerance has been shown to
improve with a dietary supplement that
contains omega-3 PUFA, which has anti-
inflammatory effects.
94

95. • Adipokines is a generic term for the
bioactive proteins that are secreted by
adipocytes. They include adiponectin,
leptin, IL-6, and TNF-alpha. They play a
vital role in influencing the nutritional status
and regulating the appetite.
95

96. • Leptin (satiety hormone) is secreted
promptly in response to food intake, and
plays a role in suppressing appetite and
enhancing energy expenditure.
• It has been suggested that measuring
levels of leptin in the sputum can be useful
in determining the severity of lung disease
because it has been shown to increase
during acute exacerbations.
96

97. • Adiponectin (a protein involved in fatty
acid breakdown and glucose regulation),
like leptin, is secreted from adipocytes, but
has an opposite effect.
• Adiponectin enhances appetite, has an
antiinflammatory, antidiabetic, and
antiatherosclerotic effect and is considered
beneficial.
97

98. • Resistin, another adipokine, induces
inflammation and insulin resistance.
• In addition to being an appetite stimulant,
ghrelin also stimulates growth hormone
secretion, with antagonistic effects to
leptin.
98

99. 99

100. Macronutrients
• In stable COPD, requirements for water,
protein, fat, and carbohydrate are determined
by the underlying lung disease, oxygen therapy,
medications, weight status, and any acute fluid
fluctuations.
• Attention to the metabolic side effects of
malnutrition and the role of individual amino
acids is necessary.
• Determination of a specific patient’s
macronutrient needs is made on an individual
basis, with close monitoring of outcomes.
100
stable and unstable

101. Energy
• Meeting energy needs can be difficult. For
patients participating in pulmonary
rehabilitation programs, energy
requirements depend on the intensity and
frequency of exercise therapy and can be
increased or decreased.
• It is crucial to remember that energy
balance and nitrogen balance are
intertwined.
101
zero or positive balance

102. • Consequently, maintaining optimal energy balance is
essential to preserving visceral and somatic proteins.
• Preferably, indirect calorimetry should be used to
determine energy needs and to prescribe and
monitor the provision of sufficient, but not excessive
calories.
• When energy equations are used for prediction of
needs, increases for physiologic stress must be
included.
• Caloric needs may vary significantly from one person
to the next and even in the same individual over time.
102

103. Fat
• Omega-3 and omega-6 are PUFAs that are
essential fatty acids.
• The simplest forms of these fatty acids are the
omega-6 linoleic acid (LA) and alpha-linolenic acid
(ALA). The body is unable to synthesize them, and
they must be consumed in the human diet.
• These fatty acids are desaturated to form long chain
omega-3 PUFAs or omega-6 PUFAs.
Docosahexaenoic acid (DHA) and eicosapentaenoic
acid (EPA) and alpha-linolenic acid (ALA) are the
major omega-3 PUFAs, and the major long-chain
omega–6 fatty acids are linoleic acid (LA) and
arachidonic acid (AA).
103
essential fatty acids
to reduce
inflammation
two omega-3 are EPA and DHA

104. • In theory, intake of long-chain omega-3
PUFAs, which reduces inflammation,
should improve the efficacy of COPD
treatments. PUFA supplementation is
beneficial in COPD, but various factors
such as supplement adherence,
comorbidities, and duration of the
supplementation play vital roles.
104

105. • Dietary supplementation of DHA and AA
has been shown to delay and reduce risk
of upper respiratory infections and asthma,
with lowering the incidence of bronchiolitis
during the first year of life.
• Data from various studies have shown the
positive impact of long-chain PUFAs in
initiating and providing resolution of
inflammation in respiratory diseases.
105

106. • It has been shown that aspirin helps to
trigger resolvin, a molecule naturally made
by the body from omega-3 fatty acids.
• Resolvin resolves or turns off the
inflammation in underlying destructive
conditions such as inflammatory lung
diseases.
106

107. Protein
• Sufficient protein of 1.2 to 1.5 g/kg of dry body
weight is necessary to maintain or restore lung
and muscle strength, as well as to promote
immune function.
• A balanced ratio of protein (15% to 20% of
calories) with fat (30% to 45% of calories) and
carbohydrate (40% to 55% of calories) is
important to preserve a satisfactory respiratory
quotient (RQ) from substrate metabolism use.
107
depends on each
case
COPD needs
more protein

108. • Repletion but not overfeeding is particularly
critical in patients with compromised ability
to exchange gases as excess feeding of
calories results in CO2 that must be
expelled.
• Other concurrent disease processes such
as cardiovascular or renal disease, cancer,
or diabetes affect the total amounts, ratios,
and kinds of protein, fat, and carbohydrate
prescribed.
108

109. Vitamins and Minerals
• As with macronutrients, vitamin and
mineral requirements for individuals with
stable COPD depend on the underlying
pathologic conditions of the lung, other
concurrent diseases, medical treatments,
weight status, and bone mineral density.
• For people continuing to smoke tobacco,
additional vitamin C is necessary.
109

110. • The role of minerals such as magnesium
and calcium in muscle contraction and
relaxation may be important for people with
COPD.
• Intakes at least equivalent to the dietary
reference intake (DRI) should be provided.
110

111. • Depending on bone mineral density test
results, coupled with food intake history
and glucocorticoid medications use,
additional vitamins D and K also may be
necessary.
111

112. • Patients with cor pulmonale and
subsequent fluid retention require sodium
and fluid restriction.
• Depending on the diuretics prescribed,
increased potassium supplementation may
be required.
• And other water soluble vitamins,
particularly thiamin, may need to be
supplemented.
112

113. • Patients are recommended to drink
adequate fluids and stay hydrated to help
sputum consistency and easier
expectoration.
• The Parenteral and Enteral Nutrition Group
(PENG) recommends a fluid intake of 35
ml/kg body weight daily for adults 18 to 60
years and 30 ml of fluid/kg body daily for
adults over 60 years.
113

114. • COPD patients report difficulties with
eating because of low appetite, increased
breathlessness when eating, difficulty
shopping and preparing meals, dry mouth,
early satiety and bloating, anxiety and
depression, and fatigue.
• In addition to the above, inefficient and
overworking respiratory muscles lead to
increased nutritional requirements.
114
best time to eat is after resting so they have energy to eat

115. Patients in the Advanced Stage of COPD
• Patients with advanced COPD are
undernourished and in a state of pulmonary
cachexia.
• The cause of cachexia in advanced COPD is
poorly understood. The role for myostatin has
been suggested. Myostatin is a member of the
transforming growth factor-beta super family
that functions as a negative regulator of muscle
growth.
• These cachectic patients have anorexia as a
typical symptom.
115

116. • Pulmonary cachexia is an independent risk
factor and is common in the advanced
stage of COPD.
• Pharmacotherapy and non pharmaco
therapeutic treatments such as respiratory
rehabilitation and nutrition counseling are
the mainstays of COPD treatment in such
patients.
116

117. • Sarcopenia and cachexia result from the
accelerated loss of lean tissue. This muscle
wasting has a detrimental effect on the
respiratory function.
• Osteoporosis exists as a significant
problem in 24% to 69% of patients with
advanced COPD. Any sudden drop in
height is a mark of developing
osteoporosis.
117
important to maintain normal weight

118. • As COPD progresses, osteoporosis results
because of immobility, which also leads to
deconditioning and dyspnea.
• Smoking, low BMI, low skeletal muscle
mass, and corticosteroid usage can lead to
bone loss along with low serum vitamin D
levels.
118

119. 119