NUTRITIONAL MANAGEMENT OF PULMONARY DISEASES

Redario C. Laygo, M.D.

Department of Biochemistry, Molecular Biology and Nutrition
UST Faculty of Medicine and Surgery
(Transcribed from the Powerpoint Presentation. Side Notes from MinionNotes)
Introduction

Lungs functions for gas exchange

Mitochondria serves as the final electron

receptor for cellular metabolic demands

Oxygen molecule

Metabolic pathways (produces CO2)

o Krebs cycle: generates CO2 by PDH
complex
o CO2 + H2O = Carbonic acid ->
subsequently dissociates into protons and
HCO3
o HCO3 enters the RBC through, in
exchange with Cl ion (Chloride shift)
Pulmonary Function

Gas exchange

Obtain O2 needed for cellular metabolic demands

Remove CO2

Filter, warm and humidify inspired air (turbinates)

Synthesize surfactant (major component:

dipalmitoyl phosphatidylcholine and dipalmitoyl
lecithin)

Regulate body acid-base balance

Synthesize arachidonic acid (precursor to

prostaglandins)

Convert angiotensin I to angiotensin II (ACE)

Nutrition and Lung Immune Defense

Cells secrete mucus

o Moist airways (regulate temperature)
o Traps particles and microorganisms

Cilia sweep particles upward toward pharynx

Macrophages of epithelial surfaces phagocytose

and digest inhaled inert materials, microorganisms
Category of Pulmonary System Disorders

Primary
o Tuberculosis
o Bronchial asthma
o Lung cancer

Secondary
o Associated with CVDs
o Obesity (and diabetes)
o AIDS
o Sickle cell disease
o Scoliosis

Acute conditions
o Aspiration of enteral feeding liquids (and
solids)
o Airway obstruction from foods (esp.
children)
o Anaphylaxis

Chronic conditions
o Cystic fibrosis (mutation in CFTR gene
that codes for ABC transporter, affecting
chloride channels)
o Emphysema (results from chronic
smoking; alpha-1 antitrypsin is affected
methionine is oxidized > elastase is
released)
Parameters Used to Assess Pulmonary Status

Imaging procedures

Pulmonary function test (i.e. spirometry)

Arterial blood gas determinations

Sputum cultures (AFB for PTB)

Biopsies (for malignancies)

Second Semester || A.Y. 20132014

CVS, renal, neurologic and hematologic systems

Cycle of Malnutrition and Lung Disease

Notes:

Mere chewing or swallowing will render the

patient breathless (deterrence due to decline in
pulmonary function)
Impairment in nutritional status if we dont take
in something like: carbohydrate intake, will
contribute to decline in pulmonary function
Diaphragm and thoracic cage - skeletal muscles
ATP is needed in the release of myosin from actin
in the power stroke (muscle contraction)

Malnutrition

Often occurs in conjunction with pulmonary

disease

Adversely affect:
o Lung structure and function (protein
molecule synthesis transcription and
translation, needs amino acids)
o Respiratory muscle strength and
endurance
o Immune defense mechanisms
(antibodies)
o Control of breathing

Increase in nutritional needs

Impact of Starvation

Frequent complication of respiratory infection (if

you dont take in anything!)

Impaired pulmonary function (Keys, et. al.)

o Decreased vital capacity
o Minute ventilation
o Efficiency of ventilation

Decline in:
o Respiratory muscle mass (which will
affect:)
o Strength
o Endurance
o Efficiency
Impact of Malnutrition

Altered pulmonary parenchymal structure:

o Lung tissue more susceptible to damage
o Repair process disrupted
o Increased compliance (distensibility)
o Decreased elasticity (elastin)
o Collapse of alveoli (lung surfactants will
decrease surface tension)
o Pulmonary edema (protein molecules
cannot be synthesized effect on oncotic
pressure)

Altered pulmonary parenchymal function:

o Decline in oxygen-carrying capacity of
blood (Hemoglobin)
o Decreased ventilatory response to
hypoxia
Impaired pulmonary defense mechanism

At The Cellular Level

Respiratory muscle function compromised by:

o Low levels of energy substrates
o Low levels of minerals and electrolytes
(iron, magnesium and potassium) (Bilbrey,
et. al., 1973; Molloy, et. al, 1984; Rochester, 1986)

Acute respiratory failure associated with

hypophosphatemia (Aubier, et. al, 1985)

Impact of Lung Disease on Nutritional Status

25-50% more energy spent in Chronic Lung

Disease (CLD) (Field, et. al, 1982; Yeh, et. al, 1989)

10% increase in Recommended Energy

Expenditure (REE) with use of salbutamol
(Vaisman, et. al, 1987)

35% increase in O2 consumption associated with

chest physical therapy for critically ill,
mechanically ventilated patients
(Weissmann, et. al, 1984)

Adverse Effects of Lung Disease on Nutritional Status

Increased energy requirement

o Increased work of breathing
o Chronic infection
o Medical treatments

Reduced nutrient intake

o Fluid restriction
o Shortness of breath
o Decreased O2 saturation when eating
o Anorexia
o GIT distress and vomiting

Additional limitations
o Difficulty of preparing food
o Lack of financial resources
o Impaired feeding skills
o Altered metabolism
Nutritional Care in Respiratory Distress Syndrome
(Hyaline Membrane Disease)

Goals of nutritional therapy

o Prevent or correct malnutrition
o Prevent overfeeding
o Replace essential fatty acids, carnitine
and other nutrients (Essential FAs:
Linoleic and Linolenic acid) (Carnitine:
transport of FAs from cytosol to matrix =
FAs broken down through betaoxidation) (Skeletal and cardiac muscles:
preferred fuel is FAs)

Specific dietary modifications

o Increase fat, add extra calories and give
palatability to diet
o Provide adequate Essential Fatty Acids
(EFA) and ADEK (Fat soluble vitamins)

Vitamin A (Retinal phosphate

and Retinoic acid): for the
repair of tissues, a lot of sulfate
is utilized

Vitamin D (Calcitriol or 1,25dihydroxycholecalciferol):

associated with calcium
bones of the thoracic cage

Vitamin E (Tocopherols):
antioxidant property, reduction
of ROS together with Selenium,
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Vitamin C and Glutathione

(NADPH + H will maintain
Glutathione in reduced state,
coming from Hexose
Monophosphate pathway
through the enzyme, Glucose6-Phosphate dehydrogenase)

Vitamin K: pre-term infants,

susceptible to periventricular
hemorrhage
o Caution with TPN-induced CO2 gas
o Weight maintenance: 1-1.2 X BEE
o Anabolism: 1.4-1.6 X BEE
o Non-Protein Calories (NPC): 50%
glucose and 50% lipid
Goal of nutritional therapy
o Meet energy and nutrient requirements
o Preserve LBM
o Maintain fluid and acid-base balance
o Provide nutritional substrates that will
not increase CO2

Nutritional Care in Acute Respiratory Failure

Specific dietary modifications

o Begin feeding ASAP
o Diet: 35-50% CHO and 30-50% lipid
cal.
Adults daily diet of:

25-35 kcal/kg maintenance

35-45 kcal/kg anabolism

o Protein: 2g/kg DBW
o Reduce sodium if with pulmonary edema
o Supplement with Vitamins A and C
o Phosphorus, if depleted: 2.5-5mg/kg BW
Nutritional Care in Chronic Pulmonary Disease

Goals of nutritional therapy

o Maintain acceptable weight-for-height
o Maintain fluid and acid-base balance
o Manage drug-nutrient interactions

Specific dietary modifications

o Provide high protein/high calorie diet:

1.2-1.5g CHON/kg

BEE X 1.5 for anabolism

o Diet: 40-55% CHO, 30-40% Fat, 1520% CHON
o Soft diet, no gas forming vegetables (i.e.
cabbage, onions, sweet potatoes, prunes)
o Small, concentrated feeds at intervals (to
prevent impingement of the diaphragm)
o Supplement with Vitamins A, C and B
complex

B1 - Thiamine (Thiamine
pyrophosphate): Pyruvate
dehydrogenase (Pyruvate to
Acetyl-CoA), Alphaketoglutarate dehydrogenase (in
Krebs Cycle); Transketolase (in
HMP Shunt)

B2 Riboflavin: FMN and FAD

(Succinate dehydrogenase)

B3 Niacin: NAD (Malate

dehydrogenase, Isocitrate
dehydrogenase, Alphaketoglutarate dehydrogenase)

B5 Pantothenic acid: synthesis

of Coenzyme A for activation
process

B6 Pyridoxine (Pyridoxal
phosphate): transamination
reactions

B7 Biotin: carboxylation
reactions (Propionyl CoA
carboxylase; Pyruvate
carboxylase first enzyme
gluconeogenesis, important
anaplerotic reaction)

B9 Folate: Thymidylate
synthase

B12 Cobalamin: Methionine

synthase and L-Methylmalonyl
CoA mutase
High fluid intake: 1mL/kcal
Restrict Na+ and increase K+ if with
pulmonary edema
Increase fiber gradually

o
o
o

Gas forming foods: Beans, Brussel sprouts, etc.

Nutritional Care in Pulmonary Tuberculosis

Goals of nutritional therapy

o Maintain weight
o Restore Ca2+ levels in serum
o Replace losses from lung bleed
(hemoptysis)
o Promote healing of pulmonary cavities
o Counteract side effects of drugs (INH,
supplement Vitamin B6 because
Pyridoxal phosphate is converted)
o Stimulate appetite
o Prevent dehydration

Specific dietary modifications

o Well-balanced diet:

Protein: 1.2-1.5g/kg

Calories: 3000 kcal

o Provide sufficient Ca2+, controlled
amounts of vitamin D (A study have
shown that a dose of 300mg INH per day
for 14 days decreases serum Calcium and
Phosphate levels)
o Provide iron and vitamins A and D
o Ensure diet provides vitamin B-complex,
especially vitamin B6
o Fluids: 2 liters unless contraindicated

Second Semester || A.Y. 20132014