NUTRITION AND RESPIRATORY PROBLEM

HARUN ALRASYID
FAC.OF MEDICINE
USU-MEDAN
“BETTER OUTCOMES
WITH
NUTRITION SUPPORT”
DUKUNGAN NUTRISI
 Lakukan penilaian nutrisi pada pasien penyakit
paru
 Evaluasi kebutuhan energi dan berikan jumlah
yang tepat
 Tidak overfeed atau underfeed
 Ada keseimbangan protein
 Monitoring cairan dan elektrolit, terutama fosfor
 Evaluasi status vitamin dan mineral
 Pemilihan makanan dengan tinggi lemak, rendah
karbohidrat pada pasien hiperkapnia
 Evaluasi nutrisi penting pada pasien penyakit
paru
 Hal ini diperlukan untuk mendeteksi malnutrisi
dan mengadakan rencana asupan makanan
 Optimalisasi asupan total energi
 Perhitungan REE sangat diperlukan (1.1-1.4)
 Pergunakan kalorimetri indirek jika ingin
menentukan estimasi kebutuhan energi dengan
tepat
 Pergunakan REE dan RQ untuk menentukan
asupan energi
 Penurunan asupan energi dibawah atau seimbang
REE dapat membantu proses weaning, tetapi
hindari pasien katabolik dan berkepanjangan
 Jika terjadi peningkatan berat badan dengan baik
dan kondisi pasien stabil maka boleh
meningkatkan asupan makan
 Dengan pemantauan fungsi pernafasan
 Pasien yang tidak hiperkapnia, kalori harus
didistribusi dengan baik:
 KH 50-60% kalori total
 Lemak 20-30% kalori total
 Protein 15-20% kalori total
 Pasien dengan hiperkapnia, apakah menggunakan
ambu atau ventilator:
 KH 25-30% kalori total
 Lemak 50-55% kalori total
 Asupan seharusnya individual untuk menentukan
persentase lemak agar pCO2 tetap terjaga
 Lebih disarankan untuk menjaga jumlah asupan
energi dibandingkan mengkombinasi persentase
KH dan lemak
THE RESPIRATORY SYSTEM

EFFECTS OF MALNUTRITION ON
 DEVELOPMENT
 STRUCTURE

 FUNCTION
EFFECTS OF MALNUTRITION
Ad.Development
#Animal models:
-fetal malnutritionpulmonary hypoplasia
-lung size disproportionately small for body size
Ad.Structure
#Inadequate protein this phasepathologic changes
similar in emphysema
Ad.Function
#Direct correlation (human):
low birth weight and subsequent decreases in pulmonary
function
RESPIRATORY MUSCLE

-Diaphragma weight ~ Body Weight

- ↓Maximal resp.muscle strenght (MIP&MEP)

loss of muscle mass & myopathy of the remain-
ing muscle
MALNUTRITION
 ↓peak pressure generation
limited impact on
endurance
VENTILATORY DRIVE
 Calory& nutrient restrictions ↓ hypoxic
respiratory drive (normal subjects)
 Severe anorexia nervosa (46% IBW)↓VE&
mouth occlusion pressure (=output of resp.
center) due to hypercapnia (reversed on
refeeding) (Ryan etal 1992)
 Malnutrition affects central resp.control and
muscle strenght
HOST DEFENSES

Malnutrition:
-alters pulmonary defense mechanisms
-animal models (severe malnourishment)
↓alveolar macrophage/phagocytosis/microbial killing
-inadequate clearance of resp.secretion (ineffective
cough from muscle weakness & alveolar collapse
/atelectase)predisposed to pulmonary infection
TUBERCULOSIS

Spectrum:
 Asymptomatic latent to disseminated disease

 Disrupts normal hostpulm.& extrapulm

 Poor nutr. & TBthe Greek term aphthisis

( “to waste away” & “consumption”)

 Network of cytokines TNF-ᾳ as the central role

in pathogenesis of TB
 Multiple micronutrient deficiencies during TB
TUBERCULOSIS

 Serum albumin & arm circumf. subnormal 12 month

after therapynot fully recovered of
body protein reserve
 Altered amino acids metabolismwasting
 TB & HIV the body cell mass depleted
 Vit.A improves immune response
(animal studies)
Solotorovsky M,1961; Ferraro,1988
 Protein deficiency:
loss of tuberculin test sensitivity
↓lymphocyte proliferation responses to
mycrobial antigens
 IL-2 production
 CD2+ lymphocytes in thymus & peripheral
Bartow,1990;Mc Murray,1992
NUTRITIONAL STATUS & PROTOTYPICAL LUNG DISEASES

Nutrition in critical illness:

 hypermetabolism
 protein catabolism
 muscle proteolysis

 insulin resistance (impaired glucose utiliz.)

 hyperglycemia
NUTRITION SUPPORT
 Appropiate amount & composition of nutrients
 Energy Requirement estimated (REEx1.2-1.5)
 Estimate Calory needs by Fick Equation
Vo2=CO+Cao2-Cvo2  invasive monitoring
(pulmonary artery catheter,relative stable pat.)
 Vo2 (ml/min) converted to kilocalories/day
calorie value O2 (4.69-5.05 kcal/L O2 consumed)
or Weir equation if Vco2 (O2 product.) known
SUBSTRATE SUPPLEMENTATION & VENTILATORY
REQUIREMENT

Acute Resp.Failure
proteolysis (endogen protein)
in fasting, glucose 100 g/d (600g/d in septic)
fat emulsion (+minimum 500 kcal/d for spare)
approp. mix.of Carb.+Proten+Fat (individual):
-CHO oxidized ~ CO2> (6 molecules) RQ=1
-Protein oxidized ~ RQ=0.8
-Fat oxidized ~ RQ = 0.7
TIMING & ROUTE OF NUTR.SUPPORT

 Enteral Feeding & Pulmonary Issues

-potential mechanical risks (tracheobronchial
tree/pleural space
-nasoduodenal route↓ risk of aspiration
-semirecumbent position
 PEN & pulmonary issues (peripheral/central)

-central veinconcentrated solution

-ARDS  improve outcome with limited fluid
-Heparin 6000 U/d ~ ↓ risk of thrombosis
ARDS/ACUTE LUNG INJURY

ARDS :
-↓ Antioxydant (vit-E,C,retinol,β carotene)↑ lipoperoxides
- Supplementation(-) change in pulm.MR, lower incidence
of MOF/LOS of intensive care/fewer days of mechanical
ventilation
- Dietary lipids ~ eicosanoids profile produced inflammatory
cells
a.linoleic acid (n-6 FA)arachidonic (precussor of many
proinflam. PG & leukotrines )
b.linolenic (n-3FA) eicosapentanoic (~eicosanoids
less inflammatory potential
MALNUTRITION & COPD
 60 % of patients with COPD
 Improvement in nutr.statussurvival >
 Malnutr.& ↓ BW (advanced lung disease)=
Pulmonary cachexia syndrome (inadequate
intake from hyperinflation)
 Generally hypermetabolic in COPD
 ↑Work of breathing & EE>  ↑REE
COPD
 Inflammatory state (malnutrition)from:
-chronic airway inflammation
-circulating inflammatory mediators
loss of skeletal muscles/weight/fat-free mass
 ↑ TNFᾳ (induce cachexia) in weight loss
(absence of an acute infection)
COPD
1.Growth hormone/anabolic steroid
 adjuvant therapy

 improvements N-balance,BW,LBM,MIP

 protein synthesis

 minimizing thermogenic effect nutritional replacement

by reducing calories needed for

anabolism
2.High fat,low CHO diet
3.Att. for ↓K/Ca/PO4resp..muscle function?
ASTHMA
 Dietary fat,rich in fish oil  alter prostanoid
released (from inflam.sel)
 Vit.C,E (antioxidants),Mgmodulate effects
of airway injury
SELESAI