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Rts2-K52-Nutrition and Respiratory Problem
Rts2-K52-Nutrition and Respiratory Problem
HARUN ALRASYID
FAC.OF MEDICINE
USU-MEDAN
“BETTER OUTCOMES
WITH
NUTRITION SUPPORT”
THE RESPIRATORY SYSTEM
EFFECTS OF MALNUTRITION ON
DEVELOPMENT
STRUCTURE
FUNCTION
EFFECTS OF MALNUTRITION
Ad.Development
#Animal models:
-fetal malnutritionpulmonary hypoplasia
-lung size disproportionately small for body size
Ad.Structure
#Inadequate protein this phasepathologic changes
similar in emphysema
Ad.Function
#Direct correlation (human):
low birth weight and subsequent decreases in pulmonary
function
RESPIRATORY MUSCLE
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
role in pathogenesis of TB
Multiple micronutrient deficiencies during TB
TUBERCULOSIS
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
RESPIRATIONAL QUOTIENT (RQ)
Substrate utilization
Allows nutrient administration to be
tailored
patient’s need
On a kcal per kcal basis:CH produce
21% more
CO2 vs fat
ASPEN 1993:CH REQ.=25-30 KCAL/BW/DAY
ASPEN 2001:
*Source of energy
*prevent EFA deficiency
*↓osmolarity peripheral TPN
* MONITORING IMMUNOLOGIC FUNCTION
FAT REQUIREMENT
To provide EFA
EFA cell
membranes,prostaglandins,immune
mediators
PROTEIN REQ.
Normal 0.5-1,0g/kg/day (in patient may
increase to 1.0-1,5 g/kg/d (ASPEN 2000)
Nitrogen consumption:
Urine ureum/24 hrx28x4000 mmol (mg/24
hr)
Protein reg : N consumption 6.25
Protein req vs Cal.req:
Metab.stress (-) 1gr prot: 30 Cal/kg/d
Metab.stress (+) 2 gr prot. : 40 Cal/kg/d
ELECTROLYTE REQ.
ElectrolytemEq/kg/d daily dose(mEq/d)
----------------------------------------------------------------
-------------------
Na 1-2 50-100
K 1-2 50-100
Mg 0.2-0.5 10-30
Ca 0.2-0.3 10-15
P 0.5-1.0 20-45
Cl 1.0-2.0 50-100
VIT.REQ.
Vit. Req/d
-----------------------------------------------------------------------------------------------------------
------------------------
Thiamin 3.0
Riboflavin 3.6
Pyridoxin 4.0
Niacin 40 mg
Pantothenic acid 15
Folic acid 400 mcg
Biotin 60 mcg
Cyanocobalamin 5 mcg
Ascorbic acid 100 g
Vit A 3300 U
Cholecalciferol 200
Tocopherol 10 mg
Phytonadione 2mg
TIMING & ROUTE OF NUTR.SUPPORT
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.statussurvival >
Malnutr.& ↓ BW (advanced lung disease)=
Pulmonary cachexia syndrome
(inadequate
intake from hyperinflation
hypermetabolic in COPD
↑Work of breathing & EE)
Generally > ↑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)
OBJECTIVE OF MNT IN COPD
improvements N-balance,BW,LBM,MIP
protein synthesis
A clinical/metabolic syndrome
characterized by:
-weight loss
-weakness
-anorexia
-depletion and derangement of body
compartments, disturbances in water
and electrolyte metabolism,progressive
impairment
of vital function
CLINICAL PRESENTATION OF CACHEXIA
PROTEIN
↑muscle protein catabolism
↑whole body protein turnover
↑liver protein synthesis
↓muscle protein synthesis
LIPID
↑lipolyisis/glycerol/fatty acid turnover, ↓lipogenesis & LPL activity
↑NEFA (nonconstant) and plasma lipid (nonconstant)
MEDITORS OF MANY METAB.ALTERATIONS
PROTEIN CARBOHYDRATE LIPID
TNFα proteolysis glycogenesis ↓lipogenis
hepatic pr.synt. gluconeogenesis ↓LPL in fat tissue
↑lactate production
--------------------------------------------------------------------------------------------------------------------------
IL-1 ↑ hepatic pr.synt. ↑gluconeogenesis ↑lipolysis
↓ LPL synthesis
↑FA synthesis
-------------------------------------------------------------------------------------------------------------------------
IL-6 ↑ hepatic pr.synt. ↑ lipolysis
↑FA synthesis
--------------------------------------------------------------------------------------------------------------------------
IFNɤ ↓lipogenesis
↑lipolysis
↓LPL activity
DISEASE-SPECIFIC FORMULAS (LUNG CANCER)
Central PEN: