kuliah respirasi gizi

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Department of Nutrition , Faculty of Medicine,University of Hasanuddin Makassar

Andi FaradilahHaerani Rasyid

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UNDERSTAND NUTRITION AND RESPIRATORY SYSTEM

UNDERSTAND NUTRITION AND PULMONARY DISEASES

APPLY NUTRITIONAL CARE IN PULMONARY DISEASES

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The respiratory system can be divided into 3 component :

- A control mechanism located in CNS

- A pump made up of respiratory muscles - A gas exchange organ : lung

Malnutrition affect all of these components and produce profound changes in respiratory homeostasis

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Imbalance between synthesis and breakdown of lung surfactants

Alteration in intra alveolar surface tension

Decrease in lung protein synthesis

The muscle of resp is subject to the catabolic effect of malnutrition

Malnutrition is an adaptive mechanism to decrease VO2 & work of breathing

Medications & co-morbidities appetite, diet selection & metabolism

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BW, diaphragmatic

muscle mass ,

contractile strength ,

endurance , VC

ability to breath

deeply, effectively

cough up secretion

atelectasis & pulmonary

infection

Ventilatory drive,

endurance, work of

breathing

Acute Resp Failure

Resp muscle weakness &

altered ventilatory drive

failure to wean from

ventilator

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Altered host immune response chronic or repeated pulmonary infection

Diminished cell mediated immunity

Alteration in immunoglobulin turnover, surfactant prod , ability for repair following injury

Chronic fatigue & hypoxia work & activity restrictions negative impact on overall quality of life

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Increased Energy Expenditure

Reduced Intake Effect medication

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CH, fat and protein each utilize specific quantity of oxygen and produce a specific quantity of CO2 during metabolism. If VCO2 is divided by VO2, we obtain the

RESPIRATORY QUOTIENT ( RQ )

RQ = VC02 / V02

◦ RQ CH = 1◦ RQ Fat = 0.7◦ RQ Protein = 0.8

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Ingestion of insufficient calories1

Hypermetabolic state (increased resting energy expenditure)2

Loss of appetite1

Malabsorption1

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VISCOUS CIRCLE BETWEEN IMPAIRMENT AND MALNUTRITION IN COPD:

COPD

Difficulty consuming food

Increased metabolic rate

Chronic inadequate intake

Impaired aerobic capacity

Malnutrition

worsening

Increased caloric needs

Decreased muscle strength

worsening

( Kwiatkowski, et al. 1999)

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COPD patients are unable to regulate blood concentrations of O2 and CO2

Respiratory failure is confirmed when PaCO2>50 mm Hg and/or when PaO2<50 mm Hg

Treatment goals are to decrease PaCO2 levels and increase oxygenation (PaO2)

Overfeeding and high carbohydrate diets can increase PaCO2

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Decrease CHO consumption to minimize respiratory quotient (RQ)

Fullfill energy requirements without overfeeding (increases CO2 production)

Avoid excessive protein intake (in some cases)

Monitor fluid requirements

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In clinically stable COPD patients, optimal efficacy of ONS is best achieved not by manipulating macronutrient composition

but by giving EN in small frequent doses thereby avoiding complications & improving compliance composition

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Any metabolic stress, including nutrient adm, will augment CO2 prod act as a ventilatory stress to pt with impaired resp function

Immune-enhancing diets : modulate the dysfunctional inflammatory response by preventing the severe delayed immuno-suppresion

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Th/ goals: 1) improve VO2 & provide hemodynamic support,2) reduce VCO2

3) individualized NS 4) optimize gas exchange

NS is essential weaning from prolong mechanical ventilator

The role of omega 3 the immune syst by competing with arachidonic acid for cyclo-oxygenase metabolism

Omega 3 minimized the reaction of T cells to inflammatory process

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ACUTE RESP FAILURE (ARF) In pt with pulmonary dysfunction resp distress inability

to wean from mech.Ventilator Moderate malnutrition & resp muscle weakness resp

failure & delay transition back to spont. ventilation

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Conservative estimate of calorie need for all critically ill :REE = 25 – 30 kcal/kg/d

Harris –Benedict equation x stress factor of 1.2 – 2.0

Greater severity of illness: indirect calorimetry

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Dextrose, PRO & fat CO2

Dextrose >> RQ RQ > 1.0 VCO2 work of breathing

Metabolic stress, nutrient adm CO2 : ventilatory stress to pt with impaired pulmonary function

Nutrient intake must be monitored closely Adjust the proportion of NPC as fat & CHO

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Nutrition care during acute illness◦ Supply adequate

energy and protein

◦ Fluid restrictions may be necessary to reverse pulmonary edema

◦ Enteral nutrition is preferred over parenteral nutrition

Energy◦ Harris-Benedict

equation

Fluids◦ Watch for

dehydration

◦ Edema may make it difficult to assess accurate weight

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Nutrition support◦Nutrient-dense

formula – if on fluid restriction

◦ Pulmonary formulas – less carbohydrate and more fat

◦Parenteral nutrition if risk of aspiration too high to continue enteral feedings

© 2006 Thomson-Wadsworth

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• Counter regulatory hormone• Pro inflammatory cytokines• Acidosis• Loss of appetite• Inactivity

BREAKDOWN of BODY PRO STORES

• Immune dysfunction• Infections rates• Tissue repair • Wound healing • Skeletal muscle function

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Increase

d protein intake

CO2 production (effects negligible)

Ventilatory-drive mechanism

Minute ventilation

-

Beneficial for patients

able to respond to stimulus

Can increase work of

breathing and dyspnea in

patients unable to increase minute

ventilation

Askanazi et al. 1984

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K, Ca, PO4, Mg should be provided in adequate amounts to meet muscle requirements & maintain optimal respiratory muscle force

Vit A, C & E favorable impact on immune defenses.

Fe, Zn, Cu, Mn

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Toxic oxygen radicals damage parenchymal and endothelial

cells

Supplemental vitamin E, vitamin C, Supplemental vitamin E, vitamin C, --carotene, taurine, selenium, molybdenum carotene, taurine, selenium, molybdenum

may attenuate lung injurymay attenuate lung injury

Endogenous antioxidant system overwhelmed

Oxidants also lead to impairment of connective tissue repair, impaired ciliary function, increased mucous

production

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Perform a complete nutrition assessment

Evaluate Energy needs (appropriate amount do not overfeeding or underfeed)

Ensure protein balance

Monitor fluids and electrolyte, especially phosphorus

Evaluate vitamin, mineral status as indicated Consider high fat, low CH feeding in patients

with persistent hypercapnia

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FLOWCHART : NUTRITIONAL SCREENING AND THERAPY

SCREENINGSCREENING

weight

Fat free mass

TREATMENTTREATMENT

FOLLOW-UPFOLLOW-UP

MAINTENANCE TREATMENT• Dietary habits• exercise

MAINTENANCE TREATMENT• Dietary habits• exercise

SUPPLEMENTAL NUTRITION• oral supplement

SUPPLEMENTAL NUTRITION• oral supplement

ANABOLIC STIMULATION• Dietary habits• exercise - type

- duration- intensity

ANABOLIC STIMULATION• Dietary habits• exercise - type

- duration- intensity

SUPPLEMENTAL NUTRITION• oral supplmental• enteral nutrition

SUPPLEMENTAL NUTRITION• oral supplmental• enteral nutrition

COMPLIANCE IMPROVEMENT

COMPLIANCE IMPROVEMENT

BMI<21 kg/m2

NUTRITIONAL THERAPYNUTRITIONAL THERAPY

responder Non-responder

FOLLOW-UPFOLLOW-UP

21<BMI<25 kg/m2 25<BMI,30 kg/m2

Weight loss Weight lossWeight stable Weight stable

FFMI<16/15 kg/m2 FFMI>16/15 kg/m2

Flowchart of nutritional screening and therapy. BMI, body mass index; FFMI, fat-free mass index

Schols AMWJ, Wouters EFMPulmonary Rehabilitation 2000 : 247-59

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Ingestion of insufficient calories1

Hypermetabolic state (increased resting energy expenditure)2

Loss of appetite1

Malabsorption1

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Multifactorial including tissue hypoxia, ageing, physical exercise, increased resting metabolic rate, chronic inflammatory processes drugs,

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COPD patients are unable to regulate blood concentrations of O2 and CO2

Respiratory failure is confirmed when PaCO2>50 mm Hg and/or when PaO2<50 mm Hg

Treatment goals are to decrease PaCO2 levels and increase oxygenation (PaO2)

Overfeeding and high carbohydrate diets can increase PaCO2

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Decrease CHO consumption to minimize respiratory quotient (RQ)

Fullfill energy requirements without overfeeding (increases CO2 production)

Avoid excessive protein intake (in some cases)

Monitor fluid requirements

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In clinically stable COPD patients, optimal efficacy of ONS is best achieved not by manipulating macronutrient composition

but by giving EN in small frequent doses thereby avoiding complications & improving compliance composition

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High CHO dietContinued erosion of tissues, resulting in:Impaired respiratory function hypoxic ventilatory response resistance to infection Deteriorated lung function

Pulmonary insufficiency

Decreased caloric intake; Increased caloric requirement

MALNUTRITION

CO2 production; RQ

Inability to excrete CO2

CO2 retention RESPIRATORY FAILURE

High fat dietImproved nutritional status; Reduced CO2 production and retention

High CHO dietIncreased CO2 production and retention

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FLOWCHART : NUTRITIONAL SCREENING AND THERAPY

SCREENINGSCREENING

weight

Fat free mass

TREATMENTTREATMENT

FOLLOW-UPFOLLOW-UP

MAINTENANCE TREATMENT• Dietary habits• exercise

MAINTENANCE TREATMENT• Dietary habits• exercise

SUPPLEMENTAL NUTRITION• oral supplement

SUPPLEMENTAL NUTRITION• oral supplement

ANABOLIC STIMULATION• Dietary habits• exercise - type

- duration- intensity

ANABOLIC STIMULATION• Dietary habits• exercise - type

- duration- intensity

SUPPLEMENTAL NUTRITION• oral supplmental• enteral nutrition

SUPPLEMENTAL NUTRITION• oral supplmental• enteral nutrition

COMPLIANCE IMPROVEMENT

COMPLIANCE IMPROVEMENT

BMI<21 kg/m2

NUTRITIONAL THERAPYNUTRITIONAL THERAPY

responder Non-responder

FOLLOW-UPFOLLOW-UP

21<BMI<25 kg/m2 25<BMI,30 kg/m2

Weight loss Weight lossWeight stable Weight stable

FFMI<16/15 kg/m2 FFMI>16/15 kg/m2

Flowchart of nutriional screening and therapy. BMI, body mass index; FFMI, fat-free mass index

Schols AMWJ, Wouters EFMPulmonary Rehabilitation 2000 : 247-59

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Malnutrition & resp failure are integrally linked

Malnutrition causes a loss of skeletal muscle mass and alteration in respiratory muscle function

Critically ill pt with resp failure is vulnerable to complication of under/over-feeding

A great deal of optimism surrounds the development of immuno-enhancing nutrient

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BODY WEIGHT LOSS IN CHRONIC PULMONARY DISEASE

• Adaptive Mechanism to reduce O2 consumption

• Body weight loss and underweight are poor prognostic, but not close related with the degree of lung function impairment

• 5% of ABW within 3 months or 10% within 6 months) is found in 25–40% of all cases when lung function is severely impaired (FEV1o50%)

• Nutritional support reduced mortality rate

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Malnutrition in outpts : 25%, inpts : 50%, critically ill pt in ICU : 60%

Nutritional depletion has been attributed to anorexia & hypermetabolism as a result of work of breathing

Inadequate intake of pro-cal primary lung parenchymal disease, immuno-compromise & resp muscle wasting & dysfunction the need for intubation & mechanical ventilation

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Th/ goals: 1) improve VO2 & provide hemodynamic support,2) reduce VCO2

3) individualized NS 4) optimize gas exchange

NS is essential for weaning from prolong mech. Ventilator The role of omega 3 to aid the immune syst by competing

with arachidonic acid for cyclo-oxygenase metabolism Omega 3 minimized the reaction of T cells to inflammatory

process

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Should be simple & follow basic concepts utilized for other critically ill pts

Earlier nutrient adm is beneficial (esp pt with malnutrition & severe stress)

The hypermetabolism muscle wasting that may be aggravated by bedrest, sedation & neuromuscular blockade. Prolonged ventilator support further deconditioning

Malnutrition can occur rapidly due to pro-catabolism + inadequate nutritional intake

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Airway wall contraction of airway smooth muscleimpairment of -adrenoceptor functionstimulation of airway secretionpulmonary vascular smooth-muscle relaxation or contractionactivation of mast cells

Antiproteases inactivation of 1-proteinase inhibitor

inactivation of secretory leukoprotease inhibitor

Lung matrix elastin synthesis ↓ and fragmentationcollagen synthesis ↓ and fragmentationdepolymerisation of proteoglycans

Pulmonary microcirculation

↑ permeabilityPMN sequestration↑ PMN adhesion to endothelium of arterioles and venules

Alveolar epithelial cell layer

↑ permeability by detachment, ↓ adherence and ↑ cell lysis

Tabel : Alterations in components of the lungs caused by oxidative stress

Dekhuijzen PNR et al, Pnews 1998 ; 1 : 3-5

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Pt with acute pulmonary failure must be given nutrition support to satisfy energy requirements and limit progressive wasting of respiratory muscle

Malnourished pt with COPD can benefit from nutrition support because it produces an increase in respiratory muscle strenght

In the case pt with lung disease who are bordering upon developing respiratory failure, nutrient intake must be monitored carefully to avoid an over production of CO2 which can trigger respiratory failure. Non protein calorie distributing can be adjusted, reducing CHO and increasing fat, which will decrease CO2 production

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Pt with respiratory failure are on mechanical ventilator should receive nutritional support from the first day of intubation, providing sufficient calorie to cover total energy expenditure

Administration of mineral such as sodium, potassium, calsium and particularly phosphorous and magnesium should be carefully monitored to maintain good muscle function

For pt with severe ooxigenation disorders, lipid in parenteral formula must be administered carefully, in a continuos 24 hour infusion. The dose should not exceed 1 gram/kg/day

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Improved respiratory function◦ Increase in weight/lean muscle mass1

◦ Increase in inspiratory and expiratory pressures1

◦ Associated with successful weaning from mechanical ventilation2

Improved quality of life◦ Reduced frequency, duration, and intensity of

pulmonary-related hospitalization2

1Irwin and Openbrier 1985; 2Larca and Greenbaum 1982

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Historical Parameters Medical Parameters Nutritional Parameters Diet history Environmental Parameters

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