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NUTRITION in Metabolic&,PULMO Stress

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© 2006 Thomson-Wadsworth Nutrition In Metabolic and Respirator y Stress NTRS 317 Chapter 22 NTRS 317 Chapter 22
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Page 1: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Nutrition In Metabolic

and Respiratory

StressNTRS 317 Chapter 22NTRS 317 Chapter 22

Page 2: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Nutrition In Metabolic and Respiratory Stress

• Metabolic stress• Respiratory stress• Hypermetabolism• Wasting• Multiple organ failure

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© 2006 Thomson-Wadsworth

The Body’s Responses to Stress and Injury

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© 2006 Thomson-Wadsworth

Hormonal Responses to Stress

Mediated by several hormones:• Catecholamines - Epinephrine –

Norepinephrine• Cortisol - Enhances protein degradation• All of the above cause: glycogenolysis;

gluconeogenesis, and lypolysis

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© 2006 Thomson-Wadsworth

Hormonal Responses to Stress

Mediated by several hormones:• Excessive cortisol

– Disrupts calcium metabolism– Causes insulin resistance and abnormal fat

deposition– Suppression of immune responses

• Aldosterone and antidiuretic hormone – help maintain blood volume

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© 2006 Thomson-Wadsworth

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© 2006 Thomson-Wadsworth

The Inflammatory ProcessThe inflammatory

response - contains and destroys infectious agents and prevents further tissue damage.

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© 2006 Thomson-Wadsworth

The Inflammatory Process• The inflammatory process causes –

– Dilation of blood vessels that deliver blood to a site of injury (arterioles)

– Constriction of small blood vessels that carry blood away from infected area (venules) – resulting in edema

– Prevents spread of infection – Encourages entry of immune cells

• Phagocytes

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© 2006 Thomson-Wadsworth

The Inflammatory Process

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© 2006 Thomson-Wadsworth

The Inflammatory Process

• Mediators of inflammation– Released from damaged tissue, blood

vessel cells and activated immune cells– Histamine – released from mast cells –

causes vasodilation and capillary permeability

– Cytokines and eicosanoids participate in the inflammatory process

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© 2006 Thomson-Wadsworth

The Inflammatory Process• Mediators of inflammation (cont’d)

– Anti-inflammatory medications act by blocking eicosanoid synthesis • Steroidal and non-steroidal anti-inflammatory

drugs– Changing dietary fat sources – have subtle

effects on inflammatory process• Replacing vegetable oils rich in omega-6 fatty

acids with sources high in omega-3 fatty acids (fish oil) helps to suppress inflammation – not a reliable treatment.

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© 2006 Thomson-Wadsworth

The Inflammatory Process• Systemic effects of inflammation

– Cytokines that are released provoke changes in the rest of the body

– Within hours or days – acute-phase response occurs – the liver increases its production of certain proteins• C-reactive protein • Blood clotting proteins – fibrinogen,

prothrombin and others• Muscle catabolism – gluconeogenesis• Negative nitrogen balance

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© 2006 Thomson-Wadsworth

The Inflammatory Process• Systemic effects of inflammation

(cont’d)– Systemic inflammatory response syndrome

(SIRS) • Increased heart and respiratory rate• Elevated white blood cell count• Increased body temperature

– Sepsis– Shock

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© 2006 Thomson-Wadsworth

SIRS, Sepsis and Multiple Organ

Failure

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© 2006 Thomson-Wadsworth

Nutrition Support for Acute Stress

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Determining Nutritional Requirements

• Estimation of energy needs– Harris-Benedict equation– Multiply body weight by a factor

appropriate for the person’s medical condition

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© 2006 Thomson-Wadsworth

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© 2006 Thomson-Wadsworth

Determining Nutritional Requirements

• Estimation of protein needs– 1 – 2 grams per kilogram body weight– Glutamine supplementation – associated

with fewer infections, shorter hospital stays, and reduced mortality rates in critically ill patients

– Arginine supplementation – beneficial effects on the immune responses of postoperative patients

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© 2006 Thomson-Wadsworth

Determining Nutritional Requirements

• Carbohydrates and lipids– Main source of energy– May provide up to 70% kcalories

depending on patient’s condition– Fat may supply up to 40% of kcalories

• Micronutrients– Zinc, vitamin C, vitamin A have critical

roles in immunity and wound healing– Blood concentrations monitored while on

parenteral nutrition

Page 20: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Determining Nutritional Requirements

• Nutrient delivery– Enteral nutrition support preferred over

parenteral nutrition in patients with normal intestinal function

– Incidence of bacterial translocation – similar in either type of nutrition support

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© 2006 Thomson-Wadsworth

Determining Nutritional Requirements

• Nutrient delivery– Parenteral nutrition –

• Sometimes used to supplement enteral feedings

• May be used as the main source of nutrients in patients who may become malnourished during critical illness

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© 2006 Thomson-Wadsworth

Patients with Burns

• Burn classification• Treatment• Metabolic changes• Nutrition support

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© 2006 Thomson-Wadsworth

Patients with Burns

• Burn classification– First-degree –

affecting epidermis – painful

– Second-degree – affecting epidermis and dermis – extremely painful

– Third-degree – full thickness burn – not painful

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© 2006 Thomson-Wadsworth

Patients with Burns

• Burn classificationBody divided into 11

parts (% Total Body Surface Area, TBSA)

– Head 9%– Neck 9%– Each arm 9%– Front torso 18%– Back torso 18%– Each leg 18%

Page 25: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Patients with Burns• Treatment

– Remove clothing, smoldering material, chemical agents

– Submerge burn and flush with copious amounts of water

– Wounds cleaned and debris removed

– Blisters and dead tissue may need debridement

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© 2006 Thomson-Wadsworth

Patients with Burns• Treatment

– Topic antibacterial agents and sterile dressings

– Fluid replacement and diagnosis of metabolic disturbances

– Possible immediate oxygen support/ mechanical ventilation

– Pain control

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© 2006 Thomson-Wadsworth

Patients with Burns• Metabolic changes

– Hypermetabolism– Tissue breakdown– Alterations in

nutrient metabolism– Loss of evaporative

water and body heat

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© 2006 Thomson-Wadsworth

Patients with Burns• Metabolic changes

– 2nd and 3rd degree – substantial losses of protein and micronutrients

– Gastrointestinal function may be disrupted – with burns covering 40-50% TBSA

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© 2006 Thomson-Wadsworth

Patients with Burns

• Nutrition support– Maintain fluid and electrolyte replacement

during the first 24 to 48 hours after injury• Goals – maintain adequate blood volume and

blood pressure• Avoid shock• Monitor urine and hemoglobin levels to ensure

adequate fluid input

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© 2006 Thomson-Wadsworth

Patients with Burns• Nutrition support

– Objectives• Achieve nitrogen balance • Minimize tissue losses• Promote wound healing• Maintain immune defenses

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Patients with Burns• Nutrition support

– Provide oral supplements and nutrient-dense snacks

– Tube feedings– If gastric ileus – nasoenteric feedings– Parenteral support – if intestinal function is

lacking

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© 2006 Thomson-Wadsworth

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© 2006 Thomson-Wadsworth

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Nutrition and Respiratory Stress

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

Two major types1. Chronic bronchitis2. EmphysemaReduced normal O2 capacity, Shortness

of breath (dyspnea), eventually respiratory or heart failure.

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© 2006 Thomson-Wadsworth

The Respiratory

System

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease

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Chronic Obstructive Pulmonary Disease - COPD

• Causes of COPD– Smoking tobacco– Occupational exposure to dusts or

chemicals– Respiratory infections– Genetic factors

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• The COPD patient– Debilitating disease– Eventually experience exhaustion or

breathlessness performing routine activities – bathing or dressing

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• The COPD patient– Weight loss – poor food intake, increased

metabolic rate, activities of certain inflammatory proteins

– Muscle wasting– Anxiety and depression

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Treatment of COPD– Prevent disease progression– Relieve major symptoms (dyspnea and

coughing)– Medications

• brochodialators – improve airflow• corticosteroids – anti-inflammatory medications

– Supplemental oxygen therapy– Exercise training

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Medical Nutrition Therapy– Maintaining a healthy body weight– Preserve muscle mass– Low body weights – correlated with

increased mortality – Weight loss often results from lower food

intake, higher metabolic needs or the inflammatory state

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Improving food intake– Small frequent meals– Liquids consumed between meals– Avoid foods that increase gas formation– Eat slowly and in a calm environment– Use oxygen at mealtimes

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Improving food intake– High-energy, high-protein diet may be

beneficial– Excessive energy intakes may increase

carbon dioxide output and increase respiratory stress

– If overweight or obese – use energy-restricted diet to promote gradual weight loss

Page 46: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Incorporating an exercise program– Prevent loss of muscle with carefully

designed exercise program

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© 2006 Thomson-Wadsworth

Chronic Obstructive Pulmonary Disease - COPD

• Use of specialized formulas– More kcalories from fat and fewer from

carbohydrate –Theoretically should lower respiratory

requirements – ratio of carbon dioxide production to oxygen consumption within cells is lower when fat is consumed

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© 2006 Thomson-Wadsworth

Respiratory FailureMay result from:• Weakness or paralysis of the muscles

involved in respiration• Embolus lodged within the lungs• Toxic substances that damage lung tissue• Surgery - anesthesia or abdominal

procedures that affect breathing• Severe trauma or infections – acute

respiratory distress syndrome (ARDS)

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© 2006 Thomson-Wadsworth

Respiratory Failure

• Consequences of respiratory failure– Hypoxemia – low blood levels of oxygen– Hypercapnia – excessive carbon dioxide in

the blood– Hypoxia – inadequate oxygen supply

within the tissues

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© 2006 Thomson-Wadsworth

Respiratory Failure• Acute respiratory distress syndrome

(ARDS)– Follows acute lung injury due to:

• Sepsis• Trauma• Severe pneumonia• Inhalation of smoke or toxic chemicals• Aspiration of gastric contents

– Requires mechanical ventilation– Later stages cause fibrosis and disrupt

lung structure– May progress to multiple organ failure

Page 51: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Respiratory Failure• Treatment of Respiratory Failure

– Oxygen therapy via face mask or nasal tubing

– Maintain fluid balance and prevent overload

– Diuretics – to mobilize fluid accumulating in lung tissue

– Medications to treat infections, keep airways open, or relieve inflammation

Page 52: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Respiratory Failure

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© 2006 Thomson-Wadsworth

Respiratory Failure

• 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

Page 54: NUTRITION in Metabolic&,PULMO Stress

© 2006 Thomson-Wadsworth

Respiratory Failure

• Energy– Harris-Benedict equation

• Fluids– Watch for dehydration– Edema may make it difficult to assess

accurate weight

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© 2006 Thomson-Wadsworth

Respiratory Failure

• Nutrition support– May need nutrition support– Tube feedings used if intestine is

functioning– Intestinal feedings preferred over gastric

feedings to reduce risk of aspiration

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© 2006 Thomson-Wadsworth

Respiratory Failure

• 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

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© 2006 Thomson-Wadsworth

Multiple Organ Failure

• Cause of death in up to ½ of intensive care patients

• Failure of 2 or more organ systems

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© 2006 Thomson-Wadsworth

Multiple Organ Failure• Development of multiple organ failure

– SIRS, if not reversed quickly, may progress to shock

– Shock can impair numerous organ systems

– The failure of one organ may place excessive demands on another, causing it to fail as well

– Typical pattern: (1) lungs; (2) liver; (3) kidneys, GI tract or heart

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Multiple Organ Failure

• Factors that influence organ failure– Age– Severity of SIRS– Infection– Blood transfusions – immunosuppressive,

so they may increase risks of developing infection or sepsis

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Multiple Organ Failure• Treatment of organ failure

– Lung support – mechanical ventilation– Fluid resuscitation – restore blood volume

and maintain electrolyte balance– Heart and blood vessel function – meds – Kidney support – hemofiltration or dialysis– Infection – antibiotic therapy– Nutrition support – enteral and parenteral

support to provide nutrients, prevent wasting and promote recovery


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