Malnutrition adversely affects the structure, elasticity, and function of the lungs as well as the mass, strength, and endurance of muscles involved in the respiration process.2–4 Malnutrition-altered lung function includes decreased strength, power, and endurance of respiratory muscles and increased respiratory muscle fatigue. In addition, skeletal muscle relaxation slows, and muscle mass is diminished due to specific reduction in muscle fiber size and type. During starvation or malnutrition, respiratory muscles and skeletal muscles are subject to catabolism, providing energy to the body. The resultant reduction in the mass of the diaphragm, diminished inspiratory and expiratory muscle strength, and decreased vital capacity and endurance result in impaired pulmonary function.^4–9 Inadequate nutrition or an increase in energy needs can result in malnutrition, leading to alterations in pulmonary muscle function.

Within days, protein deficits in the diet result in a decline in respiratory muscle function.⁷ Low levels of proteins in the blood (hypoalbuminemia) contribute to pulmonary edema as colloid osmotic pressure is decreased, allowing a fluid shift into the interstitial space. Extravascular lung water increases, resulting in a decrease in functional residual capacity and pulmonary reserve. Low serum albumin levels can result in an increase in extracellular fluid volume and a reduction in the intracellular space.^7,9 Surfactant provides the low surface tension at the air-liquid interface, preventing the atelectasis, alveolar collapse, alveolar flooding, and severe hypoxia that result in respiratory distress. Even short periods of starvation result in a decreased synthesis and secretion of surfactant.¹⁰ Reduced surfactant, which is synthesized from proteins and phospholipids, contributes to the collapse of alveoli, resulting in an increased effort of breathing. Airway mucus is composed of glycoproteins, water, and electrolytes. Malnutrition results in depletion of liver and muscle glycogen and energy-rich compounds used to provide cellular energy, resulting in metabolic and muscular endurance dysfunction. This reduction in respiratory muscle function often coexists with increased energy requirements, resulting in a deterioration of gas exchange and an increased work of breathing, which can lead to pulmonary failure.^7,9

Micronutrients consistent of vitamins and minerals. Micronutrient imbalances and deficiencies can affect pulmonary function in several ways. Iron deficiency can result in low hemoglobin levels, thus reducing the oxygen-carrying capacity of the blood. Low levels of other micronutrients, such as potassium, phosphorus, calcium, and magnesium, affect cellular processes. Collagen, composing the supporting connective tissue of the lungs, requires vitamin C for synthesis. Low levels of phosphorus result in neuromuscular dysfunction and can exacerbate pulmonary failure. A reduction in 2,3-diphosphoglycerate (2,3-DPG) in the red blood cells due to reduced phosphorus levels decreases oxygen delivery to tissues and decreases the contractibility of respiratory muscles. Muscle strength is reduced in the presence of magnesium deficiency.⁷ Deficiencies in vitamin A, pyridoxine, and zinc may impair immune status and increase risk for pulmonary infections.^5,11 Antioxidant nutrients, including vitamins A, C, and E and flavonoids, have been reviewed for their relationship to the pathogenesis or exacerbations in patients with COPD. Reduced serum or tissue levels of antioxidant vitamins were found in people with COPD; however, other studies did not show significant effects.¹² Malnutrition has been found to be an independent predictor of higher morbidity and mortality in respiratory disease.⁴

Effect of Pulmonary Disease on Nutritional Status

Diseases of the pulmonary system can increase energy requirements. In addition, complications and treatment of pulmonary disease affect the ability to ingest and digest adequate food and affect the circulation, cellular use, storage, and excretion of most nutrients. The increased work of breathing, chronic infection, and medical treatments used to treat pulmonary diseases, such as chest physical therapy and some medications, increase energy requirements. Medications such as bronchodilators, steroids, and antibiotics used to treat disease may have other nutritional implications and need to be considered in the nutritional evaluation. Patients with pulmonary disease usually present with a reduced nutritional intake attributed to fluid restrictions, gastrointestinal discomfort, vomiting, anorexia, shortness of breath, and decreased oxygen saturation when eating. A reduced ability to prepare foods because of fatigue and shortness of breath, impaired feeding skills, altered metabolism, and financial limitations all result in additional limitations in achieving adequate nutritional intake. Also, some diseases, such as cystic fibrosis, affect not only the lungs but also the pancreas, resulting in inadequate production of certain enzymes necessary in the digestion of fats. This exposes cystic fibrosis patients to certain types of malnutrition, unless certain dietary supplements are taken to compensate.

Interdependence of Respiration and Nutrition

Respiration and nutrition are interdependent (Fig. 18-1). Air and food share common pathways during ingestion and then separate only briefly during “digestion,” with air going to the lungs for distribution and food to the stomach and intestinal tract for digestion and absorption. Oxygen and nutrients then combine in the blood and are distributed to the tissues of the body. The use of food for energy at the cellular level requires oxygen to support a controlled combustion process that produces energy molecules of adenosine triphosphate (ATP), which are used in all of the body processes for energy (Fig. 18-2).

FIGURE 18-1 Nutrition and breathing are interrelated. Air and food share common pathways of entry during ingestion and then separate only briefly during “digestion,” with air going to the lungs for distribution and food to the stomach and intestinal tract for digestion and absorption. Oxygen and nutrients then combine in the blood and are distributed to the tissues of the body. The use of food for energy at the cellular level requires oxygen to support a controlled combustion process that produces energy molecules of adenosine triphosphate (ATP), which is used in all of the body processes for energy, carbon dioxide, and water.

Body heat is a result of a combustion process called metabolism. Metabolism requires fuel in the form of food. For combustion to occur, oxygen must be present, provided through the process of breathing. Unless oxygen is delivered to the cells, the food eaten cannot be used. Nutrition and respiration are truly interdependent because breathing and oxygenation are considered part of the process of providing nutrition to the body’s tissues.

Titrating the proper amount of oxygen and eliminating carbon dioxide (the metabolic “smoke” of the combustion process) is the job of the respiratory system, coupled closely with the cardiovascular system. The respiratory system must be sensitive to the metabolic needs of the entire body. This process requires the integration of several organ systems. The respiratory system consists of neurologic components, cardiovascular components, respiratory muscles, and lungs (Fig. 18-3).

FIGURE 18-3 Block diagram illustrating components of the respiratory system. The neurologic component drives and controls respiration at the lungs by the respiratory muscles. It also affects the cardiovascular system by altering heart function and circulatory resistance. All components are necessary to achieve respiration. Nutritional quality and quantity directly affect the functioning of each system.

The metabolic rates of the tissues dictate the amount of oxygen needing to be picked up in the lungs. Oxygen uptake (V˙o2) is a respiratory factor that can be measured in the laboratory or at the bedside using specialized equipment. Nutritionally speaking, it is this measure that indicates the patient’s energy requirement. If V˙o2 is measured while a person is in a resting, nonstressed state, the basal metabolic rate (BMR) or basal energy expenditure (BEE) can be calculated. The BEE is the measure obtained when a person is at absolute rest with no physical movement, which is not clinically possible in the hospitalized patient. The term resting energy expenditure (REE) is used when a person is at rest upon waking. REE is the measurement used in hospitalized patients and is about 10% higher than BEE ¹³ because measurements are done when the patient is awake and at rest but not at basal conditions. A variety of predictive equations have been developed for use in estimating REE. For the purposes of predicting energy needs through predictive equations in nonobese critically ill patients when indirect calorimetry is not available, four equations were considered precise and unbiased in this population. In patients younger than 60 years and in those older than 60 years, respectively, the equations and their accuracy are as follows: Penn State Equation (69%, 77%), Brandi equation (61%, 61%), Mifflin-St. Jeor equation × 1.25 (54%, 54%), and Faisy equation (65%, 37%). The Penn State equation was validated in 2009 and is calculated as follows¹⁴:

Restingmetabolicrate(RMR)=Mifflin(0.96)+VE(31)+Tmax(167)−6212

Because calculating the REE produces only an estimate, it is preferable to measure the actual metabolic rate by indirect calorimetry in order to know the patient’s true energy needs. This eliminates some of the guesswork, especially when treating critically ill or metabolically challenged patients.

Adequate nutrition support depends on the ability to determine a patient’s energy needs. There are several ways to determine energy needs, including direct and indirect calorimetry and whole-body potassium measurement. Total daily energy expenditure is usually divided into three components:

1. REE, which includes metabolic rate at rest while the patient is awake

2. Diet-induced thermogenesis

3. Energy cost of physical activity ¹⁵

Energy production generates heat, and heat is measured in calories. Direct calorimetry directly measures the heat given off by the body in a carefully designed room. This measurement is not practical in clinical settings and cannot be used with compromised patient populations. Indirect calorimetry is the method most commonly used in clinical environments. Indirect calorimetry is the calculation of energy expenditure using measured respiratory parameters of oxygen consumption (V˙o2) and carbon dioxide production (V˙co2).V˙o2 and V˙co2 require precise measurements of inspired and expired gas concentrations and volume. V˙o2 and V˙co2 are converted to energy expenditure through the application of the abbreviated Weir equation 13,16,17:

Energy expenditure(kcal)=[(V.O2L/min)(3.941)+(V.CO2L/min)(1.11)]1400minutes

where V˙o2 and V˙co2 are expressed in liters per minute, and 1440 is the number of minutes in a day.

Because oxygen is not stored in the body, measuring oxygen uptake (V˙o2) correlates directly with energy (ATP) creation and use. Metabolism (REE) then can be measured by oxygen consumption and is directly related to the energy (calories) used. Indirect calorimetry may be clinically beneficial in the identification of patients who will not be able to sustain spontaneous ventilation because of excessive pulmonary work.¹⁸ The work of breathing is attributable to about 2% to 3% of the REE in the normal adult; however, in the pulmonary-compromised patient, as much as 25% of the REE can be attributed to the work of breathing.¹⁹ The respiratory quotient (RQ) (V˙co2/V˙o2) is also obtained from indirect calorimetry, which is used in the interpretation of net substrate use and as an indicator of test validity. The normal RQ range in humans is 0.67 to 1.2.¹⁷ Because energy measurements by indirect calorimetry are respiratory measurements, the RT is one of the members of the patient care team who commonly performs these measures in clinical settings. The RT who is trained to perform indirect calorimetry measurements is an important contributor to the assessment of nutritional needs of patients.

Indirect calorimetry measurements are usually performed using a metabolic cart, although different types of calorimeters exist. A metabolic cart is a computer-controlled unit composed of oxygen and carbon dioxide gas analyzers and flow transducers. The cart automatically measures patients’ airflow and expiratory volumes, applies correction factors, and prints out and graphs the results. Different types of gas collection devices, such as a facemask, mouthpiece with nose clip, or canopy, can be used as long as rigorous control is used and no air leaks occur.¹⁴

Having an understanding of this procedure will help the RT better understand what is automatically calculated by a metabolic cart. The following is a summary of the traditional energy measurement procedure:

1. Collect expired gas in a bag or Tissot spirometer for several minutes.

2. Analyze for carbon dioxide and oxygen (or oxygen and nitrogen).

3. Measure the volume of the gas collected in the bag.

4. Calculate:

a. If oxygen and carbon dioxide are measured:

V˙o2(STPD)=V˙E(ATPS)×(PB−H2O)×21.55Collectiontime×(273+tempin°C)×[1−FEO2−FECO2(PH2OPB)1−FIO2FIO2]−FEO2

Note:(273°K ×60sec)760mmHg=21.55

If gas is analyzed with desiccant (a drying agent) in line, then

PH2O/PB=0

where V˙o2_(STPD) = oxygen uptake, standard conditions

V˙E(ATPS) = minute volume; ambient temperature and pressure, saturated

P_B = barometric pressure

F_Eo₂ = fraction of expired oxygen

F_Eco₂ = fraction of expired carbon dioxide

PH₂O = water vapor pressure

F_Io₂ = fraction of inspired oxygen

V˙co2=V˙E×(FECO2−0.0003)

where V˙co2 = carbon dioxide production

RQ=V˙co2/V˙o2

where RQ = respiratory quotient

d. If only oxygen and nitrogen are measured,

V˙o2=V˙E×(FEN2/FIN2)×FIO2−V˙E×FEO2)

where F_EN₂ = fraction of expired nitrogen

F_IN₂ = fraction of inspired nitrogen

For patients confined to a hospital bed, portable equipment is used. For patients who are not intubated and whose condition does not allow them to cooperate with the procedure using a nose clip and mouthpiece, a special hood or canopy apparatus becomes necessary. The RT’s interactions with the nutritional support team for metabolic measurements is most helpful because respiratory therapy departments are usually equipped and therapists are trained for such measurements.

In nutrition, energy is quantified in terms of kilocalories (kcal); 1 kcal is the amount of energy it takes to raise the temperature of 1 kg of water 1° C. (Although kilocalories have been used most frequently in clinical nutrition, the kilojoule [kJ] is often used in research because kJ is the international unit for energy. To convert kcal to kJ, multiply kcal by 4.184.) For approximately every 5 kcal burned, 1 L of oxygen is used by the tissues. Therefore, if a patient’s V˙o2 is measured as 300 mL oxygen/minute, then 300 mL oxygen × 60 minutes × 24 hours equals 432 L of oxygen required per day and 5 kcal × 432 L oxygen/day equals 2160 kcal/day that should be given to the patient. If less than this amount of energy is given, the patient must use body energy stores (glycogen, adipose tissue, and lean muscle mass), which are often already depleted in chronically ill patients. The abbreviated Weir equation is used for more precise conversion of V˙o2 to kilocalories,¹⁶ as follows:

kcal/min=(3.94×V˙o2L/min)+(1.11×V˙co2L/min)

Energyexpenditure=kcal/min×1440min(perday)

Nutritional Depletion and Respiration

A patient who is not ingesting food enterally (through the gastrointestinal tract) probably will be placed on intravenous (IV) therapy. An IV solution of 5% dextrose running at 3 L/day will provide the patient with only 600 kcal/day (0.05 × 3000 mL × 3.41 kcal/g of glucose). (Note: glucose, when given in hydrated form [IV D₅/W and so on], yields 3.41 kcal/g; otherwise the yield is about 4 kcal/g of carbohydrate.) This is far from what is needed to meet a person’s energy needs and does not include requirements for protein, vitamins, and minerals.

Blood sugar levels are maintained from liver glycogen (carbohydrate) stores between meals and during fasting. The liver’s glycogen stores come from the carbohydrates (starches and sugars) that are eaten in the diet and converted to glucose and stored as glycogen. However, liver glycogen will be depleted within 12 to 16 hours unless sufficient carbohydrate is provided again. When the liver glycogen is depleted, the body obtains sugar by converting protein (amino acids) to sugar. This process is called gluconeogenesis (gluco, meaning “glucose sugar”; neo, meaning “new”; and genesis, meaning “to create”). The protein used for gluconeogenesis is obtained from functional proteins (muscles and enzyme systems) because protein is never stored like fat in the body. Protein in the body is always a part of structural or functional tissue, organ, enzyme, or other biochemical action molecule, or is in an “amino acid pool” in circulation while waiting to be incorporated into body systems. Therefore, in patients who have a consistently inadequate nutritional intake, protein, instead of serving a functional role, must be used for more and more of the body’s energy needs. This leads to a loss of functional tissue. Skeletal muscle tissues, including the diaphragm and other respiratory muscles, lose muscle mass, with a resultant decrease in endurance and strength. The depletion of protein from the body is also reflected in lowered blood albumin levels; however, low albumin levels may be a result of other metabolic conditions, such as stress and inflammation. In starvation or semistarvation states, respiratory muscle strength can diminish, producing a decrease in forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV₁) because the muscles of respiration, as well as other skeletal muscles, are being catabolized for energy. In starvation, a decrease in carbon monoxide diffusing capacity (Dlco) also occurs, which reflects a diminished gas exchange capacity of the lungs. The decline in FEV₁ also correlates with a decreased creatinine-height index (CHI), indicative of loss of muscle mass. Because immune antibodies are composed of proteins, persistent inadequate calorie and protein intake will also compromise the immune system, thereby limiting the body’s ability to fight pneumonia or other infections.

If the calorie intake is less than needed, there will be a decrease in weight, as is commonly seen in patients with COPD. Patients with emphysema are more commonly underweight, appearing thin and often cachectic (nutritionally depleted) compared with those with chronic bronchitis, who may be of normal weight and often are overweight. Emphysema produces a catabolic state that usually results in weight loss and mild hypoxemia. Nutritional depletion is evidenced by low body weight or body mass index (BMI) and a reduced triceps skinfold thickness measurement. Lean body mass may be decreased, although weight may be stable. BMI alone may not be indicative of a patient’s nutritional status, and body composition measurement is preferred in this population to detect alterations in body compartments. Body composition can help differentiate lean body mass from adipose tissue and overhydration from dehydration because changes in hydration status can hide actual body wasting. In patients who retain fluids, it is important to carefully assess anthropometric measurements and biochemical measurements in light of fluid status.

Measures of REE are consistently higher in malnourished emphysematous patients.²⁰ This increased REE leads to nutritional depletion and eventually malnutrition. Malnutrition can exacerbate symptoms of COPD by decreasing respiratory muscle strength and exercise tolerance and can compromise immune function, leading to increased respiratory infections. Energy expenditure is usually elevated related to pulmonary complications, including the degree of airway obstruction and resultant increased work of breathing.²¹ Respiratory inflammation, carbon dioxide retention, gas diffusing capacity, and other mediators, including hormones and cytokines, affect energy expenditure. In addition, insufficient absorption of some nutrients may lead to muscle wasting and malnutrition. Adequate protein intake is needed to maintain or restore lung and muscle strength in these patients.²¹ COPD presenting with chronic hypoxia and oxidative stress could be responsible for the catabolic state seen in these patients. Systemic inflammation, anorexia, and muscle dysfunction may all relate to the hypoxia. Correction of the hypoxia by oxygen supplementation seems to allow weight gain and in the short term improve exercise tolerance.^22,23 This improvement is usually not sustained because the underlying metabolic increase is not reversed, and the patient’s appetite is not improved.

SIMPLY STATED

Chronic nutritional depletion eventually weakens the muscles of breathing and can contribute to the onset of respiratory failure, especially in patients with chronic lung disease.

If an increased amount of food is consumed, weight can begin to normalize, but emphysematous patients are not comfortable eating larger quantities of foods. In one study, it was necessary to increase intake above 140% of the BMR before improvement of the nutritional status of COPD patients was achieved.²⁴ If not continuously encouraged to do so, patients typically return to eating their normal amount, which is insufficient to maintain a normal weight. In addition, patients with chronic protein energy malnutrition (PEM), also known as protein-calorie malnutrition (PCM), experience higher morbidity and mortality rates. With loss of body protein, there is a subsequent loss not only of muscle and various enzyme systems but also of immunoglobulins (IgA, IgG, and IgM). Thus, susceptibility to respiratory infections is increased because of decreased immunocompetence.