Critically ill patients often have multisystem organ failure, commonly including the respiratory system. Respiratory dysfunction is often the result of acute respiratory distress syndrome (ARDS), a syndrome characterized by hypoxemic respiratory failure in the setting of a severe systemic critical illness or isolated pulmonary disease. This section reviews nutritional supplementation in the critically ill patient, with specific attention to ARDS.
Nutrition in Critical Illness: Metabolic Requirements
The nutritional milieu of critical illness is characterized by hypermetabolism, protein catabolism, and insulin resistance leading to impaired glucose use and hyperglycemia.
Because of the inherent complications of both underfeeding and overfeeding, proper estimation of caloric requirements is an essential but challenging task. Energy requirements can be estimated using standard populationbased regression formulas, such as the Harris-Benedict equation (21
). However, predictive formulas were derived from physiologically normal subjects at rest and do not address the stress and hypercatabolism of critical illness. “Correction stress factors,” ranging from 1.2 to 1.5 times the calculated resting energy expenditure (REE) are suggested, but their correlation with indirect calorimetry measurements is often suboptimal (22
O2 consumption ([V with dot above]O2), which can be used as an estimate of caloric needs, can be calculated by the Fick equation
[V with dot above]O2 = CO ÷ (Cao2 − Cvo2)
where CO is the cardiac output and Cao2 and Cvo2 are the O2 content of arterial and mixed venous blood, respectively. This approach requires invasive monitoring with a pulmonary artery catheter, and a relatively stable patient.
Alternatively, [V with dot above]O2 can be assessed with a metabolic cart that measures exhaled gases directly. This technique is not universally available, and it requires expensive equipment, technical expertise, and a stable fraction of inspired O2. Despite these limitations, this technique offers the advantage of continuous measurements rather than intermittent snapshots of one’s caloric needs.
The [V with dot above]O2
(mL/minute) obtained by either the Fick equation or by the gas exchange method is converted to kilocalories/day by using the caloric value of O2
(4.69 to 5.05 kcal/L of O2
consumed) or the modified Weir equation if VCO2
production) is also known (24
Substrate Supplementation: Implications for Ventilatory Requirements
Patients with acute respiratory failure typically are in a hypercatabolic state and rely in part on proteolysis of protein
stores to meet their immediate metabolic needs. Nutritional supplementation may spare consumption of endogenous protein, although the amount of glucose required differs from that needed in normal fasting adults (25
). Intravenous fat emulsions, if administered with a minimum of 500 kcal/day of carbohydrate (26
), and exogenous protein supplementation also can limit proteolysis (26
The appropriate mix of carbohydrate, fat, and protein calories must be individualized. Carbohydrates produce more CO2
during oxidation than fat or protein. For every molecule of glucose completely oxidized, six molecules of CO2
are produced, giving a respiratory quotient of 1 (Table 99.1
), whereas the oxidation of fat and protein produces less CO2
, with a respiratory quotient of 0.7 and 0.8, respectively. VA
must be increased when CO2
production increases to maintain a normal partial pressure of arterial PaCO2
. In the presence of underlying lung disease, the ability to increase VA
may be limited.
TABLE 99.1 DEFINITION OF RESPIRATORY PHYSIOLOGY TERMS AND ABBREVIATIONS
Tidal volume (VT)
Volume of gas moved during a single respiration
Minute ventilation (VE)
Amount of air moved in and out of the lungs in 1 minute; VE = VT × respiratory rate (RR) per minute
Dead-space ventilation (VD)
Amount of inspired gas that does not participate in gas exchange; ventilation of nonperfused alveoli
Fraction of each tidal volume that is dead space
Alveolar minute ventilation (VA)
Amount of inspired air able to participate in gas exchange; alveolar ventilation is the difference between total minute ventilation and dead-space ventilation
Forced vital capacity (FVC) Volume of gas that can be forcibly exhaled after a maximal inhalation Forced expiratory volume in 1 second (FEV1)
Volume of gas expired in the first second of a forced expiration
Stroke volume (SV)
Amount of blood pumped by the heart in a single beat
Cardiac output (CO)
Volume of blood pumped by the heart in 1 minute (heart rate [HR] × SV)
Partial pressure of oxygen in the arterial blood
Partial pressure of carbon dioxide in the arterial blood
[V with dot above]O2
Oxygen consumption (mL/min)
[V with dot above]CO2
Carbon dioxide production (mL/min)
Change in volume per unit change of pressure
Respiratory quotient (RQ)
Molecules of oxygen used/molecule of carbon dioxide produced
Mixed venous blood
Deoxygenated blood returned to the heart; samples for measurements are obtained from a catheter in the pulmonary artery
Timing and Route of Nutritional Support
Malnutrition at the onset of critical illness is associated with poor outcomes, and improved clinical outcomes are associated with nutritional support (27
). However, the optimal composition and timing of the initiation of feedings remains uncertain (28
Enteral Feeding and Pulmonary Issues.
Enteral feeding is most commonly accomplished through a nasogastric tube or nasoduodenal tube. Potential mechanical risks are associated with enteric feeding tubes, including misplacement in the tracheobronchial tree or pleural space; thus, radiographic confirmation of proper placement is mandatory before initiation of feeding. It is uncertain if the risk of aspiration differs between gastric and duodenal feedings (29
). Postpyloric feedings should be considered in those with significant gastroesophageal reflux disease, high risk for aspiration, on high doses of sedatives/paralytics, or intolerance to gastric feeding. Maintaining patients in a semirecumbent position, rather than supine, decreases the risk of aspiration (31
Parenteral Nutrition and Pulmonary Issues.
Parenteral nutrition is delivered through a central or peripheral vein. Central vein infusions allow for the delivery of more concentrated solutions; thus, it minimizes obligate fluid requirements. In patients with ARDS, limited fluid intake shortens the duration of mechanical ventilation (32
). The addition of heparin (33
), sterile line placement, and restriction of catheter use exclusively to alimentation (34
) may limit catheter-associated complications such as thrombosis and infection. Infusion of lipid emulsions decrease diffusing capacity and oxygen saturation by causing ventilation and perfusion mismatch; thus, its use is typically avoided if possible.
Acute Respiratory Distress Syndrome and Acute Lung Injury
Optimal nutritional support in ARDS has been investigated. Patients with ARDS have lower levels of dietary antioxidants, including vitamin E, vitamin C, retinol, and β-carotene, than healthy controls (35
). Decreased plasma concentrations of tocopherol and vitamin E and elevated lipoperoxides indicative of oxidative damage commonly are seen in patients with ARDS (36
); findings prompting speculation that antioxidant supplementation may be beneficial. Although a prospective randomized trial examining the efficacy of supplementation with α-tocopherol and vitamin C did not decrease pulmonary mortality or the development of ARDS, the intervention group did have a significantly lower incidence of multisystem organ failure, shorter duration of intensive care unit (ICU) stay, and mechanical ventilation (37
The specific dietary lipid alters the profile of eicosanoids produced by inflammatory cells, which may have clinical relevance. Linoleic acid, an n-6 fatty acid, is converted to arachidonic acid, which is the precursor of many proinflammatory prostaglandins and leukotrienes (38
). Alternatively, linolenic acid, an n-3 fatty acid, is converted
to eicosapentaenoic acid, which produces eicosanoids with much less inflammatory potential (38
Gadek et al prospectively assessed the effects of enteral feedings enriched with eicosapentaenoic acid (and fish oil), γ-linolenic acid, and antioxidants in 98 patients with ARDS. Compared with controls, the treatment group had more ventilator-free and ICU-free days, earlier improvements in oxygenation, less new organ failure development, and a nonsignificant trend toward decreased mortality (16% versus 25%; p
= .31) (39
Currently, the ARDS network is performing a prospective, randomized trial of initial trophic enteral feeding followed by advancement to full-calorie enteral feeding versus early advancement to full-calorie enteral feeding. This trial will be conducted simultaneously with a one comparing omega-3 fatty acid, γ-linolenic acid, and antioxidant supplementation with a comparator.
Chronic Lung Diseases
Chronic lung disease generally is classified as obstructive or restrictive, based on the primary physiologic abnormality, as discussed. Obstructive lung diseases include asthma, chronic bronchitis, emphysema, cystic fibrosis (CF), and bronchiectasis. Emphysema and chronic bronchitis are most commonly the result of tobacco abuse and are collectively labeled chronic obstructive pulmonary disease (COPD).
Restrictive diseases include infiltrative or fibrotic diseases of the lung parenchyma as well as extrapulmonary processes such as muscular weakness, thoracic cage abnormalities, and neurologic diseases that result in similar physiologic impairments. Investigations of the interrelationships between nutrition and chronic pulmonary disease have focused on COPD, asthma, and CF.