Quick Review: The Metabolic Cart
T Fujii, B Phillips
Citation
T Fujii, B Phillips. Quick Review: The Metabolic Cart. The Internet Journal of Internal Medicine. 2002 Volume 3 Number 2.
Abstract
This article gives a brief review of the metabolic cart.
Terms & Definitions
Calorimetry
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The metabolic cart essentially measures the oxygen consumed and the carbon dioxide produced by the patient and then calculates (using the modified Weir equation) the energy expenditure for the patient
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Weir equation: EE = (3.94 x VO2) + (1.1 x (VCO2)
Indirect calorimetry provides two pieces of information:
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A measure of energy expenditure as reflected by the resting energy expenditure (REE)
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A measure of substrate utilization as reflected in the respiratory quotient (RQ)
Resting Energy Expenditure (REE)
REE = 75 % - 95 % of total energy expenditure
(diet-induced, environmental, activity)
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Metabolism in brain, liver, heart and kidney is relatively constant (60 - 70 % REE)
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Variability in REE:
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between people
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during the day 12 %
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increases with critical illness
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day to day - 23 %
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Variability in REE can be due to:
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Size
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Gender
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Age
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Work of breathing (2 - 3 %)
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Diet-induced thermogenesis
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Sleep
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Illness
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Starvation
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Fever (13 % per degree C)
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Cold
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Activity
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Drugs
Points:
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REE correlates closely with fat free lean body mass.
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Work of breathing normally (2 - 3 %) can be as high as 25% of REE with impending respiratory failure
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Diet-induced thermogenesis normally 8-10% drops to 4-8% with continues enteral feeds
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REE drops with sleep
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Most disease states increase REE
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20-50% increase seen with elective surgery and trauma, 100% increase in REE seen with severe burns
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Increases in REE are seen in the flow phase of injury and can be effected by therapy
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Increases in REE can be expected to reflex severity of illness but the response plateaus at
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2x the REE
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Increases in REE due to acute illness usually return to base line at 7 to 10 days
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Not all critically ill patients become hypermetabolic (35-60%)
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15-20 % of ICU-patients are found to be normometabolic.
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10 -20% of ICU-patients are found to be hypometabolic.
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Hypometabolic state may be do to the disease process: specific cancers ,cachexia ,spinal cord injuries paraplegics decreased REE by 10% quadriplegics by 30%
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Long-term starvation reduces EE by 30-40%
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Fever increases REE (13 % per degree C)
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Exposure to Cold /hypothermia increases REE by shivering and nonshivering thermogenesis
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General Activity is responsible for most of the variability in REE.
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Being awake and alert increase EE by 10%.
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Routine nursing care increases EE by 20 -30%.
Medications that affect REE:
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caffeine, aspirin increase EE
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catecholamines and pressor increase EE
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sedatives,analgesics, beta blockers
* general anesthesia decreases EE
** Acute hyperventilation increases EE, while Hypoventilation decreases EE
Predicting REE
Harris-Benedict is correct 80-90% of the time in healthy, normal volunteers. In 10-14% it over-estimates EE. In obese volunteers, the equation predicts EE correctly only 40-64% of the time. In critically-ill patients the Harris-Benedict equation is correct only 50% of the time. For most disease processes Harris -Benedict underestimates EE. Multipliers for various disease states attempt to improve the accuracy of the Harris-Benedict equation (though these multipliers tend to overestimate EE when compared to indirect calorimetry).
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RQ: Derived from actual measurements of VCO2 and VO2
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RQ is the ratio of carbon dioxide produced to oxygen consumed (VCO2 / VO2)
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Reflection of which fuels are being oxidized
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“Non-protein” RQ (npRQ) excludes protein metabolism
Respiratory Quotient
Ratio of CO2 produced to O2 consumed.
(VCO2 / VO2) = RQ
Carbohydrate: 1gm C + 0.83 L 02 0.83 L CO2 + 0.56g H2O + 4.17 Kcal
RQ =1
Fat: 1gm F + 2.02 L O2 1.43 L CO2 + 1.07 g H2O + 9.3 Kcal
RQ = 0.70
Protein: 1gm P + 0.96 L O2 0.78 L CO2 + 0.41 H2O + 0.16g Nu + 4.3 Kcal RQ = 0.81
Glucose oxidation RQ = 1.0
Fat oxidation RQ = 0.7
Protein oxidation RQ 0.8
Lipogenesis RQ 1.3
(npRQ of 0.85 - 50 % fat and 50 % carbohydrate oxidation)
“Optimal RQ”
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Nutrition support should probably provide a balance between carbohydrate and lipid with an RQ in the 0.8 to 0.9 range
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Avoidance of RQ's > 1.0 which represents “overfeeding” and potential lipogenesis is a reasonable goal
Factors that affect RQ:
Those that increase RQ
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Hyperventilation
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metabolic acidosis leading to increases in carbon dioxide,
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overfeeding leading to lipogenesis
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exercise
Those that decrease RQ
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Hypoventilation
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Mild starvation with ketosis
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Diabetes with ketoacidosis or high rates of urinary glucose lose
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Gluconeogenesis
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ETOH metabolism
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Hypothermia via continued gluconeogenesis
Resting energy expenditure of critically ill patients varies widely over the course of the day and over the course of an illness. Measurements from 10 - 23% of an “average” REE can be seen within a 24 hour period. Test patient at rest in quiet, controlled environment. “Steady state” implies a 5 minute interval where the average V02 and the VC02 changes by less then 10% and the average RQ changes by less than 5%.
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Question validity of the test
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Steady state is not achieved
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RQ falls outside of the physiologic range of 0.67-1.3
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Measurements should fall with in the range of V02 (1.7 to 3.4 mL/min/kg) and VC02 (1.4 to 3.1 mL/min/kg)
Metabolic Cart Sources of error:
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FiO2 >60%
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Air leaks (chest tubes etc).
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Hemodialysis (Co2 loss via the dialysis coil )
Use of the metabolic cart can prevent over-feeding, and under-feeding by accurately measuring energy requirements. Overfeeding critically ill patients results in hyperglycemia, hepatic steatosis, R.E.S. dysfunction and increased septic complications. Under-feeding patients can lead to the complications of malnutrition. The use of a metabolic cart can reduce the amount of “unnecessary” TPN which is administered (use of a metabolic cart reduced TPN use from 33,000 liters to 26,000 liters in one study - Mullen et al., Proc Nutr Sos 1991. 50:239-44).