The aim of this study is to compare the effect of dexmedetomidine on resting energy expenditure in relation to the midazolam in critically ill patients using indirect calorimetry
Caloric needs in critically-ill patients fluctuate significantly over the course of the disease which might expose patients to either malnutrition or overfeeding. Malnutrition is associated with deterioration of lean body mass, poor wound healing, increased risk of nosocomial infection, and weakened respiratory muscles. On the other hand overfeeding in medically compromised patients can promote lipogenesis, hyperglycemia, and exacerbation of respiratory failure. Many factors may affect the resting energy expenditure (REE) through manipulation of oxygen consumption (VO2). Sedatives are important contributors to reduction of REE. The postulated mechanism of sedative-induced reduction of VO2 is inhibition of circulating catecholamine and pro-inflammatory cytokines. Dexmedetomidine is a highly selective α2-adrenoceptor agonist. Stimulation of the α2-adrenoceptor in the central nervous system causes a 60-80% reduction in sympathetic outflow and endogenous catecholamine levels. It was found that perioperative use of α2 agonists decreased sympathetic activity with subsequent reduction of VO2 and REE. Moreover, dexmedetomidine, has some anti-inflammatory effect by inhibiting the pro-inflammatory cytokines which may cause additional reduction of REE in critically ill patient. Midazolam is another important sedative that is frequently used in critically-ill patient. Terao et al. found that increasing the depth of sedation using midazolam, decreased oxygen consumption and REE. However, it remains unclear whether the effect of midazolam on REE is related to the drug itself or to the depth of sedation. There is no direct comparison in the literature between dexmedetomidine and midazolam on REE.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
TRIPLE
Enrollment
30
The drug will be administered for sedation and its effect on basal metabolic rate will be investigated
The drug will be administered for sedation and its effect on basal metabolic rate will be investigated
The drug will be administered in both groups
Cairo University
Cairo, Egypt
Change in Resting energy expenditure after drug administration
Resting energy expenditure will be measured using indirect calorimetry via metabolic module on General Electric ventilator
Time frame: The first baseline measurement will be taken before drug administration. The second measurement will be taken 24 hours after drug infusion.
Heart rate
number of heart beats per minute
Time frame: 24 hours
arterial blood pressure
arterial blood pressure measured in mmHg
Time frame: 24 hours
Richmond agitation and sedation scale
range from -5 (unarousable) to +4 (combative)
Time frame: 24 hours
Plasma interleukin-1β level
determined by ELISA using a quantitative sandwich enzyme immunoassay technique
Time frame: 24 hours
Tumor necrosis factor-α plasma concentration
Enzyme immunoassay
Time frame: 24 hours
partial pressure of oxygen in arterial blood
the partial pressure of oxygen in arterial blood measured in mmHg
Time frame: 24 hours
VO2
the oxygen consumption measured in mL/Kg/min
Time frame: 24 hours
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.
The device will be used for measurement of basal metabolic rate
VCO2
carbon dioxide production measured in mL/Kg/min
Time frame: 24 hours
end-tidal co2
the pressure of carbon dioxide in expired air measured in mmHg
Time frame: 24 hours
cardiac output
the amount of blood pumped by the heart during one minute
Time frame: 24 hours