Ali Mchaourab

Lack of Degradation of Sevoflurane by a New Carbon Dioxide Absorbent in Humans

Background Potent inhaled anesthetics degrade in the presence of the strong bases (sodium hydroxide or potassium hydroxide) in carbon dioxide (CO2) absorbents. A new absorbent, Amsorb (Armstrong Medical Ltd., Coleraine, Northern Ireland), does not employ these strong bases. This study compared the scavenging efficacy and compound A production of two commercially available absorbents (soda lime and barium hydroxide lime) with Amsorb in humans undergoing general anesthesia. Methods Four healthy volunteers were anesthetized on different days with desflurane, sevoflurane, enflurane, and isoflurane. End-tidal carbon dioxide (ETco2) and anesthetic concentrations were measured with infrared spectroscopy; blood pressure and arterial blood gases were obtained from a radial artery catheter. Each anesthetic exposure lasted 3 h, during which the three fresh (normally hydrated) CO2 absorbents were used for a period of 1 h each. Anesthesia was administered with a fresh gas flow rate of 2 l/min of air:oxygen (50:50). Tidal volume was 10 ml/kg; respiratory rate was 8 breaths/min. Arterial blood gases were obtained at baseline and after each hour. Inspired concentrations of compound A were measured after 15, 30, and 60 min of anesthetic administration for each CO2 absorbent. Results Arterial blood gases and ETco2 were not different among three CO2 absorbents. During sevoflurane, compound A formed with barium hydroxide lime and soda lime, but not with Amsorb. Conclusions This new CO2 absorbent effectively scavenged CO2 and was not associated with compound A production.

Perioperative considerations in a patient with orthostatic intolerance syndrome

ORTHOSTATIC intolerance syndrome is an unusual autonomic nervous system disorder characterized by episodic or postural tachycardia that occurs independent of alterations in arterial blood pressure and is associated with symptoms that include palpitations, tremulousness, light-headedness, fatigue, and syncope. Orthostatic intolerance syndrome is most often observed in young women and has also been described as postural orthostatic tachycardia syndrome, chronic orthostatic intolerance, or hyperadrenergic orthostatic tachycardia. This diverse terminology emphasizes the often confusing nature of this idiopathic disorder of primary autonomic failure. The medical treatment of orthostatic intolerance is controversial because the pathophysiology of the disease is complex. We describe the perioperative treatment of a patient with severe orthostatic intolerance syndrome who was scheduled for bilateral mastectomy.

Large neutral amino acids levels in primate cerebrospinal fluid do not confirm competitive transport under baseline conditions

In rodents, transport of large neutral amino acids (LNAAs) across the blood brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier is mediated by high affinity carriers. Net brain LNAA levels are thought to be determined mainly by this competitive transport from plasma. Since the affinity for LNAA transport at the BBB in primates is considerably higher than in rodents, brain influx and by extension LNAA brain levels, should be even more dependent on competitive transport. Given that LNAA levels in CSF and brain interstitial fluid are usually similar, we analyzed serum and CSF of fasted subjects (n=24) undergoing spinal anesthesia and calculated brain influx and transporter occupancy using a conventional model of transport. Despite predicted near-full transporter saturation (99.7%), correlations between CSF levels and brain influx were modest, limited to tyrosine (r=0.60, p<0.002) and tryptophan (r=0.50, p<0.01) and comparable to correlations between CSF and serum levels. We also analyzed serum and CSF in (n=5) fasted vervet monkeys. Tyrosine and phenylalanine levels in CSF were positively correlated with those in serum, but correlations with calculated brain influx, which takes competition into account, were weaker or absent. We conclude that in primates i) baseline CSF LNAA levels do not confirm competitive transport, ii) brain LNAA levels should not be estimated on the basis of serum indices alone. This has implications for amino acid challenge studies and for neuropsychiatric disorders associated with dysregulated LNAA transport in which quantitative information about brain LNAA levels is needed.