Mechanisms and implications in gene polymorphism mediated diverse reponses to sedatives, analgesics and muscle relaxants / 대한마취과학회지

Responses to sedatives, analgesics and muscle relaxants vary among patients under general anesthesia, which could be ascribed to the disparities of clinical characteristics and genetic factors of individuals. Accumulating researches have indicated that gene polymorphisms of the receptors, transporters and metabolizing enzymes associated with anesthetics play a considerable role in their efficacy. However, a systematically summarized study on the mechanisms of gene polymorphisms on pharmacodynamics and pharmacokinetics of anesthetics is still lacking. In this paper, the recent researches on pharmacogenomics of sedatives, analgesics and muscle relaxants are comprehensively reviewed, and the contributions and mechanisms of polymorphisms to the differences of individual efficacy of these drugs are discussed, so as to provide guidance for the formulation of a rational anesthesia regimen for patients with various genotypes.

[Comparison of pulseoximetry oxygen saturation and arterial oxygen saturation in open heart intensive care unit]

Pulseoximetry is widely used in the critical care setting, currently used to guide therapeutic interventions. Few studies have evaluated the accuracy of SPO[2] [pulseoximetry oxygen saturation] in intensive care unit after cardiac surgery. Our objective was to compare pulseoximetry with arterial oxygen saturation [SaO[2]] during clinical routine in such patients, and to examine the effect of mild acidosis on this relationship. In an observational prospective study 80 patients were evaluated in intensive care unit after cardiac surgery. SPO[2] was recorded and compared with SaO[2] obtained by blood gas analysis. One or serial arterial blood gas analyses [ABGs] were performed via a radial artery line while a reliable pulseoximeter signal was present. One hundred thirty seven samples were collected and for each blood gas analyses, SaO[2] and SPO[2] we recorded. O[2] saturation as a marker of peripheral perfusion was measured by Pulseoximetry [SPO[2]]. The mean difference between arterial oxygen saturation and pulseoximetry oxygen saturation was 0.12% +/- 1.6%. A total of 137 paired readings demonstrated good correlation [r=0.754; P<0.0001] between changes in SPO[2] and those in SaO[2] in samples with normal hemoglobin. Also in forty seven samples with mild acidosis, paired readings demonstrated good correlation [r=0.799; P<0.0001] and the mean difference between SaO[2] and SPO[2] was 0.05% +/- 1.5%.Data showed that in patients with stable hemodynamic and good signal quality, changes in pulseoximetry oxygen saturation reliably predict equivalent changes in arterial oxygen saturation. Mild acidosis doesn't alter the relation between SPO[2] and SaO[2] to any clinically important extent. In conclusion, the pulse oximeter is useful to monitor oxygen saturation in patients with stable hemodynamic.