• Journal of Chest Surgery
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• v.13 no.2
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• pp.85-91
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• 1980

Extracorporeal circulation by hemodilution technique has been currently used with its clinical safety and good peripheral tissue perfusion in open heart surgery. There is no doubt that $O_{2}$ carrying capacity of the blood is disturbed by decreased hemoglobin level resulting from hemodilution of the circulating blood. From the view point of the blood gas exchange, these experimental studies were undertaken to determined the sate limit of hemodilution in the condition of cardiopulmonary bypass with a constant perfusion flow rate. Twelve adult mongrel dogs weighing 10 to 13 Kg. were anesthetized with pentobarbital and then respiration was controlled with Harvard volume respirator using room air. The cardiopulmonary by pass was performed by use of Sarns heart lung machine (console 5000, 5 head and 2 roller pumps) and Travenol pediatric bubble oxygenator. The perfusion rate during bypass was maintained at a constant rate of 80 ml/min/Kg of body weight. The ratio of oxygen gas flow to blood flow was kept in 3 to 1 constantly. International hemodilution was attained by serial blood withdrawals and immediate infusion of equal volumes of diluants composed of Ringer's lactate, 5% dextrose in water and 25% mannitol solution, proportionally 60%, 30%, and 10%. Arterial and venous blood samples were obtained between 15 and 20 minutes following each hemodilution. Hematocrits and hemoglobin values, $PO_{2}$, $PCO_{2}$ and pH were measured. Oxygen and carbon dioxide contents oxygen consumption and carbon dioxide elimination were calculated groups according to different hematocrit values and the correlations were evaluated. Result were as follows. 1. the arterial $O_{2}$ tension and $O_{2}$ saturation were maintained at the physiological level irrespective of the hematocrit value. 2. The venous $O_{2}$ tension and $O_{2}$ saturation showed a tendency to decline with the decrease in hematocrit value and positive correlation between them (r = +0.49, r = +0.76), The mean values of venous $O_{2}$ tension and $O_{2}$ saturation, however, were not decreased when the hematocrit levels were lower than 20%. 3. The arterial $O_{2}$ content declined lineally in proportion to the fall of hematocrit level with a positive correlation between them (r = +0.95). 4. The venous $O_{2}$ contents were decreased gradually as the hematocrit value decreased with positive correlation between them ( r =+0.89). The trend of diminution of venous $O_{2}$ content, however, was became low according to progressive decrease of hematocrit level. 5. Systemic oxygen consumption was in higher range than $O_{2}$ requirement of basal metabolism when the hematocrit value was above 20%, but abruptly decreased when the hematocrit value became to below 20%. 6. The arterial $CO_{2}$ tension and $CO_{2}$ content showed trend of increasing with progressive decrease of hematocrit value but exhibited a rather broad range and there was no relationship between those value and the hematocrit value. 7. The venous $CO_{2}$ tension and $CO_{2}$ content have also no correlation with change of Ht. value but related directly to those value of arterial blood with positive correlation between them (r = +0.78, r = +0.95_. 8. A-V difference of $CO_{2}$ content and $CO_{2}$ elimination wasnot significantly influenced by Ht. value. From the results, we obtained that feasible limit in inteneional hemodilution is above the hematocrit value of 20% under the given experimental condition.

• Journal of Korean Biological Nursing Science
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• v.14 no.4
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• pp.275-281
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• 2012

Purpose: This study was performed to evaluate the effect of low-dose lidocaine on fentanyl-induced cough and hemodynamic changes under general anesthesia. This research was a randomized trial design and performed using a double-blind method. Methods: Data collection was performed from October 22, 2008, to May 4, 2009. One hundred and thirty two patients were randomly assigned to control group (Con G) and experimental group (Exp G) using a table of random numbers. Exp G (n=66) were administered 0.5 mg/kg lidocaine and Con G (n=66)) were administered saline. The occurrence of cough and vital sign were recorded within one minute after fentanyl bolus by an anesthesiologist. Collected data were analyzed using Repeated measures ANOVA using SPSS for Windows (Version 17.0). Results: The incidence of cough in Exp G was 13.6%, while Con G was 53%. The incidence cough in Exp G was significantly lower compared to Con G (p<.001). Lidocaine seemed not to suppress mean arterial pressure (p=.145), heart rate (p=.508), and oxygen saturation (p=.161). Conclusion: Intravenous administration of 0.5 mg/kg lidocaine seems to suppress fentanyl-induced cough without affecting mean blood pressure, heart rate and oxygen saturation. Therefore, we recommend intravenous 0.5 mg/kg lidocaine administration to suppress fentanyl-induced cough under general anesthesia.

• Journal of Yeungnam Medical Science
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• v.15 no.1
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• pp.97-113
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• 1998

The sympathoadrenal system plays an important role in homeostasis in widely varing external environments. Conflicting findings, however, have been reported on its response to hypoxia. We investigated the effect of hypoxia on the sympathoadrenal system in dogs under halothane anesthesia by measuring levels of circulating catecholamines in response to graded hypoxia. Ten healthy mongreal dogs were mechanically ventilated with different hypoxic gas mixtures. Graded hypoxia and reoxygenation were induced by progressively decreasing the oxygen fraction in the inhalation gas mixture from 21%(control) to 15%, 10% and 5% at every 5 minutes, and then reoxygenated with 60% oxygen. Mean arterial pressure, central venous pressure and mean pulmonary arterial pressure were measured directly using pressure transducers. Cardiac output was measured by the thermodilutional method. For analysis of blood gas, saturation and content, arterial and mixed venous blood were sampled via the femoral and pulmonary artery at the end of each hypoxic condition. The concentration of plasma catecholamines was determined by radioenzymatic assay. According to the exposure of graded hypoxia, not only did arterial and mixed venous oxygen tension decreased markedly at 10% and 5% oxygen, but also arterial and mixed venous oxygen saturation decreased significantly. An increased trend of the oxygen extraction ratio was seen during graded hypoxia. Cardiac output, mean arterial pressure and systemic vascular resistance were unchanged or increased slightly. Pulmonary arterial pressure(PAP) and pulmonary vascular resistance(PVR) were increased by 55%, 76% in 10% oxygen and by 82%, 95% in 5% oxygen, respectively(p<0.01). The concentrations of plasma norepinephrine, epinephrine and dopamine increased by 75%, 29%, 24% in 15% oxygen and by 382%, 350%, 49% in 5% oxygen. These data suggest that the sympathetic nervous system was activated to maintain homeostasis by modifying blood flow distribution to improve oxygen delivery to tissues by hypoxia, but hemodynamic changes might be blunted by high concentration of nitrous oxide except PAP and PVR. It would be suggested that hemodynamic changes might not be sensitive index during hypoxia induced by high concentration of nitrous oxide exposure.

• Proceedings of the IEEK Conference
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• 2000.06e
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• pp.117-120
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• 2000

Pulse oximetry is a well established non-invasive optical technique for monitoring the SpO$_2$ during anaesthesia, recovery and intensive care. Pulse oximeters determine the oxygen saturation level of blood by measuring the light absorption of arterial blood. The sensors consists of red and infrared light sources and photodetectors. In the measurement of the hemoglobin oxygen saturation, conventional method has required the technique of filtering of remove the noise, and of complex signal processing algorithm. So much time have required to signal processing. In this research, we separate AC signal and DC signal in the stage of signal detection. We filter the noise from each signal and convert A/D. We obtain the SpO$_2$ using the DSP algorithm.

• Korean Journal of Optics and Photonics
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• v.11 no.6
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• pp.452-456
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• 2000

A measurement unit and signal processing algorithm have been developed for predicting arterial oxygen saturation noninvasively. The measurement set-up was composed of a probe including light source and photodetector, optical signal processing section, LED driving circuit, PC interface software for data acquisition and data processing software. Light from the LED's was irradiated onto the finger nail bed and transmitted light was measured at different wavelengths. An effective baseline correction method was developed and measured data were analyzed by using various data processing methods and prediction algOlithms. For performance evaluation, a pulse oximeter simulator (Bio- Tek Instrument Inc.) was used as reference. The best performance in terms of the correlation coefficient and the standard deviation was obtained under the following conditions; when the arterial signals were computed in terms of area rather than peak-valley difference, and when the algorithm calculating by $In(I_p/I_v)/I_{avr}$ value for pulsation waveform was used. In in vivo test, prediction was improved when the developed baseline correction method was used. In addition, wavelengths of 660 nm and 940 nm provided better linearity and precision than wavelengths of 660 nm and 805 nm. 05 nm.

• Journal of Dental Anesthesia and Pain Medicine
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• v.20 no.2
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• pp.73-81
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• 2020

Background: The international organization for standardization (ISO) 80601-2-61 dictates that the accuracy of a pulse oximeter should be assessed by a controlled desaturation study. We aimed to characterize the relationship between the fraction of inspired oxygen (FiO₂) and peripheral oxygen saturation (SpO₂) using a turnover model by retrospectively analyzing the data obtained from previous controlled desaturation studies. Materials and Methods: Each volunteer was placed in a semi-Fowler's position and connected to a breathing circuit to administer the hypoxic gas mixture containing medical air, oxygen, nitrogen, and carbon dioxide. Volunteers were exposed to various levels of induced hypoxia over 70-100% arterial oxygen saturation (SaO₂). The study period consisted of two rounds of hypoxia and the volunteers were maintained in room air between each round. FiO₂ and SpO₂ were recorded continuously during the study period. A population pharmacodynamic analysis was performed with the NONMEM VII level 4 (ICON Development Solutions, Ellicott City, MD, USA). Results: In total, 2899 SpO₂ data points obtained from 20 volunteers were used to determine the pharmacodynamic characteristics. The pharmacodynamic parameters were as follows: k_out = 0.942 1/min, Imax = 0.802, IC₅₀ = 85.3%, γ = 27.3. Conclusion: The changes in SpO₂ due to decreases in FiO₂ well explained by the turnover model with inhibitory function as a sigmoidal model.

• Journal of Dental Anesthesia and Pain Medicine
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• v.21 no.4
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• pp.357-361
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• 2021

Methemoglobinemia is a blood disorder in which an abnormal amount of methemoglobin is produced, and prilocaine is one of the drugs that can cause this disorder. The maximum recommended dose of prilocaine is 8 mg/kg. We report a case of methemoglobinemia caused by the administration of 4.2 mg/kg of prilocaine without other methemoglobinemia-inducing drugs during general anesthesia. A 17-year-old girl with hyperthyroidism and anemia was scheduled to undergo maxillary sinus floor elevation and tooth extraction. The patient's peripheral oxygen saturation (SpO₂) decreased from 100% at arrival to 95% after receiving prilocaine with felypressin following induction of general anesthesia. However, the fraction of inspired oxygen was 0.6. Blood gas analysis showed that the methemoglobin level was 3.8% (normal level, 1%-2%), fractional oxygen saturation was 93.9%, partial pressure of oxygen was 327 mmHg, and arterial oxygen saturation was 97.6%. After administration of 1 mg/kg of methylene blue, her SpO₂ improved gradually to 99%, and the methemoglobin value decreased to 1.2%. When using prilocaine as a local anesthetic, it is important to be aware that methemoglobinemia may occur even at doses much lower than the maximum recommended dose.

• Tuberculosis and Respiratory Diseases
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• v.38 no.3
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• pp.255-261
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• 1991

Frequently patients with chronic obstructive pulmonary disease have lowered arterial oxygen saturation in daytime. During sleep, they are apt to experience additional hypoxemia. These episode of nocturnal hypoxemia are usually associated with periods of relative hypoventilation. Noctunal hypoxemia may be associated with cardiac arrhythmia and with acute increase in pulmonary arterial pressure and may be implicated in the development of chronic pulmonary hypertension and cor pulmonale. We selected 14 patients with chronic obstructive pulmonary disease, 9 with emphysema dominant type and 5 with chronic bronchitis dominant type, to examine the frequency and severity of nocturnal hypoxemia and the effect of oxygen in prevention of nocturnal hypoxemia. The results were as follows; 1) On PFT, FVC, $FEV_1$, and $FEV_1$/FVC showed no significant difference between the emphysema dominant type (pink puffers, PP) and the chronic bronchitis dominant type (blue bloaters, BB). But DLCO/VA for the PP group was $45.7{\pm}15.1%$ which was significantly different from BB group, $82.4{\pm}5.6%$. 2) The daytime arterial oxygen saturation ($SaO_2$) and the lowest $SaO_2$, during sleep for the BB group were significantly lower than for the PP group. 3) The hypoxemic episodes during sleep were more frequent in BB group and the duration of hypoxemic episode was longer in BB group. 4) In both group studied, although there was a tendency for a lower L-$SaO_2$ (the lowest $SaO_2$, during sleep), an increase in hypoxemic episodes and duration as the daytime $SaO_2$, fell lower, the only parameter which showed significant correlation was daytime $SaO_2$, and the frequency of hypoxemic episodes in the PP group (r=-0.68, P<0.05). 5) In PP group, with oxygen supplementation, L-$SaO_2$, during sleep showed significant increase, and there was a tendency for the frequency of hypoxemic episodes and duration to fall but it was not significant. 6) In BB group, oxygen supplementation significantly increased the L-$SaO_2$ during sleep and also significantly decreased the frequency and duration of hypoxemic episode. From these results, we can see that oxygen supplementation during sleep can prevent the decrease in $SaO_2$ to some extent and that this effect of oxygen can be seen more prominently in the BB group.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.379-388
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• 1994

Background : In sleep apnea syndrome, arterial oxygen saturation($SaO_2$) decreases at a variable rate and to a variable degree for a given apneic period from patient to patient, and various kinds of cardiac arrythmia are known to occur. Factors supposed to affect arterial oxygen desaturation during apnea are duration of apnea, lung voulume at which apnea occurs, and oxygen consumption rate of the subject. The lung serves as preferential oxygen source during apnea, and there have been many reports related with the influence of lung volume on $SaO_2$ during apnea, but there are few, if any, studies about the influence of oxygen consumption rate of an individual on $SaO_2$ during breath holding or about the profile of arterial oxygen resaturation after breathing resumed. Methods : To investigate the changes of $SaO_2$ and heart rate(HR) during breath holding(BH) and rebreathing(RB) and to evaluate the physiologic factors responsible for the changes, lung volume measurements, and arterial blood gas analyses were performed in 17 healthy subjects. Nasal airflow by thermistor, $SaO_2$ by pulse oxymeter and ECG tracing were recorded on Polygraph(TA 4000, Gould, U.S.A.) during voluntary BH & RB at total lung capacity(TLC), at functional residual capacity(FRC) and at residual volume(RV), respectively, for the study subjects. Each subject's basal metabolic rate(BMR) was assumed on Harris-Benedict equation. Results: The time needed for $SaO_2$ to drop 2% from the basal level during breath holding(T2%) were $70.1{\pm}14.2$ sec(mean${\pm}$standard deviation) at TLC, $44.0{\pm}11.6$ sec at FRC, and $33.2{\pm}11.1$ sec at RV(TLC vs. FRC, p<0.05; FRC vs. RV, p<0.05). On rebreathing after $SaO_2$ decreased 2%, further decrement in $SaO_2$ was observed and it was significantly greater at RV($4.3{\pm}2.1%$) than at TLC($1.4{\pm}1.0%$)(p<0.05) or at FRC($1.9{\pm}1.4%$)(p<0.05). The time required for $SaO_2$ to return to the basal level after RB(Tr) at TLC was not significantly different from those at FRC or at RV. T2% had no significant correlation either with lung volumes or with BMR respectively. On the other hand, T2% had significant correlation with TLC/BMR(r=0.693, p<0.01) and FRC/BMR (r=0.615, p<0.025) but not with RV/BMR(r=0.227, p>0.05). The differences between maximal and minimal HR(${\Delta}HR$) during the BH-RB manuever were $27.5{\pm}9.2/min$ at TLC, $26.4{\pm}14.0/min$ at RV, and $19.1{\pm}6.0/min$ at FRC which was significantly smaller than those at TLC(p<0.05) or at RV(p<0.05). The mean difference of 5 p-p intervals before and after RB were $0.8{\pm}0.10$ sec and $0.72{\pm}0.09$ sec at TLC(p<0.001), $0.82{\pm}0.11$ sec and $0.73{\pm}0.09$ sec at FRC(p<0.025), and $0.77{\pm}0.09$ sec and $0.72{\pm}0.09$ sec at RV(p<0.05). Conclusion Healthy subjects showed arterial desaturation of various rates and extent during breath holding at different lung volumes. When breath held at lung volume greater than FRC, the rate of arterial desaturation significantly correlated with lung volume/basal metabolic rate, but when breath held at RV, the rate of arterial desaturation did not correlate linearly with RV/BMR. Sinus arrythmias occurred during breath holding and rebreathing manuever irrespective of the size of the lung volume at which breath holding started, and the amount of change was smallest when breath held at FRC and the change in vagal tone induced by alteration in respiratory movement might be the major responsible factor for the sinus arrythmia.

• Journal of Chest Surgery
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• v.6 no.2
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• pp.131-142
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• 1973

Studies of cardiopulmonary function and acid-base balance were performed on 29 dogs during control period, during oligemic hypotension and following return of blood to the animals. Intravenous morphine and local anesthesia were used. Fifteen of the 29 animals survived the complete experiment. The 14 animals that failed to survive the experimental period died between 15 to 90 minutes after the onset of bleeding. The results were as follows. 1. The heart rate increased after the onset of bleeding and failed to return to control level following reinfusion. Stroke volume decreased markedly after bleeding and failed to recover after return of blood from the reservoir. Cardiac output also decreased during oligemic hypotension and was maintained at this level after re-infusion. Total peripheral resistance decreased significantly immediately after bleeding, however it increased soon over the pre-bleeding level. Central venous pressure decreased after the onset of bleeding and remained at lower level for the rest of the experimental period. Arterial blood pressure, clown to 40-45 mmHg by acute hemorrhage, was elevated near to control level. Left ventricular work decreased tremendously during oligemic hypotension and failed to return to control level with the re-infusion of blood. Hematocrit value showed no significant decrease after bleeding and increased after re-infusion. Hemoglobin decreased after the onset of bleeding and recovered to control value after re-infusion. 2. The respiratory rate fell rapidly after bleeding from 124 to 29 and remained at this lower level for the remainder of the experiment. The tidal volume increased after bleeding and was maintained at this level for the remainder of the experiment. The respiratory minute volume showed no significant changes throughout the experimental period. Oxygen consumption fell lightly in all animals during oligemic hypotension and returned to normal levels following re-infusion. Arterial oxygen content and arterial oxygen saturation decreased following bleeding and the values returned to normal levels after the return of blood from the reservoir The arterio-venous oxygen difference increased after the onset of bleeding. It failed to return to normal values following re-infusion. Arterial $Pco_2$ decreased in all animals after the beginning of the bleeding. Partial pressure of $Co_2$ continued to fall until re-infusion, after which the values returned toward normal. Animals became acidotic. The pH fell to lower level following bleeding. Lactic acid and lactate: pyruvate ratio also increased during same period. Arterial pH and lactic acid failed to return to control value and lactate: pyruvate ratio increased more after re-infusion. Sodium bicarbonate decreased after bleeding and returned to control value following re-infusion.