• Title/Summary/Keyword: 가스 측정 방법

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The Patterns of Change in Arterial Oxygen Saturation and Heart Rate and Their Related Factors during Voluntary Breath holding and Rebreathing (자발적 호흡정지 및 재개시 동맥혈 산소포화도와 심박수의 변동양상과 이에 영향을 미치는 인자)

  • Lim, Chae-Man;Kim, Woo-Sung;Choi, Kang-Hyun;Koh, Youn-Suck;Kim, Dong-Soon;Kim, Won-Dong
    • 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.

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Comparison of Effects of Normothermic and Hypothermic Cardiopulmonary Bypass on Cerebral Metabolism During Cardiac Surgery (체외순환 시 뇌 대사에 대한 정상 체온 체외순환과 저 체온 체외순환의 임상적 영향에 관한 비교연구)

  • 조광현;박경택;김경현;최석철;최국렬;황윤호
    • Journal of Chest Surgery
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    • v.35 no.6
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    • pp.420-429
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    • 2002
  • Moderate hypothermic cardiopulmonary bypass (CPB) has commonly been used in cardiac surgery. Several cardiac centers recently practice normothermic CPB in cardiac surgery, However, the clinical effect and safety of normothermic CPB on cerebral metabolism are not established and not fully understood. This study was prospectively designed to evaluate the clinical influence of normothermic CPB on brain metabolism and to compare it with that of moderate hypothermic CPB. Material and Method: Thirty-six adult patients scheduled for elective cardiac surgery were randomized to receive normothermic (nasopharyngeal temperature >34.5 $^{\circ}C$, n=18) or hypothermic (nasopharyngeal temperature 29~3$0^{\circ}C$, n=18) CPB with nonpulsatile pump. Middle cerebral artery blood flow velocity (VMCA), cerebral arteriovenous oxygen content difference (CAVO$_{2}$), cerebral oxygen extraction (COE), modified cerebral metabolic rate for oxygen (MCMRO$_{2}$), cerebral oxygen transport (TEO$_{2}$), cerebral venous desaturation (oxygen saturation in internal jugular bulb blood$\leq$50 %), and arterial and internal jugular bulb blood gas analysis were measured during six phases of the operation: Pre-CPB (control), CPB-10 min, Rewarm-1 (nasopharyngeal temperature 34 $^{\circ}C$ in the hypothermic group), Rewarm-2 (nasopharyngeal temperature 37 $^{\circ}C$ in the both groups), CPB-off and Post-CPB (skin closure after CPB-off). Postoperaitve neuropsychologic complications were observed in all patients. All variables were compared between the two groups. Result: VMCA at Rewarm-2 was higher in the hypothermic group (153.11$\pm$8.98%) than in the normothermic group (131.18$\pm$6.94%) (p<0.05). CAVO$_{2}$ (3.47$\pm$0.21 vs 4.28$\pm$0.29 mL/dL, p<0.05), COE (0.30$\pm$0.02 vs 0.39$\pm$0.02, p<0.05) and MCMRO$_{2}$ (4.71 $\pm$0.42 vs 5.36$\pm$0.45, p<0.05) at CPB-10 min were lower in the hypothermic group than in the normothermic group. The hypothermic group had higher TEO$_{2}$ than the normothermic group at CPB-10 (1,527.60$\pm$25.84 vs 1,368.74$\pm$20.03, p<0.05), Rewarm-2 (1,757.50$\pm$32.30 vs 1,478.60$\pm$27.41, p<0.05) and Post-CPB (1,734.37$\pm$41.45 vs 1,597.68$\pm$27.50, p<0.05). Internal jugular bulb oxygen tension (40.96$\pm$1.16 vs 34.79$\pm$2.18 mmHg, p<0.05), saturation (72.63$\pm$2.68 vs 64.76$\pm$2.49 %, p<0.05) and content (8.08$\pm$0.34 vs 6.78$\pm$0.43 mL/dL, p<0.05) at CPB-10 were higher in the hypothermic group than in the normothermic group. The hypothermic group had less incidence of postoperative neurologic complication (delirium) than the normothermic group (2 vs 4 patients, p<0.05). Lasting periods of postoperative delirium were shorter in the hypothermic group than in the normothermic group (60 vs 160 hrs, p<0.01). Conclusion: These results indicate that normothermic CPB should not be routinely applied in all cardiac surgery, especially advanced age or the clinical situations that require prolonged operative time. Moderate hypothermic CPB may have beneficial influences relatively on brain metabolism and postoperative neuropsychologic outcomes when compared with normothermic CPB.

Inflammatory Reponse of the Lung to Hypothermia and Fluid Therapy after Hemorrhagic Shock in Rats (흰쥐에서 출혈성 쇼크 후 회복 시 저체온법 및 수액 치료에 따른 폐장의 염증성 변화)

  • Jang, Won-Chae;Beom, Min-Sun;Jeong, In-Seok;Hong, Young-Ju;Oh, Bong-Suk
    • Journal of Chest Surgery
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    • v.39 no.12 s.269
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    • pp.879-890
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    • 2006
  • Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.