• Tuberculosis and Respiratory Diseases
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• v.39 no.1
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• pp.7-14
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• 1992

Background: Cognitive deficit by hypoxia and/or hypercapnia is one of neuropsychological impairments frequently observed in patients with chronic obstructive pulmonary disease (COPD). The degree of cognitive deficit is variable among patients with similar level of hypoxia and/or hypercapnia, although a cause of this individual difference is well not known. COPD can be divided into two characteristic clinical entities including predominant emphysema and predominant bronchitis. This study was designed to evaluate the individual difference in cognitive deficit respond to hypoxia and/or hypercapnia in patients with COPD. Method: Sixteen patients with COPD (9 emphysema-dominant and 7 bronchitis-dominant) participated in this study. On admission arterial blood gas analysis and trail-making B (TMB) test for the evaluation of cognitive function were done in all patients. Mean TMB scores and the correlations between TMB scores and arterial blood gases were compared between two clinical groups. Results: 1) Mean TMB scores and arterial blood gases between two clinical groups were not different. 2) There was a tendency to be higher TMB score in hypoxemia, acidemia, and hypercapnia. However these findings were not statistically significant. 3) In emphysema-dominant group, $PaCO_2$ was mostly well correlated with TMB score (r=0.693). 4) In bronchitis-dominant group, arterial pH was mostly well correlated with TMB score (r=-0.526). Conclusion: Our data suggest that the individual difference in cognitive deficit respond to hypoxia and/or hypercapnia in patients with COPD may be dependent on their clinical entities, and arterial blood gases mostly well correlated with cognitive function that may be different according to their clinical entities.

• Tuberculosis and Respiratory Diseases
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• v.67 no.1
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• pp.52-58
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• 2009

Pulmonary arteriovenous malformation (PAVM) is a rare pulmonary vascular anomaly due to an abnormal communication between the pulmonary artery and vein. The most common presenting symptom is a dyspnea on exertion related to this right-to-left shunt. If left untreated, PAVM has been known to result in serious complications. Incomplete pulmonary capillary network can be the cause of cerebral abscesses and other noninfectious neurological complications, such as stroke and transient ischemic attacks due to paradoxic embolism Transcatheter embolotherapy, using coils or balloons, has replaced surgical resection as the treatment of choice for PAVM. However, the risk of device embolization has limited the use of coil embolotherapy, while the size of PAVM is huge. Recently, Amplatzer$^{(R)}$ Vascular Plug has been proposed as an alternative endovascular occlusion device for arteriovenous malformation. We report a case of 81-year-old male patient with a giant PAVM, which was successfully treated by transcatheter embolotherapy using the Amplatzer$^{(R)}$ Vascular Plug.

• Sleep Medicine and Psychophysiology
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• v.14 no.1
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• pp.49-53
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• 2007

Mitochondrial myopathy is characterized by variable clinical manifestations from mild limb weakness to fatal respiratory failure and central nervous system sequela. But it is a rare event that sleep disordered breathing become a clue of diagnosis for mitochondrial myopathy. We report a case of a 21 year-old man who was diagnosed as mitochondrial myopathy during the investigation for the possible cause of chronic hypoventilation syndrome. Before being admitted to our hospital, he was suspected as having sleep apnea syndrome in another hospital. We re-evaluated the history, physical examination, laboratoy findings and polysomnography in detail. Severe hypoxemia was noted during REM sleep on nocturnal polysomnography and the diagnosis of mitochondrial myopathy was made by muscle biopsy in rectus abdominis muscle. We treated him with bilevel positive airway pressure therapy during sleep and it could reverse the hypoxemia during REM sleep. He could be discharged with improved condition and is being well with the use of this ventilatory assistance.

• Tuberculosis and Respiratory Diseases
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• v.61 no.3
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• pp.265-272
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• 2006

Background: Chest wall deformities such as kyphoscoliosis, thoracoplasty, and fibrothorax cause ventilatory insufficiency that can lead to chronic respiratory failure, with recurrent fatal acute respiratory failure(ARF). This study evaluated the frequency and outcome of ARF, the physiologic status, and the long-term prognosis of these patients. Methods: Twenty-nine patients with chest wall disorders, who experienced the first requirement of ventilatory support from ARF were examined. The mortality and recurrence rate of ARF, the pulmonary functions with arterial blood gas analysis, the efficacy of home oxygen therapy, and the long-term survival rate were investigated. Results: 1) The mortality of the first ARF was 24.1%. ARF recurred more than once in 72.7% of the remaining 22 patients, and overall rate of successful weaning was 73.2%. 2) Twenty-two patients who recovered from the first ARF showed a restrictive ventilatory impairment with a mean FVC and TLC of 37.2% and 62.4 % of predicted value, respectively, and a mean $PaCO_{2}$ of 57mmHg. Among the parameters of pulmonaty functions. the FVC(p=0.01) and VC(p=0.02) showed a significant correlation with the $PaCO_{2}$ level. 3) There were no significant differences between the patients treated with conservative medical treatment only and those with additional home oxygen therapy due to significant hypoxemia in the patients with recurrent ARF and the mortality. 4) The 1, 3, 5-year survival rates were 75%, 66%, and 57%, respectively, in the 20 patients who had recovered from the first ARF, excluding the two patients managed by non-invasive nocturnal ventilatory support. Conclusion: These results suggest that active ventilatory support should be provided to patients with ARF and chest wall disorders. However, considering recurrent ARF and weak effect of home oxygen therapy, non-invasive domiciliary ventilation is recommended in those patients with these conditions to achieve a better long-term prognosis.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.844-852
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• 1997

Background : Recent studies have documented increased release of endothelin(ET) during acute attack of asthma. The purpose of this study is to observe the link between plasma level and urinary excretion of each and changes during acute exacerbation. Method : Plasma and 24 hour urine were collected from sixteen asthmatics during acute exacerbation, twice ; first day of symptomatic exacerbation and two weeks after treatment. Controls were ten healthy normal subjects. All patients were treated with corticosteroid and beta-2 adrenergic agonist on admission. ET was determined by radioimmmunoassay and had 100% cross reactivity with ET-1, 67% with ET-2, 84% with ET-3, and 8% with Big-ET. Results : Plasma ETs were significantly elevated during acute attack of asthma compared with those in remission and controls.,However, there was no significant changes in urine ET concentrations or total ET amounts in 24 hour urine during exacerbation upto two weeks. Those levels of urine ET in asthmatics were still higher than controls. ET concentrations in plasma or urine were not correlated with pulmonary functional parameters and hypoxemia. Conclusion : The findings suggests that increased plasma ETs are related with exaggerated release during acute asthma. Urinary ET excretion is increased in asthma. However, urine ET changes during exacerbation should be observed in a larger and longer scale.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.231-238
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• 1999

Background: Nocturnal hypoxemia occurs in patients with chronic obstructive pulmonary disease(COPD) and the detection and treatment of nocturnal hypoxemia should be part of the management of COPD patients. We performed this study to evaluate the factors influencing to sleep related arterial oxygen desaturation($SaO_2$) in patients with COPD. Methods: Resting and exercise cardiopulmonary function test, polysomnography, and $SaO_2$ during resting, exercise and sleep were measured in 12 patients with COPD. Results: The $SaO_2$ fell twice as much during sleep as during maximal exercise($13.1{\pm}9.3%$ fall in nocturnal $SaO_2$ vs. $6.4{\pm}3.3%$, p<0.05). Fall in nocturnal $SaO_2$ was well correlated with mean exercise $SaO_2$(r=-0.78, p<0.05), minimum exercise $SaO_2$(r=-0.90, p<0.01), and resting $SaO_2$(Cr=-0.82, p<0.05). Lowest sleep $SaO_2$ was well correlated with mean exercise $SaO_2$(r=0.80, p<0.05), lowest exercise $SaO_2$(r=0.90, p<0.01), and resting $SaO_2$(r=0.84, p<0.05). Conclusion: Resting and exercise $SaO_2$ was well correlated with nocturnal $SaO_2$, but exercise study add no additional information to predicting the nocturnal oxygen desaturation in patients with COPD.

• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.42-49
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• 1999

Background: In patients with chronic obstructive pulmonary disease(COPD). it is well known that hypoxemia increases the frequency of VPB, which is associated with the poor prognosis such as sudden death. The aim of this study is to evaluate the effect of short and long-term low flow oxygen therapy on the development of VPBs in patients with COPD by correcting the hypoxemia. Method: In 19 patients with COPD, oxygen saturation and VPB's were monitored by pulse oxymeter and 24-hour Holter EKG, with room air and oxygen saturation and VPB's were monitored on the 1st and on the 8th day during oxygen therapy with nasal prong (2L/min). Results : The arterial oxygen saturation was significantly higher on the 1st day of oxygen therapy compared with breathing room air, and was also higher on the 8th day of oxygen therapy than on the 1st day. We found that there was significant correlation between the lowest value of the arterial oxygen saturation and the mean value of the arterial oxygen saturation. The number of VPB's per hour was significantly lower on the 1st day of oxygen therapy compared with breathing room air, and also lower on the 8th day of oxygen therapy than on the 1st day. Our results showed positive correlation between the decrease in the frequency of VPB's and the increase in the lowest arterial oxygen saturation, even though correlation was not significant(p=0.056). Conclusion: With oxygen therapy, the arterial oxygen saturation was increased and the number of VPB's was decreased. Long-term oxygen therapy more than 7days, would be helpful to decrease the number of VPB' s in patients with COPD.

• 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.