• Tuberculosis and Respiratory Diseases
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• v.63 no.3
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• pp.261-267
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• 2007

Background: The causes of the pleural effusion are remained unclear in a the substantial number of patients with exudative effusions determined by an examination of the fluid obtained via thoracentesis. Among the various tools for diagnosing exudative pleural effusions, thoracoscopy has a high diagnostic yield for cancer and tuberculosis. Medical thoracoscopy can also be carried out under local anesthesia with mild sedation. The aim of this study was to determine diagnostic accuracy and safety of medical thoracoscopy. Methods: Twenty-five patients with exudative pleural effusions of an unknown cause underwent medical thoracoscopy between October 2005 and September 2006 in Konyang University Hospital. The clinical data such as age, gender, preoperative pulmonary function, amounts of pleural effusion on lateral decubitus radiography were collected. The vital signs were recorded, and arterial blood gas analyses were performed five times during medical thoracoscopy in order to evaluate the cardiopulmonary status and acid-base changes. Results: The mean age of the patients was 56.8 years (range 22-79). The mean depth of the effusion on lateral decubitus radiography (LDR) was 27.49 mm. The medical thoracoscopic pleural biopsy was diagnostic in 24 patients (96.0%), with a diagnosis of tuberculosis pleurisy in 9 patients (36%), malignant effusions in 8 patients (32%), and parapneumonic effusions in 7 patients (28%). Medical thoracoscopy failed to confirm the cause of the pleural effusion in one patient, who was diagnosed with tuberculosis by a pericardial biopsy. There were no significant changes in blood pressure, heart rate, acid-base and no major complications in all cases during medical thoracoscopy (p>0.05). Conclusions: Medical thoracoscopy is a safe method for patients with unknown pleural effusions with a relatively high diagnostic accuracy.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.136-145
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• 1997

Background : Tracheal Gas Insufflation (TGI) is one of the newer ancillary measures in mechanical ventilation employed to enhance carbon dioxide elimination. TGI exerts its effect through reduction of deadspace ventilation, but the factors determining its effect are not well studied yet. Method : The subjects were seven mechanically-ventilated patients ($58.8{\pm}10.6$ yrs) who showed increased physiologic deadspace greater than 60%. After 30 nun of stabilization with 100% oxygen on pressure control ventilation, continuous flow TGI was administered via the insufflation lumen of Hi-Lo Jet Tracheal Tube (Mallincrodt, USA) for 15 min at 3 L/min and 5 L/min each. Results : $PaCO_2$ was decreased ($51.4{\pm}17.6$ at baseline, $49.1{\pm}18.9$ at TGJ 3 L/min $45.0{\pm}14.9$ mm Hg at TGI 5 L/min, p=0.050), and pH was increased ($7.37{\pm}0.12$, $7.38{\pm}0.13$, $7.39{\pm}0.12$, respectively, p=0.037) while mixed expired $CO_2$ ($P_ECO_2$) was not changed significantly from baseline (p=0.336) by TGI. Physiologic deadspace(Vdphy) was decreased ($73.0{\pm}7.9$% at baseline, $69.8{\pm}10.0$% at TGI 3 L/min, and $67.1{\pm}10.1$% at TGI 5 L/min, p=0.015). $AaDO_2$(p=0.147), Vt(p=0.2140), Pmean(p=0.7788) and mean arterial pressure(p=0.4169) were not changed. The correlation between % maximal decrease of Vdphy were r=0.790 with the ratio of baseline Vdana/Vdphy(p=0.035) and r=-0.754 with baseline Vdalv(p=0.050). Conclusion: TGI was effective in reducing $PaCO_2$ and deadspace, and the deadspace-reducing effect was best correlated with baseline anatomic/physiologic deadspace ratio.

• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.645-653
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• 1999

Introduction : Although myocardial ischemia tends to occur more frequently than can he documented in ventilated patients, it has not been well studied on the factors related to the occurrence of the ischemia. Methods : To investigate the related factors to ischemia development, a prospective study was done in 95 cases with consecutive 73 patients who had received mechanical ventilation(MV) in MICU. In addition to 24 h holter monitoring, echocardiogram, electrolytes, cardiac enzymes, hemodynamic, and gas exchange measurements were done within 24 h after initiation of MV in 69 cases. The measurements were repeated at weaning period in 26 cases. The ischemia was defined by the ST segment changes; up-sloping depression more than 1.5 mm or down-sloping or horizontal depression more than 1.0 mm from isoelectric baseline for 80 ms following J point. Results : Twelve patients(12.6% in 95 cases) developed ischemia in total. The incidence of ischemia development showed an increased tendency in the initial 24 hr after MV (15.9%) and in patients with left-sided heart failure found by echocardiogram (18.2%) compared with that of the weaning period (3.8%) and patients without heart failure (10.9%) (P=0.12, P=0.09, in each). There were no differences in APACHE III score, baseline ECG findings, electrolytes abnormalities, use of inotropics or bronchodilators, presence of sepsis or shock, mode of ventilation, and survival rate according to the development of ischemia. Maximal heart rates and mean arterial pressure also were not different between patients with ($137.2{\pm}30.9/min$, $82.5{\pm}15.9$ mm Hg) and without ischemia ($l29.5{\pm}29.7/min$, $83.8{\pm}17.6$ mm Hg). Conclusion : Although the incidence of myocardial ischemia was 12.6% in total, there were no clinically predictable factors to the development of ischemia during mechanical ventilation.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.506-515
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• 2003

Background : A decreased level of serum arginine vasopressin(AVP) and an increased sensitivity to an exogenous AVP is expected in patients with septic shock who often require a high infusion rate of catecholamines. The goal of the study was to determine whether an exogenous AVP infusion to the patients with septic shock would achieve a significant decrement in infusion rate of catecholamine vasopressors while maintaining hemodynamic stability and adequate urine output. Method : Eight patients with septic shock who require a high infusion rate of norepinephrine had received a trial of 4-hour AVP infusion with simultaneous titration of norepinephrine. Hemodynamic parameters and urine output were monitored during the AVP infusion and the monitoring continued up to 4 hours after the AVP infusion had stopped. Results : Mean arterial pressure showed no significant changes during the study period(p=0.197). Norepinephrine infusion rate significantly decreased with concurrent AVP administration(p=0.001). However, beneficial effects had disappeared after the AVP infusion was stopped. In addition, hourly urine output showed no significant changes throughout the trials(p=0.093). Conclusion : Concurrent AVP infusion achieved the catecholamine vasopressor sparing effect in the septic shock patients, but there was no evidence of the improvement of renal function. Further study may be indicated to determine whether AVP infusion would provide an organ-protective effect to the septic shock patients.

• Tuberculosis and Respiratory Diseases
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• v.50 no.1
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• pp.106-116
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• 2001

Background : Pulmonary thromboembolism is relatively frequent and potentially fatal. However, it is commonly misdiagnosed. The incidence of pulmonary thromboembolism is not decreasing despite advances in diagnosis and effective prophylatic measures. Its potential for significant sequela necessitates a prompt diagnosis and treatment. Unfortunately, there are many difficulties and problems regarding accurate diagnosis. There is a low prevalence of deep vein thrombosis and pulmonary thromboembolism in Korea and only few reports on this subject are available. Method : The clinical features of 36 patients, who were diagnosed with pulmonary thromboembolism at the Korea University medical center, were reviewed. Results : 1) There was no significant difference in prevalence between men an women, and the mean age was 50.9 years in men 59.2 years in women. 2) The frequent causes of pulmonary thromboembolism were malignancies (22.2%), surgery (22.2%), and heart disease(8.2%). Specific causes were not identified in 33.3%. 3) The most common symptom was dyspnea(72.2%), and the most common sign was tachypnea(61.1%). 4) The EKG findings were normal in 28.6%, an S1Q3T3 pulmonale pattern in 25.7%, ST or QRS changes in others. 5) The chest X-ray findings indicated pulmonary infiltration in 37.5%, cardiomegaly in 15.6%, pleural effusion in 12.5%, and normal in 27.8%. The perfusion lung scan showed a high probability in 66.7%, and intermediate or low probability in 33.3%. 6) The pulmonary arterial pressure(PAP) in the high probability groups was 57.9mmHg with a higher mortality rate(35%). Conclusion : Pulmonary thromboembolism is not uncommon in Korea and its clinical features do not differ greatly from thase reported in the literature. When pulmonary thromboemblism of unknown causes are diagnosed, a search for an occult malignancy is recommended. Rapid diagnosis and treatment are achieved when thromboemblism is suspected.

• Clinical and Experimental Pediatrics
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• v.49 no.3
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• pp.317-325
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• 2006

Purpose : This study was carried out to elucidate the effects of nitric oxide synthase(NOS) inhibitor, NG-monomethyl-L-arginine(L-NMMA) and nitric oxide precursor, L-arginine(L-Arg) on cerebral hemodynamics and energy metabolism during reoxygenation-reperfusion(RR) after hypoxia-ischemia(HI) in newborn piglets. Methods : Twenty-eight newborn piglets were divided into 4 groups; Sham normal control(NC), experimental control(EC), L-NMMA(HI & RR with L-NMMA), and L-Arg(HI & RR with L-Arg) groups. HI was induced by occlusion of bilateral common carotid arteries and simultaneously breathing with 8 percent oxygen for 30 mins, and followed RR by release of carotid occlusion and normoxic ventilation for one hour. All groups were monitored with cerebral hemodynamics and cytochrome $aa_3$ (Cyt $aa_3$) using near infrared spectroscopy(NIRS). $Na^+$, $K^+$-ATPase activity, lipid peroxidation products, and tissue high energy phosphate levels were determined biochemically in the cerebral cortex. Results : In experimental groups, mean arterial blood pressure, $PaO_2$, and pH decreased, and base excess and blood lactate level increased after HI compared to NC group(P<0.05). These variables subsequently returned to baseline after RR except pH. There were no differences among the experimental groups. In NIRS, oxidized hemoglobin($HbO_2$) decreased and hemoglobin(Hb) increased during HI(P<0.05) but returned to base line immediately after RR; 40 min after RR, the $HbO_2$ had decreased significantly compared to NC group(P<0.05). Changes of Cyt $aa_3$ decreased significantly compared to NC after HI and recovered at the end of the experiment. Significantly reduced cerebral cortical cell membrane $Na^+$, $K^+$-ATPase activity and increased lipid peroxidation products(P<0.05) were not improved with L-NMMA or L-Arg. Conclusion : These findings suggest that NO is not involved in the mechanism of HI and RR brain damage during the early acute phase of RR.