• Korean Journal of Clinical Laboratory Science
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• v.52 no.3
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• pp.278-283
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• 2020

Central sleep apnea (CSA) is characterized by respiratory failure of at least 10 seconds without any effort of the chest and abdomen in the absence of upper airway resistance during sleep. In this case, the patient experiences respiratory failure that does not meet the CSA diagnostic criteria and CSA symptoms. Magnetic resonance imaging diffusion-weighted imaging (MRI DWI) scans revealed a lateral medullary infarction. Continuous positive airway pressure (CPAP) was applied as a primary treatment for CSA and respiratory failure. During the titration of CPAP, the apnea-hypopnea index (AHI) and arousal index (AI) were worse than the results before its use (AHI: 42.5/hr→82.8/hr, AI: 21.7/hr→40.8h). As a result, adaptive servo-ventilation (ASV) was chosen as the secondary treatment. Compared to the night-polysomnography results before the ASV treatment, the AHI improved (42.5/hr→8.6/hr). Therefore, ASV is a potential treatment for CSA and respiratory failure in these patients.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.350-362
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• 1999

Background: Acute Respiratory failure which is developed after extubation in the weaning process from mechanical ventilation is an important cause of weaning failure. Once it was developed, endotracheal reintubation has been done for respiratory support. Noninvasive Positive Pressure Ventilation (NIPPV) has been used in the management of acute or chronic respiratory failure, as an alternative to endotracheal intubation, using via nasal or facial mask. In this study, we evaluated the usefulness of NIPPV as an alternative method of reintubation in patients who developed acute respiratory failure after extubation. Method: We retrospectively analyzed thirty one patients(eighteen males and thirteen females, mean ages $63\pm13.2$ years) who were developed acute respiratory failure within forty eight hours after extubation, or were extubated unintentionally at medical intensive care unit(MICU) of Asan Medical Center. NIPPV was applied to the patients. Ventilatory mode of NIPPV, level of ventilatory support and inspiratory oxygen concentration were adjusted according to the patient condition and results of blood gas analysis by the attending doctors at MICU. NIPPV was completely weaned when the patients maintained stable clinical condition under 8 $cmH_2O$ of pressure support level. Weaning success was defined as maintenance of stable spontaneous breathing more than forty eight hours after discontinuation of NIPPV. Respiratory rate, heart rate, arterial blood gas analysis, level of pressure support, and level of PEEP were monitored just before extubation, at thirty minutes, six hours, twenty four hours after initiation of NIPPV. They were also measured at just before weaning from NIPPV in success group, and just before reintubation in failure group. Results: NIPPV was successfully applied to thirty-one patients of thirty-two trials and one patient could not tolerated NIPPV longer than thirty minutes. Endotracheal reintubation was successfully obviated in fourteen patients (45%) among them. There was no difference in age, sex, APACHE III score on admission at MICU, duration of intubation, interval from extubation to initiation of NIPPV, baseline heart rate, respiratory rate, arterial blood gas, and $PaO_2/FiO_2$ between the success and the failure group. Heart rate and respiration rate were significantly decreased with increase $SaO_2$ after thirty minutes of NIPPV in both groups(p<0.05). However, in the patients of failure group, heart rate and respiratory rate were increased again with decrease in $SaO_2$ leading to endotracheal reintubation. The success rate of NIPPV treatment was significantly higher in the patients with COPD compared to other diseases(62% vs 39%) (p=0.007). The causes of failure were deterioration of arterial blood gas without aggravation of underlying disease(n=9), aggravation of undelying disease(n=5), mask intolerance(n=2), and retained airway secretion(n=l). Conclusion: NIPPV would be a useful therapeutic alternative which can avoid reintubation in patient who developed acute respiratory failure after extubation.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.129-139
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• 1997

The data collected to date indicate that sleep-related breathing disorders, including sleep-disordered breathing(sleep apnea) and underlying respiratory system diseases, are one of the important risk factors for cardiovascular dysfunction. Sleep-disordered breathing(sleep apnea) is now recognized as one of the leading causes of systemic hypertension, cardiac arrhythmias, coronary heart disease, pulmonary hypertension, right heart failure, and stroke. Sleep may exert a profound effect on breathing in patients with underlying respiratory system disease including bronchopumonary diseases, chest wall abnormalities, central alveolar hypoventilation syndromes or respiratory neuromuscular disorders. Chronic hypoxia and hypercapnia in these patients may accelerate the development of long term cardiovascular complications such as cardiac arrhythmias, pulmonary hypertension, and right heart failure(cor pulmonale). Several recent studies reported that sleep-related breathing disorders are associated with long-term cardiovascular morbidity and mortality. Careful assessment of respiratory and cardiovascular function in these patients is critical. Aggressive and highly effective treatment of sleep-related breathing disorders using tracheostomy, mechanical ventilation, nasal continuous positive airway pressure therapy(nCPAP), intercurrent oxygen therapy or other interventions can reduce the prevalence of cardiovascular dysfunction and the long-term mortality.

• 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.

• Journal of Chest Surgery
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• v.39 no.4 s.261
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• pp.323-327
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• 2006

Lymphangioleiomyomatosis (LAM) is a rare disease in women of childbearing ages that eventually leads to respiratory failure. Lung transplantation is the only conclusive therapeutic modality in end-stage LAM. While single-lung transplantation is the preferred operation, the graft failure or recurrence of LAM was reported. We performed a single lung transplantation on a 36-year-old woman suffering from respiratory failure due to lymphangioleiomyomatosis. After a 1-year follow up, the patient was readmitted because of graft failure with collapsed transplanted lung. The lung volume reduction surgery (LVRS), tracheostomy and ventilator care were performed. However, neither the medical nor surgical treatment had any effect. Subsequently, we performed a contralateral single lung re-transplantation and had a good postoperative results.

• Tuberculosis and Respiratory Diseases
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• v.64 no.1
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• pp.44-47
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• 2008

Gefitinib를 사용할 경우 발생할 수 있는 급성호흡부전은 주로 남성, 흡연자, 편평상피세포암 혹은 사이성 폐질환 등에서 발생하는 것으로 알려져 있다. 따라서 이와 같은 임상적 요인이 없는 경우 이 약제를 안전하게 사용할 수 있을 것이다. 연구자 등은 흡연한 적이 없고, EGFR 유전자의 19번 엑손 돌연변이를 보였던 47세 여성 선암 환자에서 gefitinib 투여 후 발생한 급성호흡부전을 보고하며, 부작용의 발생기전이 밝혀지지 않은 시점에서, 이들 임상적 특성을 보이는 환자에서도 호흡기계 부작용의 발생 가능성에 대한 임상의사의 주의를 촉구하는 바이다.

• Tuberculosis and Respiratory Diseases
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• v.61 no.6
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• pp.562-566
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• 2006

Fat embolism syndrome is a rare clinical diagnosis of dyspnea with acute respiratory failure and neurological signs caused by a traumatic long bone fracture. We report a case of fat embolism in a 22 year-old man after a traffic accident. Dyspnea and stuporous mental changes developed on the $1^{st}$ day after the external fixation operation of a left metaphyseal femur fracture. On the following day, he was transferred from a hospital to this one because of acute respiratory failure. After recovery, macrophages with fat droplets were found in the bronchoalveolar lavage fluid 1. It is important to diagnose a fat embolism as the correct cause of acute respiratory failure through the BAL in the acute state of fat embolism syndrome It is believed that clinically apparent or sometimes hidden fat embolism syndrome can be diagnosed from the BAL during the recovery state.

• Journal of Yeungnam Medical Science
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• v.10 no.1
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• pp.1-17
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• 1993

고빈도 환기법은 최근에 개발되어 임상에 응용되면서 호흡생리학, 마취학, 집중치료의 학등의 분야에서 호흡부전의 새로운 치료법으로 관심이 집중되고 있는 환기법이다. 현재까지 고빈도 환기법중 고빈도 양압 환기와 제트 환기는 비교적 많은 연구가 되고 있고 임상적으로 사용되고 있으나 고빈도 진동 환기법은 제한적으로 사용되고 있다. 앞으로 고빈도 진동 환기법에 대해서도 더 많은 연구가 되어야 할 것이다. 또한 최근 개발되고 있는 고빈도 흉벽 진동 환기와 체표면 진동 환기에도 관심을 기울이면 호흡부전 환자의 치료에 바람직한 새로운 환기법이 될 수 있을 것으로 기대된다. 현재 고빈도 환기법의 몇몇 적용형태는 기관지-늑막루등의 폐압손상으로 인한 병변의 치료외에도 기관수술, 흉부수술, 뇌수술에서 수술부위의 움직임을 최소화시키면서 충분한 가스교환율 이룩할 수 있어서 효과적으로 이용되고 있다. 그러나 응급심폐소생술, 폐쇄성 폐질환, 성인 또는 영아 호흡곤란증후군등과 같은 질환에서의 적용은 더 규명되어져야겠다. 고빈도 환기법의 여러가지 문제점중 적절한 환기빈도의 결정, 충분한 습도를 공급하는 장치, 고빈도 환기의 정확한 감시장치의 개발등은 앞으로 우선적으로 해결해야 할 문제점이다. 또한 임상에 더욱 효과적으로 응용될 수 있는 새로운 환기법이 되기 위해서는 고빈도 환기법의 호흡생리와 안정성등에 관한 연구도 병행되어야겠다.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.247-254
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• 1999

Respiratory failure is the most serious manifestation and usual cause of death in acute organophosphate poisoning, and is common in acute cholinergic crisis. But the respiratory failure may appear suddenly in a patient who is recovering from the cholinergic crisis, even while receiving conventional therapy. These are case report of 37 years old male and 24 years old female with intermediate syndrome in organophosphate poisoning. The two patients ingested organophosphate(fenthion and mixture of DDVP with chlorpyrifos respectively) incidentally and in a sucide attempt respectively. After apparent recovery from the cholinergic crisis with a conventional therapy but before the expected onset of delayed polyneuropathy, the respiratory failure appeared suddenly with a muscular weakness, affecting predominantly the proximal limb muscles, neck flexors, territories of several motor cranial nerves. The two patients needed mechanical ventilatory support and recovery from the intermediate syndrome was complete in both patients, although one subsequently developed hypoxic encephalopathy. The clinical manifestation and electrophysiologic study support the clinical diagnosis of intermediate syndrome. The syndrome carries a risk of death. because of respiratory paralysis, if not recognized early and treated adequatedly. Prompt endotrachial intubation and mechanical ventilatory support is the cornerstone of treatment of the intermediate syndrome. Therefore, all patient should be observed in a hospital for up to 5 days after poisoning.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.525-539
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• 2001