• Tuberculosis and Respiratory Diseases
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• v.58 no.3
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• pp.295-298
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• 2005

We report a case of a 48-year-old man with a paradoxic upper airway obstruction and central sleep apnea that developed after an anterior cervical spinal fusion. Nine months before being admitted to this hospital, he was diagnosed with a herniated intervertebral disc between the 5th and 6th cervical spine, and the first operation was carried out. Two months later, a pseudoarthrosis has developed and a second operation, an anterior interbody fusion of the C5 and C6 using autogenous strut bone graft, was performed. After the second operation, he began to complain of snoring, excessive daytime sleepiness, insomnia, and a bizarre sound heard near the upper airway during breathing. Nasopharyngoscope and magnetic resonance imaging disclosed a paradoxical narrowing of the nasopharynx during expiration. On the overnight polysomnography, the apnea index was 8.7/h (central apnea, 7.0/h; obstructive apnea, 1.7/h). Nasal continuous positive airway pressure was applied, but he complained of pressure-intolerance, and laser-assisted uvulopalatoplasty was then performed. Two months after surgery, clinical symptoms as well as the apneas had improved markedly. We suggest that this paradoxic upper airway obstruction might be associated with the anterior cervical spinal surgery even though the mechanism is unclear. This case also emphasizes that an upper airway obstruction can contribute to the development of central sleep apnea.

• Tuberculosis and Respiratory Diseases
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• v.46 no.4
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• pp.500-511
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• 1999

Background: Noninvasive positive pressure ventilation (NPPV) using facial or nasal mask have been widely used for several years in stable patients with chronic neuromuscular disease or central alveolar hypoventilation, and recently have been tried in patients with acute respiratory failure. In a few studies, NPPV was also used to rescue the patients with post-extubation respiratory failure. However, yet it has not been adopted as a weaning method in patients on long-term mechanical ventilation. So we performed this prospective clinical study to evaluate the usefulness of NPPV as a weaning method after removing endotracheal tube intentionally in patients on long-term mechanical ventilation. Method: Twelve patients who had been on invasive mechanical ventilation over 10 days were enrolled and 14 trials of NPPV were done. All had failed at least one weaning trial and showed ventilator dependence(pressure support requirement between 8-15cm $H_2O$, and PEEP requirement between 5-10cm $H_2O$), so tracheostomy was being considered. After removing the endotracheal tube, NPPV was applied using facial mask. Respiratory rate, arterial blood gas, pressure support level, and PEEP level were monitored just before intended extubation, at 30 minutes, 1 to 6, 6 to 12, 12 to 24 hours, 2nd day, and 3rd day following initiation of NPPV, and just before weaning from NPPV. The successful weaning was defined as spontaneous breathing off the ventilator for 48 hours or longer without respiratory distress. Results: The weaning through NPPV after intended extubation was successful in 7(50%) of 14 trials, and tracheostomy could be avoided in them. There were no differences in age, sex, APACHE III score, duration of invasive mechanical ventilation, baseline respiratory rate, $PaCO_2$ $PaO_2/FiO_2$, and ventilatory requirement(PS and PEEP) between the success and failure groups. In the success group, respiratory rate, pH, $PaCO_2$, and $PaO_2/FiO_2$ were not different between invasive MV and NPPV period. But in the failure group, pH decreased after 30 minutes of NPPV initiation compared with that of invasive MV($7.40\pm0.08$ vs. $7.34\pm0.06$, p<0.05). The causes of failure were worsening of ABG(n=3), retained tracheal secretion(n=2), mask intolerance(n=1), and flail chest(n=1). Conclusion: NPPV may be worth trying as a bridge method in weaning patients on long-term invasive mechanical ventilation.

• Journal of the korean academy of Pediatric Dentistry
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• v.31 no.4
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• pp.721-728
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• 2004

Velopharyngeal closure is a sphincter mechanism between the activities of the soft palate, lateral pharyngeal wall and the posterior pharyngeal wall, which divides the oral and nasal cavity. It participates in physiological activities such as swallowing, breathing and speech. It is called a velopharyngeal dysfunction when this mechanism malfunctions. The causes of this dysfunction are defects in (1) length, function, posture of the soft palate, (2) depth and width of the nasopharynx and (3) activity of the posterior and lateral pharyngeal wall. The purposes of this study are to analyze the nasopharynx of cleft palate patients using cephalometry and to evaluate the degree of hypernasality using nasometry to find its relationship with velopharyngeal dysfunction. The following results were obtained : 1. In cephalometry, there were significant differences in soft palate length, soft palate thickness, nasopharyngeal depth, nasopharyngeal area, and adequate ratio between two groups. 2. In nasometry, there were significant differences between two groups in vowel /o/ and sentences including oral consonants. 3. In cleft palate patients, though no general correlation was found between Anatomic VPI and nasalance scores, vowel /i/ and sentences including oral consonants were slightly correlated. In conclusion, cephalometry and nasometer results were significantly different between the two groups. Though in the cleft palate group, Anatomic VPI and nasalance scores, which are indices for velopharyngeal closure, excluding the vowel /i/ and sentences including oral consonants show generally no significance.

• 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.

• 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.