Kim, Dae Sung;Yoon, Hye Eun;Lee, Seung Jae;Kim, Yong Hyun;Song, So Hyang;Kim, Chi Hong;Moon, Hwa Sik;Song, Jeong Sup;Park, Sung Hak
Tuberculosis and Respiratory Diseases
/
v.59
no.6
/
pp.690-695
/
2005
Nitric acid is an oxidizing agent used in metal refining and cleaning, electroplating, and other industrial applications. Its accidental spillage generates oxides of nitrogen, including nitric oxide (NO) and nitrogen dioxide ($NO_2$), which cause chemical pneumonitis when inhaled. The clinical presentation of a nitric acid inhalation injury depends on the duration and intensity of exposure. In mild cases, there may be no symptoms during the first few hours after exposure, or the typical symptoms of pulmonary edema can appear within 3-24 hours. However, in cases of prolonged exposure, progressive pulmonary edema develops instantaneously and patients may not survive for more than 24 hours. We report a case of a 44-year-old male who was presented with acute respiratory distress syndrome after nitric acid inhalation. He complained of cough and dyspnea of a sudden onset after inhaling nitric acid fumes at his workplace over a four-hour period. He required endotracheal intubation and mechanical ventilation due to fulminant respiratory failure. He was managed successfully with mechanical ventilation using positive end expiratory pressure and systemic corticosteroids, and recovered fully without any deterioration in his pulmonary function.
Pulmonary clearance of Tc-99m-DTPA(PCD) has been used for the measurement of polmonary epithelial permeability. It has been reported to be increased not only in variety of polmonary diseases including ARDS, interstitial fibrosis, and smokers, but also in normal subjects on positive end expiratory pressure respirator, or after exercise. It was also noted that decrease of pulmonary blood flow due to pulmonary arterial obstruction results in delayed PCD. Normal range of PCD varies with institutes. We prospectively measured PCD in 17 normals (5 males and 12 females) consisted of staffs and trainees in the department of radiology of Kangnam St. Mary's hospital using original Bark Nebulizer (India). Age ranged from 32 to 43 years. 370 MBq of Tc-99m-DTPA was inhaled in supine position and supine posterior images were subsequently obtained with 1 min/frame, $64{\times}64$ matrix and word mode for 30min. Regions of interest were set on each lung, whole lungs, and upper, middle and lower thirds of right lung, respectively. Best fit regression curve was obtained by least square method from initial 7min after peak activity on each curve and time for half clearance of maximum activity (t1/2) was calculated. Mean t1/2 was $51{\pm}11.2min$ for whole lung. There was no significant difference between t1/ 2 of right and left lungs. Initial uptake was higher in the lower third and t1/2 was shorter in the lower third than in the upper third(P<0.05). We reviewed several reports on PCD and compared our data with the others. In this study, faster clearance in the lower third may be due to the position imaged with or the environment the subjects belong to, and further investigation is under way.
Purpose : The aim of this study was to evaluate the effect of inhaled nitric oxide(iNO) on gas exchange, hemodynamics and pulmonary inflammation in newborn piglets with E. coli induced septic lung. Methods : Twenty three instrumented and ventilated piglets were randomized into three groups : CON(n=6), PCON(n=9), and PNO(n=8). In the piglets of the PCON and PNO groups, E. coli septic lung was induced by endotracheal instillation of E. coli. Ten ppm iNO was given continuously in the PNO group after endotracheal instillation of E. coli. All animals were mechanically ventilated for six hour with a peak inspiratory pressure of 30 $cmH_2O$, frequency of 25 breaths/min, $FiO_2$ 1.0 and a positive end-expiratory pressure of 4 $cmH_2O$. All measurements were made at one hour intervals during the experiment. At the end of the experiment, lung tissue was harvested for the analysis of myeloperoxidase activity, indicative of lung inflammation. Results : All piglets with pulmonary instillation of E. coli developed E. coli sepsis. Piglets in the PCON group developed progresseve pulmonry hypertension, hypoxemia and hypercarbia compared to the CON group due to increased pulmonary vascular resistance, intrapulmonary shunt fraction and physiologic dead space fraction. iNO did not reverse pulmonary hypertension in the PNO group. However iNO significantly improved oxygenation, which was attributed to marked improvement of venous admixture and partial attenuation of increase in dead space fraction. Increased myeloperoxidase activity in PCON compared to CON was significantly attenuated in PNO. Conclusion : iNO improves oxygenation and lung inflammation in newborn piglets with E. coli induced septic lung.
Backgrounds : Because ventilator-induced lung injury is partly dependent on the intensity of vascular flow, we hypothesized that hypothermia may attenuate the degree of such an injury through a reduced cardiac output. Methods : Twenty-seven male Sprague-Dawley rats were randomly assigned to normothermia ($37{\pm}1^{\circ}C$)-injurious ventilation (NT-V) group (n=10), hypothermia ($27{\pm}1^{\circ}C$)-injurious ventilation (HT-V) group (n=10), or nonventilated control group (n=7). The two thermal groups were subjected to injurious mechanical ventilation for 20 min with peak airway pressure 30 cm $H_2O$ at zero positive end-expiratory pressure, which was translated to tidal volume $54{\pm}6\;ml$ in the NT-V group and $53{\pm}4\;ml$ in the HT-V group (p>0.05). Results : Pressure-volume (P-V) curve after the injurious ventilation was almost identical to the baseline P-V curve in the HT-V group, whereas it was shifted rightward in the NT-V group. On gross inspection, the lungs of the HT-V group appeared smaller in size, and showed less hemorrhage especially at the dependent regions, than the lungs of the NT-V group. [Wet lung weight (g)/body weight (kg)] ($1.6{\pm}0.1$ vs $2.4{\pm}1.2$ ; p=0.014) and [wet lung weight/dry lung weight] ($5.0{\pm}0.1$ vs $6.1{\pm}0.8$ ; p=0.046) of the HT-V group were both lower than those of the NT-V group, while not different from those of the control group($1.4{\pm}0.4$, $4.8{\pm}0.4$, respectively). Protein concentration of the BAL fluid of the HT-V group was lower than that of the NT-V group($1,374{\pm}726\;ug/ml$ vs $3,471{\pm}1,985\;ug/ml$;p=0.003). Lactic dehydrogenase level of the BAL fluid of the HT-V group was lower than that of the NT-V group ($0.18{\pm}0.10\;unit/ml$ vs $0.43{\pm}0.22\;unit/ml$;p=0.046). Conclusions : Hypothermia attenuated pulmonary hemorrhage, permeability pulmonary edema, and alveolar cellular injuries associated with injurious mechanical ventilation, and preserved normal P-V characteristics of the lung in rats.
Background : Reduced lung compliance and increased lung resistance are the primary lung mechanical abnormalities in acute respiratory distress syndrome (ARDS). Although there is little information regarding the mechanisms responsible for the increases in the respiratory resistance of ARDS, bronchodilators have been frequently administered in mechanically ventilated ARDS patients. To determine the effect of a bronchodilator on the respiratory mechanics depending on the level of applied positive end-expiratory pressure (PEEP), the changes in the respiratory mechanics by salbutamol inhalation was measured under the variable PEEP level in patients with ARDS. Materials and Methods : Fifteen mechanically ventilated paralyzed ARDS patients (14 of male, mean age 57 years) were enrolled in this study. The respiratory system compliance, and the maximum and minimum inspiratory resistance were obtained by the end-inspiratory occlusion method during constant flow inflation using the CP-100 pulmonary monitor (Bicore, Irvine, CA, USA). The measurements were performed at randomly applied 8, 10 and 12 cm $H_2O$ PEEP before and 30 mins after administrating salbutamol using a meter-dose-inhaler (100ug${\times}$6). Results : 1) The maximum inspiratory resistance of the lung was higher than the reported normal values due to an increase in the minimal inspiratory resistance & additional resistance. 2) The maximum inspiratory resistance and peak airway pressure were significantly higher at 12cm $H_2O$ of PEEP compared with those at 10cm $H_2O$ of PEEP. 3) Salbutamol induced a significant decrease in the maximum and the minimum inspiratory resistance but no significant change in the additional resistance only was observed at 12cm $H_2O$ of PEEP(from $15.66{\pm}1.99$ to $13.54{\pm}2.41$, from $10.24{\pm}2.98$ to $8.04{\pm}2.34$, and from $5.42{\pm}3.41$ to $5.50{\pm}3.58cm$$H_2O$/L/sec, respectively). 4)The lung compliance did not change at the applied PEEP and salbutamol inhalation levels. Conclusion : The bronchodilator response would be different depending on the level of applied PEEP despite the increased respiratory resistance in patients with ARDS.
Background: The opitmal ventilator setting during partial liquid ventilation(PLV) is controversial. This study investigated the effects of various gas exchange parameters during PLV in normal rabbit lungs in order to aid in the development of an optimal ventilator setting during PLV. Methods: Seven New-Zealand white rabbits were ventilated in pressure-controlled mode with the following settings; tidal volume($V_T$) 8 mL/kg, positive end-expiratory pressure(PEEP) 4 $cmH_2O$, inspiratory-to-expiratory ratio(I:E ratio) 1:2, fraction of inspired oxygen($F_TO_2$) 1.0. The respiration rate(RR) was adjusted to keep $PaCO_2$ between 35~45 mmHg. The ventilator settings were changed every 30 min in the following sequence : (1) Baseline, as the basal ventilator setting, (2) Inverse ratio, I:E ratio 2:1, (3) high PEEP, adjust PEEP to achieve the same mean inspiratory pressure (MIP) as in the inverse ratio, (4) High $V_T$, $V_T$ 15 mL/kg, (5) high RR, the same minute ventilation (MV) as in the High $V_T$. Subsequently, the same protocol was repeated after instilling 18 mL/kg of perfluorodecalin for PLV. The parameters of gas exchange, lung mechanics, and hemodynamics were examined. Results: (1) The gas ventilation(GV) group showed no significant changes in the $PaO_2$ at all phases. The $PaCO_2$ was lower and the pH was higher at the high $V_T$ and high RR phases(p<0.05). No significant changes in the lung mechanics and hemodynamics parameters were observed. (2) The baseline $PaO_2$ for the PLV was $312{\pm}$ mmHg. This was significantly lower when decreased compared to the baseline $PaO_2$ for GV which was $504{\pm}81$ mmHg(p=0.001). During PLV, the $PaO_2$, was significantly higher at the high PEEP($452{\pm}38$ mmHg) and high $V_T$ ($461{\pm}53$ mmHg) phases compared with the baseline phase. However, it did not change significantly during the inverse I:E ratio or the high RR phases. (3) The $PaCO_2$ was significantly lower at high $V_T$ and RR phases for both the GV and PLV. During the PLV, $PaCO_2$ were significantly higher compared to the GV (p<0.05). (4) There were no important or significant changes in of baseline and high RR phases lung mechanics and hemodynamics parameters during the PLV. Conclusion: During PLV in the normal lung, adequate $V_T$ and PEEP are important for optimal oxygenation.
Pyun, Yu Jang;Suh, Gee Young;Koh, Won-Jung;Yu, Chang-Min;Jeon, Kyeongman;Jeon, Ik Soo;Ham, Hyoung Suk;Kang, Eun Hae;Chung, Man Pyo;Kim, Hojoong;Kown, O Jung
Tuberculosis and Respiratory Diseases
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v.56
no.5
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pp.523-531
/
2004
Background : Bronchoscopy in patients on mechanical ventilation is being performed much more frequently. However, there is little data on the changes in physiologic parameters and no established mechanical ventilation protocol during bronchoscopy. A decreasing or the removal of positive end-expiratory pressure (PEEP) during bronchoscopy may precipitate severe hypoxemia and/or derecruitment. Methods : Our standardized mechanical ventilation protocol, without changing the PEEP level, was used during bronchoscopy. The physiological parameters were measured during the bronchoscopic procedure. Results : During bronchoscopy, respiratory acidosis, elevation of peak pressure, elevation of heart rate and auto-PEEP were developed, but were reversible changes. Procedure-related gross barotraumas or other severe complications did not developed. Conclusion : No serious complications developed during bronchoscopy under our standardized mechanical ventilation protocol when the PEEP level remained unchanged. The procedure time should be kept to a minimum to decrease the exposure time to undesirable physiological changes.
Background : Many inflammatory mediators and collagenases are involved in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The increase of matrix metalloproteinase-9 (MMP-9, gelatinase-B) produced mainly by inflammatory cells was reported in many ALI models and connective tissue cells. In this study, the expression of MMP-9 in ventilator-induced lung injury (VILI) model and the effects of matrix metalloproteinase inhibitor (MMPI) on VILI were investigated. Methods : Eighteen Sprague-Dawley rats were divided into three groups: low tidal Volume (LVT, 7mL/Kg tidal volume, 3 $cmH_2O$ PEEP, 40/min), high tidal volume (HVT, 30mL/Kg tidal volume, no PEEP, 40/min) and high tidal volume with MMPI (HVT+MMPI) groups. Mechanical ventilation was performed in room air for 2 hours. The 20 mg/Kg of CMT-3 (chemically modified tetracycline-3, 6-demethyl 6-deoxy 4-dedimethylamino tetracycline) was gavaged as MMPI from three days before mechanical ventilation. The degree of lung injury was measured with wet-to-dry weight ratio and acute lung injury score. Expression of MMP-9 was studied by immunohistochemical stain with a mouse monoclonal anti-rat MMP-9 $IgG_1$. Results : In the LVT, HVT and HVT+MMPI groups, the wet-to-dry weight ratio was $4.70{\pm}0.14$, $6.82{\pm}1.28$ and $4.92{\pm}0.98$, respectively. In the HVT group, the ratio was significantly higher than other groups (p<0.05). Acute lung injury score measured by five-point scale was $3.25{\pm}1.17$, $12.83{\pm}1.17$ and $4.67{\pm}0.52$, respectively. The HVT group was significantly damaged by VILI and MMPI protects injuries by mechanical ventilation (p<0.05). Expression of MMP-9 measured by four-point scale was $3.33{\pm}2.07$, $12.17{\pm}2.79$ and $3.60{\pm}1.95$, respectively, which were significantly higher in the HVT group (p<0.05). Conclusion : VILI increases significantly the expression of MMP-9 and MMPI prevents lung injury induced by mechanical ventilation through the inhibition of MMP-9.
Jeon, Ik Soo;Suh, Gee Young;Koh, Won-Jung;Pyun, Yu Jang;Kang, Eun Hae;Ham, Hyoung Suk;Oui, Misook;Chung, Man Pyo;Kim, Hojoong;Kwon, O Jung
Tuberculosis and Respiratory Diseases
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v.54
no.4
/
pp.429-438
/
2003
Background : The mortality from acute respiratory distress syndrome(ARDS) is >40-50%. Although some prospective trials have failed to demonstrate a survival benefit of steroids in the early stages of ARDS, there are some reports showing some success with steroids in the later stages. This study observed the changes in the physiologic parameters with time in late ARDS patients who were treated with steroids. Methods : The medical charts of 28 intensive care unit patients(male:female=24:4; mean age 64 years), who had been diagnosed with refractory late ARDS ($PaO_2/FIO_2$ <200) and were treated with corticosteroids from December 1999 to July 2002, were retrospectively reviewed. The patients were divided into two groups: the weaned group(n=14), which included the patients who had been successfully weaned from a ventilator after corticosteroid therapy, and the failed group(n=14), which included the patients who had failed weaning. The physiologic parameters included the $PaO_2/FIO_2$ ratio, the positive end-expiratory pressure(PEEP) level, the $PaCO_2$, compliance, the sequential organ failure assessment(SOFA) score, the acute physiologic and the chronic health evaluation(APACHE) II score, and the Murray Lung Injury Score(LIS) in the two groups were compared from the day of mechanical ventilation(Dmv) to 7 days after the corticosteroid therapy. Results : There was no significant difference in the clinical characteristics and the physiologic parameters between the two groups prior to the corticosteroid therapy except for the SOFA score at Dmv(weaned group : $6.6{\pm}2.5$ vs failed group : $8.8{\pm}2.9$, p=0.047). However, within 7 days after corticosteroid therapy, there was significant improvement in the $PaO_2/FIO_2$ ratio, the PEEP level, the $PaCO_2$, the SOFA score, the APACHE II score, and the LIS of the weaned group compared to the failed group. Conclusions : During corticosteroid therapy in late ARDS, the continuation of corticosteroid therapy should be determined carefully in patients who do not show improvement in their physiologic parameters by day 7.
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