Background : Mechanical ventilation constitutes the last therapeutic method for acute respiratory failure when oxygen therapy and medical treatment fail to improve the respiratory status of the patient. This invasive ventilation, classically administered by endotracheal intubation or by tracheostomy, is associated with significant mortality and morbidity. Consequently, any less invasive method able to avoid the use of endotracheal ventilation would appear to be useful in high risk patient. Over recent years, the efficacy of nasal mask ventilation has been demonstrated in the treatment of chronic restrictive respiratory failure, particularly in patients with neuromuscular diseases. More recently, this method has been successfully used in the treatment of acute respiratory failure due to parenchymal disease. Method : We assessed the efficacy of Bilevel positive airway pressure(BiPAP) in the treatment of acute exacerbation of chronic obstructive pulmonary disease(COPD). This study prospectively evaluated the clinical effectiveness of a treatment schedule with positive pressure ventilation via nasal mask(Respironics BiPAP device) in 22 patients with acute exacerbations of COPD. Eleven patients with acute exacerbations of COPD were treated with nasal pressure support ventilation delivered via a nasal ventilatory support system plus standard treatment for 3 consecutive days. An additional 11 control patients were treated only with standard treatment. The standard treatment consisted of medical and oxygen therapy. The nasal BiPAP was delivered by a pressure support ventilator in spontaneous timed mode and at an inspiratory positive airway pressure $6-8cmH_2O$ and an expiratory positive airway pressure $3-4cmH_2O$. Patients were evaluated with physical examination(respiratory rate), modified Borg scale and arterial blood gas before and after the acute therapeutic intervention. Results : Pretreatment and after 3 days of treatment, mean $PaO_2$ was 56.3mmHg and 79.1mmHg (p<0.05) in BiPAP group and 56.9mmHg and 70.2mmHg (p<0.05) in conventional treatment (CT) group and $PaCO_2$ was 63.9mmHg and 56.9mmHg (p<0.05) in BiPAP group and 53mmHg and 52.8mmHg in CT group respectively. pH was 7.36 and 7.41 (p<0.05) in BiPAP group and 7.37 and 7.38 in cr group respectively. Pretreatment and after treatment, mean respiratory rate was 28 and 23 beats/min in BiPAP group and 25 and 20 beats/min in CT group respectively. Borg scale was 7.6 and 4.7 in BiPAP group and 6.4 and 3.8 in CT group respectively. There were significant differences between the two groups in changes of mean $PaO_2$, $PaCO_2$ and pH respectively. Conclusion: We conclude that short-term nasal pressure-support ventilation delivered via nasal BiPAP in the treatment of acute exacerbation of COPD, is an efficient mode of assisted ventilation for improving blood gas values and dyspnea sensation and may reduce the need for endotracheal intubation with mechanical ventilation.
Background : Pressure-controlled ventilation (PCV) is frequently used recently as the initial mode of mechanical ventilation in the patients with respiratory failure. Theoretically, because of its high initial inspiratory flow, pressure-controlled ventilation has lower peak inspiratory pressure and improved gas exchange than volume-controlled ventilation (VCV). But the data from previous studies showed controversial results about the gas exchange. Moreover, the comparison study between PCV and VCV with various inspiration : expiration time ratios (I : E ratios) is rare. So this study was performed to compare the respiratory mechanics and gas exchange between PCV and VCV with various I : E raitos. Methods : Nine patients receiving mechanical ventilation for respiratory failure were enrolled. They were ventilated by both PCV and VCV with various I : E ratios (1 : 2, 1 : 1.3 and 1.7 : 1). $FiO_2$, tidal volume, respiratory rate and external positive end-expiratory pressure (PEEP) were kept constant throughout the study. After 20 minutes of each ventilation mode, arterial blood gas, airway pressures, expired $CO_2$ were measured. Results : In both PCV and VCV, as the I : E ratio increased, the mean airway pressure was increased, and $PaCO_2$ and physiologic dead space fraction were decreased. But P(A-a)$O_2$ was not changed. In all three different I : E ratios, peak inspiratory pressure was lower during PCV, and mean airway pressure was higher during PCV. But $PaCO_2$ level, physiologic dead space fraction and P(A-a)$O_2$ were not different between PCV and VCV with three different I : E ratios. Conclusion : There was no difference in gas exchange between PCV and VCV under the same tidal volume, frequency and I : E ratio.
Background: Bronchial asthma is characterized by noctunal dyspnea, cough and wheezing because of airway hyperresponsiveness to nonspecific stimuli. These symptoms and signs are also observed in patients with congestive heart failure. Therefore, this is so called "cardiac asthma". There are lots of experimental and clinical datas to suggest that airway dysfunctions occur in acute and chronic congestive heart failure. However, it is still controversial whether bronchial hyperresponsiveness is present in patients with congestive heart failure. To assess whether bronchial hyperresponsiveness is present in patients with congestive heart failure and to demonstrate the relationship between bronchial responsiveness and vascular pressure, we performed methacholine provocation test in 11 patients with mitral valvular heart disease. Methods: All patients were in the New York Heart Association functional class II and treated continuously with digoxin and/or dichlozid and/or angiotensin converting enzyme inhibitor except one patient. All patients were undergone right and left side heart catheterization for hemodynamic measurements. A 20 percent fall of peak expiratory flow rate were considered as positive response to methacholine provocation test. Results: 1) Only one patient who has normal pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index was positive in methacholine provocation test. 2) Their mean pulmonary artery pressure, pulmonary capillary wedge pressure were $21.72{\pm}9.70mmHg$, $15.45{\pm}8.69mmHg$ respectively which were significantly higher. Conclusion: It is speculated that in stable congestive heart failure patients, bronchial responsiveness as assessed by methacholine provocation test may not be increased.
Background: Positive end, expiratory pressure (PEEP) has become one of the standard therapies for adult respiratory distress syndrome (ARDS). Total static compliance has been proposed as a guide to determine the size of PEEP ('best PEEP') which is of unproven clinical benefit and remains controversial. Besides increasing functional residual capacity and thus improving oxygenation, PEEP stimulate prostacyclin secretion and was proposed for the treatment of acute pulmonary embolism. But little is known about the effect of PEEP on hemodynamic and gas exchange disturbances in acute pulmonary embolism. Methods: To study the validity of total static compliance as a predictor of 'best PEEP' in ARDS and acute pulmonary embolism, experimental ARDS was induced in mongrel dog with oleic acid and acute pulmonary embolism with autologous blood clot. Then hemodynamic and gas exchange parameters were measured with serial increment of PEEP. Results:In ARDS group, total static compliance and oxygen transport were maximal at 5 cm$H_2O$, and decreased thereafter (p<0.05). With increment of PEEP, arterial oxygen tension ($PaO_2$) and arterial carbon dioxide tension ($PaCO_2$) increased and cardiac output and physiological shunt decreased. In pulmonary embolism group, total static compliance, oxygen transport, physiological shunt and cardiac output decreased and $PaO_2$ and $PaCO_2$ increased with increment of PEEP (p<0.05). Comparing the change induced by increment of PEEP by 1 cm$H_2O$ in ARDS group with that in pulmonary embolism group, there was no significant difference between two groups except cardiac output which decreased more in pulmonary embolism group (p<0.05). In ARDS group, oxygen transport and total static compliance increased after PEEP application, and total static compliance was maximal at the PEEP level where oxygen transport was maximal. However in pulmonary embolism group, oxygen transport and total static compliance decreased after application of PEEP. There was significant correlation between change of total static compliance and change of oxygen transport in both groups. Conclusion: In both ARDS and acute pulmonary embolism, it can be concluded that total static compliance is useful as a predictor of 'best PEEP'.
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.
Cho, Young-Jae;Moon, Jae Young;Shin, Ein-Soon;Kim, Je Hyeong;Jung, Hoon;Park, So Young;Kim, Ho Cheol;Sim, Yun Su;Rhee, Chin Kook;Lim, Jaemin;Lee, Seok Jeong;Lee, Won-Yeon;Lee, Hyun Jeong;Kwak, Sang Hyun;Kang, Eun Kyeong;Chung, Kyung Soo;Choi, Won-Il
Tuberculosis and Respiratory Diseases
/
v.79
no.4
/
pp.214-233
/
2016
There is no well-stated practical guideline for mechanically ventilated patients with or without acute respiratory distress syndrome (ARDS). We generate strong (1) and weak (2) grade of recommendations based on high (A), moderate (B) and low (C) grade in the quality of evidence. In patients with ARDS, we recommend low tidal volume ventilation (1A) and prone position if it is not contraindicated (1B) to reduce their mortality. However, we did not support high-frequency oscillatory ventilation (1B) and inhaled nitric oxide (1A) as a standard treatment. We also suggest high positive end-expiratory pressure (2B), extracorporeal membrane oxygenation as a rescue therapy (2C), and neuromuscular blockage for 48 hours after starting mechanical ventilation (2B). The application of recruitment maneuver may reduce mortality (2B), however, the use of systemic steroids cannot reduce mortality (2B). In mechanically ventilated patients, we recommend light sedation (1B) and low tidal volume even without ARDS (1B) and suggest lung protective ventilation strategy during the operation to lower the incidence of lung complications including ARDS (2B). Early tracheostomy in mechanically ventilated patients can be performed only in limited patients (2A). In conclusion, of 12 recommendations, nine were in the management of ARDS, and three for mechanically ventilated patients.
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.
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.
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.
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