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Low-intensity noninvasive ventilation: Lower pressure, more exacerbations of chronic respiratory failure
In recent years, we have seen an increasing use of noninvasive ventilation (NIV) in the context of acute respiratory insufficiency (acute respiratory failure). However, adherence to treatment is not perfect; partly because of patient's complaints relating to high-pressure levels. This led to envisaging if the use of lower ventilatory pressures could lead to the same clinical results of the higher pressures, on patients with the restrictive pulmonary disease.
Background
We aimed to evaluate the ICU management and long-term outcomes of kyphoscoliosis patients with respiratory failure.
Methods
A retrospective observational cohort study was performed in a respiratory ICU and outpatient clinic from 2002–2011. We enrolled all kyphoscoliosis patients admitted to the ICU and followed-up at regular intervals after discharge. Reasons for acute respiratory failure (ARF), ICU data, mortality, length of ICU stay and outpatient clinic data, non-invasive ventilation (NIV) device settings, and compliance were recorded. NIV failure in the ICU and the long term effect of NIV on pulmonary performance were analyzed.
Results
Sixty-two consecutive ICU kyphoscoliosis patients with ARF were enrolled in the study. NIV was initially applied to 55 patients, 11 (20%) patients were intubated, and the majority had sepsis and septic shock (p < 0.001). Mortality in the ICU was 14.5% (n = 9), reduced pH, IMV, and sepsis/septic shock were significantly higher in the non-survivors (p values 0.02, 0.02, 0.028, 0.012 respectively). Among 46 patients attending the outpatient clinic, 17 were lost to follow up and six were died. The six minute walk distance was significantly increased in the final follow up (306 m versus 419 m, p < 0.001).
Conclusions
We strongly discourage the use of NIV in the case of septic shock in ICU kyphoscoliosis patients with ARF. Pulmonary performance improved with NIV during long term follow up.
Nasal intermittent positive pressure ventilation (NIPPV) is a new technique which has rapidly supplanted other non-invasive methods of ventilation over the last 5-10 years. Data on its effectiveness are limited.
The outcome of long term domiciliary NIPPV has been analysed in 180 patients with hypercapnic respiratory failure predominantly due to chest wall restriction, neuromuscular disorders, or chronic obstructive lung disease. One hundred and thirty eight patients were started on NIPPV electively, and 42 following an acute hypercapnic exacerbation. Outcome measures were survival (five year probability of continuing NIPPV), pulmonary function, and health status. A crossover study from negative pressure ventilation to NIPPV was carried out in a subgroup of patients.
Five year acturial probability of continuing NIPPV for individuals with early onset scoliosis (n = 47), previous poliomyelitis (n = 30), following tuberculous lung disease (n = 20), general neuromuscular disorders (n = 29), and chronic obstructive pulmonary disease (n = 33) was 79% (95% CI 66 to 92), 100%, 94% (95% CI 83 to 100), 81% (95% CI 61 to 100), 43% (95% CI 6 to 80), respectively. Most of the patients with bronchiectasis died within two years. One year after starting NIPPV electively the mean (SD) PaO2 compared with the pretreatment value was +1.8 (1.9) kPa, mean PaCO2 -1.4 (1.3) kPa in patients with extrapulmonary restrictive disorders, and PaO2 +0.8 (1.0) kPa, PaCO2 -0.9 (0.8) kPa in patients with obstructive lung disease. Arterial blood gas tensions improved in patients transferred from negative pressure ventilation to NIPPV. Health status was ranked highest in patients with early onset scoliosis, previous poliomyelitis, and following tuberculous lung disease. In the group as a whole health perception was comparable to outpatients with other chronic disorders.
The long term outcome of domiciliary NIPPV in patients with chronic respiratory failure due to scoliosis, previous poliomyelitis, and chest wall and pulmonary disease secondary to tuberculosis is encouraging. The results of NIPPV in patients with COPD and progressive neuromuscular disorders show benefit in some subgroups. The outcome in end stage bronchiectasis is poor.
Use of NPPV has rapidly proliferated during the past decade. Previously, body ventilators such as negative pressure devices were the main noninvasive means of assisting ventilation. After the introduction of the nasal mask to treat obstructive sleep apnea during the mid-1980s and the subsequent development of nasal ventilation, NPPV became the ventilator mode of first choice to treat patients with chronic respiratory failure. More recently, NPPV has been attaining acceptance for certain indications in the acute setting, as well. On the basis of controlled trials demonstrating marked reductions in intubation rates as well as improvements in morbidity, mortality, and complication rates, NPPV is now considered the ventilatory mode of first choice in selected patients with COPD exacerbations. The indications for NPPV are not as clear in patients with non-COPD causes of acute respiratory failure. For acute pulmonary edema, CPAP alone drastically reduces the need for intubation, although studies have not demonstrated reductions in morbidity or mortality rates. NPPV avoids intubation and reduces complication rates in patients with hypoxemic respiratory failure, but more controlled trials are needed to establish precise indications. In the meantime, NPPV administration to patients with non-COPD causes of acute respiratory failure appears to be safe as long as patients are selected carefully with particular attention to the exclusion of inappropriate candidates. A possible role is also emerging for NPPV in the facilitation of weaning patients from invasive mechanical ventilation. In this context, noninvasive ventilation can be used to permit earlier removal of invasive airways than would otherwise be the case, to prevent reintubation in patients developing post-extubation respiratory failure, and to serve a prophylactic role in postoperative patients who are at high risk for pulmonary complications. For chronic respiratory failure, a wide consensus now favors the use of NPPV as the ventilatory mode of first choice for patients with neuromuscular diseases and chest wall deformities, despite a lack of randomized controlled trials. Central hypoventilation and failure of obstructive sleep apnea to respond to CPAP are also considered acceptable indications, although evidence to support these latter applications is sparse. For patients with severe stable COPD, some evidence supports the use of NPPV in severely hypercapnic patients, particularly if there is associated nocturnal hypoventilation. However, the data are conflicting and do not permit the formulation of firm selection guidelines. NPPV has emerged as the noninvasive ventilation mode of first choice over alternatives such as negative pressure ventilation or abdominal displacement ventilators. However, these latter techniques are still used in some areas of the world and may be effective for patients who fail NPPV because of mask intolerance. Noninvasive ventilation has undergone a remarkable evolution over the past decade and is assuming an important role in the management of both acute and chronic respiratory failure. Appropriate use of noninvasive ventilation can be expected to enhance patient comfort, improve patient outcomes, and increase the efficiency of health care resource utilization. Over the next decade, continued advances in technology should make noninvasive ventilation even more acceptable to patients. Future studies should better define indications and patient selection criteria, further evaluate efficacy and effects on resource utilization, and establish optimal techniques of administration.
Patients with kyposcoliosis and chronic respiratory insufficiency are treated either with home oxygen therapy or ventilation. Kyphoscoliotic patients demonstrate impaired ventilatory mechanics, consequently ventilation seems to be the treatment of choice. Yet, no randomised controlled trials (CRT) exist to prove it. Most investigators find it difficult to ethically justify a CRT. Therefore, the current authors performed the following retrospective study: survival and pulmonary function were analysed in all consecutive kyphoscoliotic patients who started long-term oxygen therapy (LTO group; n=15, aged 62+/-11 yrs (mean+/-SD)) or LTO plus nocturnal nasal intermittent positive pressure ventilation (nNIPPV group; n=18, aged 61+/-7 yrs) in the Dept of Pulmonology (University Hospital Gasthuisberg, Leuven) between 1990-2002. Prior to treatment partial pressure of oxygen (PO2) was lower, partial pressure of carbon dioxide (PCO2) tended to be higher and vital capacity (VC) tended to be lower in the nNIPPV group than in the LTO group (PO2 5.9+/-1 versus 6.7+/-0.9 kPa (44+/-8 versus 50+/-7 mmHg), PCO2 8+/-1 versus 7.3+/-0.9 kPa (60+/-8 versus 55+/-7 mmHg), VC 32+/-12 versus 40+/-16% predicted, or 645+/-244 versus 970+/-387 mL). In the nNIPPV group the 1-yr survival was higher (100% versus 66%). nNIPPV patients demonstrated an improvement in PO2 (breathing air) +54%, PCO2 (breathing air) -21%, VC +47% and maximal static inspiratory mouth pressure +33%; these improvements were absent in the LTO group. In conclusion, nocturnal nasal intermittent positive pressure ventilation, plus long-term oxygen therapy results in more favourable survival and changes in blood gases and respiratory function than long-term oxygen therapy alone.
Background:
The significance of changes in P(aCO2) during long-term noninvasive ventilation (NIV) on prognosis remains unclear. We aimed to clarify whether stabilizing P(aCO2) during NIV had a favorable prognostic effect.
Methods:
Data from 190 subjects with restrictive thoracic disease and who received long-term NIV were studied retrospectively. The annual change in P(aCO2) during NIV was determined using a simple linear regression method for each subject who had at least 4 6-month intervals of P(aCO2) data. Annual changes in P(aCO2) during long-term NIV and possible confounders were analyzed with discontinuation of long-term NIV as the main outcome.
Results:
One hundred and twenty-five subjects who had > 4 6-month intervals of P(aCO2) data were included in the study. P(aCO2) during long-term NIV decreased in 41 subjects (group 1; < 0 mm Hg/y), increased slightly in 42 subjects (group 2; between 0 and 1.85 mm Hg/y), and increased significantly in 42 subjects (group 3; > 1.85 mm Hg/y). Smaller annual changes in P(aCO2) (P < .001) and a control ventilator mode (P = .008) were associated with a significantly higher probability of continuing NIV, compared with decreased P(aCO2) 3-6 months after the start of long-term NIV (P = .11). The 10-y probability of continuing NIV was 69% in group 1, 39% in group 2, and 12% in group 3.
Conclusions:
A decrease in the annual change of P(aCO2) during long-term NIV was shown to be a significantly prognostically favorable factor. Efforts to reduce P(aCO2) should be made if P(aCO2) increases at a greater rate during long-term NIV.
The case of 57-year-old man with chronic ventilatory insufficiency due to asbestos pleurisy and sequelae of pulmonary tuberculosis is described. Non-invasive positive pressure ventilation therapy appeared to improve the pulmonary hypertension. Ultrasonic cardiography was valuable in the serial assessment of pulmonary artery pressure.
The long-term evolution of patients with chest wall disease and chronic respiratory failure treated with noninvasive home mechanical ventilation (NIHMV) is poorly known.
The aim of this prospective observational study was to analyze the variables associated with mortality in a cohort of chest wall disease patients with chronic respiratory failure undergoing long-term follow-up after starting treatment with NIHMV.
Chest wall disease patients who began NIHMV between 1996 and 2005 were followed up, with death as the primary outcome. The patients' clinical characteristics, lung function, and arterial blood gases were recorded at the start of treatment. Patients were seen and evaluated 1 month after starting NIHMV. The prognostic value of clinical and functional variables were assessed by Cox regression analyses.
We included 110 patients, 61 with tuberculosis sequelae and 49 with kyphoscoliosis. By the end of follow-up, 34 patients (28%) had died. The 5-year survival was 69% in those with tuberculosis sequelae and 75% in kyphoscoliosis. PaCO(2) ≥50 mmHg at 1 month of home ventilation and comorbidity (Charlson Index ≥3) were independent predictors of mortality.
Our results suggest that PaCO2 levels ≥50 mmHg at 1 month after starting noninvasive home mechanical ventilation and the presence of comorbid conditions are risk factors for mortality in patients with chest wall disease. The importance of early detection of suboptimal home ventilation as well as comorbidities is highlighted.
The level at which arterial carbon dioxide tension (PaCO(2)) a few months after introduction of long-term non-invasive positive pressure ventilation (NPPV) is associated with a favorable prognosis remains uncertain.
Data on 184 post-tuberculosis patients with chronic restrictive ventilatory failure who were receiving long-term domiciliary NPPV were examined retrospectively. Average PaCO(2) 3-6 months after NPPV (3- to 6-mo PaCO(2)) and potential confounders were analyzed with discontinuation of long-term NPPV as the primary outcome. The effects of 3- to 6-mo PaCO(2) on annual hospitalization rates due to respiratory deterioration from 1 year before to 3 years after the initiation of NPPV were examined. The effect of the difference between the PaCO(2) value at the start of NPPV (0-mo PaCO(2)) and the PaCO(2) value 3- to 6-mo later (d-PaCO(2)) on continuation rates for NPPV was also assessed in patients who initiated NPPV while in a chronic state.
Patients with relatively low 3- to 6-mo PaCO(2) values maintained a relatively low PaCO(2) 6-36 months after NPPV (p < 0.0001) and had significantly better continuation rates (p < 0.03) and lower hospitalization rates from the 1st to 3rd year of NPPV (p = 0.008, 0.049, 0.009, respectively) than those with higher levels. The 0-mo PaCO(2) (p = 0.26) or d-PaCO(2) (p = 0.86) had no predictive value.
A relatively low 3- to 6-mo PaCO(2) value was predictive of long-term use of NPPV. The target values for 3- to 6-mo PaCO(2) may, therefore, be less than 60 mmHg in post-tuberculosis patients, although more studies are needed.
Long-term noninvasive positive pressure ventilation (NPPV) is associated with an excellent survival rate, especially in post-tuberculosis patients. Nothing is currently known on which method of ventilatory support is associated with a better continuation of long-term NPPV, which itself might lead to longer survival.
One hundred and eighty four post-tuberculosis patients, who started NPPV at the Kyoto University Hospital group and the National Tokyo Hospital from June 1990 to August 2007, were examined retrospectively. Ventilator mode (an assisted mode or a pure controlled mode) and potential confounders were examined with the discontinuation of NPPV as the primary outcome.
Patients treated with a pure controlled mode had significantly better continuation rates (hazard ratio, 3.09; 95% confidential interval, 1.75-5.47; p=0.0001) and better survival rates (Log-rank test; p=0.0031) than those treated with an assisted mode. Female gender and no pulmonary lesions were also associated with a significantly better probability of continuing NPPV. The five- and ten-year probabilities of continuing NPPV for 106 patients with a pure controlled mode were 68.3% and 41.4%, respectively, while those for 76 patients with an assisted mode were 46.7% and 12.7%, respectively.
Patients treated with pure controlled ventilation had significantly better continuation rates and survival rates than those treated with assisted ventilation. Prospective randomized controlled trials are needed to verify the effectiveness of a pure controlled mode in patients with not only restrictive thoracic disease but also other diseases including chronic obstructive pulmonary disease.
We tested the efficacy of nocturnal nasal ventilation (NNV) using the BIPAP ventilator in patients with restrictive thoracic diseases by withdrawing them from NNV for an average of 1 wk. One male and five female patients were enrolled in the study; four with restrictive chest wall diseases, and two with muscular dystrophies. All patients had chronic CO2 retention (PaCO2 greater than 50 mm Hg) and had been improved by using NNV for at least 2 months before the study. Four patients were switched to the BIPAP ventilator from standard portable volume ventilators at least 1 month prior to the study without changes in gas exchange or symptoms. After withdrawal of NNV, patients had no deterioration in daytime vital signs, pulmonary functions, maximal inspiratory or expiratory pressures, or arterial blood gases compared with measures made immediately before withdrawal and 1 wk after resumption. However, patients had more dyspnea at rest, increased daytime somnolence, more morning headaches, less daytime energy, and felt less rested in the morning during withdrawal of NNV. Furthermore, nocturnal monitoring demonstrated greater tachycardia, tachypnea, oxygen desaturation, and hypoventilation during withdrawal of NNV. We conclude that NNV administered by the BIPAP ventilator is effective in ameliorating nocturnal hypoventilation and daytime symptoms in patients with chronic CO2 retention caused by severe restrictive thoracic diseases. These data also suggest that the efficacy of NNV may depend more on amelioration of nocturnal hypoventilation than on resting of ventilatory muscles.
Ten patients with respiratory failure and nocturnal hypoventilation were treated for three to nine months by nasal intermittent positive pressure ventilation. Four patients had chronic obstructive lung disease (median FEV1 19% predicted) and six restrictive chest wall disorders (median FVC 25% predicted); eight of the patients also had cardiac failure. The median daytime arterial oxygen tension, measured before and after at least three months' treatment, increased from 6.2 (range 5.4-9.6) to 9.1 (7.1-9.8) kPa in those with restrictive disease (p less than 0.05), and from 6.0 (5.7-6.5) to 7.1 (6.3-7.7) kPa in the four with airflow limitation (NS). Median values for arterial carbon dioxide tension over the same time fell from 8.2 (range 6.7-9.8) to 6.5 (6.0-6.9) kPa in the group with restrictive disease (p less than 0.05) and from 8.2 (7.0-9.2) to 7.1 (4.9-7.7) kPa in those with airflow limitation (p less than 0.02). Total sleep time while patients were using nasal positive pressure ventilation varied from 155 to 379 (median 341) minutes, and included 4-26% rapid eye movement sleep (median 14%). The percentage of monitored time during the night in which the arterial oxygen saturation was less than 80% fell from a median (range) of 96 (3-100) to 4 (0-9) in the six patients with restrictive disease and from 100 (98-100) to 40 (2-51) in those with airflow limitation. There were no changes in spirometric values but exercise tolerance improved in all patients. The technique may prove an acceptable alternative to long term domiciliary oxygen therapy in selected patients.
Nasal intermittent positive pressure ventilation (NIPPV) applied during sleep has been demonstrated to be useful in the treatment of restrictive thoracic diseases (RTD). The purpose of this study was to evaluate the repercussions of a withdrawal period from NIPPV of 15 days. This would be sufficient time for patients to go on trips without the respirator. It was hypothesized that once daytime improvement was achieved and was stable, it could be maintained for this period of time. Five volunteer patients with severe RTD who had been receiving treatment with nocturnal NIPPV for at least 2 months before and who had improved at least 5 mm Hg in daytime PO2 and PCO2 were included in the study. No significant differences were disclosed clinically or with arterial blood gas levels, spirometry results, lung volumes, airway resistances, or maximal muscle pressures 15 days following the withdrawal. However, in the sleep studies, a severe worsening of gas exchange was observed, mainly during rapid eye movement (REM) sleep, as well as a trend toward a more disturbed sleep pattern and more important alterations in cardiac rhythm. Consequently, withdrawing the treatment with nocturnal NIPPV cannot be recommended, at least for this particular removal period. Moreover, alterations in daytime gas exchange were found to originate in those produced during REM sleep through the blunting of the respiratory center to CO2. The NIPPV obstructs this mechanism, preventing the deterioration of gas exchange during sleep.
Prior studies have shown that nasal intermittent positive pressure ventilation (NIPPV) can improve arterial blood gas values, prevent symptoms resulting from alveolar hypoventilation, and decrease hospitalization in patients with chronic respiratory failure. Most studies have involved small samples of patients followed up for a limited time. This study reviews our experience during 5 years use of NIPPV in 276 patients with kyphoscoliosis, posttuberculosis sequelae, Duchenne-type muscular dystrophy, COPD, and bronchiectasis followed up for > or = 3 years while receiving NIPPV. Outcomes were compared for patients who survived short term eg, died or converted to management with a tracheostomy and intermittent positive ventilation (TIPPV) during year 1 or year 2 on a regimen of NIPPV and long term, eg, survived more > or = 2 years on a regimen of NIPPV. The most favorable outcome was achieved by patients with kyphoscoliosis and posttuberculosis sequelae with improvement in PaO2 and PaCO2 (p < 0.0001) and a reduction in days of hospitalization for respiratory illness (p < 0.0001) for > or = 2 years while receiving NIPPV. Patients with Duchenne-type muscular dystrophy also had fewer hospital days during NIPPV (p < 0.003) but only 9 of 16 patients (56 percent) continued using NIPPV for the duration of followup. Benefit was also more short term for patients with COPD and bronchiectasis. NIPPV can sustain improvement in gas exchange, while reducing hospitalization for substantial periods of time. NIPPV can be an attractive and effective alternative to other methods of assisted ventilation such as TIPPV.
Some patients with chest wall diseases (CWD) without respiratory failure manifest important alterations in nocturnal gas exchange, as a previous stage to the future development of daytime respiratory failure. The purpose of this study was to evaluate the efficacy of nasal intermittent positive pressure ventilation (NIPPV) during sleep in a group of obese patients and in another group with restrictive thoracic diseases (RTD), comparing the results with those obtained from conventional nocturnal oxygen therapy. From a total of 42 patients with CWD free of daytime respiratory failure, 27 (64%) were considered nocturnal oxygen desaturators without sleep apnea and were included in the study. The study protocol was completed by 21 of these patients. After 2 weeks of treatment, symptoms of dyspnea, morning headaches, and morning obnubilation improved significantly (p<0.05) in both groups of patients after NIPPV but not with oxygen. Baseline daytime PaO2 was 68+/-7 mm Hg in the obese group of patients and 73+/-11 mm Hg in the RTD group. It improved significantly with NIPPV to 73+/-5 mm Hg in obese patients (p<0.05) and to 77+/-12 mm Hg in the RTD group (p<0.05) but did not change with oxygen (68+/-8 mm Hg in the obese group and 73+/-12 mm Hg in the RTD group). Both treatments improved oxygen saturation during sleep, but oxygenation tends to be higher with oxygen than with NIPPV. Only NIPPV was able to normalize the baseline nocturnal alveolar hypoventilation. From the 21 patients treated, 19 decided to continue with long-term NIPPV, one with oxygen, and one refused treatment. We conclude that in patients with CWD who manifest nighttime oxygen desaturation and hypoventilation, early initiation of NIPPV is preferable to supplemental oxygen. Our results also suggest that NIPPV initiated before overt ventilatory failure could prevent its onset.
Previous studies have shown the acute effects of noninvasive positive pressure ventilation (NPPV) in chronic respiratory failure; however, information on the chronic effects of NPPV is limited. We examined the acute and chronic effects of NPPV on gas exchange, functional status, and respiratory mechanics in patients with chronic respiratory failure related to restrictive ventilatory disorders or COPD.
Descriptive analysis of prospectively collected clinical data.
Inpatient noninvasive respiratory care unit and outpatient clinic of university hospital.
Forty patients with chronic respiratory failure (20 with severe COPD and 20 with restrictive ventilatory disorders).
All patients were admitted to a noninvasive respiratory care unit for 20 +/- 3 days for inpatient evaluation consisting of medical treatment, rehabilitation, and NPPV evaluation and instruction. NPPV was titrated via a ventilatory support system (BiPAP; Respironics Inc; Monroeville, PA) or a portable volume ventilator (PLV 102; Lifecare, Inc; Boulder, CO) to achieve a > or = 20% increase in baseline minute ventilation while monitoring gas exchange, expired volume, and clinical evidence of a decrease in the patient's work of breathing.
The patients' mean age (+/- SD) was 65 +/- 9.7 years, and there was a 3:1 female:male predominance. In the noninvasive respiratory care unit, 36 patients used NPPV for 7.31 +/- 0.26 h/night. Four patients (three with COPD, one with restrictive disorder) withdrew from the study during the 3-week inpatient stay because they could not tolerate NPPV. Six patients (5 with COPD, 1 with restrictive disorder) used a portable volume ventilator and 34 patients used BiPAP (15 with COPD, 19 with restrictive disorders). At discharge, compared with at admission, daytime PaO2/fraction of inspired oxygen (FIO2) increased (327 +/- 10 vs 283 +/- 13 mm Hg; p = 0.01), PaCO2 was reduced (52 +/- 2 vs 67 +/- 3 mm Hg; p = 0.0001), and functional score increased (4.76 +/- 1.16 vs 2.7 +/- 1.64 arbitrary units (AUs); p < 0.01). Six months after discharge, improvements in PaO2/FIO2 (317 +/- 10 vs 283 +/- 13; p = 0.05), PaCO2 (52 +/- 2 vs 67 +/- 3 mm Hg; p = 0.0001), and functional score (5.66 +/- 0.41 vs 2.7 +/- 0.3 AUs; p < 0.001) were maintained compared with admission values. FVC, FEV1, and maximum inspired and expired mouth pressures were unchanged before and after long-term NPPV. Ten patients (7 with COPD, 3 with restrictive disorders) discontinued NPPV at 6 months, and 3 progressed to tracheostomy. The remaining 26 patients continued to use NPPV at the 6-month follow-up. They claimed to use NPPV for 7.23 +/- 0.24 h/night, but logged metered use was 4.5 +/- 0.58 h/night. Problems that required adjustment in either the mask (36%) or ventilator source (36%) included mask leaks (43%), skin irritation (22%), rhinitis (13%), aerophagia (13%), and discomfort from mask headgear (7%).
NPPV acutely and chronically improves gas exchange and functional status in patients with chronic respiratory failure, but a significant number of patients do not tolerate NPPV on a chronic basis. Comprehensive follow-up is required to correct problems with NPPV and ensure optimal patient compliance.
To determine the effects of long-term nocturnal intermittent positive-pressure ventilation (NIPPV) on symptoms, pulmonary function test results, sleep, and respiratory muscle performance in patients with ventilatory insufficiency due to severe kyphoscoliosis.
A prospective study in which 16 severe kyphoscoliotic patients were treated with NIPPV delivered by volume-cycled and pressure-cycled ventilators, over a period of 36 months.
At baseline, pulmonary function tests, blood gas measurements, polysomnography, and respiratory muscle strength (measured by noninvasive indexes) were obtained. Symptoms and the number of hospitalizations in the previous 6 months also were recorded. Patients then began using a ventilator for > 1 to 2 days, in order to select the type of ventilator and the appropriate interface. Patients returned for evaluation (in outpatient setting) every 6 months for a follow-up period of 3 years. At 6 months, polysomnography was repeated, and by the third year clinical and functional parameters had been reassessed.
All symptoms improved significantly with NIPPV therapy, when compared with the baseline values. The mean (+/- SD) PaO(2) and FVC values increased at 36 months compared with baseline values (62.6 +/- 7.1 vs 67.8 +/- 8.8 mm Hg, respectively; and 37.9 +/- 7.2% vs 47.5 +/- 11.9%, respectively; p < 0.05 for both). There were significant improvements in mean maximal inspiratory pressure (55.8 +/- 17.4 to 78.5 +/- 17.5 cm H(2)O), maximal expiratory pressure (53.8 +/- 17.7 to 72.3 +/- 11.0 cm H(2)O), mouth pressure (0.28 +/- 0.08 to 0.22 +/- 0.02 cmH(2)O), and pressure-time index (0.18 +/- 0.05 to 0.11 +/- 0.02; p < 0.05 for all comparisons). There were no significant differences in breathing pattern and ventilatory drive. After 6 months, nocturnal oxyhemoglobin saturation improved, however, there was no significant change in sleep architecture. All patients subjectively perceived a better quality of life after beginning ventilation, which persisted over the course of the study.
Long-term NIPPV therapy improves daytime blood gas levels, respiratory muscle performance, and hypoventilation-based symptoms in patients with severe kyphoscoliosis.
Non-invasive ventilation (NIV) is widely used for acute and chronic respiratory failure. If arterial blood gas tensions do not improve, the level of support can be increased. However, there may be a limit above which increasing ventilatory support leads only to greater interface leak with no improvement in ventilation. The aim of this study was to establish whether there is such a limit.
During a daytime study in 24 ventilated stable patients (10 with chronic obstructive pulmonary disease (COPD), 14 with chest wall deformity, CWD), inspiratory pressures up to 20cmH2O and set tidal volumes up to 10mlkg⁻¹ were associated with mask leak of <5lmin⁻¹. Although leak increased with higher levels of support, there was still an increase in minute ventilation. The mean (2 sd) tolerated pressure was 24cmH2O (8–40) in both groups, and set tidal volume 12.7mlkg⁻¹ (5.0–20.4) in CWD and 9.6mlkg⁻¹ (3.9–14.8) in COPD. Measures of respiratory effort were significantly reduced at all levels with both forms of ventilatory support.
There is debate about whether the therapeutic aim of NIV should be to reduce respiratory muscle effort, or to reverse nocturnal hypoventilation. We conclude that if the primary aim is to improve arterial blood gas tensions and this is not achieved, higher levels of ventilation can be obtained using greater pressure or volume, despite additional interface leak. If the aim is to abolish muscle effort completely, there is little to be gained by increasing the level of inspiratory pressure above 20 (CWD) or 25 (COPD) cmH2O.
The aim of the study was to evaluate serum uric acid (UA) levels before and after non-invasive positive pressure ventilation (NPPV) to assess the utility of serum UA as an indicator of acute exacerbation of chronic respiratory failure (CRF) in patients treated with NPPV.
We analyzed change in the serum UA level in 29 patients with CRF due to restrictive thoracic disease and treated with NPPV.
After NPPV therapy, PaO2 was significantly increased and PaCO2 was significantly decreased in all patients. Sixty-two percent of patients (18 of 29) showed a decreased serum UA/creatinine (Cr) ratio after NPPV therapy, but, overall, there was no significant change in serum UA/Cr (P=0.0688). The change in serum UA/Cr was not correlated with the changes in PaO2 and PaCO2 after NPPV. When we compared patients in whom serum UA/Cr decreased (n=18) with patients in whom serum UA/Cr did not decrease (n=11), there were significantly fewer patients who suffered CRF exacerbation in the group with a decrease (P=0.0021). Furthermore, the cumulative proportion (Kaplan-Meier) of patients who did not suffer exacerbation of CRF was significantly higher in the group in which serum UA/Cr decreased (P=0.0003).
Our data suggest that serum UA may be a useful clinical indicator of CRF exacerbation in patients treated by NPPV.
Noninvasive Mechanical Ventilation. Philadelphia: Hanley and Belfus
- J R Bach
Bach JR. Noninvasive Mechanical Ventilation. Philadelphia:
Hanley and Belfus; 2002.