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PubMed2003

Initial responses to ventilation of premature lambs exposed to intra-amniotic endotoxin 4 days before delivery.

Preterm delivery is frequently preceded by chorioamnionitis, resulting in exposure of the fetal lung to inflammation. We hypothesized that ventilation of the antenatally inflamed lung would result in amplification of the lung injury. Therefore, we induced fetal lung inflammation with intra-amniotic endotoxin (10 mg of Escherichia coli 055:B5) 4 days before premature delivery at 130 days of gestation. Lung function and lung inflammation after surfactant treatment and 4 h of mechanical ventilation were evaluated. Inflammatory cell numbers in amniotic fluid were increased >10-fold by antenatal endotoxin exposure. Antenatal endotoxin exposure had minimal effects on blood pressure, heart rate, lung compliance, and blood gas values. The endotoxin-exposed lungs required higher ventilation pressures. Ventilation did not increase the number of inflammatory cells or the protein in bronchoalveolar lavage fluid of the endotoxin-exposed animals above that measured in endotoxin-exposed fetuses that were not ventilated. IL-1beta, IL-6, and IL-8 mRNA in cells from bronchoalveolar lavage fluid were increased by antenatal endotoxin exposure but not changed by ventilation. IL-1beta and IL-8 protein was increased in lung tissue by 4 h of ventilation. Very little inflammation was induced by ventilation in this premature lamb model of surfactant treatment and gentle ventilation. After lung inflammation was induced by intra-amniotic endotoxin injection, ventilation did not increase lung injury.

Animals↗
PubMed1989

Regional mapping of gas transport during high-frequency and conventional ventilation.

The effects of changing tidal volume (VT) and frequency (f) on the distribution of ventilation during high-frequency ventilation (HFV) were assessed from the washout of nitrogen-13 by positron emission tomography. Six dogs, anesthetized and paralyzed, were studied in the supine position during conventional ventilation (CV) and during HFV at f of 3, 6, and 9 Hz. In CV and HFV at 6 Hz, VT was selected to achieve eucapnic arterial partial pressure of CO2 (37 +/- 3 Torr). At 3 and 9 Hz, VT was proportionally changed so that the product of VT and f remained constant and equal to that at 6 Hz. Mean residence time (MRT) of nitrogen-13 during washout was calculated for apical, midheart, and basal transverse sections of the lung and further analyzed for gravity-dependent, cephalocaudal and radial gradients. An index of local alveolar ventilation per unit of lung volume, or specific ventilation (spV), was calculated as the reciprocal of MRT. During CV vertical gradients of regional spV were seen in all sections with ventral (nondependent) regions less ventilated than dorsal (dependent) regions. Regional nonuniformity in gas transport was greatest for HFV at 3 and 6 Hz and lowest at 9 Hz and during CV. During HFV, a central region at the base of the lungs was preferentially ventilated, resulting in a regional time-averaged tracer concentration equivalent to that of the main bronchi. Because the main bronchi were certainly receiving fresh gas, the presence of this preferentially ventilated area, whose ventilation increased with VT, strongly supports the hypothesis that direct convection of fresh gas is an important mechanism of gas transport during eucapnic HFV. Aside from the local effect of increasing overall lung ventilation, this central area probably served as an intermediate shuttle station for the transport of gas between mouth and deeper alveoli when VT was less than the anatomic dead space.

Animals↗
PubMed1991

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation.

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

Animals↗
PubMed1985

Effect of rapid-rate ventilation on the experimental diseased lung caused by meconium aspiration.

We compared rapid-rate ventilation using a conventional ventilator with slow-rate ventilation in the normal lung of 7 newborn pigs and in the diseased lung model instilled with 25% meconium solution into the trachea. The flow rate (7.5 1/min) and inspiratory:expiratory ratio (1:3) were kept constant during the experiments by using a constant-flow and time-cycled ventilator; the only change in settings was the rate. Transthoracic electrical impedance at end-expiration increased in the normal and in the diseased lung. Both mean intratracheal pressure and end-expiratory esophageal pressure increased significantly (p less than 0.05) in both models upon changing to rapid-rate ventilation. Following the increase in ventilatory rates from an initial frequency of 37.5 breaths/min to a rapid rate of 150 breaths/min, there was a significant rise in both PaO2 and PaCO2 in the normal and diseased lung models. Although rapid-rate ventilation was maintained for 1 h, the improvement in oxygenation progressively deteriorated and PaCO2 also increased further. This rise in PaCO2 returned to the control levels by decreasing ventilation to the initial rate of 37.5/min. This study demonstrates that rapid-rate ventilation using a constant-flow and time-cycled ventilator is inferior to slow-rate ventilation in the diseased lung model.

Animals↗
PubMed2001

Production of inflammatory cytokines in ventilator-induced lung injury: a reappraisal.

We investigated the production of proinflammatory cytokines by the lung during high mechanical stretch in vivo. To do this, we subjected rats to high-volume (42 ml/kg tidal volume [VT]) ventilation for 2 h. The animals developed severe pulmonary edema and alveolar flooding, with a high protein concentration in bronchoalveolar lavage fluid (BALF). The animals' BALF contained no tumor necrosis factor (TNF)-alpha, negligible amounts of interleukin (IL)-1beta, and less than 300 pg/ml of the chemokine macrophage inflammatory protein (MIP)-2, an amount similar to that found in rats ventilated with 7 ml/kg VT. Systemic cytokine levels were below the detection threshold. Because isolated lungs have been shown to produce high levels of proinflammatory cytokines when ventilated with a similarly high VT for the same duration (Tremblay, et al. J Clin Invest 1997;99:944-952), we reconsidered this specific issue. We ventilated isolated, unperfused rat lungs for 2 h with 7 ml/kg or 42 ml/kg VT, or maintained them in a statically inflated state. Negligible amounts of TNF-alpha were found in the BALF whatever the ventilatory condition applied. The BALF IL-1beta concentration was slightly elevated and higher in lungs ventilated with 42 ml/kg VT than in those ventilated with 7 ml/kg VT or in statically inflated lungs (p < 0.05). The BALF MIP-2 concentration was moderately elevated in all isolated lungs (200 to 300 pg/ml), and was slightly higher (p < 0.05) in lungs ventilated with 42 ml/kg VT. After lipopolysaccharide (LPS) challenge, high levels of TNF-alpha, IL-1beta, and MIP-2 were found in the animals' plasma before the lungs were removed. Negligible amounts of TNF-alpha and IL-1beta were retrieved from the BALF of statically inflated lungs. The concentrations of TNF-alpha and IL-1beta were higher in the BALF of ventilated lungs (p < 0.001). The TNF-alpha level did not differ with the magnitude of VT, whereas the level of IL-1beta was significantly higher in BALF of lungs ventilated with 42 ml/kg VT (p < 0.01). The MIP-2 concentrations were similar for the two ventilatory conditions. These results suggest that ventilation that severely injures lungs does not lead to the release of significant amounts of TNF-alpha or IL-1beta by the lung in the absence of LPS challenge but may increase lung MIP-2 production.

Analysis of Variance↗
PubMed1993

Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation.

Mechanical ventilation with high peak inspiratory pressure and large tidal volume (VT) produces permeability pulmonary edema. Whether it is mean or peak inspiratory pressure (i.e., mean or end-inspiratory volume) that is the major determinant of ventilation-induced lung injury is unsettled. Rats were ventilated with increasing tidal volumes starting from different degrees of FRC that were set by increasing end-expiratory pressure during positive-pressure ventilation. Pulmonary edema was assessed by the measurement of extravascular lung water content. The importance of permeability alterations was evaluated by measurement of dry lung weight and determination of albumin distribution space. Pulmonary edema with permeability alterations occurred regardless of the value of positive end-expiratory pressure (PEEP), provided the increase in VT was large enough. Similarly, edema occurred even during normal VT ventilation provided the increase in PEEP was large enough. Furthermore, moderate increases in VT or PEEP that were innocuous when applied alone, produced edema when combined. The effect of PEEP was not the consequence of raised airway pressure but of the increase in FRC since similar observations were made in animals ventilated with negative inspiratory pressure. However, although permeability alterations were similar, edema was less marked in animals ventilated with PEEP than in those ventilated with zero end-expiratory pressure (ZEEP) with the same end-inspiratory pressure. This "beneficial" effect of PEEP was probably the consequence of hemodynamic alterations. Indeed, infusion of dopamine to correct the drop in systemic arterial pressure that occurred during PEEP ventilation resulted in a significant increase in pulmonary edema. In conclusion, rather than VT or FRC value, the end-inspiratory volume is probably the main determinant of ventilation-induced edema. Hemodynamic status plays an important role in modulating the amount of edema during lung overinflation but does not fundamentally modify the characteristics of this edema which is consistently associated with major permeability alterations. These results may be relevant for ventilatory strategies during acute respiratory failure.

Albumins↗
PubMed1995

Mechanical ventilation with heated humidifiers or heat and moisture exchangers: effects on patient colonization and incidence of nosocomial pneumonia.

The contribution of ventilator circuit bacterial contamination to the occurrence of ventilator-associated pneumonia remains controversial. In a previous study, we found that the incidence of pneumonia was identical with ventilator circuit changes every 48 h and with no ventilator circuit changes. The present study prospectively assessed whether keeping ventilator circuits clean with a heat and moisture exchanger exhibiting antimicrobial barrier properties affects patient colonization and the incidence of nosocomial pneumonia in patients receiving mechanical ventilation for more than 48 h. Consecutive patients were randomly allocated to humidification with either a heat and moisture exchanger (Group 1, n = 61) or a heated humidifier (Group 2, n = 70). In both groups, no circuit changes were performed throughout ventilatory support. Duration of mechanical ventilation was identical in both groups (10 +/- 8.6 d (range: 2 to 47) in Group 1 and 12.5 +/- 14.2 d [range: 2 to 85] in Group 2). The incidence of pneumonia (positive quantitative culture of protected brush specimen) was similar in both groups (6/61 and 8/70 in Groups 1 and 2, respectively; p = 0.8), as was duration of ventilation prior to pneumonia (9 +/- 5.9 versus 8.2 +/- 5.7 d; p = 0.8). Ventilator tubing contamination was considerably reduced with the use of a heat and moisture exchanger. In contrast, bacterial colonization of the pharynx and trachea was identical in both groups. These results suggest that circuit colonization plays little or no role in the occurrence of ventilator-associated pneumonia, provided usual maintenance precautions are applied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

The relationship between frequency of ventilator circuit changes and infectious hazard.

The relationship between frequency of ventilator circuit changes and risk of ventilator-associated pneumonia was studied using 2 independent approaches. The first was an in-use aerosol contamination study with patients on 8-hour, 16-hour, or 24-hour ventilator changing schedules. The second approach was a study comparing the incidence of pneumonia in patients on ventilators for 2 one-year periods when the ventilator circuit changing time differed. In-use aerosol sampling of 513 ventilator treatment periods showed bacterial contamination greater than 100 organisms per aerosol in 1.8 per cent of 8-hour cycles, in 2.5 per cent of 16-hour cycles, and in 5.4 per cent of 24-hour cycles. These differences were not significant. The incidence of ventilator-associated pneumonia was the same for one-year periods when ventilator circuits were changed either every 8 or every 24 hours. It was concluded that changing ventilator circuits every 24 hours provides adequate protection from ventilator-associated pneumonia.

Bacterial Infections↗
PubMed1987

Treatment of respiratory failure during sleep in patients with neuromuscular disease. Positive-pressure ventilation through a nose mask.

Severe nocturnal hypoxemia may occur in patients with respiratory muscle weakness caused by neuromuscular disorders. Negative pressure ventilators may be partially effective in these patients but can cause upper airway obstructive apneas. We examined the effectiveness of positive pressure ventilation through a nose mask in preventing nocturnal hypoxemia and compared it with negative pressure systems. We reasoned that nasal positive pressure would provide stability for the upper airway. Five patients with neuromuscular disorders underwent a series of all-night sleep studies under control conditions, negative pressure ventilation, and positive pressure ventilation through a comfortable nose mask. Sleep staging and respiratory variables were monitored during all studies. Daytime awake lung function, respiratory muscle strength, and arterial blood gases were also measured. The severe hypoxemia and hypercapnia that occurred under control conditions were prevented by positive pressure ventilation through a nose mask. Negative pressure ventilation improved NREM ventilation in all patients, but did not prevent severe oxyhemoglobin desaturation, which occurred during REM sleep. Negative pressure ventilation appears to contribute to upper airways obstruction during REM sleep as evidenced by cessation of air flow, reduced chest wall movements, falls in arterial oxyhemoglobin saturation, and hypercapnia. With treatment, daytime PaO2 improved from a mean of 70 to 83 mm Hg, and PaCO2 decreased from a mean of 61 to 46 mm Hg. We conclude that nasally applied positive pressure ventilation is a highly effective method of providing nocturnal assisted ventilation because it stabilizes the oropharyngeal airway.

Evaluation Studies as Topic↗
PubMed1967

The effect of Pendelluft and dead space on nitrogen clearance: mathematical and experimental models and their application to the study of the distribution of ventilation.

Reinspired mixed dead space gas and Pendelluft may be considered to be part of a single process of interalveolar gas transfer. The effect of interalveolar gas transfer on nitrogen clearance from a two chamber lung model can be described by a single set of equations which hold for synchronous, and series ventilation. Interalveolar gas transfer may theoretically be either bidirectional or unidirectional. Bidirectional transfer results in an underestimation of the effective ventilation and volume of the well-ventilated compartment when nitrogen washout is analyzed by available methods. The volume of the poorly ventilated compartment is overestimated and its effective ventilation is usually overestimated but may be correctly or underestimated as distribution becomes more uneven. Unidirectional transfer has the same qualitative effect except that the ventilation of the poorly ventilated space is always overestimated. The distortions produced by both types of gas transfer become less marked as ventilation becomes more uneven.Nitrogen washout data from a model consisting of two rubber balloons connected with a Y tube agree well with the mathematical predictions. Application of the theory to data obtained from patients with advanced chronic obstructive lung disease suggests that estimates of the functional residual capacity and of the volume and ventilation of the poorly ventilated spaces are not greatly affected by interalveolar gas transfer when nitrogen washout is analyzed by usual methods.

Adult↗
PubMed1982

Studies on the regulation of secretion in Clara cells with evidence for chemical nonautonomic mediation of the secretory response to increased ventilation in rat lungs.

Using electron microscopy and morphometric methods to assess secretion, we previously found that two times tidal volume ventilation of isolated perfused rat lung stimulates secretion by bronchiolar Clara cells; this effect is not prevented by beta-adrenergic blockade (J. Clin. Invest. 1981. 67: 345-351.). In this study we used the isolated perfused rat lung and the anesthetized mechanically ventilated rat, to further study the mechanism by which large tidal volumes stimulate secretion by Clara cells. With the perfused lung we found (a) alpha-adrenergic inhibition did not block the secretory effect of ventilation at two times normal tidal volume; (b) indomethacin completely blocked the secretory action of two times tidal volume ventilation; (c) medium previously used to perfuse lungs ventilated at two times tidal volume, but not medium previously used to ventilate lungs at normal tidal volume, stimulated secretion by Clara cells when used to perfuse fresh lungs ventilated at tidal volume; (d) addition of prostacyclin to the fresh perfusate increased secretion by Clara cells of lungs ventilated at normal tidal volume. In anesthetized mechanically ventilated rats, sighs stimulated secretion by Clara cells; this increased secretion was inhibited by indomethacin but not by cholinergic blockade (bilateral vagotomy). These studies indicate that increased volume ventilation stimulates secretion by Clara cells in vivo and in vitro; they provide evidence that chemical nonadrenergic, noncholinergic mechanisms are involved in this secretion, and that prostaglandins may be the chemical messenger coupling the mechanico-secretory events.

Airway Resistance↗
PubMed2003

Increased ventilation with NiIPPV does not necessarily improve exercise capacity in COPD.

Evidence that noninvasive intermittent positive-pressure ventilation (NiIPPV) improves exercise capacity in chronic obstructive pulmonary disease (COPD) is limited. The effectiveness of different ventilators in this setting has not been studied. Three bilevel pressure support ventilators (Bipap S/T 30, Nippy2 and Vpap II ST), applied via a mouthpiece, were compared during submaximal treadmill exercise in eight subjects with COPD. Subjects walked to exhaustion with each of the ventilators and while breathing through the mouthpiece alone, in random order. In addition, four unencumbered walks were performed. The unencumbered distance (mean +/- SD) walked was 259 +/- 123 m. With the mouth-piece alone this decreased to 211 +/- 96 m and fell further to 145 +/- 76 m with NiIPPV. There was no difference between the brands of ventilator. At the break-point of exercise, significant increases were seen in tidal volume and minute ventilation in the ventilator walks compared with the mouthpiece alone. Noninvasive intermittent positive-pressure ventilation increased ventilation but did not improve exercise capacity in the subjects in this study. No significant differences were seen between the ventilators. The effectiveness of this technique and the optimal method of assistance require further clarification.

Aged↗
PubMed2001

Biphasic positive airway pressure ventilation (PeV+) in children.

BACKGROUND: Biphasic positive airway pressure (BIPAP) (also known as PeV+) is a mode of ventilation with cycling variations between two continuous positive airway pressure levels. In adults this mode of ventilation is effective and is being accepted with a decrease in need for sedatives because of the ability to breathe spontaneously during the entire breathing cycle. We studied the use of BIPAP in infants and children. METHODS: We randomized 18 patients with respiratory failure for ventilation with either BIPAP (n = 11) or assisted spontaneous breathing (ASB) (n = 7) on Evita 4. Lorazepam and, if necessary, morphine were used as sedatives and adjusted in accordance with the Comfort scale. We compared number of randomized mode failure, duration and complications of ventilation and number and dosages of sedatives administered. RESULTS: No differences in patient characteristics, ventilatory parameters, complications of ventilation or use of sedatives were noted. Ten out of eleven patients that we intended to ventilate with BIPAP were successfully ventilated with BIPAP. Four out of seven patients that we intended to ventilate with ASB could not be ventilated adequately with ASB but were successfully crossed over to BIPAP without the need for further sedatives. CONCLUSIONS: BIPAP is an effective, safe and easy to use mode of ventilation in infants and children.

Female↗
PubMed2006

Biological markers of lung injury before and after the institution of positive pressure ventilation in patients with acute lung injury.

BACKGROUND: Several biological markers of lung injury are predictors of morbidity and mortality in patients with acute lung injury (ALI). The low tidal volume lung-protective ventilation strategy is associated with a significant decrease in plasma biomarker levels compared to the high tidal volume ventilation strategy. The primary objective of this study was to test whether the institution of lung-protective positive pressure ventilation in spontaneously ventilating patients with ALI exacerbates pre-existing lung injury by using measurements of biomarkers of lung injury before and after intubation. MATERIALS AND METHODS: A prospective observational cohort study was conducted in the intensive care unit of a tertiary care university hospital. Twenty-five intubated, mechanically ventilated patients with ALI were enrolled. Physiologic data and serum samples were collected within 6 hours before intubation and at two different time points within the first 24 hours after intubation to measure the concentration of interleukin (IL)-6, IL-8, intercellular adhesion molecule 1 (ICAM-1), and von Willebrand factor (vWF). The differences in biomarker levels before and after intubation were analysed using repeated measures analysis of variance and a paired t test with correction for multiple comparisons. RESULTS: Before endotracheal intubation, all of the biological markers (IL-8, IL-6, ICAM-1, and vWF) were elevated in the spontaneously breathing patients with ALI. After intubation and the institution of positive pressure ventilation (tidal volume 7 to 8 ml/kg per ideal body weight), none of the biological markers was significantly increased at either an early (3 +/- 2 hours) or later (21 +/- 5 hours) time point. However, the levels of IL-8 were significantly decreased at the later time point (21 +/- 5 hours) after intubation. During the 24-hour period after intubation, the PaO2/FiO2 (partial pressure of arterial oxygen/fraction of the inspired oxygen) ratio significantly increased and the plateau airway pressure significantly decreased. CONCLUSION: Levels of IL-8, IL-6, vWF, and ICAM-1 are elevated in spontaneously ventilating patients with ALI prior to endotracheal intubation. The institution of a lung-protective ventilation strategy with positive pressure ventilation does not further increase the levels of biological markers of lung injury. The results suggest that the institution of a lung-protective positive pressure ventilation strategy does not worsen the pre-existing lung injury in most patients with ALI.

Adult↗
PubMed1990

Effect of mechanical ventilation and barotrauma on pulmonary clearance of 99mtechnetium diethylenetriamine pentaacetate in lambs.

We studied the effect of positive pressure mechanical ventilation on the pulmonary clearance (k) of 99mtechnetium diethylenetriamine pentaacetate (99mTc-DTPA) in lambs. Twelve lambs were anesthetized and ventilated with air at 25 breaths/min and with end expiratory airway pressure at 2 cm H2O for a minimum period of 8 h. Four lambs received normal pressure ventilation with peak airway pressure at 17 +/- 3 cm H2O and eight received high pressure ventilation with peak airway pressure at 41 +/- 2 cm H2O. Three 99mTc-DTPA clearance studies were done in each lamb; at the start and after 4 and 8 h of mechanical ventilation. All clearance measurements were made at normal peak airway pressure 16 +/- 3 cm H2O. Baseline clearance rate, k, (n = 12) was 1.2 +/- 0.5% (SD). During normal pressure ventilation, k increased from 1.0 +/- 0.5 to 2.2 +/- 0.8% after 4 h and to 2.7 +/- 0.8% after 8 h. During high pressure ventilation, k increased from 1.4 +/- 0.4 to 3.6 +/- 1.3% after 4 h and to 4.8 +/- 1.2% after 8 h. To see if 8 h of mechanical ventilation was associated with other evidence of lung epithelial injury, we determined the movement of I125 labeled albumin from the interstitium into the airspace, lung water content, lung histology, and lung lavage constituents in the lambs at the end of the study. All variables were similar between ventilated and four unventilated lambs, except the percentage of alveolar macrophages recovered by lavage, which was more in the ventilated lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Survival following mechanical ventilation for acute respiratory failure in adult men.

STUDY DESIGN: Survival following mechanical ventilation for acute respiratory failure has important implications for medical decision-making and allocation of expensive resources for critical care. PROCEDURE: We reviewed a 5-year experience with mechanical ventilation in 383 men with acute respiratory failure and studied the impact of patient age, cause of acute respiratory failure, and duration of mechanical ventilation on survival. Survival rates were 66.6 percent to weaning, 61.1 percent to ICU discharge, 49.6 percent to hospital discharge, and 30.1 percent to 1 year after hospital discharge. When our data were combined with 10 previously reported series, mean survival rates were calculated to be 62 percent to ventilator weaning, 46 percent to ICU discharge, 43 percent to hospital discharge, and 30 percent to 1 year after discharge. Of 255 patients weaned from mechanical ventilation, 44 (17.3 percent) required an additional period of mechanical ventilation during the same hospitalization. RESULTS: Age had a significant influence on survival to hospital discharge and on that to 1 year after hospital discharge, and the cause of acute respiratory failure had a significant influence on survival only to weaning. Survival was best in younger patients and those with COPD or postoperative respiratory failure and worst in patients resuscitated after cardiac or respiratory arrest. Increased duration of mechanical ventilation significantly reduced survival only to hospital discharge. Overall survival was significantly affected by age and cause of acute respiratory failure, but not by duration of mechanical ventilation. CONCLUSION: We conclude that age, cause of acute respiratory failure, and duration of mechanical ventilation have specific influences on the generally poor outcome of mechanical ventilation for acute respiratory failure.

Acute Disease↗
PubMed1998

The use of continuous i.v. sedation is associated with prolongation of mechanical ventilation.

STUDY OBJECTIVE: To determine whether the use of continuous i.v. sedation is associated with prolongation of the duration of mechanical ventilation. DESIGN: Prospective observational cohort study. SETTING: The medical ICU of Barnes-Jewish Hospital, a university-affiliated urban teaching hospital. PATIENTS: Two hundred forty-two consecutive ICU patients requiring mechanical ventilation. INTERVENTIONS: Patient surveillance and data collection. MEASUREMENTS AND RESULTS: The primary outcome measure was the duration of mechanical ventilation. Secondary outcome measures included ICU and hospital lengths of stay, hospital mortality, and acquired organ system derangements. A total of 93 (38.4%) mechanically ventilated patients received continuous i.v. sedation while 149 (61.6%) patients received either bolus administration of i.v. sedation (n=64) or no i.v. sedation (n=85) following intubation. The duration of mechanical ventilation was significantly longer for patients receiving continuous i.v. sedation compared with patients not receiving continuous i.v. sedation (185+/-190 h vs 55.6+/-75.6 h; p<0.001). Similarly, the lengths of intensive care (13.5+/-33.7 days vs 4.8+/-4.1 days; p<0.001) and hospitalization (21.0+/-25.1 days vs 12.8+/-14.1 days; p<0.001) were statistically longer among patients receiving continuous i.v. sedation. Multiple linear regression analysis, adjusting for age, gender, severity of illness, mortality, indication for mechanical ventilation, use of chemical paralysis, presence of a tracheostomy, and the number of acquired organ system derangements, found the adjusted duration of mechanical ventilation to be significantly longer for patients receiving continuous i.v. sedation compared with patients who did not receive continuous i.v. sedation (148 h [95% confidence interval: 121, 175 h] vs 78.7 h [95% confidence interval: 68.9, 88.6 h]; p<0.001). CONCLUSION: We conclude from these preliminary observational data that the use of continuous i.v. sedation may be associated with the prolongation of mechanical ventilation. This study suggests that strategies targeted at reducing the use of continuous i.v. sedation could shorten the duration of mechanical ventilation for some patients. Prospective randomized clinical trials, using well-designed sedation guidelines and protocols, are required to determine whether patient-specific outcomes (eg, duration of mechanical ventilation, patient comfort) can be improved compared with conventional sedation practices.

Adolescent↗
PubMed2003

Relation between oscillatory ventilation at rest before cardiopulmonary exercise testing and prognosis in patients with left ventricular dysfunction.

BACKGROUND: Although nocturnal Cheyne-Stokes respiration alternating between hyperpnea and hypopnea has been considered a sign of severe heart failure, the clinical status of cardiac patients who exhibit oscillatory ventilation during wakefulness has not been clarified. This study was carried out to determine the relation between oscillatory ventilation during wakefulness and exercise capacity in patients with chronic heart disease. We also evaluated retrospectively whether the presence of oscillatory ventilation influences the long-term prognosis in these patients. METHODS: A total of 164 patients with left ventricular dysfunction performed a symptom-limited incremental exercise test. Respiratory gas exchange was measured on a breath-by-breath basis throughout the test. Oscillatory ventilation was defined when clear ventilatory oscillation of at least two consecutive cycles was identified at rest before exercise testing and the difference between the peak and nadir of oscillating ventilation was > 30% of the mean value of ventilation. RESULTS: Oscillatory ventilation was noted in 45 of 164 cardiac patients (27%), and the magnitude (mean +/- SD) of oscillation in these patients was 45.5 +/- 16.9%. Patients with oscillatory ventilation had significantly lower left ventricular ejection fraction than those without it (40.7 +/- 12.7% vs 44.9 +/- 11.6%, p < 0.05). However, parameters of exercise capacity such as the peak oxygen uptake (O(2)), the slope of the increase in O(2) relative to the increase in work rate (DeltaO(2)/DeltaWR), and the ratio of the increase in ventilation to the increase in carbon dioxide output (DeltaE/DeltaCO(2)) were not significantly different between the two groups. The mortality rate during 1,797 +/- 599 days of follow-up did not differ between the groups (p = 0.65). CONCLUSIONS: Oscillatory ventilation present at rest before cardiopulmonary exercise testing is not significantly related to the peak O(2), DeltaO(2)/DeltaWR, DeltaE/DeltaCO(2), or prognosis in patients with left ventricular dysfunction.

Adult↗