Large Tidal Volumes Research Articles

An audit on ventilator management in critical care units in National Hospital Sri Lanka

Mechanical ventilation is a common life saving intervention in Intensive Care Units (ICU). Traditional approaches to mechanical ventilation use large tidal volumes which may cause volutrauma. Lung protective ventilator strategies are used to prevent this. Concept of a ventilator care bundle was introduced to improve the quality of care in ventilated patients. The main objectives of this audit were to find out the common modes and ventilator parameters used in our ICUs and whether ventilator care bundle are used. The audit was conducted in Feb 2011. Data was collected from intubated and mechanically ventilated patients in 5 critical care units at National Hospital of Sri Lanka (NHSL). Total number of patients analyzed was 100. Ethical clearance was obtained from the NHSL ethics committee. Of the 100 patients 65 were males and 35 were females. Highest number of patients belonged to age group of 51-60yrs, and the majority were from Neuro-Trauma ICUs (NT-ICU). Commonest mode of ventilation was SIMV/PC (45%) and CMV/VC(37%). Frequently used tidal volume/kg was 7.1-10ml/kg (63%) and the lung protective tidal volume/kg range of 4.1-7ml/kg was used only in 31%. Commonest reasons for ventilation were central nervous system (CNS) (32%) and respiratory causes (16%). Muscle relaxants were used in 54% of patients, mainly in NT-ICUs and AS-ICU. Reasons for muscle relaxation were CNS stabilization following head injury/ neurosurgical intervention (28%), and to control intra-cranial pressure (11%). 91% of patients were given sedation and sedation free window was practiced in 70% of patients. Head-up tilt was maintained in 89% of patients and the reasons for not maintaining that position was severe hypotension and cervical spine injury. Mouth care (100%) and antacid prophylaxis (99%) were practiced in almost all the patients. Regular ETT cuff pressure checking is not a common practice in our ICUs. This audit highlight that less than 1/3 of ICU personnel practice lung protective ventilation strategies. To improve the quality of care of ventilated patients, we recommend to conduct awareness programmes to educate the ICU staff on the importance of practicing lung protective ventilator strategies and to introduce a system for monitoring compliance to the care bundle. DOI: http://dx.doi.org/10.4038/slja.v20i2.4153 Sri Lankan Journal of Anaesthesiology.2012:20(2):78-83

A multicentre observational study of intra‐operative ventilatory management during general anaesthesia: tidal volumes and relation to body weight

We conducted an observational prospective multicenter study to describe the practices of mechanical ventilation, to determine the incidence of use of large intra-operative tidal volumes (≥10 ml.kg(-1) of ideal body weight) and to identify patient factors associated with this practice. Of the 2960 patients studied in 97 anaesthesia units from 49 hospitals, volume controlled mode was the most commonly used (85%). The mean (SD) tidal volume was 533 (82) ml; 7.7 (1.3) ml.kg(-1) (actual weight) and 8.8 (1.4) ml.kg(-1) (ideal body weight)). The lungs of 381 (18%) patients were ventilated with a tidal volume>10 ml.kg(-1) ideal body weight. Being female (OR 5.58 (95% CI 4.20-7.43)) and by logistic regression, underweight (OR 0.06 (95% CI 0.01-0.45)), overweight (OR 1.98 (95% CI 1.49-2.65)), obese (OR 5.02 (95% CI 3.51-7.16)), severely obese (OR 10.12 (95% CI 5.79-17.68)) and morbidly obese (OR 14.49 (95% CI 6.99-30.03)) were the significant (p ≤ 0.005) independent factors for the use of large tidal volumes during anaesthesia.

Reducing tidal volume and increasing positive end-expiratory pressure with constant plateau pressure during one-lung ventilation: effect on oxygenation

It is no longer safe to use large tidal volumes (V(T)) (>8 ml kg(-1)) for one-lung ventilation (OLV), and limiting plateau pressure should be a major objective. Due to the specificity of OLV, the use of positive end-expiratory pressure (PEEP) remains controversial. This study determined whether at the same low plateau pressure, reducing V(T) and increasing PEEP were not inferior to larger V(T) and lower PEEP ventilation in terms of oxygenation. This prospective, randomized, non-inferiority, cross-over trial included 88 patients undergoing open thoracotomy who received two successive ventilatory strategies in random order: V(T) (8 ml kg(-1) of ideal body weight) with low PEEP (5 cm H(2)O), or low V(T) (5 ml kg(-1)) with a high PEEP. Respiratory rate and PEEP were, respectively, adjusted to maintain constant ventilation and plateau pressure. The primary endpoint was the ratio under each ventilatory strategy. The non-inferiority of low-V(T) ventilation could not be established. The mean adjusted ratio was lower overall during low-V(T) ventilation, and differences between the two ventilatory modes varied significantly according to baseline (T0). Decreased oxygenation during low V(T) was smaller when baseline values were low. Systolic arterial pressure was not lower during low-V(T) ventilation. During OLV, lowering V(T) and increasing PEEP, with the same low plateau pressure, reduced oxygenation compared with larger V(T) and lower PEEP. This strategy may reduce the risk of lung injury, but needs to be investigated further.

Plasma membrane disruptions with different modes of injurious mechanical ventilation in normal rat lungs*

Plasma membrane disruptions are caused by excessive mechanical stress and thought to be involved in inflammatory mediator upregulation. Presently, plasma membrane disruption formation has been studied only during mechanical ventilation with large tidal volumes and limitedly to subpleural alveoli. No information is available concerning the distribution of plasma membrane disruptions within the lung or the development of plasma membrane disruptions during another modality of injurious mechanical ventilation, i.e., mechanical ventilation with eupneic tidal volume (7 mL · kg) at low end-expiratory lung volume. The aim of this study is to assess whether 1) mechanical ventilation with eupneic tidal volume at low end-expiratory lung volume causes plasma membrane disruptions; and 2) the distribution of plasma membrane disruptions differs from that of mechanical ventilation with large tidal volume at normal end-expiratory lung volume. Experimental animal model. Sprague-Dawley rats. Plasma membrane disruptions have been detected as red spots in gelatin-included slices of rat lungs stained with ethidium homodimer-1 shortly after anesthesia (control) after prolonged mechanical ventilation with eupneic tidal volume at low end-expiratory lung volume followed or not by the restoration of physiological end-expiratory lung volume and after prolonged mechanical ventilation with large tidal volumes and normal end-expiratory lung volume. Plasma membrane disruptions increased during mechanical ventilation at low end-expiratory lung volume, mainly at the bronchiolar level. Resealing of most plasma membrane disruptions occurred on restoration of normal end-expiratory lung volume. Mechanical ventilation with large tidal volume caused the appearance of plasma membrane disruptions, both bronchiolar and parenchymal, the latter to a much greater extent than with mechanical ventilation at low end-expiratory lung volume. The increase of plasma membrane disruptions correlated with the concomitant increase of airway resistance with both modes of mechanical ventilation. : Amount and distribution of plasma membrane disruptions between small airways and lung parenchyma depends on the type of injurious mechanical ventilation. This could be relevant to the release of inflammatory mediators.

Ventilator-induced lung injury

Ventilator-induced lung injury (VILI) is a ubiquitous iatrogenic clinical problem in critical care. Aside from avoiding large tidal volumes, little progress has been made in identifying effective clinical strategies to minimize this injury. With recent rapid development in bioinformatics and high-throughput molecular technology, the genetic basis of lung injury has been intensively investigated. This review will describe recent insights and potential therapies developed in the field. Much progress has been made in delineating the possible genes and gene products involved in VILI through various mechanisms such as early induced genes, capillary leak, apoptosis, fibrin deposition, inflammatory cytokines, oxidative stress, disrupted angiogenesis, and neutrophil infiltration. Some studies have translated bench findings to the bedside in an attempt to identify clinically important genetic susceptibility, which could aid in the identification of at-risk individuals who might benefit from careful titration of mechanical ventilation. Genetic insights also provide candidate pharmaceutical approaches that may ameliorate VILI in the future. Much relevant information exists for investigators and clinicians interested in VILI. Future research will interlink evolving data to provide a more integrated picture of the molecular mechanisms involved in VILI enabling translation of the most promising candidate therapies.

Effects of dynamic ventilatory factors on ventilator-induced lung injury in acute respiratory distress syndrome dogs.

Mechanical ventilation is a double-edged sword to acute respiratory distress syndrome (ARDS) including lung injury, and systemic inflammatory response high tidal volumes are thought to increase mortality. The objective of this study is to evaluate the effects of dynamic ventilatory factors on ventilator induced lung injury in a dog model of ARDS induced by hydrochloric acid instillation under volume controlled ventilation and to investigate the relationship between the dynamic factors and ventilator-induced lung injuries (VILI) and to explore its potential mechanisms. Thirty-six healthy dogs were randomly divided into a control group and an experimental group. Subjects in the experimental group were then further divided into four groups by different inspiratory stages of flow. Two mL of alveolar fluid was aspirated for detection of IL-8 and TNF-α. Lung tissue specimens were also extracted for total RNA, IL-8 by western blot and observed under an electronic microscope. IL-8 protein expression was significantly higher in group B than in groups A and D. Although the IL-8 protein expression was decreased in group C compared with group B, the difference was not statistically significant. The TNF-α ray degree of group B was significantly higher than that in the other groups (P<0.01), especially in group C (P>0.05). The alveolar volume of subjects in group B was significantly smaller, and cavity infiltration and cell autolysis were marked with a significant thicker alveolar septa, disorder of interval structures, and blurring of collagenous and elastic fiber structures. A large number of necrotic debris tissue was observed in group B. Mechanical ventilation with a large tidal volume, a high inspiratory flow and a high ventilation frequency can cause significant damage to lung tissue structure. It can significantly increase the expression of TNF-α and IL-8 as well as their mRNA expression. Furthermore, the results of our study showed that small tidal ventilation significantly reduces the release of pro-inflammatory media. This finding suggests that greater deterioration in lung injury during ARDS is associated with high inspiratory flow and high ventilation rate.

Perioperative Lung Protective Strategies

Perioperative Lung Protective Strategies

Influence of Low Tidal Volume Ventilation on Time to Extubation in Cardiac Surgical Patients

Low tidal volumes are clearly beneficial for patients with established acute respiratory distress syndrome/acute lung injury (ARDS/ALI).1–3 However, the optimal mechanical ventilation of patients at risk of ARDS/ALI remains unclear. In theory, lung overdistention could contribute to lung injury among predisposed individuals, leading to prolongation of mechanical ventilation. Gajic et al.4 conducted a retrospective analysis of patients who did not have ARDS when mechanical ventilation was initiated. They observed that high tidal volume was an independent risk factor for ALI among patients with relatively normal gas exchange. The authors4 concluded that strong consideration should be given to limiting large tidal volume, not only among patients with established ALI, but also for at-risk patients. Subsequent retrospective analyses have confirmed these findings.5,6 However, other researchers7 have suggested that low tidal volume may be unnecessary in non-ALI cases and that it may lead unnecessarily to patient discomfort, increased work during breathing, high sedation requirements, autopositive end-expiratory pressure (PEEP; high respiratory rate), hypercapnia (low respiratory rate), and atelectasis. Thus, despite biologic plausibility and considerable retrospective data to support limiting tidal volume in all ventilated patients, equipoise remains regarding optimal tidal volume in non-ALI patients. Although various groups of surgical patients, but especially cardiac surgical patients, have been observed,8–20 these investigations have focused primarily on surrogate outcomes measures, leaving a lack of clarity regarding optimal perioperative ventilator strategy. Therefore, we performed a randomized controlled trial comparing ventilation with 6 versus 10 ml/kg tidal volume for patients undergoing elective cardiac surgery. We hypothesized that using a low tidal volume ventilator strategy would reduce ventilator-associated lung injury and that this improvement would reduce time to extubation.

Intraoperative ventilation: incidence and risk factors for receiving large tidal volumes during general anesthesia

BackgroundThere is a growing concern of the potential injurious role of ventilatory over-distention in patients without lung injury. No formal guidelines exist for intraoperative ventilation settings, but the use of tidal volumes (VT) under 10 mL/kg predicted body weight (PBW) has been recommended in healthy patients. We explored the incidence and risk factors for receiving large tidal volumes (VT > 10 mL/kg PBW).MethodsWe performed a cross-sectional analysis of our prospectively collected perioperative electronic database for current intraoperative ventilation practices and risk factors for receiving large tidal volumes (VT > 10 mL/kg PBW). We included all adults undergoing prolonged (≥ 4 h) elective abdominal surgery and collected demographic, preoperative (comorbidities), intraoperative (i.e. ventilatory settings, fluid administration) and postoperative (outcomes) information. We compared patients receiving exhaled tidal volumes > 10 mL/kg PBW with those that received 8-10 or < 8 mL/kg PBW with univariate and logistic regression analyses.ResultsVentilatory settings were non-uniform in the 429 adults included in the analysis. 17.5% of all patients received VT > 10 mL/kg PBW. 34.0% of all obese patients (body mass index, BMI, ≥ 30), 51% of all patients with a height < 165 cm, and 34.6% of all female patients received VT > 10 mL/kg PBW.ConclusionsVentilation with VT > 10 mL/kg PBW is still common, although poor correlation with PBW suggests it may be unintentional. BMI ≥ 30, female gender and height < 165 cm may predispose to receive large tidal volumes during general anesthesia. Further awareness of patients' height and PBW is needed to improve intraoperative ventilation practices. The impact on clinical outcome needs confirmation.

Mechanical ventilation and volutrauma: study in vivo of a healthy pig model.

Mechanical ventilation is essential in intensive care units. However, it may itself induce lung injury. Current studies are based on rodents, using exceptionally large tidal volumes for very short periods, often after a "priming" pulmonary insult. Our study deepens a clinically relevant large animal model, closely resembling human physiology and the ventilator setting used in clinic settings. Our aim was to evaluate the pathophysiological mechanisms involved in alveolo/capillary barrier damage due to mechanical stress in healthy subjects. We randomly divided 18 pigs (sedated with medetomidine/tiletamine-zolazepam and anesthetised with thiopental sodium) into three groups (n=6): two were mechanically ventilated (tidal volume of 8 or 20 ml/kg), the third breathed spontaneously for 4 hours, then animals were sacrificed (thiopental overdose). We analyzed every 30' hemogasanalysis and the main circulatory and respiratory parameters. Matrix gelatinase expression was evaluated on bronchoalveolar lavage fluid after surgery and before euthanasia. On autoptic samples we performed zymographic analysis of lung, kidney and liver tissues and histological examination of lung. Results evidenced that high Vt evoked profound alterations of lung mechanics and structure, although low Vt strategy was not devoid of side effects, too. Unexpectedly, also animals that were spontaneously breathing showed a worsening of the respiratory functions.

Deletion of Apoptosis Signal–Regulating Kinase–1 Prevents Ventilator-Induced Lung Injury in Mice

Both hyperoxia and mechanical ventilation can independently cause lung injury. In combination, these insults produce accelerated and severe lung injury. We recently reported that pre-exposure to hyperoxia for 12 hours, followed by ventilation with large tidal volumes, induced significant lung injury and epithelial cell apoptosis compared with either stimulus alone. We also reported that such injury and apoptosis are inhibited by antioxidant treatment. In this study, we hypothesized that apoptosis signal-regulating kinase-1 (ASK-1), a redox-sensitive, mitogen-activated protein kinase kinase kinase, plays a role in lung injury and apoptosis in this model. To determine the role of ASK-1 in lung injury, the release of inflammatory mediators and apoptosis, attributable to 12 hours of hyperoxia, were followed by large tidal volume mechanical ventilation with hyperoxia. Wild-type and ASK-1 knockout mice were subjected to hyperoxia (Fi(O(2)) = 0.9) for 12 hours before 4 hours of large tidal mechanical ventilation (tidal volume = 25 μl/g) with hyperoxia, and were compared with nonventilated control mice. Lung injury, apoptosis, and cytokine release were measured. The deletion of ASK-1 significantly inhibited lung injury and apoptosis, but did not affect the release of inflammatory mediators, compared with the wild-type mice. ASK-1 is an important regulator of lung injury and apoptosis in this model. Further study is needed to determine the mechanism of lung injury and apoptosis by ASK-1 and its downstream mediators in the lung.

Invited Commentary

Invited Commentary

New images, new insights for VILI

prioritization of high-volume vs. low-volume mechanisms of ventilator-induced lung injury (VILI) is an issue that is often discussed and debated in clinical ventilator management. Abundant laboratory studies ([7][1]), as well as several prominent clinical studies ([1][2], [3][3], [14][4], [19][5]),

Lung injury caused by high tidal volume mechanical ventilation and hyperoxia is dependent on oxidant-mediated c-Jun NH2-terminal kinase activation

Both prolonged exposure to hyperoxia and large tidal volume mechanical ventilation can each independently cause lung injury. However, the combined impact of these insults is poorly understood. We recently reported that preexposure to hyperoxia for 12 h, followed by ventilation with large tidal volumes, induced significant lung injury and epithelial cell apoptosis compared with either stimulus alone (Makena et al. Am J Physiol Lung Cell Mol Physiol 299: L711-L719, 2010). The upstream mechanisms of this lung injury and apoptosis have not been clearly elucidated. We hypothesized that lung injury in this model was dependent on oxidative signaling via the c-Jun NH(2)-terminal kinases (JNK). We, therefore, evaluated lung injury and apoptosis in the presence of N-acetyl-cysteine (NAC) in both mouse and cell culture models, and we provide evidence that NAC significantly inhibited lung injury and apoptosis by reducing the production of ROS, activation of JNK, and apoptosis. To confirm JNK involvement in apoptosis, cells treated with a specific JNK inhibitor, SP600125, and subjected to preexposure to hyperoxia, followed by mechanical stretch, exhibited significantly reduced evidence of apoptosis. In conclusion, lung injury and apoptosis caused by preexposure to hyperoxia, followed by high tidal volume mechanical ventilation, induces ROS-mediated activation of JNK and mitochondrial-mediated apoptosis. NAC protects lung injury and apoptosis by inhibiting ROS-mediated activation of JNK and downstream proapoptotic signaling.

Straining to Make Mechanical Ventilation Safe and Simple

Straining to Make Mechanical Ventilation Safe and Simple

Increased apparatus dead space and tidal volume increase blood concentrations of oxygen and sevoflurane in overweight patients: a randomised controlled clinical study

General anaesthesia impairs respiratory function in overweight patients. We wanted to determine whether increased tidal volume (V(T)), with unchanged end-tidal carbon dioxide partial pressure (P(ET)CO₂), affects blood concentrations of oxygen and sevoflurane in overweight patients. The present study is a prospective, randomised, clinical study. American Society of Anesthesiologists physical status I and II patients with BMI over 25 scheduled for elective surgery of the lower abdomen were randomly assigned to one of two groups with 10 patients in each. One group was ventilated with normal V(T) (NV(T)) and one group with increased V(T) (IV(T)) achieved by increasing inspired plateau pressure 0.04 cmH₂O kg⁻¹ above initial plateau pressure. Extra apparatus dead space was added to maintain P(ET)CO₂ at 4.5 kPa. Respiratory rate was set at 15 min⁻¹, and sevoflurane was delivered to the fresh gas by a vaporiser set at 3%. Arterial oxygenation, sevoflurane tensions (P(a)sevo, F(i)sevo, P(ET)sevo), paCO₂, P(ET)CO₂, V(t) and airway pressure were measured. The two groups of patients were similar with regard to sex, age, weight, height and BMI. Arterial oxygen tension (mean ± SD) was significantly higher in the IV(T) group (15 ± 4.3 vs. 10 ± 2.7 kPa after 60 min of anaesthesia, P < 0.05). Mean PETsevo did not differ between the groups, whereas arterial sevoflurane tension (mean ± SD) was significantly higher in the IVT group (1.74 ± 0.18 vs. 1.43 ± 0.19 kPa after 60 min of anaesthesia, P < 0.05). Ventilation with larger tidal volumes with isocapnia maintained with added apparatus dead space increases the tension of oxygen and sevoflurane in arterial blood in overweight patients.

Unstable Maternal Environment, Separation Anxiety, and Heightened CO2 Sensitivity Induced by Gene-by-Environment Interplay

BackgroundIn man, many different events implying childhood separation from caregivers/unstable parental environment are associated with heightened risk for panic disorder in adulthood. Twin data show that the occurrence of such events in childhood contributes to explaining the covariation between separation anxiety disorder, panic, and the related psychobiological trait of CO2 hypersensitivity. We hypothesized that early interference with infant-mother interaction could moderate the interspecific trait of response to CO2 through genetic control of sensitivity to the environment.MethodologyHaving spent the first 24 hours after birth with their biological mother, outbred NMRI mice were cross-fostered to adoptive mothers for the following 4 post-natal days. They were successively compared to normally-reared individuals for: number of ultrasonic vocalizations during isolation, respiratory physiology responses to normal air (20%O2), CO2-enriched air (6% CO2), hypoxic air (10%O2), and avoidance of CO2-enriched environments.ResultsCross-fostered pups showed significantly more ultrasonic vocalizations, more pronounced hyperventilatory responses (larger tidal volume and minute volume increments) to CO2-enriched air and heightened aversion towards CO2-enriched environments, than normally-reared individuals. Enhanced tidal volume increment response to 6%CO2 was present at 16–20, and 75–90 postnatal days, implying the trait's stability. Quantitative genetic analyses of unrelated individuals, sibs and half-sibs, showed that the genetic variance for tidal volume increment during 6%CO2 breathing was significantly higher (Bartlett χ = 8.3, p = 0.004) among the cross-fostered than the normally-reared individuals, yielding heritability of 0.37 and 0.21 respectively. These results support a stress-diathesis model whereby the genetic influences underlying the response to 6%CO2 increase their contribution in the presence of an environmental adversity. Maternal grooming/licking behaviour, and corticosterone basal levels were similar among cross-fostered and normally-reared individuals.ConclusionsA mechanism of gene-by-environment interplay connects this form of early perturbation of infant-mother interaction, heightened CO2 sensitivity and anxiety. Some non-inferential physiological measurements can enhance animal models of human neurodevelopmental anxiety disorders.

Establishing long-term surviving model of ventilator induced lung injury in piglets by large tidal volume ventilation

Objective To establish a long-term surviving model of ventilator induced lung injury ( VILI) in piglets with large tidal volume ventilation. Methods A total of 21 piglets were randomly( random number) divided into trial experiment group (group A,n =9), injury group ( group B,n =6) and control group ( group C, n = 6). Each piglet was intubated orotracheally and intravascular cannulae were inserted both into carotid artery and external jugular vein. The tidal volume in 60 - 80 ml/kg was given to rats of group A and 50 ml/kg to rats of group B, and free breath to rats of group C. Vital signs, pneumatic mechanics, blood-gas analysis and hemodynamics were monitored every hour ( group A and group B from just after the model established 0 h, group C from 0 ～6 h). The t test or ANOVA test was used for statistical analysis. Left lung tissue was sent to biopsy after experiment. Results About 6 hours after mechanical ventilation with large tidal volume, PaO2/FiO2 lower significantly both in A and B group in comparison with control group (P ＜0.05 ) and histological changes hit the ALl criteria. Piglets ventilated with 50 ml/kg of tidal volume could survive for long-term. Conclusions The model of VILI in piglets made with 50 ml/kg of tidal volume ventilation was established successfully and survived for long-term. Key words: Ventilator induced lung injury; Acute lung injury; Large tide volume; Mechanical ventilation; Animal model; Keep surviving for long term; Pneodynamic; Hemodynamic

Clinical Testing of the Apnea Prevention Device

Narcotic-induced respiratory depression is a major cause of perioperative morbidity and mortality. Current monitoring modalities are inadequate to detect and treat respiratory depression in postoperative patients. Intermittent nursing assessments, even if conducted frequently, may not capture the rapid onset of airway obstruction, apnea, and hypoxia that can occur in many of these patients. Continuous nursing observation, as in an intensive care unit setting, is cost-prohibitive and impractical, given the large number of patients at risk. In an effort to address this problem, the author has created and tested the Apnea Prevention Device (APD), which is designed to detect the onset of hypoxia and instantly intervene to restore respiration and oxygen saturation in narcotized patients. The prototype APD used in this study consisted of a laptop computer running custom software, a pulse oximeter, and a nerve stimulator. Oxygen saturation data were acquired by the computer from the pulse oximeter, and stimuli to the patient were delivered either by headphones (verbal prompts) or a nerve stimulator (cutaneous). The APD program was written to analyze oximetry data and when indicated, deliver a series of stimuli of increasing intensity to arouse patients from narcosis. The device was tested on surgical patients in the postanesthesia care unit. An intervention delivered by the APD was scored as a success if the patient took a large tidal volume breath (as evidenced by chest rise) and there was a subsequent increase in oxygen saturation. The APD maintained a data log of oxygen saturations and interventions. In a subset of patients, it was possible to compare the functioning of the APD with routine nursing care. A total of 125 interventions were delivered by the APD to 10 patients with a 97% success rate. The depth of desaturations was less when the APD was in use than when patients received routine 1:1 nursing care. When the APD was functioning, the frequency with which nurses prompted the subjects to breathe was dramatically reduced. This study demonstrates that the prototype APD can successfully treat narcotic-induced respiratory depression in postoperative patients and does so in a manner that is superior to that provided by routine 1:1 nursing care. Such a device has the potential to decrease the morbidity associated with narcotic-induced respiratory depression in postoperative patients.

Acute Exacerbation of Idiopathic Interstitial Pneumonia Following Lung Surgery in 3 of 68 Consecutive Patients: A Retrospective Study

Acute exacerbation (AE) of idiopathic interstitial pneumonia (IIP) is occasionally observed after lung surgery. However, the risk of lung surgery in patients with IIPs is not yet clearly known. We conducted a retrospective study of consecutive patients who underwent lung surgery for cancer or for the diagnosis of interstitial pneumonia (IP) between 2000 and 2006. Patients who developed AE following the lung operation were assessed. The data of 68 consecutive patients (males: 56, females: 12) with IP who underwent lung surgery were analyzed. The lung surgery included lobectomy for lung cancer in 48 patients [idiopathic pulmonary fibrosis (IPF) 31, non-IPF 17], and lung biopsy in 20 patients [IPF 8, non-specific interstitial pneumonia (NSIP) 8, unclassified 4]. Three patients with IPF (4.4% in total) developed AE after the operation (2 lobectomy, 1 biopsy). The triggers of AE were considered to be prolonged ventilation at a large tidal volume with oxygen supplementation at a high concentration. At the time of the AE, the extent of parenchymal involvement on the HRCT images was greater on the non-operated side. All three patients died of respiratory failure 12 to 82 days after the onset of AE despite corticosteroid therapy. It is essential to be aware of the risk of AE of IPF following lung operation. Intraoperative respiratory management, such as oxygen supplementation at a high concentration and/or prolonged mechanical ventilation are likely possible etiologic factors.