Servo Ventilator 900C Research Articles

Sevoflurane Therapy for Severe Refractory Bronchospasm in Children.

To describe the effect of inhaled sevoflurane in the treatment of severe refractory bronchospasm in children. Retrospective case series. Two PICUs of tertiary general university hospitals in Spain. Ten patients ranging from 5 months to 14 years old with severe bronchospasm and acute respiratory failure requiring tracheal intubation and mechanical ventilation and treated with sevoflurane from 2008 to 2015. Inhaled sevoflurane therapy was initiated after failure of conventional medical management and mechanical ventilation. In two patients, sevoflurane was administered through a Servo 900C ventilator (Maquet, Bridgewater, NJ) equipped with a vaporizer and in the other eight patients via the Anesthetic Conserving Device (AnaConDa; Sedana medical, Uppsala, Sweden) with a critical care ventilator. Inhaled sevoflurane resulted in statistically significant decreases of PaCO2 of 34.2 torr (95% CI, 8.3-60), peak inspiratory pressure of 14.3 cm H2O (95% CI, 8.6-19.9), and improvement in pH of 0.17 (0.346-0.002) within 6 hours of administration. Only one patient presented hypotension responsive to volume administration at the beginning of the treatment. All patients could be extubated within a median time of 120 hours (interquartile range, 46-216). Inhaled sevoflurane therapy decreases the levels of PaCO2 and peak inspiratory pressure values, and it may be considered as a rescue therapy in patients with life-threatening bronchospasm refractory to conventional therapy.

No explicit memory after skin incision without anesthetic except for remifentanil infusion

To the Editor: Awareness and memory during general anesthesia is a serious problem. We experienced no explicit memory in a patient who was accidentally not administered anesthetic during skin incision before abdominal surgery. During that time, remifentanil alone was infused continuously. A 76-year-old woman, height 156.8 cm, weight 52 kg, was scheduled for peritoneal metastatic tumor resection. She had no complications or past history, except for lower anterior resection of the rectum with laparoscopic surgery 24 months prior. No premedication was administered. Anesthesia was induced with 200 mg thiopental and continuous infusion of remifentanil at the rate of 0.5 lg/kg/ min. She underwent tracheal intubation with the aid of 7 mg of vecuronium. The ventilation was controlled with 35% oxygen in air. After the induction of anesthesia, we planned to provide inhaled 3% sevoflurane during mask ventilation and 1% after tracheal intubation. We used the sevoflurane vaporizer 953 for servo 900C ventilator (MAQUET Critical Care AB, Solna, Sweden). This vaporizer requires activation of another switch in addition to adjusting the concentration dial to initiate sevoflurane inhalation (Fig. 1). We inadvertently forgot to activate the vaporizer switch to the ‘‘on’’ position. Accordingly, no sevoflurane was inhaled. After intubation, we decreased the rate of remifentanil infusion to 0.25 lg/kg/min during surgical-site sterilization and draping. Just before skin incision, we increased the rate of remifentanil infusion to 0.5 lg/kg/min. Twenty-four minutes after the administration of thiopental, skin incision was performed as usual. There was no apparent change of blood pressure or heart rate. The laparotomy was then continued, and there were no apparent changes in her vital signs. About 6 min after the skin incision, we noticed that the end-tidal concentration of sevoflurane on the monitor (S5, GE Healthcare Japan, Tokyo) was zero, and activated the vaporizer switch. We initially administered 3% sevoflurane, followed by 1–1.5% sevoflurane with 0.1–0.5 lg/kg/min of remifentanil. No other sedatives were administered. The operation was completed uneventfully with a total operation time of 1 h 39 min. The emergence from anesthesia was uneventful, with a total duration of anesthesia of 2 h 29 min. We asked the patient about her memories of the operation later on that same day and the next day. She had no explicit memory during the operation and expressed her thanks for a good anesthetic experience. The hypnotic that we administered to this patient was 200 mg of thiopental alone. Clinically, patients awaken from a single dose of thiopental about 5–10 min after administration because the drug levels in the brain decrease as a result of redistribution [1]. Accordingly, about 15 min after the end of the hypnotic action of thiopental, the patient was sedated only with remifentanil of 0.25–0.5 lg/kg/min. During the procedure, we had closed the eyelids of the patient using a sticking tape. The ears of the patient were free, but the sound in the operating room was minimal. Accordingly, it is possible that the patient was not aware of any stimuli except for the surgical procedure. Remifentanil has some sedative action and has been used for analgesia-based sedation [2, 3]. No implicit or explicit memory was found when a high concentration of remifentanil combined with low hypnotic concentration of propofol was maintained with high bispectral index (BIS) values [4]. Remifentanil 0.5 lg/kg/min might have been M. Yasuda R. Kubota T. Adachi (&) Department of Anesthesiology, Kitano Hospital, The Tazukekofukai Medical Research Institute, 2-4-20 Ohgimachi, Kita-ku, Osaka 530-8480, Japan e-mail: t-adachi@kitano-hp.or.jp

Pressure-controlled inverse ratio ventilation after cardiac surgery

Background and objective Pressure-controlled inverse ratio ventilation was compared with controlled mechanical ventilation in patients after cardiac surgery. Methods Ten patients were ventilated after sternal closure using a Siemens Servo 900C ventilator to a target end-tidal PCO2 of 4.0 kPa. They were randomized to receive controlled mechanical ventilation or pressure-controlled inverse ratio ventilation. CO2-based data were recorded on a laptop personal computer, which together with arterial PCO2 permitted measurement of the respiratory dead space. Once measurements were complete the ventilator was switched to the other mode and new measurements taken. Results PaCO2 and CO2 were virtually the same in both modes. Peak airway pressure (17.2 ± 2.7 vs. 20.8 ± 2.5 cmH2O, P < 0.01) and minute ventilation (4.9 ± 1.1 vs. 5.3 ± 1.1 cmH2O, P < 0.01) were less during pressure-controlled inverse ratio ventilation. Physiological dead space fraction (0.39 ± 0.06 vs. 0.51 ± 0.05, P < 0.001), airway dead space (56 ± 15 vs. 81 ± 15 mL, P < 0.001) and alveolar dead space fraction (0.25 ± 0.07 vs. 0.31 ± 0.09, P < 0.01) were all less during pressure-controlled inverse ratio ventilation. There were no differences in heart rate or mean arterial pressure. Conclusions The prolonged inspiratory period and pressure-controlled flow pattern of pressure-controlled inverse ratio ventilation reduce the alveolar and airway dead spaces, and give lower peak airway pressures, compared with conventional ventilation, in cardiac surgical patients.

Respiratory physiopathology in surgical repair for large incisional hernias of the abdominal wall

Background: The computerized noninvasive measurement of respiratory mechanics enables new prospects in the study of respiratory physiopathology in surgical repair of large incisional hernias. Study design: We studied 10 patients with COPD ventilated with a Servo Ventilator 900C. We measured inspiratory flow by means of a pneumotacograph, the volume by integrating the flow signal, and esophageal and airway opening pressure by means of two differential pressure transducers (an esophageal balloon measures, separately, chest wall and lung mechanical properties). The signals were sent by an analogic-digital converter to a personal portable computer to be analyzed. We calculated compliance of total respiratory system (Crs), chest wall (Ccw), and lung (Cl); maximum resistance of the total respiratory system (Rmax, Rs), chest wall (Rmax, w), and lung (Rmax, L); and work of breathing (Wob). Statistics were performed using one-way analysis of variance and p = 0.05 was considered significant. Results: At the closure of the peritoneum a reduction of Crs and Wob was recorded in seven patients in whom a PTFE prosthesis widening the abdominal cavity was used to restore the baseline value. Variations in respiratory compliance are from variations in Ccw with unaffected Cl (Ccw varied from 0.180 to 0.130 L/cmH 2O at peritoneal closure and from 0.130 to 0.170 L/cmH 2O by prosthetic peritoneal widening). Respiratory resistances remained unchanged (11.3 cmH 2O/L/s) at any time of measurement. Conclusions: The intraoperative assessment of respiratory mechanics is useful to evaluate and eventually to decrease the mechanical workload (prosthesis widening peritoneum or fascia incisions). The passive mechanical work performed by the ventilator needs to be kept constant or no higher than 10% basic data: if these conditions are maintained, mostly in patients with COPD, there is no risk of respiratory muscular fatigue during the postoperative period.

Second gas effect of N2O on oxygen uptake.

The concept of the second gas effect is well known, however, there have been no studies that showed the relationship between alveolar oxygen concentration and arterial oxygen tension (PaO2) after the inhalation of nitrous oxide (N2O) in humans. The purpose of this study was to examine the changes in both end-tidal oxygen fraction (F(ET)O2) and PaO2 after N2O inhalation in patients under general anesthesia. Fifteen patients scheduled for elective orthopedic surgery were enrolled in this study. Anesthesia was maintained with the continuous infusion of propofol and with nitrogen (N2) and oxygen (O2) (6 L x min(-1), F1O2, 0.33). In all patients, the lungs were ventilated with a Servo 900C ventilator equipped with a gas mixer for O2, N2O, and N2. After obtaining baseline data, N2 was replaced with N2O maintaining FIO2 constant at 0.33. The changes in fractional concentration of O2, N2O, and N2 were continuously measured using mass spectrometer in a breath-by-breath basis. PaO2 and hemodynamic data were obtained at 1, 5, 10, 30 and 60 min after the start of N2O inhalation. Five minutes after N2O inhalation, F(ET)O2 increased from 0.27+/-0.01 to 0.31+/-0.02 (P<0.01) and PaO2 increased from 172.0+/-22.5 mm Hg to 201.0+/-10.3 mm Hg (P<0.01). These effects produced by N2O were observed for 30 min. These results confirm the concept of second gas effect of N2O on oxygen uptake in humans and provide evidence that the PaO2 increase correlated with the increase in F(ET)O2 after N2O inhalation.

Comparison of NAD 6000 and Servo 900C Ventilators in an Infant Lung Model

Comparison of NAD 6000 and Servo 900C Ventilators in an Infant Lung Model

Reliability of Noninvasive Measurement of Cardiac Output Using Partial CO2 Rebreathing: A Comparison with Thermodilution Method

Background: A noninvasive method for estimating cardiac output was tested in dogs. The technique is based on a differential CO₂ Fick equation applied during normal ventilation and 50 seconds of partial rebreathing using additional dead space. We compared the cardiac output measured by the CO₂ rebreathing method vs. the thermodilution technique. Methods: Seven mongrel-dogs (24.6 ± 0.4 kg) were studied, anesthesia was induced and maintained with a pentobarbital 25 mg/kg IV bolus injection followed by an infusion of 5 mg/kg/h. Mechanical ventilation was accomplished with a Servo 900C ventilator with FiO₂ 0.6 to maintain normocarbia. A fiberoptic pulmonary artery catheter was introduced via an external jugular vein for continuous monitoring of the cardiac output by the thermodilution method. Also cardiac output was measured by using partial CO₂ rebreathing method. A continuous infusion of 0.5% bupivacaine was started at 0.5 mg/kg/min via the venous infusion port of the pulmonary catheter. Bupivacaine was infused continuously until mean arterial pressure decreased to 60 mmHg or less for at least 5 seconds. Results: The total measured cardiac outputs (n = 72) were distributed over the range of 1.03 7.72 L/min by thermodilution method and 1.6 7.3 L/min by CO₂ rebreathing. The correlation coefficients between both cardiac outputs was 0.6, the mean difference was 0.27 ± 0.81 L/min. Conclusions: The cardiac output measured by CO₂ rebreathing method was well correlated with cardiac output by thermodilution method.

Lung volume and oxygenation changes with a closed suction system (CSS) in patients undergoing volume controlled ventilation (VCV)

We wished to measure changes in lung volume (Δ LV), airway pressures, and oxygenation during tracheal suctioning performed with a CSS and with an open suction system (OSS). We enrolled 7 adult patients, sedated and paralyzed, VCV ventilated by a SERVO 900C ventilator (Siemens, Sweden) with PEEP ≥ 5 cmH2O and FiO2 ≥ 0.4. Keeping all remaining ventilarory settings unchanged, we set trigger sensitivity at -2 cmH2O, inspiratory time at 25%, inspiratory pause at 10%. We performed four suctioning manouvers at 20 min intervals using alternatively a CSS and an OSS. With both systems, we used 12 F size catheters. We performed no pre-oxygenation manouvers. Suction was applied for 20 s at a pressure of 100 cmH2O. We continuously recorded signals of respiratory inductance pletismography (RIP. Respitrace Plus. NIMS, FL), arterial oxygen saturation (O2Sat) by pulse oxymetry, and airway pressures. We obtained Δ LV as the change in the RIP signal measured during VCV and during suction. We measured Respiratory Rate (RR), peak inspiratory pressure (PIP), positive end-expiratory pressure (PEEP), and mean airway pressure(MAP) during VCV and during suction with the CSS.

Implementation of a respiratory drive monitor on a Servo Ventilator.

To design and evaluate a clinical monitor of respiratory drive (P0.1) and other respiratory variables in a simple way, using a commercial ventilator. Nine healthy males were studied as they were breathing spontaneously in a Servo 900C Ventilator, at rest and during light exercise (50 W). The ventilator was slightly modified to improve its mechanical performance during spontaneous breathing, and was used as a measuring instrument. All the relevant information was retrieved, calculated and monitored by a PC. Respiratory drive was assessed as occlusion pressures from the inspiratory airway pressure signal. The equipment was compared with a two-way non-rebreathing laboratory system. Furthermore, negative and positive inspiratory pressures were applied from the ventilator, to study respiratory responses to mechanical loads. At rest, the ventilator introduced a minor influence on inspiratory time and P0.1, but not in ventilation, tidal volume, expiratory duration and respiratory frequency. During exercise, the influence was more evident. This effect could also be noticed in the coefficients of variation. The responses to mechanical loads were easily recorded and can be used as a simple test of central load-compensating mechanisms. CONCLUSIONS. The ventilator, with limitations, may be an alternative to conventional techniques, especially in clinical studies of the central inspiratory activity with and without respiratory loading.

A single computer-controlled mechanical insufflation allows determination of the pressure-volume relationship of the respiratory system.

To evaluate and further develop a method for determination and mathematical characterisation of the elastic pressure-volume (Pel-V) relationship in mechanically ventilated human subjects during one single modified insufflation with simultaneous determination of resistance of the respiratory system. Eight adult non-smoking human subjects without heart, lung, or thoracic cage disease scheduled for non-thoracic surgery. The study was performed in anaesthetised and muscle-relaxed subjects. The Pel-V curve was determined with a computer-controlled Servo Ventilator 900C during a modified insufflation with either constant or sinusoidally varying flow. Pressure and flow were measured with the built-in sensors of the ventilator. Tracheal pressure (Ptr) was calculated by subtracting the pressure drop over the tracheal tube. The elastic recoil pressure in the peripheral lung, Pel, was obtained from the calculated Ptr by subtracting the pressure drop over the airways. Ptr was also directly measured through a catheter. The calculated Ptr gave similar results as the directly measured Ptr, thus indicating the reliability of the signal originating from the ventilator sensor for computation of downstream pressures. The inflection points of the sigmoidal Pel-V curve and the compliance of the linear segment were determined with high reproducibility. Using one single modified insufflation allows a fast and accurate determination of respiratory mechanics. The Pel-V curves were determined with high reproducibility and were adequately described by a three-segment model of the curve incorporating a linear segment between two asymmetrical non-linear segments.

Respiratory Muscle Performance, Pulmonary Mechanics, and Gas Exchange Between the BiPAP S/T-D System and the Servo Ventilator 900C With Bilevel Positive Airway Pressure Ventilation Following Gradual Pressure Support Weaning

Our objective was to compare respiratory muscle performance, pulmonary mechanics, and gas exchange between the BiPAP S/T-D ventilation system (Respironics Inc; Murrysville, PA) and the Servo Ventilator 900C (Siemens-Elma AB; Sweden) with similar inspiratory and expiratory airway pressure in patients who are recovering from acute respiratory failure. A prospective, randomized, clinical trial. Medical ICU. We studied 27 medical patients on mechanical ventilators following gradual pressure support weaning. Each patient breathed while in the following equivalent modes: (a) an inspiratory pressure preset (pressure support mode) of 5 cm H2O with an external positive end-expiratory pressure (PEEP) of 5 cm H2O on the Servo Ventilator 900C and (b) an inspiratory pressure preset of 10 cm H2O with an expiratory pressure preset of 5 cm H2O on the BiPAP S/T-D. Using the CP-100 pulmonary monitor, we compared the total work of breathing (WOB), the pressure-time index (PTP), and other pulmonary mechanics and gas exchange parameters between the two modes. The WOB injoules per liter (mean +/- SE) (0.76+/-0.08 vs 0.73+/-0.08, p = 0.70), the WOB in joules per minute (8.62+/-1.06 vs 8.11+/-0.96, p = 0.60), and the PTP in cm H2O/s/min (187+/-18 vs 167+/-18, p = 0.21) between the BiPAP S/T-D and the Servo Ventilator 900C were not statistically different. There were statistically significant differences between the two ventilators in auto-PEEP (1.34+/-0.37 vs 0.88+/-0.30 cm H2O, p = 0.03), duty cycle (0.44+/-0.01 vs 0.37+/-0.01, p < 0.001), and expiratory airway resistance (11.81+/-1.53 vs 8.75+/-1.22 cm H2O/L/s, p < 0.001), but not in respiratory rate (27.48+/-1.54 vs 28.06+/-1.61 breaths/min, p = 0.40) or in minute ventilation (10.43+/-0.59 vs 10.27+/-0.37 L/min, p = 0.66). There was a statistically significant difference in the ratio of Pa(O2) to the fraction of inspired oxygen (F(IO2)) (333+/-21 vs 300+/-22, p < 0.03) but not in Pa(CO2) (48+/-2 vs 47+/-2 mm Hg, p = 0.59) between the BiPAP S/T-D and the Servo Ventilator 900C. Despite differences in initiating and maintaining the inspiratory and expiratory phases, in breathing circuits, and in ventilator circuits between the two ventilators, the performance of the BiPAP S/T-D is equally efficacious to that of a conventional mechanical ventilator in supporting respiratory muscles. Thus, the BiPAP S/T-D is safe and effective when used in mechanically ventilated patients recovering from acute respiratory failure who do not require total ventilatory support.

A rat model of acute respiratory distress syndrome (ARDS): part 1. time dependency of histological and pathological changes

The time course of histopathological changes in a rat lung lavage model of the acute respiratory distress syndrome (ARDS) was analyzed by sacrificing animals 10, 30, 60, 180, and 210 min after the last lung parenchyma lavage which was performed with physiological saline solution. This lavage depleted the lung from its natural surfactant resources leading into a pathophysiological cascade similar to that of the acute respiratory distress syndrome. Tracheotomized rats (12 animals per time point) were pressure-controlled ventilated (Siemens Servo Ventilator 900C) with 100% oxygen at a respiratory rate of 30 breaths/min, inspiration–expiration ratio of 1:2, peak inspiratory pressure of 28 cm H 2O at positive end-expiratory pressure (PEEP) of 8 cm H 2O. During the whole experimental period, the ventilation was not changed. Blood gases (partial arterial oxygen pressures [PaO 2, mmHg] and partial arterial carbon dioxide pressures [PaCO 2, mmHg]) were estimated before, directly after, and 10, 30, 60, 90, 120, 150, 180, and 210 min after the last lavage. For grading lung lavage-induced histopathological changes associated with the time-dependent development of ARDS, slides were coded and evaluated without any knowledge of the sacrifice time. A semiquantitative grading was performed with respect to the severity of the following parameters: hyaline membrane formation (HM), interstitial and intraalveolar edema edema (E), and margination and infiltration of polymorphonuclear neutrophil leukocytes (PMNL) into the lung alveoli. The severity of these parameters showed a time-dependent increase after the last lavage. This was accompanied by a time-dependent decrease in partial arterial oxygen pressure (PaO 2) values during the early postlavage period (up to 30 min). Thereafter, PaO 2 levels remained fairly stable. The severity of intraalveolar and/or perivascular hemorrhages within the lung was not time dependent. The rat lavage model shows similarities to the pathophysiological sequelae occuring during the acute phase of the acute respiratory distress syndrome in humans. Most of the characteristic pathognomic histological changes seen in humans can be observed in this lung lavage model. This ARDS model is brief and easy in its experimental design, showed a good and homogeneous reproducibility of pathophysiological and histopathological parameters, and is therefore a useful model to estimate the influence of therapeutic pharmacological treatments of ARDS.

Computer-aided learning--a solution for the training needs of users & maintainers of medical equipment.

It can be argued that the strategic role of training and assessment in the use and maintenance of medical equipment for the delivery of safe and efficient healthcare is underestimated. While there has been frequent comment on this issue, the resources provided for this activity are most often insufficient. New methods are required to deliver regular, cost-effective training within the working environment, at the time and place of need. Similarly, the administrative workload has to be automated--and thus reduced--if training is to improve in both frequency and content. Computer-aided learning has had increasing and diverse application in education and training over the past few decades. The sophistication of software tools and the reduced cost of the necessary hardware makes this a viable and appropriate method for application in the field of Clinical Engineering. However, this technology has not yet been fully exploited to provide instruction in the use and maintenance of equipment. In this paper, it is proposed that computer-based training packages should not only be a source of interactive instruction and assessment, but also act as rapidly accessible reference materials or simulators of the actual device for the purpose of fault finding or troubleshooting. Brief details of a sample package are given for training in the use and maintenance of the Siemens Elema Servo Ventilator 900C.

Nitrogen dioxide production in a nitric oxide inhalation system using the Servo Ventilator 900C.

During nitric oxide (NO) inhalation therapy, toxicity may be produced by the reactive metabolite nitrogen dioxide (NO2). The purpose of the present study was to determine the NO2 concentration in a NO inhalation system used for respiratory failure in children at relatively low concentrations of NO (< 20 ppm). The production of NO2 in the NO inhalation system using the Servo Ventilator 900C connected to the test lung under each of 30 combinations of NO concentrations (0, 4, 8, 12, 16, and 19 ppm) and inspired oxygen (O2) concentrations (21, 40, 60, 80, and 100%). Pressure controlled ventilation was used with a respiratory rate of 20 breaths/min. NO and NO2 measurements were obtained on the inspiratory side of the Y-piece connected to the test lung. At a given NO level, increases in the concentration of inspired O2 resulted in increases in the concentration of NO2 produced, as did increases in the amount of NO at a given concentration of O2. The mean NO concentration at the inspiratory site of the Y-piece did not exceed 0.05 ppm (the limit of NO2 as an outdoor air pollutant in the United States) when the NO concentration did not exceed 8 ppm, regardless of the O2 concentration. NO inhalation therapy for children with severe respiratory failure using the Servo Ventilator 900C can be performed safely when the concentration of NO does not exceed 8 ppm.

Generation of nitrogen dioxide during nitric oxide therapy and mechanical ventilation of children with a Servo 900C ventilator.

To determine the combinations of nitric oxide (NO), oxygen (O2), minute ventilation (MV) and total gas flow (TGF) which generate toxic concentrations of nitrogen dioxide (NO2) during mechanical ventilation with a Servo 900C ventilator. The measurement of NO2 generated with NO (20, 40, 60, 80, 100 ppm) and O2 [fractional inspired oxygen (FIO2) 0.21, 0.4, 0.6, 0.9] during mechanical ventilation with MVs of 2.5, 5.0 and 7.5 l/min and TGFs from 2 to 14 l/min. Laboratory of intensive care unit in paediatric tertiary hospital. Toxic concentrations of NO2 (> 5 ppm) were generated in the ventilator circuit when NO was 80 ppm or 100 ppm in FIO2 of 0.6 or 0.9 with MVs of 2.5, 5.0 and 7.5 l/ min; and with 80 ppm NO in FIO2 of 0.6 at all TGFs from 2.0 to 13.6 l/min and MVs of 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.4). NO2 1.5-2.6 ppm was generated with 40 ppm NO in FIO2 of 0.6, TGFs 2.1-13.7 l/ min, and MVs 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.5). NO2 0.9-0.6 ppm was generated with 20 ppm NO in FIO2 of 0.6, TGFs 2.5-13.8 and MVs 2.5, 5.0 and 7.5 (TGF/MV 0.3-5.5). NO2 generation was not affected significantly by the TGF/MV ratio. The generation of NO2 in the ventilator circuit is directly proportional to concentration of NO and O2 and inversely proportional to the TGF and MV but uninfluenced by the TGF/MV ratio. NO 80 ppm, but neither 20 nor 40 ppm in FIO2 of 0.6, generates toxic NO2 irrespective of TGF, MV or the TGF/MV ratio.

Evaluation of a delivery system and monitors for ventilator administration of nitric oxide

The aim of this study was to compare nitric oxide (NO) and nitrogen dioxide (NO2) measurements obtained by chemiluminescence and electrochemical monitors using a delivery system for ventilator administration of NO. The formation of NO2 in this system and the efficacy of a soda-lime absorber to scavenge NO2 from inspiratory gas were also evaluated. Various concentrations of NO without and with soda lime were administered to a model lung via a Servo ventilator 900C with controlled ventilation by setting mass-flow regulators to maintain desired concentrations of NO in 80% O2. Close correlations were found between NO concentrations, as well as NO2 concentrations, measured using electrochemical monitors (TM100; 1002, PACII) and a chemiluminescence monitor (CLA-510SS). Soda-lime removed NO2 almost completely during administration of 0-25 p.p.m. NO, although a high concentration of NO2 appeared in the breathing circuit without soda lime. Four hundred grams of soda lime continued to absorb NO2 effectively during long-term administration of inhaled NO.These findings suggest that electrochemical monitoring is accurate and clinically useful for measurements of NO and NO2 concentrations, and that low doses of inhaled NO can be administered safely and reliably with the NO delivery system using a soda-lime absorber and mass-flow regulators.

Nitrogen Dioxide Production during Mechanical Ventilation with Nitric Oxide in Adults

Inhaled nitric oxide (NO) may be useful in the treatment of adult respiratory distress syndrome and other diseases characterized by pulmonary hypertension and hypoxemia. NO is rapidly converted to nitrogen dioxide (NO2) in oxygen (O2) environments. We hypothesized that in patients whose lungs are mechanically ventilated and in those with a long residence time for NO in the lungs, a clinically important [NO2] may be present. We therefore determined the rate constants for NO conversion in adult mechanical ventilators and in a test lung simulating prolonged intrapulmonary residence of NO. NO (800 ppm) was blended with nitrogen (N2), delivered to the high-pressure air inlet of a Puritan-Bennett 7200ae or Siemens Servo 900C ventilator, and used to ventilate a test lung. The ventilator settings were varied: minute ventilation (VE) from 5 to 25 l/min, inspired O2 fraction (FIO2) from 0.24 to 0.87, and [NO] from 10 to 80 ppm. The experiment was then repeated with air instead of N2 as the dilution gas. The effect of pulmonary residence time on NO2 production was examined at test lung volumes of 0.5-4.0 l, VE of 5-25 l/min, FIO2 of 0.24-0.87, and [NO] of 10-80 ppm. The inspiratory gas mixture was sampled 20 cm from the Y-piece and from within the test lung. NO and NO2 were measured by chemiluminescence. The rate constant (k) for the conversion of NO to NO2 was determined from the relation 1/[NO]t-1/[NO]o = k x [O2] x t, where t = residence time. No NO2 was detected during any trial with VE 20 or 25 l/min. With N2 dilution and the Puritan-Bennett 7200ae, NO2 (< or = 1 ppm) was detected only at a VE of 5 l/min with an FIO2 of 0.87 and [NO] > or = 70 ppm. In contrast, [NO2] values were greater with the Servo 900C ventilator than with the Puritan-Bennett 7200ae at similar settings. When NO was diluted with air, clinically important [NO2] values were measured with both ventilators at high [NO] and FIO2. Rate constants were 1.46 x 10(-9) ppm-2.min-1 when NO was mixed with N2, 1.17 x 10(-8) ppm-2.min-1 when NO was blended with air, and 1.44 x 10(-9) ppm-2.min-1 in the test lung. [NO2] increased with increased FIO2 and [NO], decreased VE, blending with air, and increased lung volumes. Higher [NO2] was produced with the Servo 900C ventilator than the Puritan-Bennett 7200ae because of the greater residence time. With long intrapulmonary residence times for NO, there is a potential for NO2 production within the lungs. The rate constants determined can be used to estimate [NO2] in adult mechanical ventilation systems.

Helium/Oxygen Breathing Improved Hypoxemia After Cardiac Surgery

Helium/Oxygen Breathing Improved Hypoxemia After Cardiac Surgery

Helium/Oxygen Breathing Improved Hypoxemia After Cardiac Surgery

14 breaths/min under volume-controlled ventilation without muscle relaxants, which was sufficient to maintain normocapnea) and Pao, did not improve. After admission to the intensive care unit (ICU), her arterial blood oxygenation failed to improve despite vigorous therapy, including nebulization of a bronchodilator, an 1:E ratio of 0.75, and PEEP of up to 10 cm H,O. Use of high PEEP (15-20 cm H,O) was avoided in order to prevent hemodynamic deterioration. (Her cardiac index [CI] and central venous pressure were 2.0-2.3 L * min-’ * m-’ and 9-13 mm Hg, respectively, with support by intravenous dopamine and dobutamine at a rate of 5 Fg * kg-’ . min-’ each.) Bronchial secretion was not pathologic, and her chest radiograph showed no significant change (Fig. 1). On the second postoperative day, when Pao, had decreased to 56 mm Hg with a FIO, of 1.0 and the intrapulmonary shunt fraction (Qs/Qt) was calculated to be 35%, He/O, was initiated. Helium (purity, 99.9%) was connected to the compressed-air port of a Servo-ventilator 900-C. The required FIO, decreased and the fraction of helium thus increased: Pao, was 50 mm Hg with a FIO, of 40.5 and Qs/Qt of 31% some 15 min after the initiation of He/O, (Fig. 2). Pace, was slightly decreased (42 + 37 mm Hg). Peak inspiratory pressure (PIP, 24 + 24 cm H,O), CI (2.4 + 2.5 L * min-’ * m-‘), and a systolic systemic blood pressure (127 + 129 mm Hg) showed no change. After 2 h of inhaling He/O,, oxygenation remained good and reached the normal range after 12 h.

A new application of an old method for respiratory mechanics measurements: The passive inflation method in newborn infants during pressure‐controlled ventilation

We have previously described a passive inflation method during constant inspiratory flow for measuring total respiratory elastance and resistance during mechanical ventilation in newborns. The simple method for measuring respiratory mechanics had been assessed during decelerating inspiratory flow obtained with pressure controlled ventilation (PCV). We report an application of this method to preterm and full-term mechanically ventilated newborn infants and a comparison with the occlusion method. Twenty-one newborn infants (birth weight 1,060 to 3,650 g; gestational age 26 to 41 weeks), between 1 to 55 days of postnatal age, were enrolled in the study. They were ventilated with a "Servo ventilator 900C," first set in the pressure-controlled mode and then in the volume-controlled mode without changing the tidal volume (VT), inspiratory time or ventilator rate. Flow was measured through a pneumotachograph inserted between the endotracheal tube (ETT) and the breathing circuit; VT was obtained by integration of flow and airway pressure measured directly at the airway opening. Flow, volume, and pressure were plotted on analog X/Y tables to obtain pressure-volume (P/V) and flow-volume (V/V) loops, as well as pressure-time curves. Occlusion was performed by using the end-inspiratory and the end-expiratory pause buttons of the ventilator. The passive inflation method during PCV was based on the analysis of P/V and V/V loops and provided compliance (Crs(PC)infl.), resistance Rrs(PC)infl.) of the respiratory system, and intrinsic positive end-expiratory pressure (PEEP(PC)i,infl.). These values were compared with (1) compliance (Crs(PC)occl.) and intrinsic positive end-expiratory pressure (PEEP(PC)i,occl.) measured by the occlusion method during PCV; (2) static (Crs(VC),occl.) and dynamic (Crs(VC),dyn.) compliance, airway (R(aw)(VC),), tissue (Rrs(VC),visc.) and total resistance (Rrs(VC),occl.), and intrinsic positive end-expiratory pressure (PEEP(VC)i,occl.) measured by the occlusion method during volume-controlled ventilation. Crs(PC),infl. correlated well with Crs(PC),occl., Crs(VC),occl., and Crs(VC),dyn.. Furthermore, Crs(PC),infl. and Crs(VC),dyn. did not differ significantly. Rrs(PC),infl. correlated well and did not differ significantly from total inspiratory resistance, i.e., the sum of R(aw)(VC) and Rrs(VC),vis. PEEPPC,i,infl. correlated well and did not differ significantly from PEEP(PC)i.occl. and from PEEP(VC),i,occl. The passive inflation method can be used during PCV with a decelerating flow waveform. It provides dynamic compliance, inspiratory resistance of the respiratory system, and intrinsic PEEP from the analysis of V/V and P/V loops recorded at the airway opening. This technique is simple to use and well tolerated by preterm and full-term ventilated newborn infants. It can be a good alternative to occlusion methods.