Clinical trials of an intravenous oxygenator in patients with adult respiratory distress syndrome.

In patients with severe adult respiratory distress syndrome, mechanical ventilation may not be able to ensure gas exchange sufficient to sustain life. We report the use of an intravenous oxygenator (IVOX) in five patients who were suffering from severe adult respiratory distress syndrome as a result of aspiration, fat embolism, or pneumonia. IVOX was used in an attempt to provide supplemental transfer of CO2 and O2 and thereby reduce O2 toxicity and barotrauma. All patients were tracheally intubated, sedated, and chemically paralyzed and had a PaO2 < 60 mmHg when the lungs were ventilated with an FIO2 = 1.0 and a positive end expiratory pressure of > or = 5 cmH2O. The right common femoral vein was located surgically, and the patient was systemically anticoagulated with heparin. A hollow introducer tube was inserted into the right common femoral vein, and the furled IVOX was passed into the inferior vena cava and advanced until the tip was in the lower portion of the superior vena cava. IVOX use ranged from 2 h to 4 days. In this group of patients, IVOX gas exchange ranged from 21 to 87 ml x min-1 of CO2 and from 28 to 85 ml x min-1 of O2. One of the five patients survived and was discharged from the hospital. The IVOX transferred up to 28% of metabolic gas-exchange requirements. One patient with a small vena cava showed signs of caval obstruction. Three other patients demonstrated signs of a septic syndrome after the device was inserted.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravascular Membrane Oxygenation and Carbon Dioxide Removal with IVOX: Can Improved Design and Permissive Hypercapnia Achieve Adequate Respiratory Support During Severe Respiratory Failure?

Abstract: The intravenacaval oxygenator and carbon dioxide removal device (IVOX) conceived by Mortensen at CardioPulmonics is a diffusion–limited device capable of removing 30% of CO₂ production of an adult at normocapnia with minimal reduction in ventilator requirements. Through mathematical modeling, an ex vivo venovenous bypass circuit to model the vena cava and animal models of severe smoke inhalation injury, the practice of permissive hypercapnia has been established to enhance CO₂ removal by IVOX. By allowing the blood PCO₂ to rise gradually, the CO₂ excretion by IVOX can be linearly increased in a 1: 1 relationship. Experimental and clinical studies have shown that CO₂ removal by IVOX increased from 30–40 ml/min at normal blood PCO₂ to 80–90 ml/min at PCO₂ of 90 mm Hg. In addition, IVOX with permissive hypercapnia allowed a significant reduction in minute ventilation and peak airway pressure. Design changes could also improve the performance of IVOX. Increased surface area and mixing with more fibers and crimping in new prototypes of IVOX significantly increased CO₂ removal and oxygen transfer. Active mixing in the blood to decrease the boundary layer resistance can further enhance gas exchange of IVOX. In conclusion, gas exchange by the current design of IVOX is limited, and improvements in design are needed for it to become a more clinically applicable device. Permissive hypercapnia can significantly enhance CO, removal by IVOX as well as significantly reduce ventilator requirements.     

Major Findings from the Clinical Trials of the Intravascular Oxygenator

Abstract: Major clinically relevant findings have been extracted and summarized from the database developed from the international multicenter clinical trials of the intravascular oxygenator (IVOX) as a means for augmenting the deficient blood gas transfer of patients in advanced acute respiratory failure (ARF). Between February 1990 and May 1993, a total of 164 IVOX devices were utilized in 160 clinical trial patients who were hypoxemic and/or hypercarbic while receiving closed system positive pressure mechanical ventilator support at or exceeding generally accepted minimum safe levels of intensity. The average rates of oxygen and carbon dioxide transfer into and out of circulating venous blood by means of the IVOX device varied from 40–70 ml/min. Evidence of patient benefit during IVOX utilization includes improvement in blood gas partial pressures associated with decreased intensity of mechanical ventilation, improved hemodynamics in patients with mechanical ventilator depressed cardiovascular function, and decreased indices of lung dysfunction. Clinically recognized IVOX–related complications or adverse events were reported in 24. 5% of the clinical trials patients. At necropsy examination of 68 clinical trials patients who died during or after I VOX utilization, forensic pathologists reported 4 cases in which IVOX utilization could have been a primary or contributing cause of death. Significant IVOX device mechanical and/or performance malfunction problems were recognized in 29 (17. 7%) of the IVOX devices utilized in clinical trials. IVOX clinical trials data collected and analyzed to date indicate IVOX utilization has a favorable risk/benefit ratio in patients in severe, acute, potentially reversible ARF.     

Rate of Thrombus Accumulation on Intravenacaval IVOX Devices Explanted from Human Clinical Trial Patients with Acute Respiratory Failure

Abstract: The weight gain of IVOX devices removed from the first 49 human clinical trials patients after from 1 to 29 days of implantation into the venae caval blood stream has been assessed. Each patient had received sufficient systemic heparin to maintain activated clotting times between 150 and 200 s while the IVOX device was indwelling. The nature of the material accumulating on the IVOX device was documented histologically as being thrombus in various stages of development. The weight gain findings indicate that an average of 2. 0 g of thrombus accumulates per 24 h on IVOX devices indwelling in the venous blood stream of moderately anticoagulated human acute respiratory failure patients. The rate of weight gain per 24 h of the IVOX device was more rapid during the first 96 h after its implantation than during its second, third, or fourth week of implantation. The accumulated thrombus on the IVOX hollow fibers was associated with a small but measurable decrease (˜ 1%/day) in gas transfer efficiency of the implanted device. The data support the conclusion that IVOX can function effectively and safely without major thrombus formation for up to 29 days in moderately anticoagulated human acute respiratory failure patients.     

Late Pathophysiologic Sequelae after Utilization of an Intravenacaval Oxygenator in Experimental Animals

Abstract: The intravenacaval hollow fiber oxygenator (IVOX) has been shown to be remarkably free from acute adverse effects on the venae cavae, right heart, and lungs when indwelling experimentally in sheep and in human clinical trial patients. However, all pathophysiologic assessments reported to date have been carried out during or immediately after IVOX utilization. It is recognized that IVOX indwelling in the venae cavae for up to 3 weeks could produce minor or unrecognized acute injury that could become more evident or more harmful after several weeks had elapsed following removal of the device. Therefore, this current study was designed and carried out to assess any pathophysiologic sequelae that could be recognized on follow–up examination 4 months after removal of an IVOX device that had been indwelling in the venae cavae for from 7 to 13 days. Extensive clinical and physiologic assessments of the blood, hemody namics, and pulmonary functional status of 8 sheep were carried out 4 months after removal of IVOX devices that had been indwelling for 7 to 13 days. Each animal was then euthanized and complete necropsy examination was conducted looking especially for gross or histologic lesions in the venae cavae, access veins, right heart, and lungs. Findings indicated that all animals were normal, without clinically or pathologically significant pathophysiologic abnormalities or adverse effects from the IVOX utilization. Detailed hematologic, hemodynamic, blood chemistry, pulmonary function, and gross and histopathologic findings, presented in graphic, tabular, and photographic form, document the conclusion that utilization of an IVOX device in normal sheep for from 7 to 13 days produces no significant adverse late pathophysiologic sequelae.     

In Vivo Gas Transfer Performance of the Intravascular Oxygenator in Acute Respiratory Failure

Abstract: The intravascular oxygenator (IVOX) has undergone both animal and clinical trials. Data from the animal studies have demonstrated that the device is capable of transferring up to approximately 100 ml/min of oxygen and carbon dioxide. Initial data from the human trials suggest that gas transfer, although approaching these levels, varied widely in patients with respiratory failure. We studied the factors affecting gas exchange in 26 patients with severe acute respiratory failure who underwent intravenacaval support of gas exchange with IVOX. The patients underwent monitoring of IVOX gas transfer rates, hemodynamics, blood gases, and ventilation parameters at scheduled intervals following device insertion. All devices functioned following implantation. The mean value for O₂ transfer was 64 ± 21 SD ml/min (range 15–114 ml/min) and for CO₂ transfer was ± 17 ml min^–1 (range 14–112 ml/min). CO₂ transfer correlated positively with device surface area, cardiac output, and mixed venous PCO₂ and negatively with duration of implantation. O₂ transfer did not correlate with any patient factors probably due to error inherent in the measurement of this variable. Independent measurements of IVOX gas transfer by respiratory gas exchange in a subset of patients with normal values of mixed venous PCO₂ were in good agreement with the routine measurements and indicated that the device provided up to 26% of gas exchange requirements in this subset. We conclude that IVOX transfers clinically useful amounts of oxygen and carbon dioxide in vivo. Factors that influence gas transfer include device surface area, PVCO₂, cardiac output, and duration of implantion. Optimization of these factors (such as with permissive hypercapnea) could result in enhanced performance in vivo     

下腔静脉内氧合器的实验研究

检测静脉内氧合器（ＩＶＯＸ）的气体交换能力,了解ＩＶＯＸ植入体内后血栓形成、气检发生的情况。方法杂种大１２条,采用扩大死腔、气道给Ｎ２的方法造成低氧血症后,经髂总静脉向下腔静脉内植入ＩＶＯＸ,ＩＶＯＸ通Ｏ２。结果使用ＩＶＯＸ后ＰａＣＯ２明显降低（１９％,Ｐ＜０．０５）,但ＰａＯ２无明显升高（Ｐ＞０．０５）。８例ＩＶＯＸ有少许纤维蛋白形成,４例右房内有少许气栓形成。结论ＩＶＯＸ能较为有效地清除体内ＣＯ２,其加氧能力尚需进一步证实。     

Permissive Hypercapnia and Intravascular Oxygenator in the Treatment of Patients with ARDS

Abstract: This open clinical study was aimed at testing the hypothesis that an intravascular oxygenator (IVOX) may help to perform permissive hypoventilation in 10 patients with severe ARDS. After initial evaluation, we tried to reduce ventilator settings before and after IVOX implantation. Before IVOX, poor clinical tolerance and worsening oxygenation did not allow for a significant decrease in ventilator settings. With IVOX, peak inspiratory pressure (PIP) was reduced from 47 to 39 cm H₂O (p = 0. 005) and minute ventilation from 13 ± 3. 5 to 11 ± 3 L/min. CO₂ removal by IVOX allowed a significant decrease in Paco₂ from 66 ± 15 to 59 ± 13 mm Hg. Improvement of oxygenation with IVOX was not signify cant. Furthermore, interruption of oxygen flow through IVOX did not change oxygenation variables. Tolerance of the IVOX device was good, but insertion of the device was followed by a significant decrease in both cardiac index and pulmonary wedge pressure. In conclusion, IVOX improves tolerance of hypoventilation by limiting hypercapnia in ARDS patients. These preliminary results must be confirmed by a randomized controlled study     

The influence of meperidine and nitrous oxide on respiratory depression in rats.

Narcotic sedation is commonly accomplished with nitrous oxide (N2O) coadministration. Concerns regarding respiratory morbidity and mortality with drug combinations have been reported in the literature, particularly in patients not receiving supplemental oxygen (O2). The purpose of this investigation was to determine the effect of meperidine alone and in combination with N2O on respiration in laboratory rats by evaluating cardiovascular and arterial blood gas data. Fifty-four Sprague-Dawley rats were assigned to one of six groups (nine per group). Groups were allocated based upon the dosage of meperidine administered (0, 4.0, or 8.0 mg/kg intraperitoneally [i.p.]) and exposure to N2O (50% with oxygen) or O2 (100%). Following meperidine administration, animals were placed into a sealed chamber through which flowed either N2O or O2. Arterial blood was obtained, at baseline and at 15-min intervals, from a femoral artery catheter and pH, O2, CO2 (mm Hg), and oxygen saturation (%) were determined. Plasma samples were analyzed using a System 1306 pH/blood gas analyzer. Group comparisons demonstrated that: (a) N2O coadministration, in animals pretreated with meperidine, did not result in increased arterial CO2 levels, and (b) as expected, arterial O2 levels in all groups increased significantly from preexposure baseline values (P < 0.05). This investigation demonstrated that the coadministration of N2O to meperidine-sedated animals did not enhance respiratory depression.     

Increases in cardiac output can reverse flow deficits from vasospasm independent of blood pressure: a study using xenon computed tomographic measurement of cerebral blood flow

INTRODUCTION: Vasospasm after subarachnoid hemorrhage remains a management challenge. The accepted treatment involves hypertensive, hypervolemic, hemodilution therapy. However, there is variation in the application of this treatment. Most authors increase mean arterial pressure (MAP), which can be associated with significant morbidity. Others increase cardiac output (CO). In this study, we examined the relationship between volume status, CO, and MAP and cerebral blood flow (CBF) in the setting of vasospasm. METHODS: A xenon blood flow tomography-based system was used to quantitate CBF. Sixteen patients with vasospasm after subarachnoid hemorrhage were treated with hypervolemia, phenylephrine to increase MAP, or dobutamine to increase CO. Direct CBF measurements were obtained before and after treatment. A strength of this study is that only one variable (central venous pressure, MAP, or CO) was manipulated in each patient, and the effect of this change was measured immediately. RESULTS: With phenylephrine, mean MAP increased from 102.4 to 132.1 mm Hg. In regions of diminished CBF due to vasospasm, mean CBF increased from 19.2 to 33.7 ml/100 g/min. Similarly, dobutamine increased the cardiac index from a mean of 4.1 to 6.0 L/min/m(2) and slightly decreased MAP. CBF increased from a mean of 24.8 to 35.4 ml/100 g/min. Both were statistically significant changes. With hypervolemia, the average central venous pressure increased from a mean of 5.4 to 7.3 cm H(2)O; no changes in mean CBF were noted. CONCLUSION: This article reports the first human study that shows with direct measurements the independent influence of CO in the setting of vasospasm. Increases in CO without changes in MAP can elevate CBF. This finding has immediate clinical application because CO manipulation is much safer than increasing MAP. Because both interventions were equally efficacious, our protocol has been changed to augment CO as a first measure. Induced hypertension is reserved for patients in whom this initial treatment fails.     

Clinical Strategies in Intravascular Gas Exchange

Abstract: Specific therapies in the management of acute pulmonary failure remain elusive, with attention being focused instead on novel supportive measures. The benefits of extracorporeal gas exchange support remain uncertain, and the perceived simplicity of intravascular gas exchange has, therefore, attracted much interest. Initial clinical experience with the intravascular oxygenator (IVOX) device confirms its safety and simplicity, but estimated mean gas-transfer values represent only 25% of basal gas-exchange requirements. The inherent limitations of IVOX as an oxygenator are discussed, providing a rationale for considering IVOX as primarily a CO, removal device. Reappraisal of the clinical place of intravascular gas exchange and the identification of specific applications most likely to yield benefit to patients are suggested. Design modifications enhancing efficacy are anticipated, further strengthening the potential of intravascular gas-exchange devices in selected patients with pulmonary failure.     

Whole body oxygen utilization during acute carbon monoxide poisoning and isocapneic nitrogen hypoxia

Carbon monoxide (CO) poisoning occurs frequently in victims of enclosed space fires, resulting in the formation of carboxyhemoglobin (COHb). Based on in vitro studies it has been suggested that CO poisoning causes a left shift of the oxyhemoglobin dissociation curve, decreasing peripheral oxygen extraction and exacerbating hypoxic injury. Formation of carboxycytochrome oxidase has also been postulated to act as a toxin by blocking cellular oxygen utilization. The effects of in vitro CO poisoning were evaluated in studies of 12 anesthetized, paralyzed dogs ventilated at 150 cc/kg/min. Six were subjected to CO poisoning by ventilation with a 0.5% CO in air inspirate. Six were ventilated with a mixture of air and nitrogen (N2) to produce a similar decrement of arterial oxyhemoglobin (aO2Hb) saturation. Arterial and mixed venous blood gases, thermal dilution cardiac output, and spectrophotometric arterial and mixed venous O2Hb and COHb saturation were measured. Oxygen consumption (VO2) and extraction (EXT) were calculated from these measurements and the CO and N2 groups were compared by ANOVA and Wilcoxon sign rank test as oxyhemoglobin was progressively decreased. There were no significant differences in VO2 or O2 EXT in these two sets of animals subjected to equivalent reductions of arterial oxyhemoglobin despite the fact that CO poisoning was the mode of desaturation in one group. These findings suggest that CO poisoning is primarily a hypoxic lesion caused by replacement of O2Hb by COHb. Effects predicted from in vitro studies may not be manifest in vivo due to physiologic responses active in the whole organism. This may have implications for the resuscitation of CO-injured patients.     

Development of a novel polyimide hollow-fiber oxygenator

We have developed a membrane oxygenator using a novel asymmetric polyimide hollow fiber. The hollow fibers are prepared using a dry/wet phase-inversion process. The gas transfer rates of O(2) and CO(2) through the hollow fibers are investigated in gas-gas and gas-liquid systems. The polyimide hollow fiber has an asymmetric structure characterized by the presence of macrovoids, and the outer diameter of the hollow fiber is 330 microm. It is found that the polyimide hollow-fiber oxygenator can enhance the gas transfer rates of O(2) and CO(2), and that the hollow fiber provides excellent blood compatibility in vitro and in vivo.     

Safe transplantation of blood type A2 livers to blood type O recipients

BACKGROUND: Transplantation of blood type A subgroup 2 (A2) livers into non-A recipients has not been reported previously. A2 to O renal transplantation has been reported, with early results including some accelerated rejections and graft losses. This has led some to selectively offer A2 renal transplantation only for patients with low anti-A titers. Given the different clinical behavior of liver allografts to preformed antibody, we felt that such restriction was unnecessary. METHODS: We performed six cases of A2 to O liver transplantation with no augmented immunomodulation or restriction with regard to antibody titers. Clinical courses, anti-A titers, rejection rates, and graft and patient survival were evaluated. RESULTS: All six patients had high pretransplant anti-A titers (>1:8), and all six grafts functioned normally. There were nine rejections in the six patients, of which three were severe (steroid-resistant) and five were late (>90 days). No rejection was vascular, and no grafts were lost, with mean follow-up of 665 days. In one patient who had anti-A antibody measured at the time of rejection IGM titers increased from baseline. Currently all patients are home with normal function. CONCLUSIONS: We found that transplantation of blood group A2 livers into blood group O recipients is safe and can be performed without graft loss and without regard to anti-A titer level. The rate of acute cellular rejection is high in this small series, and a significant proportion of these events were late or required OKT-3. We did not rely on plasmapheresis or anti-A titer determinations. However, the potential for late rejection prompts us to consider the addition of a third immunosuppressive agent. The transplantation of A2 livers into O recipients can partially compensate for the more frequent use of O livers in recipients from other blood groups.     

The PaCO2 rate of rise in anesthetized patients with airway obstruction

Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO2 because it requires a continuous O2 flow. The CO2 rate of rise in anesthetized humans with airway obstruction was measured. Fourteen consenting healthy adults were monitored continuously with pulse oximetry and EKG. Enflurane--O2 anesthesia was established for at least 10 minutes with normal PaCO2 without neuromuscular blockade so that anesthesia was deep enough to prevent spontaneous ventilation. Then, patients' tracheal tubes were clamped. Arterial blood samples were obtained before and after 0, 20, 40, 60, 120, 180, 240, and 300 seconds after clamping, provided that oxyhemoglobin saturation exceeded 0.92. The equation that best described the PaCO2 rise was a logarithmic function. Piecewise linear approximation yielded a PaCO2 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg/minute thereafter. These values should be employed when estimating the duration of apnea from PaCO2 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant CO2 quantities.     

Development of a New Hollow Fiber Silicone Membrane Oxygenator: In Vitro Study

An experimental silicone hollow fiber membrane oxygenator for long-term extracorporeal membrane oxygenation (ECMO) was developed in our laboratory using an ultrathin silicone hollow fiber. However, the marginal gas transfer performances and a high-pressure drop in some cases were demonstrated in the initial models. In order to improve performance the following features were incorporated in the most recent oxygenator model: increasing the fiber length and total surface area, decreasing the packing density, and modifying the flow distributor. The aim of this study was to evaluate the gas transfer performances and biocompatibility of this newly improved model with in vitro experiments. According to the established method in our laboratory, in vitro studies were performed using fresh bovine blood. Gas transfer performance tests were performed at a blood flow rate of 0.5 to 6 L/min and a V/Q ratio (V = gas flow rate, Q = blood flow rate) of 2 and 3. Hemolysis tests were performed at a blood flow rate of 1 and 5 L/min. Blood pressure drop was also measured. At a blood flow rate of 1 L/min and V/Q = 3, the O2 and CO2 gas transfer rates were 72.45 +/- 1.24 and 39.87 +/- 2.92 ml/min, respectively. At a blood flow rate of 2 L/min and V/Q = 3, the O2 and CO2 gas transfer rates were 128.83 +/- 1.09 and 47.49 +/- 5.11 ml/min. Clearly, these data were superior to those obtained with previous models. As for the pressure drop and hemolytic performance, remarkable improvements were also demonstrated. These data indicate that this newly improved oxygenator is superior to the previous model and may be clinically acceptable for long-term ECMO application.     

The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide

The reduction in cerebral blood flow (CBF) caused by hypocapnia is an important element of neuroanesthetic techniques. While it has been demonstrated previously that the CO2 response of the cerebral circulation (CO2 X R) is enhanced (i.e., greater delta CBF/delta PaCO2) during halothane administration, the effect of isoflurane on CO2 X R has not been evaluated completely. Accordingly, the authors examined CO2 X R in cats during anesthesia with 1.0 MAC isoflurane (with 75% N2O) and compared it with CO2 X R during anesthesia with 1.0 MAC halothane (with 75% N2O) and with CO2 X R during the administration of 75% N2O alone. CO2 X R during anesthesia with isoflurane-N2O was enhanced relative to that observed during administration of both halothane-N2O (P less than 0.025) and N2O alone (P less than .001). CO2 X R during anesthesia with halothane-N2O was, in turn, greater than that observed during the administration of N2O alone (P less than 0.025). Furthermore, at similar levels of hypocapnia (PaCO2 18-20 mmHg), CBF was significantly lower (P less than 0.01) during administration of isoflurane-N2O (29.0 +/- 4.5 ml X 100 g-1 X min-1) than during administration of either N2O (40.6 +/- 5.5 ml X 100 g-1 X min-1) or halothane-N2O (39.6 +/- 7.8 ml X 100 g-1 X min-1). CBF values during administration of the N2O alone and halothane-N2O were not different during hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thoughts and Progress

In recent years, extracorporeal membrane oxygenation (ECMO) has been used for treatment of neonates with respiratory failure. A prototype of a compact ECMO system for neonates was developed. A single-lumen catheter, inserted into the right atrium via a jugular vein, was used for withdrawal and infusion of blood through the catheter. An extracapillary flow hollow-fiber membrane lung made of microporous polypropylene has a total surface area of 0.6 m2. To prevent the increase of plasma free hemoglobin, the ratio of withdrawal/infusion is controlled by a microcomputer. The system is compact in size with a low priming volume (less than 90 ml), which allows for ECMO with no additional blood transfusions. Its potential application as a respiratory support system is evaluated in animal experiments. The total intermittent veno-veno bypass flow was 15-30 ml/min/kg. The O2 transfer rate was 20 ml/min and the CO2 transfer rate was 33 ml/min at a blood flow rate of 300 ml/min. The O2 and CO2 exchange with the ECMO system was efficient enough to eliminate the respiratory failure induced by mechanical ventilation. The increase in plasma free hemoglobin was only 4 mg/dl after 6 h of ECMO. The system was considered applicable to respiratory aid for neonates.     

Monitoring functional residual capacity (FRC) by quantifying oxygen/carbon dioxide fluxes during a short apnea

BACKGROUND: Clinically applicable methods for measuring FRC are currently lacking. This study presents a new method for FRC monitoring based on quantification of metabolic gas fluxes of O2 and CO2 during a short apnea. METHODS: Base line exchange of oxygen and carbon dioxide was measured with indirect calorimetry. End-tidal ( approximately alveolar) O2 and CO2 concentrations were measured before and after a short apnea, 8-12 s, and FRC was calculated according to standard washin/washout formulas taking into account the increased solubility of CO2 in blood when the tension is increased during the apnea. The method was tested in a lung model with CO2 excretion and O2 consumption achieved by combustion of hydrogen and implemented in six ventilator-treated patients with acute respiratory failure (ARF). RESULTS: In the lung model the method showed excellent correlation (r = 0.98) with minimal bias (34 ml) and a good precision, limits of agreement being 160 and -230 ml, respectively, compared to the reference method. In six ARF patients changes in FRC induced by increase or decrease in PEEP and measured with the O2/CO2 flux FRC method corresponded well with changes in reference values of FRC (r = 0.76-0.94). CONCLUSIONS: A new method has been proposed in which FRC could be monitored from measurements of physiological fluxes of gases during a short apnea with the use of standard ICU equipment and some calculations. We anticipate that with further development, this technique could provide a new tool for monitoring respiratory changes and ventilator management in the ICU.     

Modified nasal cannula for simultaneous oxygen delivery and end-tidal CO2 monitoring during spontaneous breathing

BACKGROUND AND OBJECTIVES: Supplemental oxygen is commonly given via nasal cannulae in spontaneously breathing patients. Our modified nasal cannula with a clamp between the nasal prongs can provide O2 via one nostril and CO2 can be sampled through the other one. We have studied whether this cannula can provide oxygenation similar to a standard cannula without affecting end-tidal CO2 monitoring. METHODS: Eighty-six patients were studied during spinal anaesthesia and sedation. In 15 patients, arterial blood was sampled while O2 was delivered at flow rates of 0, 2 and 4 L min(-1), with or without clamping between the prongs of our modified nasal cannula. In the remaining 71 patients, arterial O2 was measured while using our modified nasal cannula with the clamp applied. End-tidal CO2 was recorded on a capnograph and the correlation between end-tidal and arterial values with our modified nasal cannula was investigated. RESULTS: No end-tidal CO2 waveforms were found with oxygen flow greater than 2L min(-1) without clamping between the prongs. With clamping there was a significant correlation (r = 0.83) between arterial and end-tidal CO2. A Bland-Altman analysis revealed a bias of 0.49 kPa with precision of +/-0.76 kPa. Arterial oxygenation was not affected by our modified nasal prongs with clamp as compared to the standard cannula. CONCLUSION: Our modified nasal cannula can provide continuous monitoring of end-tidal CO2 without affecting oxygen delivery in sedated, spontaneously breathing patients.