Comparison of volume-controlled, pressure-controlled, and pressure-controlled volume-guaranteed ventilation during robot-assisted laparoscopic gynecologic surgery in the Trendelenburg position.

Background: Pressure-controlled ventilation volume-guaranteed (PCV-VG) is being increasingly used for ventilation during general anesthesia. Carbon dioxide (CO2) pneumoperitoneum in the Trendelenburg position is routinely used during robot-assisted laparoscopic gynecologic surgery. Here, we hypothesized that PCV-VG would reduce peak inspiratory pressure (Ppeak), compared to volume-controlled ventilation (VCV) and pressure-controlled ventilation (PCV). Methods: In total, 60 patients were enrolled in this study and randomly assigned to receive VCV, PCV, or PCV-VG. Hemodynamic variables, respiratory variables, and arterial blood gases were measured in the supine position 15 minutes after the induction of anesthesia (T0), 30 and 60 minutes after CO2 pneumoperitoneum and Trendelenburg positioning (T1 and T2, respectively), and 15 minutes after placement in the supine position at the end of anesthesia (T3). Results: The Ppeak was higher in the VCV group than in the PCV and PCV-VG groups (p=0.011). Mean inspiratory pressure (Pmean) was higher in the PCV and PCV-VG groups than in the VCV group (p<0.001). Dynamic lung compliance (Cdyn) was lower in the VCV group than in the PCV and PCV-VG groups (p=0.001). Conclusion: Compared to VCV, PCV and PCV-VG provided lower Ppeak, higher Pmean, and improved Cdyn, without significant differences in hemodynamic variables or arterial blood gas results during robot-assisted laparoscopic gynecologic surgery with Trendelenburg position.

Feasibility and safety of extracorporeal CO2 removal to enhance protective ventilation in acute respiratory distress syndrome: the SUPERNOVA study.

PURPOSE: We assessed feasibility and safety of extracorporeal carbon dioxide removal (ECCO2R) to facilitate ultra-protective ventilation (VT 4 mL/kg and PPLAT ≤ 25 cmH2O) in patients with moderate acute respiratory distress syndrome (ARDS). METHODS: Prospective multicenter international phase 2 study. Primary endpoint was the proportion of patients achieving ultra-protective ventilation with PaCO2 not increasing more than 20% from baseline, and arterial pH > 7.30. Severe adverse events (SAE) and ECCO2R-related adverse events (ECCO2R-AE) were reported to an independent data and safety monitoring board. We used lower CO2 extraction and higher CO2 extraction devices (membrane lung cross-sectional area 0.59 vs. 1.30 m2; flow 300-500 mL/min vs. 800-1000 mL/min, respectively). RESULTS: Ninety-five patients were enrolled. The proportion of patients who achieved ultra-protective settings by 8 h and 24 h was 78% (74 out of 95 patients; 95% confidence interval 68-89%) and 82% (78 out of 95 patients; 95% confidence interval 76-88%), respectively. ECCO2R was maintained for 5 [3-8] days. Six SAEs were reported; two of them were attributed to ECCO2R (brain hemorrhage and pneumothorax). ECCO2R-AEs were reported in 39% of the patients. A total of 69 patients (73%) were alive at day 28. Fifty-nine patients (62%) were alive at hospital discharge. CONCLUSIONS: Use of ECCO2R to facilitate ultra-protective ventilation was feasible. A randomized clinical trial is required to assess the overall benefits and harms. CLINICALTRIALS.GOV: NCT02282657.

The choroid plexus sodium-bicarbonate cotransporter NBCe2 regulates mouse cerebrospinal fluid pH.

KEY POINTS: Normal pH is crucial for proper functioning of the brain, and disorders increasing the level of CO2 in the blood lead to a decrease in brain pH. CO2 can easily cross the barriers of the brain and will activate chemoreceptors leading to an increased exhalation of CO2 . The low pH, however, is harmful and bases such as HCO3- are imported across the brain barriers in order to normalize brain pH. We show that the HCO3- transporter NBCe2 in the choroid plexus of the blood-cerebrospinal fluid barrier is absolutely necessary for normalizing CSF pH during high levels of CO2 . This discovery represents a significant step in understanding the molecular mechanisms behind regulation of CSF pH during acid-base disturbances, such as chronic lung disease. ABSTRACT: The choroid plexus epithelium (CPE) is located in the brain ventricles where it produces the majority of the cerebrospinal fluid (CSF). The hypothesis that normal brain function is sustained by CPE-mediated CSF pH regulation by extrusion of acid-base equivalents was tested by determining the contribution of the electrogenic Na+ -HCO3- cotransporter NBCe2 to CSF pH regulation. A novel strain of NBCe2 (Slc4a5) knockout (KO) mice was generated and validated. The base extrusion rate after intracellular alkalization was reduced by 77% in NBCe2 KO mouse CPE cells compared to control mice. NBCe2 KO mice and mice with CPE-targeted NBCe2 siRNA knockdown displayed a reduction in CSF pH recovery during hypercapnia-induced acidosis of approximately 85% and 90%, respectively, compared to control mice. NBCe2 KO did not affect baseline respiration rate or tidal volume, and the NBCe2 KO and wild-type (WT) mice displayed similar ventilatory responses to 5% CO2 exposure. NBCe2 KO mice were not protected against pharmacological or heating-induced seizure development. In conclusion, we establish the concept that the CPE is involved in the regulation of CSF pH by demonstrating that NBCe2 is necessary for proper CSF pH recovery after hypercapnia-induced acidosis.

Venoarterial Extracorporeal Membrane Oxygenation in Cardiogenic Shock.

Venoarterial extracorporeal membrane oxygenation has emerged as a viable treatment for patients in cardiogenic shock with biventricular failure and pulmonary dysfunction. Advances in pump and oxygenator technology, cannulation strategies, patient selection and management, and durable mechanical circulatory support have contributed to expanded utilization of this technology. However, challenges remain that require investigation to improve outcomes.

[Effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 in rat lung tissues following ischemia/reperfusion].

OBJECTIVE: To establish rat model of lung ischemia/reperfusion (IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 (MMP-9) and the possible mechanisms.
 Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group (S group), a IR group, and an experiment group (RA group) (n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide (PETCO2) reached 56-65 mmHg (1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry (W/D) and lung permeability index (LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured.
 Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion (both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group (P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group (both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly (both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group (P<0.01).
 Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.

Assessment of the optimal operating parameters during extracorporeal CO2 removal with the Abylcap® system.

PURPOSE: Lung protective ventilation is recommended in patients with acute respiratory distress syndrome (ARDS) needing mechanical ventilation. This can however be associated with hypercapnia and respiratory acidosis, such that extracorporeal CO2 removal (ECCO2R) can be applied. The aim of this study was to derive optimal operating parameters for the ECCO2R Abylcap® system (Bellco, Italy). METHODS: We included 4 ARDS patients with a partial arterial oxygen tension over the fraction of inspired oxygen (PaO2/FiO2) lower than 150 mmHg, receiving lung-protective ventilation and treated with the Abylcap® via a double lumen 13.5-Fr dialysis catheter in the femoral vein. Every 24 hours during 5 consecutive days, blood was sampled at the Abylcap® inlet and outlet for different blood flows (QB:200-300-400 mL/min) with 100% O2 gas flow (QG) of 7 L/min, and for different QG (QG: 0.5-1-1.5-3-6-8 L/min) with QB400 mL/min. CO2 and O2 transfer remained constant over 5 days for a fixed QB. RESULTS: We found that, for a fixed QG of 7 L/min, CO2 transfer linearly and significantly increased with QB (i.e. from 58 ± 8 to 98 ± 16 mL/min for QB 200 to 400 mL/min). For a fixed QB of 400 mL/min, CO2 transfer non-linearly increased with QG (i.e. from 39 ± 9 to 98 ± 16 mL/min for QG 0.5 to 8 L/min) reaching a plateau at QG of 6 L/min. CONCLUSIONS: Hence, when using the Abylcap® ECCO2R in the treatment of ARDS patients the O2 flow should be at least 6 L/min while QB should be set at its maximum.

Novel CO2 removal device driven by a renal-replacement system without hemofilter. A first step experimental validation.

OBJECTIVES: To study the technical effectiveness of a novel extracorporeal CO2 removal device in removing CO2 from blood. STUDY DESIGN: Prospective animal study. ANIMALS: Five adult female healthy pigs. METHODS: Hypercapnic pigs were equipped with a low-flow CO2 removal device (PrismaLung(®), Hospal(®)) integrated on a CRRT platform. The rate of CO2 elimination was examined in vivo using a hollow fiber gas exchanger under various conditions (blood flow rates: 200, 300 and 400 mL/min; sweep gas flows: 2, 5, 10 and 50 L/min; FsO2: 0.21 and 1). Statistical analysis was performed with Student t-test. RESULTS: The extracorporeal device produced CO2 removal rates ranging from 35 to 75 mL/min. Efficiency was increased with higher blood and sweep gas flows: reduction of PCO2 of 40.2 ± 13.0 mmHg (relative decrease of 46%, P < 0.001) and increase in pH of 0.24 ± 0.06 (7.21 before and 7.46 after filter, P < 0.001). Animals' blood gases were significantly modified after 10 minutes of treatment: PaCO2 decreased from 81.2 to 70.0 mmHg (relative decrease of 14%, P < 0.001) and pH increased from 7.17 to 7.22 (P < 0.001). No significant changes in arterial blood oxygenation were observed when using pure oxygen (increase of PaO2 from 106 to 107 mmHg, P = 0.36), allowing the use of ambient air as sweep gas through the membrane. CONCLUSIONS: A device based on a Prismaflex(®) platform was technically effective in removing CO2 from the blood, thus decreasing PaCO2 and acidosis in hypercapnic pigs.

Utility of Prehospital Quantitative End Tidal CO2?

INTRODUCTION: End tidal CO2 (ETCO2) has been established as a standard for confirmation of an airway, but its role is expanding. In certain settings ETCO2 closely approximates the partial pressure of arterial CO2 (PaCO2) and has been described as a tool to optimize a patient's ventilatory status. ETCO2 monitors are increasingly being used by EMS personnel to guide ventilation in the prehospital setting. Severely traumatized and burn patients represent a unique population to which this practice has not been validated. HYPOTHESIS: The sole use of ETCO2 to monitor ventilation may lead to avoidable respiratory acidosis. METHODS: A consecutive series of patients with burns or trauma intubated in the prehospital setting over a 24-month period were evaluated. Prehospital arrests were excluded. Absence of ETCO2 transport data and patients without an arterial blood gas (ABG) within 15 minutes of arrival were also excluded. Data collected included demographics, place and time of intubation, service performing intubation, ETCO2 maintained en-route to hospital, and ABG upon arrival. Further data included length of stay, mortality, and injury severity scores. RESULTS: One hundred sixty patients met the inclusion criteria. Prehospital ETCO2 did not correlate with measured PaCO2 (R2 = 0.08). Mean ETCO2 was significantly lower than mean PaCO2 (34 mmHg vs 44 mmHg, P < .005). Patients arriving acidotic were more likely to die. Mean pH on arrival for survivors and decedents was 7.32 and 7.19 respectively (P < .001). Mortality, acidosis, higher base deficits, and more severe injury patterns were all predictors for a worse correlation between ETCO2 and PaCO2 and increased mean difference between the two values. Decedents and patients presenting with a pH <7.2 demonstrated the greatest discrepancy between ETCO2 and PaCO2. The data suggest that patients may be hypoventilated by prehospital providers in order to obtain a prescribed ETCO2. CONCLUSION: ETCO2 is an inadequate tool for predicting PaCO2 or optimizing ventilation in severely injured patients. Adherence to current ETCO2 guidelines in the prehospital setting may contribute to acidosis and increased mortality. Consideration should be given to developing alternate protocols to guide ventilation of the severely injured in the prehospital setting.

Extracorporeal carbon dioxyde removal for additional pulmonary resection after pneumonectomy.

Additional pulmonary surgery in a previously pneumonectomized patient requires apnea during surgical manipulation of the surviving lung. We report on a novel approach to manage the intraoperative apnea period, combining apneic oxygenation and minimally invasive, low flow extracorporeal CO2 removal. A 69-year-old man previously submitted to left pneumonectomy was scheduled for wedge resection of a single right upper lobe lesion. During the intraoperative apnea period, oxygenation was maintained through apneic oxygenation with continuous positive airway pressure (CPAP) of 5 cmH2O and inspiratory oxygen fraction (FiO2) of 1 and respiratory acidosis was prevented through extracorporeal CO2 removal, performed with the Decap® system (Hemodec, Salerno, Italy), a veno¬venous pump-driven extracorporeal circuit including a neonatal membrane lung. The extracorporeal circuit was connected to the right femoral vein, accessed via a 14 Fr double lumen catheter. The blood flow through the circuit was 350 mL/min and the sweep flow of oxygen through the membrane lung was 8 L/min. The intraoperative apnea period lasted 13 minutes. Our approach allowed maintaining normocapnia (PaCO2 38,5 and 40 mmHg before and at the end of the apnea period, respectively), preserving oxygenation (P/F ratio 378, 191, 198 and 200 after 3, 6, 9 and 12 min of apnea, respectively). Our report suggests that the minimally invasive CO2 removal associated with apneic oxygenation is an useful technique for managing anesthesiological situations requiring moderate apnea periods.

Hypercapnic acidosis in ventilator-induced lung injury.

RATIONALE: Permissive hypercapnia is established in lung injury management. Therapeutic hypercapnia causes benefit or harm, depending on the context. Ventilator-associated lung injury has a wide spectrum of candidate mechanisms, affording multiple opportunities for intervention such as hypercapnia to exert benefit or harm. OBJECTIVES: To confirm (1) that hypercapnia attenuates in vivo ventilator-induced lung injury (VILI); (2) biological plausibility of such protection (e.g., dose-response, time series, inflammatory profile); and (3) that the associated biochemical events are consistently beneficial. METHODS: A mouse model of VILI was established in vivo. Injurious ventilation was established, hypercapnia applied and markers of inflammation measured. MEASUREMENTS: Lung injury was quantified by gas exchange, elastance, microvascular leak, histology and levels of cytokines and eicosanoids, cyclooxygenase and tissue nitrotyrosine. MAIN RESULTS: Injurious ventilation caused significant lung injury (mechanics, microvascular leak, histology) and release of inflammatory cytokines, chemokines and eicosanoids. Hypercapnia attenuated these responses, with dose-response and time-dependent effects. No adverse effects of hypercapnia were observed in controls. Hypercapnia suppressed the transcription (mRNA) and translation (protein) of the major inducible prostanoid-generating enzyme (COX-2), but the effects on the downstream eicosanoids were modest. However, hypercapnia significantly increased lung tissue nitrotyrosine-at PaCO(2) levels that were protective. CONCLUSIONS: Hypercapnia provided consistent and biologically plausible in vivo protection against VILI, but elevated lung tissue levels of nitro-tyrosine as previously described in sepsis. Clinicians and those designing clinical trials need to be aware of the potential for detrimental effects when using hypercapnia in order to balance benefits versus harm with this approach.

Damage control resuscitation for the Special Forces medic: simplifying and improving prolonged trauma care: Part One.

Current operational theaters have developed to where medical evacuation and surgical assets are accessible in times comparable to the United States. While this has been an essential tool in achieving the best survivability on a battlefield in our history, the by-product of this experience is a recognized shortcoming in current protocols and capabilities of Special Forces medics for prolonged care. The purpose of this article is to provide a theory of care, identify training and support requirements, and to capitalize on current successful resuscitation theories in developing a more efficient and realistic capability under the worst conditions.

Mechanical determinants of early acute ventilatory failure in COPD patients: a physiologic study.

OBJECTIVE: The purpose of this study is to investigate the respiratory mechanics, breathing pattern, and pressure-generating capacity of respiratory muscles during the early phases of an acute exacerbation of COPD. DESIGN: Prospective study. SETTING: Division of Emergency Critical Care and Chronic Ventilator Unit. PATIENTS: A total of 24 COPD patients: nine patients requiring ventilatory support because of acute respiratory acidosis due to COPD exacerbation (NPPV group, pH 7.28 +/- 0.02); seven patients successfully managed with medical therapy only (SB group, pH 7.39 +/- 0.04); eight clinically stable, long term mechanically ventilated, COPD patients (IPPV group). MEASUREMENTS: Respiratory mechanics during a period of unsupported breathing. RESULTS: A rapid shallow breathing, in the presence of a high drive to breath and a high diaphragmatic tension-time index (TT(di)), was found in NPPV and IPPV groups compared to the SB group (f/V (T) ratio: 118 +/- 43 and 137 +/- 65, respectively, versus 37 +/- 12 breaths/min/L; P (0.1): 5.0 +/- 1.0 and 5.4 +/- 1.4, respectively, versus 2.2 +/- 0.2 cmH(2)O, TT(di): 0.168 +/- 0.035 and 0.161 +/- 0.039, respectively, versus 0.057 +/- 0.033); at variance, PEEPi(dyn) was greater in IPPV compared to the other two groups. A significant relationship was observed between TT(di) ratio and f/V (T) (Rho 0.756). CONCLUSION: During the early phases of an acute exacerbation, patients with COPD and acute respiratory failure had an imbalance between the decreased capacity of the respiratory muscles to generate pressure and the increased respiratory load. This imbalance was similar to that recorded in patients with COPD and chronic ventilatory failure. In both groups, the imbalance was associated with rapid shallow breathing. Among the mechanical constraints to ventilation, only PEEPi,dyn was different between acute and chronic patients with ventilatory failure.

Monitoring of the ventilatory status of anesthetized birds of prey by using end-tidal carbon dioxide measured with a microstream capnometer.

The relationship between end-tidal partial pressure of carbon dioxide (PETCO2), arterial partial pressure of carbon dioxide (PaCO2), and blood pH in isoflurane-anesthetized raptors was evaluated. PaCO2 and pH were determined in serial arterial samples from isoflurane anesthetized birds and compared with concurrent end-tidal partial pressure of carbon dioxide measured with a Microstream sidestream capnograph. Forty-eight paired samples, taken from 11 birds of prey (weighing 416-2,062 g), were used to determine correlations coefficients between PaCO2 and PETCO2, and between PETCO2 and pH. Limits of agreement between PaCO2 and PETCO2 also were calculated. Strong correlations were observed between PaCO2 and PETCO2 (r = 0.94; P < 0.0001) as well as between PETCO2 and pH (r = -0.90; P < 0.0001). However, the level of agreement between PaCO2 and PETCO2 varied considerably. Low values of PETCO2, ranging from 18 to 29 mm Hg, exceeded the concomitantly measured values of PaCO2 by an average of 6.0 mm Hg (6.0 +/- 1.9 mm Hg; mean +/- SD). Conversely, high values of PETCO2, ranging from 50 to 63 mm Hg, were on average 7.6 mm Hg (7.6 +/- 9.8 mm Hg) lower than values of PaCO2. In the 30 to 49 mm Hg range for PETCO2, the difference between PETCO2 and PaCO2 was on average 1.0 mm Hg (1.0 +/- 8.5 mm Hg). These results suggest that the capnograph used provided a sufficiently accurate estimation of arterial partial pressure of carbon dioxide for birds weighing > 400 g and receiving manual positive ventilation with a Bain system. In our study, the linear relationship observed between the pH and the end-tidal partial pressure of carbon dioxide suggested that the monitoring of end-tidal partial pressure of carbon dioxide also can be useful to prevent respiratory acidosis.

Oxygen alert cards and controlled oxygen: preventing emergency admissions at risk of hypercapnic acidosis receiving high inspired oxygen concentrations in ambulances and A&E departments.

BACKGROUND: Appropriate resuscitation of hypoxic patients is fundamental in emergency admissions. To achieve this, it is standard practice of ambulance staff to administer high concentrations of oxygen to patients who may be in respiratory distress. A proportion of patients with chronic respiratory disease will become hypercapnic on this. OBJECTIVES AND METHODS: A scheme was agreed between the authors' hospital and the local ambulance service, whereby patients with a history of previous hypercapnic acidosis with a Pao2 >10.0 kPa--indicating that oxygen may have worsened the hypercapnia--are issued with "O2 Alert" cards and a 24% Venturi mask. The patients are instructed to show these to ambulance and A&E staff who will then use the mask to avoid excessive oxygenation. The scheme was launched in 2001 and this paper present the results of an audit of the scheme in 2004. RESULTS: A total of 18 patients were issued with cards, and 14 were readmitted on 69 occasions. Sufficient documentation for auditing purposes was available for 52 of the 69 episodes. Of these audited admissions, 63% were managed in the ambulance, in line with card-holder protocol. This figure rose to 94% in the accident and emergency department. CONCLUSION: These data support the usability of such a scheme to prevent iatrogenic hypercapnia in emergency admissions.

Comparison of pH-stat versus Alpha-stat during hypothermic cardiopulmonary bypass in the prevention and control of acidosis in cardiac surgery.

OBJECTIVES: To compare the effects of blood-gas management using either alpha-stat (temperature-uncorrected blood-gas management) or pH-stat (temperature-corrected blood-gas management) strategies, 30 patients undergoing coronary artery bypass surgery allocated randomly to either one of the approaches were studied. Acid-base balance, tissue oxygenation, and biochemical parameters were measured at distinct times: before bypass, after 15 min of hypothermia at 32 degrees C, after 45 min of hypothermia at 32 degrees C, after 15 min of rewarming at 37 degrees C, and 45 min after the end of bypass in normothermic conditions. RESULTS: The groups were similar with regard to physical characteristics, physiological parameters, and bypass time. In the pH-stat group, CO2 administered with the aim of correcting pH for the patients hypothermic temperature caused a significant increase in temperature-uncorrected PaCO2 and a decrease in arterial temperature-uncorrected pH at 45 min. During the rewarming period and following bypass, the pH was lower and PaCO2 higher in the pH-stat group (P < 0.001). CONCLUSION: It was found that during the rewarming period and following bypass, the resulting acidosis caused by the procedure was less in the alpha-stat group. It was found that there were no difference between the two groups, with regard to tissue perfusion, as is seen by the tissue oxygenation parameters and lactic acid concentration.

Tracheal double-lumen ventilation attenuates hypercapnia and respiratory acidosis in lung injured pigs.

OBJECTIVE: Evaluation of ventilatory and circulatory effects with coaxial double-lumen tube ventilation for dead-space reduction as compared with standard endotracheal tube ventilation. DESIGN: Experimental study in a pig model of lung lavage induced acute lung injury. SETTING: University research laboratory. MEASUREMENTS AND RESULTS: Tidal volumes of 6, 8 and 10 ml/kg body weight with a set respiratory rate of 20 breaths per minute were used in a random order with both double-lumen ventilation and standard endotracheal tube ventilation. Measurements of ventilatory and circulatory parameters were obtained after steady state at each experimental stage. With a tidal volume of 6 ml/kg, PaCO(2) was reduced from 10.9 kPa (95% CI 9.0-12.9) with a standard endotracheal tube to 8.2 kPa (95% CI 7.0-9.4) with double-lumen ventilation. This corresponds to a reduction in carbon dioxide levels by 25%. At 6 ml/kg, pH increased from 7.17 (95% CI 7.09-7.24) with a standard endotracheal tube to 7.27 (95% CI 7.21-7.32) with double-lumen ventilation. Tracheal pressure was monitored continuously and no difference between single- or double-lumen ventilation was noted at corresponding levels of ventilation. There was no formation of auto-PEEP. Partial tube obstruction due to secretions was not observed during the experiments. CONCLUSIONS: Coaxial double-lumen tube ventilation is an effective adjunct to reduce technical dead space. It attenuates hypercapnia and respiratory acidosis in a lung injury pig model.

Permissive hypercapnia--role in protective lung ventilatory strategies.

"Permissive hypercapnia" is an inherent element of accepted protective lung ventilation. However, there are no clinical data evaluating the efficacy of hypercapnia per se, independent of ventilator strategy. In the absence of such data, it is necessary to determine whether the potential exists for an active role for hypercapnia, distinct from the demonstrated benefits of reduced lung stretch. In this review, we consider four key issues. First, we consider the evidence that protective lung ventilatory strategies improve survival and we explore current paradigms regarding the mechanisms underlying these effects. Second, we examine whether hypercapnic acidosis may have effects that are additive to the effects of protective ventilation. Third, we consider whether direct elevation of CO(2), in the absence of protective ventilation, is beneficial or deleterious. Fourth, we address the current evidence regarding the buffering of hypercapnic acidosis in ARDS. These perspectives reveal that the potential exists for hypercapnia to exert beneficial effects in the clinical context. Direct administration of CO(2) is protective in multiple models of acute lung and systemic injury. Nevertheless, several specific concerns remain regarding the safety of hypercapnia. At present, protective ventilatory strategies that involve hypercapnia are clinically acceptable, provided the clinician is primarily targeting reduced tidal stretch. There are insufficient clinical data to suggest that hypercapnia per se should be independently induced, nor do outcome data exist to support the practice of buffering hypercapnic acidosis. Rapidly advancing basic scientific investigations should better delineate the advantages, disadvantages, and optimal use of hypercapnia in ARDS.

Carbon dioxide added late in inspiration reduces ventilation-perfusion heterogeneity without causing respiratory acidosis.

We have shown previously that inspired CO2 (3-5%) improves ventilation-perfusion (Va/Q) matching but with the consequence of mild arterial hypercapnia and respiratory acidosis. We hypothesized that adding CO2 only late in inspiration to limit its effects to the conducting airways would enhance Va/Q matching and improve oxygenation without arterial hypercapnia. CO2 was added in the latter half of inspiration in a volume aimed to reach a concentration of 5% in the conducting airways throughout the respiratory cycle. Ten mixed-breed dogs were anesthetized and, in a randomized order, ventilated with room air, 5% CO2 throughout inspiration, and CO2 added only to the latter half of inspiration. The multiple inert-gas elimination technique was used to assess Va/Q heterogeneity. Late-inspired CO2 produced only very small changes in arterial pH (7.38 vs. 7.40) and arterial CO2 (40.6 vs. 39.4 Torr). Compared with baseline, late-inspired CO2 significantly improved arterial oxygenation (97.5 vs. 94.2 Torr), decreased the alveolar-arterial Po2 difference (10.4 vs. 15.7 Torr) and decreased the multiple inert-gas elimination technique-derived arterial-alveolar inert gas area difference, a global measurement of Va/Q heterogeneity (0.36 vs. 0.22). These changes were equal to those with 5% CO2 throughout inspiration (arterial Po2, 102.5 Torr; alveolar-arterial Po2 difference, 10.1 Torr; and arterial-alveolar inert gas area difference, 0.21). In conclusion, we have established that the majority of the improvement in gas exchange efficiency with inspired CO2 can be achieved by limiting its application to the conducting airways and does not require systemic acidosis.

pH-stat ventilation management: a simple method of achieving this regimen.

Since the advent of extracorporeal circulation for life support during cardiac surgery, there have been varied opinions as to the best method of ventilating an oxygenator to achieve the optimum arterial blood gas. With respect to the optimum pCO2, clinical investigators have focused primarily on the pros and cons of the alpha-stat and pH-stat ventilation schemes. pH-stat is a ventilation scheme that attempts to maintain the temperature corrected pH of the arterial blood at 7.40, no matter what the actual temperature of the blood. This paper does not attempt to elucidate the benefits of one scheme over the other, but is offered to provide perfusionists with a simple method of achieving pH-stat ventilation, using a CO2 source and materials readily available in any operating room. Strict adherence to a few cautionary notes should enable any perfusionist to safely deliver pH-stat ventilation when indicated. This technique of providing pH-stat ventilation has been used at our institution for over three years. It has proven to be easy to accomplish, adjust and maintain.

Ability and safety of a heated humidifier to control hypercapnic acidosis in severe ARDS.

OBJECTIVE: To assess the ability of a heated humidifier to improve CO(2) clearance in ARDS patients submitted to protective ventilation. DESIGN: Prospective clinical study. SETTING: University hospital intensive care unit. PATIENTS: During a 12-month period, we studied 11 ARDS patients under protective mechanical ventilation with severe hypercapnia. INTERVENTION: When PaCO(2) was above 55 mmHg, the heat and moisture exchanger (HME) was removed and patients were ventilated using a heated humidifier (HH) until their recovery or death. The heated humidifier was inserted on the inspiratory limb of the respirator and the inspirated air was saturated to achieve a temperature of 40 degrees C at the Y connector of ventilator tubing and of 37 degrees C at the outlet of the endotracheal tube. MEASUREMENTS AND RESULTS: Mechanical measurements and blood gas analysis were performed just before removal of the HME, and 30 min after mechanical ventilation using HH. Ventilator parameters were kept constant in the two conditions. Using HH instead of HME, PaCO(2) was safely decreased by 11+/-5 mmHg, without any need to change respiratory rate. No significant difference was noted in intrinsic PEEP or airway plateau pressure. Decrease in PaCO(2) after HME removal was strongly correlated with the initial value of PaCO(2). CONCLUSION: Supposing there is an interest in correcting or limiting hypercapnic acidosis in ARDS patients submitted to protective ventilation, HME removal and use of HH appears to be an efficient and safe way of increasing CO(2) clearance.