Finger photopletysmography detects early acute blood loss in compensated blood donors: a pilot study.

Objective.Diagnosis of incipient acute hypovolemia is challenging as vital signs are typically normal and patients remain asymptomatic at early stages. The early identification of this entity would affect patients' outcome if physicians were able to treat it precociously. Thus, the development of a noninvasive, continuous bedside monitoring tool to detect occult hypovolemia before patients become hemodynamically unstable is clinically relevant. We hypothesize that pulse oximeter's alternant (AC) and continuous (DC) components of the infrared light are sensitive to acute and small changes in patient's volemia. We aimed to test this hypothesis in a cohort of healthy blood donors as a model of slight hypovolemia.Approach.We planned to prospectively study blood donor volunteers removing 450 ml of blood in supine position. Noninvasive arterial blood pressure, heart rate, and finger pulse oximetry were recorded. Data was analyzed before donation, after donation and during blood auto-transfusion generated by the passive leg-rising (PLR) maneuver.Main results.Sixty-six volunteers (44% women) accomplished the protocol successfully. No clinical symptoms of hypovolemia, arterial hypotension (systolic pressure < 90 mmHg), brady-tachycardia (heart rate <60 and >100 beats-per-minute) or hypoxemia (SpO2< 90%) were observed during donation. The AC signal before donation (median 0.21 and interquartile range 0.17 a.u.) increased after donation [0.26(0.19) a.u;p< 0.001]. The DC signal before donation [94.05(3.63) a.u] increased after blood extraction [94.65(3.49) a.u;p< 0.001]. When the legs' blood was auto-transfused during the PLR, the AC [0.21(0.13) a.u.;p= 0.54] and the DC [94.25(3.94) a.u.;p= 0.19] returned to pre-donation levels.Significance.The AC and DC components of finger pulse oximetry changed during blood donation in asymptomatic volunteers. The continuous monitoring of these signals could be helpful in detecting occult acute hypovolemia. New pulse oximeters should be developed combining the AC/DC signals with a functional hemodynamic monitoring of fluid responsiveness to define which patient needs fluid administration.

Effects of apparatus dead space on volumetric capnograms in neonates with healthy lungs: a simulation study.

BACKGROUND: Volumetric capnography in healthy ventilated neonates showed deformed waveforms, which are supposedly due to technological limitations of flow and carbon dioxide sensors. AIMS: This bench study analyzed the role of apparatus dead space on the shape of capnograms in simulated neonates with healthy lungs. METHODS: We simulated mechanical breaths in neonates of 2, 2.5, and 3 kg of body weight using a neonatal volumetric capnography simulator. The simulator was fed by a fixed amount of carbon dioxide of 6 mL/kg/min. Such simulator was ventilated in a volume control mode using fixed ventilatory settings with a tidal volume of 8 mL/kg and respiratory rates of 40, 35, and 30 breaths per minute for the 2, 2.5 and 3 kg neonates, respectively. We tested the above baseline ventilation with and without an additional apparatus dead space of 4 mL. RESULTS: Simulations showed that adding the apparatus dead space to baseline ventilation increased the amount of re-inhaled carbon dioxide in all neonates: 0.16 ± 0.01 to 0.32 ± 0.03 mL (2 kg), 0.14 ± 0.02 to 0.39 ± 0.05 mL (2.5 kg), and 0.13 ± 0.01 to 0.36 ± 0.05 mL (3 kg); (p < .001). Apparatus dead space was computed as part of the airway dead space, and therefore, the ratio of airway dead space to tidal volume increased from 0.51 ± 0.04 to 0.68 ± 0.06, from 0.43 ± 0.04 to 0.62 ± 0.01 and from 0.38 ± 0.01 to 0.60 ± 0.02 in the 2, 2.5 and 3 kg simulated neonates, respectively (p < .001). Compared to baseline ventilation, adding apparatus dead space decreased the ratio of the volume of phase III to VT size from 31% to 11% (2 kg), from 40% to 16% (2.5 kg) and from 50% to 18% (3 kg); (p < .001). CONCLUSIONS: The addition of a small apparatus dead space artificially deformed the volumetric capnograms in simulated neonates with healthy lungs.

Dynamic Relative Regional Lung Strain Estimated by Electrical Impedance Tomography in an Experimental Model of ARDS.

BACKGROUND: To analyze the role of PEEP on dynamic relative regional strain (DRRS) in a model of ARDS, respective maps were generated by electrical impedance tomography (EIT). METHODS: Eight ARDS pigs submitted to PEEP steps of 0, 5, 10, and 15 cm H2O at fixed ventilation were evaluated by EIT images. DRRS was calculated as (VT-EIT/EELI)/(VT-EIT[15PEEP]/EELI[15PEEP]), where the tidal volume (VT)-EIT and end-expiratory lung impedance (EELI) are the tidal and end-expiratory change in lung impedance, respectively. The measurement at 15 PEEP was taken as reference (end-expiratory transpulmonary pressure > 0 cm H2O). The relationship between EIT variables (center of ventilation, EELI, and DRRS) and airway pressures was assessed with mixed-effects models using EIT measurements as dependent variables and PEEP as fixed-effect variable. RESULTS: At constant ventilation, respiratory compliance increased progressively with PEEP (lowest value at zero PEEP 10 ± 3 mL/cm H2O and highest value at 15 PEEP 16 ± 6 mL/cm H2O; P < .001), whereas driving pressure decreased with PEEP (highest value at zero PEEP 34 ± 6 cm H2O and lowest value at 15 PEEP 21 ± 4 cm H2O; P < .001). The mixed-effect regression models showed that the center of ventilation moved to dorsal lung areas with a slope of 1.81 (1.44-2.18) % points by each cm H2O of PEEP; P < .001. EELI increased with a slope of 0.05 (0.02-0.07) (arbitrary units) for each cm H2O of PEEP; P < .001. DRRS maps showed that local strain in ventral lung areas decreased with a slope of -0.02 (-0.24 to 0.15) with each cm H2O increase of PEEP; P < .001. CONCLUSIONS: EIT-derived DRRS maps showed high strain in ventral lung zones at low levels of PEEP. The findings suggest overdistention of the baby lung.

Multimodal non-invasive monitoring to apply an open lung approach strategy in morbidly obese patients during bariatric surgery.

To evaluate the use of non-invasive variables for monitoring an open-lung approach (OLA) strategy in bariatric surgery. Twelve morbidly obese patients undergoing bariatric surgery received a baseline protective ventilation with 8 cmH2O of positive-end expiratory pressure (PEEP). Then, the OLA strategy was applied consisting in lung recruitment followed by a decremental PEEP trial, from 20 to 8 cmH2O, in steps of 2 cmH2O to find the lung's closing pressure. Baseline ventilation was then resumed setting open lung PEEP (OL-PEEP) at 2 cmH2O above this pressure. The multimodal non-invasive variables used for monitoring OLA consisted in pulse oximetry (SpO2), respiratory compliance (Crs), end-expiratory lung volume measured by a capnodynamic method (EELVCO2), and esophageal manometry. OL-PEEP was detected at 15.9 ± 1.7 cmH2O corresponding to a positive end-expiratory transpulmonary pressure (PL,ee) of 0.9 ± 1.1 cmH2O. ROC analysis showed that SpO2 was more accurate (AUC 0.92, IC95% 0.87-0.97) than Crs (AUC 0.76, IC95% 0.87-0.97) and EELVCO2 (AUC 0.73, IC95% 0.64-0.82) to detect the lung's closing pressure according to the change of PL,ee from positive to negative values. Compared to baseline ventilation with 8 cmH2O of PEEP, OLA increased EELVCO2 (1309 ± 517 vs. 2177 ± 679 mL) and decreased driving pressure (18.3 ± 2.2 vs. 10.1 ± 1.7 cmH2O), estimated shunt (17.7 ± 3.4 vs. 4.2 ± 1.4%), lung strain (0.39 ± 0.07 vs. 0.22 ± 0.06) and lung elastance (28.4 ± 5.8 vs. 15.3 ± 4.3 cmH2O/L), respectively; all p < 0.0001. The OLA strategy can be monitored using noninvasive variables during bariatric surgery. This strategy decreased lung strain, elastance and driving pressure compared with standard protective ventilatory settings.Clinical trial number NTC03694665.

Effect of PEEP on Dead Space in an Experimental Model of ARDS.

BACKGROUND: The difference between Bohr and Enghoff dead space are not well described in ARDS patients. We aimed to analyze the effect of PEEP on the Bohr and Enghoff dead spaces in a model of ARDS. METHODS: 10 pigs submitted to randomized PEEP steps of 0, 5, 10, 15, 20, 25 and 30 cm H2O were evaluated with the use of lung ultrasound images, alveolar-arterial oxygen difference (P(A-a)O2 ), transpulmonary mechanics, and volumetric capnography at each PEEP step. RESULTS: At PEEP ≥ 15 cm H2O, atelectasis and P(A-a)O2 progressively decreased while end-inspiratory transpulmonary pressure (PL), end-expiratory PL, and driving PL increased (all P < .001). Bohr dead space (VDBohr /VT), airway dead space (VDaw /VT), and alveolar dead space (VDalv /VTalv ) reached their highest values at PEEP 30 cm H2O (0.69 ± 0.10, 0.53 ± 0.13 and 0.35 ± 0.06, respectively). At PEEP <15 cm H2O, the increases in atelectasis and P(A-a)O2 were associated with negative end-expiratory PL and highest driving PL. VDBohr /VT and VDaw /VT showed the lowest values at PEEP 0 cm H2O (0.51 ± 0.08 and 0.32 ± 0.08, respectively), whereas VDalv /VTalv increased to 0.27 ± 0.05. Enghoff dead space and its derived VDalv /VTalv showed high values at low PEEPs (0.86 ± 0.02 and 0.79 ± 0.04, respectively) and at high PEEPs (0.84 ± 0.04 and 0.65 ± 0.12), with the lowest values at 15 cm H2O (0.77 ± 0.05 and 0.61 ± 0.11, respectively; all P < .001). CONCLUSIONS: Bohr dead space was associated with lung stress, whereas Enghoff dead space was partially affected by the shunt effect.

Photoplethysmographic characterization of vascular tone mediated changes in arterial pressure: an observational study.

To determine whether a classification based on the contour of the photoplethysmography signal (PPGc) can detect changes in systolic arterial blood pressure (SAP) and vascular tone. Episodes of normotension (SAP 90-140 mmHg), hypertension (SAP > 140 mmHg) and hypotension (SAP < 90 mmHg) were analyzed in 15 cardiac surgery patients. SAP and two surrogates of the vascular tone, systemic vascular resistance (SVR) and vascular compliance (Cvasc = stroke volume/pulse pressure) were compared with PPGc. Changes in PPG amplitude (foot-to-peak distance) and dicrotic notch position were used to define 6 classes taking class III as a normal vascular tone with a notch placed between 20 and 50% of the PPG amplitude. Class I-to-II represented vasoconstriction with notch placed > 50% in a small PPG, while class IV-to-VI described vasodilation with a notch placed < 20% in a tall PPG wave. 190 datasets were analyzed including 61 episodes of hypertension [SAP = 159 (151-170) mmHg (median 1st-3rd quartiles)], 84 of normotension, SAP = 124 (113-131) mmHg and 45 of hypotension SAP = 85(80-87) mmHg. SAP were well correlated with SVR (r = 0.78, p < 0.0001) and Cvasc (r = 0.84, p < 0.0001). The PPG-based classification correlated well with SAP (r = - 0.90, p < 0.0001), SVR (r = - 0.72, p < 0.0001) and Cvasc (r = 0.82, p < 0.0001). The PPGc misclassified 7 out of the 190 episodes, presenting good accuracy (98.4% and 97.8%), sensitivity (100% and 94.9%) and specificity (97.9% and 99.2%) for detecting episodes of hypotension and hypertension, respectively. Changes in arterial pressure and vascular tone were closely related to the proposed classification based on PPG waveform.Clinical Trial Registration NTC02854852.

Postural lung recruitment assessed by lung ultrasound in mechanically ventilated children.

BACKGROUND: Atelectasis is a common finding in mechanically ventilated children with healthy lungs. This lung collapse cannot be overcome using standard levels of positive end-expiratory pressure (PEEP) and thus for only individualized lung recruitment maneuvers lead to satisfactory therapeutic results. In this short communication, we demonstrate by lung ultrasound images (LUS) the effect of a postural recruitment maneuver (P-RM, i.e., a ventilatory strategy aimed at reaerating atelectasis by changing body position under constant ventilation). RESULTS: Data was collected in the operating room of the Hospital Privado de Comunidad, Mar del Plata, Argentina. Three anesthetized children undergoing mechanical ventilation at constant settings were sequentially subjected to the following two maneuvers: (1) PEEP trial in the supine position PEEP was increased to 10 cmH2O for 3 min and then decreased to back to baseline. (2) P-RM patient position was changed from supine to the left and then to the right lateral position for 90 s each before returning to supine. The total P-RM procedure took approximately 3 min. LUS in the supine position showed similar atelectasis before and after the PEEP trial. Contrarily, atelectasis disappeared in the non-dependent lung when patients were placed in the lateral positions. Both lungs remained atelectasis free even after returning to the supine position. CONCLUSIONS: We provide LUS images that illustrate the concept and effects of postural recruitment in children. This maneuver has the advantage of achieving recruitment effects without the need to elevate airways pressures.

Doppler images of intra-pulmonary shunt within atelectasis in anesthetized children.

BACKGROUND: Doppler images of pulmonary vessels in pulmonary diseases associated with subpleural consolidations have been described. Color Doppler easily identifies such vessels within consolidations while spectral Doppler analysis allows the differentiation between pulmonary and bronchial arteries. Thus, Doppler helps in diagnosing the nature of consolidations. To our knowledge, Doppler analysis of pulmonary vessels within anesthesia-induced atelectasis has never been described before. The aim of this case series is to demonstrate the ability of lung ultrasound to detect the shunting of blood within atelectatic lung areas in anesthetized children. FINDINGS: Three anesthetized and mechanically ventilated children were scanned in the supine position using a high-resolution linear probe of 6-12 MHz. Once subpleural consolidations were detected in the most dependent posterior lung regions, the probe was rotated such that its long axis followed the intercostal space. In this oblique position, color Doppler mapping was performed to detect blood flow within the consolidation. Thereafter, pulsed waved spectral Doppler was applied in the previously identified vessels during a short expiratory pause, which prevented interferences from respiratory motion. Different flow patterns were identified which corresponded to both, pulmonary and bronchial vessels. Finally, a lung recruitment maneuver was performed which leads to the complete resolution of the aforementioned consolidation thereby confirming the pathophysiological entity of anesthesia-induced atelectasis. CONCLUSIONS: Lung ultrasound is a non-invasive imaging tool that not only enables the diagnosis of anesthesia-induced atelectasis in pediatric patients but also analysis of shunting blood within this consolidation.

Real-time images of tidal recruitment using lung ultrasound.

BACKGROUND: Ventilator-induced lung injury is a form of mechanical damage leading to a pulmonary inflammatory response related to the use of mechanical ventilation enhanced by the presence of atelectasis. One proposed mechanism of this injury is the repetitive opening and closing of collapsed alveoli and small airways within these atelectatic areas-a phenomenon called tidal recruitment. The presence of tidal recruitment is difficult to detect, even with high-resolution images of the lungs like CT scan. The purpose of this article is to give evidence of tidal recruitment by lung ultrasound. FINDINGS: A standard lung ultrasound inspection detected lung zones of atelectasis in mechanically ventilated patients. With a linear probe placed in the intercostal oblique position. We observed tidal recruitment within atelectasis as an improvement in aeration at the end of inspiration followed by the re-collapse at the end of expiration. This mechanism disappeared after the performance of a lung recruitment maneuver. CONCLUSIONS: Lung ultrasound was helpful in detecting the presence of atelectasis and tidal recruitment and in confirming their resolution after a lung recruitment maneuver.

Volumetric capnography: the time has come.

PURPOSE OF REVIEW: Volumetric capnography (VCap) measures the kinetics of carbon dioxide (CO2) elimination on a breath-by-breath basis. A volumetric capnogram contains extensive physiological information about metabolic production, circulatory transport and CO2 elimination within the lungs. VCap is also the best clinical tool to measure dead spaces allowing a detailed analysis of the functional components of each tidal volume, thereby providing clinically useful hints about the lung's efficiency of gas exchange. Difficulties in its bedside measurement, oversimplifications of its interpretation along with prevailing misconceptions regarding dead space analysis have, however, limited its adoption as a routine tool for monitoring mechanically ventilated patients. RECENT FINDINGS: Improvements in CO2 measuring technologies and more advanced algorithms for faster and more accurate analysis of volumetric capnograms have increased our physiological understanding and thus the clinical usefulness of VCap. The recently validated VCap-based method for estimating alveolar partial pressure of CO2 provided a breakthrough for a fully noninvasive breath-by-breath measurement of physiological dead space. SUMMARY: Recent advances in VCap and our improved understanding of its clinical implications may help in overcoming the known limitations and reluctances to include expired CO2 kinetics and dead space analysis in routine bedside monitoring. It is about time to start using this powerful monitoring tool to support decision making in the intensive care environment.

Reference values for volumetric capnography-derived non-invasive parameters in healthy individuals.

The aim of this study was to determine typical values for non-invasive volumetric capnography (VCap) parameters for healthy volunteers and anesthetized individuals. VCap was obtained by a capnograph connected to the airway opening. We prospectively studied 33 healthy volunteers 32 ± 6 years of age weighing 70 ± 13 kg at a height of 171 ± 11 cm in the supine position. Data from these volunteers were compared with a cohort of similar healthy anesthetized patients ventilated with the following settings: tidal volume (VT) of 6-8 mL/kg, respiratory rate 10-15 bpm, PEEP of 5-6 cmH2O and FiO2 of 0.5. Volunteers showed better clearance of CO2 compared to anesthetized patients as indicated by (median and interquartile range): (1) an increased elimination of CO2 per mL of VT of 0.028 (0.005) in volunteers versus 0.023 (0.003) in anesthetized patients, p < 0.05; (2) a lower normalized slope of phase III of 0.26 (0.17) in volunteers versus 0.39 (0.38) in anesthetized patients, p < 0.05; and (3) a lower Bohr dead space ratio of 0.23 (0.05) in volunteers versus 0.28 (0.05) in anesthetized patients, p < 0.05. This study presents reference values for non-invasive volumetric capnography-derived parameters in healthy individuals. Mechanical ventilation and anesthesia altered these values significantly.

States of low pulmonary blood flow can be detected non-invasively at the bedside measuring alveolar dead space.

We tested whether the ratio of alveolar dead space to alveolar tidal volume (VD(alv)/VT(alv)) can detect states of low pulmonary blood flow (PBF) in a non-invasive way. Fifteen patients undergoing cardiovascular surgeries with cardiopulmonary bypass (CPB) were studied. CPB is a technique that excludes the lungs from the general circulation. The weaning of CPB is a model that manipulates PBF in vivo because each time blood flow through the CPB decreases, expected PBF (ePBF) increases. Patients were liberated from CPB in steps of 20 % every 2' starting from 100 % CPB (very low ePBF) to 0 % CPB (100 % ePBF). During constant ventilation, volumetric capnograms were recorded and Bohr's dead space ratio (VD(Bohr)/VT), VD(alv)/VT(alv) and the ratio of airway dead space to tidal volume (VD(aw)/VT) were calculated. Before CPB, VD(Bohr)/VT was 0.36 ± 0.05, VD(aw)/VT 0.21 ± 0.04 and VD(alv)/VT(alv) 0.18 ± 0.06 (mean ± SD). During weaning from CPB, VD(aw)/VT remained unchanged while VD(Bohr)/VT and VD(alv)/VT(alv) decreased with increasing ePBF. At CPB of 80, 60, 40 and 20 % VD(Bohr)/VT was 0.64 ± 0.06, 0.55 ± 0.06, 0.47 ± 0.05 and 0.40 ± 0.04, respectively; p < 0.001 and VD(alv)/VT(alv) 0.53 ± 0.07, 0.40 ± 0.07, 0.29 ± 0.06 and 0.25 ± 0.04, respectively; p < 0.001). After CPB, VD(Bohr)/VT and VD(alv)/VT(alv) reached values similar to baseline (0.37 ± 0.04 and 0.19 ± 0.06, respectively). At constant ventilation the alveolar component of VD(Bohr)/VT increased in proportion to the deficit in lung perfusion.

Rationale of dead space measurement by volumetric capnography.

Dead space is the portion of a tidal volume that does not participate in gas exchange because it does not get in contact with blood flowing through the pulmonary capillaries. It is commonly calculated using volumetric capnography, the plot of expired carbon dioxide (CO(2)) versus tidal volume, which is an easy bedside assessment of the inefficiency of a particular ventilatory setting. Today, Bohr's original dead space can be calculated in an entirely noninvasive and breath-by-breath manner as the mean alveolar partial pressure of CO(2) (Paco(2)) which can now be determined directly from the capnogram. The value derived from Enghoff's modification of Bohr's formula (using Paco(2) instead of PACO(2)) is a global index of the inefficiency of gas exchange rather than a true "dead space" because it is influenced by all causes of ventilation/perfusion mismatching, from real dead space to shunt. Therefore, the results obtained by Bohr's and Enghoff's formulas have different physiological meanings and clinicians must be conscious of such differences when interpreting patient data. In this article, we describe the rationale of dead space measurements by volumetric capnography and discuss its main clinical implications and the misconceptions surrounding it.

Atelectasis and perioperative pulmonary complications in high-risk patients.

PURPOSE OF REVIEW: This review evaluates the link between perioperative lung atelectasis and postoperative pulmonary complications (PPCs) and how appropriate ventilatory strategies could mitigate this problem. RECENT FINDINGS: Atelectasis may contribute to serious PPCs including respiratory failure and pneumonia. Ventilator settings during anesthesia, especially with higher tidal volumes (V(T)) (>10  ml/kg), high plateau pressures (>30  cmH(2)O) and without positive end expiratory pressure (PEEP), are associated with lung injury even in healthy, but partially collapsed, lungs. These injurious settings may cause inflammation which is related to repetitive tidal recruitment and alveolar overdistension. Such ventilator-induced lung injury can be attenuated by using low V(T) and plateau pressures at sufficient PEEP, ideally after actively recruiting the lungs. The use of continuous positive airway pressure and 'lower' FiO(2) during anesthetic induction, intraoperative use of lower FiO(2), low V(T), lung recruitment and PEEP ('protective ventilatory strategy') in conjunction with postoperative early mobilization, breathing exercises and continuous positive airway pressure may help in maintaining lung aeration, thereby decreasing hypoxemia and risk of postoperative pneumonia. Evidence is accumulating suggesting that the incidence of postoperative pulmonary complication could be markedly reduced if an 'open lung' philosophy was adopted for the perioperative care. SUMMARY: A goal-directed ventilatory approach keeping an 'open lung' condition during the perioperative period may reduce the incidence of PPCs.

Validation of Bohr dead space measured by volumetric capnography.

PURPOSE: Bohr's dead space (VD(Bohr)) is commonly calculated using end-tidal CO(2) instead of the true alveolar partial pressure of CO(2) (PACO(2)). The aim of this work was to validate VD(Bohr) using PACO(2) derived from volumetric capnography (VC) against VD(Bohr) with PACO(2) values obtained from the standard alveolar air formula. METHODS: Expired gases of seven lung-lavaged pigs were analyzed at different lung conditions using main-stream VC and multiple inert gas elimination technique (MIGET). PACO(2) was determined by VC as the midpoint of the slope of phase III of the capnogram, while mean expired partial pressure of CO(2) (PeCO(2)) was calculated as the mean expired fraction of CO(2) times the barometric minus the water vapor pressure. MIGET estimated expired CO(2) output (VCO(2)) and PeCO(2) by its V/Q algorithms. Then, PACO(2) was obtained applying the alveolar air formula (PACO(2) = VCO(2)/alveolar ventilation). RESULTS: We found close linear correlations between the two methods for calculating both PACO(2) (r = 0.99) and VD(Bohr) (r = 0.96), respectively (both p < 0.0001). Mean PACO(2) from VC was very similar to the one obtained by MIGET with a mean bias of -0.10 mmHg and limits of agreement between -2.18 and 1.98 mmHg. Mean VD(Bohr) from VC was close to the value obtained by MIGET with a mean bias of 0.010 ml and limits of agreement between -0.044 and 0.064 ml. CONCLUSIONS: VD(Bohr) can be calculated with accuracy using volumetric capnography.

Lung recruitment and positive end-expiratory pressure have different effects on CO2 elimination in healthy and sick lungs.

BACKGROUND: We studied the effects that the lung recruitment maneuver (RM) and positive end-expiratory pressure (PEEP) have on the elimination of CO(2) per breath (Vtco(2,br)). METHODS: In 7 healthy and 7 lung-lavaged pigs at constant ventilation, PEEP was increased from 0 to 18 cm H(2)O and then decreased to 0 in steps of 6 cm H(2)O every 10 minutes. Cycling RMs with plateau pressure/PEEP of 40/20 (healthy) and 50/25 (lavaged) cm H(2)O were applied for 2 minutes between 18-PEEP steps. Volumetric capnography, respiratory mechanics, blood gas, and hemodynamic data were recorded. RESULTS: In healthy lungs before the RM, Vtco(2,br) was inversely proportional to PEEP decreasing from 4.0 (3.6-4.4) mL (median and interquartile range) at 0-PEEP to 3.1 (2.8-3.4) mL at 18-PEEP (P < 0.05). After the RM, Vtco(2,br) increased from 3.3 (3-3.6) mL at 18-PEEP to 4.0 (3.5-4.5) mL at 0-PEEP (P < 0.05). In lavaged lungs before the RM, Vtco(2,br) increased initially from 2.0 (1.7-2.3) mL at 0-PEEP to 2.6 (2.2-3) mL at 12-PEEP (P < 0.05) but then decreased to 2.4 (2-2.8) mL when PEEP was increased further to 18 cm H(2)O (P < 0.05). After the RM, the highest Vtco(2,br) of 2.9 (2.1-3.7) mL was observed at 12-PEEP and then decreased to 2.5 (1.9-3.1) mL at 0-PEEP (P < 0.05). Vtco(2,br) was directly related to changes in lung perfusion, the area of gas exchange, and alveolar ventilation but inversely related to changes in dead space. CONCLUSIONS: CO(2) elimination by the lungs was dependent on PEEP and recruitment and showed major differences between healthy and lavaged lungs.

Prevention and reversal of lung collapse during the intra-operative period.

General anaesthesia induces ventilation/perfusion mismatch by lung collapse. Such lung collapse predisposes patients to preoperative complications since it can persist for several hours or days after surgery. Atelectasis can be partially prevented by using continuous positive airway pressure (CPAP) and/or by lowering FiO2 during anaesthesia induction. However, these manoeuvres are dangerous for patients presenting with challenging airway or ventilator conditions. Lung recruitment manoeuvres (RMs) are ventilatory strategies that aim to restore the aeration of normal lungs. They consist of a brief and controlled increment in airway pressure to open up collapsed areas of the lungs and sufficient positive end-expiratory pressure (PEEP) to keep them open afterward. The application of RMs during anaesthesia normalises lung function along the intraoperative period. There is physiological evidence that patients of all ages and any kind of surgery benefit from such an active intervention. The effect of RMs on patient outcome in the postoperative period is, however, not yet known.

Model fitting of volumetric capnograms improves calculations of airway dead space and slope of phase III.

BACKGROUND: This study assessed the performance of a Functional Approximation based on a Levenberg-Marquardt Algorithm (FA-LMA) to calculate airway dead space (VD(aw)) and the slope of phase III (S(III)) from capnograms. METHODS: We performed mathematical simulations to test the effect of noises on the calculation of VD(aw) and S(III). Data from ten mechanically ventilated patients at 0, 5 and 10 cmH(2)O of PEEP were also studied. FA-LMA was compared with the traditional Fowler's method (FM). RESULTS: Simulations showed that: (1) The FM determined VD(aw) with accuracy only if the capnogram approximated a symmetrical curve (S(III) = 0). When capnograms became asymmetrical (S(III) > 0), the FM underestimated VD(aw) (-3.1% to -0.9%). (2) When adding noises on 800 capnograms, VD(aw) was underestimated whenever the FM was used thereby creating a bias between -5.54 and -1.28 ml at standard deviations (SD) of 0.1-1.8 ml (P < 0.0001). FA-LMA calculations of VD(aw) were close to the simulated values with the bias ranging from -0.21 to 0.16 ml at SD from 0.1 to 0.4 ml. The FM overestimated S(III) and showed more bias (0.0041-0.0078 mmHg/ml, P < 0.0001) than the FA-LMA (0.0002-0.0030 mmHg/ml). When calculating VD(aw) from patients, variability was less with the FA-LMA leading to mean variation coefficients of 0.0102, 0.0111 and 0.0123 compared to the FM (0.0243, 0.0247 and 0.0262, P < 0.001) for 0, 5 and 10 cmH(2)O of PEEP, respectively. The FA-LMA also showed less variability in S(III) with mean variation coefficients of 0.0739, 0.0662 and 0.0730 compared to the FM (0.1379, 0.1208 and 0.1246, P < 0.001) for 0, 5 and 10 cmH(2)O of PEEP, respectively. CONCLUSIONS: The Functional Approximation based on a Levenberg-Marquardt Algorithm showed less bias and dispersion compared to the traditional Fowler's method when calculating VD(aw) and S(III).

Pulmonary blood flow generates cardiogenic oscillations.

Cardiogenic oscillations are small waves produced by heartbeats, which are superimposed on the pressure and flow signals at the airway opening. The aim of this study was to investigate the role of the two main factors believed to generate these oscillations: (1) contact between heart and lungs and (2) pulmonary blood flow. We studied 15 heart surgery patients on cardiopulmonary bypass so both factors could be manipulated independently. At minimal heart-lung contact pressure and flow oscillations were larger than during maximal contact (1.20+/-0.17 cmH(2)O and 2.36+/-0.08 L min(-1) vs 0.92+/-0.15 cmH(2)O and 1.78+/-0.26 L min(-1), mean+/-SD, p<0.05). Cardiogenic oscillations for pressure and flow were smaller at 50% compared to 100% pulmonary blood flow (0.80+/-0.12 cmH(2)O and 1.56+/-0.34 L min(-1) vs 1.19+/-0.14 cmH(2)O and 2.38+/-0.19 L min(-1)). We conclude that the amount of pulmonary blood flow and not the contact between heart and lungs is the main factor determining the amplitude of cardiogenic oscillations.