Volumetric capnography in acute respiratory distress syndrome / Capnografia volumétrica na síndrome do desconforto respiratório agudo

Volumetric capnography is especially sensitive to disturbances affecting the efficiency of ventilation for gas exchange. Because lung homogeneity is a very fragile property, it is endangered in the majority of diseases that affect the airways, lung parenchyma, or alveolar microcirculation. Acute lung injury and acute respiratory distress syndrome can be conveniently monitored with volumetric capnography. The combination of two advanced technologies—airway flow monitoring and mainstream capnography—allows breath-by-breath bedside computerized determination of the physiological dead space, alveolar heterogeneity, and CO2 elimination. The use of volumetric capnography at the bedside can provide clinicians with important physiological and prognostic data, as well as allowing the effects of therapeutic interventions to be evaluated in critical ill patients receiving mechanical ventilation.

A capnografia volumétrica é especialmente sensível aos problemas que afetam a eficiência da ventilação para a troca gasosa. Uma vez que a homogeneidade do pulmão é uma propriedade muito frágil, a medida da capnografia é um desafio na maioria das doenças que comprometem as vias aéreas, o parênquima pulmonar e a microcirculação alveolar. A lesão pulmonar aguda e síndrome do desconforto respiratório agudo são situações que devem ser monitoradas com a capnografia volumétrica. Essa tecnologia avançada é uma combinação da medida do fluxo aéreo e a capnografia convencional, fazendo com que seja possível computar, à beira do leito, parâmetros como espaço morto, heterogeneidade alveolar e eliminação do CO2. O uso da capnografia volumétrica à beira do leito pode fornecer aos clínicos importantes informações fisiológicas e sobre o prognóstico, assim como seguir o efeito de intervenções terapêuticas nos doentes críticos ventilados mecanicamente.

Different strains of mice present distinct lung tissue mechanics and extracellular matrix composition in a model of chronic allergic asthma.

The impact of genetic factors on asthma is well recognized but poorly understood. We tested the hypothesis that different mouse strains present different lung tissue strip mechanics in a model of chronic allergic asthma and that these mechanical differences may be potentially related to changes of extracellular matrix composition and/or contractile elements in lung parenchyma. Oscillatory mechanics were analysed before and after acetylcholine (ACh) in C57BL/10, BALB/c, and A/J mice, subjected or not to ovalbumin sensitization and challenge. In controls, tissue elastance (E) and resistance (R), collagen and elastic fibres' content, and alpha-actin were higher in A/J compared to BALB/c mice, which, in turn, were more elevated than in C57BL/10. A similar response pattern was observed in ovalbumin-challenged animals irrespective of mouse strain. E and R augmented more in ovalbumin-challenged A/J [E: 22%, R: 18%] than C57BL/10 mice [E: 9.4%, R: 11%] after ACh In conclusion, lung parenchyma remodelled differently yielding distinct in vitro mechanics according to mouse strain.

Mouse strain dependence of lung tissue mechanics: role of specific extracellular matrix composition.

This study analyses the differences between C57BL/10 and BALB/c mice in lung tissue micromechanical behaviour and whether specific histological characteristics are related to the mechanical profile. C57BL/10 and BALB/c subpleural lung strips were submitted to multisinusoidal deformation with frequencies ranging between 0.2 and 3.1 Hz. Tissue resistance (R), elastance (E), and hysteresivity (eta) at each frequency were determined before and 30s, 1, 2, and 3 min after acetylcholine (ACh) treatment. BALB/c mice showed higher E and R, at baseline, as well as greater amount of collagen and elastic fibres, and alpha-actin than C57BL/10 mice. However, E, R, and eta augmented with the same magnitude after ACh treatment in both strains. Baseline R was correlated with collagen fibre content and with the volume proportion of alpha-actin, while E was correlated with elastic and collagen fibres, and alpha-actin contents. In conclusion, BALB/c and C57BL/10 mice present distinct tissue mechanical properties that are accompanied by specific extracellular matrix composition and contractile structures.

What increases type III procollagen mRNA levels in lung tissue: stress induced by changes in force or amplitude?

We hypothesized that stress determined by force could induce higher type III procollagen (PCIII) mRNA expression than the stress determined by amplitude. To that end, rat lung tissue strips were oscillated for 1h under different amplitudes [1, 5 and 10% of resting length (L(B)), at 0.5 x 10(-2) N] and forces (0.25 x 10(-2), 0.5 x 10(-2) and 10(-2)N, at 5% L(B)). Resistance (R), elastance (E) and hysteresivity (eta) were analysed during sinusoidal oscillations at 1Hz. After 1h of oscillation, PCIII mRNA expression was determined by Northern-blot and semiquantitative RT-PCR. Control value of PCIII mRNA was obtained from unstressed strips. E and R increased with augmenting force and decreased with increasing amplitude, while eta remained unaltered. PCIII mRNA expression increased significantly after 1h of oscillation at 10(-2)N and 5% L(B) and remained unchanged for 6h. In conclusion, the stress induced by force but not by amplitude led to the increment in PCIII mRNA expression.

On the preparation of lung strip for tissue mechanics measurement.

It is widely believed that it is fundamental to degas and/or rinse the lung prior to the measurement of the tissue mechanics, so that the undesirable effects of surfactant and localized gas trapping are eliminated. However, one could hypothesize that these mechanisms are bound to disappear in the in vitro preparation since the small tissue sample remains suspended oscillating in an organ bath. To investigate the real necessity to follow these procedures, dynamic mechanical properties were studied in strips of lungs previously rinsed with saline, degassed by ventilation with 100% O(2), or without any of these prior procedures. Resistance, elastance, hysteresivity, and the amounts of airway, blood vessel, and alveolar wall were computed. There was no difference in either tissue mechanics or morphology among the groups. In conclusion, the time-consuming degassing and rinsing steps are not necessary to adequately prepare lung tissue for in vitro mechanical analysis, and eliminating these steps potentially helps preserving the intact microstructure of the tissue.

Evaluation of a noninvasive method for cardiac output measurement in critical care patients.

OBJECTIVE: Thermodilution (TD) is the gold standard to monitor cardiac output (CO) in critical care. However, there is concern about the safety of right-ventricular catheterization. The CO(2) rebreathing technique allows noninvasive CO determination by means of the indirect Fick principle. Our objectives were: (a) to assess the accuracy of a new system of CO measurement using the CO(2) partial rebreathing method (PRCO); (b) to evaluate whether the PRCO itself may induce changes in CO. DESIGN AND SETTING: Prospective study in the intensive care department in a university-affiliated hospital. PATIENTS: Twenty-two mechanically ventilated critically ill patients. INTERVENTIONS: CO measured simultaneously by PRCO and TDCO. MEASUREMENTS AND RESULTS: PRCO and TDCO values were compared by concordance analysis. Stability of cardiac output during PRCO was evaluated by comparing the TDCO measurements before, during, and after the partial rebreathing period using analysis of variance. From a total of 79 valid sets of measurements, bias and precision was calculated at -0.18+/-1.39 l/min. The concordance analysis of lower and intermediate CO values (<7 l/min) yielded a bias and precision calculation of -0.07+/-0.91 l/min. No changes in hemodynamics were observed during the partial rebreathing period. CONCLUSIONS: The noninvasive partial CO(2) rebreathing technique may be an alternative method for CO determination in mechanically ventilated critically ill patients. The rebreathing maneuver alone does not induce changes in CO.