19 research outputs found
Effect of PEEP and Tidal Volume on Ventilation Distribution and End-Expiratory Lung Volume: A Prospective Experimental Animal and Pilot Clinical Study
<div><p>Introduction</p><p>Lung-protective ventilation aims at using low tidal volumes (V<sub>T</sub>) at optimum positive end-expiratory pressures (PEEP). Optimum PEEP should recruit atelectatic lung regions and avoid tidal recruitment and end-inspiratory overinflation. We examined the effect of V<sub>T</sub> and PEEP on ventilation distribution, regional respiratory system compliance (C<sub>RS</sub>), and end-expiratory lung volume (EELV) in an animal model of acute lung injury (ALI) and patients with ARDS by using electrical impedance tomography (EIT) with the aim to assess tidal recruitment and overinflation.</p><p>Methods</p><p>EIT examinations were performed in 10 anaesthetized pigs with normal lungs ventilated at 5 and 10 ml/kg body weight V<sub>T</sub> and 5 cmH<sub>2</sub>O PEEP. After ALI induction, 10 ml/kg V<sub>T</sub> and 10 cmH<sub>2</sub>O PEEP were applied. Afterwards, PEEP was set according to the pressure-volume curve. Animals were randomized to either low or high V<sub>T</sub> ventilation changed after 30 minutes in a crossover design. Ventilation distribution, regional C<sub>RS</sub> and changes in EELV were analyzed. The same measures were determined in five ARDS patients examined during low and high V<sub>T</sub> ventilation (6 and 10 (8) ml/kg) at three PEEP levels.</p><p>Results</p><p>In healthy animals, high compared to low V<sub>T</sub> increased C<sub>RS</sub> and ventilation in dependent lung regions implying tidal recruitment. ALI reduced C<sub>RS</sub> and EELV in all regions without changing ventilation distribution. Pressure-volume curve-derived PEEP of 21±4 cmH<sub>2</sub>O (mean±SD) resulted in comparable increase in C<sub>RS</sub> in dependent and decrease in non-dependent regions at both V<sub>T</sub>. This implied that tidal recruitment was avoided but end-inspiratory overinflation was present irrespective of V<sub>T</sub>. In patients, regional C<sub>RS</sub> differences between low and high V<sub>T</sub> revealed high degree of tidal recruitment and low overinflation at 3±1 cmH<sub>2</sub>O PEEP. Tidal recruitment decreased at 10±1 cmH<sub>2</sub>O and was further reduced at 15±2 cmH<sub>2</sub>O PEEP.</p><p>Conclusions</p><p>Tidal recruitment and end-inspiratory overinflation can be assessed by EIT-based analysis of regional C<sub>RS</sub>.</p></div
Respiratory and hemodynamic data of the studied patients.
<p>Data are shown as mean values ± standard deviation. V<sub>T</sub>: tidal volume, F<sub>I</sub>o<sub>2</sub>: fraction of inspired oxygen, PEEP: positive end-expiratory pressure, PIP, peak inspiratory pressure, C<sub>RS</sub>: respiratory system compliance, P<sub>a</sub>co<sub>2</sub>: end-expiratory partial pressure of carbon dioxide, HR: heart rate.</p><p>*The measurement at LIP+7 and high V<sub>T</sub> was not conducted in patient 1 due to excess of peak inspiratory pressure limit of 40 cm H<sub>2</sub>O (see Methods for further details).</p
Regional ventilation and respiratory system compliance.
<p>Ventrodorsal profiles of regional tidal volume (V<sub>T</sub>) (A), regional respiratory system compliance (C<sub>RS</sub>) (C) and differences in regional V<sub>T</sub> (ÎV<sub>T</sub>) (B) and regional C<sub>RS</sub> (ÎC<sub>RS</sub>) (D) with respect to baseline (mean values ±SD in 10 animals). Panel A (V<sub>T</sub> [%]) shows the relative distribution of V<sub>T</sub> in 32 horizontal layers in% of overall V<sub>T</sub> in the chest cross-section. Panel B (ÎV<sub>T</sub> [%]) indicates the respective differences in regional V<sub>T</sub> compared with baseline. It shows a shift in ventilation toward the dorsal regions already with higher V<sub>T</sub> at time point 1 in normal lung and more pronounced shifts at points 3 through 6 with a PEEP set 2 cm H<sub>2</sub>O above the lower inflection point in acute lung injury (ALI). Panel C (C<sub>RS</sub> [ml/kg H<sub>2</sub>O]) shows regional C<sub>RS</sub> in the same 32 layers with the respective differences to baseline provided in panel D (ÎC<sub>RS</sub> [ml/kg H<sub>2</sub>O]). The differences in regional C<sub>RS</sub> indicate slightly lower and higher C<sub>RS</sub> in the ventral and dorsal regions at time point 1. Significantly lower values were found in layers 7 to 12 and significantly higher ones in layers 16 to 25 (layers counting from 1 to 32 in the ventrodorsal direction). ALI (time point 2) resulted in significant decrease in C<sub>RS</sub> in all layers. A small increase in C<sub>RS</sub> in the dorsal regions (significant in layers 23 and 24) with the decreased C<sub>RS</sub> in the ventral regions (significant in layers 1 to 17 and 27 and 28) at time point 3/5. At all other three time points, the findings were comparable. High V<sub>T</sub>, ventilation with 10 ml/kg BW, low V<sub>T</sub>, ventilation with 5 ml/kg BW.</p
End-expiratory lung volume.
<p>Changes in end-expiratory lung volume (ÎEELV) at individual measurement time points in comparison to baseline. The median, the 25th and the 75th percentile, minimum and maximum values of ten animals are shown. The gray areas in the diagram show the positive end-expiratory pressure (PEEP) values during the individual time points. Significant differences between the measurements are indicated. Left Y axis: ÎEELV, right Y axis: PEEP. High V<sub>T</sub>, ventilation with 10 ml/kg BW, low V<sub>T</sub>, ventilation with 5 ml/kg BW.</p
Respiratory and hemodynamic data.
<p>Data are shown as mean values ± standard deviation. V<sub>T</sub>: tidal volume, F<sub>I</sub>o<sub>2</sub>: fraction of inspired oxygen, PEEP: positive end-expiratory pressure, PIP: peak inspiratory pressure, C<sub>RS</sub>: respiratory system compliance, Pco<sub>2</sub>: end-expiratory partial pressure of carbon dioxide, MAP: mean arterial pressure, HR: heart rate. Due to the crossover design data obtained at identical V<sub>T</sub>/ILA settings were combined resulting in the merged time points 5/3 and 6/4 for low V<sub>T</sub> and 3/5 and 4/6 for high V<sub>T</sub> ventilation.</p><p>*: vs. baseline (P<0.05).</p>âĄ<p>: vs. baseline (P<0.01).</p>â <p>: vs. baseline (P<0.0001).</p>â â <p>: vs. time point 1 (P<0.05).</p>âĄâĄ<p>: vs. time point 1 (P<0.001).</p>§<p>: vs. time point 1 (P<0.0001).</p><p>$: vs. time point 2 (P<0.01).</p><p>&: vs. time point 2 (P<0.05).</p
Gas exchange data.
<p>Data are shown as mean values ± standard deviation. ALI: acute lung injury, F<sub>I</sub>o<sub>2</sub>: arterial oxygen saturation, P<sub>a</sub>o<sub>2</sub>: arterial partial pressure of oxygen, P<sub>a</sub>co<sub>2</sub>: arterial partial pressure of carbon dioxide, P: pressure, V: volume.</p><p>At the time point âPV maneuverâ, data was obtained immediately after the low-flow inflation maneuver during ventilation with high V<sub>T</sub> and with PEEP set 2 cmH<sub>2</sub>O above the lower inflection point.</p><p>*: vs. time point 1 (P<0.05).</p><p>**: vs. time point 1 (P<0.001).</p>â <p>: vs. PV maneuver (P<0.0001).</p
Study flowchart.
<p>Ten animals were studied during volume-controlled ventilation during ventilation with 5 ml/kg (baseline) and 10 ml/kg tidal volume (V<sub>T</sub>) (measurement time point 1) in the normal lung (NL) as well as after induction of acute lung injury (ALI) (time point 2) at inspired fractions of oxygen of 0.5 and 1.0, respectively. Then a constant low-flow inflation maneuver (pressure-volume (PV) maneuver) was performed and positive end-expiratory pressure (PEEP) was set 2 cm H<sub>2</sub>O above the lower inflection point (LIP) identified in the PV curve. Using a crossover design, further measurements were performed 5 and 30 min after ventilation with low V<sub>T</sub> and active interventional lung assist (ILA) and after another 5 and 30 min with high V<sub>T</sub> and inactive ILA (no ILA) (time points 3â6). Five animals were randomly ventilated in the reversed chronological order. Ventilator settings of V<sub>T</sub> and PEEP at each measurement time point are shown in the lower part of the Figure. *, time elapsed after the change in ventilator and ILA settings.</p
Regional ventilation distribution.
<p>Examples of functional EIT scans of regional lung ventilation in animal 2 during all measurement time points (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072675#pone-0072675-g001" target="_blank">Figure 1</a> for explanation). The orientation of the scans is indicated (ant., anterior; post., posterior). Panel A: Ventilated areas within the chest cross-section exhibit higher values of relative impedance change and are shown in red tones. In normal lungs (NL), symmetrical ventilation distribution between the right and left lung regions was found. With induction of acute lung injury (ALI), higher ventilation in the right lung region with pronounced ventilation in its ventral part and reduced left lung ventilation especially in its dorsal part were found. After PEEP was set 2 cm H<sub>2</sub>O above the lower inflection point (LIP) according to the pressure-volume curve, a shift in ventilation toward the dependent (dorsal) lung regions was observed. No obvious difference between ventilation with 10 ml/kg V<sub>T</sub> and inactive interventional lung assist (ILA) (high V<sub>T</sub>, no ILA) and ventilation with 5 ml/kg V<sub>T</sub> and active ILA (low V<sub>T</sub>, ILA) was detected. Panel B: Ventilation difference scans of the same animal. Red color indicates increase in regional ventilation, blue color shows the decrease in ventilation compared with baseline.</p
Center of ventilation.
<p>Ventilation distribution during individual measurement time points represented by the geometrical center of ventilation. The center of ventilation is given in percent of the anteroposterior chest diameter. Values above 50 indicate a location in the dorsal half of the chest cross-section. The median, the 25th and the 75th percentile, minimum and maximum values of ten animals are shown. The gray areas in the diagram show the positive end-expiratory pressure (PEEP) values during the individual measurement time points. Significant differences between corresponding high V<sub>T</sub> and low V<sub>T</sub> are indicated. Every group with ALI and high PEEP is significantly different from normal lung and ALI with PEEP 10 cm H<sub>2</sub>O (Time point 2). Left Y axis: center of ventilation, right Y axis: PEEP. High V<sub>T</sub>, ventilation with 10 ml/kg BW, low V<sub>T</sub>, ventilation with 5 ml/kg BW.</p
Acid Sphingomyelinase Serum Activity Predicts Mortality in Intensive Care Unit Patients after Systemic Inflammation: A Prospective Cohort Study
<div><p>Introduction</p><p>Acid sphingomyelinase is involved in lipid signalling pathways and regulation of apoptosis by the generation of ceramide and plays an important role during the host response to infectious stimuli. It thus has the potential to be used as a novel diagnostic marker in the management of critically ill patients. The objective of our study was to evaluate acid sphingomyelinase serum activity (ASM) as a diagnostic and prognostic marker in a mixed intensive care unit population before, during, and after systemic inflammation.</p><p>Methods</p><p>40 patients admitted to the intensive care unit at risk for developing systemic inflammation (defined as systemic inflammatory response syndrome <i>plus</i> a significant procalcitonin [PCT] increase) were included. ASM was analysed on ICU admission, before (<i>PCT<sub>before</sub>)</i>, during (<i>PCT<sub>peak</sub></i>) and after (<i>PCT<sub>low</sub>)</i> onset of SIRS. Patients undergoing elective surgery served as control (Nâ=â8). Receiver-operating characteristics curves were computed.</p><p>Results</p><p>ASM significantly increased after surgery in the eight control patients. Patients from the intensive care unit had significantly higher ASM on admission than control patients after surgery. 19 out of 40 patients admitted to the intensive care unit developed systemic inflammation and 21 did not, with no differences in ASM between these two groups on admission. In patients with SIRS and PCT peak, ASM between admission and <i>PCT<sub>before</sub></i> was not different, but further increased at <i>PCT<sub>peak</sub></i> in non-survivors and was significantly higher at <i>PCT<sub>low</sub></i> compared to survivors. Survivors exhibited decreased ASM at <i>PCT<sub>peak</sub></i> and <i>PCT<sub>low</sub></i>. Receiver operating curve analysis on discrimination of ICU mortality showed an area under the curve of 0.79 for ASM at <i>PCT<sub>low</sub></i>.</p><p>Conclusions</p><p>In summary, ASM was generally higher in patients admitted to the intensive care unit compared to patients undergoing uncomplicated surgery. ASM did not indicate onset of systemic inflammation. In contrast to PCT however, it remained high in non-surviving ICU patients after systemic inflammation.</p></div