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Purpose: Regulation of spontaneous breathing is highly complex and may be influenced by drugs administered during the perioperative period. Because of their different pharmacological properties we hypothesized that midazolam and s-ketamine exert different effects on the variability of minute ventilation (MV), tidal volume (TV) and respiratory rate (RR). Methods: Patients undergoing procedural sedation (PSA) with propofol and remifentanil received a single dose of midazolam (1–3 mg, n = 10) or s-ketamine (10–25 mg, n = 10). We used non-invasive impedance-based respiratory volume monitoring to record RR as well as changes in TV and MV. Variability of these three parameters was calculated as coefficients of variation. Results: TV and MV decreased during PSA to a comparable extent in both groups, whereas there was no significant change in RR. In line with our hypothesis we observed marked differences in breathing variability. The variability of MV (– 47.5% ± 24.8%, p = 0.011), TV (– 42.1% ± 30.2%, p = 0.003), and RR (– 28.5% ± 29.3%, p = 0.011) was significantly reduced in patients receiving midazolam. In contrast, variability remained unchanged in patients receiving s-ketamine (MV + 16% ± 45.2%, p = 0.182; TV +12% ± 47.7%, p = 0.390; RR +39% ± 65.2%, p = 0.129). After termination of PSA breathing variables returned to baseline values. Conclusions: While midazolam reduces respiratory variability in spontaneously breathing patients undergoing procedural sedation, s-ketamine preserves variability suggesting different effects on the regulation of spontaneous breathing. [ABSTRACT FROM AUTHOR]

Monitoring of postoperative pulmonary function usually includes respiratory rate and oxygen saturation measurements. We hypothesized that changes in postoperative respiratory rate do not correlate with changes in tidal volume or minute ventilation. In addition, we hypothesized that variability of minute ventilation and tidal volume is larger than variability of respiratory rate. Respiratory rate and changes in tidal volume and in minute ventilation were continuously measured in 27 patients during 24 h following elective abdominal surgery, using an impedance-based non-invasive respiratory volume monitor (ExSpiron, Respiratory Motion, Waltham, MA, US). Coefficients of variation were used as a measure for variability of respiratory rate, tidal volume and minute ventilation. Data of 38,149 measurements were analyzed. We found no correlation between respiratory rate and tidal volume or minute ventilation (r2 = 0.02 and 0.01). Mean respiratory rate increased within the first 24 h after abdominal surgery from 13.9 ± 2.5 to 16.2 ± 2.4 breaths/min (p = 0.008), while tidal volume and minute ventilation remained unchanged (p = 0.90 and p = 0.18). Of interest, variability of respiratory rate (0.21 ± 0.06) was significantly smaller than variability of tidal volume (0.37 ± 0.12, p < 0.001) and minute ventilation (0.41 ± 0.12, p < 0.001). Changes in postoperative respiratory rate do not allow conclusions about changes in tidal volume or minute ventilation. We suggest that postoperative alveolar hypoventilation may not be recognized by monitoring respiratory rate alone. Variability of respiratory rate is smaller than variability in tidal volume and minute ventilation, suggesting that adaptations of alveolar ventilation to metabolic needs may be predominately achieved by variations in tidal volume. [ABSTRACT FROM AUTHOR]

Purpose: Most randomized controlled trials (RCTs) in patients with acute respiratory distress syndrome (ARDS) revealed indeterminate or conflicting study results. We aimed to systematically evaluate between-trial heterogeneity in reporting standards and trial outcome.Methods: A systematic review of RCTs published between 2000 and 2019 was performed including adult ARDS patients receiving lung-protective ventilation. A random-effects meta-regression model was applied to quantify heterogeneity (non-random variability) and to evaluate trial and patient characteristics as sources of heterogeneity.Results: In total, 67 RCTs were included. The 28-day control-group mortality rate ranged from 10 to 67% with large non-random heterogeneity (I2 = 88%, p < 0.0001). Reported baseline patient characteristics explained some of the outcome heterogeneity, but only six trials (9%) reported all four independently predictive variables (mean age, mean lung injury score, mean plateau pressure and mean arterial pH). The 28-day control group mortality adjusted for patient characteristics (i.e. the residual heterogeneity) ranged from 18 to 45%. Trials with significant benefit in the primary outcome reported a higher control group mortality than trials with an indeterminate outcome or harm (mean 28-day control group mortality: 44% vs. 28%; p = 0.001).Conclusion: Among ARDS RCTs in the lung-protective ventilation era, there was large variability in the description of baseline characteristics and significant unexplainable heterogeneity in 28-day control group mortality. These findings signify problems with the generalizability of ARDS research and underline the urgent need for standardized reporting of trial and baseline characteristics. [ABSTRACT FROM AUTHOR]

Purpose: Traumatic brain injury (TBI) is a major cause of trauma-related visits to emergency departments (ED). Determination of monitoring requirements of patients with apparently mild TBI is challenging. Patients may turn out to be more severely injured than initially assumed, and failure to identify these patients constitutes a serious threat to patient safety. We, therefore, aimed to identify clinical risk factors for more severe injuries in patients with apparently mild TBI.Methods: In a retrospective cohort analysis performed at two level I trauma centers, 808 patients aged ≥ 16 presenting to the ED with head trauma and a Glasgow Coma Scale (GCS) score 13-15 who received a head CT scan were studied. Discrepancies between the initial TBI severity as determined by GCS and severity as determined post hoc by the Head Abbreviated Injury Score were assessed. Multiple logistic regression was used to identify risk factors of such discrepancies.Results: 104 (12.9%) patients were more severely injured than initially classified. A GCS < 15 at presentation (GCS 13: OR 6.2, [95% CI 3.8-9.9]; GCS 14: OR 2.7, [2.0-3.7]), an SpO2 < 90% (OR 5.4, [1.2-23.4]), loss of consciousness (OR 2.3, [1.5-3.5]), absence of equal and reactive pupils (OR 2.1, [1.6-2.7]), transport by ambulance (OR 2.0, [1.7-2.4]), and use of anticoagulant drugs (OR 1.2, [1.1-1.3]) were independent risk factors of more severe injury.Conclusions: Six risk factors of more severe injury in patients presenting with apparently mild TBI were identified. Patients with any of these factors should be thoroughly monitored for signs of neurologic deterioration. [ABSTRACT FROM AUTHOR]

Objective: Erythrocytes influence the magnitude of hypoxia-induced pulmonary artery pressure increase. It is, however, unknown to what extent haemoconcentration and haemodilution affect this response and whether intrapulmonary blood volume (and thus vessel dimensions) alters the magnitude of pressure increase. Furthermore, it is unclear whether the haemodilution/ haemoconcentration-dependent pressure increase is flow-related, via flow-dependent changes in vasomotor tone or rheologic effects, or can also be observed under no-flow conditions.Design: Experimental study in isolated rabbit lungs (n = 12) perfused with autologous blood at constant flow (100 ml/min) and ventilated with 5% carbon dioxide in air.Setting: Laboratory for experimental studies.Interventions: Haemoconcentration (centrifugation) and haemodilution (Krebs-Henseleit/albumin) were carried out, resulting in haematocrits between 50% and 0%. During hypoxic ventilation, inspiratory oxygen fraction was reduced from 0.20 to 0.03.Measurements and Results: Under constant flow conditions, haemodilution (from a Hct of 34-36% to 0-1%) decreased hypoxic pulmonary artery pressure response to one-third (from 10.8 +/- 2.3 cmH2O to 3.1 +/- 1.0 cmH2O, P < 0.05), while haemoconcentration did not affect the magnitude of hypoxic response (10.5 +/- 2.0 cmH2O). For all haematocrit values an increase in pulmonary blood volume (by 5 ml) decreased the magnitude of pressure response. Hypoxia-induced changes in static vascular filling pressure (double occlusion pressure) and vascular compliance were used to assess the strength of hypoxic vasoconstriction under static conditions. Neither haemoconcentration nor haemodilution altered hypoxia-induced changes in either variable.Conclusions: The magnitude of the acute hypoxic pressure response is not altered by haemoconcentration, but significantly reduced by haemodilution. In contrast, neither haemoconcentration nor haemodilution influenced hypoxia-induced changes in static vascular filling pressure and compliance. This suggests that the degree of hypoxic pulmonary vasoconstriction is not affected under static conditions and that the red blood cell-dependence of the magnitude of hypoxic pressure response is based on flow-related mechanisms. [ABSTRACT FROM AUTHOR]

Objective: Transcapillary heat transfer after injections of cold saline into the right atrium generates bronchial thermodilution curves resembling those observed in the aorta. Under the assumption that no indicator is lost or gained within the pulmonary capillary bed and changes in blood temperature are instantaneously recorded in the bronchial system, we tested the hypothesis that flow rates calculated from bronchial temperature-time curves are similar to those from aortic curves.Design: Comparative study of two cardiac output estimates in five dogs.Setting: Research laboratory for Experimental Anaesthesiology.Interventions: Cardiac output was decreased (repeated withdrawal of blood) and increased (infusion of colloids or dobutamine) in order to study a wide range of cardiac outputs.Measurements and Results: Thermistors were placed in a bronchiole (wedge position) and in the ascending aorta of anaesthetized dogs. Bronchial and aortic thermodilution curves were recorded after injection of 5 ml ice-cold saline into the right atrium. We found that bronchial thermodilution yields flow estimates similar to those from aortic curves. Correlation between the two flow estimates was acceptable (r = 0.84) with a mean difference between the two of less than 2%.Conclusion: We conclude that the Stewart-Hamilton equation may be extended to bronchial temperature-time curves for estimations of cardiac output. At this time, however, we do not advocate bronchial thermistors as suitable and less invasive alternatives to pulmonary arterial catheters for routine cardiac output measurements in patients. [ABSTRACT FROM AUTHOR]

Quantitative information about the effects of pulmonary blood volume ( Qp) on pulmonary haemodynamics is lacking since Qp changes inevitably with flow. To separate flow-dependent from volume-dependent changes in intravascular pressures we imposed changes in Qp (measured continuously) by altering outflow pressure in seven isolated, blood-perfused rabbit lungs and studied the effects of Qp on the relations between arteriovenous pressure gradient (Δ P) and blood flow ( Q·) under two conditions: flow-dependent volume changes were either permitted or compensated. In the latter circumstances, Δ P changed more for a given change in Q·. The Δ P/ Q· relations were shifted to smaller Δ P when Qp was increased. Hence, the calculated flow resistance ( R = Δ P/ Q·) decreased with increasing Qp at a given Q·. Assuming constant viscosity, changes in R can be predicted from changes in vessel geometry and thus Qp. We found that R increased less than expected (by a factor of 3–7.5 instead of 9) when Qp was reduced to one-third. This discrepancy may be explained by a change in blood distribution within the lung despite constant Qp and by a change in apparent blood viscosity with Q·. Regardless of these speculations we have shown that Qp determines Δ P at each flow and thus flow resistance. [ABSTRACT FROM AUTHOR]

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Objective: Pulmonary vascular flow resistance depends on blood viscosity, mainly due to haematocrit, and on vessel dimensions determining blood volume in this highly compliant vascular bed. We, therefore, evaluated the interaction between haematocrit, blood flow, and transpulmonary vascular pressure gradient under conditions of controlled pulmonary blood volume.Design: Experimental study in isolated zone-III rabbit lungs perfused with autologous blood.Setting: Laboratory for experimental studies.Interventions: Stepwise and independent variation of flow (50, 100, and 200 ml/min), pulmonary blood volume (increments of 2.5 ml and 5 ml imposed by changes of left atrial pressure), and haematocrit (0-50%) varied by haemodilution (Krebs-Henseleit/albumin) or haemoconcentration (centrifugation).Measurements: Pulmonary arterial, left atrial, and airway pressures as well as reservoir volume (reflecting reciprocal changes of lung blood volume) and lung weight.Results: Haemodilution from the normal haematocrit (32%) to 10% at constant pulmonary blood volume and flow decreased flow resistance only slightly, whereas haemoconcentration (50%) increased flow resistance up to 130%. At the same time increments of in pulmonary blood volume of 2.5 and 5 ml (approx. 15 and 30% of normal pulmonary blood volume) at constant haematocrit significantly shifted downwards pressure-flow relationships for all investigated haematocrits (0-50%).Conclusions: Because of the multiple interrelationships between haematocrit, blood flow and pulmonary blood volume, haematocrit effects on pulmonary flow resistance and pressure-flow relationships in the pulmonary vasculature should be studied at controlled blood volume. While haemodilution only has minor effects, haemoconcentration changes pressure-flow relationships markedly. Pulmonary blood volume has a major impact on slope and position of pressure-flow relationships for all haematocrits investigated. [ABSTRACT FROM AUTHOR]

The terminal airways are separated from the surrounding pulmonary capillaries by a tissue layer of a few micrometers in thickness only. Therefore, it should be possible to gain information about in vivo transcapillary heat transport of the interior pulmonary vascular bed by recording the terminal bronchial temperature. For this purpose, we studied temperature-time curves in the pulmonary artery, bronchial system and the aorta of six anaesthetized dogs permanently instrumented for measuring pulmonary blood flow. Thermistors recorded temperature changes at the three locations after injection of 5 ml cold solution into the right atrium. From the observed temperature-time curves mean transit times between the three recording sites were calculated for various pulmonary blood flows (integral of delta Ttdt/integral of delta Tdt) (range 1.1-3.5 1/ min). We found that the temperature-time curves of the bronchial system resemble typical "dilution" curves and are interspaced between those in the pulmonary artery and those in the aorta. Regardless of pulmonary blood flow, mean transit times from the pulmonary artery to the distal bronchial system and from there to the aorta were about equal. We conclude that transcapillary heat transfer generates bronchial temperature-time curves which permit an estimation of the relation of precapillary to postcapillary mean transit times in the interior of the lung. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Consensus statement of the ESICM task force on colloid volume therapy in critically ill patients," by Konrad Reinhart and colleagues in the July 2012 issue.