Limb Remote Ischemic Preconditioning Applied During Sevoflurane Anesthesia Does Not Protect the Lungs in Patients Undergoing Adult Heart Valve Surgery

Background: Two consistent overall cell protective preconditioning treatments should provide more protection. We hypothesized that limb remote ischemic preconditioning (RIPC, second preconditioning stimulus) applied during sevoflurane inhalation (first preconditioning stimulus) would provide more protection to the lungs of patients undergoing adult heart valve surgery. Methods: In this randomized, placebo-controlled, double-blind trial, 50 patients were assigned to the RIPC group or the placebo group (1:1). Patients in the RIPC group received three 5-min cycles of 300 mmHg cuff inflation/deflation of the left-side lower limb before aortic cross-clamping. Anesthesia consisted of opioids and propofol for induction and sevoflurane for maintenance. The primary end point was comparison of the postoperative arterial–alveolar oxygen tension ratio (a/A ratio) between groups. Secondary end points included comparisons of pulmonary variables, postoperative morbidity and mortality and regional and systemic inflammatory cytokines between groups. Results: In the RIPC group, the a/A ratio and other pulmonary variables exhibited no significant differences throughout the study period compared with the placebo group. No significant differences in either plasma or bronchoalveolar lavage levels of TNF- α were noted between the groups at 10 min after anesthetic induction and 1 h after cross-clamp release. The percentage of neutrophils at 12 h postoperation was significantly increased in the RIPC group compared with the placebo group (91.34±0.00 vs. 89.42±0.10, P = 0.023). Conclusions: Limb RIPC applied during sevoflurane anesthesia did not provide additional significant pulmonary protection following adult valvular cardiac surgery.

The Hen or the Egg: Impaired Alveolar Oxygen Diffusion and Acute High-altitude Illness?

Individuals ascending rapidly to altitudes >2500 m may develop symptoms of acute mountain sickness (AMS) within a few hours of arrival and/or high-altitude pulmonary edema (HAPE), which occurs typically during the first three days after reaching altitudes above 3000–3500 m. Both diseases have distinct pathologies, but both present with a pronounced decrease in oxygen saturation of hemoglobin in arterial blood (SO2). This raises the question of mechanisms impairing the diffusion of oxygen (O2) across the alveolar wall and whether the higher degree of hypoxemia is in causal relationship with developing the respective symptoms. In an attempt to answer these questions this article will review factors affecting alveolar gas diffusion, such as alveolar ventilation, the alveolar-to-arterial O2-gradient, and balance between filtration of fluid into the alveolar space and its clearance, and relate them to the respective disease. The resultant analysis reveals that in both AMS and HAPE the main pathophysiologic mechanisms are activated before aggravated decrease in SO2 occurs, indicating that impaired alveolar epithelial function and the resultant diffusion limitation for oxygen may rather be a consequence, not the primary cause, of these altitude-related illnesses.

Effects of inspired oxygen fractions in rabbits anesthetized with isoflurane or sevoflurane, maintained on spontaneous ventilation

ABSTRACT It is important to identify the best inspired fraction of oxygen in a variety of situations, including sevoflurane or isoflurane anesthesia, in spontaneously breathing rabbits. For this, 64 rabbits were assigned to eight groups: GI100 (FiO2= 1,0 + isoflurane), GS100 (FiO2= 1,0 + sevoflurane), GI80 (FiO2= 0,8 + isoflurane), GS80 (FiO2= 0,8 + sevoflurane), GI60 (FiO2= 0,6 + isoflurane), GS60 (FiO2= 0,6 + sevoflurane), GI21 (FiO2= 0,21 + isoflurane), GS21 (FiO2= 0,21 + sevoflurane). The induction was performed with (2.5MAC) of the anesthetic. The vaporizer was setted at 1.5 MAC and FiO2 as attributed for each group. After the induction, the concentration was changed to 1 MAC. Measurements of parameters were performed 30 minutes after induction (T0), and then at 15 minute intervals (from T15 to T60). The arterial partial pressures of oxygen (PaO2), alveolar oxygen partial pressure (PAO2) and alveolar-arterial oxygen gradient [P(A-a)O2] were higher with the use of high FiO2. The GI80 showed higher levels of PaO2 FiO2 ratio and respiratory index (RI). In conclusion, the FiO2 of 0.21 is not indicated, because it causes hypoxemia. The isoflurane determines better ventilation when compared to sevoflurane, but isoflurane associated with 80% of oxygen promotes intrapulmonary shunt increase.

Outcomes of Patients Presenting with Mild Acute Respiratory Distress Syndrome

Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Patients with initial mild acute respiratory distress syndrome are often underrecognized and mistakenly considered to have low disease severity and favorable outcomes. They represent a relatively poorly characterized population that was only classified as having acute respiratory distress syndrome in the most recent definition. Our primary objective was to describe the natural course and the factors associated with worsening and mortality in this population. Methods This study analyzed patients from the international prospective Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG SAFE) who had initial mild acute respiratory distress syndrome in the first day of inclusion. This study defined three groups based on the evolution of severity in the first week: “worsening” if moderate or severe acute respiratory distress syndrome criteria were met, “persisting” if mild acute respiratory distress syndrome criteria were the most severe category, and “improving” if patients did not fulfill acute respiratory distress syndrome criteria any more from day 2. Results Among 580 patients with initial mild acute respiratory distress syndrome, 18% (103 of 580) continuously improved, 36% (210 of 580) had persisting mild acute respiratory distress syndrome, and 46% (267 of 580) worsened in the first week after acute respiratory distress syndrome onset. Global in-hospital mortality was 30% (172 of 576; specifically 10% [10 of 101], 30% [63 of 210], and 37% [99 of 265] for patients with improving, persisting, and worsening acute respiratory distress syndrome, respectively), and the median (interquartile range) duration of mechanical ventilation was 7 (4, 14) days (specifically 3 [2, 5], 7 [4, 14], and 11 [6, 18] days for patients with improving, persisting, and worsening acute respiratory distress syndrome, respectively). Admissions for trauma or pneumonia, higher nonpulmonary sequential organ failure assessment score, lower partial pressure of alveolar oxygen/fraction of inspired oxygen, and higher peak inspiratory pressure were independently associated with worsening. Conclusions Most patients with initial mild acute respiratory distress syndrome continue to fulfill acute respiratory distress syndrome criteria in the first week, and nearly half worsen in severity. Their mortality is high, particularly in patients with worsening acute respiratory distress syndrome, emphasizing the need for close attention to this patient population.

Smoking and Flap Survival

Purpose: The aim of this study was to compare the complications of flap surgery in non-smokers and smokers and to determine how the incidence of complications was affected by the abstinence period from smoking before and after flap surgery. Methods: In PubMed and Scopus, terms “smoking” and “flap survival” were used, which resulted in 113 papers and 65 papers, respectively. After excluding 6 duplicate titles, 172 titles were reviewed. Among them, 45 abstracts were excluded, 20 full papers were reviewed, and finally 15 papers were analyzed. Results: Post-operative complications such as flap necrosis ( P < .001), hematoma ( P < .001), and fat necrosis ( P = .003) occurred significantly more frequently in smokers than in non-smokers. The flap loss rate was significantly higher in smokers who were abstinent for 24 hours post-operatively than in non-smokers (n = 1464, odds ratio [OR] = 4.885, 95% confidence interval [CI] = 2.071-11.524, P < .001). The flap loss rate was significantly lower in smokers who were abstinent for 1 week post-operatively than in those who were abstinent for 24 hours post-operatively (n = 131, OR = 0.252, 95% CI = 0.074-0.851, P = .027). No significant difference in flap loss was found between non-smokers and smokers who were abstinent for 1 week preoperatively (n = 1519, OR = 1.229, 95% CI = 0.482-3.134, P = .666) or for 4 weeks preoperatively (n = 1576, OR = 1.902, 95% CI = 0.383-2.119, P = .812). Conclusion: Since smoking decreases the alveolar oxygen pressure and subcutaneous wound tissue oxygen, and nicotine causes vasoconstriction, smokers are more likely to experience flap loss, hematoma, or fat necrosis than non-smokers. Preoperative and post-operative abstinence period of at least 1 week is necessary for smokers who undergo flap operations.

Standardisation and application of the single-breath determination of nitric oxide uptake in the lung

Diffusing capacity of the lung for nitric oxide (DLNO), otherwise known as the transfer factor, was first measured in 1983. This document standardises the technique and application of single-breathDLNO. This panel agrees that 1) pulmonary function systems should allow for mixing and measurement of both nitric oxide (NO) and carbon monoxide (CO) gases directly from an inspiratory reservoir just before use, with expired concentrations measured from an alveolar “collection” or continuously sampledviarapid gas analysers; 2) breath-hold time should be 10 s with chemiluminescence NO analysers, or 4–6 s to accommodate the smaller detection range of the NO electrochemical cell; 3) inspired NO and oxygen concentrations should be 40–60 ppm and close to 21%, respectively; 4) the alveolar oxygen tension (PAO2) should be measured by sampling the expired gas; 5) a finite specific conductance in the blood for NO (θNO) should be assumed as 4.5 mL·min-1·mmHg-1·mL-1of blood; 6) the equation for 1/θCO should be (0.0062·PAO2+1.16)·(ideal haemoglobin/measured haemoglobin) based on breath-holdingPAO2and adjusted to an average haemoglobin concentration (male 14.6 g·dL−1, female 13.4 g·dL−1); 7) a membrane diffusing capacity ratio (DMNO/DMCO) should be 1.97, based on tissue diffusivity.