| 1. |
- Frestadius, Andrea, et al.
(författare)
-
Intranasal dexmedetomidine and rectal ketamine for young children undergoing burn wound procedures
- 2022
-
Ingår i: Burns. - : Elsevier. - 0305-4179 .- 1879-1409. ; 48:6, s. 1445-1451
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Safe and effective methods for sedation and analgesia in pediatric burn patients are strongly warranted. This retrospective study of electronic health care records aims to evaluate the safety and efficacy of intranasal dexmedetomidine combined with rectal ketamine as procedural sedation for young children undergoing dressing changes and debridement of burn wounds.Methods: Documentation was analyzed from 90 procedures in 58 pediatric patients aged <5 years. Safety and efficacy of the method were assessed based on documentation for complications, adverse effects, pain level, level of sedation and preoperative and recovery time.Results: All 90 sedations were completed without significant adverse events with acute airway management or medical intervention. The combination of dexmedetomidine-ketamine produced acceptable analgesia during the procedure and effectively relieved postoperative pain. However, the approach was insufficient for 7/58 patients (7.8%); these patients were converted from the dexmedetomidine-ketamine combination to intravenous anesthesia. In 23% of the cases an extra dose of either ketamine of dexmedetomidine was administered. Moreover, there were two cases of delayed awakening with recovery time >120 min.Conclusion: The drug combination intranasal dexmedetomidine and rectal ketamine is a safe and reliable approach for procedural sedation and analgesia in pediatric patients undergoing burn wound procedures, producing a clinically stable sedative condition requiring only basic monitoring.
|
|
| 2. |
|
|
| 3. |
- Bergquist, Maria, et al.
(författare)
-
Altered adrenal and gonadal steroids biosynthesis in patients with burn injury
- 2016
-
Ingår i: Clinical Mass Spectrometry. - : Elsevier BV. - 2213-8005 .- 2376-9998. ; 1, s. 19-26
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction: Burn injury inevitably leads to changes in the endogenous production of cytokines, as well as adrenal and gonadal steroids. Previous studies have reported gender-related differences in outcome following burn injury, which suggests that gonadal steroids may play a role. The aim of this study was to assess alterations in concentration of endogenous steroids in patients with burn injury.Methods: For this single-center, prospective descriptive study, high-sensitivity liquid chromatography tandem mass spectrometry (LC-MS/MS)-based steroid quantification was used to determine longitudinal profiles of the concentrations of endogenous steroids in plasma from sixteen adult male patients with burn injury (14.5-72% of total body surface area). Steroids were extracted from plasma samples and analyzed using multiple reaction monitoring acquisition, with electrospray ionization on a triple quadruple mass spectrometer. Total protein concentration was measured in the samples using spectrophotometry.Results: Steroid and total protein concentration distributions were compared to reference intervals characteristic of healthy adult men. Concentrations of the following steroids in plasma of burn injured patients were found to correlate positively to the area of the burn injury: cortisol (r = 0.84), corticosterone (r = 0.73), 11-deoxycortisol (r = 0.72), androstenedione (r = 0.72), 17OH-progesterone (r = 0.68), 17OH-pregnenolone (r = 0.64) and pregnenolone (r = 0.77). Concentrations of testosterone decreased during the acute phase and were up to ten-times lower than reference values for healthy adult men, while concentrations of estrone were elevated. By day 21 after injury, testosterone concentrations were increased in younger, but not older, patients. The highest concentrations of estrone were observed on day 3 after the injury and then declined by day 21 to concentrations comparable to those observed on the day of the injury.Conclusion: Burn injury alters endogenous steroid biosynthesis, with decreased testosterone concentrations and elevated estrone concentrations, during the first 21 days after the injury. Concentrations of glucocorticoids, progestagens and androgen precursors correlated positively with the area of burn injury. The finding of increased estrone following burn injury needs to be confirmed in a larger hypothesis driven study.
|
|
| 4. |
- Bergquist, Maria, et al.
(författare)
-
Glucocorticoid receptor expression and binding capacity in patients with burn injury.
- 2016
-
Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 60:2, s. 213-221
-
Tidskriftsartikel (refereegranskat)abstract
- Burn injuries are associated with strong inflammation and risk of secondary sepsis which both may affect the function of the glucocorticoid receptor (GR). The aim of this study was to determine GR expression and binding capacity in leucocytes from patients admitted to a tertiary burn center.
|
|
| 5. |
- Bergquist, Maria, et al.
(författare)
-
The time-course of the inflammatory response to major burn injury and its relation to organ failure and outcome
- 2019
-
Ingår i: Burns. - : Elsevier BV. - 0305-4179 .- 1879-1409. ; 45:2, s. 354-363
-
Tidskriftsartikel (refereegranskat)abstract
- Burn injury causes major inflammatory activation and cytokine release, however, the temporal resolution of the acute and sub-acute inflammatory response has not yet been fully delineated. To this end, we have quantified 20 inflammatory mediators in plasma from 44 adult patients 0-21 days after burn injury and related the time course of these mediators to % total body surface area (TBSA) burned, clinical parameters, organ failure and outcome. Of the cytokines analyzed in these patients, interleukin 6 (IL-6), IL-8, IL-10 and monocyte chemoattractant protein 1 (MCP-1) correlated to the size of the injury at 24-48h after burn injury. In our study, the concentration of IL-10 had prognostic value in patients with burn injury both measured at admission and at 24-48h after injury. However, simple demographic data such as age, % burned TBSA, inhalation injury and their combination, the Baux score and modified Baux score, outperform most of the cytokines, with the exception of IL-8 and MCP1 levels on admission, in predicting death.
|
|
| 6. |
- Chen, Luni, et al.
(författare)
-
Endothelin-1 and nitric oxide synthase in short rebound reaction to short exposure to inhaled nitric oxide
- 2001
-
Ingår i: American Journal of Physiology. Heart and Circulatory Physiology. - 0363-6135 .- 1522-1539. ; 281, s. H124-31
-
Tidskriftsartikel (refereegranskat)abstract
- On withdrawal of inhalation of nitric oxide (INO) administered after lung injury, pulmonary artery pressure (PAP) and arterial oxygen tension (Pa(O(2))) may deteriorate more than before INO (rebound response). In this study, we investigated the possible roles of endothelin (ET)-1 and nitric oxide (NO) synthase (NOS) activity in the short rebound reaction to short-term inhalation of NO. Twenty-six anesthetized mechanically ventilated piglets were given endotoxin infusion. Twelve animals then received INO (30 parts per million) for two 30-min periods. Nine controls were not given NO. Measurements were made of blood gases and hemodynamic parameters, lung tissue ET-1 expression and NOS activity, and plasma ET-1 concentration. INO decreased PAP and increased Pa(O(2)), but INO withdrawal caused a short rebound reaction with an increase in PAP. Lung tissue expression and plasma concentration of ET-1 increased during INO, and plasma ET-1 increased further after its withdrawal. Activity of constitutive NOS decreased during INO, whereas that of inducible NOS was unchanged. Upregulation of ET-1 and downregulation of NOS activity may have influenced the short rebound reaction to short-term INO.
|
|
| 7. |
- Fransén, Jian, et al.
(författare)
-
A proof-of-concept study on mortality prediction with machine learning algorithms using burn intensive care data
- 2022
-
Ingår i: Scars, Burns & Healing. - : Sage Publications. - 2059-5131.
-
Tidskriftsartikel (refereegranskat)abstract
- IntroductionBurn injuries are a common traumatic injury. Large burns have high mortality requiring intensive care and accurate mortality predictions. To assess if machine learning (ML) could improve predictions, ML algorithms were tested and compared with the original and revised Baux score.MethodsAdmission data and mortality outcomes were collected from patients at Uppsala University Hospital Burn Centre from 2002 to 2019. Prognostic variables were selected, ML algorithms trained and predictions assessed by analysis of the area under the receiver operating characteristic curve (AUC). Comparison was made with Baux scores using DeLong test.ResultsA total of 17 prognostic variables were selected from 92 patients. AUCs in leave-one-out cross-validation for a decision tree model, an extreme boosting model, a random forest model, a support-vector machine (SVM) model and a generalised linear regression model (GLM) were 0.83 (95% confidence interval [CI] = 0.72–0.94), 0.92 (95% CI = 0.84–1), 0.92 (95% CI = 0.84–1), 0.92 (95% CI = 0.84–1) and 0.84 (95% CI = 0.74–0.94), respectively. AUCs for the Baux score and revised Baux score were 0.85 (95% CI = 0.75–0.95) and 0.84 (95% CI = 0.74–0.94). No significant differences were observed when comparing ML algorithms with Baux score and revised Baux score. Secondary variable selection was made to analyse model performance.ConclusionThis proof-of-concept study showed initial credibility in using ML algorithms to predict mortality in burn patients. The sample size was small and future studies are needed with larger sample sizes, further variable selections and prospective testing of the algorithms.
|
|
| 8. |
- Fredén, Filip, et al.
(författare)
-
Inhalation of a nitric oxide synthase inhibitor to a hypoxic or collapsed lung lobe in anaesthetized pigs : effects on pulmonary blood flow distribution
- 1996
-
Ingår i: British Journal of Anaesthesia. - : Elsevier BV. - 0007-0912 .- 1471-6771. ; 77:3, s. 413-418
-
Tidskriftsartikel (refereegranskat)abstract
- I.v. administration of the nitric oxide synthase inhibitor, nitro-L-arginine methyl ester (L-NAME), not only reduces blood flow in a hypoxic lung region but also causes systemic vasoconstriction and a decrease in cardiac output. In this study, we delivered nebulized L-NAME 0.2-1 mg kg-1 to the left lower lobe of 10 anaesthetized pigs. The left lower lobe was made hypoxic by selective inhalation of 5% oxygen or collapsed by interrupted ventilation, or both. Inhalation of L-NAME reduced fractional blood flow to the left lower lobe from 5.3 (SD 3.1)% to 1.7 (1.4)% (P < 0.05) in lobar hypoxia and from 6.0 (3.3) to 2.7 (2.7)% (P < 0.05) in lobar collapse. These reductions were accompanied by a significant increase in PaO2. There were no significant changes in arterial pressure, cardiac output or heart rate. We have shown that selective inhalation of L-NAME reduced blood flow to a hypoxic or collapsed lung region without systemic effects. The possible role for nitric oxide synthase inhibition in reducing shunt during one-lung ventilation, however, requires further study.
|
|
| 9. |
|
|
| 10. |
- Glas, Gerie J., et al.
(författare)
-
Ventilation practices in burn patients-an international prospective observational cohort study
- 2021
-
Ingår i: BURNS & TRAUMA. - : Oxford University Press. - 2321-3868 .- 2321-3876. ; 9
-
Tidskriftsartikel (refereegranskat)abstract
- Background: It is unknown whether lung-protective ventilation is applied in burn patients and whether they benefit from it. This study aimed to determine ventilation practices in burn intensive care units (ICUs) and investigate the association between lung-protective ventilation and the number of ventilator-free days and alive at day 28 (VFD-28). Methods: This is an international prospective observational cohort study including adult burn patients requiring mechanical ventilation. Low tidal volume (V-T) was defined as V-T <= 8 mL/kg predicted body weight (PBW). Levels of positive end-expiratory pressure (PEEP) and maximum airway pressures were collected. The association between V-T and VFD-28 was analyzed using a competing risk model. Ventilation settings were presented for all patients, focusing on the first day of ventilation. We also compared ventilation settings between patients with and without inhalation trauma. Results: A total of 160 patients from 28 ICUs in 16 countries were included. Low V-T was used in 74% of patients, median V-T size was 7.3 [interquartile range (IQR) 6.2-8.3] mL/kg PBW and did not differ between patients with and without inhalation trauma (p= 0.58). Median VFD-28 was 17 (IQR 0-26), without a difference between ventilation with low or high V-T (p= 0.98). All patients were ventilated with PEEP levels >= 5 cmH(2)O; 80% of patients had maximum airway pressures <30 cmH(2)O. Conclusion: In this international cohort study we found that lung-protective ventilation is used in the majority of burn patients, irrespective of the presence of inhalation trauma. Use of low V-T was not associated with a reduction in VFD-28.
|
|
| 11. |
- Hambraeus-Jonzon, Kristina, et al.
(författare)
-
Pulmonary Vasoconstriction during Regional Nitric Oxide Inhalation : Evidence of a Blood-borne Regulator of Nitric Oxide Synthase Activity
- 2001
-
Ingår i: Anesthesiology. - : Ovid Technologies (Wolters Kluwer Health). - 0003-3022 .- 1528-1175. ; 95:1, s. 102-112
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect. METHODS: Nitric oxide concentration was measured in exhaled air (NO(E)), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [FIO2] = 0.05), with and without INO to HL (FIO2 = 0.8), and during cross-circulation of blood from pigs with and without INO. RESULTS: Left lower lobar hypoxia increased exhaled NO from the LLL (NO(E)LLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P < 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86] vs. 162 [96] pmol x g(-1) x min(-1), P < 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol x g(-1) x min(-1) (P < 0.01), and NO(E)LLL to 2.0 [0.8] ppb (P < 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NO(E)LLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P < 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol x g(-1) x min(-1) (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P < 0.05), but more so in hypoxic (P < 0.01) than in hyperoxic (P < 0.05) lung regions, resulting in a further redistribution (P < 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions. CONCLUSIONS: Inhaled nitric oxide downregulates endogenous NO production in other, predominantly hypoxic, lung regions. This distant effect is blood-mediated and causes vasoconstriction in lung regions that do not receive INO.
|
|
| 12. |
- Hastbacka, Johanna, et al.
(författare)
-
Matrix Metalloproteinases-8 and-9 and Tissue Inhibitor of Metalloproteinase-1 in Burn Patients. A Prospective Observational Study
- 2015
-
Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:5
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction Matrix metalloproteinases (MMPs) -8 and -9 are released from neutrophils in acute inflammation and may contribute to permeability changes in burn injury. In retrospective studies on sepsis, levels of MMP-8, MMP-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) differed from those of healthy controls, and TIMP-1 showed an association with outcome. Our objective was to investigate the relationship between these proteins and disease severity and outcome in burn patients. Methods In this prospective, observational, two-center study, we collected plasma samples from admission to day 21 post-burn, and burn blister fluid samples on admission. We compared MMP-8, -9, and TIMP-1 levels between TBSA<20% (N = 19) and TBSA>20% (N = 30) injured patients and healthy controls, and between 90-day survivors and non-survivors. MMP-8, -9, and TIMP-1 levels at 24-48 hours from injury, their maximal levels, and their time-adjusted means were compared between groups. Correlations with clinical parameters and the extent of burn were analyzed. MMP-8, -9, and TIMP-1 levels in burn blister fluids were also studied. Results Plasma MMP-8 and -9 were higher in patients than in healthy controls (P<0.001 and P = 0.016), but only MMP-8 differed between the TBSA<20% and TBSA>20% groups. MMP-8 and -9 were not associated with clinical severity or outcome measures. TIMP-1 differed significantly between patients and controls (P<0.001) and between TBSA<20% and TBSA>20% groups (P<0.002). TIMP-1 was associated with 90-day mortality and correlated with the extent of injury and clinical measures of disease severity. TIMP-1 may serve as a new biomarker in outcome prognostication of burn patients.
|
|
| 13. |
- Holm, Sebastian, et al.
(författare)
-
Cutaneous steam burns and steam inhalation injuries : a literature review and a case presentation
- 2022
-
Ingår i: European journal of plastic surgery. - : Springer Nature. - 0930-343X .- 1435-0130. ; 45:6, s. 881-896
-
Tidskriftsartikel (refereegranskat)abstract
- Scald is one type of burn that s often mentioned alone and occurs mostly in the paediatric population. Inhaled steam is mostly cooled off in the airways, why thermal damage is rarely seen. A sudden exposure to hot steam/inhalation can cause a thermal inhalation injury. A scoping review was performed, with the aim to summarize all published papers in English, about steam-related injuries. The search was conducted using the PubMed (R) and Cochrane libraries on 19th of May 2021, without a set time period. Out of a total of 1186 identified records, 31 were chosen for review. Burns related to the contact with steam are generally rare and can be both minor and severe. The more severe cases related to steam exposure are mostly workplace accidents and the minor injuries reported in the literature are often related to steam inhalation therapy, especially in the paediatric population. This review describes the challenges that can be found dealing with patients suffering from cutaneous steam burns and/or steam inhalation injuries. A steam injury to the airways or the skin can be directly life-threatening and should be treated with caution. This type of injury can lead to acute respiratory insufficiency and sometimes death. A case of a male patient with extensive cutaneous steam burns and a steam inhalation injury who passed away after 11 days of treatment is also presented to illustrate this review. Level of evidence: Level V, Therapeutic; Risk/Prognostic Study.
|
|
| 14. |
- Hultström, Michael, 1978-, et al.
(författare)
-
Limitations of the ARDS criteria during high-flow oxygen or non-invasive ventilation : evidence from critically ill COVID-19 patients
- 2022
-
Ingår i: Critical Care. - : Springer Nature. - 1364-8535 .- 1466-609X. ; 26
-
Tidskriftsartikel (refereegranskat)abstract
- Background: The ratio of partial pressure of arterial oxygen to inspired oxygen fraction (PaO2/FIO2) during invasive mechanical ventilation (MV) is used as criteria to grade the severity of respiratory failure in acute respiratory distress syndrome (ARDS). During the SARS-CoV2 pandemic, the use of PaO2/FIO2 ratio has been increasingly used in non-invasive respiratory support such as high-flow nasal cannula (HFNC) and non-invasive ventilation (NIV). The grading of hypoxemia in non-invasively ventilated patients is uncertain. The main hypothesis, investigated in this study, was that the PaO2/FIO2 ratio does not change when switching between MV, NIV and HFNC.Methods: We investigated respiratory function in critically ill patients with COVID-19 included in a single-center prospective observational study of patients admitted to the intensive care unit (ICU) at Uppsala University Hospital in Sweden. In a steady state condition, the PaO2/FIO2 ratio was recorded before and after any change between two of the studied respiratory support techniques (i.e., HFNC, NIV and MV).Results: A total of 148 patients were included in the present analysis. We find that any change in respiratory support from or to HFNC caused a significant change in PaO2/FIO2 ratio. Changes in respiratory support between NIV and MV did not show consistent change in PaO2/FIO2 ratio. In patients classified as mild to moderate ARDS during MV, the change from HFNC to MV showed a variable increase in PaO2/FIO2 ratio ranging between 52 and 140 mmHg (median of 127 mmHg). This made prediction of ARDS severity during MV from the apparent ARDS grade during HFNC impossible.Conclusions: HFNC is associated with lower PaO2/FIO2 ratio than either NIV or MV in the same patient, while NIV and MV provided similar PaO2/FIO2 and thus ARDS grade by Berlin definition. The large variation of PaO2/FIO2 ratio indicates that great caution should be used when estimating ARDS grade as a measure of pulmonary damage during HFNC.
|
|
| 15. |
- Karlsson, Victoria, 1968-
(författare)
-
Aspects of neonatal intensive care and anesthesia : Thermal balance and respiratory management
- 2018
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- This thesis is based on four articles originating from three studies conducted in the neonatal intensive care unit and the children’s operating deparment at Uppsala University Hospital, Sweden.The overall aim was to obtain new knowledge about thermal balance and care environment in extremely preterm infants during skin-to-skin care (SSC), evaluate different methods of intraoperative monitoring of carbon dioxide (CO2), and to investigate how different levels of inhaled oxygen affect infants’ oxygenation during anesthesia and surgery. Study I investigated infant thermal balance and the physical environment for extremely preterm infants during SSC. Study II formed part of a prospective study to assess the performance of non-invasive transcutaneous and end-tidal technique to continuously monitor CO2 levels in the infants blood during anesthesia. Study III was a prospective randomized trial to investigate oxygenation during induction of anesthesia with room air versus high fraction (80%) of oxygen in healthy newborn infants.The infants maintained normal body temperature during SSC. In comparison to care in an incubator, during SSC ambient humidity was lower and insensible water loss through the skin was higher. Compared to blood gas Pco2, transcutaneous carbon dioxide monitoring yielded a bias of 0.3 ± 0.7 kPa, and end-tidal technique a bias of -1.9 ± 0.9 kPa. After intubation, saturation measured by pulse oximetry was lower (p < .05) in the group breathing room air than in the group with high oxygen (93% ± 6.7 and 99% ± 1.5). None of the infants spent time below the pre-specified safety oxygen saturation targets to mandate supplemental oxygen.This thesis provides new knowledge about early initiation of SSC after birth for extremely preterm infants, the results will be useful to guide safe routines for implementation of early SSC. These results suggest that during anesthesia would transcutaneous monitoring of carbon dioxide be beneficial, end-tidal monitoring correlated poorly to blood gas and induction of general anesthesia in newborn infants can be safely performed without the use of high levels of supplemental oxygen. Taken together, this new knowledge has the potential to improve intraoperative respiratory management.
|
|
| 16. |
- Karlsson, Victoria, et al.
(författare)
-
Randomized controlled trial of low vs high oxygen during neonatal anesthesia : Oxygenation, feasibility, and oxidative stress
- 2022
-
Ingår i: Pediatric Anaesthesia. - : John Wiley & Sons. - 1155-5645 .- 1460-9592. ; 32:9, s. 1062-1069
-
Tidskriftsartikel (refereegranskat)abstract
- Background To reduce risk for intermittent hypoxia a high fraction of inspired oxygen is routinely used during anesthesia induction. This differs from the cautious dosing of oxygen during neonatal resuscitation and intensive care and may result in significant hyperoxia. Aim In a randomized controlled trial, we evaluated oxygenation during general anesthesia with a low (23%) vs a high (80% during induction and recovery, and 40% during maintenance) fraction of inspired oxygen, in newborn infants undergoing surgery. Method Thirty-five newborn infants with postconceptional age of 35-44 weeks were included (17 infants in low and 18 in high oxygen group). Oxygenation was monitored by transcutaneous partial pressure of oxygen, pulse oximetry, and cerebral oxygenation. Predefined SpO2 safety targets dictated when to increase inspired oxygen. Results At start of anesthesia, oxygenation was similar in both groups. Throughout anesthesia, the high oxygen group displayed significant hyperoxia with higher (difference-20.3 kPa, 95% confidence interval (CI)-28.4 to 12.2, p < .001) transcutaneous partial pressure of oxygen values than the low oxygen group. While SpO2 in the low oxygen group was lower (difference - 5.8%, 95% CI -9.3 to -2.4, p < .001) during anesthesia, none of the infants spent enough time below SpO(2) safety targets to mandate supplemental oxygen, and cerebral oxygenation was within the normal range and not statistically different between the groups. Analysis of the oxidative stress biomarker urinary F-2-Isoprostane revealed no differences between the low and high oxygen group. Conclusion We conclude that in healthy newborn infants, use of low oxygen during general anesthesia was feasible, while the prevailing practice of using high levels of inspired oxygen resulted in significant hyperoxia. The trade-off between careful dosing of oxygen and risks of hypo- and hyperoxia in neonatal anesthesia should be further examined.
|
|
| 17. |
|
|
| 18. |
- Kozian, Alf, 1969-, et al.
(författare)
-
One-lung ventilation induces hyperperfusion and alveolar damage in the ventilated lung : an experimental study
- 2008
-
Ingår i: British Journal of Anaesthesia. - : Elsevier BV. - 0007-0912 .- 1471-6771. ; 100:4, s. 549-559
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: One-lung ventilation (OLV) increases mechanical stress in the lung and affects ventilation and perfusion (V, Q). There are no data on the effects of OLV on postoperative V/Q matching. Thus, this controlled study evaluates the influence of OLV on V/Q distribution in a pig model using a gamma camera technique [single-photon emission computed tomography (SPECT)] and relates these findings to lung histopathology after OLV. METHODS: Eleven anaesthetized and ventilated pigs (V(T)=10 ml kg(-1), Fio2=0.40, PEEP=5 cm H2O) were studied. After lung separation, OLV and thoracotomy were performed in seven pigs (OLV group). During OLV and in a two-lung ventilation (TLV), control group (n=4) ventilation settings remained unchanged. SPECT with (81m)Kr (ventilation) and (99m)Tc-labelled macro-aggregated albumin (perfusion) was performed before, during, and 90 min after OLV/TLV. Finally, lung tissue samples were harvested and examined for alveolar damage. RESULTS: OLV affected ventilation and haemodynamic variables, but there were no differences between the OLV group and the control group before and after OLV/TLV. SPECT revealed an increase of perfusion in the dependent lung compared with baseline (49-56%), and a corresponding reduction of perfusion (51-44%) in non-dependent lungs after OLV. No perfusion changes were observed in the control group. This resulted in increased low V/Q regions and a shift of V/Q areas to 0.3-0.5 (10(-0.5)-10(-0.3)) in dependent lungs of OLV pigs and was associated with an increased diffuse alveolar damage score. CONCLUSIONS: OLV in pigs results in a substantial V/Q mismatch, hyperperfusion, and alveolar damage in the dependent lung and may thus contribute to gas exchange impairment after thoracic surgery.
|
|
| 19. |
- Kozian, Alf, 1969-
(författare)
-
Pathophysiological and Histomorphological Effects of One-Lung Ventilation in the Porcine Lung
- 2009
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Thoracic surgical procedures require partial or complete airway separation and the opportunity to exclude one lung from ventilation (one-lung ventilation, OLV). OLV is commonly associated with profound pathophysiological changes that may affect the postoperative outcome. It is injurious in terms of increased mechanical stress including alveolar cell stretch and overdistension, shear forces secondary to repeated tidal collapse and reopening of alveolar units and compression of alveolar vessels. Ventilation and perfusion distribution may thus be affected during and after OLV. The present studies investigated the influence of OLV on ventilation and perfusion distribution, on the gas/tissue distribution and on the lung histomorphology in a pig model of thoracic surgery.Anaesthetised and mechanically ventilated piglets were examined. The ventilation and perfusion distribution within the lungs was assessed by single photon emission computed tomography. Computed tomography was used to establish the effects of OLV on dependent lung gas/tissue distribution. The pulmonary histopathology of pigs undergoing OLV and thoracic surgery was compared with that of two-lung ventilation (TLV) and spontaneous breathing.OLV induced hyperperfusion and significant V/Q mismatch in the ventilated lung persistent in the postoperative course. It increased cyclic tidal recruitment that was associated with a persistent increase of gas content in the ventilated lung. OLV and thoracic surgery as well resulted in alveolar damage. In the present model of OLV and thoracic surgery, alveolar recruitment manoeuvre (ARM) and protective ventilation approach using low tidal volume preserved the ventilated lung density distribution and did not aggravate cyclic recruitment of alveoli in the ventilated lung.In conclusion, the present model established significant alveolar damage in response to OLV and thoracic surgery. Lung injury could be related to the profound pathophysiological consequences of OLV including hyperperfusion, ventilation/perfusion mismatch and increased tidal recruitment of lung tissue in the dependent, ventilated lung. These mechanisms may contribute to the increased susceptibility for respiratory complications in patients undergoing thoracic surgery. A protective approach including sufficient ARM, application of PEEP, and the use of lower tidal volumes may prevent the ventilated lung from deleterious consequences of OLV.
|
|
| 20. |
- Lattuada, Marco, 1974-, et al.
(författare)
-
Effect of increased intra-abdominal pressure (IAP) on lung function in a sepsis model
-
Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- We have previously shown that mechanical ventilation with positive pressure increases abdominal edema formation and causes an increase in intra-abdominal pressure (IAP) in a sepsis-like porcine model. In this study we investigated, in the same animal model effects of increase in IAP on the cardiovascular and respiratory system. Twelve pigs of Swedish country breed with a mean weight 28 kg were anesthetized and mechanically ventilated. Six animals received a continuous infusion of endotoxin and the other six served as controls. Catheters were inserted for vascular pressure recordings and cardiac output was measured by thermo-dilution. In both groups IAP was temporarily elevated to 20 mmHg by insufflation of CO2 into the abdominal cavity. Endotoxin infusion caused significant increases in pulmonary artery and central venous pressures and increase in shunt with fall in PaO2. Respiratory compliance was reduced. IAP elevation by CO2 insufflation increased these pressures as well as shunt further and caused additional decrease in compliance. Deflation of the abdomen returned vascular pressures to pre-insufflation but shunt remained increased and PaO2 was still reduced as was compliance. In control animals similar but smaller changes were seen on increase in IAP but with deflation not only vascular pressures but also shunt and PaO2 returned to normal. This suggests that in the sepsis-like condition, increased IAP causes persisting deterioration of lung function even when IAP has been normalized. We propose this to be caused by lung collapse that remains, at least for some time, after deflation.
|
|
| 21. |
- Lattuada, Marco, 1974-
(författare)
-
Effect of Ventilatory Support on Abdominal Fluid Balance in a Sepsis Model
- 2013
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- In patients affected by acute respiratory failure or acute respiratory distress syndrome (ARDS) the leading cause of death is failure of different vital organs other than the lungs, so called multiple organ dysfunction syndrome (MODS). The abdominal organs have a crucial role in the pathogenesis of this syndrome.There is a lack of knowledge regarding the mechanisms by which mechanical ventilation can affect the abdominal compartment. One hypothesis is that mechanical ventilation can interfere with abdominal fluid balance causing edema and inflammation.We addressed the question whether different levels of ventilatory support (mechanical ventilation with different levels of positive end-expiratory pressure, PEEP, and spontaneous breathing with or without PEEP) can influence abdominal edema and inflammation in both healthy and endotoxin-exposed animals.The effect on lymphatic drainage from the abdomen exerted by different degrees of ventilatory support was evaluated (paper I). We demonstrated that endotoxin increases abdominal lymph production, that PEEP and mechanical ventilation increase lymph production but also impede lymphatic drainage; spontaneous breathing improves lymphatic drainage from the abdomen.By adapting a non-invasive nuclear medicine imaging technique and validating it (paper II), we have been able to evaluate extravascular fluid accumulation (edema formation) in the abdomen over time (paper III) demonstrating that edema increases during endotoxemia, mimicking a sepsis-like condition, and that spontaneous breathing, compared to mechanical ventilation, reduces extravascular fluid. Pro-inflammatory cytokines TNF-α and IL-6 in intestinal biopsies are reduced during spontaneous breathing compared to mechanical ventilation.Abdominal edema results in increased intra-abdominal pressure (IAP): in paper IV we analyzed the effect of increased intra-abdominal pressure on the respiratory system. Pulmonary shunt fraction increased with high IAP both in healthy and LPS animals, resulting in decreased level of oxygenation. These changes are only partially reversible by reducing IAP.In conclusion, mechanical ventilation is a life-saving tool but the possible side effect at the extra-pulmonary level should be considered, and the introduction of some degree of spontaneous breathing when clinically possible is a suggested choice.
|
|
| 22. |
|
|
| 23. |
- Nilsson, Manja C. A., 1966-, et al.
(författare)
-
Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction in anesthetized pigs, without affecting the endogenous pulmonary nitric oxide production.
- 2012
-
Ingår i: Intensive Care Medicine. - : Springer Science and Business Media LLC. - 0342-4642 .- 1432-1238. ; 38:3, s. 509-517
-
Tidskriftsartikel (refereegranskat)abstract
- Purpose Hypercapnic acidosis often occurs in critically ill patients and during protective mechanical ventilation; however, the effect of hypercapnic acidosis on endogenous nitric oxide (NO) production and hypoxic pulmonary vasoconstriction (HPV) presents conflicting results. The aim of this study is to test the hypothesis that hypercapnic acidosis augments HPV without changing endogenous NO production in both hyperoxic and hypoxic lung regions in pigs. Methods Sixteen healthy anesthetized pigs were separately ventilated with hypoxic gas to the left lower lobe (LLL) and hyperoxic gas to the rest of the lung. Eight pigs received 10% carbon dioxide (CO2) inhalation to both lung regions (hypercapnia group), and eight pigs formed the control group. NO concentration in exhaled air (ENO), nitric oxide synthase (NOS) activity, cyclic guanosine monophosphate (cGMP) in lung tissue, and regional pulmonary blood flow were measured. Results There were no differences between the groups for ENO, Ca2+-independent or Ca2+-dependent NOS activity, or cGMP in hypoxic or hyperoxic lung regions. Relative perfusion to LLL (Q LLL/Q T) was reduced similarly in both groups when LLL hypoxia was induced. During the first 90 min of hypercapnia, Q LLL/Q T increased from 6% (1%) [mean (standard deviation, SD)] to 9% (2%) (p < 0.01), and then decreased to the same level as the control group, where Q LLL/Q T remained unchanged. Cardiac output increased during hypercapnia (p < 0.01), resulting in increased oxygen delivery (p < 0.01), despite decreased PaO2 (p < 0.01). Conclusions Hypercapnic acidosis does not potentiate HPV, but rather transiently weakens HPV, and does not affect endogenous NO production in either hypoxic or hyperoxic lung regions.
|
|
| 24. |
- Nilsson, Manja C, et al.
(författare)
-
Distant effects of nitric oxide inhalation in endotoxemic pigs
- 2010
-
Ingår i: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 38:1, s. 242-248
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Inhalation of nitric oxide (INO) has distant effects. By a blood- borne factor, INO down-regulates endogenous nitric oxide production in healthy pig lungs, resulting in vasoconstriction in lung regions not directly reached by INO. The aim of this study was to investigate whether INO has distant effects in endotoxemic pig lungs. The hypothesis was that INO down-regulates endogenous NO production in lung regions not reached by INO. DESIGN: Prospective, randomized animal study. SETTING: University hospital research laboratory. SUBJECTS: Twenty-two pairs of domestic pigs. INTERVENTIONS: Cross-circulation was established in 22 pairs of anesthetized pigs. Nine pairs received endotoxin (control group) and 13 pairs received endotoxin, with one pig inhaling NO (80 ppm) and one pig receiving blood from that pig (NO-blood recipient group). MEASUREMENTS AND MAIN RESULTS: NO in exhaled air, NO synthase activity in lung tissue, endothelin-1 in the blood, ETA and ETB receptor immunoreactivity in lung tissue, vital parameters, and blood gases were measured. Endotoxin per se increased NO in exhaled air by 100% compared to baseline (control group). In the NO-blood recipient group, i.e., pigs receiving blood from the NO-inhaling pigs, NO in exhaled air increased by 300% (p = .03). The Ca-dependent NO synthase activity was higher in these pigs (p = .02), indicating increased endogenous NO production. The ET B receptor immunoreactivity was higher in the NO-blood recipient group (p = .004). CONCLUSIONS: As opposed to findings in healthy pigs, INO in endotoxemic pigs causes an increase in endogenous NO production in lung regions not reached by INO. Increased NO production in nonventilated lung regions may cause vasodilatation, counteracting the INO-induced increase in blood flow to the ventilated lung regions.
|
|
| 25. |
- Nilsson, Manja, et al.
(författare)
-
Distant effects of nitric oxide inhalation in lavage induced lung injury in anaesthetised pigs
- 2013
-
Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 57:3, s. 326-333
-
Tidskriftsartikel (refereegranskat)abstract
- Background Inhalation of nitric oxide (INO) exerts both local and distanteffects. INO in healthy pigs causes down-regulation of endogenous nitric oxide(NO) production and vasoconstriction in lung regions not reached by INO, especially in hypoxic regions, which augments hypoxic pulmonary vasoconstriction. In contrast, in pigs with endotoxemia-induced lung injury, INO causes increased NO production in lung regions not reached by INO. The aim ofthis study was to investigate whether INO exerts distant effects in surfactant-depleted lungs. Methods Twelve pigs were anaesthetised, and the left lower lobe (LLL) was separately ventilated. Lavage injury was induced in all lung regions, except the LLL. In six pigs, 40 ppm INO was given to the LLL (INO group), and theeffects on endogenous NO production and blood flow in the lavage-injured lungregions were studied. Six pigs served as a control group. NO concentration inexhaled air (ENO), NO synthase (NOS) activity and cyclic guanosine monophosphate (cGMP) in lung tissue, and regional pulmonary blood flow were measured. Results The calcium (Ca2+)-dependent NOS activity was lower (P<0.05) in the lavage-injured lung regions in the INO group than in the control group. There were no measurable differences between the groups for Ca2+-independent NOS activity, cGMP, ENO, or regional pulmonary blood flow. Conclusions Regional INO did not increase endogenous NO production in lavage-injured lung regions not directly reached by INO, but instead down-regulated the constitutive calcium-dependent nitric oxide synthase activity, indicating that NO may inhibit its own synthesis.
|
|
| 26. |
- Nilsson, Manja
(författare)
-
Endogenous Nitric Oxide Production and Pulmonary Blood Flow : during different experimental lung conditions
- 2011
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Nitric oxide (NO) is an important regulator of pulmonary blood flow and attenuates hypoxic pulmonary vasoconstriction (HPV). Nitric oxide is synthesized enzymatically in a number of tissues, including the lungs, and can also be generated from reduction of nitrite during hypoxia and acidosis. Inhaled nitric oxide (INO) is a selective pulmonary vasodilator, with no effects on systemic arterial blood pressure due to inactivation by hemoglobin in the blood. INO has distant effects both within the lungs and in other organs, since NO can be transported to remote tissues bound to proteins, or as more stable molecules of nitrite and nitrate. In healthy pigs, INO causes vasoconstriction and down regulation of endogenous NO production in lung regions not reached by INO, and predominantly so in hypoxic lung regions, i.e. augmentation of HPV. In this thesis, distant effects of INO in pigs with endotoxemic- and lavage-induced lung injuries were studied. INO increased the NO production in lung regions not reached by INO in endotoxemic pigs, whereas endogenous NO production was unaffected in pigs with lavage-induced injury. Metabolic and/or hypercapnic acidosis frequently occurs in critically ill patients, but whether acidosis affects the endogenous pulmonary NO production is unclear. The regional NO production and blood flow in hyperoxic and hypoxic lung regions, were studied during metabolic and hypercapnic acidosis. Neither metabolic, nor hypercapnic acidosis changed the endogenous NO production in hyperoxic or hypoxic lung regions. Metabolic acidosis potentiated HPV, whereas hypercapnic acidosis transiently attenuated HPV. In conclusion, the present thesis has demonstrated that INO in experimental sepsis increases the endogenous NO production in lung regions not reached by INO, which may cause increased shunt and poor response to INO. This distant effect is not seen in lavage injuried lungs, an experimental model with less inflammation. Acidosis does not affect the endogenous pulmonary NO production in hyperoxic or hypoxic lung regions. Whereas metabolic acidosis potentiates HPV, hypercapnic acidosis transiently attenuates HPV, due to a combination of hypercapnia-induced increase in cardiac output and a probable vasodilating effect of the CO2-molecule.
|
|
| 27. |
- Nilsson, Manja, et al.
(författare)
-
No effect of metabolic acidosis on nitric oxide production in hypoxic and hyperoxic lung regions in pigs
- 2011
-
Ingår i: Acta Physiologica. - : Wiley. - 1748-1708 .- 1748-1716. ; 202:1, s. 59-68
-
Tidskriftsartikel (refereegranskat)abstract
- Aim: In the severely ill intensive care patients metabolic acidosis and hypoxia often co-exist. We studied the effects of metabolic acidosis on nitric oxide synthase (NOS) dependent and NOS independent nitric oxide (NO) production in hypoxic and hyperoxic lung (HL) regions in a pig model. Methods: Eighteen healthy anaesthetized pigs were separately ventilated with hypoxic gas to the left lower lobe (LLL) and hyperoxic gas to the rest of the lung. Six pigs received HCl infusion (HCl group), six pigs received the non-specific NOS inhibitor N omega-nitro-l-arginine methyl ester (l-NAME) and HCl infusions (l-NAME + HCl group) and six pigs received buffered Ringer's solution (control group). NO concentration in exhaled air (ENO), NOS activity in lung tissue, and regional pulmonary blood flow were measured. Results: Metabolic acidosis, induced by infusion of HCl, decreased the relative perfusion to the hypoxic LLL from 7 (3) [mean (SD)] to 3 (1) % in the HCl group (P < 0.01), and from 4 (1) to 1 (1) % in the l-NAME + HCl group (P < 0.05), without any measurable significant changes in ENO from hypoxic or HL regions There were no significant differences between the HCl and control groups for Ca2+-dependent (cNOS) or Ca2+-independent NOS (iNOS) activity in hypoxic or HL regions. Conclusions: Metabolic acidosis augmented the hypoxic pulmonary vasoconstriction, without any changes in pulmonary NOS dependent or NOS independent NO production. When acidosis was induced during ongoing NOS blockade, the perfusion of hypoxic lung regions was almost abolished, indicating acidosis-induced pulmonary vasoconstriction was not NO dependent.
|
|
| 28. |
|
|
| 29. |
- Pellegrini, Mariangela, et al.
(författare)
-
Expiratory Resistances Prevent Expiratory Diaphragm Contraction, Flow Limitation, and Lung Collapse
- 2020
-
Ingår i: American Journal of Respiratory and Critical Care Medicine. - : AMER THORACIC SOC. - 1073-449X .- 1535-4970. ; 3:7
-
Tidskriftsartikel (refereegranskat)abstract
- Rationale: Tidal expiratory flow limitation (tidal-EFL) is not completely avoidable by applying positive end-expiratory pressure and may cause respiratory and hemodynamic complications in ventilated patients with lungs prone to collapse. During spontaneous breathing, expiratory diaphragmatic contraction counteracts tidal-EFL. We hypothesized that during both spontaneous breathing and controlled mechanical ventilation, external expiratory resistances reduce tidal-EFL.Objectives: To assess whether external expiratory resistances 1) affect expiratory diaphragmatic contraction during spontaneous breathing, 2) reduce expiratory flow and make lung compartments more homogeneous with more similar expiratory time constants, and 3) reduce tidal atelectasis, preventing hyperinflation.Methods: Three positive end-expiratory pressure levels and four external expiratory resistances were tested in 10 pigs after lung lavage. We analyzed expiratory diaphragmatic electric activity and respiratory mechanics. On the basis of computed tomography scans, four lung compartments-not inflated (atelectasis), poorly inflated, normally inflated, and hyperinflated-were defined.Measurements and Main Results: Consequently to additional external expiratory resistances, and mainly in lungs prone to collapse (at low positive end-expiratory pressure), 1) the expiratory transdiaphragmatic pressure decreased during spontaneous breathing by >10%, 2) expiratory flow was reduced and the expiratory time constants became more homogeneous, and 3) the amount of atelectasis at end-expiration decreased from 24% to 16% during spontaneous breathing and from 32% to 18% during controlled mechanical ventilation, without increasing hyperinflation.Conclusions: The expiratory modulation induced by external expiratory resistances preserves the positive effects of the expiratory brake while minimizing expiratory diaphragmatic contraction. External expiratory resistances optimize lung mechanics and limit tidal-EFL and tidal atelectasis, without increasing hyperinflation.
|
|
| 30. |
- Pellegrini, Mariangela, et al.
(författare)
-
Expiratory Resistances Prevent Expiratory Diaphragm Contraction, Flow Limitation, and Lung Collapse.
- 2020
-
Ingår i: American journal of respiratory and critical care medicine. - 1535-4970. ; 201:10, s. 1218-1229
-
Tidskriftsartikel (refereegranskat)abstract
- Rationale: Tidal expiratory flow limitation (tidal-EFL) is not completely avoidable by applying positive end-expiratory pressure and may cause respiratory and hemodynamic complications in ventilated patients with lungs prone to collapse. During spontaneous breathing, expiratory diaphragmatic contraction counteracts tidal-EFL. We hypothesized that during both spontaneous breathing and controlled mechanical ventilation, external expiratory resistances reduce tidal-EFL.Objectives: To assess whether external expiratory resistances 1) affect expiratory diaphragmatic contraction during spontaneous breathing, 2) reduce expiratory flow and make lung compartments more homogeneous with more similar expiratory time constants, and 3) reduce tidal atelectasis, preventing hyperinflation.Methods: Three positive end-expiratory pressure levels and four external expiratory resistances were tested in 10 pigs after lung lavage. We analyzed expiratory diaphragmatic electric activity and respiratory mechanics. On the basis of computed tomography scans, four lung compartments-not inflated (atelectasis), poorly inflated, normally inflated, and hyperinflated-were defined.Measurements and Main Results: Consequently to additional external expiratory resistances, and mainly in lungs prone to collapse (at low positive end-expiratory pressure), 1) the expiratory transdiaphragmatic pressure decreased during spontaneous breathing by >10%, 2) expiratory flow was reduced and the expiratory time constants became more homogeneous, and 3) the amount of atelectasis at end-expiration decreased from 24% to 16% during spontaneous breathing and from 32% to 18% during controlled mechanical ventilation, without increasing hyperinflation.Conclusions: The expiratory modulation induced by external expiratory resistances preserves the positive effects of the expiratory brake while minimizing expiratory diaphragmatic contraction. External expiratory resistances optimize lung mechanics and limit tidal-EFL and tidal atelectasis, without increasing hyperinflation.
|
|
| 31. |
|
|
| 32. |
|
|
| 33. |
- Reinius, Henrik, 1968-
(författare)
-
Open lung concept in high risk anaesthesia : Optimizing mechanical ventilation in morbidly obese patients and during one lung ventilation with capnothorax
- 2016
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Formation of atelectasis, defined as reversible collapse of aerated lung, often occurs after induction of anaesthesia with mechanical ventilation. As a consequence, there is a risk for hypoxemia, altered hemodynamics and impaired respiratory system mechanics. In certain situations, the risk for atelectasis formation is increased and its consequences may also be more difficult to manage. Anesthesia for bariatric surgery in morbidly obese patients and surgery requiring one-lung ventilation (OLV) with capnothorax are examples of such situations.In Paper I (30 patients with BMI > 40 kg/m2 scheduled for bariatric surgery) a recruitment maneuver followed by positive end-expiratory pressure (PEEP) reduced the amount of atelectasis and improved oxygenation for a prolonged period of time. PEEP or a recruitment maneuver alone did not reduce the amount of atelectasis.In paper II we investigated whether it is possible to predict respiratory function impairment in morbidly obese patients without pulmonary disease from a preoperative lung function test. Patients with mild signs of airway obstruction (reduced end-expiratory flow) in the preoperative spirometry developed less atelectasis during anaesthesia.In paper III we developed an experimental model of sequential OLV with capnothorax using electrical impedance tomography (EIT) that in real-time detected lung separation and dynamic changes in pulmonary ventilation and perfusion distributions. OLV to the left side caused a decrease in cardiac output, arterial oxygenation and mixed venous saturation.In paper IV we used our model of OLV with capnothorax and applied a CO2-insufflation pressure of 16 cm H2O. We demonstrated that a PEEP level of 12-16 cm H2O is needed for optimal oxygenation and lowest possible driving pressure without compromising hemodynamic variables. Thus, the optimal PEEP was closely related to the level of the capnothorax insufflation pressure. With insufficient PEEP, ventilation/perfusion mismatch in the ventilated lung and redistribution of blood flow to the non-ventilated lung occurred.
|
|
| 34. |
- Reinius, Henrik, 1968-, et al.
(författare)
-
Optimal PEEP during one-lung ventilation with capnothorax : An experimental study
- 2019
-
Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 63:2, s. 222-231
-
Tidskriftsartikel (refereegranskat)abstract
- Background: One‐lung ventilation (OLV) with induced capnothorax carries the risk of severely impaired ventilation and circulation. Optimal PEEP may mitigate the physiological perturbations during these conditions.Methods: Right‐sided OLV with capnothorax (16 cm H2O) on the left side was initiated in eight anesthetized, muscle‐relaxed piglets. A recruitment maneuver and a decremental PEEP titration from PEEP 20 cm H2O to zero end‐expiratory pressure (ZEEP) was performed. Regional ventilation and perfusion were studied with electrical impedance tomography and computer tomography of the chest was used. End‐expiratory lung volume and hemodynamics were recorded and.Results: PaO2 peaked at PEEP 12 cm H2O (49 ± 14 kPa) and decreased to 11 ± 5 kPa at ZEEP (P < 0.001). PaCO2 was 9.5 ± 1.3 kPa at 20 cm H2O PEEP and did not change when PEEP step‐wise was reduced to 12 cm H2O PaCO2. At lower PEEP, PaCO2 increased markedly. The ventilatory driving pressure was lowest at PEEP 14 cm H2O (19.6 ± 5.8 cm H2O) and increased to 38.3 ± 6.1 cm H2O at ZEEP (P < 0.001). When reducing PEEP below 12‐14 cm H2O ventilation shifted from the dependent to the nondependent regions of the ventilated lung (P = 0.003), and perfusion shifted from the ventilated to the nonventilated lung (P = 0.02).Conclusion: Optimal PEEP was 12‐18 cm H2O and probably relates to capnothorax insufflation pressure. With suboptimal PEEP, ventilation/perfusion mismatch in the ventilated lung and redistribution of blood flow to the nonventilated lung occurred.
|
|
| 35. |
- Reinius, Henrik, 1968-, et al.
(författare)
-
Preoperative lung function tests as a predictor for atelectasis in morbidly obese patients during anesthesia
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Rationale: Pulmonary function is regularly impaired during general anesthesia and paralysis in morbidly obese patients. The aim of this study was to compare preoperative lung function with the alterations in respiratory function after induction of anesthesia in patients with BMI > 40 kg/m2.Methods: 23 women and 7 men (38 ± 9 years, (mean ± SD)), with a body mass index of 45 ± 4 kg/m2 were studied. 20 patients were active smokers (20 ± 12 pack years). All patients underwent preoperative lung functiontests. Arterial blood gases were collected before and after induction of anesthesia and either a single slice CT or a spiral CT was made for assessment of the amount of lung collapse. Respiratory system compliance was measured during anesthesia.Results: Lung volumes were within normal limits, however forced expiratory gas flow was reduced during the latter part of expiration. The arterial oxygen tension divided by the inspired O2 fraction (PaO2/FIO2 ratio) decreased from 409 ± 47 mmHg awake to 238 ± 80 mmHg after induction of anesthesia. The higher FEV1 was, the larger was the fall in oxygenation during anesthesia. At 5 min after induction, atelectasis in a CT cut 1 cm above the diaphragm was 7 ± 2 % of the lung area. The amount of atelectasis during anesthesia correlated with FEF75 in a regression analysis (p = 0.03).Conclusion: In morbidly obese patients without clinical signs of pulmonary disease a preoperative spirometry with mild signs of airway obstruction (reduced late expiratory flow) may predict reduced formation of atelectasis during anesthesia.
|
|
| 36. |
- Reinius, Henrik, et al.
(författare)
-
Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis : a computerized tomography study
- 2009
-
Ingår i: Anesthesiology. - 0003-3022 .- 1528-1175. ; 111:5, s. 979-987
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Morbidly obese patients show impaired pulmonary function during anesthesia and paralysis, partly due to formation of atelectasis. This study analyzed the effect of general anesthesia and three different ventilatory strategies to reduce the amount of atelectasis and improve respiratory function. METHODS: Thirty patients (body mass index 45 +/- 4 kg/m) scheduled for gastric bypass surgery were prospectively randomized into three groups: (1) positive end-expiratory pressure of 10 cm H2O (PEEP), (2) a recruitment maneuver with 55 cm H2O for 10 s followed by zero end-expiratory pressure, (3) a recruitment maneuver followed by PEEP. Transverse lung computerized tomography scans and blood gas analysis were recorded: awake, 5 min after induction of anesthesia and paralysis at zero end-expiratory pressure, and 5 min and 20 min after intervention. In addition, spiral computerized tomography scans were performed at two occasions in 23 of the patients. RESULTS: After induction of anesthesia, atelectasis increased from 1 +/- 0.5% to 11 +/- 6% of total lung volume (P < 0.0001). End-expiratory lung volume decreased from 1,387 +/- 581 ml to 697 +/- 157 ml (P = 0.0014). A recruitment maneuver + PEEP reduced atelectasis to 3 +/- 4% (P = 0.0002), increased end-expiratory lung volume and increased Pao2/Fio2 from 266 +/- 70 mmHg to 412 +/- 99 mmHg (P < 0.0001). PEEP alone did not reduce the amount of atelectasis or improve oxygenation. A recruitment maneuver + zero end-expiratory pressure had a transient positive effect on respiratory function. All values are presented as mean +/- SD. CONCLUSIONS: A recruitment maneuver followed by PEEP reduced atelectasis and improved oxygenation in morbidly obese patients, whereas PEEP or a recruitment maneuver alone did not.
|
|
| 37. |
- Reinius, Henrik, et al.
(författare)
-
Real-time ventilation and perfusion distributions by electrical impedance tomography during one-lung ventilation with capnothorax
- 2015
-
Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 59:3, s. 354-368
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Carbon dioxide insufflation into the pleural cavity, capnothorax, with one-lung ventilation (OLV) may entail respiratory and hemodynamic impairments. We investigated the online physiological effects of OLV/capnothorax by electrical impedance tomography (EIT) in a porcine model mimicking the clinical setting.Methods: Five anesthetized, muscle-relaxed piglets were subjected to first right and then left capnothorax with an intra-pleural pressure of 19cm H2O. The contra-lateral lung was mechanically ventilated with a double-lumen tube at positive end-expiratory pressure 5 and subsequently 10cm H2O. Regional lung perfusion and ventilation were assessed by EIT. Hemodynamics, cerebral tissue oxygenation and lung gas exchange were also measured.Results: During right-sided capnothorax, mixed venous oxygen saturation (P=0.018), as well as a tissue oxygenation index (P=0.038) decreased. There was also an increase in central venous pressure (P=0.006), and a decrease in mean arterial pressure (P=0.045) and cardiac output (P=0.017). During the left-sided capnothorax, the hemodynamic impairment was less than during the right side. EIT revealed that during the first period of OLV/capnothorax, no or very minor ventilation on the right side could be seen (33% vs. 97 +/- 3%, right vs. left, P=0.007), perfusion decreased in the non-ventilated and increased in the ventilated lung (18 +/- 2% vs. 82 +/- 2%, right vs. left, P=0.03). During the second OLV/capnothorax period, a similar distribution of perfusion was seen in the animals with successful separation (84 +/- 4% vs. 16 +/- 4%, right vs. left).Conclusion: EIT detected in real-time dynamic changes in pulmonary ventilation and perfusion distributions. OLV to the left lung with right-sided capnothorax caused a decrease in cardiac output, arterial oxygenation and mixed venous saturation.
|
|
| 38. |
- Strang, Christof M., et al.
(författare)
-
Development of atelectasis and arterial to end-tidal PCO2-difference in a porcine model of pneumoperitoneum
- 2009
-
Ingår i: British Journal of Anaesthesia. - : Elsevier BV. - 0007-0912 .- 1471-6771. ; 103:2, s. 298-303
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Intraperitoneal insufflation of carbon dioxide (CO2) may promote collapse of dependent lung regions. The present study was undertaken to study the effects of CO2-pneumoperitoneum (CO2-PP) on atelectasis formation, arterial oxygenation, and arterial to end-tidal PCO2-gradient (Pa-E'(CO2)). METHODS: Fifteen anaesthetized pigs [mean body weight 28 (SD 2) kg] were studied. Spiral computed tomography (CT) scans were obtained for analysis of lung tissue density. In Group 1 (n=5) mechanical ventilation (V(T)=10 ml kg (-1), FI(O2)=0.5) was applied, in Group 2 (n=5) FI(O2) was increased for 30 min to 1.0 and in Group 3 (n=5) negative airway pressure was applied for 20 s in order to enhance development of atelectasis. Cardiopulmonary and CT data were obtained before, 10, and 90 min after induction of CO2-PP at an abdominal pressure of 12 mmHg. RESULTS: Before CO2-PP, in Group 1 non-aerated tissue on CT scans was 1 (1)%, in Group 2 3 (2)% (P<0.05, compared with Group 1), and in Group 3 7 (3)% (P<0.05, compared with Group 1 and Group 2). CO2-PP significantly increased atelectasis in all groups. PaO2/FI(O2) fell and venous admixture ('shunt') increased in proportion to atelectasis during anaesthesia but CO2-PP had a varying effect on PaO2/FI(O2) and shunt. Thus, no correlation was seen between atelectasis and PaO2/FI(O2) or shunt when all data before and during CO2-PP were pooled. Pa-E'(CO2), on the other hand correlated strongly with the amount of atelectasis (r2=0.92). CONCLUSIONS: Development of atelectasis during anaesthesia and PP may be estimated by an increased Pa-E'(CO2).
|
|
| 39. |
- Strang, Christof M., et al.
(författare)
-
Improved ventilation-perfusion matching with increasing abdominal pressure during CO(2)-pneumoperitoneum in pigs
- 2011
-
Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 55:7, s. 887-896
-
Tidskriftsartikel (refereegranskat)abstract
- Background: CO(2)-pneumoperitoneum (PP) is performed at varying abdominal pressures. We studied in an animal preparation the effect of increasing abdominal pressures on gas exchange during PP. Methods: Eighteen anaesthetized pigs were studied. Three abdominal pressures (8, 12 and 16mmHg) were randomly selected in each animal. In six pigs, single-photon emission computed tomography (SPECT) was used for the analysis of V / Q distributions; in another six pigs, multiple inert gas elimination technique (MIGET) was used for assessing V / Q matching. In further six pigs, computed tomography (CT) was performed for the analysis of regional aeration. MIGET, CT and central haemodynamics and pulmonary gas exchange were recorded during anaesthesia and after 60min on each of the three abdominal pressures. SPECT was performed three times, corresponding to each PP level. Results: Atelectasis, as assessed by CT, increased during PP and in proportion to abdominal pressure [from 9 +/- 2% (mean +/- standard deviation) at 8mmHg to 15 +/- 2% at 16mmHg, P <0.05]. SPECT during increasing abdominal CO(2) pressures showed a shift of blood flow towards better ventilated areas. V / Q analysis by MIGET showed no change in shunt during 8 mmHg PP (9 +/- 1.9% compared with baseline 9 +/- 1.2%) but a decrease during 12mmHg PP (7 +/- 0.9%, P <0.05) and 16mmHg PP (5 +/- 1%, P <0.01). PaO(2) increased from 39 +/- 10 to 52 +/- 9 kPa (baseline to 16 mmHg PP, P <0.01). Arterial carbon dioxide (PCO(2)) increased during PP and increased further with increasing abdominal pressures. Conclusion: With increasing abdominal pressure during PP perfusion was redistributed more than ventilation away from dorsal, collapsed lung regions. This resulted in a better V / Q match. A possible mechanism is enhanced hypoxic pulmonary vasoconstriction mediated by increasing PCO(2).
|
|
| 40. |
- Strang, Christof M., et al.
(författare)
-
Ventilation-perfusion distributions and gas exchange during carbon dioxide-pneumoperitoneum in a porcine model
- 2010
-
Ingår i: British Journal of Anaesthesia. - : Elsevier BV. - 0007-0912 .- 1471-6771. ; 105:5, s. 691-697
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: /st> Carbon dioxide (CO(2))-pneumoperitoneum (PP) of 12 mm Hg increases arterial oxygenation, but it also promotes collapse of dependent lung regions. This seeming paradox prompted the present animal study on the effects of PP on ventilation-perfusion distribution (V/Q) and gas exchange. METHODS: /st> Fourteen anaesthetized pigs were studied. In seven pigs, single photon emission computed tomography (SPECT) was used for spatial analysis of ventilation and perfusion distributions, and in another seven pigs, multiple inert gas elimination technique (MIGET) was used for detailed analysis of V/Q matching. SPECT/MIGET and central haemodynamics and pulmonary gas exchange were recorded during anaesthesia before and 60 min after induction of PP. RESULTS: /st> SPECT during PP showed no or only poorly ventilated regions in the dependent lung compared with the ventilation distribution during anaesthesia before PP. PP was accompanied by redistribution of blood flow away from the non- or poorly ventilated regions. V/Q analysis by MIGET showed decreased shunt from 9 (sd 2) to 7 (2)% after induction of PP (P<0.05). No regions of low V/Q were seen either before or during PP. Almost no regions of high V/Q developed during PP (1% of total ventilation). Pa(o(2)) increased from 33 (1.2) to 35.7 (3.2) kPa (P<0.01) and arterial to end-tidal Pco(2) gradient (Pae'(co(2))) increased from 0.3 (0.1) to 0.6 (0.2) kPa (P<0.05). CONCLUSIONS: /st> Perfusion was redistributed away from dorsal, collapsed lung regions when PP was established. This resulted in a better V/Q match. A possible mechanism is enhanced hypoxic pulmonary vasoconstriction.
|
|
