| 1. |
- 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.
|
|
| 2. |
- 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.
|
|
| 3. |
|
|
| 4. |
- 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.
|
|
| 5. |
- 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).
|
|
