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Respiratory Function During Anesthesia: Effects on Gas Exchange

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Abstract

Anaesthesia causes a respiratory impairment, whether the patient is breathing spontaneously or is ventilated mechanically. This impairment impedes the matching of alveolar ventilation and perfusion and thus the oxygenation of arterial blood. A triggering factor is loss of muscle tone that causes a fall in the resting lung volume, functional residual capacity. This fall promotes airway closure and gas adsorption, leading eventually to alveolar collapse, that is, atelectasis. The higher the oxygen concentration, the faster will the gas be adsorbed and the aleveoli collapse. Preoxygenation is a major cause of atelectasis and continuing use of high oxygen concentration maintains or increases the lung collapse, that typically is 10% or more of the lung tissue. It can exceed 25% to 40%. Perfusion of the atelectasis causes shunt and cyclic airway closure causes regions with low ventilation/perfusion ratios, that add to impaired oxygenation. Ventilation with positive end‐expiratory pressure reduces the atelectasis but oxygenation need not improve, because of shift of blood flow down the lung to any remaining atelectatic tissue. Inflation of the lung to an airway pressure of 40 cmH2O recruits almost all collapsed lung and the lung remains open if ventilation is with moderate oxygen concentration (< 40%) but recollapses within a few minutes if ventilation is with 100% oxygen. Severe obesity increases the lung collapse and obstructive lung disease and one‐lung anesthesia increase the mismatch of ventilation and perfusion. CO2 pneumoperitoneum increases atelectasis formation but not shunt, likely explained by enhanced hypoxic pulmonary vasoconstriction by CO2. Atelectasis may persist in the postoperative period and contribute to pneumonia. © 2012 American Physiological Society. Compr Physiol 2:69‐96, 2012.

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Figure 1. Figure 1.

Influence of age on functional residual capacity (FRC) awake in different body positions (sitting and supine) and during anesthesia (supine). Closing capacity (CC), the lung volume at which airways begin to close during expiration, is also shown. Note the increase in FRC with increasing age, provided that body height and weight are constant. Note also the decrease in FRC by approximately 0,7‐0,8 l when lying down from upright and the further decrease by another 0,4‐0,5 l during anesthesia. Closing capacity increases faster with age so that a certain amount of airway closure occurs above FRC in upright position at ages above 65 years and at around 50 years in the supine position. During anesthesia most patients older than 30 years will suffer from airway closure. Composite drawing, with permission, with data from .

Figure 2. Figure 2.

Change in thoracic volume during anesthesia and consequences for lung volume and respiratory mechanics. During anesthesia functional residual capacity (FRC) is reduced by approximately 0,4‐0,5 l and lung compliance is reduced and airway resistance increased. Loss of respiratory muscle tone causes a decrease in FRC and the fall in compliance might be attributed to lung collapse and airway closure. The increase in airway resistance may be related to the reduced lung volume and the decrease in airway dimensions.

Figure 3. Figure 3.

Transverse computed tomography (CT) images of the chest with the cut just above the top of the diaphragm in an awake subject and during anesthesia (right panels). Corresponding ventilation‐perfusion distributions by multiple inert gas elimination technique (MIGET) are shown to the left. Note the appearance of atelectasis in the bottom of both lungs during anesthesia and the slight broadening of the a/ distribution with some increase in low a/ and shunt. A cardiac catheter causes the radiating beams that can be seen in the heart contour of the CT. Adapted, with permission, from reference .

Figure 4. Figure 4.

Three‐dimensional reconstruction of atelectasis in an anesthetized subject. The chest wall is shown in grey and the atelectasis in black. Note the rather uneven distribution in the dependent regions of the atelectasis that is larger to the left (near the diaphragm) and decreases to the right toward the apex. Adapted, with permission, from reference .

Figure 5. Figure 5.

Dependence of the critical inspired ventilation‐perfusion ratio (a/) and inspired O2 concentration on minimum time to collapse [from , with permission]. The calculations have been made on the assumption that the blood flow has been 2 ml/min/ml lung unit. Adapted from reference , with permission by the editor of JAP.

Figure 6. Figure 6.

Lung model used for calculating the kinetics of adsorption atelectasis during induction of anesthesia. Note that one lung model is being used before induction of anesthesia and another model with an additional unventilated lung region after induction of anesthesia. To enable calculations during dynamic events and to eliminate the need of steady state, a peripheral tissue compartment consisting of four regions has been added to the model (VRG: vessel rich group, MG: muscle group, FG: fat group, and VPG: vessel poor group). Moreover, the ventilated lung compartment (lower panel) consists of an alveolar gas and a lung tissue subcompartment with gas exchange between the two subcompartments and with air and lung blood. Adapted from reference , with permission by the editor of JAP.

Figure 7. Figure 7.

Time to collapse of unventilated lung compartment with and without preoxygenation (pre‐O2) for 3 min and when breathing either nitrogen (N2, 60%) or nitrous oxide (N2O, 60%) in oxygen (40%). Note the much faster collapse after preoxygenation and the minimal difference between the effect of N2 or N2O. Adapted from reference , with permission by the editor of JAP.

Figure 8. Figure 8.

Influence of oxygen concentration during induction of anesthesia on atelectasis formation. Black symbols show individual patients. Twelve patients received 100% O2 during 3 to 4 min before induction, their expired O2 (FETO2) being shown. Another 12 patients were preoxygenated with 80% O2 and still another 12 patients with 60% O2. Note the varying amount of atelectasis and the considerable dependence on inspired oxygen concentration. The open symbol (circle) demonstrates the almost complete absence of atelectasis in 10 patients who were preoxygenated with an inspired oxygen concentration of 30%. Data adapted, with permission, from and . Adapted from reference , with permission by the editor of Anesthesiology.

Figure 9. Figure 9.

Decrease in arterial oxygen saturation, as measured by pulse oximetry during apnea after preceding preoxygenation with different inspired oxygen concentrations for 3 to 4 min. Note the fairly stable oxygen saturation for the first 2 to 4 or 5 min and the rapid decline thereafter. Adapted from reference , with permission by the editor of Anesthesiology.

Figure 10. Figure 10.

The effect of different inspiratory pressures on recruitment of collapsed lung tissue. Note the presence of atelectasis during anesthesia at functional residual capacity (FRC) level (airway pressure 0 cmH2O) with no effect at all after inspiration to 10 cmH2O (corresponding to a normal tidal volume) or at an airway pressure of 20 cmH2O (corresponding to a sigh or double tidal volume). Not until airway pressure has reached 30 cmH2O a certain reduction of atelectasis can be seen. Complete elimination of atelectasis in most but not all patients can be seen at an airway pressure of 40 cmH2O. The inflation pressure was kept for 15 s before computed tomography (CT) measurements were made. Adapted from reference , with permission by the editor of Br J Anesth.

Figure 11. Figure 11.

Shunt (filled column) and low a/ regions (open column) before and after recruitment maneuver (vital capacity with an inflation of the lung to an airway pressure of 40 cmH2O for 15 s. Note that awake there is a minimal shunt and some low a/. During anesthesia significant shunt can be seen with some low a/. After a recruitment maneuver most of the shunt is eliminated but an increase in low a/ can be seen. This suggests that the atelectasis producing shunt has been reopened with elimination of shunt but with reduced ventilation in proportion to perfusion (low a/). Redrawn, with permission, from data in reference .

Figure 12. Figure 12.

Computed tomography (CT) scan (left panel) and vertical distributions of ventilation (open squares) and perfusion (closed circles) in an anesthetized subject. Note the appearance of atelectasis in the bottom of both lungs. Note also that most of the ventilation is distributed to the upper half of the lung and is decreasing in the lower half until the bottom where the ventilation has ceased. Perfusion on the other hand increases down the lung except for the lowermost part where a certain decrease can be seen. This causes a considerable ventilation/perfusion mismatch with high a/ in the upper half of the lung, mimicking dead space ventilation, and low a/ and shunt in the lowermost regions. Redrawn, with permission, from reference .

Figure 13. Figure 13.

Inhibition of the hypoxic pulmonary vasoconstrictor response by inhalational anesthetics. Data from humans and animals have been plotted. Adapted from reference , with permission by the editor.

Figure 14. Figure 14.

Theoretical analysis of the effect on a/ of different vertical distributions of lung blood flow. Left upper panel: blood flow curves (x) similar to those obtained during mechanical ventilation without and with positive end‐expiratory pressure (PEEP) in reference . In addition, the dotted curve in the uppermost part along the vertical axis shows a theoretical situation where blood flow is increasing continuously down the lung (and thus slightly different from what actually was found (the continuous line). Right upper panel: distribution of regional lung volume (y) from top to bottom of the lung (distance) as found in reference . Assuming even distribution of ventilation, regional ventilation will be proportional to regional volume, k x Y. Left lower panel: vertical distribution of a/ calculated as k x Y / X x Y or k/X. Right lower panel: a plot of ventilation, k x Y, against logarithmic distribution of a/ (log k/X). Note the unimodal a/ distribution without PEEP and bimodal distribution with PEEP. Also, if perfusion had been continuously increasing down the lung in the topmost part, as indicated by the dotted line in the right upper panel, a/ distribution would have been broad but unimodal (dotted line). Adapted from reference , with permission by the editor of JAP.

Figure 15. Figure 15.

Computed tomography (CT) scans and inert gas‐a/ distributions of ventilation (open squares) and perfusion (closed rhomboids) in a patient awake (upper panels) and during anesthesia and muscle paralysis (mid panels) as well as corresponding single photon emission computed tomography (SPECT) scan and a/ distribution during anesthesia (lower panels). Note the appearance of atelectasis (gray densities) in the bottom of both lungs during anesthesia and the appearance of shunt approximately corresponding to the atelectatic regions (lower left panel). Also, note the rather similar a/ distribution with inert gas and isotope techniques except for much smaller dead space (VD) with the isotope technique. The latter can not separate alveolar ventilation from dead space ventilation explaining the virtual absence of “dead space.” Adapted from reference , with permission by the editor of JAP.

Figure 16. Figure 16.

Dependence of shunt and of shunt plus low a/ on age in awake and anesthetized subjects. Note the constant minor shunt with increasing age awake and a small, still insignificant, increase during anesthesia. Note also the significant increase in shunt plus low a/ both awake and during anesthesia with increasing age. Redrawn, with permission, from data from reference .

Figure 17. Figure 17.

Computed tomography (CT) in anesthetized obese patients with the cut 1 cm above the diaphragm. A recruitment maneuver (RM) (airway pressure of 55 cmH2O for 10 s) + PEEP of 10 cmH2O reduced atelectasis and this effect was sustained for 20 min. RM + ZEEP caused a reduction of atelectasis, but this effect could not be seen after 20 min. PEEP had no effect on the amount of atelectasis. *P < 0.05 versus anesthesia, †P < 0.05 versus PEEP and RM + ZEEP. PEEP = positive end expiratory pressure, RM = recruitment maneuver, ZEEP = zero end expiratory pressure. Adapted from reference , with permission by the editor of Anesthesiology.

Figure 18. Figure 18.

Ventilation perfusion distributions and CT scans in a patient with severe obstructive lung disease awake and during anesthesia. Note the increased dispersion of a/ ratios but absence of shunt in the waking condition and the further broadening of the a/ distribution during anesthesia but still without any shunt. Note also the hyperinflated lung (large transverse lung area) with no atelectasis awake and also no atelectasis during anesthesia, opposite to the finding in lung healthy subjects. Adapted from reference , with permission by the editor of Eur Respir J.

Figure 19. Figure 19.

Perfusion of the left lower lobe (LL/T in percent of cardiac otput) in dogs (n = 6). Control: anesthesia with controlled mechanical ventilation, FIO2 = 1.0; atelectasis: atelectasis, induced by clamping the left lower lung lobe; N2/CO2: left lower lobe ventilated with inspiratory gas of 95% N2 and 5% CO2; O2: left lwover lobe ventilated with FIO2 = 1.0. Data suggest, that the change in regional perfusion is due to hypoxic pulmonary vasoconstriction, no effect of passive mechanical forces was found. Data are mean ± SEM. Adapted from reference , with permission by the editor of JAP.



Figure 1.

Influence of age on functional residual capacity (FRC) awake in different body positions (sitting and supine) and during anesthesia (supine). Closing capacity (CC), the lung volume at which airways begin to close during expiration, is also shown. Note the increase in FRC with increasing age, provided that body height and weight are constant. Note also the decrease in FRC by approximately 0,7‐0,8 l when lying down from upright and the further decrease by another 0,4‐0,5 l during anesthesia. Closing capacity increases faster with age so that a certain amount of airway closure occurs above FRC in upright position at ages above 65 years and at around 50 years in the supine position. During anesthesia most patients older than 30 years will suffer from airway closure. Composite drawing, with permission, with data from .



Figure 2.

Change in thoracic volume during anesthesia and consequences for lung volume and respiratory mechanics. During anesthesia functional residual capacity (FRC) is reduced by approximately 0,4‐0,5 l and lung compliance is reduced and airway resistance increased. Loss of respiratory muscle tone causes a decrease in FRC and the fall in compliance might be attributed to lung collapse and airway closure. The increase in airway resistance may be related to the reduced lung volume and the decrease in airway dimensions.



Figure 3.

Transverse computed tomography (CT) images of the chest with the cut just above the top of the diaphragm in an awake subject and during anesthesia (right panels). Corresponding ventilation‐perfusion distributions by multiple inert gas elimination technique (MIGET) are shown to the left. Note the appearance of atelectasis in the bottom of both lungs during anesthesia and the slight broadening of the a/ distribution with some increase in low a/ and shunt. A cardiac catheter causes the radiating beams that can be seen in the heart contour of the CT. Adapted, with permission, from reference .



Figure 4.

Three‐dimensional reconstruction of atelectasis in an anesthetized subject. The chest wall is shown in grey and the atelectasis in black. Note the rather uneven distribution in the dependent regions of the atelectasis that is larger to the left (near the diaphragm) and decreases to the right toward the apex. Adapted, with permission, from reference .



Figure 5.

Dependence of the critical inspired ventilation‐perfusion ratio (a/) and inspired O2 concentration on minimum time to collapse [from , with permission]. The calculations have been made on the assumption that the blood flow has been 2 ml/min/ml lung unit. Adapted from reference , with permission by the editor of JAP.



Figure 6.

Lung model used for calculating the kinetics of adsorption atelectasis during induction of anesthesia. Note that one lung model is being used before induction of anesthesia and another model with an additional unventilated lung region after induction of anesthesia. To enable calculations during dynamic events and to eliminate the need of steady state, a peripheral tissue compartment consisting of four regions has been added to the model (VRG: vessel rich group, MG: muscle group, FG: fat group, and VPG: vessel poor group). Moreover, the ventilated lung compartment (lower panel) consists of an alveolar gas and a lung tissue subcompartment with gas exchange between the two subcompartments and with air and lung blood. Adapted from reference , with permission by the editor of JAP.



Figure 7.

Time to collapse of unventilated lung compartment with and without preoxygenation (pre‐O2) for 3 min and when breathing either nitrogen (N2, 60%) or nitrous oxide (N2O, 60%) in oxygen (40%). Note the much faster collapse after preoxygenation and the minimal difference between the effect of N2 or N2O. Adapted from reference , with permission by the editor of JAP.



Figure 8.

Influence of oxygen concentration during induction of anesthesia on atelectasis formation. Black symbols show individual patients. Twelve patients received 100% O2 during 3 to 4 min before induction, their expired O2 (FETO2) being shown. Another 12 patients were preoxygenated with 80% O2 and still another 12 patients with 60% O2. Note the varying amount of atelectasis and the considerable dependence on inspired oxygen concentration. The open symbol (circle) demonstrates the almost complete absence of atelectasis in 10 patients who were preoxygenated with an inspired oxygen concentration of 30%. Data adapted, with permission, from and . Adapted from reference , with permission by the editor of Anesthesiology.



Figure 9.

Decrease in arterial oxygen saturation, as measured by pulse oximetry during apnea after preceding preoxygenation with different inspired oxygen concentrations for 3 to 4 min. Note the fairly stable oxygen saturation for the first 2 to 4 or 5 min and the rapid decline thereafter. Adapted from reference , with permission by the editor of Anesthesiology.



Figure 10.

The effect of different inspiratory pressures on recruitment of collapsed lung tissue. Note the presence of atelectasis during anesthesia at functional residual capacity (FRC) level (airway pressure 0 cmH2O) with no effect at all after inspiration to 10 cmH2O (corresponding to a normal tidal volume) or at an airway pressure of 20 cmH2O (corresponding to a sigh or double tidal volume). Not until airway pressure has reached 30 cmH2O a certain reduction of atelectasis can be seen. Complete elimination of atelectasis in most but not all patients can be seen at an airway pressure of 40 cmH2O. The inflation pressure was kept for 15 s before computed tomography (CT) measurements were made. Adapted from reference , with permission by the editor of Br J Anesth.



Figure 11.

Shunt (filled column) and low a/ regions (open column) before and after recruitment maneuver (vital capacity with an inflation of the lung to an airway pressure of 40 cmH2O for 15 s. Note that awake there is a minimal shunt and some low a/. During anesthesia significant shunt can be seen with some low a/. After a recruitment maneuver most of the shunt is eliminated but an increase in low a/ can be seen. This suggests that the atelectasis producing shunt has been reopened with elimination of shunt but with reduced ventilation in proportion to perfusion (low a/). Redrawn, with permission, from data in reference .



Figure 12.

Computed tomography (CT) scan (left panel) and vertical distributions of ventilation (open squares) and perfusion (closed circles) in an anesthetized subject. Note the appearance of atelectasis in the bottom of both lungs. Note also that most of the ventilation is distributed to the upper half of the lung and is decreasing in the lower half until the bottom where the ventilation has ceased. Perfusion on the other hand increases down the lung except for the lowermost part where a certain decrease can be seen. This causes a considerable ventilation/perfusion mismatch with high a/ in the upper half of the lung, mimicking dead space ventilation, and low a/ and shunt in the lowermost regions. Redrawn, with permission, from reference .



Figure 13.

Inhibition of the hypoxic pulmonary vasoconstrictor response by inhalational anesthetics. Data from humans and animals have been plotted. Adapted from reference , with permission by the editor.



Figure 14.

Theoretical analysis of the effect on a/ of different vertical distributions of lung blood flow. Left upper panel: blood flow curves (x) similar to those obtained during mechanical ventilation without and with positive end‐expiratory pressure (PEEP) in reference . In addition, the dotted curve in the uppermost part along the vertical axis shows a theoretical situation where blood flow is increasing continuously down the lung (and thus slightly different from what actually was found (the continuous line). Right upper panel: distribution of regional lung volume (y) from top to bottom of the lung (distance) as found in reference . Assuming even distribution of ventilation, regional ventilation will be proportional to regional volume, k x Y. Left lower panel: vertical distribution of a/ calculated as k x Y / X x Y or k/X. Right lower panel: a plot of ventilation, k x Y, against logarithmic distribution of a/ (log k/X). Note the unimodal a/ distribution without PEEP and bimodal distribution with PEEP. Also, if perfusion had been continuously increasing down the lung in the topmost part, as indicated by the dotted line in the right upper panel, a/ distribution would have been broad but unimodal (dotted line). Adapted from reference , with permission by the editor of JAP.



Figure 15.

Computed tomography (CT) scans and inert gas‐a/ distributions of ventilation (open squares) and perfusion (closed rhomboids) in a patient awake (upper panels) and during anesthesia and muscle paralysis (mid panels) as well as corresponding single photon emission computed tomography (SPECT) scan and a/ distribution during anesthesia (lower panels). Note the appearance of atelectasis (gray densities) in the bottom of both lungs during anesthesia and the appearance of shunt approximately corresponding to the atelectatic regions (lower left panel). Also, note the rather similar a/ distribution with inert gas and isotope techniques except for much smaller dead space (VD) with the isotope technique. The latter can not separate alveolar ventilation from dead space ventilation explaining the virtual absence of “dead space.” Adapted from reference , with permission by the editor of JAP.



Figure 16.

Dependence of shunt and of shunt plus low a/ on age in awake and anesthetized subjects. Note the constant minor shunt with increasing age awake and a small, still insignificant, increase during anesthesia. Note also the significant increase in shunt plus low a/ both awake and during anesthesia with increasing age. Redrawn, with permission, from data from reference .



Figure 17.

Computed tomography (CT) in anesthetized obese patients with the cut 1 cm above the diaphragm. A recruitment maneuver (RM) (airway pressure of 55 cmH2O for 10 s) + PEEP of 10 cmH2O reduced atelectasis and this effect was sustained for 20 min. RM + ZEEP caused a reduction of atelectasis, but this effect could not be seen after 20 min. PEEP had no effect on the amount of atelectasis. *P < 0.05 versus anesthesia, †P < 0.05 versus PEEP and RM + ZEEP. PEEP = positive end expiratory pressure, RM = recruitment maneuver, ZEEP = zero end expiratory pressure. Adapted from reference , with permission by the editor of Anesthesiology.



Figure 18.

Ventilation perfusion distributions and CT scans in a patient with severe obstructive lung disease awake and during anesthesia. Note the increased dispersion of a/ ratios but absence of shunt in the waking condition and the further broadening of the a/ distribution during anesthesia but still without any shunt. Note also the hyperinflated lung (large transverse lung area) with no atelectasis awake and also no atelectasis during anesthesia, opposite to the finding in lung healthy subjects. Adapted from reference , with permission by the editor of Eur Respir J.



Figure 19.

Perfusion of the left lower lobe (LL/T in percent of cardiac otput) in dogs (n = 6). Control: anesthesia with controlled mechanical ventilation, FIO2 = 1.0; atelectasis: atelectasis, induced by clamping the left lower lung lobe; N2/CO2: left lower lobe ventilated with inspiratory gas of 95% N2 and 5% CO2; O2: left lwover lobe ventilated with FIO2 = 1.0. Data suggest, that the change in regional perfusion is due to hypoxic pulmonary vasoconstriction, no effect of passive mechanical forces was found. Data are mean ± SEM. Adapted from reference , with permission by the editor of JAP.

References
 1. Agusti AG, Barbera JA. Contribution of multiple inert gas elimination technique to pulmonary medicine. 2. Chronic pulmonary diseases: Chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Thorax 49: 924‐932, 1994.
 2. Albert SP, DiRocco J, Allen GB, Bates JH, Lafollette R, Kubiak BD, Fischer J, Maroney S, Nieman GF. The role of time and pressure on alveolar recruitment. J Appl Physiol 106: 757‐765, 2009.
 3. Andersson L, Lagerstrand L, Thorne A, Sollevi A, Brodin LA, Odeberg‐Wernerman S. Effect of CO(2) pneumoperitoneum on ventilation‐perfusion relationships during laparoscopic cholecystectomy. Acta Anaesthesiol Scand 46: 552‐560, 2002.
 4. Andersson LE, Baath M, Thorne A, Aspelin P, Odeberg‐Wernerman S. Effect of carbon dioxide pneumoperitoneum on development of atelectasis during anesthesia, examined by spiral computed tomography. Anesthesiology 102: 293‐299, 2005.
 5. Anjou‐Lindskog E, Broman L, Broman M, Holmgren A, Settergren G, Ohqvist G. Effects of intravenous anesthesia on VA/Q distribution: a study performed during ventilation with air and with 50% oxygen, supine and in the lateral position. Anesthesiology 62: 485‐492, 1985.
 6. Ansermino JM, Magruder W, Dosani M. Spontaneous respiration during intravenous anesthesia in children. Curr Opin Anaesthesiol 22: 383‐387, 2009.
 7. Appelberg J, Pavlenko T, Bergman H, Rothen HU, Hedenstierna G. Lung aeration during sleep. Chest 131: 122‐129, 2007.
 8. Arozullah AM, Khuri SF, Henderson WG, Daley J. Development and validation of a multifactorial risk index for predicting postoperative pneumonia after major noncardiac surgery. Ann Intern Med 135: 847‐857, 2001.
 9. Bablekos GD, Michaelides SA, Roussou T, Charalabopoulos KA. Changes in breathing control and mechanics after laparoscopic vs open cholecystectomy. Arch Surg 141: 16‐22, 2006.
 10. Ballard RD, Irvin CG, Martin RJ, Pak J, Pandey R, White DP. Influence of sleep on lung volume in asthmatic patients and normal subjects. J Appl Physiol 68: 2034‐2041, 1990.
 11. Baraka AS, Taha SK, Siddik‐Sayyid SM, Kanazi GE, El‐Khatib MF, Dagher CM, Chehade JM, Abdallah FW, Hajj RE. Supplementation of pre‐oxygenation in morbidly obese patients using nasopharyngeal oxygen insufflation. Anaesthesia 62: 769‐773, 2007.
 12. Bardoczky GI, Yernault JC, Houben JJ, d'Hollander AA. Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg 81: 385‐388, 1995.
 13. Bendixen HH, Hedley‐Whyte J, Laver MB. Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. A concept of atelectasis. N Engl J Med 269: 991‐996, 1963.
 14. Benoit Z, Wicky S, Fischer JF, Frascarolo P, Chapuis C, Spahn DR, Magnusson L. The effect of increased FIO(2) before tracheal extubation on postoperative atelectasis. Anesth Analg 95: 1777‐1781, 2002.
 15. Benumof JL. Mechanism of decreased blood flow to atelectatic lung. J Appl Physiol 46: 1047‐1048, 1979.
 16. Berggren SM. The oxygen deficit of arterial blood caused by non‐ventilating parts of the lung. Acta Physiol Scand 4(Suppl 11): 1‐92, 1942.
 17. Berthoud MC, Peacock JE, Reilly CS. Effectiveness of preoxygenation in morbidly obese patients. Br J Anaesth 67: 464‐466, 1991.
 18. Bindslev L, Hedenstierna G, Santesson J, Gottlieb I, Carvallhas A. Ventilation‐perfusion distribution during inhalation anaesthesia. Effects of spontaneous breathing, mechanical ventilation and positive end‐expiratory pressure. Acta Anaesthesiol Scand 25: 360‐371, 1981.
 19. Bindslev L, Hedenstierna G, Santesson J, Norlander O, Gram I. Airway closure during anaesthesia, and its prevention by positive end expiratory pressure. Acta Anaesthesiol Scand 24: 199‐205, 1980.
 20. Bjertnaes LJ. Hypoxia‐induced vasoconstriction in isolated perfused lungs exposed to injectable or inhalation anesthetics. Acta Anaesthesiol Scand 21: 133‐147, 1977.
 21. Boriek AM, Rodarte JR. Inferences on passive diaphragm mechanics from gross anatomy. J Appl Physiol 77: 2065‐2070, 1994.
 22. Brar MS, Brar SS, Dixon E. Perioperative supplemental oxygen in colorectal patients: A meta‐analysis. J Surg Res, 2009.
 23. Brismar B, Hedenstierna G, Lundquist H, Strandberg A, Svensson L, Tokics L. Pulmonary densities during anesthesia with muscular relaxation–a proposal of atelectasis. Anesthesiology 62: 422‐428, 1985.
 24. Broccard AF, Hotchkiss JR, Suzuki S, Olson D, Marini JJ. Effects of mean airway pressure and tidal excursion on lung injury induced by mechanical ventilation in an isolated perfused rabbit lung model. Crit Care Med 27: 1533‐1541, 1999.
 25. Brodsky JB. Approaches to hypoxemia during single‐lung ventilation. Curr Opin Anaesthesiol 14: 71‐76, 2001.
 26. Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A, Wiedemann HP, Arroliga AC, Fisher CJ, Komara JJ, Perez‐Trepichio P, Parsons PE, Wolkin R, Welsh C, Fulkerson WJ, MacIntyre N, Mallatratt L, Sebastian M, McConnell R, Wilcox C, Govert J, Thompson D, Clemmer T, Davis R, Orme J, Weaver L, Grissom C, Eskelson M, Young M, Gooder V, McBride K, Lawton C, d'Hulst J, Peerless JR, Smith C, Brownlee J, Pluss W, Kallet R, Luce JM, Gottlieb J, Elmer M, Girod A, Park P, Daniel B, Gropper M, Abraham E, Piedalue F, Glodowski J, Lockrem J, McIntyre R, Reid K, Stevens C, Kalous D, Silverman HJ, Shanholtz C, Corral W, Toews GB, Arnoldi D, Bartlett RH, Dechert R, Watts C, Lanken PN, Anderson H, Finkel B, Hanson CW, Barton R, Mone M, Hudson LD, Lee C, Carter G, Maier RV, Steinberg KP, Bernard G, Stroud M, Swindell B, Stone L, Collins L, Mogan S, Ancukiewicz M, Hayden D, Molay F, Ringwood N, Wenzlow G, Kazeroonian AS, Gail DB, Bosken CH, Randall P, Waclawiw M, Spragg RG, Boyett J, Kelley J, Leeper K, Secundy MG, Slutsky A, Hyers TM, Emerson SS, Garcia JGN, Marini JJ, Pingleton SK, Shasby MD, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 342: 1301‐1308, 2000.
 27. Bures E, Fusciardi J, Lanquetot H, Dhoste K, Richer JP, Lacoste L. Ventilatory effects of laparoscopic cholecystectomy. Acta Anaesthesiol Scand 40: 566‐573, 1996.
 28. Chalhoub V, Yazigi A, Sleilaty G, Haddad F, Noun R, Madi‐Jebara S, Yazbeck P. Effect of vital capacity manoeuvres on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery. Eur J Anaesthesiol 24: 283‐288, 2007.
 29. Chiumello D, Cressoni M, Chierichetti M, Tallarini F, Botticelli M, Berto V, Mietto C, Gattinoni L. Nitrogen washout/washin, helium dilution and computed tomography in the assessment of end expiratory lung volume. Crit Care 12: R150, 2008.
 30. Choi YS, Bang SO, Shim JK, Chung KY, Kwak YL, Hong YW. Effects of head‐down tilt on intrapulmonary shunt fraction and oxygenation during one‐lung ventilation in the lateral decubitus position. J Thorac Cardiovasc Surg 134: 613‐618, 2007.
 31. Chu EK, Whitehead T, Slutsky AS. Effects of cyclic opening and closing at low‐ and high‐volume ventilation on bronchoalveolar lavage cytokines. Crit Care Med 32: 168‐174, 2004.
 32. Claxton BA, Morgan P, McKeague H, Mulpur A, Berridge J. Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia 58: 111‐116, 2003.
 33. Cohen E. Recommendations for airway control and difficult airway management in thoracic anesthesia and lung separation procedures. Are we ready for the challenge? Minerva Anestesiol 75: 3‐5, 2009.
 34. Constantinopol M, Jones JH, Weibel ER, Taylor CR, Lindholm A, Karas RH. Oxygen transport during exercise in large mammals. II. Oxygen uptake by the pulmonary gas exchanger. J Appl Physiol 67: 871‐878, 1989.
 35. Coussa M, Proietti S, Schnyder P, Frascarolo P, Suter M, Spahn DR, Magnusson L. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesth Analg 98: 1491‐1495, 2004.
 36. Crotti S, Mascheroni D, Caironi P, Pelosi P, Ronzoni G, Mondino M, Marini JJ, Gattinoni L. Recruitment and derecruitment during acute respiratory failure: A clinical study. Am J Respir Crit Care Med 164: 131‐140, 2001.
 37. Dalibon N, Moutafis M, Liu N, Law‐Koune JD, Monsel S, Fischler M. Treatment of hypoxemia during one‐lung ventilation using intravenous almitrine. Anesth Analg 98: 590‐594, 2004.
 38. Damgaard‐Pedersen K, Qvist T. Pediatric pulmonary CT‐scanning. Anaesthesia‐induced changes. Pediatr Radiol 9: 145‐148, 1980.
 39. Damia G, Mascheroni D, Croci M, Tarenzi L. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anaesth 60: 574‐578, 1988.
 40. Dantzker DR, Wagner P, West JB. Instability of lung untis with low VA/Q ratios during O2 breathing. J Appl Physiol 38: 886‐895, 1975.
 41. Daudel F, Gorrasi J, Bracht H, Brandt S, Krejci V, Jakob SM, Takala J, Rothen HU. Effects of lung recruitment maneuvers on splanchnic organ perfusion during endotoxin‐induced pulmonary arterial hypertension. Shock 34: 488‐494, 2010.
 42. Dembinski R, Henzler D, Rossaint R. Modulating the pulmonary circulation: An update. Minerva Anestesiol 70: 239‐243, 2004.
 43. Determann RM, Royakkers A, Wolthuis EK, Vlaar AP, Choi G, Paulus F, Hofstra JJ, de Graaff MJ, Korevaar JC, Schultz MJ. Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: A preventive randomized controlled trial. Crit Care 14: R1, 2010.
 44. Dixon BJ, Dixon JB, Carden JR, Burn AJ, Schachter LM, Playfair JM, Laurie CP, O'Brien PE. Preoxygenation is more effective in the 25 degrees head‐up position than in the supine position in severely obese patients: A randomized controlled study. Anesthesiology 102: 1110‐1115, 2005.
 45. Don H. The mechanical properties of the respiratory system during anesthesia. Int Anesthesiol Clin 15: 113‐136, 1977.
 46. Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich CW. Respiration during sleep in normal man. Thorax 37: 840‐844, 1982.
 47. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end‐expiratory pressure. Am Rev Respir Dis 137: 1159‐1164, 1988.
 48. Drummond GB, Milic‐Emili J. Forty years of closing volume. Br J Anaesth 99: 772‐774, 2007.
 49. Dueck R, Prutow RJ, Davies NJ, Clausen JL, Davidson TM. The lung volume at which shunting occurs with inhalation anesthesia. Anesthesiology 69: 854‐861, 1988.
 50. Dueck R, Rathbun M, Greenburg AG. Lung volume and VA/Q distribution response to intravenous versus inhalation anesthesia in sheep. Anesthesiology 61: 55‐65, 1984.
 51. Dueck R, Wagner PD, West JB. Effects of positive end‐expiratory pressure on gas exchange in dogs with normal and edematous lungs. Anesthesiology 47: 359‐366, 1977.
 52. Dueck R, Young I, Clausen J, Wagner PD. Altered distribution of pulmonary ventilation and blood flow following induction of inhalation anesthesia. Anesthesiology 52: 113‐125, 1980.
 53. Dyhr T, Laursen N, Larsson A. Effects of lung recruitment maneuver and positive end‐expiratory pressure on lung volume, respiratory mechanics and alveolar gas mixing in patients ventilated after cardiac surgery. Acta Anaesthesiol Scand 46: 717‐725, 2002.
 54. Dyhr T, Nygard E, Laursen N, Larsson A. Both lung recruitment maneuver and PEEP are needed to increase oxygenation and lung volume after cardiac surgery. Acta Anaesthesiol Scand 48: 187‐197, 2004.
 55. Edmark L, Kostova‐Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 98: 28‐33, 2003.
 56. Eichenberger A, Proietti S, Wicky S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Morbid obesity and postoperative pulmonary atelectasis: An underestimated problem. Anesth Analg 95: 1788‐1792, 2002.
 57. Enghoff H, Holmdahl MH, Risholm L. Diffusion respiration in man. Nature 168: 830, 1951.
 58. Erlandsson K, Odenstedt H, Lundin S, Stenqvist O. Positive end‐expiratory pressure optimization using electric impedance tomography in morbidly obese patients during laparoscopic gastric bypass surgery. Acta Anaesthesiol Scand 50: 833‐839, 2006.
 59. Feihl F, Broccard AF. Interactions between respiration and systemic hemodynamics. Part I: Basic concepts. Intensive Care Med 35: 45‐54, 2009.
 60. Fernandez‐Perez ER, Keegan MT, Brown DR, Hubmayr RD, Gajic O. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology 105: 14‐18, 2006.
 61. Fernandez‐Perez ER, Sprung J, Afessa B, Warner DO, Vachon CM, Schroeder DR, Brown DR, Hubmayr RD, Gajic O. Intraoperative ventilator settings and acute lung injury after elective surgery: A nested case control study. Thorax 64: 121‐127, 2009.
 62. Froese AB, Bryan AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 41: 242‐255, 1974.
 63. Gama de Abreu M, Heintz M, Heller A, Szechenyi R, Albrecht DM, Koch T. One‐lung ventilation with high tidal volumes and zero positive end‐expiratory pressure is injurious in the isolated rabbit lung model. Anesthesia and analgesia 96: 220‐228, 2003.
 64. Garutti I, Cruz P, Olmedilla L, Barrio JM, Cruz A, Fernandez C, Perez‐Pena JM. Effects of thoracic epidural meperidine on arterial oxygenation during one‐lung ventilation in thoracic surgery. J Cardiothorac Vasc Anesth 17: 302‐305, 2003.
 65. Garutti I, Martinez G, Cruz P, Pineiro P, Olmedilla L, de la Gala F. The impact of lung recruitment on hemodynamics during one‐lung ventilation. J Cardiothorac Vasc Anesth 23: 506‐508, 2009.
 66. Gattinoni L, Caironi P, Cressoni M, Chiumello D, Ranieri VM, Quintel M, Russo S, Patroniti N, Cornejo R, Bugedo G. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 354: 1775‐1786, 2006.
 67. Gehr P, Mwangi DK, Ammann A, Maloiy GM, Taylor CR, Weibel ER. Design of the mammalian respiratory system. V. Scaling morphometric pulmonary diffusing capacity to body mass: Wild and domestic mammals. Respir Physiol 44: 61‐86, 1981.
 68. Gilbert R, Auchincloss JH Jr., Kuppinger M, Thomas MV. Stability of the arterial/alveolar oxygen partial pressure ratio. Effects of low ventilation/perfusion regions. Crit Care Med 7: 267‐272, 1979.
 69. Glenny RW, Bernard S, Robertson HT, Hlastala MP. Gravity is an important but secondary determinant of regional pulmonary blood flow in upright primates. J Appl Physiol 86: 623‐632, 1999.
 70. Glenny RW, Lamm WJ, Albert RK, Robertson HT. Gravity is a minor determinant of pulmonary blood flow distribution. J Appl Physiol 71: 620‐629, 1991.
 71. Glenny RW, Polissar NL, McKinney S, Robertson HT. Temporal heterogeneity of regional pulmonary perfusion is spatially clustered. J Appl Physiol 79: 986‐1001, 1995.
 72. Glenny RW, Robertson HT. Fractal modeling of pulmonary blood flow heterogeneity. J Appl Physiol 70: 1024‐1030, 1991.
 73. Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Supplemental perioperative oxygen to reduce the incidence of surgical‐wound infection. Outcomes Research Group. N Engl J Med 342: 161‐167, 2000.
 74. Gunnarsson L, Strandberg A, Brismar B, Tokics L, Lundquist H, Hedenstierna G. Atelectasis and gas exchange impairment during enflurane/nitrous oxide anaesthesia. Acta Anaesthesiol Scand 33: 629‐637, 1989.
 75. Gunnarsson L, Tokics L, Gustavsson H, Hedenstierna G. Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. Br J Anaesth 66: 423‐432, 1991.
 76. Gunnarsson L, Tokics L, Lundquist H, Brismar B, Strandberg A, Berg B, Hedenstierna G. Chronic obstructive pulmonary disease and anaesthesia: Formation of atelectasis and gas exchange impairment. Eur Respir J 4: 1106‐1116, 1991.
 77. Gutt CN, Oniu T, Mehrabi A, Schemmer P, Kashfi A, Kraus T, Buchler MW. Circulatory and respiratory complications of carbon dioxide insufflation. Dig Surg 21: 95‐105, 2004.
 78. Hachenberg T, Brussel T, Roos N, Lenzen H, Mollhoff T, Gockel B, Konertz W, Wendt M. Gas exchange impairment and pulmonary densities after cardiac surgery. Acta Anaesthesiol Scand 36: 800‐805, 1992.
 79. Hachenberg T, Tenling A, Hansson HE, Tyden H, Hedenstierna G. The ventilation‐perfusion relation and gas exchange in mitral valve disease and coronary artery disease. Implications for anesthesia, extracorporeal circulation, and cardiac surgery. Anesthesiology 86: 809‐817, 1997.
 80. Halbertsma FJ, Vaneker M, Pickkers P, Neeleman C, Scheffer GJ, Hoeven van der JG. A single recruitment maneuver in ventilated critically ill children can translocate pulmonary cytokines into the circulation. J Crit Care 25: 10‐15, 2010.
 81. Hall LW. Cardiovascular and pulmonary effects of recumbency in two conscious ponies. Equine Vet J 16: 89‐92, 1984.
 82. Hall LW, Clarke KW. Anaesthesia of the Horse, in Veterinary Anaesthesia. In: Hall LW, Clarke KW, editors. 9th ed. Baillière Tindall, London, 1983.
 83. Hansen LK, Koefoed‐Nielsen J, Nielsen J, Larsson A. Are selective lung recruitment maneuvers hemodynamically safe in severe hypovolemia? An experimental study in hypovolemic pigs with lobar collapse. Anesth Analg 105: 729‐734, 2007.
 84. Hardman JG, Aitkenhead AR. Estimating alveolar dead space from the arterial to end‐tidal CO(2) gradient: A modeling analysis. Anesth Analg 97: 1846‐1851, 2003.
 85. Hedenstierna G. Contribution of multiple inert gas elimination technique to pulmonary medicine. 6. Ventilation‐perfusion relationships during anaesthesia. Thorax 50: 85‐91, 1995.
 86. Hedenstierna G. Alveolar collapse and closure of airways: Regular effects of anaesthesia. Clin Physiol Funct Imaging 23: 123‐129, 2003.
 87. Hedenstierna G, Baehrendtz S, Klingstedt C, Santesson J, Soderborg B, Dahlborn M, Bindslev L. Ventilation and perfusion of each lung during differential ventilation with selective PEEP. Anesthesiology 61: 369‐376, 1984.
 88. Hedenstierna G, Edmark L. The effects of anesthesia and muscle paralysis on the respiratory system. Intensive Care Med 31: 1327‐1335, 2005.
 89. Hedenstierna G, Hammond M, Mathieu‐Costello O, Wagner PD. Functional lung unit in the pig. Respir Physiol 120: 139‐149, 2000.
 90. Hedenstierna G, Jarnberg PO, Gottlieb I. Thoracic gas volume measured by body plethysmography during anesthesia and muscle paralysis: Description and validation of a method. Anesthesiology 55: 439‐443, 1981.
 91. Hedenstierna G, Lofstrom B, Lundh R. Thoracic gas volume and chest‐abdomen dimensions during anesthesia and muscle paralysis. Anesthesiology 55: 499‐506, 1981.
 92. Hedenstierna G, Lundh R, Johansson H. Alveolar stability during anaesthesia for reconstructive vascular surgery in the leg. Acta Anaesthesiol Scand 27: 26‐34, 1983.
 93. Hedenstierna G, Lundquist H, Lundh B, Tokics L, Strandberg A, Brismar B, Frostell C. Pulmonary densities during anaesthesia. An experimental study on lung morphology and gas exchange. Eur Respir J 2: 528‐535, 1989.
 94. Hedenstierna G, McCarthy GS. Airway closure and closing pressure during mechanical ventilation. Acta Anaesthesiol Scand 24: 299‐304, 1980.
 95. Hedenstierna G, Nyman G, Kvart C, Funkquist B. Ventilation‐perfusion relationships in the standing horse: An inert gas elimination study. Equine Vet J 19: 514‐519, 1987.
 96. Hedenstierna G, Sandhagen B. Assessing dead space. A meaningful variable? Minerva Anestesiol 72: 521‐528, 2006.
 97. Hedenstierna G, Tokics L, Lundquist H, Andersson T, Strandberg A, Brismar B. Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis. Anesthesiology 80: 751‐760, 1994.
 98. Hedenstierna G, White FC, Mazzone R, Wagner PD. Redistribution of pulmonary blood flow in the dog with PEEP ventilation. J Appl Physiol 46: 278‐287, 1979.
 99. Heil M, Hazel AL, Smith JA. The mechanics of airway closure. Respir Physiol Neurobiol 163: 214‐221, 2008.
 100. Heinonen EHG, Meriläinen P, Högman M, Nyman G. Pulsed delivery of nitric oxide counteracts hypoxaemia in the anaesthetized horse. Vet Anaesth Analg 28: 3‐11, 2001.
 101. Heneghan CP, Bergman NA, Jones JG. Changes in lung volume and (PAO2‐PaO2) during anaesthesia. Br J Anaesth 56: 437‐445, 1984.
 102. Hewlett AM, Hulands GH, Nunn JF, Milledge JS. Functional residual capacity during anaesthesia III: Artificial ventilation. Br J Anaesth 46: 495‐503, 1974.
 103. Hirvonen EA, Nuutinen LS, Kauko M. Ventilatory effects, blood gas changes, and oxygen consumption during laparoscopic hysterectomy. Anesth Analg 80: 961‐966, 1995.
 104. Hlastala MP, Bernard SL, Erickson HH, Fedde MR, Gaughan EM, McMurphy R, Emery MJ, Polissar N, Glenny RW. Pulmonary blood flow distribution in standing horses is not dominated by gravity. J Appl Physiol 81: 1051‐1061, 1996.
 105. Hudgel DW, Devadatta P. Decrease in functional residual capacity during sleep in normal humans. J Appl Physiol 57: 1319‐1322, 1984.
 106. Hugh‐Jones P, Barter CE, Hime JM, Rusbridge MM. Dead space and tidal volume of the giraffe compared with some other mammals. Respir Physiol 35: 53‐58, 1978.
 107. Hughes JM, Glazier JB, Maloney JE, West JB. Effect of lung volume on the distribution of pulmonary blood flow in man. Respir Physiol 4: 58‐72, 1968.
 108. Hulands GH, Greene R, Iliff LD, Nunn JF. Influence of anaesthesia on the regional distribution of perfusion and ventilation in the lung. Clin Sci 38: 451‐460, 1970.
 109. Ide T, Sakurai Y, Aono M, Nishino T. Contribution of peripheral chemoreception to the depression of the hypoxic ventilatory response during halothane anesthesia in cats. Anesthesiology 90: 1084‐1091, 1999.
 110. Inomata S, Nishikawa T, Saito S, Kihara S. “Best” PEEP during one‐lung ventilation. Br J Anaesth 78: 754‐756, 1997.
 111. Jeon K, Yoon JW, Suh GY, Kim J, Kim K, Yang M, Kim H, Kwon OJ, Shim YM. Risk factors for post‐pneumonectomy acute lung injury/acute respiratory distress syndrome in primary lung cancer patients. Anaesth Intensive care 37: 14‐19, 2009.
 112. Johansson MJ, Wiklund A, Flatebo T, Nicolaysen A, Nicolaysen G, Walther SM. Positive end‐expiratory pressure affects regional redistribution of ventilation differently in prone and supine sheep. Crit Care Med 32: 2039‐2044, 2004.
 113. Jones RL, Nzekwu MM. The effects of body mass index on lung volumes. Chest 130: 827‐833, 2006.
 114. Jonmarker C, Jansson L, Jonson B, Larsson A, Werner O. Measurement of functional residual capacity by sulfur hexafluoride washout. Anesthesiology 63: 89‐95, 1985.
 115. Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anesthesia: A mathematical model. J Appl Physiol 86: 1116‐1125, 1999.
 116. Kaditis AG, Motoyama EK, Zin W, Maekawa N, Nishio I, Imai T, Milic‐Emili J. The effect of lung expansion and positive end‐expiratory pressure on respiratory mechanics in anesthetized children. Anesth Analg 106: 775‐785, 2008.
 117. Karzai W, Schwarzkopf K. Hypoxemia during one‐lung ventilation: Prediction, prevention, and treatment. Anesthesiology 110: 1402‐1411, 2009.
 118. Klingstedt C, Hedenstierna G, Baehrendtz S, Lundqvist H, Strandberg A, Tokics L, Brismar B. Ventilation‐perfusion relationships and atelectasis formation in the supine and lateral positions during conventional mechanical and differential ventilation. Acta Anaesthesiol Scand 34: 421‐429, 1990.
 119. Klingstedt C, Hedenstierna G, Lundquist H, Strandberg A, Tokics L, Brismar B. The influence of body position and differential ventilation on lung dimensions and atelectasis formation in anaesthetized man. Acta Anaesthesiol Scand 34: 315‐322, 1990.
 120. Kozian A, Schilling T, Freden F, Maripuu E, Rocken C, Strang C, Hachenberg T, Hedenstierna G. One‐lung ventilation induces hyperperfusion and alveolar damage in the ventilated lung: An experimental study. Br J Anaesth 100: 549‐559, 2008.
 121. Kozian A, Schilling T, Schutze H, Heres F, Hachenberg T, Hedenstierna G. Lung computed tomography density distribution in a porcine model of one‐lung ventilation. Br J Anaesth 102: 551‐560, 2009.
 122. Kroenke K, Lawrence VA, Theroux JF, Tuley MR, Hilsenbeck S. Postoperative complications after thoracic and major abdominal surgery in patients with and without obstructive lung disease. Chest 104: 1445‐1451, 1993.
 123. Kubo S Kapitan TG, Wagner PD. Effect of metacholine (MCH) inhalation on pulmonary gas exchange in pigs. Fed Proc 44, 1985.
 124. Kuwabara S, Duncalf D. Effect of anatomic shunt on physiologic deadspace‐to‐tidal volume ratio–a new equation. Anesthesiology 31: 575‐577, 1969.
 125. Lagerstrand L, Hedenstierna G. Gas‐exchange impairment: Its correlation to lung mechanics in acute airway obstruction (studies on a rabbit asthma model). Clin Physiol 10: 363‐380, 1990.
 126. Landmark SJ, Knopp TJ, Rehder K, Sessler AD. Regional pulmonary perfusion and V/Q in awake and anesthetized‐paralyzed man. J Appl Physiol 43: 993‐1000, 1977.
 127. Larsson A, Linnarsson D, Jonmarker C, Jonson B, Larsson H, Werner O. Measurement of lung volume by sulfur hexafluoride washout during spontaneous and controlled ventilation: Further development of a method. Anesthesiology 67: 543‐550, 1987.
 128. Licker M, de Perrot M, Spiliopoulos A, Robert J, Diaper J, Chevalley C, Tschopp JM. Risk factors for acute lung injury after thoracic surgery for lung cancer. Anesth Analg 97: 1558‐1565, 2003.
 129. Licker M, Diaper J, Villiger Y, Spiliopoulos A, Licker V, Robert J, Tschopp JM. Impact of intraoperative lung‐protective interventions in patients undergoing lung cancer surgery. Crit Care 13: R41, 2009.
 130. Lindberg P, Gunnarsson L, Tokics L, Secher E, Lundquist H, Brismar B, Hedenstierna G. Atelectasis and lung function in the postoperative period. Acta Anaesthesiol Scand 36: 546‐553, 1992.
 131. Luginbuhl M, Vuilleumier P, Schumacher P, Stuber F. Anesthesia or sedation for gastroenterologic endoscopies. Curr Opin Anesthesiol 22: 524‐531, 2009.
 132. Lundh R, Hedenstierna G, Johansson H. Ventilation‐perfusion relationships during epidural analgesia. Acta Anaesthesiol Scand 27: 410‐416, 1983.
 133. Lundquist H, Hedenstierna G, Ringertz H. Barbiturate anaesthesia does not cause pulmonary densities in dogs: a study using computerized axial tomography. Acta Anaesthesiol Scand 32: 162‐165, 1988.
 134. Lundquist H, Hedenstierna G, Strandberg A, Tokics L, Brismar B. CT‐assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 36: 626‐632, 1995.
 135. Magder S. Clinical usefulness of respiratory variations in arterial pressure. Am J Respir Crit Care Med 169: 151‐155, 2004.
 136. Magnusson L, Zemgulis V, Tenling A, Wernlund J, Tyden H, Thelin S, Hedenstierna G. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study. Anesthesiology 88: 134‐142, 1998.
 137. Magnusson L, Zemgulis V, Wicky S, Tyden H, Thelin S, Hedenstierna G. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: An experimental study. Anesthesiology 87: 1153‐1163, 1997.
 138. Magnusson P, Larsson L, Englund G, Larsson B, Strang P, Selin‐Sjogren L. Differences of bone alkaline phosphatase isoforms in metastatic bone disease and discrepant effects of clodronate on different skeletal sites indicated by the location of pain. Clin Chem 44: 1621‐1628, 1998.
 139. Maisch S, Reissmann H, Fuellekrug B, Weismann D, Rutkowski T, Tusman G, Bohm SH. Compliance and dead space fraction indicate an optimal level of positive end‐expiratory pressure after recruitment in anesthetized patients. Anesth Analg 106: 175‐181, 2008.
 140. Makinen MT, Yli‐Hankala A. Respiratory compliance during laparoscopic hiatal and inguinal hernia repair. Can J Anaesth 45: 865‐870, 1998.
 141. Malmberg P, Hedenstrom H, Fridriksson HV. Reference values for gas‐exchange during exercise in healthy nonsmoking and smoking men. Bull Eur Physiopathol Respir 23: 131‐138, 1987.
 142. Mansell A, Bryan C, Levison H. Airway closure in children. J Appl Physiol 33: 711‐714, 1972.
 143. Marshall BE. Anesthetic influences on the pulmonar circulation. In: Stanley TH, Sperry RJ, editor. Anesthesia and the Lung (1st ed). London: Kluwer Academic Publishers, 1989, p. 69‐77.
 144. Marshall BE. Regulation of the pulmonary circulation. In: Stanley TH, Sperry RJ, editor. Anesthesia and the Lung (1st ed). London: Kluver Academic Publishers, 1989, p. 3‐15.
 145. Marshall BE. Hypoxic pulmonary vasoconstriction. Acta Anaesthesiol Scand Suppl 94: 37‐41, 1990.
 146. McCarthy GS. The effect of thoracic extradural analgesia on pulmonary gas distribution, functional residual capacity and airway closure. Br J Anaesth 48: 243‐248, 1976.
 147. McDonell WN, Hall LW, Jeffcott LB. Radiographic evidence of impaired pulmonary function in laterally recumbent anaesthetised horses. Equine Vet J 11: 24‐32, 1979.
 148. McLaughlin RF, Tyler WS, Canada RO. A study of the subgross pulmonary anatomy in various mammals. Am J Anat 108: 149‐165, 1961.
 149. McMahon AJ, Fischbacher CM, Frame SH, MacLeod MC. Impact of laparoscopic cholecystectomy: A population‐based study. Lancet 356: 1632‐1637, 2000.
 150. Meier T, Lange A, Papenberg H, Ziemann M, Fentrop C, Uhlig U, Schmucker P, Uhlig S, Stamme C. Pulmonary cytokine responses during mechanical ventilation of noninjured lungs with and without end‐expiratory pressure. Anesth Analg 107: 1265‐1275, 2008.
 151. Melot C. Contribution of multiple inert gas elimination technique to pulmonary medicine. 5. Ventilation‐perfusion relationships in acute respiratory failure. Thorax 49: 1251‐1258, 1994.
 152. Mertens M, Tabuchi A, Meissner S, Krueger A, Schirrmann K, Kertzscher U, Pries AR, Slutsky AS, Koch E, Kuebler WM. Alveolar dynamics in acute lung injury: heterogeneous distension rather than cyclic opening and collapse. Crit Care Med 37: 2604‐2611, 2009.
 153. Meyhoff CS, Wetterslev J, Jorgensen LN, Henneberg SW, Hogdall C, Lundvall L, Svendsen PE, Mollerup H, Lunn TH, Simonsen I, Martinsen KR, Pulawska T, Bundgaard L, Bugge L, Hansen EG, Riber C, Gocht‐Jensen P, Walker LR, Bendtsen A, Johansson G, Skovgaard N, Helto K, Poukinski A, Korshin A, Walli A, Bulut M, Carlsson PS, Rodt SA, Lundbech LB, Rask H, Buch N, Perdawid SK, Reza J, Jensen KV, Carlsen CG, Jensen FS, Rasmussen LS. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: The PROXI randomized clinical trial. JAMA 302: 1543‐1550, 2009.
 154. Michelet P, Roch A, Brousse D, D'Journo XB, Bregeon F, Lambert D, Perrin G, Papazian L, Thomas P, Carpentier JP, Auffray JP. Effects of PEEP on oxygenation and respiratory mechanics during one‐lung ventilation. Br J Anaesth 95: 267‐273, 2005.
 155. Milic‐Emili J. Ventilation distribution. In: Hammid QSJ, Marini J, editors. Physiologic Basis of Respiratory Disease. Hamilton BC: Decker Inc, 2005, p. 133‐141.
 156. Milic‐Emili J, Torchio R, D'Angelo E. Closing volume: A reappraisal (1967‐2007). Eur J Appl Physiol 99: 567‐583, 2007.
 157. Miller FL, Chen L, Malmkvist G, Marshall C, Marshall BE. Mechanical factors do not influence blood flow distribution in atelectasis. Anesthesiology 70: 481‐488, 1989.
 158. Miserocchi G, Mariani E, Negrini D. Role of the diaphragm in setting liquid pressure in serous cavities. Respir Physiol 50: 381‐392, 1982.
 159. Misthos P, Katsaragakis S, Milingos N, Kakaris S, Sepsas E, Athanassiadi K, Theodorou D, Skottis I. Postresectional pulmonary oxidative stress in lung cancer patients. The role of one‐lung ventilation. Eur J Cardiothorac Surg 27: 379‐382; discussion 382‐373, 2005.
 160. Moerman AT, Herregods LL, De Vos MM, Mortier EP, Struys M. Manual versus target‐controlled infusion remifentanil administration in spontaneously breathing patients. Anesth Analg 108: 828‐834, 2009.
 161. Moller JT, Johannessen NW, Berg H, Espersen K, Larsen LE. Hypoxaemia during anaesthesia–an observer study. Br J Anaesth 66: 437‐444, 1991.
 162. Morton CP, Drummond GB. Change in chest wall dimensions on induction of anaesthesia: A reappraisal. Br J Anaesth 73: 135‐139, 1994.
 163. Moudgil R, Michelakis ED, Archer SL. Hypoxic pulmonary vasoconstriction. J Appl Physiol 98: 390‐403, 2005.
 164. Moutafis M, Liu N, Dalibon N, Kuhlman G, Ducros L, Castelain MH, Fischler M. The effects of inhaled nitric oxide and its combination with intravenous almitrine on Pao2 during one‐lung ventilation in patients undergoing thoracoscopic procedures. Anesth Analg 85: 1130‐1135, 1997.
 165. Mure M, Glenny RW, Domino KB, Hlastala MP. Pulmonary gas exchange improves in the prone position with abdominal distension. Am J Respir Crit Care Med 157: 1785‐1790, 1998.
 166. Mure M NS, Radell P. Regional lung perfusion is more uniform in the rone than in the supine posture in healthy subjects duringanesthesia and mechanical ventilation. 9th Congress of the World Federation of Societies of Intensive and Critical Care Medicine, Buenos Aires, Argentinia, 2006, 2006.
 167. Murphy GS, Szokol JW, Curran RD, Votapka TV, Vender JS. Influence of a vital capacity maneuver on pulmonary gas exchange after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 15: 336‐340, 2001.
 168. Nagendran J, Stewart K, Hoskinson M, Archer SL. An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: Implications for managing single‐lung anesthesia and atelectasis. Curr Opin Anaesthesiol 19: 34‐43, 2006.
 169. Naureckas ET, Dawson CA, Gerber BS, Gaver DPIII, Gerber HL, Linehan JH, Solway J, Samsel RW. Airway reopening pressure in isolated rat lungs. J Appl Physiol 76: 1372‐1377, 1994.
 170. Neudecker J, Sauerland S, Neugebauer E, Bergamaschi R, Bonjer HJ, Cuschieri A, Fuchs KH, Jacobi C, Jansen FW, Koivusalo AM, Lacy A, McMahon MJ, Millat B, Schwenk W. The European Association for Endoscopic Surgery clinical practice guideline on the pneumoperitoneum for laparoscopic surgery. Surg Endosc 16: 1121‐1143, 2002.
 171. Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Positive end‐expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 43: 295‐301, 1999.
 172. Nicholas TE, Power JH, Barr HA. The pulmonary consequences of a deep breath. Respir Physiol 49: 315‐324, 1982.
 173. Nielsen J, Ostergaard M, Kjaergaard J, Tingleff J, Berthelsen PG, Nygard E, Larsson A. Lung recruitment maneuver depresses central hemodynamics in patients following cardiac surgery. Intensive Care Med 31: 1189‐1194, 2005.
 174. Nunes S, Rothen HU, Brander L, Takala J, Jakob SM. Changes in splanchnic circulation during an alveolar recruitment maneuver in healthy porcine lungs. Anesth Analg 98: 1432‐1438, 2004.
 175. Nunn JF, Bergman NA, Coleman AJ. Factors influencing the arterial oxygen tension during anaesthesia with artificial ventilation. Br J Anaesth 37: 898‐914, 1965.
 176. Nunn JF, Hill DW. Respiratory dead space and arterial to end‐tidal CO2 tension difference in anesthetized man. J Appl Physiol 15: 383‐389, 1960.
 177. Nyman G, Funkquist B, Kvart C, Frostell C, Tokics L, Strandberg A, Lundquist H, Lundh B, Brismar B, Hedenstierna G. Atelectasis causes gas exchange impairment in the anaesthetised horse. Equine Vet J 22: 317‐324, 1990.
 178. Nyman G, Hedenstierna G. Ventilation‐perfusion relationships in the anaesthetised horse. Equine Vet J 21: 274‐281, 1989.
 179. Nyren S, Mure M, Jacobsson H, Larsson SA, Lindahl SG. Pulmonary perfusion is more uniform in the prone than in the supine position: Scintigraphy in healthy humans. J Appl Physiol 86: 1135‐1141, 1999.
 180. Olegard C, Sondergaard S, Houltz E, Lundin S, Stenqvist O. Estimation of functional residual capacity at the bedside using standard monitoring equipment: A modified nitrogen washout/washin technique requiring a small change of the inspired oxygen fraction. Anesth Analg 101: 206‐212, 2005.
 181. Pagel PS, Fu JL, Damask MC, Davis RF, Samuelson PN, Howie MB, Warltier DC. Desflurane and isoflurane produce similar alterations in systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing one‐lung ventilation during thoracotomy. Anesth Analg 87: 800‐807, 1998.
 182. Pattinson KT. Opioids and the control of respiration. Br J Anaesth 100: 747‐758, 2008.
 183. Pelosi P, Croci M, Calappi E, Cerisara M, Mulazzi D, Vicardi P, Gattinoni L. The prone positioning during general anesthesia minimally affects respiratory mechanics while improving functional residual capacity and increasing oxygen tension. Anesth Analg 80: 955‐960, 1995.
 184. Pelosi P, Croci M, Calappi E, Mulazzi D, Cerisara M, Vercesi P, Vicardi P, Gattinoni L. Prone positioning improves pulmonary function in obese patients during general anesthesia. Anesth Analg 83: 578‐583, 1996.
 185. Pelosi P, Croci M, Ravagnan I, Cerisara M, Vicardi P, Lissoni A, Gattinoni L. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 82: 811‐818, 1997.
 186. Pelosi P, Croci M, Ravagnan I, Tredici S, Pedoto A, Lissoni A, Gattinoni L. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 87: 654‐660, 1998.
 187. Pelosi P, Croci M, Ravagnan I, Vicardi P, Gattinoni L. Total respiratory system, lung, and chest wall mechanics in sedated‐paralyzed postoperative morbidly obese patients. Chest 109: 144‐151, 1996.
 188. Pelosi P, Ravagnan I, Giurati G, Panigada M, Bottino N, Tredici S, Eccher G, Gattinoni L. Positive end‐expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology 91: 1221‐1231, 1999.
 189. Pelosi P, Rocco PR. Effects of mechanical ventilation on the extracellular matrix. Intensive Care Med 34: 631‐639, 2008.
 190. Perilli V, Sollazzi L, Modesti C, Annetta MG, Sacco T, Bocci MG, Tacchino RM, Proietti R. Comparison of positive end‐expiratory pressure with reverse Trendelenburg position in morbidly obese patients undergoing bariatric surgery: Effects on hemodynamics and pulmonary gas exchange. Obes Surg 13: 605‐609, 2003.
 191. Perlman CE, Bhattacharya J. Alveolar expansion imaged by optical sectioning microscopy. J Appl Physiol 103: 1037‐1044, 2007.
 192. Pesola GR, Magari RT, Dartey‐Hayford S, Coelho‐D'Costa V, Chinchilli VM. Total lung capacity: single breath methane dilution versus plethysmography in normals. Respirology 12: 291‐294, 2007.
 193. Pinsky MR. Cardiovascular issues in respiratory care. Chest 128: 592S‐597S, 2005.
 194. Pinsky MR. Heart‐lung interactions. Curr Opin Crit Care 13: 528‐531, 2007.
 195. Prutow RJ, Dueck R, Davies NJ, Clausen J. Shunt development in young adult surgical patients due to inhalational anesthesia. Anesthesiology 57: A477, 1982.
 196. Pryor KO, Fahey TJ III, Lien CA, Goldstein PA. Surgical site infection and the routine use of perioperative hyperoxia in a general surgical population: A randomized controlled trial. JAMA 291: 79‐87, 2004.
 197. Puls A, Pollok‐Kopp B, Wrigge H, Quintel M, Neumann P. Effects of a single‐lung recruitment maneuver on the systemic release of inflammatory mediators. Intensive Care Med 32: 1080‐1085, 2006.
 198. Reber A, Engberg G, Sporre B, Kviele L, Rothen HU, Wegenius G, Nylund U, Hedenstierna G. Volumetric analysis of aeration in the lungs during general anaesthesia. Br J Anaesth 76: 760‐766, 1996.
 199. Reber A, Nylund U, Hedenstierna G. Position and shape of the diaphragm: Implications for atelectasis formation. Anaesthesia 53: 1054‐1061, 1998.
 200. Rehder K, Knopp TJ, Sessler AD, Didier EP. Ventilation‐perfusion relationship in young healthy awake and anesthetized‐paralyzed man. J Appl Physiol 47: 745‐753, 1979.
 201. Reinius H, Jonsson L, Gustafsson S, Sundbom M, Duvernoy O, Pelosi P, Hedenstierna G, Fredén F. PEEP and recruitment maneuver in morbidly obese patients during general anesthesia and muscle paralysis: A computed tomography study. Anesthesiology 111: 979‐987, 2009.
 202. Richard JC, Decailliot F, Janier M, Annat G, Guerin C. Effects of positive end‐expiratory pressure and body position on pulmonary blood flow redistribution in mechanically ventilated normal pigs. Chest 122: 998‐1005, 2002.
 203. Robertson HT, Hlastala MP. Microsphere maps of regional blood flow and regional ventilation. J Appl Physiol 102: 1265‐1272, 2007.
 204. Rothen HU. Oxygen: Avoid too much of a good thing. Eur J Anaesthesiol 27: 493‐494, 2010.
 205. Rothen HU, Neumann P, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Dynamics of re‐expansion of atelectasis during general anaesthesia. Br J Anaesth 82: 551‐556, 1999.
 206. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re‐expansion of atelectasis during general anaesthesia: A computed tomography study. Br J Anaesth 71: 788‐795, 1993.
 207. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand 39: 118‐125, 1995.
 208. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Airway closure, atelectasis and gas exchange during general anaesthesia. Br J Anaesth 81: 681‐686, 1998.
 209. Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 82: 832‐842, 1995a.
 210. Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G. Prevention of atelectasis during general anaesthesia. Lancet 345: 1387‐1391, 1995b.
 211. Roussos C. Ventilatory muscle fatigue governs breathing frequency. Bull Eur Physiopathol Respir 20: 445‐451, 1984.
 212. Rubinfeld AR, Wagner PD, West JB. Gas exchange during acute experimental canine asthma. Am Rev Respir Dis 118: 525‐536, 1978.
 213. Sakai EM, Connolly LA, Klauck JA. Inhalation anesthesiology and volatile liquid anesthetics: Focus on isoflurane, desflurane, and sevoflurane. Pharmacotherapy 25: 1773‐1788, 2005.
 214. Schilling T, Kozian A, Huth C, Buhling F, Kretzschmar M, Welte T, Hachenberg T. The pulmonary immune effects of mechanical ventilation in patients undergoing thoracic surgery. Anesth Analg 101: 957‐965, 2005.
 215. Scholten DJ, Novak R, Snyder JV. Directed manual recruitment of collapsed lung in intubated and nonintubated patients. Am Surg 51: 330‐335, 1985.
 216. Schultz MJ, Determann RM, Juffermans NP. Ventilator‐associated pneumonia prevention: WHAP, positive end‐expiratory pressure, or both? Crit Care Med 36: 2441‐2442, 2008.
 217. Schwarzkopf K, Klein U, Schreiber T, Preussetaler NP, Bloos F, Helfritsch H, Sauer F, Karzai W. Oxygenation during one‐lung ventilation: The effects of inhaled nitric oxide and increasing levels of inspired fraction of oxygen. Anesth Analg 92: 842‐847, 2001.
 218. Shambaugh GE, Harrison WG, Farrell JI. Treatment of the respiratory paralysis of poliomyelitis in a respirator chamber. JAMA 94: 1371‐1373, 1930.
 219. Sharma KC, Brandstetter RD, Brensilver JM, Jung LD. Cardiopulmonary physiology and pathophysiology as a consequence of laparoscopic surgery. Chest 110: 810‐815, 1996.
 220. Shimizu T, Abe K, Kinouchi K, Yoshiya I. Arterial oxygenation during one lung ventilation. Can J Anaesth 44: 1162‐1166, 1997.
 221. Silva‐Costa‐Gomes T, Gallart L, Valles J, Trillo L, Minguella J, Puig MM. Low‐ vs high‐dose almitrine combined with nitric oxide to prevent hypoxia during open‐chest one‐lung ventilation. Br J Anaesth 95: 410‐416, 2005.
 222. Slinger PD, Kruger M, McRae K, Winton T. Relation of the static compliance curve and positive end‐expiratory pressure to oxygenation during one‐lung ventilation. Anesthesiology 95: 1096‐1102, 2001.
 223. Sorenson PR, Robinson NE. Postural effects on lung volumes and asynchronous ventilation in anesthetized horses. J Appl Physiol 48: 97‐103, 1980.
 224. Sprung J, Whalley DG, Falcone T, Wilks W, Navratil JE, Bourke DL. The effects of tidal volume and respiratory rate on oxygenation and respiratory mechanics during laparoscopy in morbidly obese patients. Anesth Analg 97: 268‐274, 2003.
 225. Strandberg A, Hedenstierna G, Tokics L, Lundquist H, Brismar B. Densities in dependent lung regions during anaesthesia: Atelectasis or fluid accumulation? Acta Anaesthesiol Scand 30: 256‐259, 1986.
 226. Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiol Scand 30: 154‐158, 1986.
 227. Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Constitutional factors promoting development of atelectasis during anaesthesia. Acta Anaesthesiol Scand 31: 21‐24, 1987.
 228. Strang CM Fredén F, Maripuu E, Hachenberg T, Hedenstierna G. Ventilation‐perfusion distributions and gas exchange during CO2‐pneumoperitoneum in a porcine model. Brit J Anaesth 105: 691‐697, 2010.
 229. Strang CM, Hachenberg T, Freden F, Hedenstierna G. Development of atelectasis and arterial to end‐tidal PCO2‐difference in a porcine model of pneumoperitoneum. Br J Anaesth 103: 298‐303, 2009.
 230. Suter PM, Fairley B, Isenberg MD. Optimum end‐expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 292: 284‐289, 1975.
 231. Sykes MK, Loh L, Seed RF, Kafer ER, Chakrabarti MK. The effect of inhalational anaesthetics on hypoxic pulmonary vasoconstriction and pulmonary vascular resistance in the perfused lungs of the dog and cat. Br J Anaesth 44: 776‐788, 1972.
 232. Sykes MK, Young WE, Robinson BE. Oxygenation during anaesthesia with controlled ventilation. Br J Anaesth 37: 314‐325, 1965.
 233. Takala J. Hypoxemia due to increased venous admixture: Influence of cardiac output on oxygenation. Intensive Care Med 33: 908‐911, 2007.
 234. Talmor D, Sarge T, Legedza A, O'Donnell CR, Ritz R, Loring SH, Malhotra A. Cytokine release following recruitment maneuvers. Chest 132: 1434‐1439, 2007.
 235. Tenling A, Hachenberg T, Tyden H, Wegenius G, Hedenstierna G. Atelectasis and gas exchange after cardiac surgery. Anesthesiology 89: 371‐378, 1998.
 236. Thorsteinsson A, Werner O, Jonmarker C, Larsson A. Airway closure in anesthetized infants and children: Influence of inspiratory pressures and volumes. Acta Anaesthesiol Scand 46: 529‐536, 2002.
 237. Tiddens HA, Hofhuis W, Bogaard JM, Hop WC, de Bruin H, Willems LN, de Jongste JC. Compliance, hysteresis, and collapsibility of human small airways. Am J Respir Crit Care Med 160: 1110‐1118, 1999.
 238. Tokics L, Hedenstierna G, Strandberg A, Brismar B, Lundquist H. Lung collapse and gas exchange during general anesthesia: Effects of spontaneous breathing, muscle paralysis, and positive end‐expiratory pressure. Anesthesiology 66: 157‐167, 1987.
 239. Tokics L, Hedenstierna G, Svensson L, Brismar B, Cederlund T, Lundquist H, Strandberg A. V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. J Appl Physiol 81: 1822‐1833, 1996.
 240. Tokics L, Strandberg A, Brismar B, Lundquist H, Hedenstierna G. Computerized tomography of the chest and gas exchange measurements during ketamine anaesthesia. Acta Anaesthesiol Scand 31: 684‐692, 1987.
 241. Torres A, Reyes A, Roca J, Wagner PD, Rodriguez‐Roisin R. Ventilation‐perfusion mismatching in chronic obstructive pulmonary disease during ventilator weaning. Am Rev Respir Dis 140: 1246‐1250, 1989.
 242. Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS. Injurious ventilatory strategies increase cytokines and c‐fos m‐RNA expression in an isolated rat lung model. J Clin Invest 99: 944‐952, 1997.
 243. Tucker A, McMurtry IF, Reeves JT, Alexander AF, Will DH, Grover RF. Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude. Am J Physiol 228: 762‐767, 1975.
 244. Tusman G, Bohm SH, Melkun F, Nador CR, Staltari D, Rodriguez A, Turchetto E. Effects of the alveolar recruitment manoeuver and PEEP on arterial oxygenation in anesthetized obese patients. Rev Esp Anestesiol Reanim 49: 177‐183, 2002.
 245. Tusman G, Bohm SH, Melkun F, Staltari D, Quinzio C, Nador C, Turchetto E. Alveolar recruitment strategy increases arterial oxygenation during one‐lung ventilation. Ann Thorac Surg 73: 1204‐1209, 2002.
 246. Tusman G, Bohm SH, Sipmann FS, Maisch S. Lung recruitment improves the efficiency of ventilation and gas exchange during one‐lung ventilation anesthesia. Anesth Analg 98: 1604‐1609, 2004.
 247. Tusman G, Bohm SH, Suarez‐Sipmann F, Turchetto E. Alveolar recruitment improves ventilatory efficiency of the lungs during anesthesia. Can J Anaesth 51: 723‐727, 2004.
 248. Tusman G, Bohm SH, Tempra A, Melkun F, Garcia E, Turchetto E, Mulder PG, Lachmann B. Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology 98: 14‐22, 2003.
 249. Tusman G, Bohm SH, Vazquez de Anda GF, do Campo JL, Lachmann B. ‘Alveolar recruitment strategy’ improves arterial oxygenation during general anaesthesia. Br J Anaesth 82: 8‐13, 1999.
 250. Unzueta MC, Casas JI, Moral MV. Pressure‐controlled versus volume‐controlled ventilation during one‐lung ventilation for thoracic surgery. Anesth Analg 104: 1029‐1033, 2007.
 251. Wagner PD, Dantzker DR, Dueck R, Clausen JL, West JB. Ventilation‐perfusion inequality in chronic obstructive pulmonary disease. J Clin Invest 59: 203‐216, 1977.
 252. Wahba RM. Airway closure and intraoperative hypoxaemia: twenty‐five years later. Can J Anaesth 43: 1144‐1149, 1996.
 253. Wahba RW. Perioperative functional residual capacity. Can J Anaesth 38: 384‐400, 1991.
 254. Wahba RW, Beique F, Kleiman SJ. Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 42: 51‐63, 1995.
 255. Wahba WM, Craig DB, Don HF, Becklake MR. The cardio‐respiratory effects of thoracic epidural anaesthesia. Can Anaesth Soc J 19: 8‐19, 1972.
 256. Van Euler US Liljestrand G. Observation on the pulmonary arterial blood pressure in the cat. Acta Physiol Scand 12: 302‐318, 1946.
 257. van Kaam AH, Lachmann RA, Herting E, De Jaegere A, van Iwaarden F, Noorduyn LA, Kok JH, Haitsma JJ, Lachmann B. Reducing atelectasis attenuates bacterial growth and translocation in experimental pneumonia. Am J Respir Crit Care Med 169: 1046‐1053, 2004.
 258. Warner DO, Joyner MJ, Ritman EL. Anesthesia and chest wall function in dogs. J Appl Physiol 76: 2802‐2813, 1994.
 259. Warner DO, Warner MA. Human chest wall function while awake and during halothane anesthesia. II. Carbon dioxide rebreathing. Anesthesiology 82: 20‐31, 1995.
 260. Warner DO, Warner MA, Ritman EL. Atelectasis and chest wall shape during halothane anesthesia. Anesthesiology 85: 49‐59, 1996a.
 261. Warner DO, Warner MA, Ritman EL. Human chest wall function during epidural anesthesia. Anesthesiology 85: 761‐773, 1996b.
 262. West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures. J Appl Physiol 19: 713‐724, 1964.
 263. Westbrook PR, Stubbs SE, Sessler AD, Rehder K, Hyatt RE. Effects of anesthesia and muscle paralysis on respiratory mechanics in normal man. J Appl Physiol 34: 81‐86, 1973.
 264. Victorino JA, Borges JB, Okamoto VN, Matos GF, Tucci MR, Caramez MP, Tanaka H, Sipmann FS, Santos DC, Barbas CS, Carvalho CR, Amato MB. Imbalances in regional lung ventilation: A validation study on electrical impedance tomography. Am J Respir Crit Care Med 169: 791‐800, 2004.
 265. Villar J, Herrera‐Abreu MT, Valladares F, Muros M, Perez‐Mendez L, Flores C, Kacmarek RM. Experimental ventilator‐induced lung injury: Exacerbation by positive end‐expiratory pressure. Anesthesiology 110: 1341‐1347, 2009.
 266. Villar J, Slutsky AS. Is acute respiratory distress syndrome an iatrogenic disease? Crit Care 14: 120, 2010.
 267. Von Dossow V, Welte M, Zaune U, Martin E, Walter M, Ruckert J, Kox WJ, Spies CD. Thoracic epidural anesthesia combined with general anesthesia: the preferred anesthetic technique for thoracic surgery. Anesth Analg 92: 848‐854, 2001.
 268. von Ungern‐Sternberg BS, Frei FJ, Hammer J, Schibler A, Doerig R, Erb TO. Impact of depth of propofol anaesthesia on functional residual capacity and ventilation distribution in healthy preschool children. Br J Anaesth 98: 503‐508, 2007.
 269. Wrigge H, Zinserling J, Neumann P, Defosse J, Magnusson A, Putensen C, Hedenstierna G. Spontaneous breathing improves lung aeration in oleic acid‐induced lung injury. Anesthesiology 99: 376‐384, 2003.
 270. Wysocki M, Delclaux C, Roupie E, Langeron O, Liu N, Herman B, Lemaire F, Brochard L. Additive effect on gas exchange of inhaled nitric oxide and intravenous almitrine bismesylate in the adult respiratory distress syndrome. Intensive Care Med 20: 254‐259, 1994.
 271. Yamakage M, Namiki A, Tsuchida H, Iwasaki H. Changes in ventilatory pattern and arterial oxygen saturation during spinal anaesthesia in man. Acta Anaesthesiol Scand 36: 569‐571, 1992.

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Göran Hedenstierna, Hans Ulrich Rothen. Respiratory Function During Anesthesia: Effects on Gas Exchange. Compr Physiol 2012, 2: 69-96. doi: 10.1002/cphy.c080111