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Respiratory Function During Anesthesia: Effects on Gas Exchange

Göran Hedenstierna, Hans Ulrich Rothen

10.1002/cphy.c080111

Source: Volume 2, Issue 1, January 2012

Published online: January 2012

Full Article on Wiley Online Library



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 156,209,254.
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 240.
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 200.
Figure 5. Figure 5.

Dependence of the critical inspired ventilation‐perfusion ratio (a/) and inspired O2 concentration on minimum time to collapse [from 40, 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 40, 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 115, 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 115, 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 55 and 211. Adapted from reference 55, 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 55, 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 207, 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 209.
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 240.
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 143, 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 98. 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 98. 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 98, 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 240, 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 75.
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 202, 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 76, 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 15, 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 156,209,254.



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 240.



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 200.



Figure 5.

Dependence of the critical inspired ventilation‐perfusion ratio (a/) and inspired O2 concentration on minimum time to collapse [from 40, 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 40, 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 115, 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 115, 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 55 and 211. Adapted from reference 55, 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 55, 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 207, 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 209.



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 240.



Figure 13.

Inhibition of the hypoxic pulmonary vasoconstrictor response by inhalational anesthetics. Data from humans and animals have been plotted. Adapted from reference 143, 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 98. 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 98. 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 98, 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 240, 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 75.



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 202, 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 76, 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 15, with permission by the editor of JAP.

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Article Title: Respiratory Function During Anesthesia: Effects on Gas Exchange
 

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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