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Respiratory Mechanics During Anesthesia and Mechanical Ventilation

Kai Rehder, H. Michael Marsh

10.1002/cphy.cp030343

Source: Supplement 12: Handbook of Physiology, The Respiratory System, Mechanics of Breathing

Originally published: 1986

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Effects of Anesthesia on the Chest Wall
1.1 Anesthesia With Spontaneous Breathing
1.2 Anesthesia‐Paralysis With Mechanical Ventilation of the Lungs
2 Effects of Anesthesia on FRC
3 Effects of Anesthesia on Pressure‐Volume Relationships
3.1 Total Respiratory System
3.2 Lungs
3.3 Chest Wall
3.4 Mechanisms for Changes in Pressure‐ Volume Relationships
4 Effects of Anesthesia on Pressure‐Flow Relationships
5 Effects of Anesthesia on Intrapulmonary Inspired‐Gas Distribution
5.1 Anesthesia With Spontaneous Breathing
5.2 Anesthesia‐Paralysis With Mechanical Ventilation of the Lungs
6 Conclusions
Figure 1. Figure 1.

Diagram of end‐expiratory position and pattern of motion of diaphragm in subject lying supine. Dashed line, end‐expiratory position of diaphragm in awake state; left margin of stippled area, end‐expiratory position of diaphragm in anesthetized state; stippled area, motion of diaphragm during active inspiration (spontaneous) or passive inflation (paralyzed). Note altered pattern of motion with passive inflation of lungs (paralyzed).

From Froese and Bryan 32
Figure 2. Figure 2.

Diagram of relative contribution to tidal volume from rib cage and abdomen in 3 states: awake, anesthetized, and anesthetized‐paralyzed. Equal contributions from rib cage and abdomen would result in a loop with a slope of 1. Note that relative contribution from rib cage to tidal volume is larger during anesthesia‐paralysis with mechanical ventilation and smaller during anesthesia with spontaneous breathing than in awake state.
Figure 3. Figure 3.

Contributions of rib cage (RC) and abdomen‐diaphragm (ABD) to inspiratory minute volume () at various partial pressures of CO2 () for 1 subject studied. Note lack of increase of rib cage contribution but normal increase of abdomen‐diaphragm contribution to with CO2 stimulation under anesthesia (0.8% halothane).

From Tusiewicz et al. 85
Figure 4. Figure 4.

Dynamic transpulmonary pressure [Δ(Pao – Pes)]‐lung volume change (ΔV) loops from dog lying prone, first awake and then anesthetized with halothane. Pao, airway opening pressure; Pes, esophageal pressure. During anesthesia loop is reversed (runs clockwise). To avoid possible artifacts, Pao was measured in the trachea 12,55.

From Rich et al. 72
Figure 5. Figure 5.

Possible mechanism for reversal of transpulmonary pressure‐lung volume (PV) loop. Only elastic pressure changes are considered. Pes, esophageal pressure; Pao, airway opening pressure; ΔV, lung volume change; FRC, functional residual capacity; VT, tidal volume. Assume Pes reflects radial stress on lung. During uniform expansion of lung (top) from FRC (A) to FRC + VT (B), radial stress increases from 2 to 6 cmH2O. Deflation from FRC + VT (B) to FRC (A) is also uniform. Thus the expiratory PV relationship is defined (dashed line, middle). During anesthesia the lung is assumed to be expanded uniaxially by contraction of diaphragm (A, bottom to B′, middle). Under these conditions when width does not change, radial stress increases less (in this example from 2 to 4 cmH2O) than during uniform expansion 74. This partly defines the inspiratory PV relationship (A to B′, middle). If at end inspiration the diaphragm relaxes and allows the lung to undergo an isovolume radial expansion (B′ to B, bottom), radial stress will increase (in this example from 4 to 6 cmH2O). This part of the inspiratory PV relationship is defined as B′ to B (middle). If uniform deflation then occurs (B to A, bottom), a reversed PV relationship results (middle).

From Rich et al. 72
Figure 6. Figure 6.

Top, diagram of changes in chest wall shape (thorax, A; abdomen, B) on going from awake (solid line) to anesthetized‐paralyzed (dashed line) state in humans lying supine. Note that at end expiration during anesthesia‐paralysis, anteroposterior diameters of both thorax and abdomen decrease, while lateral diameters increase. Bottom, with mechanical ventilation of lungs initiated from functional residual capacity (dashed line) going to functional residual capacity plus tidal volume (dotted line), anteroposterior diameters of both thorax and abdomen increase, while lateral diameters decrease.
Figure 7. Figure 7.

A: comparative measurements of functional residual capacity (FRC) (n = 128) between awake and anesthetized states for recumbent humans 24,25,41,42,49,66,68,70,90. Mean FRC awake is 2.68 ± 0.08 (SE) liters, whereas mean FRC anesthetized or anesthetized‐paralyzed is 2.17 ± 0.06 liters. B: frequency distribution of change in FRC (n = 128) associated with induction of anesthesia or anesthesia‐paralysis in recumbent humans.
Figure 8. Figure 8.

A: spirogram obtained from subject lying supine who was anesthetized with 400 mg of thiopental sodium (arrows). Tracing should be read from right to left. Note almost immediate reduction of functional residual capacity of about 200 ml after injection of thiopental sodium. B: spirogram obtained from anesthetized subject lying supine who was paralyzed with 100 mg of succinylcholine chloride (arrow). Again, tracing should be read from right to left. Note unchanged end‐expiratory level during ensuing period of apnea.

From Howell and Peckett 47
Figure 9. Figure 9.

Mean deflation pressure‐volume relationships for total respiratory system, lung, and chest wall, obtained from 5 subjects lying supine. Pao, airway opening pressure; Ptp, transpulmonary pressure; Pes, esophageal pressure.

From Westbrook et al. 90
Figure 10. Figure 10.

Mean transpulmonary pressure (PL) measured at 50% of total lung capacity (TLC) awake from 5 subjects lying supine, plotted as function of the ratio of functional residual capacity (FRC) in the awake (▪), anesthetized (•), or anesthetized‐paralyzed (▴) states to residual volume (RV) awake.
Figure 11. Figure 11.

Mean deflation pressure‐volume (PV) relationship for isolated dog lung before (○) and after (•) ventilation for 30 min with nitrous oxide (N2O, n = 7), chloroform (CHCl3, n = 8), or halothane (n = 11) in air. Note large rightward shift of PV curve with chloroform and halothane and minimal change with nitrous oxide.

From Woo et al. 92
Figure 12. Figure 12.

Mean ventilation index () plotted as function of vertical distance down the lung in awake (solid line) and anesthetized‐paralyzed (dashed line) subjects. , ratio of measured regional 133Xe concentration to that predicted if inspired‐gas distribution had been uniform. Inspiration was initiated from functional residual capacity and tidal volume equaled 10% of total lung capacity. There is virtually uniform inspired‐gas distribution in right lateral decubitus position during anesthesia‐paralysis. Inspired‐gas distribution becomes more uniform in supine position but less uniform in seated subjects after induction of anesthesia‐paralysis. Anesthesia‐paralysis has little effect on gas distribution in subjects lying prone.

From Rehder et al. 66
Figure 13. Figure 13.

Regional lung volumes plotted as function of overall lung volume for 1 dependent and 1 nondependent lung region oriented along same vertical axis. D, vertical distance down the lung; TLC, total lung capacity; TLCr, regional TLC. Data are from 1 subject studied first awake and then anesthetized‐paralyzed while lying in lateral decubitus position. Note large increase in vertical gradient of regional lung volumes in anesthetized‐paralyzed state and curvilinear relationship between regional and overall lung volume.

From Rehder et al. 70
Figure 14. Figure 14.

Mean multiple‐breath nitrogen clearances for individual lungs from awake 53 and anesthetized‐paralyzed subjects 64 lying in right lateral decubitus position. Note more uniform clearances of individual lungs during anesthesia‐paralysis; because these were 2 different groups of subjects, absolute values for functional residual capacity (FRC) should not be compared. Note also altered distributions of tidal volume between the 2 lungs, which are indicated by the arrow length in airways of diagrammatic inserts in each panel.

From Rehder et al. 64


Figure 1.

Diagram of end‐expiratory position and pattern of motion of diaphragm in subject lying supine. Dashed line, end‐expiratory position of diaphragm in awake state; left margin of stippled area, end‐expiratory position of diaphragm in anesthetized state; stippled area, motion of diaphragm during active inspiration (spontaneous) or passive inflation (paralyzed). Note altered pattern of motion with passive inflation of lungs (paralyzed).

From Froese and Bryan 32


Figure 2.

Diagram of relative contribution to tidal volume from rib cage and abdomen in 3 states: awake, anesthetized, and anesthetized‐paralyzed. Equal contributions from rib cage and abdomen would result in a loop with a slope of 1. Note that relative contribution from rib cage to tidal volume is larger during anesthesia‐paralysis with mechanical ventilation and smaller during anesthesia with spontaneous breathing than in awake state.



Figure 3.

Contributions of rib cage (RC) and abdomen‐diaphragm (ABD) to inspiratory minute volume () at various partial pressures of CO2 () for 1 subject studied. Note lack of increase of rib cage contribution but normal increase of abdomen‐diaphragm contribution to with CO2 stimulation under anesthesia (0.8% halothane).

From Tusiewicz et al. 85


Figure 4.

Dynamic transpulmonary pressure [Δ(Pao – Pes)]‐lung volume change (ΔV) loops from dog lying prone, first awake and then anesthetized with halothane. Pao, airway opening pressure; Pes, esophageal pressure. During anesthesia loop is reversed (runs clockwise). To avoid possible artifacts, Pao was measured in the trachea 12,55.

From Rich et al. 72


Figure 5.

Possible mechanism for reversal of transpulmonary pressure‐lung volume (PV) loop. Only elastic pressure changes are considered. Pes, esophageal pressure; Pao, airway opening pressure; ΔV, lung volume change; FRC, functional residual capacity; VT, tidal volume. Assume Pes reflects radial stress on lung. During uniform expansion of lung (top) from FRC (A) to FRC + VT (B), radial stress increases from 2 to 6 cmH2O. Deflation from FRC + VT (B) to FRC (A) is also uniform. Thus the expiratory PV relationship is defined (dashed line, middle). During anesthesia the lung is assumed to be expanded uniaxially by contraction of diaphragm (A, bottom to B′, middle). Under these conditions when width does not change, radial stress increases less (in this example from 2 to 4 cmH2O) than during uniform expansion 74. This partly defines the inspiratory PV relationship (A to B′, middle). If at end inspiration the diaphragm relaxes and allows the lung to undergo an isovolume radial expansion (B′ to B, bottom), radial stress will increase (in this example from 4 to 6 cmH2O). This part of the inspiratory PV relationship is defined as B′ to B (middle). If uniform deflation then occurs (B to A, bottom), a reversed PV relationship results (middle).

From Rich et al. 72


Figure 6.

Top, diagram of changes in chest wall shape (thorax, A; abdomen, B) on going from awake (solid line) to anesthetized‐paralyzed (dashed line) state in humans lying supine. Note that at end expiration during anesthesia‐paralysis, anteroposterior diameters of both thorax and abdomen decrease, while lateral diameters increase. Bottom, with mechanical ventilation of lungs initiated from functional residual capacity (dashed line) going to functional residual capacity plus tidal volume (dotted line), anteroposterior diameters of both thorax and abdomen increase, while lateral diameters decrease.



Figure 7.

A: comparative measurements of functional residual capacity (FRC) (n = 128) between awake and anesthetized states for recumbent humans 24,25,41,42,49,66,68,70,90. Mean FRC awake is 2.68 ± 0.08 (SE) liters, whereas mean FRC anesthetized or anesthetized‐paralyzed is 2.17 ± 0.06 liters. B: frequency distribution of change in FRC (n = 128) associated with induction of anesthesia or anesthesia‐paralysis in recumbent humans.



Figure 8.

A: spirogram obtained from subject lying supine who was anesthetized with 400 mg of thiopental sodium (arrows). Tracing should be read from right to left. Note almost immediate reduction of functional residual capacity of about 200 ml after injection of thiopental sodium. B: spirogram obtained from anesthetized subject lying supine who was paralyzed with 100 mg of succinylcholine chloride (arrow). Again, tracing should be read from right to left. Note unchanged end‐expiratory level during ensuing period of apnea.

From Howell and Peckett 47


Figure 9.

Mean deflation pressure‐volume relationships for total respiratory system, lung, and chest wall, obtained from 5 subjects lying supine. Pao, airway opening pressure; Ptp, transpulmonary pressure; Pes, esophageal pressure.

From Westbrook et al. 90


Figure 10.

Mean transpulmonary pressure (PL) measured at 50% of total lung capacity (TLC) awake from 5 subjects lying supine, plotted as function of the ratio of functional residual capacity (FRC) in the awake (▪), anesthetized (•), or anesthetized‐paralyzed (▴) states to residual volume (RV) awake.



Figure 11.

Mean deflation pressure‐volume (PV) relationship for isolated dog lung before (○) and after (•) ventilation for 30 min with nitrous oxide (N2O, n = 7), chloroform (CHCl3, n = 8), or halothane (n = 11) in air. Note large rightward shift of PV curve with chloroform and halothane and minimal change with nitrous oxide.

From Woo et al. 92


Figure 12.

Mean ventilation index () plotted as function of vertical distance down the lung in awake (solid line) and anesthetized‐paralyzed (dashed line) subjects. , ratio of measured regional 133Xe concentration to that predicted if inspired‐gas distribution had been uniform. Inspiration was initiated from functional residual capacity and tidal volume equaled 10% of total lung capacity. There is virtually uniform inspired‐gas distribution in right lateral decubitus position during anesthesia‐paralysis. Inspired‐gas distribution becomes more uniform in supine position but less uniform in seated subjects after induction of anesthesia‐paralysis. Anesthesia‐paralysis has little effect on gas distribution in subjects lying prone.

From Rehder et al. 66


Figure 13.

Regional lung volumes plotted as function of overall lung volume for 1 dependent and 1 nondependent lung region oriented along same vertical axis. D, vertical distance down the lung; TLC, total lung capacity; TLCr, regional TLC. Data are from 1 subject studied first awake and then anesthetized‐paralyzed while lying in lateral decubitus position. Note large increase in vertical gradient of regional lung volumes in anesthetized‐paralyzed state and curvilinear relationship between regional and overall lung volume.

From Rehder et al. 70


Figure 14.

Mean multiple‐breath nitrogen clearances for individual lungs from awake 53 and anesthetized‐paralyzed subjects 64 lying in right lateral decubitus position. Note more uniform clearances of individual lungs during anesthesia‐paralysis; because these were 2 different groups of subjects, absolute values for functional residual capacity (FRC) should not be compared. Note also altered distributions of tidal volume between the 2 lungs, which are indicated by the arrow length in airways of diagrammatic inserts in each panel.

From Rehder et al. 64
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Article Title: Respiratory Mechanics During Anesthesia and Mechanical Ventilation
 

How to Cite

Kai Rehder, H. Michael Marsh. Respiratory Mechanics During Anesthesia and Mechanical Ventilation. Compr Physiol 2011, Supplement 12: Handbook of Physiology, The Respiratory System, Mechanics of Breathing: 737-752. First published in print 1986. doi: 10.1002/cphy.cp030343