Effects of positive end-expiratory pressure on anesthesia-induced atelectasis and gas exchange in anesthetized and mechanically ventilated sheep

Francesco Staffieri Dipartimento delle Emergenze e dei Trapianti d'Organo, Sezione di Chirurgia Veterinaria, Università degli Studi di Bari, 70010 Valenzano, Bari, Italy; and Department of Clinical Studies, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348.

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Bernd Driessen Department of Anesthesiology, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA 90095; and Department of Clinical Studies, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348.

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Valentina De Monte Dipartimento delle Emergenze e dei Trapianti d'Organo, Sezione di Chirurgia Veterinaria, Università degli Studi di Bari, 70010 Valenzano, Bari, Italy.

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Salvatore Grasso Dipartimento delle Emergenze e dei Trapianti d'Organo, Sezione Anestesia e Terapia Intensiva, Università degli Studi di Bari, Ospedale Policlinico, 70124 Bari, Italy.

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Antonio Crovace Dipartimento delle Emergenze e dei Trapianti d'Organo, Sezione di Chirurgia Veterinaria, Università degli Studi di Bari, 70010 Valenzano, Bari, Italy.

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Abstract

Objective—To evaluate the effects of 10 cm H2O of positive end-expiratory pressure (PEEP) on lung aeration and gas exchange in mechanically ventilated sheep during general anesthesia induced and maintained with propofol.

Animals—10 healthy adult Bergamasca sheep.

Procedures—Sheep were sedated with diazepam (0.4 mg/kg, IV). Anesthesia was induced with propofol (5 mg/kg, IV) and maintained with propofol via constant rate infusion (0.4 mg/kg/min). Muscular paralysis was induced by administration of vecuronium (25 μg/kg, bolus IV) to facilitate mechanical ventilation. After intubation, sheep were positioned in right lateral recumbency and mechanically ventilated with pure oxygen and zero end-expiratory pressure (ZEEP). After 60 minutes, 10 cm H2O of PEEP was applied for 20 minutes. Spiral computed tomography of the thorax was performed, and data were recorded for hemodynamic and gas exchange variables and indicators of respiratory mechanics after 15 (T15), 30 (T30), and 60 (T60) minutes of ZEEP and after 20 minutes of PEEP (TPEEP). Computed tomography images were analyzed to determine the extent of atelectasis before and after PEEP application.

Results—At TPEEP, the volume of poorly aerated and atelectatic compartments was significantly smaller than at T15, T30, and T60, which indicated that there was PEEP-induced alveolar recruitment and clearance of anesthesia-induced atelectasis. Arterial oxygenation and static respiratory system compliance were significantly improved by use of PEEP.

Conclusions and Clinical Relevance—Pulmonary atelectasis can develop in anesthetized and mechanically ventilated sheep breathing pure oxygen; application of 10 cm H2O of PEEP significantly improved lung aeration and gas exchange.

Abstract

Objective—To evaluate the effects of 10 cm H2O of positive end-expiratory pressure (PEEP) on lung aeration and gas exchange in mechanically ventilated sheep during general anesthesia induced and maintained with propofol.

Animals—10 healthy adult Bergamasca sheep.

Procedures—Sheep were sedated with diazepam (0.4 mg/kg, IV). Anesthesia was induced with propofol (5 mg/kg, IV) and maintained with propofol via constant rate infusion (0.4 mg/kg/min). Muscular paralysis was induced by administration of vecuronium (25 μg/kg, bolus IV) to facilitate mechanical ventilation. After intubation, sheep were positioned in right lateral recumbency and mechanically ventilated with pure oxygen and zero end-expiratory pressure (ZEEP). After 60 minutes, 10 cm H2O of PEEP was applied for 20 minutes. Spiral computed tomography of the thorax was performed, and data were recorded for hemodynamic and gas exchange variables and indicators of respiratory mechanics after 15 (T15), 30 (T30), and 60 (T60) minutes of ZEEP and after 20 minutes of PEEP (TPEEP). Computed tomography images were analyzed to determine the extent of atelectasis before and after PEEP application.

Results—At TPEEP, the volume of poorly aerated and atelectatic compartments was significantly smaller than at T15, T30, and T60, which indicated that there was PEEP-induced alveolar recruitment and clearance of anesthesia-induced atelectasis. Arterial oxygenation and static respiratory system compliance were significantly improved by use of PEEP.

Conclusions and Clinical Relevance—Pulmonary atelectasis can develop in anesthetized and mechanically ventilated sheep breathing pure oxygen; application of 10 cm H2O of PEEP significantly improved lung aeration and gas exchange.

In veterinary practice, a high Fio2 is commonly administered during general anesthesia in an attempt to minimize the possibility of low Pao2.1 Several studies2–4 in humans and in nonhuman animals revealed that high Fio2 promotes pulmonary atelectasis during induction and maintenance of anesthesia. Moreover, pulmonary atelectasis persists for several hours after surgery in humans, which exposes the affected lung parenchyma to a higher likelihood of microbial growth.5 Compression of lung tissue (compression atelectasis) and absorption of the alveolar gas (absorption atelectasis) are the main pathogenic mechanisms leading to pulmonary atelectasis during general anesthesia.5 A high Fio2 promotes the development of absorption atelectasis by increasing the rate and amount of gas absorbed into pulmonary capillary blood.6,7 Atelectasis has been proposed as the major cause of impaired pulmonary gas exchange and decreased lung compliance in anesthetized human patients independent of the anesthetic protocol and technique used.8,9 Therefore, increasing Fio2 during general anesthesia may improve anesthetic safety only at the cost of aggravating 1 mechanism responsible for gas exchange derangement.

The application of PEEP aimed at reopening (ie, recruiting) collapsed alveolar units has been proposed to treat anesthesia-induced atelectasis.10 Several studies11–14 in human patients revealed that low values of PEEP (5 to 10 cm H2O) are effective in reducing lung atelectasis during anesthesia. The effects of PEEP on gas exchange are more controversial; investigators in some studies13,14 reported improved gas exchange, and others failed to identify this effect or even detected reduced arterial oxygenation.15 The inconsistency with which PEEP affects gas exchange in humans and nonhuman animals has been associated with the impact PEEP may have on pulmonary and systemic blood circulation.15,16

Sheep are often anesthetized in clinical and research environments.17 Information regarding the effects of anesthesia on lung function in sheep is limited, although these animals have been used in a study18 to investigate physiologic and pathophysiologic characteristics of human lungs. Computed tomography is the preferred method of imaging the lungs. Analysis of the densities obtained in conventional CT images allows measurement of whole and regional lung volumes, distribution of lung aeration, and assessment of alveolar recruitment and hyperinflation,19,20 and CT has been proposed as the criterion-referenced standard technique for non-invasive estimation of FRC during mechanical ventilation.21 The first evidence of pulmonary atelectasis was detected by use of CT during a study22 of pulmonary densities in anesthetized humans.

The study reported here was conducted to evaluate the results of mechanical ventilation with pure oxygen in lateral-recumbent sheep anesthetized for 1 hour with propofol administered IV, including effects on atelectasis generation, gas exchange, and mechanical properties of the lungs. Additionally, the authors sought to determine the effects of the subsequent application of PEEP at 10 cm H2O on the same variables. We hypothesized that mechanical ventilation with pure oxygen in propofol-anesthetized sheep would result in lung atelectasis, impaired pulmonary mechanics, and reduced gas exchange and that application of 10 cm H2O of PEEP would substantially improve these functions by reopening small airways and recruiting collapsed alveoli.

Materials and Methods

Animals—Ten healthy female Bergamasca sheep from a research herd at the University of Bari (mean ± SD weight, 56 ± 9 kg [range, 45 to 68 kg]; mean ± SD age, 17 ± 2 months [range, 14 to 22 months]) were included in the study. The sheep were housed and all experiments were conducted at the School of Veterinary Medicine at Bari. During the experimental period, the sheep were housed together in 1 indoor stall (size, approx 40 m2). The diet consisted of grass and hay, and the sheep had free access to water; they were acclimated to these conditions for 1 month prior to the start of the study. Food was withheld for 24 hours before anesthetic induction. The sheep were considered healthy on the basis of the results of physical examination, which included hematologic, arterial blood gas, and serum biochemical analyses. The study protocol was approved by the Italian Ethical Committee of the Ministry of Health, Bari.

Anesthetic protocol and monitoring—All anesthetic inductions were performed in the CT suite. Skin at the site of venipuncture was surgically prepared and infiltrated with 1 mL of a 2% solution of lidocaine hydrochloride,a and a 14-gauge catheter was placed in a jugular vein of each sheep. Midazolam hydrochlorideb (0.4 mg/kg, IV) was administered for sedation. After 5 minutes, anesthesia was induced with propofolc (5 mg/kg, IV), and tracheal intubation was accomplished by use of a cuffed endotracheal tube (inner diameter, 12 mm). Sheep were positioned in sternal recumbency for intubation and subsequently moved into right lateral recumbency for the remainder of the study. Anesthesia was maintained by use of a constant rate infusion of propofol (0.4 mg/kg/min), and lactated Ringer's solution was infused at a rate of 10 mL/kg/h during the entire anesthetic procedure. Muscular paralysis was induced by administration of vecuroniumd (25 μg/kg, bolus IV) to facilitate mechanical ventilation and to avoid any interference of chest wall muscle tone on lung mechanics measurements.

The median auricular artery of the left pinna was percutaneously catheterized by use of a 20-gauge catheter to record arterial blood pressures (systolic, diastolic, and MAP)e and to facilitate collection of arterial blood samples. Hemoglobin oxygen saturation (via pulse oximetry), Petco2 (via a capnometer), heart rate (via ECG), and rectal temperature (via a digital thermometer) were continuously recorded.

Neuromuscular function was monitored with a peripheral nerve stimulatorf operating in the train-of-4 stimulation mode. Complete neuromuscular blockade (absence of any twitch response during train-of-4 nerve stimulation) was confirmed before the respiratory maneuvers were performed; on completion of the experiment after edrophonium and atropine administration23,g, 4 responses (twitches) to train-of-4 nerve stimulations were required before the constant rate infusion of propofol was discontinued and sheep were allowed to recover from anesthesia with appropriate monitoring and assistance.

Mechanical ventilation and experimental protocol—Immediately after intubation, sheep were connected to a nonrebreathing circuit and mechanically ventilatedh by use of a respirator operated in a volume-controlled, time-cycled mode with a constant fresh gas flow, Fio2 of 1 (ie, 100% oxygen), VT of 12 mL/kg, and inspiratory-to-expiratory ratio of 1:3 with ZEEP. The respiratory rate was adjusted to maintain Petco2 at 35 to 45 mm Hg. The Fio2 (maintained at 1) was continuously monitored during the experiment by use of an oxygen sensor located inside the ventilator.

Sheep were positioned in right lateral recumbency; this was considered time 0 (ie, T0). Spiral CT scan of the thorax was performed at 15, 30, and 60 minutes with ZEEP (ie, T15, T30, and T60, respectively), and arterial blood gas analysis was performed from samples obtained at each time point. Sixty minutes after positioning the sheep in right lateral recumbency, 10 cm H2O of PEEP was applied for 20 minutes, without changing the ventilatory pattern settings. The CT and blood gas analysis were repeated after PEEP was applied for 20 minutes (ie, TPEEP).

Evaluation of respiratory system mechanics— Measurement of respiratory system mechanics was performed at T15, T30, T60, and TPEEP according to the following methods. Flow was measured with a heated pneumotachograph,i which was connected to a differential pressure transducerj inserted between the Y-piece of the ventilator circuit and the endotracheal tube. The response to the pneumotachograph was linear over the experimental range of gas flows. The transducer was calibrated before each experiment via a 1-point calibration procedure. Volume was determined via numerical integration of the flow signal. The Pao was measured proximal to the endotracheal tube by use of a pressure transducer.j All variables for respiratory system mechanics were displayed and collected on a personal computer through a 12-bit analogue-to-digital converter boardk at a sampling rate of 200 Hz.l The difference between the PEEP set on the ventilator (ie, the Pao value at the end of a regular breath [PEEPexternal]) and the pressure in Pao during a 3- to 5-second end-expiratory pause (ie, PEEPtotal) was measured, and this value was regarded as the static intrinsic PEEP (ie, PEEPintrinsic).24 The end-expiratory pause was performed by use of the expiratory hold on the ventilator. The CSTATrs was calculated at T15, T30, T60, and TPEEP as: CSTATrs = VT/Paoplat − PEEPtotal, where Paoplat is the value of Pao measured at the end of an end-inspiratory pause of 4 seconds by use of the inspiratory hold of the ventilator. After confirming complete neuromuscular blockade, the end-inspiratory and end-expiratory pauses were performed sequentially at each experimental time point, with 1 or 2 regular mechanical tidal breaths delivered between the 2 pauses (Figure 1).

Figure 1—
Figure 1—

Concurrent tracings of oxygen flow (top) and airway opening pressure (bottom) obtained from a representative healthy adult sheep mechanically ventilated with pure oxygen during anesthesia induced and maintained with propofol (5 mg/ kg and 0.4 mg/kg/min, respectively, IV); muscular paralysis was induced via bolus administration of vecuronium (25 μg/kg, IV). Tracings indicate the end-inspiratory and end-expiratory pauses separated by a regular breath (ie, without an occlusive pause). Paoplat = Airway plateau pressure corresponding to the value of Pao after an end-inspiratory pause of 3 to 4 seconds. PEEPexternal = PEEP (applied by the ventilator) corresponding to the value of the Pao at the end of a regular breath. PEEPtotal = PEEP value that takes into account the possible intrinsic PEEP and corresponds to the value of the Pao at the end of an end-expiratory pause of 3 to 4 seconds.

Citation: American Journal of Veterinary Research 71, 8; 10.2460/ajvr.71.8.867

Collection and analysis of CT images—Frontal topograms and helical CT images of the thorax were obtained by use of a third-generation spiral CT scanner.m The CT images were acquired at a setting of 120 kVp and 160 mA (1 second • time) by use of a lung algorithm; matrix size was 512 × 512, field of view was 50, and pitch was 10 mm. All CT images were obtained during an end-expiration apnea, which was induced by briefly disconnecting the endotracheal tube from the ventilator circuit at T15, T30, and T60; at TPEEP, the ventilator was configured in a continuous positive-pressure mode at 10 cm H2O. Mechanical ventilation was resumed immediately after the CT image was obtained (60 to 70 seconds after disconnection from the ventilator). All CT images were analyzed for lung abnormalities; pathological changes were considered cause to exclude sheep from the study.

The CT images were analyzed by use of a commercially available computer program.n The right and left lungs were chosen as ROIs for analysis; portions of the pulmonary hila containing the trachea, main bronchi, and hilar blood vessels were excluded from the ROIs. Distributions of radiographic attenuations (expressed in HUs) among the selected ROIs were plotted by use of the computer software. In accordance with a previous study4 in dogs, the following regions or compartments were identified within the lungs: hyperinflated (ie, composed of pixels with CT numbers of −1,000 to −901 HUs), normally aerated (ie, composed of pixels −900 to −501 HUs), poorly aerated (ie, composed of pixels with CT numbers of −500 to −101 HUs), and nonaerated (ie, atelectatic; composed of pixels with CT numbers of −100 to 100 HUs).

The gas volume of each ROI (ie, ROIV) was computed by including pixels with density values of −1,000 to 100 HUs according to the following formula: gas volume (mL) = CT number/(–1,000) • voxel volume,21 where each voxel is a pixel (ie, parallelogram with a square base [0.59 mm/side]) and a height corresponding to the CT slice thickness (10 mm); this was calculated as the area of the pixel times the CT slice thickness. The volume of each compartment (ie, hyperinflated, normally aerated, poorly aerated, and atelectatic) within the ROI was calculated by use of the same formula.

The EELV for each sheep was calculated as the sum of all ROIV for all CT images obtained, and the total volume of each lung compartment was calculated as the sum of all volumes for a specified compartment in all CT slices. The total volume of each compartment was expressed as a percentage of the EELV.

The PEEP-induced alveolar recruitment was calculated25 as the difference in the volume of the atelectatic lung compartment in the entire lung between T60 and TPEEP and expressed as a percentage of the value at T60. The right and left lungs were also considered separately as ROIs, in accordance with the same method. To determine the craniocaudal distribution of atelectasis within both lungs, 26 slices (equally distributed throughout each lung in each sheep) were selected for evaluation at T60 and TPEEP and the number of voxels with an HU value between −100 and 100 was calculated for each slice.

Blood gas measurements—Blood gas measurements and related analyses were performed by use of an automated arterial blood gas analyzer.o The analyzer was calibrated each day and prior to each experiment. Arterial blood samples were collected anaerobically at T15, T30, T60, and TPEEP before CT images were obtained; samples were analyzed immediately. The pH of arterial blood, Pao2, and Paco2 were measured. All arterial blood gas values were corrected within the analyzer for body temperature of the sheep (measured per rectum at the time of sampling). The Pao2-Pao2 was calculated for each sheep, according to the alveolar gas equation: Pao2-Pao2 = ([PB − PH2O] × Fio2 − Paco2) − Pao2, where PB is the barometric pressure and PH2O is the water vapor pressure. The PB was recorded by the arterial blood gas analyzer during each analysis, and the PH2O was corrected for the rectal temperature of the sheep recorded at the time of arterial blood collection. The Vdsalv was estimated as a percentage of Vt by use of the following equation: Vdsalv/VT = ([Paco2 − Petco2]/Paco2) × 100, where Petco2 is the value measured at the moment of arterial blood collection.

Statistical analysis—The mean ± SD was determined for each numeric variable. Normal distribution of data was verified by use of a Shapiro-Wilk test. Variables for lung function, lung aeration, and cardiovascular function obtained at T15, T30, T60, and TPEEP were compared among time points. Statistical analysis included a 1-way ANOVA for repeated measures followed by Student-Newman-Keuls test. Values of P < 0.05 were considered significant.

Results

Experimental procedures were completed in all sheep without complications. Mean ± SD scanning time per helical CT was 65 ± 5 seconds. No pathologically altered lung parenchyma was detected in any sheep during preliminary examination of CT images; thus, no sheep were excluded from the study.

Heart rate, MAP, respiratory rate, Petco2, and hemoglobin oxygen saturation measured during mechanical ventilation at T15, T30, T60, and TPEEP did not differ significantly among time points (Table 1). The EELV was significantly greater at TPEEP (3.0 ± 0.4 L), compared with values recorded at T15 (2.1 ± 0.3 L), T30 (2.2 ± 0.5 L), or T60 (2.2 ± 0.6 L). The relative sizes of lung compartments (ie, hyperinflated, normally aerated, poorly aerated, and atelectatic) were determined for the various experimental conditions (Figure 2). The volume of the normally aerated compartment represented a significantly greater percentage and the poorly aerated and atelectatic compartments represented a significantly lesser percentage of the EELV at TPEEP, compared with the volumes at ZEEP (ie, T15, T30, and T60). Notably, the volume of the hyperinflated compartment did not change among the different experimental conditions.

Table 1—

Mean ± SD hemodynamic and respiratory values in 10 healthy adult sheep mechanically ventilated with pure oxygen during anesthesia induced and maintained with propofol (5 mg/kg and 0.4 mg/kg/min, respectively, IV); muscular paralysis was induced via bolus administration of vecuronium (25μ/kg, IV).

VariableT15T30T60TPEEP
HR (beats/min)108 ± 8106 ± 11113 ± 17.4111 ± 18
MAP (mm Hg)109 ± 11110 ± 9111 ± 17108 ± 11
RR (breaths/min)9 ± 29 ± 29 ± 29 ± 2
PETCO2 (mm Hg)35.6 ± 3.236.3 ± 2.536.2 ± 5.037.0 ± 5.3
Spo2 (%)99.8 ± 0.199.2 ± 5.399.1 ± 1.199.3 ± 0.7

Sheep were positioned in right lateral recumbency (time of positioning = time 0). Data were recorded at predetermined intervals (15 minutes [T30], 30 minutes [T30] and 60 minutes [T60]) with ZEEP and after application of 10 cm H2O of PEEP for 20 minutes (TPEEP).

HR = Heart rate. RR = Respiratory rate. Spo2 = Oxygen saturation as measured via pulse oximetry.

Figure 2—
Figure 2—

Relative sizes of 4 functional lung compartments identified via analysis of CT images obtained from 10 propofol-anesthetized sheep positioned in right lateral recumbency (time of positioning = time 0). Bars represent mean ± SD percentage of the EELV. Data were recorded at predetermined intervals (15 minutes [T15, white bars], 30 minutes [T30, gray bars], and 60 minutes [T60, vertically dotted line bars]) with ZEEP and after application of 10 cm H2O of PEEP for 20 minutes (TPEEP; black bars). a,bWithin each anatomic compartment, values with different letters are significantly (P < 0.05) different among time points on the basis of a 1-way ANOVA for repeated measures and a Student-Newman-Keuls test. See Figure 1 for remainder of key.

Citation: American Journal of Veterinary Research 71, 8; 10.2460/ajvr.71.8.867

When both lungs were considered together as an ROI, the volume of the atelectatic compartment (ie, atelectatic lung) was decreased by 5.8 ± 3.2%, compared with the value at T60. When each individual lung was considered as an ROI, the volume of the atelectatic compartment was significantly (P = 0.01) decreased by 33.8 ± 6.3% in the right (ie, dependent) lung (from 0.143 ± 0.002 L at T60 to 0.095 ± 0.009 L at TPEEP) and by 6.62 ± 2.32% in the left lung (from 0.045 ± 0.003 L at T60 to 0.042 ± 0.004 L at TPEEP). The distribution of atelectatic lung tissue (detected as voxels with an HU value between −100 and 100) across the entire length of both lungs in a craniocaudal direction revealed increased atelectasis formation in the caudal (slices 12 through 26) lung fields (Figure 3).

Figure 3—
Figure 3—

Distribution of atelectasis throughout the lungs in 10 propofol-anesthetized sheep. One voxel is a pixel (ie, parallelogram with a square base [0.59 mm/side]) and a height corresponding to the CT slice thickness (10 mm); bars represent the mean number of voxels with an HU value between −100 and 100 (ie, the HU range indicative of atelectasis). Transverse CT slices were equally distributed across the entire lung; CT slice numbers represent images obtained serially as the scan proceeded in a cranial to caudal direction (slices with low numbers were obtained from the most cranial lung fields, and slices with high numbers were obtained from the most caudal lung fields). Data were recorded at T60 with ZEEP (white bars) and at TPEEP (black bars). See Figures 1 and 2 for remainder of key.

Citation: American Journal of Veterinary Research 71, 8; 10.2460/ajvr.71.8.867

Transverse CT images of the thorax (at the level of the body of T8) were obtained (Figure 4). Atelectasis of the parenchyma in the dependent lung was detectable in the CT images obtained at T15, T30, and T60; at TPEEP, the amount of atelectasis was reduced.

Figure 4—
Figure 4—

Transverse CT images of the thorax obtained at the level of the body of T8 from the same propofol-anesthetized representative sheep used to obtain the tracing in Figure 1. Images were obtained at T15 (A), T30 (B), and T60 (C) with ZEEP and at TPEEP (D). Atelectatic lung parenchyma (black arrows) is apparent in the dependent (right) lung at T15, T30, and T60; at TPEEP, the amount of atelectasis is reduced (white arrow). See Figure 2 for remainder of key.

Citation: American Journal of Veterinary Research 71, 8; 10.2460/ajvr.71.8.867

The Pao2 was significantly increased and Pao2-Pao2 was significantly decreased at TPEEP, compared with the respective values at T15, T30, and T60 (Table 2). Because pure oxygen was used for ventilation throughout the experiment (ie, the Fio2 remained constant at 1), the effects of PEEP on the Pao2-to-Fio2 ratio were identical to those on Pao2. The CSTATrs was significantly increased at TPEEP, compared with values calculated at T15, T30, and T60 (Table 3).

Table 2—

Mean ± SD values for pulmonary gas exchange and respiratory dead space variables in 10 propofol-anesthetized sheep during mechanical ventilation.

VariableT15T30T60TPEEP
Pao2 (mm Hg)    
PAo2-Pao2 (mm Hg)>230 ± 57a228 ± 46a237 ± 49a61 ± 8b
Paco, (mm Hg)42.0 ± 3.2a40.1 ± 3.1a39.1 ± 4.3a38.3 ± 3.5a
VDSalv/VT (%)8.52 ± 2.31a9.20 ± 3.11a7.96 ± 3.21a8.31 ± 2.21a

Within a row, values with different superscript letters are significantly (P < 0.05) different among time points as determined on the basis of a 1-way ANOVA for repeated measures and a Student-Newman-Keuls test.

See Table 1 for remainder of key.

Table 3—

Mean ± SD values for indicators of respiratory system mechanics in 10 propofol-anesthetized sheep during mechanical ventilation.

VariableT15T30T60TPEEP
Paopeak(cm H2O)17.0 ± 4.2a16.9 ± 3.6a17.2 ± 4.0a26.0 ± 4.0b
Paoplat(cm H2O)13.9 ± 3.1a14.6 ± 2.9a14.4 ± 3.2a20.0 ± 4.0b
PEEPtotal (cm H2O)0.22 ± 0.02a0.09 ± 0.03a0.13 ± 0.05a10.1 ± 0.20b
PEEPintrinsic (cm H2O)0.22 ± 0.020.09 ± 0.03a0.13 ± 0.05a0.11 ± 0.02a
CSTATrs (mL/cm H2O)40.6 ± 3.3a40.4 ± 2.5a40.2 ± 4.4a55.1 ± 2.8b

Paopeak = Peak airway opening pressure. Paoplat = Inspiratory plateau airway opening pressure. PEEPintrinsic = Intrinsic positive end-expiratory pressure. PEEPtotal = Total positive end-expiratory pressure.

See Tables 1 and 2 for remainder of key.

Statistical analysis was performed for the remaining data (rectal temperature, pH, PaCO2, and Vdsalv) obtained during the experiments. Results of this analysis did not indicate any significant differences among time points.

Discussion

Results of the study reported here supported our hypothesis that mechanical ventilation with pure oxygen in propofol-anesthetized sheep would result in lung atelectasis, impaired pulmonary mechanics, and reduced gas exchange and that application of 10 cm H2O of PEEP would substantially improve these functions by reopening small airways and recruiting previously collapsed alveoli. Even in healthy sheep, poorly aerated and atelectatic lung compartments begin to form rapidly during anesthesia when animals are mechanically ventilated and inspire pure oxygen.26 Our data indicate that the change in lung aeration in sheep is not necessarily the result of a slowly progressive process but develops quickly and may then remain fairly static throughout the anesthetic procedure (Figures 2 and 4). This observation is consistent with the results of a study2 in anesthetized humans ventilated with pure oxygen, in which pulmonary atelectasis was detected within the first 5 to 10 minutes of anesthesia but did not increase with advancing time. The results of the present study revealed that the percentages of poorly aerated and atelectatic lung parenchyma detected during the initial anesthetic period (ie, T15) were approximately 30% and 7%, respectively, indicating that nearly 40% of the lung tissue was not properly aerated. Atelectases were predominant in the more caudal lung fields (ie, slices 12 through 26), close to the diaphragm, where the main abdominal compression forces are localized.

In sheep and in ruminants in general, the compression exerted by the rumen can substantially impair lung function during anesthesia, compared with the lung function of anesthetized monogastric animals.27 Indeed, the rumen frequently remains filled with content, even after feed is withheld for an extended period prior to anesthesia. Fermentation also continues during general anesthesia and eructation usually ceases, which promotes tympanic expansion of the rumen and further impairment of lung inflation during inspiration.27,28 We determined that actelectases were more pronounced in the dependent lung of sheep in lateral recumbency (Figure 4). This finding was similar to the results of a study29 in anesthetized, mechanically ventilated human patients in lateral recumbency, which indicated that the dependent lung, although better perfused, is subject to more widespread small-airway closure and atelectasis formation and thus to increased V/Q mismatching. Furthermore, the Vt distributes preferentially in the nondependent lung; this increases the risks of alveolar hyperinflation and further impairment of gas exchange (caused by increased dead space) and may result in lung injury.29

The principal consequence of poorly aerated and atelectatic lung tissue is impaired gas exchange with intrapulmonary shunt formation and a low V/Q.9 In the present study, the high Pao2-Pao2 gradient (Table 2) detected during the first 60 minutes of anesthesia with mechanical ventilation was compatible with impaired lung aeration; this possibility was considered even more likely because the MAP and heart rate were within respective reference ranges17 reported for sheep (Table 1). The fact that Paco2 and Vdsalv/VT remained within the physiologic range possibly indicates that minute ventilation was adequate and alveolar dead space remained constant throughout the experiments.

Prevention of alveolar collapse and recruitment of alveoli in atelectatic and poorly aerated tissue are important objectives that may prevent pulmonary complications during and after general anesthesia.30–32 Administration of a low Fio2 (ie, 0.3 to 0.6; 30% to 60% oxygen) significantly reduces atelectasis formation in humans and nonhuman animals.2–4 However, ventilation with a low Fio2 is not always applicable in a clinical setting because of technical (eg, lack of a second gas source, lack of control over the oxygen mixture, or inability to monitor Fio2) or clinical reasons (eg, compromise of lung function prior to surgery). In those circumstances, PEEP and recruitment maneuvers are the only ventilatory techniques available for treatment of anesthesia-related airway closure and atelectasis during surgery.30–36 The term PEEP describes an increased pressure in the airways relative to ambient pressure at the end of expiration. The desired effect of PEEP on the pulmonary parenchyma is to increase FRC as a result of the opening of closed bronchioli and collapsed alveolar units.10,36,37

In the study reported here, the application of 10 cm H2O of PEEP for 20 minutes significantly reduced anesthesia-induced atelectasis (Figures 2 to 4). As expected, alveolar recruitment was primarily in the more caudal lung fields that were most affected by airway closure and atelectasis (Figure 3). Given the lack of any significant time-dependent change in lung aeration, gas exchange, and lung compliance from T15 through T60, it is extremely unlikely that lung function would have improved without the application of PEEP during the 20 minutes after T60. Interestingly, alveolar recruitment was predominant in the dependent (right) lung. Our finding confirms the results of a study38 in anesthetized horses, in which addition of PEEP to positive-pressure ventilation significantly improved aeration of the dependent lung; in that study, the improvement was attributed to a reversible shift of inspired gas from the nondependent toward the dependent lung. Similar results were reported in a study39 in anesthetized humans.

It is important to distinguish between PEEP-induced recruitment and Vt-induced alveolar recruitment; these are different events that have different impacts on lung function. Positive end-expiratory pressure is an end-expiratory treatment that is persistent throughout the respiratory cycle. This ensures that alveolar units recruited by PEEP participate fully in gas exchange (provided that the lung parenchyma is physiologically normal). In contrast, Vt recruitment is a temporary (ie, inspiratory phase only) event. Although VT recruitment may contribute to the improvement of gas exchange, the previously opened lung units collapse again (referred to as derecruitment) during the expiratory phase. The application of PEEP can influence VT recruitment as a result of the increase in airway pressure; thus, it is likely that, in the sheep in the present study, there was further improvement of lung aeration during inspiration at TPEEP. To accomplish the objective of this study, however, the authors included an evaluation of PEEP-induced alveolar recruitment. For this reason, CT was performed at end expiration.

The improved gas exchange observed at TPEEP (Table 2) in sheep in the study reported here emphasizes the positive effect PEEP ventilation has on lung function. In studies10,15 in humans, however, it is cautioned that PEEP-induced improvement of lung aeration may not always be associated with better gas exchange because of the potentially negative impact of PEEP on the pulmonary (ie, redistribution of pulmonary blood flow) and systemic (ie, reduction of cardiac output) circulation. Regarding redistribution of the pulmonary blood flow, even if the V/Q ratio had not been specifically determined in the present study, the significant improvement in oxygenation and in CSTATrs at TPEEP supported the premise that 10 cm H2O of PEEP improved the V/Q. Regarding systemic hemodynamic function, a possible limitation of the study reported here is that no data were obtained to indicate whether cardiac output was impaired in the sheep. Hemodynamic impairment is an important potential limitation for the application of PEEP during mechanical ventilation in anesthetized patients. In particular, the persistent increase in intrathoracic pressure causes a reduction in venous return; thus, blood flow in the pulmonary and systemic circulation could potentially be reduced.16 However, clinical studies10 in humans and nonhuman animals revealed that in healthy subjects, the cardiovascular compromise imposed by relatively low PEEP (≤ 10 cm H2O) can usually be counteracted with administration of adequate fluids, inotropic drugs, or both. Because MAPs and heart rates remained constant in sheep in the study reported here, we speculate that application of a low PEEP had only minor effects on cardiac output, but we recognize that this aspect deserves further investigation. Moreover, we cannot exclude that the reduction of the Pao2-Pao2 detected in the present study may have been partly attributed to a reduction in the shunt fraction as a consequence of a small reduction in cardiac output induced by PEEP.

Collapsed airways and atelectatic alveoli are usually characterized by higher opening pressures than those required for physiologically normal alveoli; to be recruited (ie, reopened), they require a PEEP high enough to increase the inspiratory airway pressure above the required opening pressure and to prevent recollapse of those units at end of expiration.10 If the PEEP applied is insufficient to accomplish this and alveoli in the atelectatic lung regions cannot be opened, PEEP ventilation fails to recruit lung parenchyma and can potentially result in pulmonary hyperinflation, with PEEP and Vt disproportionally redistributed to normally aerated lung parenchyma, thereby reducing lung compliance further and impairing gas exchange.15 On the basis of clinical studies32–35 in human patients, the most rational and successful approach during those circumstances (ie, failure to recruit the atelectatic alveolar units) is to perform a recruitment maneuver via inflation of the lungs with high inspiratory pressures (eg, 30 to 40 cm H2O) for a brief period to recruit as many previously collapsed alveolar units as possible, then to apply a PEEP titrated to a value that will keep alveoli and small airways open. In the group of sheep in the present study, it appeared that the use of PEEP did not induce pulmonary hyperinflation (Figure 2). The opening pressures of alveolar units in atelectatic lung parenchyma are heterogeneous; these vary with the factors described as contributing to atelectasis formation as well as with pathological changes in the lung tissue.12 It is important to stress the notion that anesthesia-induced atelectasis usually consists of collapsed alveolar units in healthy lung parenchyma that can easily be recruited and returned to physiologic function.8,40 The situation is different for pathological pulmonary atelectasis (eg, that which results from acute lung injury, acute respiratory distress syndrome, pneumonia, or tumors), in which inflammatory cell infiltrates, degenerative processes, or both decrease compliance and impair alveolar recruitment.40

The application of PEEP should be considered a temporary treatment that is limited to the time that a patient is receiving mechanical ventilation, acting primarily during the end-expiratory phase to address temporary changes of the respiratory system (eg, decreased FRC, airway closure, and pulmonary atelectasis) induced by the anesthetic drugs and techniques. The results of the present study indicated that PEEP improved oxygenation during anesthesia induced and maintained with propofol in healthy sheep ventilated with pure oxygen; application of PEEP also increased FRC via recruitment of atelectatic lung regions. The possible clinical impact of these results in veterinary medicine deserves further investigation, but human data clearly suggest that limiting atelectasis formation during anesthesia is an important step in limiting pulmonary complications during and after surgery.5

ABBREVIATIONS

CSTATrs

Static compliance of the respiratory system

CT

Computed tomography

EELV

End-expiratory lung volume

Fio2

Fraction of inspired oxygen

FRC

Functional residual capacity

HU

Hounsfield unit

MAP

Mean arterial blood pressure

Pao

Airway opening pressure

Pao2-Pao2

Alveolar-arterial oxygen partial pressure difference

PEEP

Positive end-expiratory pressure

Petco2

End-tidal partial pressure of carbon dioxide

ROI

Region of interest

Vdsalv

Volume of alveolar dead space

V/Q

Ventilation-to-perfusion ratio

Vt

Tidal volume

ZEEP

Zero end-expiratory pressure

a.

Lidocaine 2%, Angelini SpA, Ancona, Italy.

b.

Midazolam PHG, Hospira, Naples, Italy.

c.

PropoVet 1%, Esteve Hospira Inc, North Chicago, Ill.

d.

Norcuron 10 mg, NV Organon, Oss, Holland.

e.

Edwards Lifesciences LLC, Irvine, Calif.

f.

MiniStim, model MS-II, Life-Tech Inc, Houston, Tex.

g.

Camsilon, Cambridge Laboratories, Newcastle-Upon-Tyne, England.

h.

Servo 300, Siemens-Elema, Electromedical System Division, Solna, Sweden.

i.

Fleish No. 2, Fleish, Lausanne, Switzerland.

j.

Diff-Cap, Special Instruments, Nordlingen, Germany.

k.

DAQCard-700, National Instruments, Austin, Tex.

l.

ICU Lab, KleisTEK Engineering, Bari, Italy.

m.

GE ProSpeed SX, General Electric, New York, NY.

n.

DicomWorks, version 1.3.5, Cité Internationale, Lyon, France.

o.

VetStat, IDEXX Laboratories Inc, Westbrook, Me.

References

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    McDonell W. Respiratory system. In: Thurmon JCTranquilli WJBenson GJ, eds. Lumb and Jones' veterinary anesthesia. 4th ed. Baltimore: Williams & Wilkins, 2007;117151.

    • Search Google Scholar
    • Export Citation
  • 2.

    Rothen HUSporre BEngberg G, et al.Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995;82:832842.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Staffieri FBauquier SHMoate PJ, et al.Pulmonary gas exchange in anaesthetised horses mechanically ventilated with oxygen or a helium/oxygen mixture. Equine Vet J 2009;41:747752.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4.

    Staffieri FFranchini DCarella GL, et al.Computed tomographic analysis of the effects of two inspired oxygen concentrations on pulmonary aeration in anesthetized and mechanically ventilated dogs. Am J Vet Res 2007;68:925931.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Duggan MKavanag BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005;102:838854.

  • 6.

    Dale WARahn H. Rate of gas absorption during atelectasis. J Appl Physiol 1952;70:606613.

  • 7.

    Dantzker DRWagner PDWest JB. Instability of lung units with low Va/Q ratios during O2 breathing. J Appl Physiol 1975;38:886895.

  • 8.

    Lumb AB. Applied physiology. Anaesthesia. In: Lumb AB, ed. Nunn's applied respiratory physiology. 6th ed. St Louis: Elsevier, 2005;297326.

    • Search Google Scholar
    • Export Citation
  • 9.

    Tokics LHedenstierna GSvensson L, et al.V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. J Appl Physiol 1996;81:18221833.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Haitsma JJ. Physiology of mechanical ventilation. Crit Care Clin 2007;23:117134.

  • 11.

    Neumann PRothen HUBerglund JE, et al.Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of high inspired oxygen concentration. Acta Anaesthesiol Scand 1999;43:295301.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Rothen HUSporre BEngberg G, et al.Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71:788795.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Serafini GCornara GCavalloro F, et al.Pulmonary atelectasis during paediatric anaesthesia: CT scan evaluation and effect of positive end-expiratory pressure (PEEP). Paediatr Anaesth 1999;9:225228.

    • Search Google Scholar
    • Export Citation
  • 14.

    Tokics LHedenstierna GStrandberg A, et al.Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987;66:157167.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Horton WGCheney FW. Variability of effect of positive end expiratory pressure. Arch Surg 1975;110:395398.

  • 16.

    Tittley JGFremes SEWeisel RD, et al.Hemodynamic and myocardial metabolic consequences of PEEP. Chest 1985;86:496502.

  • 17.

    Riebold TW. Ruminants. In: Thurmon JCTranquilli WJBenson GJ, eds. Lumb and Jones' veterinary anesthesia. 4th ed. Baltimore: Williams & Wilkins, 2007;731746.

    • Search Google Scholar
    • Export Citation
  • 18.

    Hedenstierna GLundquist HLundh B, et al.Pulmonary densities during anaesthesia. An experimental study on lung morphology and gas exchange. Eur Respir J 1989;2:528535.

    • Search Google Scholar
    • Export Citation
  • 19.

    Drummond GB. Computed tomography and pulmonary measurements. Br J Anaesth 1998;80:665671.

  • 20.

    Reber AEngberg GSporre B, et al.Volumetric analysis of aeration in the lung during general anaesthesia. Br J Anaesth 1996;76:760766.

  • 21.

    Patroniti NBellani GManfio A, et al.Lung volume in mechanically ventilated patients: measurement by simplified helium dilution compared to quantitative CT scan. Intensive Care Med 2004;30:282289.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Brismar BHedenstierna GLundquist H, et al.Pulmonary densities during anesthesia with muscular relaxation. A proposal of atelectasis. Anesthesiology 1985;62:422428.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Clutton REGlasby MA. Cardiovascular and autonomic nervous effects of edrophonium and atropine combinations during neuromuscular blockade antagonism in sheep. Vet Anaesth Analg 2008;35:191200.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Pepe PEMarini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Respir Dis 1982;126:166170.

    • Search Google Scholar
    • Export Citation
  • 25.

    Lu QMalbouisson LMMourgeon E, et al.Assessment of PEEP-induced reopening of collapsed lung regions in acute lung injury: are one or three CT sections representative of the entire lung? Intensive Care Med 2001;27:15041510.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Mundie TGDodd KTLagutchik M. Relationship of functional residual capacity and various body measurements in normal sheep. Lab Anim Sci 1992;42:589592.

    • Search Google Scholar
    • Export Citation
  • 27.

    Pypendop BHSteffey EP. Focused supportive care: ventilation during ruminant anesthesia. In: Steffey EP, ed. Recent advances in anesthetic management of large domestic animals. Ithaca, NY: International Veterinary Information Service, 2001.

    • Search Google Scholar
    • Export Citation
  • 28.

    Desmecht DLinden ALekeux P. Pathophysiological response of bovine diaphragm function to gastric distension. J Appl Physiol 1995;78:15371546.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Cohen E. Physiology of the lateral position and one-lung ventilation. Chest Surg Clin N Am 1997;7:753771.

  • 30.

    Johnson D. Lung recruitment during general anesthesia. Can J Anaesth 2004;51:649653.

  • 31.

    Tusman GBohm SSuarez-Sipman F, et al.Alveolar recruitment improves ventilatory efficiency of the lungs during anesthesia. Can J Anaesth 2004;51:723727.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Tusman GBohm SHVazquez de Anda GF, et al.“Alveolar recruitment strategy” improves arterial oxygenation during general anaesthesia. Br J Anaesth 1999;82:813.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Dyhr TLaursen NLarsson A. Effect 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 2002;46:717725.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Dyhr TNygard ELaursen N, et al.Both lung recruitment maneuver and PEEP are needed to increase oxygenation and lung volume after cardiac surgery. Acta Anaesthesiol Scand 2004;48:187197.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 35.

    Tusman GBohm SHTempra A, et al.Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology 2003;98:1422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 36.

    von Ungern-Sternberg BSRegli ASchibler A, et al.The impact of positive end-expiratory pressure on functional residual capacity and ventilation homogeneity impairment in anesthetized children exposed to high levels of inspired oxygen. Anesth Analg 2007;104:13641368.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 37.

    Wahba RWM. Perioperative functional residual capacity. Can J Anaesth 1991;38:384400.

  • 38.

    Moens YLagerweij EGootjes P, et al.Influence of tidal volume and positive end-expiratory pressure on inspiratory gas distribution and gas exchange during mechanical ventilation in horses positioned in lateral recumbency. Am J Vet Res 1998;59:307312.

    • Search Google Scholar
    • Export Citation
  • 39.

    Rehder KWenthe FSessler AD. Function of each lung during mechanical ventilation with ZEEP and with PEEP in men anesthetized with thiopental-meperidine. Anesthesiology 1973;39:597606.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 40.

    Magnusson LSpahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003;91:6172.

  • Figure 1—

    Concurrent tracings of oxygen flow (top) and airway opening pressure (bottom) obtained from a representative healthy adult sheep mechanically ventilated with pure oxygen during anesthesia induced and maintained with propofol (5 mg/ kg and 0.4 mg/kg/min, respectively, IV); muscular paralysis was induced via bolus administration of vecuronium (25 μg/kg, IV). Tracings indicate the end-inspiratory and end-expiratory pauses separated by a regular breath (ie, without an occlusive pause). Paoplat = Airway plateau pressure corresponding to the value of Pao after an end-inspiratory pause of 3 to 4 seconds. PEEPexternal = PEEP (applied by the ventilator) corresponding to the value of the Pao at the end of a regular breath. PEEPtotal = PEEP value that takes into account the possible intrinsic PEEP and corresponds to the value of the Pao at the end of an end-expiratory pause of 3 to 4 seconds.

  • Figure 2—

    Relative sizes of 4 functional lung compartments identified via analysis of CT images obtained from 10 propofol-anesthetized sheep positioned in right lateral recumbency (time of positioning = time 0). Bars represent mean ± SD percentage of the EELV. Data were recorded at predetermined intervals (15 minutes [T15, white bars], 30 minutes [T30, gray bars], and 60 minutes [T60, vertically dotted line bars]) with ZEEP and after application of 10 cm H2O of PEEP for 20 minutes (TPEEP; black bars). a,bWithin each anatomic compartment, values with different letters are significantly (P < 0.05) different among time points on the basis of a 1-way ANOVA for repeated measures and a Student-Newman-Keuls test. See Figure 1 for remainder of key.

  • Figure 3—

    Distribution of atelectasis throughout the lungs in 10 propofol-anesthetized sheep. One voxel is a pixel (ie, parallelogram with a square base [0.59 mm/side]) and a height corresponding to the CT slice thickness (10 mm); bars represent the mean number of voxels with an HU value between −100 and 100 (ie, the HU range indicative of atelectasis). Transverse CT slices were equally distributed across the entire lung; CT slice numbers represent images obtained serially as the scan proceeded in a cranial to caudal direction (slices with low numbers were obtained from the most cranial lung fields, and slices with high numbers were obtained from the most caudal lung fields). Data were recorded at T60 with ZEEP (white bars) and at TPEEP (black bars). See Figures 1 and 2 for remainder of key.

  • Figure 4—

    Transverse CT images of the thorax obtained at the level of the body of T8 from the same propofol-anesthetized representative sheep used to obtain the tracing in Figure 1. Images were obtained at T15 (A), T30 (B), and T60 (C) with ZEEP and at TPEEP (D). Atelectatic lung parenchyma (black arrows) is apparent in the dependent (right) lung at T15, T30, and T60; at TPEEP, the amount of atelectasis is reduced (white arrow). See Figure 2 for remainder of key.

  • 1.

    McDonell W. Respiratory system. In: Thurmon JCTranquilli WJBenson GJ, eds. Lumb and Jones' veterinary anesthesia. 4th ed. Baltimore: Williams & Wilkins, 2007;117151.

    • Search Google Scholar
    • Export Citation
  • 2.

    Rothen HUSporre BEngberg G, et al.Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995;82:832842.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Staffieri FBauquier SHMoate PJ, et al.Pulmonary gas exchange in anaesthetised horses mechanically ventilated with oxygen or a helium/oxygen mixture. Equine Vet J 2009;41:747752.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4.

    Staffieri FFranchini DCarella GL, et al.Computed tomographic analysis of the effects of two inspired oxygen concentrations on pulmonary aeration in anesthetized and mechanically ventilated dogs. Am J Vet Res 2007;68:925931.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Duggan MKavanag BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005;102:838854.

  • 6.

    Dale WARahn H. Rate of gas absorption during atelectasis. J Appl Physiol 1952;70:606613.

  • 7.

    Dantzker DRWagner PDWest JB. Instability of lung units with low Va/Q ratios during O2 breathing. J Appl Physiol 1975;38:886895.

  • 8.

    Lumb AB. Applied physiology. Anaesthesia. In: Lumb AB, ed. Nunn's applied respiratory physiology. 6th ed. St Louis: Elsevier, 2005;297326.

    • Search Google Scholar
    • Export Citation
  • 9.

    Tokics LHedenstierna GSvensson L, et al.V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. J Appl Physiol 1996;81:18221833.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Haitsma JJ. Physiology of mechanical ventilation. Crit Care Clin 2007;23:117134.

  • 11.

    Neumann PRothen HUBerglund JE, et al.Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of high inspired oxygen concentration. Acta Anaesthesiol Scand 1999;43:295301.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Rothen HUSporre BEngberg G, et al.Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71:788795.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Serafini GCornara GCavalloro F, et al.Pulmonary atelectasis during paediatric anaesthesia: CT scan evaluation and effect of positive end-expiratory pressure (PEEP). Paediatr Anaesth 1999;9:225228.

    • Search Google Scholar
    • Export Citation
  • 14.

    Tokics LHedenstierna GStrandberg A, et al.Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987;66:157167.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Horton WGCheney FW. Variability of effect of positive end expiratory pressure. Arch Surg 1975;110:395398.

  • 16.

    Tittley JGFremes SEWeisel RD, et al.Hemodynamic and myocardial metabolic consequences of PEEP. Chest 1985;86:496502.

  • 17.

    Riebold TW. Ruminants. In: Thurmon JCTranquilli WJBenson GJ, eds. Lumb and Jones' veterinary anesthesia. 4th ed. Baltimore: Williams & Wilkins, 2007;731746.

    • Search Google Scholar
    • Export Citation
  • 18.

    Hedenstierna GLundquist HLundh B, et al.Pulmonary densities during anaesthesia. An experimental study on lung morphology and gas exchange. Eur Respir J 1989;2:528535.

    • Search Google Scholar
    • Export Citation
  • 19.

    Drummond GB. Computed tomography and pulmonary measurements. Br J Anaesth 1998;80:665671.

  • 20.

    Reber AEngberg GSporre B, et al.Volumetric analysis of aeration in the lung during general anaesthesia. Br J Anaesth 1996;76:760766.

  • 21.

    Patroniti NBellani GManfio A, et al.Lung volume in mechanically ventilated patients: measurement by simplified helium dilution compared to quantitative CT scan. Intensive Care Med 2004;30:282289.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Brismar BHedenstierna GLundquist H, et al.Pulmonary densities during anesthesia with muscular relaxation. A proposal of atelectasis. Anesthesiology 1985;62:422428.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Clutton REGlasby MA. Cardiovascular and autonomic nervous effects of edrophonium and atropine combinations during neuromuscular blockade antagonism in sheep. Vet Anaesth Analg 2008;35:191200.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Pepe PEMarini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Respir Dis 1982;126:166170.

    • Search Google Scholar
    • Export Citation
  • 25.

    Lu QMalbouisson LMMourgeon E, et al.Assessment of PEEP-induced reopening of collapsed lung regions in acute lung injury: are one or three CT sections representative of the entire lung? Intensive Care Med 2001;27:15041510.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Mundie TGDodd KTLagutchik M. Relationship of functional residual capacity and various body measurements in normal sheep. Lab Anim Sci 1992;42:589592.

    • Search Google Scholar
    • Export Citation
  • 27.

    Pypendop BHSteffey EP. Focused supportive care: ventilation during ruminant anesthesia. In: Steffey EP, ed. Recent advances in anesthetic management of large domestic animals. Ithaca, NY: International Veterinary Information Service, 2001.

    • Search Google Scholar
    • Export Citation
  • 28.

    Desmecht DLinden ALekeux P. Pathophysiological response of bovine diaphragm function to gastric distension. J Appl Physiol 1995;78:15371546.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Cohen E. Physiology of the lateral position and one-lung ventilation. Chest Surg Clin N Am 1997;7:753771.

  • 30.

    Johnson D. Lung recruitment during general anesthesia. Can J Anaesth 2004;51:649653.

  • 31.

    Tusman GBohm SSuarez-Sipman F, et al.Alveolar recruitment improves ventilatory efficiency of the lungs during anesthesia. Can J Anaesth 2004;51:723727.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Tusman GBohm SHVazquez de Anda GF, et al.“Alveolar recruitment strategy” improves arterial oxygenation during general anaesthesia. Br J Anaesth 1999;82:813.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Dyhr TLaursen NLarsson A. Effect 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 2002;46:717725.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Dyhr TNygard ELaursen N, et al.Both lung recruitment maneuver and PEEP are needed to increase oxygenation and lung volume after cardiac surgery. Acta Anaesthesiol Scand 2004;48:187197.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 35.

    Tusman GBohm SHTempra A, et al.Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology 2003;98:1422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 36.

    von Ungern-Sternberg BSRegli ASchibler A, et al.The impact of positive end-expiratory pressure on functional residual capacity and ventilation homogeneity impairment in anesthetized children exposed to high levels of inspired oxygen. Anesth Analg 2007;104:13641368.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 37.

    Wahba RWM. Perioperative functional residual capacity. Can J Anaesth 1991;38:384400.

  • 38.

    Moens YLagerweij EGootjes P, et al.Influence of tidal volume and positive end-expiratory pressure on inspiratory gas distribution and gas exchange during mechanical ventilation in horses positioned in lateral recumbency. Am J Vet Res 1998;59:307312.

    • Search Google Scholar
    • Export Citation
  • 39.

    Rehder KWenthe FSessler AD. Function of each lung during mechanical ventilation with ZEEP and with PEEP in men anesthetized with thiopental-meperidine. Anesthesiology 1973;39:597606.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 40.

    Magnusson LSpahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003;91:6172.

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