'Alveolar recruitment strategy' improves arterial oxygenation during general anaesthesia

Abnormalities in gas exchange during general anaesthesia are caused partly by atelectasis. Inspiratory pressures of approximately 40 cm H2O are required to fully re-expand healthy but collapsed alveoli. However, without PEEP these re-expanded alveoli tend to collapse again. We hypothesized that an initial increase in pressure would open collapsed alveoli; if this inspiratory recruitment is combined with sufficient end-expiratory pressure, alveoli will remain open during general anaesthesia. We tested the effect of an 'alveolar recruitment strategy' on arterial oxygenation and lung mechanics in a prospective, controlled study of 30 ASA II or III patients aged more than 60 yr allocated to one of three groups. Group ZEEP received no PEEP. The second group received an initial control period without PEEP, and then PEEP 5 cm H2O was applied. The third group received an increase in PEEP and tidal volumes until a PEEP of 15 cm H2O and a tidal volume of 18 ml kg-1 or a peak inspiratory pressure of 40 cm H2O was reached. PEEP 5 cm H2O was then maintained. There was a significant increase in median PaO2 values obtained at baseline (20.4 kPa) and those obtained after the recruitment manoeuvre (24.4 kPa) at 40 min. This latter value was also significantly higher than PaO2 measured in the PEEP (16.2 kPa) and ZEEP (18.7 kPa) groups. Application of PEEP also had a significant effect on oxygenation; no such intra-group difference was observed in the ZEEP group. No complications occurred. We conclude that during general anaesthesia, the alveolar recruitment strategy was an efficient way to improve arterial oxygenation.      

RE-EXPANSION OF ATELECTASIS DURING GENERAL ANAESTHESIA: A COMPUTED TOMOGRAPHY STUDY

Formation of atelectasis is one mechanism of impaired gas exchangeduring general anaesthesia. We have studied manoeuvres to re-expandsuch atelectasis in 16 consecutive, anaesthetized adults withhealthy lungs. In group 1 (10 patients), the lungs were inflatedstepwise to an airway pressure (Paw) of 10, 20, 30 and 40 cmH₂O In group 2 (six patients), three repeated inflations upto Paw = 30 cm H₂O were followed by one inflation to 40 cm H₂O.Atelectasis was assessed by analysis of computed x-ray tomography(CT). In group 1 the mean area of atelectasis in the CT scanat the level of the right diaphragm was 6.4 cm² at Paw = 0 cmH₂O, 5.9 cm² at 20 cm H₂O, 3.5 cm ² at 30 cm H₂O and 0.8 cm²at 40 cm H₂O, A Paw of 20 cm H₂O corresponds approximately toinflation with twice the tidal volume. In group 2 the mean areaof atelectasis was 9.0 cm² at Paw = 0 cm H₂O and 4.2 cm² afterthe first inflation to 30 cm H₂O. Repeated inflations did notadd to re-expansion of atelectasis. The final inflation (Paw= 40 cm H₂O) virtually eliminated the atelectasis. We concludethat, after induction of anaesthesia, the amount of atelectasiswas not reduced by inflation of the lungs with a conventionaltidal volume or with a double tidal volume ("sigh"). An inflationto vital capacity (Paw = 40 cm H₂O, however, re-expanded virtuallyall atelectatic lung tissue. (Br. J. Anaesth. 1993; 71: 788–795)     

The effect of increased FIO(2) before tracheal extubation on postoperative atelectasis

General anesthesia promotes pulmonary atelectasis, which can be eliminated by a vital capacity (VC) maneuver (inflation of the lungs to 40 cm H(2)O for 15 s). High-inspired oxygen concentration favors recurrence of atelectasis. Therefore, 100% oxygen before tracheal extubation may contribute to atelectasis. To evaluate whether the use of 100% oxygen before extubation increases the amount of postoperative atelectasis, we studied 30 adults scheduled for elective surgery of the extremities. Ten minutes before the presumed end of surgery, patients were randomly assigned to (a) a fraction of inspired oxygen (FIO(2)) = 1.0 (n = 10), (b) VC maneuver + FIO(2) = 1.0 (n = 10), or (c) VC maneuver + FIO(2) = 0.4 (n = 10). The amount of atelectasis was measured by computed tomography scan, and oxygenation was studied by arterial blood gas analysis. Data were analyzed by one-way analysis of variance with Bonferroni correction. Results are presented as mean +/- SD; P < 0.05 was considered significant. In the VC maneuver + FIO(2) = 0.4 group, postoperative atelectasis was smaller (2.6% +/- 1.1% of total lung surface, P < 0.05) than in the FIO(2) = 1.0 group (8.3% +/- 6.2%) and in the VC maneuver + FIO(2) = 1.0 group (6.8% +/- 3.4%). Oxygen 100% at the end of general anesthesia promotes postoperative atelectasis. A safety margin in terms of oxygenation during tracheal extubation is essential, and further studies should therefore evaluate whether atelectasis formation could be prevented despite the use of 100% oxygen. IMPLICATIONS: For safety reasons, it is common to ventilate patients with 100% oxygen before tracheal extubation. This study demonstrates that this practice favors postoperative atelectasis.     

Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass

Atelectasis occurs during general anaesthesia. This is partly responsible for the impairment of gas exchange that occurs peri-operatively. During cardiopulmonary bypass, this atelectasis is exacerbated by the physical collapse of the lungs. As a result, poor arterial oxygenation is often seen postoperatively. We tested the effect of an 'alveolar recruitment strategy' on arterial oxygenation in a prospective randomised study of 78 patients undergoing cardiopulmonary bypass. Patients were divided equally into three groups of 26. Group 'no PEEP' received a standard post bypass manual lung inflation, and no positive end-expiratory pressure was applied until arrival at intensive care unit. Group '5 PEEP' received a standard post bypass manual inflation, and then 5 cmH2O of positive end-expiratory pressure was applied and maintained until extubation on intensive care. The third group, 'recruitment group', received a pressure-controlled stepwise increase in positive end-expiratory pressure up to 15 cmH2O and tidal volumes of up to 18 ml x kg(-1) until a peak inspiratory pressure of 40 cmH2O was reached. This was maintained for 10 cycles; the positive end-expiratory pressure of 5 cmH2O was maintained until extubation on intensive care. There was a significantly better oxygenation in the recruitment group at 30 min and 1 h post bypass when compared with the no PEEP and 5 PEEP groups. There was no significant difference in any of the groups beyond 1 h. Application of 5 cmH2O positive end-expiratory pressure alone had no significant effect on oxygenation. No complications due to the alveolar recruitment manoeuvre occurred. We conclude that the application of an alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass surgery.     

Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration

BACKGROUND: General anaesthesia impairs the gas exchange in the lungs, and moderate desaturation (SaO2 86-90%) occurred in 50% of anaesthetised patients in a blinded pulse oximetry study. A high FiO2 might reduce the risk of hypoxaemia, but can also promote atelectasis. We hypothesised that a moderate positive end-expiratory pressure (PEEP) level of 10 cmH2O can prevent atelectasis during ventilation with an FiO2 = 1.0. METHODS: Atelectasis was evaluated by computed tomography (CT) in 13 ASA I-II patients undergoing elective surgery. CT scans were obtained before and 15 min after induction of anaesthesia. Then, recruitment of collapsed lung tissue was performed as a "vital capacity manoeuvre" (VCM, inspiration with Paw = 40 cmH2O for 15 s), and a CT scan was obtained at the end of the VCM. Thereafter, PEEP = 0 cmH2O was applied in group 1, and PEEP = 10 cmH2O in group 2. Additional CT scans were obtained after the VCM. Oxygenation was measured before and after the VCM. RESULTS: Atelectasis (> 1 cm2) was present in 12 of the 13 patients after induction of anaesthesia. At 5 and 10 min after the VCM, atelectasis was significantly smaller in group 2 than group 1 (P < 0.005). A significant inverse correlation was found between PaO2 and atelectasis. CONCLUSIONS: PEEP = 10 cmH2O reduced atelectasis formation after a VCM, when FiO2 = 1.0 was used. Thus, a VCM followed by PEEP = 10 cmH2O should be considered when patients are ventilated with a high FiO2 and gas exchange is impaired.     

Reexpansion of atelectasis during general anaesthesia may have a prolonged effect

Pulmonary atelectasis, as found during general anaesthesia, may be reexpanded by hyper-inflation of the lungs. The purpose of this study was to determine whether such a recruitment is maintained and whether this is accompanied by an improved gas exchange. We studied a consecutive sample of twelve lung healthy adults, scheduled for elective surgery. After induction of intravenous anaesthesia, the lungs were hyperinflated manually. The ventilationperfusion relationship (Va/Q) was estimated with the multiple inert gas method, and in six patients atelectasis was assessed by computed x-ray tomography. The mean pulmonary shunt was 7.5% of cardiac output after induction of anaesthesia and this decreased to 1.0% and 2.8% at 20 and 40 min after the recruitment manoeuvre. Perfusion of poorly ventilated lung regions (low Va/Q), however, increased from 3.7% to 10.6% and 7.8% at 20 and 40 min after the recruitment, respectively. The mean alveolar-arterial oxygen tension difference (P_A-ao₂) was 14.3 kPa after induction of anaesthesia and 11.1 kPa immediately after recruitment. Forty minutes later P_A-ao₂ was still 2.0 kPa lower than after induction of anaesthesia (95% conficence interval [CI] 0.3 to 3.8 kPa). P_A-ao₂ decreased more in obese patients. The mean area of atelectasis decreased from 9.0 cm² after induction of anaesthesia to 0.1 cm² immediately after recruitment, and there was a slow increase to 1.9 cm² (95% CI 0.0 to 3.9 cm²) 40 min later. During general anaesthesia in lung healthy patients, most of the reexpanded atelectatic lung tissue remains inflated for at least 40 min. The recruitment manoeuvre decreases pulmonary shunt, but increases low Va/Q. The net effect on gas exchange is a small reduction of P_A-ao₂.     

Oxygen concentration and characteristics of progressive atelectasis formation during anaesthesia

Background: Atelectasis is a common consequence of pre‐oxygenation with 100% oxygen during induction of anaesthesia. Lowering the oxygen level during pre‐oxygenation reduces atelectasis. Whether this effect is maintained during anaesthesia is unknown. Methods: During and after pre‐oxygenation and induction of anaesthesia with 60%, 80% or 100% oxygen concentration, followed by anaesthesia with mechanical ventilation with 40% oxygen in nitrogen and positive end‐expiratory pressure of 3 cmH₂O, we used repeated computed tomography (CT) to investigate the early (0–14 min) vs. the later time course (14–45 min) of atelectasis formation. Results: In the early time course, atelectasis was studied awake, 4, 7 and 14 min after start of pre‐oxygenation with 60%, 80% or 100% oxygen concentration. The differences in the area of atelectasis formation between awake and 7 min and between 7 and 14 min were significant, irrespective of oxygen concentration (P<0.05). During the late time course, studied after pre‐oxygenation with 80% oxygen, the differences in the area of atelectasis formation between awake and 14 min, between 14 and 21 min, between 21 and 28 min and finally between 21 and 45 min were all significant (P<0.05). Conclusion: Formation of atelectasis after pre‐oxygenation and induction of anaesthesia is oxygen and time dependent. The benefit of using 80% oxygen during induction of anaesthesia in order to reduce atelectasis diminished gradually with time.     

Repeated vital capacity manoeuvres after cardiopulmonary bypass: effects on lung function in a pig model

Respiratory failure following cardiopulmonary bypass (CPB) is a major complication after cardiac surgery. A vital capacity inflation of the lungs, performed before the end of CPB, may improve gas exchange, but the necessity to repeat it is unclear. Therefore, we studied 18 pigs undergoing hypothermic CPB. A vital capacity manoeuvre (VCM) was performed in two groups and consisted of inflating the lungs for 15 s to 40 cm H2O at the end of CPB. In one group, VCM was repeated every hour. The third group served as controls. Atelectasis was studied by CT scan. Intrapulmonary shunt increased after bypass in the controls and improved spontaneously 3 h later without returning to baseline values. From 3 to 6 h after CPB, there was no more improvement and more than 10% atelectasis remained at 6 h. In contrast, the two groups treated before termination of CPB with VCM showed only minor atelectasis and no abnormal changes in gas exchange directly after bypass or later. We conclude that the protective effect of VCM remained for 6 h after bypass, and there was no extra benefit on gas exchange by repeating the VCM.      

Effect of vital capacity manoeuvres on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery

BACKGROUND: Arterial oxygenation may be compromised in morbidly obese patients undergoing bariatric surgery. The aim of this study was to evaluate the effect of a vital capacity manoeuvre (VCM), followed by ventilation with positive end-expiratory pressure (PEEP), on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery. METHODS: Fifty-two morbidly obese patients (body mass index >40 kg m-2) undergoing open bariatric surgery were enrolled in this prospective and randomized study. Anaesthesia and surgical techniques were standardized. Patients were ventilated with a tidal volume of 10 mL kg-1 of ideal body weight, a mixture of oxygen and nitrous oxide (FiO2 = 40%) and respiratory rate was adjusted to maintain end-tidal carbon dioxide at a level of 30-35 mmHg. After abdominal opening, patients in Group 1 had a PEEP of 8 cm H2O applied and patients in Group 2 had a VCM followed by PEEP of 8 cm H2O. This manoeuvre was defined as lung inflation by a positive inspiratory pressure of 40 cm H2O maintained for 15 s. PEEP was maintained until extubation in the two groups. Haemodynamics, ventilatory and arterial oxygenation parameters were measured at the following times: T0 = before application of VCM and/or PEEP, T1 = 5 min after VCM and/or PEEP and T2 = before abdominal closure. RESULTS: Patients in the two groups were comparable regarding patient characteristics, surgical, haemodynamic and ventilatory parameters. In Group 1, arterial oxygen partial pressure (PaO2) and arterial haemoglobin oxygen saturation (SaO2) were significantly increased and alveolar-arterial oxygen pressure gradient (A-aDO2) decreased at T2 when compared with T0 and T1. In Group 2, PaO2 and SaO2 were significantly increased and A-aDO2 decreased at T1 and T2 when compared with T0. Arterial oxygenation parameters at T1 and T2 were significantly improved in Group 2 when compared with Group 1. CONCLUSION: The addition of VCM to PEEP improves intraoperative arterial oxygenation in morbidly obese patients undergoing open bariatric surgery.     

Optimal Mean Airway Pressure during High-frequency Oscillation: Predicted by the Pressure-Volume Curve

Background: A number of groups have recommended setting positive end-expiratory pressure during conventional mechanical ventilation in adults at 2 cm H2O above the lower corner pressure (PCL) of the inspiratory pressure-volume (P-V) curve of the respiratory system. No equivalent recommendations for the setting of the mean airway pressure (Paw) during high-frequency oscillation (HFO) exist. The authors questioned if the Paw resulting in the best oxygenation without hemodynamic compromise during HFO is related to the static P-V curve in a large animal model of acute respiratory distress syndrome.

Methods: Saline lung lavage was performed in seven sheep (28 +/- 5 kg, mean +/- SD) until the arterial oxygen partial pressure/fraction of inspired oxygen ratio decreased to 85 +/- 27 mmHg at a positive end-expiratory pressure of 5 cm H2O (initial injury). The PCL (20 +/- 1 cm H2O) on the inflation limb and the point of maximum curvature change (PMC; 26 +/- 1 cm H2O) on the deflation limb of the static P-V curve were determined. The sheep were subjected to four 1-h cycles of HFO at different levels of Paw (PCL + 2, + 6, + 10, + 14 cm H2O), applied in random order. Each cycle was preceded by a recruitment maneuver at a sustained Paw of 50 cm H2O for 60 s.

Results: High-frequency oscillation with a Paw of 6 cm H2O above PCL (PCL + 6) resulted in a significant improvement in oxygenation (P < 0.01 vs. initial injury). No further improvement in oxygenation was observed with higher Paw, but cardiac output decreased, pulmonary vascular resistance increased, and oxygen delivery decreased at Paw greater than PCL + 6. The PMC on the deflation limb of the P-V curve was equal to the PCL + 6 (r = 0.77, P < 0.05).     

Beatmung eines ungeschützten Atemwegs

BACKGROUND: Currently 30 chest compressions and 2 ventilations with an inspiratory time of 1 s are recommended during cardiopulmonary resuscitation with an unprotected airway, thus spending about 15% instead of 40% of resuscitation time on ventilation. Time could be gained for chest compressions when reducing inspiratory time from 2 s to 1 s, however, stomach inflation may increase as well. METHODS: In an established bench model we evaluated the effect of reducing inspiratory time from 2 s to 1 s at different lower oesophageal sphincter pressure (LOSP) levels using a novel peak inspiratory-flow and peak airway-pressure-limiting bag-valve-mask device (Smart-Bag). RESULTS: A reduction of inspiratory time from 2 s to 1 s resulted in significantly lower peak airway pressure with LOSP of 0.49 kPa (5 cm H2O), 0.98 kPa (10 cm H2O) and 1.47 kPa (15 cm H2O) and an increase with 1.96 kPa (20 cm H2O). Lung tidal volume was reduced with 1 s compared to 2 s. When reducing inspiratory time from 2 s to 1 s, stomach inflation occurred only at a LOSP of 0.49 kPa (5 cm H2O). CONCLUSIONS: In this model of a simulated unprotected airway, a reduction of inspiratory time from 2 s to 1 s using the Smart-Bag resulted in comparable inspiratory peak airway pressure and lower, but clinically comparable, lung tidal volume. Stomach inflation occurred only at a LOSP of 0.49 kPa (5 cm H2O), and was higher with an inspiratory time of 2 s vs 1 s.     

Optimal mean airway pressure during high-frequency oscillation: predicted by the pressure-volume curve

BACKGROUND: A number of groups have recommended setting positive end-expiratory pressure during conventional mechanical ventilation in adults at 2 cm H2O above the lower corner pressure (P(CL)) of the inspiratory pressure-volume (P-V) curve of the respiratory system. No equivalent recommendations for the setting of the mean airway pressure (Paw) during high-frequency oscillation (HFO) exist. The authors questioned if the Paw resulting in the best oxygenation without hemodynamic compromise during HFO is related to the static P-V curve in a large animal model of acute respiratory distress syndrome. METHODS: Saline lung lavage was performed in seven sheep (28+/-5 kg, mean +/- SD) until the arterial oxygen partial pressure/fraction of inspired oxygen ratio decreased to 85+/-27 mmHg at a positive end-expiratory pressure of 5 cm H2O (initial injury). The PCL (20+/-1 cm H2O) on the inflation limb and the point of maximum curvature change (PMC; 26+/-1 cm H2O) on the deflation limb of the static P-V curve were determined. The sheep were subjected to four 1-h cycles of HFO at different levels of Paw (P(CL) + 2, + 6, + 10, + 14 cm H2O), applied in random order. Each cycle was preceded by a recruitment maneuver at a sustained Paw of 50 cm H2O for 60 s. RESULTS: High-frequency oscillation with a Paw of 6 cm H2O above P(CL) (P(CL) + 6) resulted in a significant improvement in oxygenation (P < 0.01 vs. initial injury). No further improvement in oxygenation was observed with higher Paw, but cardiac output decreased, pulmonary vascular resistance increased, and oxygen delivery decreased at Paw greater than P(CL) + 6. The PMC on the deflation limb of the P-V curve was equal to the P(CL) + 6 (r = 0.77, P < 0.05). CONCLUSION: In this model of acute respiratory distress syndrome, optimal Paw during HFO is equal to P(CL) + 6, which correlates with the PMC.     

Oxygen and anesthesia: what lung do we deliver to the post‐operative ward?

Anesthesia is safe in most patients. However, anesthetics reduce functional residual capacity (FRC) and promote airway closure. Oxygen is breathed during the induction of anesthesia, and increased concentration of oxygen (O(2) ) is given during the surgery to reduce the risk of hypoxemia. However, oxygen is rapidly adsorbed behind closed airways, causing lung collapse (atelectasis) and shunt. Atelectasis may be a locus for infection and may cause pneumonia. Measures to prevent atelectasis and possibly reduce post-operative pulmonary complications are based on moderate use of oxygen and preservation or restoration of FRC. Pre-oxygenation with 100% O(2) causes atelectasis and should be followed by a recruitment maneuver (inflation to an airway pressure of 40 cm H(2) O for 10 s and to higher airway pressures in patients with reduced abdominal compliance (obese and patients with abdominal disorders). Pre-oxygenation with 80% O(2) may be sufficient in most patients with no anticipated difficulty in managing the airway, but time to hypoxemia during apnea decreases from mean 7 to 5 min. An alternative, possibly challenging, procedure is induction of anesthesia with continuous positive airway pressure/positive end-expiratory pressure to prevent fall in FRC enabling use of 100% O(2) . A continuous PEEP of 7-10 cm H(2) O may not necessarily improve oxygenation but should keep the lung open until the end of anesthesia. Inspired oxygen concentration of 30-40%, or even less, should suffice if the lung is kept open. The goal of the anesthetic regime should be to deliver a patient with no atelectasis to the post-operative ward and to keep the lung open.     

Hyperinflation during lung preservation and increased reperfusion injury

BACKGROUND: Reperfusion injury after lung transplantation remains a perplexing and unpredictable problem. Most surgeons preserve the lung inflated, but the amount of inflation that should be used is not well documented. Therefore, we studied the effect of high inflation during organ preservation on lung function during reperfusion. Our hypothesis is that donor lung hyperinflation during storage contributes to early allograft dysfunction during reperfusion. METHODS: To test our hypothesis we used an isolated, blood-perfused, ventilated rabbit lung model. Group I lungs (control) underwent immediate reperfusion after harvest. Group II lungs (low-inflation, maintained at 6 mmHg airway pressure) and group III lungs (high-inflation, maintained at 20 mmHg airway pressure) were stored for 4 h in 4 degrees C Euro-Collins solution after harvest. All lungs were then reperfused with whole blood for 1 h, and measurements of arterial oxygenation (PO2, mmHg), pulmonary artery pressure (PAP, mmHg), peak inspiratory pressure (PIP, cm H2O), and wet-to-dry weight ratio (WTD) were obtained. RESULTS: Throughout the 1 h reperfusion period group III lungs had significantly lower oxygenation compared to groups I and II. In addition, throughout reperfusion, group III lungs showed significantly higher PAP and PIP compared to group II. WTD did not differ significantly between groups, however, there was a trend toward increased edema in group III. CONCLUSIONS: These results indicate that high inflation during cold storage results in acute pulmonary dysfunction. Careful monitoring of airway inflation pressure during storage, especially to prevent hyperinflation, should be maintained in the current practice for lung transplantation.     

Effects of an alveolar recruitment manoeuvre guided by lung ultrasound on anaesthesia‐induced atelectasis in infants: a randomised,controlled trial

Atelectasis occurs in the majority of children undergoing general anaesthesia. Lung ultrasound has shown reliable sensitivity and specificity for diagnosing anaesthesia‐induced atelectasis. We assessed the effects of a recruitment manoeuvre on atelectasis using lung ultrasound in infants undergoing general anaesthesia. Forty infants, randomly allocated to either a recruitment manoeuvre group or a control group, received volume‐controlled ventilation with 5 cmH₂O positive end‐expiratory pressure. Lung ultrasound examination was performed twice in each patient, the first a minute after starting mechanical ventilation of the lungs and the second at the end of surgery. Patients in the recruitment manoeuvre group received ultrasound‐guided recruitment manoeuvres after each lung ultrasound examination. The incidence of significant anaesthesia‐induced atelectasis at the second lung ultrasound examination was less in the recruitment manoeuvre group compared with the control group (25% vs. 80%; p = 0.001; odds ratio (OR ) 0.083; 95% confidence interval (CI ): 0.019–0.370). The median (IQR [range]) lung ultrasound scores for consolidation and B‐lines on the second examination were lower in the recruitment manoeuvre group compared with the control group; 6.0 (3.0–9.3 [0.0–14.0]) vs. 13.5 (11.0–16.5 [8.0–23.0]); p < 0.001 and 6.5 (3.0–12.0 [0.0–28.0]) vs. 15.0 (10.8–20.5 [7.0–28.0]); p < 0.001, respectively. The lung ultrasound scores for consolidation on the first and second examinations showed a negative correlation with age (r = ?0.340, p = 0.008; r = ?0.380, p = 0.003). We conclude that ultrasound‐guided recruitment manoeuvres with positive end‐expiratory pressure proved useful in reducing the incidence of anaesthesia‐induced atelectasis in infants, although 5 cmH₂O positive end‐expiratory pressure alone was not sufficient to eliminate it. In addition, the younger the patient, the more susceptible they were to atelectasis.     

Airway closure, atelectasis and gas exchange during general anaesthesia

Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV- ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related.      

AN ALTERNATIVE METHOD OF INCREASING PCO2 USING APNOEA AND CONTINUOUS POSITIVE AIRWAY PRESSURE

We have examined the use of continuous positive airway pressure(CPAP) and apnoeic oxygenation for restoration of spontaneousbreathing at the end of anaesthesia after controlled ventilation.We studied 45 adult patients without a history of acute or chronicrespiratory disturbances. Anaesthesia wos inducsd with thiopentoneor prnnnfnl and maintained with nitrous oxide and enfluranein oxygen. The patients were normocapnic during artificial ventilation.At the end of surgery, the lungs were ventilated for 5 min withoxygen and then given a CPAP of 8 cm H₂O. Spontaneous ventilationwas regained after a mean of 5 min and an arterial blood samplewas obtained at the third breath. All patients were well oxygenated(PO₂ mean 43.5 kPa, range 21–76 kPa) when spontaneousventilation started. The pH was close to 7.28 in most cases(mean 7.28, range 7.21–7.32), and PCO2 varied in the range6.6–9.9 kPa (mean 7.9 kPa). It is concluded that the methodis safe with regard to oxygenation and acid-base balance. (Br.J. naesth. 1993; 70: 411–413)     

Vital capacity manoeuvre in general anaesthesia: useful or useless?

As atelectasis occurs in most patients during general anaesthesia and may be one of the major causes for the development of hypoxaemia and nosocomial pneumonia, its prevention may be considered as an important objective in perioperative management. The major causative mechanisms are the loss of respiratory muscle tone, compression and gas absorption. Vital capacity manoeuvres have been proposed as a means to eliminate atelectasis in the vast majority of patients and restore normal pulmonary gas exchange during general anaesthesia. In this review we describe the pathogenesis of atelectasis in the perioperative period and discuss in the light of recent published investigations the suitability of the vital capacity manoeuvre as a tool during general anaesthesia. Reviewing the current literature, a vital capacity manoeuvre during general anaesthesia may only be useful under specific circumstances when mechanical ventilation with a high inspiratory fraction of oxygen is required or during cardiac surgery at the end of cardiopulmonary bypass to reduce the amount of atelectasis and to maintain adequate gas exchange.     

Atelectasis and lung function in the postoperative period

Thirteen patients with healthy hearts and lungs, and with a mean age of 68 years, who were scheduled for lower abdominal surgery during isoflurane anaesthesia with muscular paralysis, were investigated with arterial blood gases, spirometry, pulmonary x-ray and computed tomography (CT) of the chest before and during anaesthesia, as well as during the first 4 postoperative days. Before anaesthesia, lung function and gas exchange were normal in all patients. Pulmonary x-ray and CT scans of the lungs were also normal. During anaesthesia, 6 of 13 patients developed atelectasis (mean 1.0% of intrathoracic transverse area in all patients). Two hours postoperatively, 11 of 13 patients had atelectasis and the mean atelectatic area was 1.8%. Pao2 was significantly reduced by 2.1 kPa to 9.8 kPa. On the first postoperative day, the mean atelectasis was unaltered (1.8%). None of the atelectasis found on CT scanning could be detected on standard pulmonary x-ray. Forced vital capacity (FVC) and forced expired volume in 1 s (FEV1) were significantly decreased to 2/3 of preoperative level. Pao2 was significantly reduced to less than 80% of the preoperative level (mean 9.4 kPa). There were significant correlations between the atelectatic area and the impairment in FVC, FEV1, and Pao2. Spirometry and blood gases improved during the succeeding postoperative days, and atelectasis decreased. No patient suffered from pulmonary complications, as judged from clinical criteria and pulmonary x-ray, in contrast to the findings of atelectasis in 85% of the patients by computed tomography.     

A randomised controlled trial comparing transnasal humidified rapid insufflation ventilatory exchange (THRIVE) pre‐oxygenation with facemask pre‐oxygenation in patients undergoing rapid sequence induction of anaesthesia

Pre‐oxygenation is an essential part of rapid sequence induction of general anaesthesia for emergency surgery, in order to increase the oxygen reservoir in the lungs. We performed a randomised controlled trial of transnasal humidified rapid insufflation ventilatory exchange (THRIVE) pre‐oxygenation or facemask pre‐oxygenation in patients undergoing emergency surgery. Twenty patients were allocated to each group. No patient developed arterial oxygen saturation < 90% during attempted tracheal intubation. Arterial blood gases were sampled from an arterial catheter immediately after intubation. The mean (SD) PaO₂ was 43.7 (15.2) kPa in the THRIVE group vs. 41.9 (16.2) kPa in the facemask group (p = 0.722); PaCO₂ was 5.8 (1.1) kPa in the THRIVE group vs. 5.6 (1.0) kPa in the facemask group (p = 0.631); arterial pH was 7.36 (0.05) in the THRIVE group vs. 7.34 (0.06) in the facemask group (p = 0.447). No airway rescue manoeuvres were needed, and there were no differences in the number of laryngoscopy attempts between the groups. In spite of this, patients in the THRIVE group had a significantly longer apnoea time of 248 (71) s compared with 123 (55) s in the facemask group (p < 0.001). Transnasal humidified rapid insufflation ventilatory exchange is a practicable method for pre‐oxygenating patients during rapid sequence induction of general anaesthesia for emergency surgery; we found that it maintained an equivalent blood gas profile to facemask pre‐oxygenation, in spite of a significantly longer apnoea time.