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.     

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.     

Alveolar recruitment maneuver in refractory hypoxemia and lobar atelectasis after cardiac surgery: A case report

ABSTRACT: OBJECTIVE: This case report describes an unusual presentation of right upper lobe atelectasis associated with refractory hypoxemia to conventional alveolar recruitment maneuvers in a patient soon after coronary artery bypass grafting surgery. METHOD: Case-report. RESULTS: The alveolar recruitment with PEEP = 40cmH2O improved the patient's atelectasis and hypoxemia. CONCLUSION: In the present report, the unusual alveolar recruitment maneuver with PEEP 40cmH2O showed to be safe and efficient to reverse refractory hypoxemia and uncommon atelectasis in a patient after cardiac surgery.     

Protective Effect of Stroma-free Methemoglobin during Cyanide Poisoning in Dogs

Background: During fire exposure, cyanide toxicity can block aerobic metabolism. Oxygen and sodium thiosulfate are accepted therapy. However, nitrite-induced methemoglobinemia, which avidly binds cyanide, decreases oxygen-carrying capacity that is already reduced by the presence of carboxyhemoglobin (inhalation of carbon monoxide in smoke). This study tested whether exogenous stroma-free methemoglobin (SFmetHb) can prevent depression of hemodynamics and metabolism during canine cyanide poisoning.

Methods: In 10 dogs (weighing 18.8 plus/minus 3.5 kg) anesthetized with chloralose-urethane and mechanically ventilated with air, baseline hemodynamic and metabolic measurements were made. Then, 137 plus/minus 31 ml of 12 g% SFmetHb was infused into five dogs (SFmetHb group). Finally, the SFmetHb group and the control group (n = 5, no SFmetHb) received an intravenous potassium cyanide infusion (0.072 mg *symbol* kg sup -1 *symbol* min sup -1) for 20 min. Oxygen consumption (V with dot sub O2) was measured with a Datex Deltatrac (Datex Instruments, Helsinki, Finland) metabolic monitor and cardiac output (Q with dot T) was measured by pulmonary artery thermodilution.

Results: From baseline to cyanide infusion in the control group, Q with dot T decreased significantly (p < 0.05) from 2.9 plus/minus 0.8 to 1.5 plus/minus 0.4 l/min, mixed venous PCO2 (Pv with barCO2) tended to decrease from 35 plus/minus 4 to 23 plus/minus 2 mmHg, Pv with barO2 increased from 43 plus/minus 4 to 62 plus/minus 8 mmHg, V with dotO2 decreased from 93 plus/minus 8 to 64 plus/minus 19 ml/min, and lactate increased from 2.3 plus/minus 0.5 to 7.1 plus/minus 0.7 mM. In the SFmetHb group, cyanide infusion did not significantly change these variables. From baseline to infused cyanide, the increases in blood cyanide (4.8 plus/minus 1.0 to 452 plus/minus 97 micro Meter) and plasma thiocyanate cyanide (18 plus/minus 5 to 65 plus/minus 22 micro Meter) in the SFmetHb group were significantly greater than those increases in the control group. SFmetHb itself caused no physiologic changes, except small decreases in heart rate and Pv with barO2. Peak SFmetHb reached 7.7 plus/minus 1.0% of total hemoglobin.     

Positive End-Expiratory Pressure Ventilation Elicits Increases in Endogenously Formed Nitric Oxide as Detected in Air Exhaled by Rabbits

Background: Nitric oxide (NO) formed from L-arginine is exhaled by mammals and regulates pulmonary vascular tone. Little is known about how its formation is stimulated.

Methods: The concentration of NO in exhaled air was monitored by chemiluminescence in pentobarbital-anesthetized rabbits receiving mechanical ventilation by tracheostomy with graded positive end-expiratory pressure (PEEP).

Results: Introduction of PEEP (2.5-15 cmH2 O) elicited dose-dependent and reproducible increments in exhaled NO and in arterial oxygen tension (PaO2). The increase in exhaled NO exhibited a biphasic pattern, with an initial peak followed by a partial reversal during the 4-min period at each level of PEEP. Thus, at a PEEP of 10 cmH sub 2 O, exhaled NO initially increased from 19 plus/minus 4 to 30 plus/minus 5 parts per billion (ppb) (P < 0.001, n = 9) and then decreased to 27 plus/minus 5 ppb (P < 0.005) at the end of the 4-min observation period. Simultaneously, PaO2 increased from 75 plus/minus 12 mmHg in the control situation to 105 plus/minus 11 mmHg (P < 0.05) at a PEEP of 10 cmH2 O. After bilateral vagotomy, including bilateral transection of the depressor nerves, the increase in exhaled NO in response to PEEP was significantly reduced (P < 0.01). Thus, after vagotomy, a PEEP of 10 cmH2 O elicited an increase in the concentration of exhaled NO from 13 plus/minus 3 to 17 plus/minus 3 ppb (n = 7). Vagotomy did not affect the baseline concentration of NO in exhaled air. The PEEP-induced increments in PaO2 were not affected by the NO synthase inhibitor L-Nomega-arginine-methylester (30 mg *symbol* kg sup -1 intravenously). In open-chest experiments, PEEP (10 cmH2 O) induced a reduction in cardiac output from 317 plus/minus 36 to 235 plus/minus 30 ml *symbol* min sup -1 and an increase in exhaled NO from 23 plus/minus 6 to 30 plus/minus 7 ppb (P < 0.05, n = 5). Reduction in cardiac output from 300 plus/minus 67 to 223 plus/minus 52 ml *symbol* min sup -1 by partial obstruction of the pulmonary artery did not significantly increase exhaled NO (from 23 plus/minus 7 to 25 plus/minus 6, difference not significant; n = 3).     

Oral Clonidine Premedication Blunts the Heart Rate Response to Intravenous Atropine in Awake Children

Background: Clonidine, which is known to have analgesic and sedative properties, has recently been shown to be an effective preanesthetic medication in children. The drug may cause side effects, including bradycardia and hypotension. This study was conducted to evaluate the ability of intravenous atropine to increase the heart rate (HR) in awake children receiving clonidine preanesthetic medication.

Methods: We studied 96 otherwise healthy children, 8-13 yr old, undergoing minor surgery. They received, at random, oral clonidine 2 or 4 micro gram *symbol* kg sup -1 or placebo 105 min before scheduled induction of anesthesia. Part I (n = 48, 16 per group): When hemodynamic parameters after insertion of a venous catheter had been confirmed to be stable, atropine was administered in incremental doses of 2.5, 2.5, and 5 micro gram *symbol* kg sup -1 every 2 min. The HR and blond pressure were recorded at 1-min intervals. Part II (n = 48, 16 per group): After the recording of baseline hemodynamic values, successive doses of atropine (5 micro gram *symbol* kg sup -1 every 2 min, to 40 micro gram *symbol* kg sup -1), were administered until HR increased by 20 beats *symbol* min sup -1. The HR and blood pressure were recorded at 1-min intervals.

Results: Part I: The increases in HR in response to a cumulative dose of atropine 10 micro gram *symbol* kg sup -1 were 33 plus/minus 3%, 16 plus/minus 3%, and 8 plus/minus 2% (mean plus/minus SEM) in children receiving placebo, clonidine 2 micro gram *symbol* kg sup -1, and clonidine 4 micro gram *symbol* kg sup -1, respectively (P < 0.05). Part II: The HR in the control group increased by more than 20 beats *symbol* min sup -1 in response to atropine 20 micro gram *symbol* kg sup -1 or less. In two patients in the clonidine 4 micro gram *symbol* kg sup -1 group, HR did not increase by 20 beats *symbol* min sup -1 even after 40 micro gram *symbol* kg sup -1 of atropine.     

Plasma Inorganic Fluoride Concentrations after Sevoflurane Anesthesia in Children

Background: Sevoflurane is degraded in vivo in adults yielding plasma concentrations of inorganic fluoride [Fluorine sup -] that, in some patients, approach or exceed the 50-micro Meter theoretical threshold for nephrotoxicity. To determine whether the plasma concentration of inorganic fluoride [Fluorine sup -] after 1-5 MAC *symbol* h sevoflurane approaches a similar concentration in children, the following study in 120 children scheduled for elective surgery was undertaken.

Methods: Children were randomly assigned to one of three treatment groups before induction of anesthesia: group 1 received sevoflurane in air/oxygen 30% (n = 40), group 2 received sevoflurane in 70% N2 O/30% O2 (n = 40), and group 3 received halothane in 70% N2 O/30% O sub 2 (n = 40). Mapleson D or F circuits with fresh gas flows between 3 and 6 l/min were used. Whole blood was collected at induction and termination of anesthesia and at 1, 4, 6, 12, and 18 or 24 h postoperatively for determination of the [Fluorine sup -]. Plasma urea and creatinine concentrations were determined at induction of anesthesia and 18 or 24 h postoperatively.

Results: The mean (+/-SD) duration of sevoflurane anesthesia, 2.7+/-1.6 MAC *symbol* h (range 1.1-8.9 MAC *symbol* h), was similar to that of halothane, 2.5+/-1.1 MAC *symbol* h. The peak [Fluorine sup -] after sevoflurane was recorded at 1 h after termination of the anesthetic in all but three children (whose peak values were recorded between 4 and 6 h postanesthesia). The mean peak [Fluorine sup -] after sevoflurane was 15.8+/-4.6 micro Meter. The [Fluorine sup -] decreased to < 6.2 micro Meter by 24 h postanesthesia. Both the peak [Fluorine sup -] (r2 = 0.50) and the area under the plasma concentration of inorganic fluoride-time curve (r2 = 0.57) increased in parallel with the MAC *symbol* h of sevoflurane. The peak [Fluorine sup -] after halothane, 2.0+/-1.2 micro Meter, was significantly less than that after sevoflurane (P < 0.0001) and did not correlate with the duration of halothane anesthesia (MAC *symbol* h; r2 = 0.007). Plasma urea concentrations decreased 24 h after surgery compared with preoperative values for both anesthetics (P < 0.01), whereas plasma creatinine concentrations did not change significantly with either anesthetic.     

Nitrogen Dioxide Production during Mechanical Ventilation with Nitric Oxide in Adults: Effects of Ventilator Internal Volume, Air Versus Nitrogen Dilution, Minute Ventilation, and Inspired Oxygen Fraction

Background: Inhaled nitric oxide (NO) may be useful in the treatment of adult respiratory distress syndrome and other diseases characterized by pulmonary hypertension and hypoxemia. NO is rapidly converted to nitrogen dioxide (NO2) in oxygen (Oxygen2) environments. We hypothesized that in patients whose lungs are mechanically ventilated and in those with a long residence time for NO in the lungs, a clinically important [NO2] may be present. We therefore determined the rate constants for NO conversion in adult mechanical ventilators and in a test lung simulating prolonged intrapulmonary residence of NO.

Methods: NO (800 ppm) was blended with nitrogen (Nitrogen2), delivered to the high-pressure air inlet of a Puritan-Bennett 7200ae or Siemens Servo 900C ventilator, and used to ventilate a test lung. The ventilator settings were varied: minute ventilation (VE) from 5 to 25 l/min, inspired Oxygen2 fraction (FIO2) from 0.24 to 0.87, and [NO] from 10 to 80 ppm. The experiment was then repeated with air instead of Nitrogen2 as the dilution gas. The effect of pulmonary residence time on NO2 production was examined at test lung volumes of 0.5-4.0 l, V with dotE of 5-25 l/min, FIO2 of 0.24-0.87, and [NO] of 10-80 ppm. The inspiratory gas mixture was sampled 20 cm from the Y-piece and from within the test lung. NO and NO sub 2 were measured by chemiluminescence. The rate constant (k) for the conversion of NO to NO2 was determined from the relation 1/[NO]1 1/[NO]0 k x [Oxygen2] x t, where t = residence time.

Results: No NO2 was detected during any trial with V with dot sub E 20 or 25 l/min. With Nitrogen2 dilution and the Puritan- Bennett 7200ae, NO2 (less or equal to 1 ppm) was detected only at a V with dotE of 5 l/min with an FIO2 of 0.87 and [NO] greater or equal to 70 ppm. In contrast, [NO2] values were greater with the Servo 900C ventilator than with the Puritan-Bennett 7200ae at similar settings. When NO was diluted with air, clinically important [NO sub 2] values were measured with both ventilators at high [NO] and FI sub O2. Rate constants were 1.46 x 109 ppm2 *symbol* min sup -1 when NO was mixed with Nitrogen2, 1.17 x 108 ppm sup - 2 *symbol* min sup -1 when NO was blended with air, and 1.44 x 109 ppm sup -2 *symbol* min sup -1 in the test lung.     

pH-Stat Management Reduces the Cerebral Metabolic Rate for Oxygen during Profound Hypothermia (17 degrees Celsius): A Study during Cardiopulmonary Bypass in Rabbits

Background: Greater cerebral metabolic suppression may increase the brain's tolerance to ischemia. Previous studies examining the magnitude of metabolic suppression afforded by profound hypothermia suggest that the greater arterial carbon dioxide tension of pH-stat management may increase metabolic suppression when compared with alpha-stat management.

Methods: New Zealand White rabbits, anesthetized with fentanyl and diazepam, were maintained during cardiopulmonary bypass (CPB) at a brain temperature of 17 degrees Celsius with alpha-stat (group A, n = 9) or pH-stat (group B, n = 9) management. Measurements of brain temperature, systemic hemodynamics, arterial and cerebral venous blood gases and oxygen content, cerebral blood flow (CBF) (radiolabeled microspheres), and cerebral metabolic rate for oxygen (CMRO2) (Fick) were made in each animal at 65 and 95 min of CPB. To control for arterial pressure and CBF differences between techniques, additional rabbits underwent CPB at 17 degrees Celsius. In group C (alpha-stat, n = 8), arterial pressure was decreased with nitroglycerin to values observed with pH-stat management. In group D (pH-stat, n = 8), arterial pressure was increased with angiotensin II to values observed with alpha-stat management. In groups C and D, CBF and CMRO2 were determined before (65 min of CPB) and after (95 min of CPB) arterial pressure manipulation.

Results: In groups A (alpha-stat) and B (pH-stat), arterial pressure; hemispheric CBF (44 plus/minus 17 vs. 21 plus/minus 4 ml *symbol* 100 g sup -1 *symbol* min sup -1 [median plus/minus quartile deviation]; P = 0.017); and CMRO2 (0.54 plus/minus 0.13 vs. 0.32 plus/minus 0.10 ml Oxygen2 *symbol* 100 g sup -1 *symbol* min sup -1; P = 0.0015) were greater in alpha-stat than in pH-stat animals, respectively. As a result of arterial pressure manipulation, in groups C (alpha-stat) and D (pH-stat) neither arterial pressure (75 plus/minus 2 vs. 78 plus/minus 2 mm Hg) nor hemispheric CBF (40 plus/minus 10 vs. 48 plus/minus 6 ml *symbol* 100 g sup -1 *symbol* min sup -1; P = 0.21) differed between alpha-stat and pH-stat management, respectively. Nevertheless, CMRO2 was greater in alpha-stat than in pH-stat animals (0.71 plus/minus 0.10 vs. 0.45 plus/minus 0.10 ml Oxygen2 *symbol* 100 g sup -1 *symbol* min sup -1, respectively; P = 0.002).     

Effects of Recruitment Maneuver on Atelectasis in Anesthetized Children

Background: General anesthesia is known to promote atelectasis formation. High inspiratory pressures are required to reexpand healthy but collapsed alveoli. However, in the absence of positive end-expiratory pressure (PEEP), reexpanded alveoli collapse again. Using magnetic resonance imaging, the impact of an alveolar recruitment strategy on the amount and distribution of atelectasis was tested.

Methods: The authors prospectively randomized 24 children who met American Society of Anesthesiologists physical status I or II criteria, were aged 6 months-6 yr, and were undergoing cranial magnetic resonance imaging into three groups. After anesthesia induction, in the alveolar recruitment strategy (ARS) group, an alveolar recruitment maneuver was performed by manually ventilating the lungs with a peak airway pressure of 40 cm H2O and a PEEP of 15 cm H2O for 10 breaths. PEEP was then reduced to and kept at 5 cm H2O. The continuous positive airway pressure (CPAP) group received 5 cm H2O of continuous positive airway pressure without recruitment. The zero end-expiratory pressure (ZEEP) group received neither PEEP nor the recruitment maneuver. All patients breathed spontaneously during the procedure. After cranial magnetic resonance imaging, thoracic magnetic resonance imaging was performed.

Results: The atelectatic volume (median, first and third standard quartiles) detected in the ZEEP group was 1.25 (0.75-4.56) cm3 in the right lung and 4.25 (3.2-13.9) cm3 in the left lung. The CPAP group had 9.5 (3.1-23.7) cm3 of collapsed lung tissue in the right lung and 8.8 (5.3-28.5) cm3 in the left lung. Only one patient in the ARS group presented an atelectasis of less than 2 cm3. An uneven distribution of the atelectasis was observed within each lung and between the right and left lungs, with a clear predominance of the left basal paradiaphragmatic regions.     

Effects of recruitment maneuver on atelectasis in anesthetized children

BACKGROUND: General anesthesia is known to promote atelectasis formation. High inspiratory pressures are required to reexpand healthy but collapsed alveoli. However, in the absence of positive end-expiratory pressure (PEEP), reexpanded alveoli collapse again. Using magnetic resonance imaging, the impact of an alveolar recruitment strategy on the amount and distribution of atelectasis was tested. METHODS: The authors prospectively randomized 24 children who met American Society of Anesthesiologists physical status I or II criteria, were aged 6 months-6 yr, and were undergoing cranial magnetic resonance imaging into three groups. After anesthesia induction, in the alveolar recruitment strategy (ARS) group, an alveolar recruitment maneuver was performed by manually ventilating the lungs with a peak airway pressure of 40 cm H2O and a PEEP of 15 cm H2O for 10 breaths. PEEP was then reduced to and kept at 5 cm H2O. The continuous positive airway pressure (CPAP) group received 5 cm H2O of continuous positive airway pressure without recruitment. The zero end-expiratory pressure (ZEEP) group received neither PEEP nor the recruitment maneuver. All patients breathed spontaneously during the procedure. After cranial magnetic resonance imaging, thoracic magnetic resonance imaging was performed. RESULTS: The atelectatic volume (median, first and third standard quartiles) detected in the ZEEP group was 1.25 (0.75-4.56) cm3 in the right lung and 4.25 (3.2-13.9) cm3 in the left lung. The CPAP group had 9.5 (3.1-23.7) cm3 of collapsed lung tissue in the right lung and 8.8 (5.3-28.5) cm3 in the left lung. Only one patient in the ARS group presented an atelectasis of less than 2 cm3. An uneven distribution of the atelectasis was observed within each lung and between the right and left lungs, with a clear predominance of the left basal paradiaphragmatic regions. CONCLUSION: Frequency of atelectasis was much less following the alveolar recruitment strategy, compared with children who did not have the maneuver performed. The mere application of 5 cm H2O of CPAP without a prior recruitment did not show the same treatment effect and showed no difference compared to the control group without PEEP.     

Comparison of the Effects of Etomidate, Propofol, and Thiopental on Respiratory Resistance after Tracheal Intubation

Background: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia.

Methods: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction.

Results: Respiratory resistance at 2 min was 8.1+/-3.4 cmH sub 2 O *symbol* l sup -1 *symbol* s (mean+/-SD) for patients receiving propofol versus 11.3+/-5.3 for patients receiving etomidate and 12.3+/-7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental).     

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.     

Tourniquet-induced Exsanguination in Patients Requiring Lower Limb Surgery: An Ischemia-Reperfusion Model of Oxidant and Antioxidant Metabolism

Background: Surgically induced ischemia and reperfusion is frequently accompanied by local and remote organ injury. It was hypothesized that this procedure may produce injurious oxidants such as hydrogen peroxide (H2 O2), which, if unscavenged, will generate the highly toxic hydroxyl radical (*symbol* OH). Accordingly, it was proposed that tourniquet-induced exsanguination for limb surgery may be a useful ischemia-reperfusion model to investigate the presence of oxidants, particularly H2 O2.

Methods: In ten patients undergoing knee surgery, catheters were placed in the femoral vein of the limb operated on for collection of local blood and in a vein of the arm for sampling of systemic blood. Tourniquet-induced limb exsanguination was induced for about 2 h. After tourniquet release (reperfusion), blood samples were collected during a 2-h period for measurement of H2 O2, xanthine oxidase activity, xanthine, uric acid (UA), glutathione, and glutathione disulfide.

Results: At 30 s of reperfusion, H2 O2 concentrations increased ([nearly equal] 90%) from 133+/-5 to 248+/-8 nmol *symbol* ml sup -1 (P < 0.05) in local blood samples, but no change was evident in systemic blood. However, in both local and systemic blood, xanthine oxidase activity increased [nearly equal] 90% (1.91+/- 0.07 to 3.93+/-0.41 and 2.19+/-0.07 to 3.57+/- 0.12 nmol UA *symbol* ml sup -1 *symbol* min sup -1, respectively) as did glutathione concentrations (1.27+/-0.04 to 2.69+/-0.14 and 1.27+/-0.03 to 2.43+/-0.13 micro mol *symbol* ml sup -1, respectively). At 5 min reperfusion, in local blood, H2 O2 concentrations and xanthine oxidase activity peaked at 796+/-38 nmol *symbol* ml sup -1 ([nearly equal] 500%) and 11.69+/-1.46 nmol UA *symbol* ml sup -1 *symbol* min sup -1 ([nearly equal] 520%), respectively. In local blood, xanthine and UA increased from 1.49 +/-0.07 to 8.36+/-0.33 nmol *symbol* ml sup -1 and 2.69 +/-0.16 to 3.90+/-0.18 micro mol *symbol* ml sup -1, respectively, whereas glutathione and glutathione disulfide increased to 5.13+/-0.36 micro mol *symbol* ml sup -1 and 0.514+/- 0.092 nmol *symbol* ml sup -1, respectively. In systemic blood, xanthine oxidase activity peaked at 4.75+/-0.20 UA nmol *symbol* ml sup -1 *symbol* min sup -1. At 10 min reperfusion, local blood glutathione and UA peaked at 7.08+/-0.46 micro mol *symbol* ml sup -1 and 4.67 +/-0.26 micro mol *symbol* ml sup -1, respectively, while the other metabolites decreased significantly toward pretourniquet levels. From 20 to 120 min, most metabolites returned to pretourniquet levels; however, local and systemic blood xanthine oxidase activity remained increased 3.76+/-0.29 and 3.57+/-0.37 nmol UA *symbol* ml sup -1 *symbol* min sup -1, respectively. Systemic blood H2 O2 was never increased during the study. During the burst period ([nearly equal] 5-10 min), local blood H2 O2 concentrations and xanthine oxidase activities were highly correlated (r = 0.999).     

Evaluation of a recruitment maneuver with positive inspiratory pressure and high PEEP in patients with severe ARDS

BACKGROUND: To evaluate the effect of a recruitment maneuver (RM) with constant positive inspiratory pressure and high positive end-expiratory pressure (PEEP) on oxygenation and static compliance (Cs) in patients with severe acute respiratory distress syndrome (ARDS). METHODS: Eight patients with ARDS ventilated with lung-protective strategy and an arterial partial pressure of oxygen to inspired oxygen fraction ratio (PaO2/FIO2) < or =100 mmHg regardless of PEEP were prospectively studied. The RM was performed in pressure-controlled ventilation at FIO2 of 1.0 until PaO2 reached 250 mmHg or a maximal plateau pressure/PEEP of 60/45 cmH2O was achieved. The RM was performed with stepwise increases of 5 cmH2O of PEEP every 2 min and thereafter with stepwise decreases of 2 cmH2O of PEEP every 2 min until a drop in PaO2 >10% below the recruitment PEEP level. Data was collected before (preRM), during and after 30 min (posRM). RESULTS: The PaO2/FIO2 increased from 83 +/- 22 mmHg preRM to 118 +/- 32 mmHg posRM (P = 0.001). The Cs increased from 28 +/- 10 ml cmH2O(-1) preRM to 35 +/- 12 ml cmH2O(-1) posRM (P = 0.025). The PEEP was 12 +/- 3 cmH2O preRM and was set at 15 +/- 4 cmH2O posRM (P = 0.025). The PEEP of recruitment was 36 +/- 9 cmH2O and the collapsing PEEP was 13 +/- 4 cmH2O. The PaO2 of recruitment was 225 +/- 105 mmHg, with five patients reaching a PaO2 > or = 250 mmHg. The FIO2 decreased from 0.76 +/- 0.16 preRM to 0.63 +/- 0.15 posRM (P = 0.001). No major complications were detected. CONCLUSION: Recruitment maneuver was safe and useful to improve oxygenation and Cs in patients with severe ARDS ventilated with lung-protective strategy.     

Anesthetic Potency of Remifentanil in Dogs

Background: Remifentanil is an opioid that is rapidly inactivated by esterases in blood and tissues. This study examined the anesthetic potency and efficacy of remifentanil in terms of its reduction of enflurane minimum alveolar concentration (MAC) in dogs.

Methods: Twenty-five dogs were anesthetized with enflurane. One group received incremental infusion rates of remifentanil from 0.055 to 5.5 micro gram *symbol* kg sup -1 *symbol* min sup -1. A second group received constant rate infusions of remifentanil of 1.0 micro gram *symbol* kg sup -1 *symbol* min sup -1 for 6-8 h. Enflurane MAC was measured before, hourly during remifentanil infusion, and at the end of the experiment after naloxone administration. A third group received alternating infusions of 0.5 and 1.0 micro gram *symbol* kg sup -1 *symbol* min sup -1 with MAC determinations made 30 min after each change in the infusion rate. Heart rate, mean arterial pressure, and remifentanil blood concentrations were measured during MAC determinations.

Results: Enflurane MAC was reduced up to a maximum of 63.0+/- 10.4% (mean+/-SD) in a dose-dependent manner by remifentanil infusion. The dose producing a 50% reduction in the enflurane MAC was calculated as 0.72 micro gram *symbol* kg sup -1 *symbol* min sup -1 and the corresponding blood concentration was calculated as 9.2 ng/ml. Enflurane MAC reduction remained stable during continuous, constant rate infusions for periods of 6-8 h without any signs of tolerance. Recovery of enflurane MAC to baseline occurred in 30 min (earliest measurement) after stopping the remifentanil infusion.     

The pressure at the lower inflexion point has no relation to airway collapse in surfactant-treated premature lambs

BACKGROUND: The lower inflexion point (LIP) on the inspiratory part of the pressure-volume (PV) loop has been suggested to be related to the pressure at which air spaces collapse. Our hypothesis is that airway collapse might instead be assessed from the upper inflexion point on the expiratory part of the PV-loop (UIPexp), where lung volume starts to decrease significantly. We therefore examined whether there was a relation between LIP and UIPexp in premature surfactant-treated lambs. METHODS: Ten lambs, at 119-141 days of gestational age, were delivered by cesarean section and given 200 mg/kg modified natural porcine surfactant before the first breath. The lambs were then connected to a ventilator and PV-loops using airway pressures of 0-35-0 (ZEEP-loop) and 5-35-5 cmH2O (PEEP-loop) were obtained after lung recruitment at 15, 60 and 120 min after birth. From the loops, LIP, UIPexp, upper inflexion point of the inspiratory part of the loop (UIP insp), inspiratory capacity (IC) as well as inspiratory and expiratory maximal compliance of the respiratory system (Crs(insp) and Crs(exp)) were calculated. RESULTS: The ZEEP-loop showed a substantial hysteresis with a distinct LIP at 19+/-2 cmH2O (mean+/-SD), which was different (P<0.001) from UIPexp (9+/-2 cmH2O). The pressures at LIP and UIPexp were unrelated (r2=0.06). UIPinsp was located at 28+/-2 cmH2O. Crs(insp) was 2.1+/-0.6 ml x cmH2O(-1) x kg(-1), which was lower (P<0.001) than Crs(exp) (2.8+/-0.6 ml x cmH2O(-1) x kg(-1)). IC was 26+/-6 ml/kg. The PEEP-loop had a minimal hysteresis with an expiratory part coinciding with that of the ZEEP-loop. CONCLUSION: In surfactant-treated premature lambs the pressures at LIP and UIPexp are not related, showing that LIP does not indicate the pressure at which airways collapse.     

Circulatory Effects of Hypoxia, Acute Normovolemic Hemodilution, and Their Combination in Anesthetized Pigs

Background: Because hemodilution decreases the oxygen-carrying capacity of blood, it was hypothesized that severe hemodilution would decrease the tolerance to alveolar hypoxia.

Methods: Hemodynamics, oxygen transport, and blood lactate concentrations were compared in ten pigs with normal hematocrit (33 +/-4%), and ten hemodiluted pigs (hematocrit 11+/-1%; mean+/-SD) anesthetized with ketamine-fentanyl-pancuronium during stepwise decreases in inspired oxygen fraction (FIO2; 1.0, 0.35, 0.21, 0.15, 0.10, 0.05).

Results: Median systemic oxygen delivery (DO2 SY) became critical (the DO2 SY value when arterial lactate exceeded 2.0 mmol *symbol* l sup -1) at 10.4 ml *symbol* kg sup -1 min sup -1 (range 6.9-16.1) in hemodiluted animals and at 11.8 ml *symbol* kg sup -1 *symbol* min sup -1 (5.9-32.2) in animals with normal hematocrits (NS). The relationship between mixed venous oxygen saturation and arterial lactate values was less consistent and median critical mixed venous oxygen saturation was higher (P < 0.05) in the hemodiluted group (35%, range 21-64), than in animals with normal hematocrits (21%, 7-68%). In animals with normal hematocrit, decreasing FIO2 from 1.0 to 0.10 resulted in a decrease in DO2 SY from 26.3+/-9.1 to 9.3 +/-3.9 ml *symbol* kg sup -1 *symbol* min sup -1 (P < 0.01). Cardiac output did not change, systemic oxygen extraction ratio increased from 0.23+/-0.08 to 0.68+/-0.13 (P < 0.01), and arterial lactate from 0.9+/-0.2 to 3.4+/-3.0 mmol *symbol* l sup -1 (P < 0.05). Cardiac venous blood flow, as measured by retrograde thermodilution, increased from 5.7+/-2.9 to 12.6+/-5.7 ml *symbol* kg sup -1 *symbol* min sup -1 (P < 0.01). When FIO2 was reduced to 0.05, three animals became hypotensive and died. In the second group, hemodilution increased cardiac output and systemic oxygen extraction ratio (P < 0.01). Cardiac venous blood flow increased from 4.1 +/-1.7 to 9.8+/-5.1 ml *symbol* kg sup -1 *symbol* min sup -1 (P < 0.01), and cardiac venous oxygen saturation from 22+/- 5 to 41+/-10% (P < 0.01). During the subsequent hypoxia, cardiac output and DO2 SY were maintained until FIO2 = 0.15 (DO2 SY = 10.1+/-3.3 ml *symbol* kg sup -1 *symbol* min sup -1). Cardiac venous blood flow was then 18.5+/-10.7 ml *symbol* kg sup -1 *symbol* min sup -1 (P < 0.01), but in spite of this, myocardial lactate production occurred. At FIO2 = 0.10 (DO2 SY = 7.7 +/-3.0 ml *symbol* kg sup -1 *symbol* min sup -1), arterial lactate concentration increased to 8.5+/-2.3 mmol *symbol* l sup -1 (P < 0.01), and most animals became hypotensive. All hemodiluted animals died when FIO2 was decreased to 0.05 (P < 0.01 when compared to animals with normal hematocrit).     

Recruitment maneuver and high PEEP in a patient with severe reperfusion pulmonary edema after pulmonary thromboendarterectomy

Recently open lung approach such as recruitment maneuver and high PEEP has been applied in patients with acute respiratory distress syndrome. We report here a 29-year-old man with chronic pulmonary thromboembolism (CPTE). In this case, recruitment maneuver and high PEEP relieved postoperative respiratory failure. The major complications after pulmonary thromboendarterectomy (PTE) for CPTE are: reperfusion pulmonary edema (RPE), pulmonary hypertension (PH), hypoxia and bronchial bleeding, all of which the patient has demonstrated. Preoperative examination showed high pulmonary artery pressure (85/41, mean 50 mmHg), and high pulmonary vascular resistance predicted poor postoperative course. After PTE, he developed severe RPE, PH, hypoxia and bronchial bleeding, resulting in failed weaning from cardiopulmonary bypass. Therefore he required mechanical support of percutaneous cardiopulmonary support (PCPS). In ICU we repeated recruitment maneuver (PEEP: 30 cmH2O, peak inspiratory pressure: 42 cmH2O, respiratory rate; 15 breaths.min-1, for 1 min) and kept high PEEP (15 cmH2O). After initiating this ventilatory strategy, RPE was gradually relieved, followed by improvement of oxygenation and PH. We successfully weaned him from PCPS 38 hr after surgery and he was discharged alive on the 90 post-operative day. We conclude that recruitment maneuver and high PEEP may be useful for RPE developed after PTE.     

Effects of lung recruitment maneuver and positive end-expiratory pressure on lung volume,respiratory mechanics and alveolar gas mixing in patients ventilated after cardiac surgery

BACKGROUND: It is unclear whether positive end-expiratory pressure (PEEP) is needed to maintain the improved oxygenation and lung volume achieved after a lung recruitment maneuver in patients ventilated after cardiac surgery performed in the cardiopulmonary bypass (CPB). METHODS: A prospective, randomized, controlled study in a university hospital intensive care unit. Sixteen patients who had undergone cardiac surgery in CPB were studied during the recovery phase while still being mechanically ventilated with an inspired fraction of oxygen (FiO2) 1.0. Eight patients were randomized to lung recruitment (two 20-s inflations to 45 cmH2O), after which PEEP was set and kept for 2.5 h at 1 cmH2O above the pressure at the lower inflexion point (14+/-3 cmH2O, mean +/-SD) obtained from a static pressure-volume (PV) curve (PEEP group). The remaining eight patients were randomized to a recruitment maneuver only (ZEEP group). End-expiratory lung volume (EELV), series dead space, ventilation homogeneity, hemodynamics and PaO2 (oxygenation) were measured every 30 min during a 3-h period. PV curves were obtained at baseline, after 2.5 h, and in the PEEP group at 3 h. RESULTS: In the ZEEP group all measures were unchanged. In the PEEP group the EELV increased with 1220+/-254 ml (P<0.001) and PaO2 with 16+/-16 kPa (P<0.05) after lung recruitment. When PEEP was discontinued EELV decreased but PaO2 was maintained. The PV curve at 2.5 h coincided with the curve obtained at 3 h, and both curves were both steeper than and located above the baseline curve. CONCLUSIONS: Positive end-expiratory pressure is required after a lung recruitment maneuver in patients ventilated with high FiO2 after cardiac surgery to maintain lung volumes and the improved oxygenation.