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 (O2) 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% O2 causes atelectasis and should be followed by a recruitment maneuver (inflation to an airway pressure of 40 cm H2O for 10 s and to higher airway pressures in patients with reduced abdominal compliance (obese and patients with abdominal disorders). Pre‐oxygenation with 80% O2 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% O2. A continuous PEEP of 7–10 cm H2O 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.
The recording of esophageal pressure (Pes) in supine position as a substitute for pleural pressure is difficult and fraught with potential errors. Pes is affected by the: 1) elastance and weight of ...the lung; 2) elastance and weight of the rib cage; 3) weight of the mediastinal organs; 4) elastance and weight of the diaphragm and abdomen; 5) elastance of the esophageal wall; and 6) elastance of the esophageal balloon (if filled with too much air). If the purpose is to measure lung compliance in the intensive care patient, reasonably useful information might be obtained by measuring airway pressure alone, considering chest wall compliance to be a weight that is forced away by the ventilation. Such weight requires a constant pressure for displacement. The transpulmonary pressure, whether calculated with Pes or by another measure of abdominal pressure, may guide in PEEP titration. It may also enable calculation of stresses applied to the lung and these may be more important in guiding an optimal ventilator setting than an optimum compliance or oxygenation of blood. Diaphragm function can be estimated by esophageal minus gastric pressure and with even more precision, when combined with diaphragm electromyography.
Inhalation of nitric oxide (NO) improved arterial oxygenation and enabled the reduction of inspired oxygen therapy and airway pressure support in patients with severe acute respiratory syndrome ...(SARS). In addition, chest radiography showed decreased spread or density of lung infiltrates, and the physiological effects remained after termination of inhaled NO therapy. These findings suggest not only a pulmonary vasodilator effect of inhaled NO, but also an effect on SARS.
Tidal recruitment/derecruitment (R/D) of collapsed regions in lung injury has been presumed to cause respiratory oscillations in the partial pressure of arterial oxygen (PaO2). These phenomena have ...not yet been studied simultaneously. We examined the relationship between R/D and PaO2 oscillations by contemporaneous measurement of lung-density changes and PaO2.
Five anaesthetised pigs were studied after surfactant depletion via a saline-lavage model of R/D. The animals were ventilated with a mean fraction of inspired O2 (FiO2) of 0.7 and a tidal volume of 10 ml kg−1. Protocolised changes in pressure- and volume-controlled modes, inspiratory:expiratory ratio (I:E), and three types of breath-hold manoeuvres were undertaken. Lung collapse and PaO2 were recorded using dynamic computed tomography (dCT) and a rapid PaO2 sensor.
During tidal ventilation, the expiratory lung collapse increased when I:E <1 mean (standard deviation) lung collapse=15.7 (8.7)%; P<0.05, but the amplitude of respiratory PaO2 oscillations 2.2 (0.8) kPa did not change during the respiratory cycle. The expected relationship between respiratory PaO2 oscillation amplitude and R/D was therefore not clear. Lung collapse increased during breath-hold manoeuvres at end-expiration and end-inspiration (14% vs 0.9–2.1%; P<0.0001). The mean change in PaO2 from beginning to end of breath-hold manoeuvres was significantly different with each type of breath-hold manoeuvre (P<0.0001).
This study in a porcine model of collapse-prone lungs did not demonstrate the expected association between PaO2 oscillation amplitude and the degree of recruitment/derecruitment. The results suggest that changes in pulmonary ventilation are not the sole determinant of changes in PaO2 during mechanical ventilation in lung injury.
Aeroatelectasis has developed in aircrew flying routine peacetime flights on the latest generation high-performance aircraft, when undergoing excessive oxygen supply. To single out the effects of ...hyperoxia and hypergravity on lung tissue compression, and on ventilation and perfusion, eight subjects were studied before and after 1 h 15 min exposure to +1 to +3.5 Gz in a human centrifuge. They performed the protocol three times, breathing air, 44.5% O2, or 100% O2 and underwent functional and topographical imaging of the whole lung by ultrasound and single-photon emission computed tomography combined with computed tomography (SPECT/CT). Ultrasound lung comets (ULC) and atelectasis both increased after exposure. The number of ULC was <1 pre protocol (i.e., normal lung) and larger post 100% O2 (22 ± 3, mean ± SD) than in all other conditions (P < 0.001). Post 44.5% O2 differed from air (P < 0.05). Seven subjects showed low- to medium-grade atelectasis post 100% O2 There was an effect on grade of gas mixture and hypergravity, with interaction (P < 0.001, respectively); 100% O2, 44.5% O2, and air differed from each other (P < 0.05). SPECT ventilation and perfusion were always normal. Ultrasound concurred with CT in showing normal lung in the upper third and ULC/atelectasis in posterior and inferior areas, not for other localizations. In conclusion, hyperoxia and hypergravity are independent risk factors of reversible atelectasis formation. Ultrasound is a useful screening tool. Together with electrical impedance tomography measurements (reported separately), these findings show that zones with decreased ventilation prone to transient airway closure are present above atelectatic areas.
Background
Studies aimed at maintaining intraoperative lung volume to reduce post‐operative pulmonary complications have been inconclusive because they mixed up the effect of general anesthesia and ...the surgical procedure. Our aims were to study: (1) lung volume during the entire course of anesthesia without the confounding effects of surgical procedures; (2) the combination of three interventions to maintain lung volume; and (3) the emergence phase with focus on the restored activation of the respiratory muscles.
Methods
Eighteen ASA I–II patients undergoing ENT surgery under general anesthesia without muscle relaxants were randomized to an intervention group, receiving lung recruitment maneuver (LRM) after induction, 7 cmH2O positive end‐expiratory pressure (PEEP) during anesthesia and continuous positive airway pressure (CPAP) during emergence with 0.4 inspired oxygen fraction (FiO2) or a control group, ventilated without LRM, with 0 cmH2O PEEP, and 1.0 FiO2 during emergence without CPAP application. End‐expiratory lung volume (EELV) was continuously estimated by opto‐electronic plethysmography. Inspiratory and expiratory ribcage muscles electromyography was measured in a subset of seven patients.
Results
End‐expiratory lung volume decreased after induction in both groups. It remained low in the control group and further decreased at emergence, because of active expiratory muscle contraction. In the intervention group, EELV increased after LRM and remained high after extubation.
Conclusion
A combined intervention consisting of LRM, PEEP and CPAP during emergence may effectively maintain EELV during anesthesia and even after extubation. An unexpected finding was that the activation of the expiratory muscles may contribute to EELV reduction during the emergence phase.
Background
Carbon dioxide insufflation into the pleural cavity, capnothorax, with one‐lung ventilation (OLV) may entail respiratory and hemodynamic impairments. We investigated the online ...physiological effects of OLV/capnothorax by electrical impedance tomography (EIT) in a porcine model mimicking the clinical setting.
Methods
Five anesthetized, muscle‐relaxed piglets were subjected to first right and then left capnothorax with an intra‐pleural pressure of 19 cm H2O. The contra‐lateral lung was mechanically ventilated with a double‐lumen tube at positive end‐expiratory pressure 5 and subsequently 10 cm H2O. Regional lung perfusion and ventilation were assessed by EIT. Hemodynamics, cerebral tissue oxygenation and lung gas exchange were also measured.
Results
During right‐sided capnothorax, mixed venous oxygen saturation (P = 0.018), as well as a tissue oxygenation index (P = 0.038) decreased. There was also an increase in central venous pressure (P = 0.006), and a decrease in mean arterial pressure (P = 0.045) and cardiac output (P = 0.017). During the left‐sided capnothorax, the hemodynamic impairment was less than during the right side. EIT revealed that during the first period of OLV/capnothorax, no or very minor ventilation on the right side could be seen (3 ± 3% vs. 97 ± 3%, right vs. left, P = 0.007), perfusion decreased in the non‐ventilated and increased in the ventilated lung (18 ± 2% vs. 82 ± 2%, right vs. left, P = 0.03). During the second OLV/capnothorax period, a similar distribution of perfusion was seen in the animals with successful separation (84 ± 4% vs. 16 ± 4%, right vs. left).
Conclusion
EIT detected in real‐time dynamic changes in pulmonary ventilation and perfusion distributions. OLV to the left lung with right‐sided capnothorax caused a decrease in cardiac output, arterial oxygenation and mixed venous saturation.
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.
Tidal recruitment/derecruitment (R/D) of collapsed regions in lung injury has been presumed to cause respiratory oscillations in the partial pressure of arterial oxygen (PaO
). These phenomena have ...not yet been studied simultaneously. We examined the relationship between R/D and PaO
oscillations by contemporaneous measurement of lung-density changes and PaO
.
Five anaesthetised pigs were studied after surfactant depletion via a saline-lavage model of R/D. The animals were ventilated with a mean fraction of inspired O
(FiO
) of 0.7 and a tidal volume of 10 ml kg
. Protocolised changes in pressure- and volume-controlled modes, inspiratory:expiratory ratio (I:E), and three types of breath-hold manoeuvres were undertaken. Lung collapse and PaO
were recorded using dynamic computed tomography (dCT) and a rapid PaO
sensor.
During tidal ventilation, the expiratory lung collapse increased when I:E <1 mean (standard deviation) lung collapse=15.7 (8.7)%; P<0.05, but the amplitude of respiratory PaO
oscillations 2.2 (0.8) kPa did not change during the respiratory cycle. The expected relationship between respiratory PaO
oscillation amplitude and R/D was therefore not clear. Lung collapse increased during breath-hold manoeuvres at end-expiration and end-inspiration (14% vs 0.9-2.1%; P<0.0001). The mean change in PaO
from beginning to end of breath-hold manoeuvres was significantly different with each type of breath-hold manoeuvre (P<0.0001).
This study in a porcine model of collapse-prone lungs did not demonstrate the expected association between PaO
oscillation amplitude and the degree of recruitment/derecruitment. The results suggest that changes in pulmonary ventilation are not the sole determinant of changes in PaO
during mechanical ventilation in lung injury.
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