Atelectasis: anesthesia-induced
Pretest
True or false
Question 1
1. That anesthesia and surgery are regularly accompanied by impaired oxygenation of the blood has been known for more than 50 years.
2. Atelectasis was early suspected as a cause of the impaired oxygenation, but it was not until the 1980s that atelectasis was demonstrated by means of computed tomography.
3. Atelectasis can be seen in 9 of 10 patients during anesthesia. It may look small on a computed tomography scan, covering on average 3-4% of the transverse thoracic area, but this corresponds to 10-15% of the lung tissue, since there is more tissue in the atelectatic zone per picture element (pixel) than in the aerated lung area.
4. The atelectasis can easily exceed 25% of the total lung tissue, even in an uneventful anesthesia, and it can involve one-half of the lung tissue postoperatively after cardiac surgery.
Question 2
True or false
1. The atelectasis remains for a couple of days after surgery. One may thus conclude that what can be seen as a postoperative atelectasis most likely was formed before surgery.
2. The mechanism of the anesthesia-induced atelectasis needs two prerequisites:
A decrease in lung volume [functional residual capacity (FRC)], so that a closed gas pocket is created; and absorption of gas from the pocket.
3. The decrease in FRC seems to be caused by loss of respiratory muscle tone. An anesthetic that preserves tone, ketamine, appears not to lower FRC and does not cause atelectasis.
4. Tensing of the diaphragm by phrenic nerve stimulation reduces the atelectasis; also, atelectasis is not produced if preoxygenation is avoided, even though the anesthetic may have reduced muscle tone and FRC.
Keyword
The preoxygenation is well established and well founded as a precaution to prevent severe hypoxia in case of a difficult and prolonged intubation of the airway.
However, since preoxygenation is a major cause of atelectasis during the ensuing anesthesia, it may be appropriate to discuss how it should be done.
Breathing 30% oxygen during induction of anesthesia eliminates atelectasis formation, but it certainly increases the risk of hypoxia if the access to the airway is troubled.
Because the fall in FRC is another prerequisite for collapse to occur, it can be of interest to know when FRC falls and whether the fall can be prevented.
Continuous measurement of the end-expiratory level during induction of anesthesia shows that there is an almost immediate drop in the expiratory level, within seconds, when anesthesia is commenced.
The breathing against a positive end-expiratory pressure (PEEP) or continuous positive airway pressure can counter the fall, but a continuous pressure will be difficult to maintain, e.g., during the intubation of the airway.
FRC can, of course, be rapidly restored as soon as the intubation has been ensured. The application of a PEEP of 10 cmH2O can reduce the atelectasis, as might be expected, but the effect is not lasting if the PEEP is discontinued: the atelectasis recurs within 1 min.
If the atelectasis is eliminated by a vital capacity maneuver, the effect lasts for 0.5 h or more, provided that the oxygen fraction is low (0.4 has been tested).
A vital capacity maneuver stimulates the release and/or the distribution of the surfactant material out on the alveolar surface and peripheral ducts, restoring the stability of the tissue.
PEEP, on the other hand, does not promote the release and distribution of the surfactant and, therefore, does not restore the stability of the tissue.
Once the PEEP is discontinued, the lung recollapses.
http://jap.physiology.org/cgi/content/full/86/4/1114
Post test
Question 1
TTTT
Question 2
TTTT