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fiO2

Discussion in 'Anesthesiology' started by Precedex, 02.20.10.

  1. Precedex

    Precedex New Member

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    Was wondering what your thoughts are on fiO2 management for routine cases in reasonably healthy patients. So not talking about pneumonectomies or bronchs or laser airway surgery or the patient with pulmonary fibrosis on home O2. Also I am only referring to cases where you are NOT using nitrous, just air/oxygen. But curious about what reasoning/literature guides your thinking. Specifically, do you think that 100% O2 is bad and what evidence supports that? I have had a hard time finding answers to that question. I know there is some data supporting using 80% fiO2 to reduce wound infection but how strong do you think that is?

    Thanks
  2. aredoubleyou

    aredoubleyou Senior Member

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    For a pt in the ICU on the vent for days, no doubt o2 toxicity is a concern. For a routine case, I believe, the extrapolation of o2 toxicity (in adults) is an academic concern. I think it doesnt make any diffenrece if you use 30% or 100% for 6 hours.
  3. Matty44

    Matty44 AA-C

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    [​IMG][​IMG]This is a good read...

    http://0-www.rcjournal.com.novacat.nova.edu/contents/06.03/06.03.0611.pdf

    I don't know if the link will work for sure, but its an article by John Downs, who gives an interesting take on FiO2. He also has another article titled "Fallacies regarding oxygen therapy" which I have a PDF version of but couldn't find a link. Definitely worth reading IMHO.
  4. Noyac

    Noyac SDN Advisor SDN Advisor

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    I typically use 100% O2 on healthy pts for routine cases. Less nausea possibly and I am at elevation so I am starting off behind the eightball. I start mixing in air as the cases get more lengthy and the pts get more sick.
  5. proman

    proman Member Moderator

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    100% oxygen unless there's a reason not to. For patients remaining intubated I try to wean the FiO2 to 40% at the end so that the RTs set the vent there (it's the only way I've found that they'll go straight to 40).
  6. Planktonmd

    Planktonmd Moderator Emeritus Lifetime Donor

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    80% on all
  7. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    Sometimes you are just spot on! 80% is significantly "better" than 100% for helping to reduce atelectasis. While I usually use 40-55% that is preference and not backed up by any hard data. One could argue that 30-80% for routine cases is fine.

    See my next post for data.
  8. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    © The Board of Management and Trustees of the British Journal of Anaesthesia 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

    Just a little oxygen to breathe as you go off to sleep...is it always a good idea?

    Administration of oxygen 100% to patients before inducing anaesthesia provides a reserve of oxygen, mostly in the patient's functional residual capacity (FRC), to extend the time before hypoxia occurs, should there be difficulties achieving adequate ventilation after induction. Preoxygenation is now widely used, and in the operating theatres in which I work, the practice has extended beyond the anaesthetists to nursing staff and operating department practitioners, who now automatically apply a face mask to the patient while I administer the induction agents. An editorial in 2004 argued that routine preoxygenation ‘could be recommended to the profession regardless of the experience, expertise or grade of the practitioner, and mandated for trainees’.1 The author of this recommendation, and the enthusiastic theatre staff, all make the assumption that administering oxygen 100% is harmless. In his translation of the Hippocratic oath, Galen put great emphasis on the phrase primum non nocere (first, do no harm) and this tenet should be applied to the use of oxygen 100% before it becomes an accepted practice in all patients.

    Oxygen toxicity has been known to occur for many decades. Despite ubiquitous and multiple cellular defence mechanisms, all mammals are sensitive to high concentrations of oxygen, with death occurring within a few days of exposure to oxygen 100%,2 although among mammalian species humans tolerate hyperoxia relatively well. The likelihood of toxicity is a function of both oxygen partial pressure and duration of exposure. Breathing oxygen 100% at one atmosphere absolute pressure for <12 h has no known detrimental effects in humans. Beyond 12 h, the classic symptoms of an urge to take deep breaths, chest pain, and cough occur, and after 24 h forced vital capacity is reduced, indicating early lung injury. In terms of causing pulmonary oxygen toxicity, preoxygenation in the anaesthetic room for 3–5 min is, therefore, harmless.
    Indirect adverse effects of breathing oxygen 100% are far more applicable to anaesthetic practice. Atelectasis, or collapse of small regions of lung, occurs in a majority of patients having a general anaesthetic involving muscle relaxation and artificial ventilation.2 This results from changes in the shape of the chest wall, spine, and diaphragm, causing a reduction in FRC and the volume of specific areas of the chest, particularly in the dependent areas of lung and behind the diaphragm. Three mechanisms contribute to lung collapse. First, compression atelectasis occurs when lung regions are reduced in volume to such an extent that the air is effectively squeezed out. Secondly, absorption atelectasis when airway closure is followed by absorption of the gases distal to the airway leading to complete collapse of the alveoli. Thirdly, atelectasis may occur when airways are extremely narrow, but not closed, when the rate at which alveolar gas is absorbed into the blood exceeds the rate at which gas can flow through the narrow airway to replace it, accelerating airway closure and alveolar collapse. When breathing oxygen 100%, this is likely to occur in lung regions with a [​IMG]/[​IMG] ratio of <0.05.3 Using the multiple inert gas elimination technique, areas of lung with [​IMG]/[​IMG] ratios this low are easily demonstrated in the elderly when awake, and during general anaesthesia in patients of all ages. In vivo it is likely that all three mechanisms are at work simultaneously in different lung regions. In dependent regions behind the diaphragm, compression atelectasis will occur as a result of the weight of the abdominal contents in the absence of diaphragmatic muscle tone, a situation more likely to occur in obesity and in the presence of increased intra-abdominal pressure. In other dependent areas of the lung, the reduced FRC during anaesthesia will lead to resting lung volumes falling below the closing capacity, leading to airway closure and absorption atelectasis. In regions of lung bordering these dependent areas, airway narrowing will reduce the [​IMG]/[​IMG] ratio below the threshold needed for collapse to occur.
    Atelectasis during anaesthesia can be detected using computerized tomography (CT) scans, usually involving a single lung slice taken immediately cranial to the dome of the right diaphragm. The amount of atelectasis is quantified by measuring the cross-sectional area of the atelectasis, expressed as a percentage of the total cross-section of lung on that CT slice. The percentages obtained by this technique seem small, but it must be remembered that each 1% of atelectasis on a cross-sectional CT scan represents around 3% of normally expanded lung volume. Surrogate measures of the amount of atelectasis during anaesthesia are often used, such as calculating the alveolar-arterial Po2 difference or PaO2:F[SIZE=-2]I[/SIZE]O2 ratio.
    When airway closure or narrowing occurs, absorption atelectasis is greatly influenced by the gas mixture present in the alveolus. When breathing air, the partial pressure of all gases present in mixed venous blood is about 87 kPa, compared with 95 kPa in the alveolar gas.2 This difference of 8 kPa arises because water vapour is only present in alveolar gas, carbon dioxide carriage in the blood is mostly as dissolved bicarbonate rather than carbon dioxide gas in solution, and because of the small alveolar to arterial P[SIZE=-2]O[/SIZE]2 difference caused by venous admixture. To keep the alveoli open in the normal healthy lung, this difference of 8 kPa must be countered by the elastic recoil of the respiratory system. When breathing oxygen 100%, the alveolar P[SIZE=-2]N[/SIZE]2 will fall quickly, and for a short time nitrogen will diffuse from the blood into the alveolus and so mitigate against alveolar collapse. However, once blood P[SIZE=-2]N[/SIZE]2 becomes negligible, the total partial pressure of gas in the mixed venous blood, even when breathing oxygen 100%, decreases to just 12.5 kPa (P[SIZE=-2]O[/SIZE]2 of 6.4 kPa and P[SIZE=-2]CO[/SIZE]2 of 6.1 kPa) whereas that of the alveolus remains unchanged, so introducing a pressure gradient of more than 80 kPa resulting in rapid transfer of oxygen across the alveolar-capillary barrier and alveolar collapse. Mathematical modelling of absorption atelectasis during anaesthesia has been used to predict the time taken for an area of unventilated lung to collapse after induction of anaesthesia.4 This model supports the physiological principles already described by predicting that the rate at which collapse occurs is related to the F[SIZE=-2]I[/SIZE]O2 during anaesthesia and that preoxygenation for 3 min substantially reduces the time taken for collapse to occur irrespective of the F[SIZE=-2]I[/SIZE]O2 used after induction.
    Do these physiological principles impact on clinical practice, in particular the role of oxygen 100% and absorption atelectasis? It is now more than a decade since CT studies first demonstrated that preoxygenation leads to greater areas of atelectasis after induction.5 For example, if F[SIZE=-2]I[/SIZE]O2 before induction is 0.3, 0.6, 0.8, or 1.0, the mean percentage of atelectasis seen on CT scans post-induction is 0.2%, 0.2%, 1.3%, and 5.6% respectively.5 6 Re-expansion of atelectasis during anaesthesia (discussed later), usually provoked by falling oxygen saturation, is another time when oxygen 100% is often used. In a study, again using CT scanning, use of an F[SIZE=-2]I[/SIZE]O2 of 1.0 during the re-expansion manoeuvre led to recurrence of the atelectasis in 5 min whereas the lung remained expanded for more than 40 min when F[SIZE=-2]I[/SIZE]O2 was 0.4.7 Finally, administering oxygen 100% before extubation also worsens atelectasis. CT scans performed 20 min post-extubation in groups randomly assigned to be ventilated with an F[SIZE=-2]I[/SIZE]O2 of 0.4 or 1.0 before extubation were found to have 2.6% and 8.3% atelectasis, respectively.8 The presence of more than 8% atelectasis immediately after operation is clinically very significant as re-expansion of this collapsed lung after major surgery may take some days.
    Not all studies of atelectasis and anaesthesia have given such a clear link between F[SIZE=-2]I[/SIZE]O2 and atelectasis. Maintenance of anaesthesia with an F[SIZE=-2]I[/SIZE]O2 of either 0.3 or 0.8 found no significant difference in the amount of atelectasis 24 h after operation (2.5% vs 3.0%, respectively).9 However, despite the lack of statistical difference between the groups in this small study, only four of 14 patients with an intraoperative FIO2 of 0.3 had more than 2% atelectasis after operation compared with 10 of 14 in the FIO2 of 0.8 group. These results also provide some reassurance that the atelectasis seen so commonly during anaesthesia may be partially resolved 24 h after the anaesthetic.
    Collectively, these studies offer good evidence that the amount of atelectasis during anaesthesia increases significantly with increasing FIO2 and that the use of oxygen 100% at any stage of an anaesthetic is associated with significant pulmonary collapse. Reducing FIO2, even by a small amount to 0.8, seems to be substantially better than using oxygen alone.
    Either nitrogen or nitrous oxide may be used to reduce the F[SIZE=-2]I[/SIZE]O2. Mathematical modelling predicts that the two gases should have similar effects on the time taken for gas to be absorbed from an unventilated lung unit.4 However, this prediction over-simplifies the clinical situation, which will be influenced by the timing of the closure of the airway during the anaesthetic. If nitrous oxide is used immediately after induction and airway closure occurs in the first few minutes of the anaesthetic, when the alveolar to arterial P[SIZE=-2]N[/SIZE]2[SIZE=-2]O[/SIZE] gradient is large, then absorption of N2O from the alveolus will be rapid and faster than the diffusion of any remaining nitrogen from the blood into the alveolus. Under this combination of circumstances, atelectasis is likely to occur. Should airway closure occur later in the anaesthetic when alveolar and arterial P[SIZE=-2]N[/SIZE]2[SIZE=-2]O[/SIZE] are similar, then little gas exchange will occur between the blood and alveolus beyond the closed airway, and the alveolus should remain expanded. Clinical support for these observations is sparse, with only one study comparing F[SIZE=-2]I[/SIZE]O2 of 0.4 in nitrogen or N2O.10 This study, which used PaO2:F[SIZE=-2]I[/SIZE]O2 ratio to indirectly estimate the amount of atelectasis 30 min after induction, found that nitrous oxide at this early stage of an anaesthetic did indeed behave in a similar fashion to oxygen 100%. Thus, it seems that if N2O is part of the anaesthetic technique from the outset, then atelectasis may be more frequent than when ventilation is with oxygen and air.
    Re-expansion of atelectasis is possible for a patient who has a tracheal tube, and two techniques are described. The first involves increasing positive end-expiratory pressure (PEEP) to 15 cm H2O, followed by an increase in tidal volume until peak inspiratory pressure reaches 40 cm H2O. This pattern of ventilation is then maintained for 10 breaths, before returning to standard ventilator settings.11 The second involves a vital capacity manoeuvre to a sustained airway pressure of 40 cm H2O, which in the original studies was maintained for either 15 or 25 s.12 13 On the basis of subsequent CT scan studies, when using this technique half the atelectasis is re-expanded after just 2 s, and in three-quarters of patients all the atelectasis is re-expanded in 8 s.13 At these high inflation pressures, there are benefits to minimizing the duration, particularly to reduce the cardiovascular effects of this prolonged and severe Valsalva manoeuvre and to minimize the small risk of pulmonary barotrauma. Prevention of atelectasis can be achieved with modest levels of PEEP, with 10 cm H2O preventing atelectasis formation even when high F[SIZE=-2]I[/SIZE]O2 is used.14 Continuous positive airway pressure (CPAP) of 6 cm H2O applied via a tight fitting facemask before induction is also effective at preventing atelectasis formation, again despite using oxygen 100%, although this is a rather invasive technique to be used routinely.15
    Use of oxygen 100% before and during anaesthesia will always be necessary in some patients. These include patients with a known difficult airway, a reduced FRC and therefore oxygen reserve (term pregnancy, obesity, abdominal distension, and lung pathology), an increased oxygen consumption (pregnancy, paediatrics, and sepsis), or pre-existing hypoxia from lung pathology. In these situations, an effective technique of preoxygenation16 should continue to be used and should always be followed, whenever possible, by a properly administered re-expansion manoeuvre and PEEP then used to prevent atelectasis reforming. In patients who are hypoxic before induction, the use of CPAP before and during induction should be considered.
    In other groups of patients, where the reasons for using oxygen 100% are less compelling but the anaesthetist wants the security provided by greater oxygen reserves than found when breathing air, use of FIO2 of 0.8 or 0.6 should be considered. Several minutes of protection from desaturation will still be obtained, and the possibility of atelectasis during anaesthesia and into the postoperative period will be reduced. In practice, the casual preoxygenation referred to at the start of this editorial usually involves a short exposure to an inadequate flow of oxygen with an ineffective seal between the mask and the patient. This type of preoxygenation will rarely achieve an F[SIZE=-2]I[/SIZE]O2 high enough to contribute to atelectasis formation, but neither will it significantly prolong the time to hypoxia if ventilation should prove impossible. If breathing additional oxygen is considered desirable before induction and the anaesthetist is content to avoid oxygen 100%, then the required F[SIZE=-2]I[/SIZE]O2 should still be delivered using the same technique as for preoxygenation1617 but with some added air.
    The same considerations should be applied to the use of oxygen 100% during re-expansion manoeuvres and before extubation. Unfortunately, the groups of patients in whom atelectasis may be particularly detrimental are the same groups as listed above in whom use of oxygen 100% is more strongly indicated, so as usual clinicians must compromise between two opposing requirements.
    A. B. Lumb St James's University Hospital Leeds UK
  9. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    Collectively, these studies offer good evidence that the amount of atelectasis during anaesthesia increases significantly with increasing FIO2 and that the use of oxygen 100% at any stage of an anaesthetic is associated with significant pulmonary collapse. Reducing FIO2, even by a small amount to 0.8, seems to be substantially better than using oxygen alone.


    Thus, it seems that if N2O is part of the anaesthetic technique from the outset, then atelectasis may be more frequent than when ventilation is with oxygen and air.
  10. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    [SIZE=+1]References[/SIZE]
    1 Bell MDD. Routine pre-oxygenation—a new ‘minimum standard’ of care? Anaesthesia (2004) 59:943–5.[CrossRef][Web of Science][Medline]
    2 Lumb AB. Nunn's Applied Respiratory Physiology (2005) 6th Edn. London: Elsevier Butterworth Heinemann.
    3 Dantzker DR, Wagner PD, West JB. Instability of lung units with low VA/Q ratios during O2 breathing. J Appl Physiol (1975) 38:886–95.[Web of Science]
    4 Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anesthesia: a mathematical model. J Appl Physiol (1999) 86:1116–25.[Abstract/Free Full Text]
    5 Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology (2003) 98:28–33.[CrossRef][Web of Science][Medline]
    6 Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G. Prevention of atelectasis during general anaesthesia. Lancet (1996) 345:1387–91.[CrossRef][Web of Science]
    7 Rothen HU, Sporre B, Engberg G, Wegenius G, Högman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuvre during general anesthesia. Anesthesiology (1995) 82:832–42.[CrossRef][Web of Science][Medline]
    8 Benoit Z, Wicky S, Fischer J-F, et al. The effect of increased F[SIZE=-2]I[/SIZE]O2 before tracheal extubation on postoperative atelectasis. Anesth Analg (2002) 95:1777–81.[Abstract/Free Full Text]
    9 Akça O, Podolsky A, Eisenhuber E, et al. Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology (1999) 91:991–8.[CrossRef][Web of Science][Medline]
    10 Agarwal A, Singh PK, Dhiraj S, Pandey CM, Singh U. Oxygen in air (FiO2 0.4) improves gas exchange in young healthy patients during general anesthesia. Can J Anaesth (2002) 49:1040–3.[Web of Science][Medline]
    11 Tusman G, Böhm SH, Vazquez de Anda GF, do Campo JL, Lachmann B. ‘Alveolar recruitment strategy’ improves arterial oxygenation during general anaesthesia. Br J Anaesth (1999) 82:8–13.[Abstract/Free Full Text]
    12 Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth (1993) 71:788–95.[Abstract/Free Full Text]
    13 Rothen HU, Neumann P, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Dynamics of re-expansion of atelectasis during general anaesthesia. Br J Anaesth (1999) 82:551–6.[Abstract/Free Full Text]
    14 Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand (1999) 43:295–301.[CrossRef][Web of Science][Medline]
    15 Rusca M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg (2003) 97:1835–9.[Abstract/Free Full Text]
    16 Benumof JL. Preoxygenation. Best method for both efficacy and efficiency? Anesthesiology (1999) 91:603–5.[CrossRef][Web of Science][Medline]
    17 McGowan P, Skinner A. Preoxygenation—the importance of a good face mask seal. Br J Anaesth (1995) 75:777–8.[Abstract/Free Full Text] [​IMG]
  11. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    It is now more than a decade since CT studies first demonstrated that preoxygenation leads to greater areas of atelectasis after induction.5 For example, if FIO2 before induction is 0.3, 0.6, 0.8, or 1.0, the mean percentage of atelectasis seen on CT scans post-induction is 0.2%, 0.2%, 1.3%, and 5.6% respectively

    The presence of more than 8% atelectasis immediately after operation is clinically very significant as re-expansion of this collapsed lung after major surgery may take some days.
  12. BLADEMDA

    BLADEMDA SDN Gold Donor Gold Donor

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    IT seems that nitrous oxide fans should consider starting out with Air/02 then dialing in the nitrous later in the anesthetic IF THE GOAL IS TO AVOID ATELECTASIS.
    The use of Nitrous Oxide with Oxygen from the start is likely to cause as much atelectasis as high oxygen alone.



    "This study, which used PaO2:F[SIZE=-2]I[/SIZE]O2 ratio to indirectly estimate the amount of atelectasis 30 min after induction, found that nitrous oxide at this early stage of an anaesthetic did indeed behave in a similar fashion to oxygen 100%"
  13. fakin' the funk

    fakin' the funk CA-2

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    Just thought I'd post one of the only anesthesia RCT's in the last 10 years to make it into a leading journal:

    JAMA. 2005 Oct 26;294(16):2035-42.

    Supplemental perioperative oxygen and the risk of surgical wound infection: a randomized controlled trial.

    CONTEXT: Supplemental perioperative oxygen has been variously reported to halve or double the risk of surgical wound infection. OBJECTIVE: To test the hypothesis that supplemental oxygen reduces infection risk in patients following colorectal surgery. DESIGN, SETTING, AND PATIENTS: A double-blind, randomized controlled trial of 300 patients aged 18 to 80 years who underwent elective colorectal surgery in 14 Spanish hospitals from March 1, 2003, to October 31, 2004. Wound infections were diagnosed by blinded investigators using Centers for Disease Control and Prevention criteria. Baseline patient characteristics, anesthetic treatment, and potential confounding factors were recorded. INTERVENTIONS: Patients were randomly assigned to either 30% or 80% fraction of inspired oxygen (FIO2) intraoperatively and for 6 hours after surgery. Anesthetic treatment and antibiotic administration were standardized. MAIN OUTCOME MEASURES: Any surgical site infection (SSI); secondary outcomes included return of bowel function and ability to tolerate solid food, ambulation, suture removal, and duration of hospitalization. RESULTS: A total of 143 patients received 30% perioperative oxygen and 148 received 80% perioperative oxygen. Surgical site infection occurred in 35 patients (24.4%) administered 30% FIO2 and in 22 patients (14.9%) administered 80% FIO2 (P=.04). The risk of SSI was 39% lower in the 80% FIO2 group (relative risk [RR], 0.61; 95% confidence interval [CI], 0.38-0.98) vs the 30% FIO2 group. After adjustment for important covariates, the RR of infection in patients administered supplemental oxygen was 0.46 (95% CI, 0.22-0.95; P = .04). None of the secondary outcomes varied significantly between the 2 treatment groups. CONCLUSIONS: Patients receiving supplemental inspired oxygen had a significant reduction in the risk of wound infection. Supplemental oxygen appears to be an effective intervention to reduce SSI in patients undergoing colon or rectal surgery.
  14. fakin' the funk

    fakin' the funk CA-2

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    And while we're on the topic of atelectasis...



    Chest. 1995 Jan;107(1):81-4.

    Lack of association between atelectasis and fever.
    Engoren M.

    Department of Anesthesiology, Saint Vincent Medical Center, Toledo, Ohio.

    Postoperative fever occurs in many patients. If no infection is found, atelectasis, if present, may be blamed. This study of 100 postoperative cardiac surgery patients followed up from day of surgery through the second postoperative day with daily portable chest radiographs and continuous bladder thermometry was designed to look for an association between atelectasis and fever. The daily incidence of atelectasis increased from 43 to 69 to 79%. However, the incidence of fever, defined as temperature > or = 38.0 degrees C fell from 37 to 21 to 17%. When defined as temperature > or = 38.5 degrees C, the daily incidence of fever fell daily from 14 to 3 to 1%. Using chi 2 analysis, no association could be found between fever and amount of atelectasis. This contradicts common textbook dogma but agrees with previous human study and animal experiments.
  15. Sergio99

    Sergio99

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    Hello,

    Yes, those who posted above are right in everything they say. The data can be seen in ICU literature and scuba diving literature (scuba diving people have investigated this topic a lot).

    To summarize it in a few words , we can say the following:

    1 ATM oxygen may be tolerated for 24-48 hr without serious damage. There is first a carinal irritation on deep inspiration, with cough; later a more intense carinal irritation, tracheobronchitis, chest pain and dyspnea. In this first stage, cessation of exposure usually reverts the symptoms within 4 hours.

    More prolonged exposures cause parenchymal lung injury, ARDS and pulmonary interstitial fibrosis.

    Then there is the issue of atelectasis, very well described above by Blademda.
  16. Narcotized

    Narcotized

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    In a healthy patient I prefer to not run O2 above 50-60 percent (below 40% in ENT cases). I have no data to back this, but intuitively you will spot a problem faster that may be masked for a while with 100% O2, and you will have a reserve (turning up the O2) to buy you time while you search for the problem. If you first notice the problem at 100% O2 you have no extra reserve. Again, no hard data; just makes sense to me.

    This is in addition to the problems of 100% O2 such as atelectasis and the rare fire in ENT cases with ESU's. These fires are extremely rare, but I would have a hard time forgiving myself for an airway fire in a perfectly healthy kid for tonsillectomy that had no need or benefit for 100% O2.
  17. Bertelman

    Bertelman Maverick!

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    I split my flows 50/50 air/O2 because it's easier to chart. Works out to about 0.6.
  18. GoodmanBrown

    GoodmanBrown is walking down the path.

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    Not that this should be a primary concern, but doesn't running lower O2 save money as well as you're burning fewer tanks per week?
  19. rsgillmd

    rsgillmd

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    O2 supply in the OR comes from the hospital pipeline. I may be mistaken, but I think I recall being told that most major hospitals have their own O2 generation facilities. If they didn't, that would be a lot of tank changing going on in the background and would likely result in inconsistent pipeline pressures.
  20. GoodmanBrown

    GoodmanBrown is walking down the path.

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    That makes a lot of sense. Thanks for the info!
  21. Dejavu

    Dejavu ASA Member

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    What do you bet that in a decade or two, Nitrous won't even be on an anesthesia machine anymore.

    Just a thought...
  22. Planktonmd

    Planktonmd Moderator Emeritus Lifetime Donor

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    Yes, I agree.
    One place where I still like nitrous is OB when you have to do a c section under GA and you can't give a high concentration of vapors.
  23. IN2B8R

    IN2B8R Junior Member

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    Status:
    Attending Physician
    SDN 7+ Year Member
    Lotsa dental anesthesia out there, I don't think that it will all together be gone... As for hospital use, you guys maybe right.... I like to use it to wash out volatiles, 70/30 (nitrous, O2) at flows of 12L/min. Works well, only if patient is adequately narcotized....:thumbup:

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