Three Airway Disasters

[BLADEMDA]

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I have thought about this exact question. Edmark et al 2003 in Anesthesiology showed that you can gain roughly 100 seconds each going from preoxygenate with 60%, 80% and 100% before SpO2 drops to 90. The same group in 2011 also showed that atelectasis occurs rapidly after induction regardless of FiO2 during preoxygenation, but especially fast with 100%. So yes, preoxygenate with less than 100% may be beneficial.

However, atelectasis under anesthesia can occur quickly at various stages, but is reversible and preventable with recruitment manuver and the avoidance of 100% FiO2 intraop. A lost airway and anoxic brain injury are not. So I may preoxygenate with less than 100% if patient is healthy and my attending is chill. But with a suspect airway, full preoxygenate with 100% and deal with atelectasis later.

Absolutely!! The point is to THINK about each patient and your approach. I have tried explaining these concepts to the Advanced Anesthesia Nurses and most still don't get it.

 

[RT2MD]

I have thought about this exact question. Edmark et al 2003 in Anesthesiology showed that you can gain roughly 100 seconds each going from preoxygenate with 60%, 80% and 100% before SpO2 drops to 90. The same group in 2011 also showed that atelectasis occurs rapidly after induction regardless of FiO2 during preoxygenation, but especially fast with 100%. So yes, preoxygenate with less than 100% may be beneficial.

However, atelectasis under anesthesia can occur quickly at various stages, but is reversible and preventable with recruitment manuver and the avoidance of 100% FiO2 intraop. A lost airway and anoxic brain injury are not. So I may preoxygenate with less than 100% if patient is healthy and my attending is chill. But with a suspect airway, full preoxygenate with 100% and deal with atelectasis later.

I really liked this post. Obviously I have never given an anesthetic, so my opinion doesn't really matter here... but I really like this post. I will be sure to file it away for a much more glorious time of my life (ie. out of the classroom). Thank you.

 

[epidural man]

I have thought about this exact question. Edmark et al 2003 in Anesthesiology showed that you can gain roughly 100 seconds each going from preoxygenate with 60%, 80% and 100% before SpO2 drops to 90. The same group in 2011 also showed that atelectasis occurs rapidly after induction regardless of FiO2 during preoxygenation, but especially fast with 100%. So yes, preoxygenate with less than 100% may be beneficial.

However, atelectasis under anesthesia can occur quickly at various stages, but is reversible and preventable with recruitment manuver and the avoidance of 100% FiO2 intraop. A lost airway and anoxic brain injury are not. So I may preoxygenate with less than 100% if patient is healthy and my attending is chill. But with a suspect airway, full preoxygenate with 100% and deal with atelectasis later.

I don't think 30-50 secs buys you much. It's not like 30 more seconds of hypoxia is the difference between brain dead and playing jeopardy succesfully again. (It may be the difference between being able to do anesthesia - or 50 more sec of hypoxia and you can only do ortho or neurosurgery) - but who knows.

I say preoxygenate to 90%. The question then comes, how much nitrogen is needed to prevent absorbtion atelectasis?

 

[Idiopathic]

How do you know?

PMID: 12503004
"Ventilation at maximal voluntary reduction of lung volume caused significant desaturation in some healthy subjects breathing air. Saturation rapidly returned to control levels when normal lung volume was regained. These changes are probably due to reversible airway obstruction. During the inhalation of oxygen, ventilation at maximal voluntary reduction of lung volume caused, in one subject, a reduction of arterial Po2 of 243 mmHg. Normal arterial Po2 was not immediately restored on regaining normal lung volume. Chest radiographs showed extensive atelectasis, which persisted for several hours in an ambulant subject. These changes are probably due to absorption of oxygen from alveoli beyond obstructed airways. Reduction of lung volume may be harmful for patients who are breathing oxygen. Caution is therefore necessary in the use of a subatmospheric pressure phase during artificial ventilation and during suction of the tracheobronchial tree."

PMID: 10194192
"Recent computed tomography studies show that inspired gas composition affects the development of anesthesia-related atelectasis. This suggests that gas absorption plays an important role in the genesis of the atelectasis. A mathematical model was developed that combined models of gas exchange from an ideal lung compartment, peripheral gas exchange, and gas uptake from a closed collapsible cavity. It was assumed that, initially, the lung functioned as an ideal lung compartment but that, with induction of anesthesia, the airways to dependent areas of lung closed and these areas of lung behaved as a closed collapsible cavity. The main parameter of interest was the time the unventilated area of lung took to collapse; the effects of preoxygenation and of different inspired gas mixtures during anesthesia were examined. Preoxygenation increased the rate of gas uptake from the unventilated area of lung and was the most important determinant of the time to collapse. Increasing the inspired O2 fraction during anesthesia reduced the time to collapse. Which inert gas (N2 or N2O) was breathed during anesthesia had minimal effect on the time to collapse."

 

[Idiopathic]

theres also a study i cant find the reference for which showed CT evidence of worsening atalectasis with 100% FiO2. It resonated with me, so Ill try and find it.

 

[dhb]

PMID: 12503004
"Ventilation at maximal voluntary reduction of lung volume caused significant desaturation in some healthy subjects breathing air. Saturation rapidly returned to control levels when normal lung volume was regained. These changes are probably due to reversible airway obstruction. During the inhalation of oxygen, ventilation at maximal voluntary reduction of lung volume caused, in one subject, a reduction of arterial Po2 of 243 mmHg. Normal arterial Po2 was not immediately restored on regaining normal lung volume. Chest radiographs showed extensive atelectasis, which persisted for several hours in an ambulant subject. These changes are probably due to absorption of oxygen from alveoli beyond obstructed airways. Reduction of lung volume may be harmful for patients who are breathing oxygen. Caution is therefore necessary in the use of a subatmospheric pressure phase during artificial ventilation and during suction of the tracheobronchial tree."

PMID: 10194192
"Recent computed tomography studies show that inspired gas composition affects the development of anesthesia-related atelectasis. This suggests that gas absorption plays an important role in the genesis of the atelectasis. A mathematical model was developed that combined models of gas exchange from an ideal lung compartment, peripheral gas exchange, and gas uptake from a closed collapsible cavity. It was assumed that, initially, the lung functioned as an ideal lung compartment but that, with induction of anesthesia, the airways to dependent areas of lung closed and these areas of lung behaved as a closed collapsible cavity. The main parameter of interest was the time the unventilated area of lung took to collapse; the effects of preoxygenation and of different inspired gas mixtures during anesthesia were examined. Preoxygenation increased the rate of gas uptake from the unventilated area of lung and was the most important determinant of the time to collapse. Increasing the inspired O2 fraction during anesthesia reduced the time to collapse. Which inert gas (N2 or N2O) was breathed during anesthesia had minimal effect on the time to collapse."

You're not convincing me...

 

[Idiopathic]

im not trying to. there is data to support what i say. do what you want.

PMID: 7760608
"Atelectasis is an important cause of impaired gas exchange during general anaesthesia; it causes pulmonary shunting. We studied the effects of gas composition on the formation of atelectasis and on gas exchange during the induction of general anaesthesia. In 12 adult patients, the lungs were ventilated with 30% oxygen in nitrogen during anaesthesia induction, and in another 12, a conventional technique was used (100% oxygen during induction and 40% oxygen in nitrogen thereafter). Extent of atelectasis was estimated by computed tomography and the ventilation-perfusion relation (VA/Q) by the multiple inert gas elimination technique. After anaesthesia induction, there was little atelectasis in the 30% oxygen group (mean 0.2 [SD 0.4] cm2) and a significantly greater amount (4.2 [5-6] cm2; p < 0.001) in the 100% oxygen group. Patients in the 30% oxygen group were observed for another 40 min. 6 continued to receive 30% oxygen (subgroup A) and 6 were ventilated with 100% oxygen (subgroup B). During this time, the amount of atelectasis increased to 1.6 (1.6) cm2 in subgroup A and to 4.7 (4.5) cm2 in subgroup B (p = 0.047 for difference between groups). In subgroup A, the shunt (VA/Q < 0.005) increased from 1.6 (2.0)% of cardiac output to 3.2 (2.7)%, but the arterial oxygen tension did not change. In subgroup B, the shunt increased from 2.6 (5.2)% to 9.8 (5.7)% of cardiac output. These results suggest that the composition of inspired gas is important in atelectasis formation during general anaesthesia. Use of a lower oxygen concentration than is now standard practice might prevent the early formation of atelectasis." (Lancet)

 

[dhb]

im not trying to.

Thanks for clearing that up

We have studied 51 patients who were allocated randomly and prospectively to receive either 100% oxygen (n = 16), 70% nitrous oxide in oxygen (n = 18) or 30% oxygen in nitrogen (n = 17) as the inspired gas during anaesthesia for abdominal hysterectomy. Lung volumes were measured before and after surgery. TLC, VC, FVC and FEV1 but not RV or FRC were reduced after surgery. There were no significant differences between the three treatment groups in any of the lung volumes measured. We conclude that absorption atelectasis during anaesthesia is not the main cause of perioperative changes in lung volume after abdominal hysterectomy. Any effect of the inspired gas is likely to be of limited clinical significance.
Br J Anaesth. 1995 Oct;75(4):417-21.

 

[BLADEMDA]

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 &#8216;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&#8211;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

/

ratio of <0.05.3 Using the multiple inert gas elimination technique, areas of lung with

/

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

/

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

 

[BLADEMDA]

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.

 

[pgg]

We had a related discussion about high FiO2s and absorption atelectasis in this thread a couple years ago.


To sum up what I think and posted in that thread - I am not a believer in clinically significant atelectasis under GA, with PPV and appropriate PEEP in effect.


I have started extubating people on 80% oxygen though, because once extubated and off the vent, PPV and PEEP obviously aren't helping any more.

 

[BLADEMDA]

[SIZE=+1]References[/SIZE]
1 Bell MDD. Routine pre-oxygenation&#8212;a new &#8216;minimum standard' of care? Anaesthesia (2004) 59:943&#8211;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&#8211;95.[Web of Science]
4 Joyce CJ, Williams AB. Kinetics of absorption atelectasis during anesthesia: a mathematical model. J Appl Physiol (1999) 86:1116&#8211;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&#8211;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&#8211;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&#8211;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&#8211;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&#8211;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&#8211;3.[Web of Science][Medline]
11 Tusman G, Böhm SH, Vazquez de Anda GF, do Campo JL, Lachmann B. &#8216;Alveolar recruitment strategy' improves arterial oxygenation during general anaesthesia. Br J Anaesth (1999) 82:8&#8211;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&#8211;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&#8211;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&#8211;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&#8211;9.[Abstract/Free Full Text]
16 Benumof JL. Preoxygenation. Best method for both efficacy and efficiency? Anesthesiology (1999) 91:603&#8211;5.[CrossRef][Web of Science][Medline]
17 McGowan P, Skinner A. Preoxygenation&#8212;the importance of a good face mask seal. Br J Anaesth (1995) 75:777&#8211;8.[Abstract/Free Full Text]

 

[BLADEMDA]

We had a related discussion about high FiO2s and absorption atelectasis in this thread a couple years ago.


To sum up what I think and posted in that thread - I am not a believer in clinically significant atelectasis under GA, with PPV and appropriate PEEP in effect.


I have started extubating people on 80% oxygen though, because once extubated and off the vent, PPV and PEEP obviously aren't helping any more.

Yes, I understand your point (see reference number 14 above). Still, why do you need 100% FiO2? Why isn't 80% good enough 98% of the time?
Why do you need 100% FiO2 pre-oxygenation for most of your cases?
The simple FACT is that you Don't.

 

[BLADEMDA]

Reducing FIO2, even by a small amount to 0.8, seems to be substantially better than using oxygen alone.

 

[Idiopathic]

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.

I think this is from the article i was trying to find. essentially 50% better than 100%

 

[btbam]

This thread was going through my head today as we had a floor intubation go horribly wrong and it ended up with a trauma resident doing a cric as the patient coded 😱

At least we got her back...

 

[Arch Guillotti]

This thread was going through my head today as we had a floor intubation go horribly wrong and it ended up with a trauma resident doing a cric as the patient coded 😱

At least we got her back...

what happened?

 

[BobBarker]

Got her back to get pneumonia, infarct her bowel, get septic and die in the ICU.

 

[btbam]

Got her back to get pneumonia, infarct her bowel, get septic and die in the ICU.

👍

what happened?

Woman was in a MVC a week ago, intubated in the field and remained so for about a week (not sure why they didn't trach her), she's in a C-collar with C6 fracture, hx of "cardiac issues", COPD, RAD. She was extubated earlier today, 2 hours later ICU pages me (3rd call anesthetist responding to airway issues on the floors).

I respond to find this woman gasping for air on a non-rebreather, stridorous, fingernails blue, genius nurses are trying to get a sat from those fingers. I run to get the code cart and call my attending, when I come back the RT is bagging her with an AMBU and she has a sat of 95.

There are no predictors of a difficult airway other than her recent extubation, and we are not in a situation where we can fumble around with a fiber optic for 15-20 min. I try to intubate with a Mac 3, lots of secretions/junk in the airway, suction some, see no identifiable structures, grade IV view.

Attending takes a look with Mil 3, sees nothing from the edema (very experienced guy, I respect him a lot). In between attempts, we are able to bag her but can't really get her sats above 90. He tries a bougie with no luck. Finally, he blindly intubates. We hear breath sounds, condensation in tube, everything seems ok. About 30 seconds later her lips are blue, sat is non-existent...we are unsure what happened...bronchospasm? mucus plug? Either way, we are unable to ventilate. At this point trauma attending/residents are in the room, her pulse drops to 30, wide QRS complexes. Trauma resident grabs a scalpel and does a cric and slides a 7.5 tube in.

Immediately after patient goes into PEA, we start compressions, give epi and atropine...After 2 rounds of this with some calcium, we get her back and she is emergently rushed to the OR for a trach with an ETT basically dangling out of her neck. All a little overwhelming for a new anesthetist, but I have to say reading this board prepares you for a lot of stuff!!

 

[nycitygas]

What PGY was the trauma resident that did the slash trach? Thats pretty impressive, I dont many gen surgery resident who can do it especially under that kind of pressure.

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Woman was in a MVC a week ago, intubated in the field and remained so for about a week (not sure why they didn't trach her), she's in a C-collar with C6 fracture, hx of "cardiac issues", COPD, RAD. She was extubated earlier today, 2 hours later ICU pages me (3rd call anesthetist responding to airway issues on the floors).

I respond to find this woman gasping for air on a non-rebreather, stridorous, fingernails blue, genius nurses are trying to get a sat from those fingers. I run to get the code cart and call my attending, when I come back the RT is bagging her with an AMBU and she has a sat of 95.

There are no predictors of a difficult airway other than her recent extubation, and we are not in a situation where we can fumble around with a fiber optic for 15-20 min. I try to intubate with a Mac 3, lots of secretions/junk in the airway, suction some, see no identifiable structures, grade IV view.

Attending takes a look with Mil 3, sees nothing from the edema (very experienced guy, I respect him a lot). In between attempts, we are able to bag her but can't really get her sats above 90. He tries a bougie with no luck. Finally, he blindly intubates. We hear breath sounds, condensation in tube, everything seems ok. About 30 seconds later her lips are blue, sat is non-existent...we are unsure what happened...bronchospasm? mucus plug? Either way, we are unable to ventilate. At this point trauma attending/residents are in the room, her pulse drops to 30, wide QRS complexes. Trauma resident grabs a scalpel and does a cric and slides a 7.5 tube in.

Immediately after patient goes into PEA, we start compressions, give epi and atropine...After 2 rounds of this with some calcium, we get her back and she is emergently rushed to the OR for a trach with an ETT basically dangling out of her neck. All a little overwhelming for a new anesthetist, but I have to say reading this board prepares you for a lot of stuff!!

 

[Arch Guillotti]

Sounds like it was in the goose. Was there an ETCO2 detector?

Woman was in a MVC a week ago, intubated in the field and remained so for about a week (not sure why they didn't trach her), she's in a C-collar with C6 fracture, hx of "cardiac issues", COPD, RAD. She was extubated earlier today, 2 hours later ICU pages me (3rd call anesthetist responding to airway issues on the floors).

I respond to find this woman gasping for air on a non-rebreather, stridorous, fingernails blue, genius nurses are trying to get a sat from those fingers. I run to get the code cart and call my attending, when I come back the RT is bagging her with an AMBU and she has a sat of 95.

There are no predictors of a difficult airway other than her recent extubation, and we are not in a situation where we can fumble around with a fiber optic for 15-20 min. I try to intubate with a Mac 3, lots of secretions/junk in the airway, suction some, see no identifiable structures, grade IV view.

Attending takes a look with Mil 3, sees nothing from the edema (very experienced guy, I respect him a lot). In between attempts, we are able to bag her but can't really get her sats above 90. He tries a bougie with no luck. Finally, he blindly intubates. We hear breath sounds, condensation in tube, everything seems ok. About 30 seconds later her lips are blue, sat is non-existent...we are unsure what happened...bronchospasm? mucus plug? Either way, we are unable to ventilate. At this point trauma attending/residents are in the room, her pulse drops to 30, wide QRS complexes. Trauma resident grabs a scalpel and does a cric and slides a 7.5 tube in.

Immediately after patient goes into PEA, we start compressions, give epi and atropine...After 2 rounds of this with some calcium, we get her back and she is emergently rushed to the OR for a trach with an ETT basically dangling out of her neck. All a little overwhelming for a new anesthetist, but I have to say reading this board prepares you for a lot of stuff!!

 

[BobBarker]

Glidescope

 

[btbam]

Sounds like it was in the goose. Was there an ETCO2 detector?

Yea and it wasn't really picking up, but we theorized that was from the decreased CO...thoughts?

What PGY was the trauma resident that did the slash trach? Thats pretty impressive, I dont many gen surgery resident who can do it especially under that kind of pressure.

Not exactly sure, definitely senior level 4 or 5. It was quick and impressive...then again our hospital is a level 1 trauma center so I think they get a fair amount of practice.

 

[Arch Guillotti]

Yea and it wasn't really picking up, but we theorized that was from the decreased CO...thoughts?

Major red flags all around this scenario. May have been from decreased CO but may have still been in the goose. This is a very hectic scene, I am not saying this was an recognized esophageal intubation but it is possible certainly.

 

[BLADEMDA]

Remember to keep an LMA in your back pocket for those "floor" intubations.
It may save your arse one day.

I agree Glidescope would have been real nice for this airway but an LMA may have bought you precious time; however, if the edema was the primary issue (as it seems) the LMA wouldn't have helped here.

 

[BLADEMDA]

Major red flags all around this scenario. May have been from decreased CO but may have still been in the goose. This is a very hectic scene, I am not saying this was an recognized esophageal intubation but it is possible certainly.

GOOSE! Always assume the esophagus in these airway codes unless confirmation by evidence (ETCO2) is present. Breath sounds aren't enough.
Of course, if the Saturation comes back, chest rises, etc. then it is reasonable to assume correct ET placement (CXR confirmation next).

The edema likely caused the ET tube to bounce off the glottic opening and end up in the old goose.

 

[BLADEMDA]

GOOSE! Always assume the esophagus in these airway codes unless confirmation by evidence (ETCO2) is present. Breath sounds aren't enough.
Of course, if the Saturation comes back, chest rises, etc. then it is reasonable to assume correct ET placement (CXR confirmation next).

The edema likely caused the ET tube to bounce off the glottic opening and end up in the old goose.

 

[ssmallz]

This....

Woman was in a MVC a week ago, intubated in the field and remained so for about a week (not sure why they didn't trach her), she's in a C-collar with C6 fracture, hx of "cardiac issues", COPD, RAD. She was extubated earlier today, 2 hours later ICU pages me (3rd call anesthetist responding to airway issues on the floors).

and this....

There are no predictors of a difficult airway other than her recent extubation

don't go together.

This patient was s/p neck fracture and intubated for a week. Was she still in a c-collar or was she s/p neck surgery? Either way this is a predictor of a difficult intubation. Combine that w/the fact that this pt was intubated for a week prior w/all the edema and swelling that can develop and you've got a set up for a difficult airway.

I would have called for a glidescope STAT or at least had an intubating LMA on the ready. The nurses were able to maintain her sat at 95% so while this is an urgent situation you're not at the point of emergent yet. Take your time, have all the tools at your disposal and go into it expecting the worst.

 

[Idiopathic]

Major red flags all around this scenario. May have been from decreased CO but may have still been in the goose. This is a very hectic scene, I am not saying this was an recognized esophageal intubation but it is possible certainly.

this is 100% an oral boards scenario. you listen, check breath sounds, treat bronchospasm, treat decreased cardiac output, check with fiberoptic and then pull the tube. obviously some of those things go by the wayside when you have a code, but ive actually pulled the tube out of the trachea in a situation exactly like this, and regretted it very quickly.

 

[CambieMD]

Remember to keep an LMA in your back pocket for those "floor" intubations.
It may save your arse one day.

I agree Glidescope would have been real nice for this airway but an LMA may have bought you precious time; however, if the edema was the primary issue (as it seems) the LMA wouldn't have helped here.

I would have attempted an LMA. This patient sounds like a patient that was not going to do well no matter what.

This patient should have been trached. After a week of being intubated swelling will develop. For some reason there is a reluctance to trach patients.Maybe it is viewed as a sign of weakness by the team caring for the patient on the wards. The thinking seems to be,"let's give extubation a shot, we can always reintubate if we have to."

Cambie

 

[Arcan57]

Yea and it wasn't really picking up, but we theorized that was from the decreased CO...thoughts?

At the time intubation was attempted, did the patient still have a BP? Also, was it a capnometer or a colorimetric device? While lack of color change secondary to cardiac output problems do occur, it's MUCH less common than you'd expect. For patients in cardiac arrest coming in from the pre-hospital setting, 9 times out of 10 absence of color change means a goosed tube. The other 10% is a mix of suboptimal CPR or patient with prolonged down-time. For those of you that respond to floor codes, is your experience the same?

 

[btbam]

This....



and this....



don't go together.

This patient was s/p neck fracture and intubated for a week. Was she still in a c-collar or was she s/p neck surgery? Either way this is a predictor of a difficult intubation. Combine that w/the fact that this pt was intubated for a week prior w/all the edema and swelling that can develop and you've got a set up for a difficult airway.

I would have called for a glidescope STAT or at least had an intubating LMA on the ready. The nurses were able to maintain her sat at 95% so while this is an urgent situation you're not at the point of emergent yet. Take your time, have all the tools at your disposal and go into it expecting the worst.

Sorry yes you are correct, I meant she didn't have any other predictors i.e. short TMD, etc..

At the time intubation was attempted, did the patient still have a BP? Also, was it a capnometer or a colorimetric device? While lack of color change secondary to cardiac output problems do occur, it's MUCH less common than you'd expect. For patients in cardiac arrest coming in from the pre-hospital setting, 9 times out of 10 absence of color change means a goosed tube. The other 10% is a mix of suboptimal CPR or patient with prolonged down-time. For those of you that respond to floor codes, is your experience the same?

Yes she still had a pressure when we were trying to DL...it was one of the colorimetric devices.

 

[DrN2O]

Remember to keep an LMA in your back pocket for those "floor" intubations.
It may save your arse one day

Evan better, an air-q. Your chance of blind intubation success is better than 50/50.

Don't know why the rush to intubate when you could bag her above 95. also, blind nasal, if that's what your attending did, sounds risky as bleeding might burn the bridge with the fiber.