[2014ASA知识更新] 挑战传统！十大麻醉呼吸管理中的“错误做法”

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1.“无用的”预给氧

麻醉诱导前预先给氧有着悠久的历史。如果被正确的实施，它可以延长呼吸暂停到发生低氧的间隔，当我们遇到预计外的困难气道时，可以为我们争取到宝贵的时间。不过，很多时候我们却没有正确的实施它。譬如：有时我们只是轻轻的象征性的把面罩放在病人脸上，这样的后果是：大量面罩周围的室内空气也同时被吸入。正确的做法是：面罩应当被充分密闭从而只让回路中的纯氧被吸入。

原因如下：在吸气相时，人的峰值吸入气流可以达到60L/min，如果面罩没有被很好的密封，当以新鲜气体流量为6L/min吸入纯氧时，实际吸入的有效氧浓度只有大约40%，实际上并不能有效的起到“给氧去氮”的作用。预给氧有多种方法，正常潮气量呼吸法或深呼吸法都可以，效果都差别不大。不过前提是必须使用合适的面罩！有一种检验预給氧是否有效的方法是：测量呼出气的氧浓度，至少在插管前应该达到80%。

要做就按正确的方式做--并且有可能的话对做法的有效性进行检测。

1. Wimpy preoxygenation Preoxygenation prior to anesthesia induction is a time-honored procedure applied routinely in anesthesia practice. When properly performed, it prolongs the duration that apnea can be maintained without arterial oxygen desaturation, a useful outcome if unanticipated airway difficulties arise. However, proper technique is often not applied. For example, the facemask is lightly placed on the patient’s face, such that there is significant entrainment of room air around the edges of the mask. The facemask seal must be sufficient so that all the inspired gas comes from the anesthesia circuit and bag, rather than via room air entrainment. .Because peak airflow during inspiration may approach 60 L/min, with typical fresh gas flows of 6 L/min the effective inspired oxygen fraction is approximately 40% if a proper seal is not obtained. This will significantly reduce the apneic time prior to desaturation. Many ventilatory maneuvers during preoxygenation have been described, ranging from normal tidal breathing to vital capacity inspiration, most of them equally efficacious, but all depend on an adequate mask fit. One way to objectively evaluate the quality of preoxygenation is to monitor the end-tidal oxygen fraction – aim for at least 80% prior to proceeding. So take the time to do it right, every time – and monitor the efficacy of your technique.

2.“千篇一律“的呼吸参数设置

许多老师会教你把呼吸参数设置成如下所示：潮气量=10ml/kg，频率=10-12次/min。如果这样设置，大多情况下会导致过度通气。“老师们”这样设置的理由如下：

1）大潮气量可以防止肺不张并提高氧合。

2）10--12次/min的频率符合人的生理。

3）宁愿过度通气的低碳酸血症，不要通气不足的高碳酸血症

事实果真如此吗？。。。

1）高潮气量（至少在我们实际用于维持通气的范围内）并不能预防或逆转肺不张，也不能增加肺部气体交换。术中肺不张的解决方式应当是“膨肺法”（持续，高压），而不是高潮气量（在第5点我们会具体讨论这个问题）。实际上，高潮气量会伤害那些已经有肺损伤的病人，并且对没有肺疾患的患者也可能会有害。

2）处于麻醉状态人体代谢减低，所以不必将呼吸频率设定为和清醒状态时一样。即使是清醒时，每个人的呼吸频率也存在个体差异。

3）除开某些神经外科手术，低碳酸血症并无益处。事实是，有些证据表明高碳酸血症反而有益。譬如：高碳酸血症引起外周血管扩张从而增加组织氧合，可以预防伤口感染（这点还有待进一步研究）。此外还有实验（不过据我所知这项实验还没有可重复性）表明术中低碳酸血症会导致苏醒延迟。

因此我建议采用低潮气量的通气策略（5--6ml/kg），并且降低呼吸频率，将呼气末二氧化碳保持在正常范围内即可。

2. “Routine” ventilator settings

Many anesthesiologists were taught in training to use the following ventilator settings intraoperatively: tidal volume = 10 ml/kg and rate = 10-12/min. These settings will routinely produce significant hyperventilation. The rationale for these settings includes:
1) higher tidal volumes will prevent atelectasis and improve oxygenation;
2) respiratory rates of 10-12 are physiologic, and;
3) hypocarbia is good, hypercarbia is bad.
However…..
1) High tidal volumes, at least in the ranges used to maintain ventilation in modern practice, do not prevent or reverse atelectasis and do not consistently improve gas exchange. Resolution of intraoperative atelectasis requires “recruitment maneuvers” (prolonged, high airway pressures), not higher tidal volumes – as we will see in point #5 below. Indeed, higher tidal volumes certainly hurt lungs that are already injured, and may have deleterious effects in even normal lungs;
2) Because metabolic demands are decreased during anesthesia, it is not necessary to maintain an “awake” respiratory rate…which in any event widely varies among individuals;
3) Other than for some neurosurgical cases, hypocapnia is not beneficial. Indeed, there is some evidence that hypercarbia may be beneficial. For example, hypercarbia causes peripheral vasodilation and increases tissue oxygenation, which could help prevent wound infection (although this remains to be shown). There is also fascinating study (which to my knowledge has not been repeated) suggesting that intraoperative hypocapnia delays emergence
So consider using lower tidal volumes (in the 5-6 ml/kg range) and lower breathing frequencies that will maintain at least normocarbia.

3.常规使用机械通气及肌松药

在美国，麻醉医生会经常使用肌松药并实施机械通气。对于那些无须肌松的手术，或者那些很容易让患者保持自主呼吸的手术，他们也这么干。一旦在诱导之后患者发生体动，很多人的第一想法是给予肌松药。毕竟这样做可以取悦手术医生，避免他们大喊大叫。而且这样做的另一个好处是可以避免使用更多的麻醉药导致低血压，还能让病人更快的苏醒。实际上，很多时候我们都会这样做。当我们心安理得地进行机械通气后，我们无须担心病人是否通气不足--“瞧，用着呼吸机呢，没问题”。

是该对常规行机械通气及使用肌松药进行再思考了：

1）要实施正压通气，或多或少得保证有一个相对安全的气道。气管插管是对人体是一个恶性的刺激。如果插管仅仅是为了提供机械通气的话，你应当考虑是否真正需要它。很多人用喉罩，不过要记住：一旦定位不良，气体会跑到你不想让它去的地方去（譬如胃）。

2）术中患者一旦发生体动，他想要传递给你的信息是“请给我加深麻醉”而不是“请给我肌松药让我不要动”。使用肌松药是导致术中知晓的危险因素，相反，对于那些没使用肌松药的患者，术中知晓却很少发生（不过也不是没有）。此外，使用肌松药还可能导致过敏或类过敏反应，以及术后肌松药拮抗不全引起的呼吸并发症。

3）像我们的麻醉前辈们所做的那样，我们可以从观察患者的呼吸中得到很多信息。比如：自主呼吸时的呼气末二氧化碳就和麻醉深度相关，因此，我们可以把中枢呼吸控制机制作为一项完美的综合神经生理监测手段，用它来监测麻醉效果，从而帮助我们更好的实施麻醉。举个例子：在手术结束前，我们可以用它来帮助我们决定补充给予芬太尼的量，以便让病人更平稳且无痛的醒来。还有一个好处是：如果生理性的膈肌收缩得以保留，那么气体交换可以更好的进行，理由是在自主呼吸的情况下，通气血流比值能更好的匹配。

当病人有明确的指针存在时才实施机械通气或使用肌松药，不要把它们作为常规。。。也不要认为有了它们麻醉就完全了。。。

3. “Routine” use of mechanical ventilation and paralysis

Anesthesiologists in the US frequently employ pharmacologic paralysis and mechanical ventilation, even for cases in which neuromuscular blockade is not required to accomplish the procedure, or cases in which patients could easily maintain spontaneous breathing. Indeed, when patients move after the induction of anesthesia, the first response is often to administer a neuromuscular blocking drug. After all, the surgeons will be happier and won’t yell if the patients don’t move, I can use less anesthetic drugs which avoids hypotension and hastens emergence, and in fact we always do it that way. And if I just turn on the ventilator, I don’t have to worry about whether the patient will be adequately ventilated – it’s a “ventilator”, right? Plus, succinylcholine is now “persona non grata” at many institutions, committing patients to extended paralysis if nondepolarizing neuromuscular blocking drugs are used to facilitate endotracheal intubation.

Here are a few reasons to reconsider “routine” mechanical ventilation/paralysis:

1) Positive pressure ventilation requires a more-or-less secure airway. Endotracheal intubation is not a benign intervention; if the only indication for an endotracheal tube is to provide mechanical ventilation, consider whether you really need mechanical ventilation. Many use positive pressure ventilation with supraglottic airways such as the LMA, but remember that unless properly seated, the gas may be delivered to locations you do not wish to receive it (e.g., the stomach).

2) When patients move, they are generally telling you “please give me more anesthesia” rather than “please paralyze me”. Use of neuromuscular blocking drugs is a risk factor for intraoperative awareness, which is rare (but not unheard of) in a patient who is not paralyzed. There are many other risks associated with neuromuscular blocking drugs, including anaphylactic and anaphylactoid reactions and postoperative respiratory complications associated with incomplete reversal of block.

3) Just like our anesthetic forefathers (and foremothers), you can learn a lot by watching patients breathe. For example, parameters such as end-tidal CO2 maintained during spontaneous breathing depend on anesthetic depths, such that central respiratory control mechanisms can serve as an excellent integrated neurophysiology monitor for overall anesthetic effects. This can be a useful tool to help administer anesthesia, for example to titrate opioid supplementation at the end of cases to facilitate smooth, painless emergence. There also may be situations in which gas exchange is better maintained if physiologic diaphragmatic contraction is also maintained, as spontaneous breathing can be associated with improved ventilation-perfusion matching during anesthesia.

So use mechanical ventilation/paralysis because it is specifically indicated for a patient, not as a matter of routine….or as a substitute for adequate anesthesia…

mlchenjia

请问有人找到原文了吗？求原文

mlchenjia

请问有人找到原文了吗
可否发一份给我，谢谢

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7 挥发罐有问题？

现在对吸入和呼出气体的监测越来越广泛，有的麻醉医生会注意到设定的吸入麻醉气体浓度和实际吸入的浓度之间存在明显的差异，有时他们会怀疑是不是设备出什么问题了。

不过事实是这样的：麻醉呼吸回路允许呼出气体的重复吸入，重复吸入的量取决于进入回路的新鲜气体量以及分钟通气量。流量越低，重复吸入越多。如果这种情况在早期诱导时就发生，可供重复吸入的麻醉气体会相对更少，就会导致实际吸入气体浓度小于设定的浓度。相反的情况会在苏醒期时出现。这种现象自我们开始使用呼吸回路及吸入气体进行麻醉那时起就已经存在--不过直到最近这些年我们才有条件常规对其进行监测。

记住如果你想快速改变吸入麻醉药物的浓度（或者在手术结束前想将麻醉气体快速洗出），你应当加大新鲜气体的流量--还有，不用担心，你的挥发罐没有问题。。。

7. Why is my vaporizer broken?

Now that the monitoring of inhaled and exhaled gases is widespread, anesthesia personnel have noted apparent discrepancies between the set volatile anesthetic concentration and the actual inspired anesthetic concentration, sometimes prompting concerns that there is a malfunction of the machine.

However….remember that anesthesia circle systems allow rebreathing of exhaled gas, with the amount of rebreathing dependent on the balance between fresh gas flow into the circuit and minute ventilation. With lower flows, more rebreathing occurs. If this happens say early in induction, the rebreathed gas will be relatively poor in anesthetic, and the inhaled anesthetic concentration will be less than the set anesthetic concentration. The opposite consideration applies during emergence. This phenomenon is as old as the use of volatile agents and circle systems – but only recently have we had the technology to see it routinely!

So remember that if you wish to rapidly change the inspired concentration of a volatile anesthetic (or to wash out agent at the end of the case), you need to use high fresh gas flows – and don’t worry, the vaporizer is fine…..

8 什么，不需要小儿螺纹管？！

对于儿童患者，“老师”们通常会使用管径较小的小儿螺纹管和较小的呼吸球囊。你问为什么要这样做？他们总是会含混不清的给你解释诸如死腔之类的理论。。。

不过等等。。。书上不是说呼吸回路系统中的死腔到Y型接头和气管导管连接处就结束了吗？和之后的螺纹管的直径有什么关系？--其实半毛钱关系都没有！真正相关的是一个叫做“压缩容量”的概念，其含义是当实施机械正压通气时，越是呼吸回路远端，压力会越大，气体会被压缩而造成所谓的“丢失”的现象。回路远端容量越低，被压缩而导致丢失的“压缩容量”就相应越少。不过，在我们常规用于机械通气的压力下，这种效应产生的影响微乎其微--只会导致约2%的通气量“丢失”。所以，使用小儿螺纹管实无必要。不过小的呼吸球囊倒是应该提倡，它更容易让我们的手部感知到肺的顺应性以及潮气量的变化。

对于小儿患者，随便你使用哪种螺纹管都行--不过在实在是找不到小儿螺纹管时，你也大可不必纠结。

8. What, no pediatric circuit?

For smaller children, we often use anesthesia circuits with small diameters, and smaller anesthesia bags. Do we really need to use smaller circuit equipment for smaller people? When asked why, people often mumble something about dead space….

However….remember that the dead space in a circle system extends only distal to the Y-junction – the diameter of the tubing leading to and from the Y-junction makes no difference to dead space. There is the concept of “compression volume” that applies during positive pressure ventilation. This represents ventilation that is “lost” due to the increase in pressure that occurs in the limbs of the ventilator circuit. The lower the volume of each limb of the circuit, the lower the “compression volume”. However, the magnitude of this effect is trivial – for normal airway pressures used during intraoperative ventilation, only about 2% of the delivered volume is “lost”. So this is not much of a reason to use smaller circuit equipment. It is true that with a smaller anesthesia bag, it is easier for the “educated hand” to detect changes in compliance, tidal volume, etc.

So use whatever circuit you wish for your smaller patients – but don’t panic if the “pediatric” circuits are not available.

9 只喷两下就够了

当术中患者发生支气管痉挛时，我们常常会使用沙丁胺醇之类的药物进行雾化治疗。不过对于全麻插管病人，这会是一个很大的挑战。因为即使对于那些情况良好的非卧床病人，使用喷雾瓶也仅仅只能将少量药物真正送到远端小气道。插管病人通过气管导管进入的药物会更少，只有约5-10%的药物会进入气道。因此只是简单的往气管导管里喷两下的做法并不能产生足够的治疗效应。改良的方法有：1）如果可能，考虑使用雾化装置2）在回路吸入端使用spacer device（一种增大空间便于吸入的装置，三言两语解释不清楚，可自行 Google） 3）多喷几下。

按部就班仅仅只喷两下远远不够--记得多喷几下才会有治疗效果。

9. Two puffs is enough
When patients develop intraoperative bronchospasm, they are often treated using aerosolized drugs such as albuterol. However, it can be quite challenging to administer aerosols to anesthetized patients via an endotracheal tube. Even under the best of conditions in ambulatory patients, only a minority of the total amount of drug administered by a metered dose inhaler actually reaches the small airways. Even less is delivered when administered via an endotracheal tube, with only 5-10% of an administered dose being delivered to the airways. Thus, simply attaching a metered dose inhaler to the elbow of the breathing circuit and administered two puffs (hopefully at the right portion of the respiratory cycle) is unlikely to produce an adequate therapeutic effect.
Suggestions to improve drug delivery include:

1) consider using nebulizers rather than metered dose inhalers if available in a timely fashion;

2) use a spacer device in the inspiratory limb of the circuit, and;

3) increase the number of puffs to account for decreased efficiency of delivery.
Usually two puffs is not enough – so don’t be afraid to administer more puffs to obtain the necessary therapeutic effect.

10 术前应当继续吸烟
长久以来在围术期治疗中存在一种秘而不宣的极端错误的观点:术前短时间内突击戒烟会增加肺部并发症的风险。持这种观点人的理由是：突击戒烟会导致患者咳嗽，还会使得痰液生产增多。是时候对此种谬论说不了！很多研究已经证实:术前任何时候戒烟都不会增加并发症。相反，它会减少肺部并发症的风险，虽然这种效果可能要戒烟数周后才能完全显现。麻醉医生在帮助患者戒烟的过程中有着独特的地位，应当竭尽全力劝说患者戒烟。手术对于患者起着一个“警戒”的作用，越是大的手术，患者戒烟成功的几率越高。无论是对于短期围术期结局的改善或是长期的健康而言，这都是有好处的。

不管什么时候都应该让患者禁烟--即便是术前很短的时间。

10. Don’t stop smoking!
One of the most pernicious and persistent myths in perioperative medicine is that quitting smoking shortly before surgery will actually increase the risk of pulmonary complications, supposedly because of increased cough and sputum production. Multiple studies have now shown that this is absolutely not true – quitting smoking at any time prior to surgery will not increase the rate of any complication, although it is true that it may take several weeks to realize the full benefits of smoking cessation in terms of reducing the risk of pulmonary complications.
Anesthesiologists are in a unique position to help their patients quit smoking, and should take every opportunity to help them do so. Surgery serves as a “teachable moment” for smoking cessation, as having major surgery can double the chances that patients can quit successfully. This will improve both immediate perioperative outcomes and long term health. For more information, see www.asahq.org/stopsmoking.
So any time is the right time for patients to quit smoking – even shortly before surgery.

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(出自丁香园 netfish513 新青年麻醉论坛)

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4 “辅助”呼吸

对于那些麻醉期间保留自主呼吸的患者，我们经常会“忍不住”去帮助他们“呼吸”---有一下没一下的捏一下皮球以增加潮气量。许多厂商也“顺应民心”，设计出了新的压力支持呼吸模式。藏在背后的逻辑依然是增加潮气量可以避免肺不张，可以避免高碳酸血症。

然而在事实面前，这种逻辑却站不住脚。前面我们已经讨论过增加潮气量（仅仅靠手动捏皮球那几下增加的潮气量相对较少），并不能改善肺不张或提高氧合。

那么对于保留自主呼吸的麻醉患者，有没有可能在不影响其自主呼吸功能的情况下明显增加其分钟通气量？当患者在吸入麻醉下保留自主呼吸时，存在一个“呼吸暂停临界值”--当动脉血中PCO2低于这个值时，呼吸功能（比如呼吸肌活动）就会停止。此临界值比正常自主呼吸时动脉血ＰＣＯ２低４－５cm，和使用的麻醉药物及麻醉深度无关。因此如果你想保留患者的自主呼吸功能，在你忍不住想帮助患者呼吸时，你只能让PCO2轻度下降。

“辅助”病人呼吸除了可以让你的手（或者呼吸机）有点事做以至于让你感到不那么无所事事之外，其实并无多少道理可言。

4. “Assisted” ventilation
Patients breathing spontaneously under anesthesia often receive “assistance” – a squeeze on the bag every now and then to augment tidal volume, or in today’s world one of numerous modes of pressure support, again designed to augment tidal volumes. The rationales behind this practice are that increased tidal volumes will improve atelectasis, and that this practice will augment minute ventilation and improve hypercapnia. However, there are inconvenient truths that make this reasoning suspect. We have already discussed that increasing tidal volumes, at least to the relatively modest degree used in “assisted” ventilation, does not improve atelectasis or oxygenation. And is it possible to significantly augment minute ventilation during spontaneous breathing underanesthesia, and still maintain spontaneous ventilatory effort? When patients are breathing spontaneously under volatile anesthesia, there is an “apneic threshold” – a value of arterial PCO2 below which ventilatory effort (i.e., respiratory muscle activity) ceases. This threshold is 4-5 cm below the arterial PCO2 maintained during spontaneous breathing, largely independent of anesthetic or the depth of anesthesia. So if you want to maintain your patient’s respiratory effort, you can only achieve modest decreases in PCO2 with “assisted” ventilation. So although “assisted” ventilation may keep your hand (or your anesthesia ventilator) busy and make you feel like you are doing something useful, the reasoning supporting its use is questionable at best.

5 PEEP

全麻期间几乎不可避免会发生肺不张，这是导致气体交换异常的主要原因(但不是唯一原因）。当合并其它诸如肥胖等引起的胸壁顺应性异常时，术中低氧就会发生。此时我们习惯性的反应是给予5--250px H2O的呼气末正压通气。在ICU使用时有时似乎有用，那么麻醉中我们为什么不用？不过事实却是：单独使用PEEP并不能逆转已经发生的肺不张。正确的做法是应当首先采用“膨肺法”：以约1000pxH2O的压力持续膨肺30-40秒，然后在给予PEEP，这样才能阻止肺不张再次发生。此外，高浓度的吸入氧浓度会加快肺不张的复发，因此如果有可能应将吸入FiO2降到80%以下。术中发生的肺不张在术后可能会持续存在而导致气体交换障碍，所以在手术结束拔管之前进行膨肺值得推荐。

术中低氧血症常常是由肺不张导致，治疗它的最好方法是膨肺后再进行PEEP--而不是仅仅单纯的给予PEEP。

5. PEEPed out
General anesthesia nearly always causes atelectasis in dependent areas of the lung, which represents a major (but not the only) source of gas exchange abnormalities during anesthesia. When combined with other abnormalities of chest wall mechanics such as obesity, intraoperative hypoxemia may occur. A frequent response is to simply dial in 5-10 cm H2O of positive end-expiratory pressure (PEEP) – which sometimes seems to help in ICU patients, right?

Unfortunately, the isolated application of PEEP is unlikely to reverse intraoperative atelectasis. Rather,
“recruitment” maneuvers are required, involving sustained (30-40 seconds), high (approximately 40 cm H2O) airway pressures. PEEP applied after recruitment maneuvers can help prevent the reformation of atelectasis. Also, a high inspired fraction of O2 can accelerate the reoccurrence of atelectasis – so keep the FIO2 below 80% if possible.
Intraoperative atelectasis can also persist into the postoperative period and cause impairment of gas exchange, so it is worth considering recruitment maneuvers prior to extubation at the end of the case.
So intraoperative hypoxemia is often caused by dependent lung atelectasis, which is best treated by recruitment maneuvers followed by PEEP – don’t just turn on the PEEP.

6“通气模式”选择困难症

现在高档麻醉机的通气模块正在向ICU所使用的呼吸机靠拢，提供了许多可供选择的通气模式。这成为了厂商推销吹嘘的资本。同时也满足了那些迷信器械的麻醉医生，他们整天沉迷于麻醉机上的各种仪表盘不能自拔。

不过HEY醒醒（正埋头捣鼓麻醉机的家伙，说你呢！），有三件事你得牢记于心：
1)尽管有许多人尝试去证明最近流行的“mode-of-the-month"可能会有益，不过目前几乎没有证据表明有哪一种通气模式对患者的结局会产生任何影响。即使在ICU这一点在很大程度上也同样适用。唯一已经明确的一点是大潮气量有害。
2）现在麻醉机上存在的大量复杂的通气模式在给予我们许多选择的同时，也增加了我们的迷惑以及误用的几率。有些操作者在使用时并没有真正理解各种通气模式的原理，从而导致不好的后果。比如在压力支持通气模式下，你可能会误认为患者自主呼吸良好而此时患者其实呼吸功能并不好。一旦你此时给患者拔管，可能一些”有趣“的事情就会发生。
3）厂商在不断对呼吸模块进行优化的过程中，却忽略了麻醉机的一些基本功能（个人观点）。比如一些麻醉机在允许儿童患者自主呼吸的同时却导致了明显的CO2重复吸入。

在你热衷于摆弄麻醉机的各种通气模式时，很多时候你只是为了自己的兴趣而不是为了病人。记得在选择通气模式之前一定要搞清楚它的原理是什么。
6. Mode madness
Newer generations of anesthesia machines are equipped with sophisticated ventilators that provide many of the same features of those ventilators utilized in intensive care units. These are touted by their manufacturers as major advances in anesthesia technology, and it is indeed fun to play with the dials (or rather the touchscreen) for those who are mechanically inclined.
However, keep three things in mind.
1) There is little to no evidence that any mode of intraoperative ventilation has any effect on outcomes, despite multiple attempts to prove benefits of the latest “mode-of-the-month”. This has largely been true even in the intensive care unit – all we really know is that high tidal volumes are bad.
2) The multiple modes of ventilation available on modern anesthesia machines provide multiple opportunities for confusion and misuse. Anecdotal experience suggests that many providers do not really understand how the ventilators operate, and this lack of knowledge can have consequences. For example, providers may assume that the patient is breathing spontaneously with a pressure-support mode, and not recognize the absence of spontaneous ventilatory effort. This can make for an interesting extubation experience.
3) In their zeal to optimize the performance of their ventilators, manufacturers have compromised abilities basic to the functioning of the anesthesia machine (in my opinion). For example, allowing pediatric patients to breathe spontaneously with some modern machines results in significant rebreathing of CO2. So if you choose to indulge in mode madness, please recognize that it is for your benefit, generally not for the benefit of your patients, and make sure you understand how that fancy ventilator works.