Thursday, November 6, 2014

Out with the Bad Air, in with the Good Air

Oxygen. It’s a little funny to me that we’re still talking about this, even a little. Story after story of poor airway management that leads to death permeate medical publications and professional journals, so much so that they routinely spill over into social media and mainstream news. How is it possible that something so simple that we as a medical community understand so clearly still results in even one death in 2014? Yet it does, and here we are.

I would argue that deaths from hypoxia related to airway management are less about ignorance than they are about arrogance. Any 4 year old knows if you hold your breath, you’ll turn blue and pass out. Where the toddler has the advantage in this situation is they are smart enough not to forcibly do that to another person. Those of us tasked with airway management often suspend that particle of wisdom and inflict such serious harm that I heard it recently described by a medical director as “one or two clean kills a month”. That is crazy and, more importantly, totally preventable.

The key to preventing a hypoxic death during rapid sequence induction and intubation (RSII) is to prevent hypoxia. The easiest way to do that to avoid RSII altogether. However, clinical conditions often preclude that choice. So, if we can’t not RSII, then we must do something that comes as close to guaranteeing adequate oxygenation as is humanly possible.

Many RSII protocols simply include a step that includes some variation of the language “Preoxygeanate”. While this is technically accurate, it is miserably vague without proper direction on tools, techniques or timeframes for getting this done. This is especially sad since there is a plethora of evidence to explain exactly how best to do this for the majority of patients.

The history: The concept of RSII is not new to medicine or even to prehospital and transport medicine. Anesthesiologists developed the procedure to safely induce anesthesia and secure the airway of surgical obstetrical patients who were not ideal candidates for general anesthesia induction due to hemodynamic instability or an undocumented fast prior to surgery (1). The process involves the injection of a fast acting sedative and neuromuscular blocker in rapid succession to induce unconsciousness and gross muscle relaxation, thus creating the most hospitable intubating conditions. In transport, we electively perform RSII for patients who meet criteria based on mental status, unstable airways, worsening respiratory status or anticipated clinical course. RSII is not without risks of course, some those being medication allergy, hypotension and failure to achieve the stated goal which is a secured airway. The most common risk, and one of the most dangerous, is hypoxia associated with the requisite apnea that comes with global neuromuscular blockade, and this was one of the first problems that anesthesiologists had to solve.

Science and evidence: Once the paralytic is administered and takes effect, the patient can no longer spontaneously breathe, guaranteeing rapid desaturation and tissue hypoxia unless purposeful steps are taken to actively provide oxygen. This can be done with a BVM and attached reservoir during the apneic period, which will provide up to 97% FiO2. However, positive pressure ventilation increases the risk of gastric insufflation and subsequent vomiting which is particularly dangerous for the patient now unable to swallow or cough. The best prevention for all of these unwanted effects is to proactively build adequate alveolar and plasma oxygen reserves to last through the apneic period during which laryngoscopy and intubation will take place; and do so prior to the induction. This step, simply referred to as preoxygenation, is taught in many airway courses, RSII programs and difficult airway management classes as part of the “P’s of RSII”(2). The idea is simple: displace the carbon dioxide and nitrogen in the patient’s lungs by instilling high flow, high concentration oxygen for a minimum period of time prior to the induction. As part of the process, blood PO2 and oxygen saturation will rise, though these effects will be lesser over the short term. Then, as apnea ensues post induction, the patient will have significant stores available to maintain blood oxygen levels without breathing or, in most cases, any active ventilation at all. Early pioneers of RSI found that safe apnea times could be significantly extended by providing patients with oxygen concentrations greater than room air prior to intubation. Later studies found that a properly preoxygenated healthy patient can maintain oxygen saturations of greater than 90% for up to eight minutes, affording the intubator ample time to perform laryngoscopy and secure the airway before reoxygenation becomes necessary. The problem with reliance on this method is twofold. First, while desaturation occurs relatively slowly in the beginning, once SpO2 falls below 90% the decline towards zero oxygen saturation occurs very rapidly as the patients enters the “steep side” of the oxyhemoglobin disassociation curve. Without the provision of additional oxygen, the risk of secondary brain injury, cardiac dysfunction and death increase greatly. Secondly, the original studies about safe apnea time used healthy volunteers, while the patients who require emergent RSII are usually by definition not healthy at all. For example, morbidly obese patients can lose up to 25% of their functional residual capacity when they are lain supine. When they undergo anesthesia, they can lose an additional 25% (3) Therefore, the steps we take to preoxygenate these patients that would provide safe apnea times of up to eight minutes in “healthy” adults would allow for less than half of that time in this population.

To protect against this desaturation and the negative effects that result, Drs. Weingart and Levitan make several recommendations for RSII preoxygenation in the emergency department that are equally applicable to the transport environment.

1.       NO DESAT (Nasal Oxygen During Efforts to Secure A Tube) In a 2010 article (4) ,Dr. Levitan summarized the old notion of providing oxygen via nasal cannula before and after induction to prolong the safe apnea period. This is not unlike methods used to oxygenate patients passively during brain death testing. In these studies, patients are disconnected from the ventilator to allow their PCO2 to rise while oxygen is instilled without positive pressure via a catheter in the ET tube. While the carbon dioxide levels in the blood continue to climb, oxygen saturations remain at or near 100% and allow for a safe assessment of respiratory drive (5). This works based on two principles. First, oxygen instilled into the nasopharynx at high flow rates (> 15 lpm) flushes the upper airways with oxygen (1) concentrations much higher than we normally think possible with a nasal cannula at lower flow rates. This greatly increases the FiO2 of each inspired breath that the patient takes on their own or that is delivered via PPV. Secondly, because of the solubility of the oxygen and relative negative pressure of oxygen in the alveoli during the apneic period, nasally delivered oxygen will be drawn downward through the trachea and into alveoli where it can diffuse into the capillaries at up to 250 ml/min (1). Studies with apneic oxygenation have shown a near doubling of safe apnea time (SpO2 >92%) vs room air. The nasal cannula can be applied as soon as the decision is made to intubate as part of the preoxygenation regimen; and it can be left in place and flowing regardless of the other devices used to oxygenate (BVM, NiPPV, NRB, etc). Also, it can and should be left in place for the duration of the RSII until the ETT is placed, confirmed and secured.

2.       Two oxygen sources for every intubation attempt. This is not expressly mentioned in the article, but it is implied by the mention of NO DESAT and other oxygenation adjuncts used simultaneously. At a minimum, you should be able to generate enough flow to run two of these devices at 15 lpm. A two port adapter on a high flow source may be adequate, but the best practice would be to have two separate oxygen sources to maximize flow and available oxygen resources. This doesn't differ much from the proper RSII preparation already in place.

3.       Avoid BVM if at all possible.  Before the induction, and especially after, it is best to allow the patient to oxygenate themselves if their respiratory effort is adequate enough to do so. Pressures of as little as 25 cm/H20 can open the esophageal sphincter and allow air to enter the stomach and pressurize the gastric contents, increasing the risk of vomiting and aspiration during the RSII (1). Therefore, if the patient is breathing at all, a standard partial rebreather mask with reservoir (commonly called a non-rebreather mask by EMS and ED personnel) delivering oxygen at >30 lpm is preferable. This, combined with NO DESAT at >15 lpm will provide nearly 100% FiO2 without generating any PPV at all. It is understood; however, that some patients simply cannot breath adequately enough to achieve the necessary level of oxygenation. For these people, see #4.

4.       If you have to BVM; do it slowly, at low volume and use a PEEP valve.  As stated above, it doesn’t take much pressure from a BVM to push air into the stomach, especially for excited or inexperienced providers and in the absence of optimal airway positioning. So it is preferable to wait to start bagging until after the ET tube is in place. But if your patient is so acutely ill that independent oxygenation with a mask and NO DESAT is not possible, you will likely have to use positive pressure to achieve acceptable pre induction saturations. If bagging is your only option, remember these things:

·         Ensure a good, tight mask seal: This is probably the most important step to ensure adequate oxygenation with a BVM. Ideally this is a two person job: one to hold the mask seal and open the airway; the other to squeeze the bag. It is preferable to use nasal and oral airways if possible to maximize BVM effectiveness.
·         Go Slow: Delivering BVM ventilation at a rate of 6-8 bpm with each breath over 1-2 seconds will help to keep the inspiratory pressure below the threshold that would open the esophageal sphincter. The long inspiratory time will also increase mean airway pressure (MAP), a vital component in maintaining oxygenation.

·         Low Volume: Aim for a tidal volume (Vt) of 6-7 ml/kg of ideal body weight (IBW). The lower volume coupled with long inspiratory time should help keep the pressure right about where it should be to avoid aspiration dangers. So how do you set a desired Vt on a BVM? Unless you can measure exhaled Vt through an anesthesia machine, it’s difficult. But, you can know how much Vt your BVM is capable of delivering and work from there. Here is the package insert from a typical BVM:

The most air you can squeeze out of this bag is 850 ml (Maximum Stroke Volume). This is much more than any patient would need based on IBW.  And, by the “Delivered Oxygen Concentration” table at the bottom, you can also see that a volume that large is pretty inefficient for the purposes of oxygenation.  Even volumes of 600 ml as noted in the table would be pretty large related to the IBW of most patients we transport. With that in mind, remember long, slow squeezes of the bag that are enough to make the chest rise.
·         Use a PEEP valve: The purpose of PEEP is to increase MAP, a fundamental component of oxygenation. By applying pressure to the end of expiration, the alveoli are never allowed to fully empty and collapse, leaving oxygen rich air in contact with the alveolar capillary membrane longer and allowing it to diffuse under this pressure. When coupled with NO DESAT, the extra oxygen + pressure will provide a CPAP effect and ultimately extend safe apnea times. 

5.       Stop the intubation attempt when SpO2 reaches 93%, not 90%.  Peripheral pulse ox sensors tell you less about the patient’s hemoglobin saturation now than it tells you about what the saturation was 30-45 seconds ago thanks a concept known as pulse ox lag or latency. And, if your patient is poorly perfused, hypothermic, or in a cold environment, that lag time could be up to two minutes (6). Therefore, when the SpO2 from the right index finger probe reads 90%, the actual percentage of bound hemoglobin is probably closer to 85% and dropping fast. And, from what we know about the oxyhemoglobin disassociation curve, we know that that oxygen saturation will fall precipitously after it drops below 90%, making it difficult to recover before severe hypoxic injury becomes likely. With these two ideas in mind, it is much safer to think of a peripheral SpO2 of 93% as the lowest acceptable before ceasing an intubation attempt and resuming oxygenation. In the literature and in practice this has led to fewer critical desaturations and better outcomes. 

Clinical considerations:  Good RSII training and drills already involve much discussion of preparation and preoxygenation, so adding these steps should be pretty easy. Logistically, we can add a nasal cannula to the intubation kit inventory and PEEP valve either to the same inventory or to every BVM. The protocols can also be updated to reflect specific methods, devices and times for proper preoxygenation.

Discussion: It is often presumed and expected within our industry that critical care transport clinicians are experts in RSII and general airway management. That is something that we can be truly proud of, but something that we also must earn every time we are called upon to transport a patient in need of this important, time critical skillset. In order to maintain the confidence placed onto us by our peers, we must continually train, drill and educate ourselves to make sure we’re taking the best care of our patients. The methods detailed above represent the most current, evidence based techniques for improving oxygenation during the requisite apneic period following neuromuscular blockade and should be employed with every RSII. The techniques cited in these studies differ somewhat from our current practice, suggesting by the research and results that our standards need to be reviewed and updated to reflect industry best practices. Whatever your feelings about the bougie or video laryngoscopy or any other tool, it’s pretty hard to argue with the value of oxygen, or more importantly the negative value of its absence. There has been much in the news lately of patients suffering anoxic brain injury that can be directly linked to poor airway management by EMS and transport crews. This possibility is real each time we care for a patient with an advanced airway in place, but it is especially applicable to those patients in whom we perform the induction and place the airway ourselves. By employing our sound clinical judgment, following our protocols and providing oxygenation in the manner described above, we should be able to avoid oxygen desaturation in nearly all of our patients. 

1.       Weingart S, Levitan R. Preoxygenation and prevention of desaturation during emergency airway management. Annals of Emergency Medicine. 2012; 59: 165-75
2.       Walls R, Murphy M. Manual of Difficult Airway Management, Fourth Edition. Philadelphia, PA: Lippincott. 2012
3.       Damia G, Mascheroni D, Croci M. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anesth. 1988; 5: 574-78
4.       Levitan R. NO DESAT!. Emergency Physicians Monthly. Published December 9 2010. Accessed October 2, 2014
5.       Wijdicks E, Varelas P, Gronseth G. Evidence-based guideline update: determining brain death in adults. American Academy of Neurology. 2010; 74: 1911-18
6.       David D, Aguilar S, Sonnleitner C. Latency and loss of pulse oximetry signal with the use of digital probes during prehospital rapid-sequence intubation. Prehospital emergency care. 2011; 15: 18-22

No comments:

Post a Comment