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Patient Care

The Perils of Peri-Intubation Hypoxia

Mrs. Smith is a 68-year-old wife, mother, and grandmother. She has been feeling “punky” for a few days—nothing specific, just not quite right. Today she starts to get a bit short of breath.

Because of her history of medical problems, this isn’t unusual for Mrs. Smith. She takes her albuterol inhaler and continues to take her daily furosemide as prescribed. Unfortunately her breathing gets worse, eventually becoming bad enough that she calls 9-1-1. 

A medic unit and field supervisor respond to her home. They find her sitting upright in her living room in obvious respiratory distress. She is sweaty and anxious. They begin their assessment and find her to be tachycardic, mildly hypertensive, and afebrile, with a saturation of 90%. They apply a nonrebreather mask while assessing breath sounds. Hearing expiratory wheezes, they administer nebulized albuterol and ipratropium. Her pulse oximetry does not improve. In fact, it begins falling. 

Realizing the nebulizer alone isn’t working, they place her on CPAP. Unfortunately Mrs. Smith is becoming agitated and confused. She starts trying to push the CPAP mask off her face. She isn’t tolerating their attempts to help her. After a brief discussion the crew collectively decides she has failed noninvasive ventilation and proceeds to intubation with rapid-sequence induction (RSI). They push 2 mg/kg of IV ketamine, rapidly followed by 2 mg/kg of IV succinylcholine. 

As Mrs. Smith relaxes and becomes apneic, they lower her to a supine position on the ground. Medics begin to intubate her using a video laryngoscope. Everyone watches the display as what was anticipated to be an easy intubation becomes difficult. Nobody, however, is watching the monitor.

86%. 80%. 75%. 60%.

Mrs. Smith, who had an initial heart rate of 120, is becoming bradycardic. Her rate drops faster and faster. 80. 50. 30.


Mrs. Smith is now in asystole. Recognizing this, medics abort the intubation attempt, begin compressions, and ventilate with a BVM. Her saturation improves to 90%, and they get pulses back. A second paramedic attempts intubation and is successful. Her saturations rise to 96%, and her pulse and blood pressure stabilize. Whew! 

The medics tell themselves Mrs. Smith is very sick, and sometimes these things just happen. “Nothing we could have done differently.” Fortunately all is well now, so no harm, no foul. 

However, Mrs. Smith never wakes up. She has permanent hypoxic brain injury and remains in a vegetative state. Her husband, children, and grandchildren won’t get her back. All because of an unforeseeable and inevitable illness.

But was it really unforeseeable? Was it really inevitable?

Mrs. Smith suffered a peri-intubation hypoxic cardiac arrest—a rapid-sequence death. This is not only predictable but preventable. By systematically changing the way we approach intubation, we can prevent this and assure that future Mrs. Smiths get to go home to their families. 

Peri-Intubation Hypoxia

Intubation has been a part of paramedic training since the first national curriculum. Training materials have always mentioned some variety of the P’s of intubation: preparation, preoxygenation, pretreatment, and paralysis. Unfortunately most of these P’s have been glossed over in both training and practice. Many medics (and physicians) skip straight to the “sexy” step of inserting the endotracheal tube. This disregard for the fundamentals has made peri-intubation hypoxia common in both EMS and the hospital. 

In a 2003 study of EMS RSI in patients with traumatic brain injuries, 57% of patients had at least one hypoxic episode during intubation.1 The majority of these (81%) were not hypoxic to begin with and were felt by the intubating medics to be “easy tubes.” Nine percent of these patients also experienced bradycardia. 

More recently a team led by investigators from Physio-Control found 43% of patients undergoing EMS RSI experienced peri-intubation hypoxia; 68% were severe (SpO2 less than 80%).2 The median attempt nadir (lowest saturation) was 71%, and the 25th percentile was a shocking 36%. This means a quarter of all intubations had saturations during intubation of less than 36%! These were not brief episodes; the median duration was two minutes. This was also in a system with an above-average first-pass success rate (FPS) of 82%. In fact, 70% of all desaturations occurred on first pass. Clearly FPS alone is not sufficient to prevent hypoxia. 

This doesn’t just occur in the field. Of 166 emergency department RSI intubations, 36% experienced a peri-intubation hypoxic episode. Of these, 93% were not hypoxic to begin with.3 

This isn’t a function of bad paramedics or physicians. As humans, we are prone to becoming task-saturated during critical events, such as intubating a sick patient (and we don’t exactly intubate nonsick patients). Of 100 directly observed ED intubations, physicians underestimated both how many patients had desaturation (23% observed vs. 13% perceived) and how long the intubation attempt took (45 seconds vs. 23 seconds).4 This is a function of being human, not a bad provider. We are not able to reliably intubate and monitor patients during an emergency. We need to systematically change how we intubate to avoid this. 

Peri-intubation hypoxia is not only common, it is also harmful, particularly in patients with conditions that do not tolerate hypoxia and tissue ischemia well—traumatic brain injury, for example. The odds ratio for death in these patients with one episode of hypoxia in a prehospital study was 3.9.5 This means the odds of death were 290% higher for patients with hypoxia than those without.

This wasn’t an isolated finding; in a large state registry of TBI patients, the odds ratio of death in patients with hypoxia was even higher, 6.6.6 This study also looked at the effects of hypotension and found that a single episode of hypotension was associated with 340% higher odds of death and, shockingly, the odds of death in patients with both hypotension and hypoxia were 1,220% (OR 13.2) higher than for patients who had neither. 

Hypoxia is also associated with hemodynamically significant bradycardia and cardiac arrest. In an academic ED study, 2% of all RSIs had a peri-intubation cardiac arrest, and more than 80% of these were from hypoxia.7 

The Importance of First-Pass Success

Much attention has been paid to achieving first-pass success when intubating. Why is this important? Because failure to achieve it is associated with an increase in adverse events, the most common of which is peri-intubation hypoxia. 

In a study of more than 1,800 ED intubations, the rate of all adverse events was 14% with FPS but increased to 47% with two attempts and 64% with three.8 The most common of these events was hypoxia (9.2% seen with FPS, 38% with two attempts). The odds of having an adverse event with more than one attempt were 652% higher than with FPS. These odds were also seen in an even larger study of 2,616 patients undergoing intubation in 11 Japanese EDs, where the OR for major adverse events was 8.9 with two attempts and 13.9 with three compared with FPS.9 

In addition to increasing the odds of adverse events, multiple attempts are also less likely to succeed. There is a “plateau point” above which further attempts are statistically futile.10 For prehospital ETI that point is 3–4, but each additional attempt comes at a clinical “cost,” so the actual attempt limit likely should be lower. 

If peri-intubation hypoxia is common and harmful, it would be nice if it were predictable too. Fortunately it often is. The classic oxyhemoglobin dissociation curve is a plot of different SpO2 values at varying PaO2 levels.11 Figure 1 shows this is a sigmoidal curve, not a linear one. It demonstrates that the rate of desaturation is different at different points on the curve. Above a PaO2 of around 90, the curve is flat, at a saturation approaching 100%. Once PaO2 drops below 60 (SpO2 around 90%), small drops in PaO2 are associated with large drops in SpO2. This is the steep part of the curve. 

This physiologic curve manifests itself in clinical practice. If your patient has an SpO2 of 100% at the time of paralysis, they will slowly desaturate until reaching an SpO2 of around 93%, at which point they desaturate progressively faster.

In other words, they “fall off the curve.” Of prehospital patients undergoing RSI intubation, 100% had peri-intubation hypoxia if their starting saturation was less than 93%.12 This is an indication of how rapidly patients desaturate once they become hypoxic.

In another study patients with a starting saturation between 98%–100% had a rate of peri-intubation hypoxia of only 20%.2,12 This indicates that patients with starting saturations above 93% can tolerate a longer period of apnea without desaturating, allowing more safe time for a controlled intubation attempt. 

So it is predictable that patients with starting saturations of less than 93% are at very high risk of peri-intubation hypoxia.13 Preventing desaturation, then, depends at least partially on having good data on your patient’s saturation. Unfortunately pulse oximetry data tends to go missing, especially during hectic intubations. Of patients with TBI undergoing RSI, 79% had at least one SpO2 “dropout” during the intubation—there was simply no oximetry value displayed.14 Additionally, the actual value displayed is a bit delayed. In 55% of intubations the intra-attempt SpO2 nadir occurred after resumption of ventilations with oxygen. 

We can use this information to improve the safety of our intubations. First, do everything possible to assure the pulse oximetry probe is firmly affixed to the patient somewhere other than distal to the BP cuff and is not inadvertently dislodged. Next, don’t wait to abort an intubation attempt until the SpO2 drops below 90%. We must assume that because of “pulse ox lag,” the patient has already desaturated. The safe place to bail out of an attempt is when the SpO2 hits 93%.


To fully maximize preoxygenation we need to not only increase the SpO2 to above 93% but keep it there long enough to completely fill up the patient’s physiologic “buffer.” In most healthy patients this is accomplished by normal-tidal-volume breathing for three minutes.15 So we need to raise the oxygen saturation above 94% and keep it there for at least three minutes.

The point of this is to replace the inert gas in the lungs and blood with oxygen. Because the atmosphere contains 21% oxygen and 78% nitrogen, our lungs contain the same ratio. Breathing 100% oxygen will come close to completely replacing all the nitrogen in the lungs with oxygen in about three minutes. This process of gas replacement is known as denitrogenation. This term is often used synonymously with preoxygenation. Keep in mind that this three-minute guideline is based on healthy patients. We are not typically intubating healthy patients, so consider extending your preoxygenation time.

If the SpO2 drops below 94% during the three minutes of denitrogenation, change something to get the saturation back above 93% and reset the three-minute period. Likewise, if the SpO2 drops below 94% during an intubation attempt, bail out and do whatever is needed to get the saturations back above 93% for another three minutes prior to the next attempt.

Preventing Peri-Intubation Hypoxia

If peri-intubation hypoxia is common and harmful, how do we prevent it? Fortunately the answer is not all that complex: Stop intubating hypoxic patients—it really is that simple. That doesn’t imply not doing anything; it means fix the problem first, then proceed with intubation. Frequently this is a matter of taking simple steps to optimize preintubation saturation. 

EMS educator Jason Cook coined the term SEXY bagging to describe several components of a “preoxygenation toolbox”:

  • S—Use a Second provider when making a mask seal;
  • E—Place the patient in an Ear-to-sternal-notch position;
  • X—Use the eXtra stuff available to you; 
  • Y—Have a Yankauer suction catheter ready for use.

Unfortunately most EMTs and paramedics are not adequately trained and don’t practice making a good face mask seal. We were all taught to use a one-handed “EC” seal. Stop doing this. We should instead use the more effective two-handed, thumbs-down seal, with your fingers lifting the mandible up into the mask while your thumbs, facing down toward the patient’s feet, hold the seal (Figure 2). This two-handed seal delivers higher tidal volumes with less air leak than the traditional one-handed method.16 

All too often, when we realize we don’t have an adequate seal, we simply press the mask down harder onto the patient’s face. This is actually counterproductive: It presses the mandible posteriorly, inadvertently occluding the airway. Lift, don’t push (the mandible). If the patient needs assistance with ventilation, the second provider will provide these gentle ventilations. 

Proper positioning is key to effective ventilation, oxygenation, and intubation. While we often pride ourselves on being able to intubate patients in very difficult positions, we really shouldn’t. Just because we can do something doesn’t mean we should. Positioning is a perfect example of this. There is no law that says we must intubate the patient where we find them. Instead, move your patient into a position where you are more likely to succeed. For oxygenation, ventilation, and intubation, this means elevating the patient’s head and placing them in an ear-to-sternal-notch position (Figure 3). This position has the neck extended and the face parallel with the ceiling. The ear canal will be level with the sternal notch. 

Because we come prepared with all manner of equipment to aid our patients, we should use these extras, including lots of oxygen. While too much oxygen can be harmful, this doesn’t apply when preoxygenating a patient. Give them as much as you can temporarily during the intubation, then titrate down to the lowest fraction of inspired oxygen (FiO2) needed to maintain your goal saturation. Use two sources of oxygen, one for the BVM and another for a nasal cannula. Turn both sources up as far as the regulator will go. Often this is past the highest number on the dial. Using a nasal cannula under a BVM does two things: It provides an extra source of oxygen to further increase the FiO2, and, most important, it allows you to easily transition to apneic oxygenation during the intubation attempt.

Use waveform capnography before, during, and after the intubation attempt. In addition to confirming tube placement, the waveform can also be used as an indirect measure of tidal volume. We typically try to assess chest rise to judge the adequacy of ventilations; however, because of large patient size, truly judging chest rise is often a bit of a crapshoot. Waveform capnography allows us to estimate tidal volume and is the most sensitive and specific means of verifying ET tube placement. 

Have a PEEP valve attached to your BVM. With PEEP attached and on to at least 5 cm H2O, a BVM is capable of delivering oxygen without squeezing. Our goal is to avoid squeezing the BVM in spontaneously breathing patients with adequate tidal volumes. Doing so leads to increased intrathoracic pressure, decreased cardiac preload, lower blood pressure, and gastric insufflation of the stomach. All of these are to be avoided. If you are still unable to achieve adequate saturations despite good tidal volume, maximal oxygen flow through two sources, a good seal, good positioning, and an adequate respiratory rate, increase the PEEP. This often increases alveolar recruitment sufficiently to raise saturations.

A common cause of failed airway attempts is secretions/vomit in the airway. Fortunately we have suction for this, provided it is available and turned on, and we are using a large-bore suction catheter. While we use the term Yankauer synonymously with all suction catheters, we really shouldn’t. Not all catheters are created equal. Use a large-bore catheter for the industrial-strength airway material we frequently encounter. 

Use all the SEXY bagging tricks in your toolbox to adequately preoxygenate your patients and prevent peri-intubation hypoxia. 

Evidence for the Preoxygenation Toolbox

Placing the patient in a head-up position improves the percentage of glottic opening (POGO) as the head elevation increases, improving intubation.17 Head elevation also prolongs the safe apnea period, delaying the time until SpO2 begins to drop.18

Using a BVM or noninvasive positive-pressure ventilation (NIPPV) provides better preoxygenation than a nonrebreather mask.19,20 Using a nasal cannula under the NIPPV mask does not increase air leakage and eases the transition from preoxygenation to apneic oxygenation.21,22 Using NIPPV, which includes BiPAP, CPAP, or BVM with flush-rate oxygen and PEEP, provides improved oxygenation and less peri-intubation hypoxia compared with NRM alone.23

Implementing a bundle of care aimed at good preoxygenation was associated with decreased rates of desaturation from 58% to 14% and improved intubation success from 89% to 98%.24 Maintaining a preintubation SpO2 greater than 93% for more than three minutes was associated with 380% higher odds of FPS without hypoxia.25 

Apneic oxygenation works. It was associated with decreased desaturation in healthy OR patients after paralysis for up to 55 minutes (do not try this at home; each of these patients had a pH less than 7),26 is associated with 120% higher odds of FPS without hypoxia,27 and decreased the rate of peri-intubation hypoxia from 29% to 7%.25 In a systematic review and meta-analysis, apneic oxygenation was associated with 34% lower odds of peri-intubation hypoxia.28 

Delayed-sequence intubation (DSI) is the process of giving ketamine followed by a delay in inducing paralysis to allow for better preoxygenation. DSI improved the SpO2 from 89% after maximal efforts at preoxygenation to 98% in ICU patients29 and has been safely implemented in EMS.30 

Implementing It in Texas

After experiencing a sentinel event with a critical patient involving peri-intubation hypoxia, Texas’ Williamson County EMS undertook a continuous quality improvement project aimed at changing the environment, culture, and processes around intubating nonarrest patients. The aim of the project was to prevent peri-intubation hypoxia.

First we went back and looked at our data to make sure our critical event wasn’t isolated. It was not. In fact, 44% of our RSIs had a peri-intubation hypoxic event, and we found two additional cases of peri-intubation cardiac arrest, putting us in line with existing literature on the frequency of these occurrences.31 

We implemented a bundle of care that consisted of a mandatory checklist-driven protocol that included proper positioning, goal-directed preoxygenation, apneic oxygenation, and DSI for all patients. Positioning required the head of the bed to be elevated at least 15 degrees and the patient placed in an E2SN position.

Goal-directed preoxygenation required the use of a BVM with PEEP and reservoir with flush-rate oxygen held in a two-person, two-thumbs-down seal, achieving a SpO2 of greater than 93% for at least three minutes. Nasal cannulas were placed and increased to flush rate after sedation. DSI was performed with ketamine and rocuronium on all patients. If we could not achieve our goal saturation, intubation was not allowed under any circumstances. If the patient needed airway protection and could not achieve this goal, an i-gel could be placed. 

We published the results earlier this year, comparing 104 intubations performed before implementing this bundle to 87 done after.32 Patient characteristics of the two groups were the same. The primary outcome of the study was the proportion of patients who experienced peri-intubation hypoxia. This rate decreased from 44.2% to 3.5% after implementing the bundle. The 25th-percentile peri-intubation nadir increased from 73.8% to 96%, and the rate of bradycardia decreased from 18.3% to 2.3%. We graphically represented the change in the SpO2 at the beginning of the intubation attempt (after maximal preoxygenation efforts) and the SpO2 nadir in Figure 4. 

A Call to Action

Our experience clearly demonstrates that paying attention to the details of intubation, particularly achieving adequate preoxygenation, proper patient positioning, apneic oxygenation, goal-directed oxygen saturations, and using delayed sequence intubation, can decrease peri-intubation hypoxia. This isn’t the only way to achieve this goal, but it worked well for us and can work for others. 

If all agencies adopt this or a similar approach, we can collectively ensure there are no more cases like Mrs. Smith’s. Help make intubation safer by avoiding peri-intubation hypoxia.  


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30. Waack J, Shepherd M, Andrew E, Bernard S, Smith K. Delayed Sequence Intubation by Intensive Care Flight Paramedics in Victoria, Australia. Prehosp Emerg Care, 2018 Feb 6; 1–7.

31. Mort TC. The incidence and risk factors for cardiac arrest during emergency tracheal intubation: A justification for incorporating the ASA Guidelines in the remote location. J Clin Anesth, 2004; 16: 508–16.

32. Jarvis JL, Gonzales J, Johns D, Sager L. Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia. Ann Emerg Med, 2018 Mar 9 [epub ahead of print].

Jeffrey L. Jarvis, MD, MS, EMT-P, FACEP, FAEMS, is EMS medical director for the Williamson County EMS system and Marble Falls Area EMS and an emergency physician at Baylor Scott & White Hospital in Round Rock, Tex. He is board-certified in emergency medicine and EMS. He began his career as a paramedic with Williamson County EMS in 1988 and continues to maintain his paramedic license.  

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