The ICU Gotchas: Peri-intubation arrest

Newcomers to critical care are often uncertain what they need to “know.” This is particularly the case for providers like APPs, for whom the training process is often informal and without clear competencies. As a result, many people feel a sort of wariness, a foreboding sense of an infinite body of unknown hazards lurking.

While this is true, many of the unknowns will wait for you to find them. Zebras usually stay in their pastures. However, there are some pitfalls that simply must be taught. They exist at the treacherous combination of being non-obvious (their truth, or at least their importance, can’t be guessed or derived from first principles), yet also precipitously hazardous. These are the hidden surprises of our field, and you just gotta learn ’em— because sometimes the most important parts of this job aren’t knowing what to do, but knowing what can go wrong.

Here, then, is the first in a short series on ICU “gotchas,” starting with peri-intubation hypotension and cardiac arrest.

The scene

When you first laid eyes on the septic patient an hour ago, you suspected they were headed towards intubation. Though awake, they were lethargic; and though breathing, they were fatiguing. Their blood gas was barely adequate and a repeat now shows worsening acidosis. Time to pull the trigger.

You set up your blades, tubes, drugs, and backup devices. The airway looks anatomically straightforward and you feel confident, so you proceed to induce and paralyze. You pass the tube without difficulty and the end-tidal CO2 gives you a visual high-five. Yahtzee!

But as you’re turning away to order an x-ray and tidy up, the nurse calls your attention to the monitor, where the blood pressure has fallen from 96/45 to 40/20. Alarmed, you call for a fluid bolus and cycle the cuff, but this time it just hums and hums until finally registering as undetectable. The nurse now informs you that he cannot feel a carotid pulse. With a sinking feeling, you start chest compressions.

What happened?

Peri-intubation hypotension isn’t mysterious; in fact, it’s a good demonstration of basic physiology we know and love. Let’s look at the key components.

(One thing we won’t discuss today is refractory hypoxemia. If a patient needs intubation for respiratory failure, and you’re unable to preoxygenate their SpO2 above 80%, your safe apnea window to intubate before their sat bottoms out is going to be negligible. Hopefully that risk is fairly obvious, however. Let’s look at the less obvious problems.)

Conversion to positive pressure

As we breathe spontaneously, our diaphragm drops and thoracic wall expands, creating negative intrapleural pressure. This suction expands the lungs, but it also sucks outward at the vena cavae and right heart, improving their preload—particularly important during states of shock. When we switch this physiology to positive pressure breaths—whether by intubation, non-invasive ventilation, even bag-mask breathing—the intrapleural pressure suddenly becomes positive, crushing the right heart rather than assisting its preload. The combination of hypovolemia (which might otherwise be tolerated due to compensatory mechanisms) and positive pressure can be especially dire.


It’s no surprise that many of the drugs used for induction can have hypotensive effects. Propofol is the most classic vasodilator and should be used with great caution in shock. However, less obvious is the impact of ostensibly “hemodynamically neutral” agents. Harken back to the distinction between sympatholytic and parasympathomimetic effects. A drug like etomidate or midazolam may have little direct parasympathomimetic impact, and if given to a healthy patient might not affect their blood pressure. Yet they’re still sedatives, and all sedatives will blunt the sympathetic response to shock, which in some patients is the only thing keeping their head above water. Take that compensation away, and they drop like a rock.


A less common but still important contributor, hypercarbia occurs when an already-acidotic patient becomes apneic. You’re the reason, of course, because of your paralytics, or from sedation alone. We usually focus on avoiding hypoxia during intubation, presuming that mild increases in PCO2 will be tolerated. However, in a patient whose pH is already 7.05—and would be much lower were they not vigorously hyperventilating their PCO2 down to 9—even a brief period of apnea during intubation can kick the legs out from their compensation, causing overwhelming acidosis and cardiovascular collapse.

What’s the solution?

The prescription is simple, if not necessarily easy.

  1. Be wary. Every time you consider intubation, your mind should scan through a checklist of potential dangers, beyond the mere anatomic challenges. What physiologic processes might be exacerbated, such as poorly-resuscitated shock or acidosis? Importantly, don’t just look for obvious or decompensated signs of such things; look for underlying problems currently being masked by compensation, such as tachycardia, a grossly underfilled heart on ultrasound, or a dramatically varying pulse pressure.
  2. Resuscitate before you intubate. Despite Tyler Christifulli‘s law that “if it rhymes, it can’t be true,” this one holds up. While some critically ill patients require intubation to be fully stabilized, in most cases, it can wait a few minutes. If you’re intubating someone for shock or obtundation, take a breath first, pause, and optimize hemodynamics before you think about touching their mandible. For bleeding patients, get some blood on board. For septic patients, bolus fluid, and have more at hand in case it’s needed post-intubation. (In fact, leaving a free-flowing IV is good general intubation practice anyway, to confirm IV patency and carry your meds.) If the blood pressure has been borderline, hang a pressor drip, even if it’s not needed yet—if it drops, you can just switch it on, rather than losing time while drugs are found, mixed, and hung.
  3. Intubate delicately. Your approach to induction and intubation should respect the underlying physiology and aim to perturb it as little as possible. Shocked patients should have their sedative dose reduced significantly. While these folks still deserve sedation, their hemodynamics are unlikely to tolerate the “normal” doses found in textbooks. Fortunately, shock itself is a sedative, so using the math of shockiness + drug dose = sedation, the worse the shock, the lower the dose. Select the most hemodynamically stable agents, such as ketamine or etomidate. Be prepared with pressors, whether as a hanging bag or syringes of phenylephrine or epinephrine. For the acidotic patient, minimize their apnea time, perhaps even by avoiding paralytics and using an induction drug that spares the respiratory drive (such as ketamine); or consider a fully awake intubation, which often involves assistance from our anesthesia colleagues.


Intubation is a high-risk event that should always be done thoughtfully and respectfully. However, for the incautious, it’s easy to start to think of it as a purely mechanical process, where the only possible challenges are finding the right hole and shoving plastic inside it. Instead, view it as a fundamental alteration in the patient’s homeostasis, one that changes the basic foundation of their cardiorespiratory system by putting brakes on what the patient is doing for themselves and saying, “I’m going to do this for you.”

That’s no problem—but you’d better be up to the task. Bodies are pretty good at compensation, so don’t underestimate the magnitude of what you’re taking on, or you’ll drop the ball, and drop it fast.

Now go forth, and intubate delicately.

[Read the second Gotcha here: Pulmonary hypertension and right heart failure]