We often times recognize a successful intubation as passing the tube through the cords. In reality, there’s a lot more to it than just that. A successful intubation includes adequately resuscitating your patient prior to the intubation, successfully delivering the tube, and providing proper monitoring and care after delivering the tube. Often times a great deal of emphasis is placed on the anatomically difficult airway with little regard given to the physiologically difficult airway. In the words of Scott Weingart… “Every time you pick up a laryngoscope you’re essentially being given a license to kill. How you go about using that license depends on how much you care about your patients.” Everybody loves the term “resuscitate before you intubate”, but what does that really mean?

You arrive on scene at a vehicle vs pedestrian. You note one male patient that appears to be in his 20s lying supine on the ground. He’s breathing 8 times a minute and you note copious amounts of blood coming from his mouth. He’s clenched and responds slightly to pain. You’ve exhausted all other airway management options using an escalating approach and then elect to move down the RSI pathway. No surgical airway options are available. Vitals are as follows:

• Blood pressure: 80/40 mmHg
• Heart Rate: 130
• SpO2: 85%
• Respirations 8

You prep your equipment and draw up a 2 mg/kg dose of ketamine and a 1.5 mg/kg dose of succinylcholine. You spike a bag of not so normal saline and run it wide open. You push your ketamine and follow it up after roughly one minute with the succs. You’re able to successfully deliver the tube. Vitals reassessment reveals the following:

• Blood pressure: Unable to obtain due to low perfusion status

• Heart Rate: 30 (with no palpable pulses present)

• SpO2: Unable to obtain due to low perfusion status

• Respirations: 10 per minute (assisted)

Your patient has deteriorated into a PEA arrest. SO WHAT THE HELL HAPPENED….

• 

Okay let’s break it down..

  When hypotension exists within the peri-intubation period this is an incredibly risky situation. Starting off hypotensive is the biggest predictor of patients coding during the intubation. Allow me to repeat… Starting off hypotensive is the biggest predictor of patients coding during the intubation! So what does this tell us? Once again, in the words of Scott Weingart: “the ways that patients perish are predictable and often times preventable.”

What are some ways to combat this?

• Volume resuscitation
• Push dose pressors
• Dosing medications appropriately

  I’m a strong advocate of permissive hypotension, but unfortunately permissive hypotension doesn’t apply when you’re trying to manage an airway. If you’re backed into a corner trying to manage a hypotensive trauma patient’s airway, you have to recall that airway is still the A of the ABCs. Unfortunately, most prehospital ground ambulance transport systems don’t carry blood product. If you’re equipped with blood product, then it becomes necessary to pound these patients with product in an effort to stabilize their pressure before progressing down the RSI pathway. Resuscitation with whole blood product is most ideal to restore the much needed circulating blood volume. As stated in a previous post, normal saline is bad so please don’t flood your patients with it if at all possible.

  In general, there’s not strong evidence to support giving pressors to patients in hemorrhagic shock.  When attempting to manage the airway of the hemodynamically unstable trauma patient, we’re seeking rapid changes/improvement in the hemodynamic status to facilitate safe delivery of an advance airway. Push dose pressors seem to be the best route towards achieving this with push dose epi most likely being the best option. But what if my patient is already tachycardic? Won’t epi make them more tachycardic? There’s nothing that causes tachycardia like shock. I would seldomly withhold giving push dose epi in trauma because of heart rate. One of the most important factors in restoring adequate perfusion is inotropy. The goal is to get these patients around the corner until we can get them resuscitated with blood. In some patients, such as an elderly patient with significant cardiac history, it becomes necessary to weigh the risk vs benefit.

There are two ways we can kill the shocked patient with induction agents:

• Direct pharmacodynamics of the drug where the drug wipes out your cardiac output.
• Sympatholysis

Let’s talk about sympatholysis. When you experience pain, your body experiences a catecholamine surge which drives up your heart rate and blood pressure. The injured trauma patient is pounding out their sympathetic drive. When we give these patients drugs that take away their pain, we run the risk of eliminating their sympathetic drive indirectly. We’re chilling them out and taking them from a heavy metal state to a slow reggae state. This is where ketamine can be dangerous. Ketamine is a sympathomimetic. There’s some truth in that it increases the heart rate and blood pressure which therefore increases the mean arterial pressure. We have to remember though that most trauma patients are experiencing pain. Due to ketamine reducing pain, this agent can reduce sympathetic drive and cause hypotension. Though ketamine is probably the best agent for intubating the shocked patient, it’s not a get out of jail free card. Often times it’s not the drug as much as it’s the dose.

Before I dive into what I’m going to say next, please note that I’m an advocate of patients having no memory or awareness during intubation if possible. In the instance of the hemodynamically unstable trauma patient, the goal of no memory or awareness at times needs to take a back seat to keeping them alive. With that said, reducing the dose of ketamine to 0.5 – 1 mg/kg may be necessary. Yes they might maintain some degree of awareness but this will aid in curbing sympatholysis. Administer your ketamine slowly over a minute and monitor your patient’s hemodynamic status.

When dosing paralytics, it’s important to remember that the full onset may be delayed due to the shocked state. Hypotension causes a delay in the paralytic reaching the more distal musculature. We combat this by dosing our paralytics high. Additionally, utilizing push-dose epinephrine to augment the delivery of the paralytic to the distal musculature might be a reasonable option.

When we intubate patients we reverse their natural physiology. We convert their beautiful negative pressure ventilations which do wonderful things for preload by augmenting venous return, over to positive pressure ventilations. Every time you take a breath your heart essentially receives a bolus of blood. With that being said, if we’re not cautious with our ventilation strategy, we can cause further hypotension and a decline in our patient’s overall status.

Additional Pearls:

• When a pulse oximetry is placed on a finger, there’s a predictable lag from what’s happening centrally to what’s being reflected peripherally. It’s as simple as the blood in the finger not being in central circulation for 20-30 seconds. In severe shock, pulse ox lagging can be significantly longer… like up to 3 minutes.

• A pre-intubation shock index ≥ 0.90 may be utilized as an indication that your patient is more likely to suffer from post intubation hypotension. Check out the video posted below for more on shock index.

The following was to highlight some of the areas we go wrong when attempting to intubate our hemodynamically unstable trauma patients. The ultimate goal is elegant resuscitation that subsequently leads to improved patient outcomes. I believe a big part of approaching these patients appropriately is moving away from the traditional RSI approach (which implies a crash airway) and moving down the DSI pathway. Check out Weingart’s video below on DSI.

Below is another fantastic video put together by Williamson County EMS on DSI.

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This site is meant to be used for educational use only. We strive to push evidence based medicine with no bias to help you obtain all the important information. You should always follow your protocols that have been set in place.

References

Scott Weingart, MD FCCM. Podcast 104 – Laryngoscope as a Murder Weapon (LAMW) Series – Hemodynamic Kills. EMCrit Blog. Published on August 5, 2013. Accessed on December 12th 2020. Available at [https://emcrit.org/emcrit/intubation-patient-shock/ ]

https://read.qxmd.com/read/27130803/hemodynamic-response-after-rapid-sequence-induction-with-ketamine-in-out-of-hospital-patients-at-risk-of-shock-as-defined-by-the-shock-index

Kim WY, Kwak MK, Ko BS, Yoon JC, Sohn CH, Lim KS, Andersen LW, Donnino MW. Factors associated with the occurrence of cardiac arrest after emergency tracheal intubation in the emergency department. PLoS One. 2014 Nov 17;9(11):e112779. doi: 10.1371/journal.pone.0112779. PMID: 25402500; PMCID: PMC4234501.