Previously, I wrote a blog on pre-oxygenation, referencing my personal “weapon of choice” as chosen from the 7 Ps of RSI. I discuss that pre-oxygenation, to me, is ONE of the most important Ps of the 7, also mentioning physiologic optimization as a same-tier choice. But, putting them both into one blog would make for a read far too long to maintain even my attention span (which honestly is pretty short). This entry is about me selecting a new weapon. This time physiologic optimization with a primary focus on hemodynamics.
As of recent, some changes to the 7 Ps of RSI have been made. Namely, the third P, previously known as pre-intubation optimization, now known as physiologic optimization. Physiologic optimization involves identifying and mitigating areas of cardiopulmonary vulnerability that may complicate resuscitative efforts, even if tracheal intubation goes quickly and smoothly, further stating that if the need for intubation is not immediate, abnormal hemodynamic parameters should be normalized as much as possible prior to intubation . This blog will focus on this new “P” and ways to identify and mitigate those areas of cardiopulmonary vulnerability as it applies to hemodynamics.
What about the 8 Ps, or the 9 Ps of RSI? (Dropdown)
While I believe FlightBridgeED was the first to use the 8 Ps (to the best of my knowledge) and Life in the Fast Lane used the 9 Ps of RSI, all of the information is pretty well the same 💩 , just broken up in a different manner.
Why is Physiologic Optimization Important?
As reported within the 6th edition Manual of Emergency Airway Management, there are cardiac arrest rates between 1% and 4%, with other complications (mostly hypoxemia and hypotension) as high as 30% in patients with first-pass success [1, pg 29; 4-10]. Up to 44% per other sources . And according to a paper from Russotto et al. titled “Intubation Practices and Adverse Peri-intubation Events in Critically Ill Patients from 29 Countries,” at least one major critical event occurred after intubation in 45.2% of patients, which included cardiovascular instability, severe hypoxia, and cardiac arrest . Of note, in the paper by Russotto et al., the patients had to have an oxygen saturation greater than 80%, a blood pressure of 90 SYS/MAP 65 or higher, and not have required intubation due to cardiac arrest prior to the intubation procedure for inclusion. This means that if the patient was dead, critically hypoxic, or hemodynamically unstable, they were not included. So… these patients were meeting near the criteria many of our pre-hospital guidelines require before intubating our patients (e.g., MAP > 65 mmHg, SYS BP > 90 mmHg) — You know, patients with normal or near normal parameters still experiencing major critical events… 😱😱😱
Depending on the research you look up, these numbers and statements vary as well. Likely due to different definitions for hypotension and adverse/major critical events, but the numbers remain higher than we would ever like — Kinda scary 💩 when you think about it. Either way you look at it, the words cardiac arrest, death, morbidity, mortality, adverse events, major critical events, and complications appear in the literature far too often.
With approximately 1 in 3 patients suffering cardiovascular collapse and nearly 1 in 30 experiencing cardiac arrest, emergency airway management MUST include peri-intubation management of hemodynamics with an overarching goal to safely transition the patient, often with little to no reserve, through apnea and laryngoscopy to PPV [1, pg 26].
RSI is dangerous for a host of reasons, and optimization is an important component of the procedure. We should take purposeful measures for the mitigation of cardiovascular collapse.
How Do I Predict Physiologically Difficult Airways?
For a host of reasons, the patient can decompensate from physiologic abnormalities during the intubation procedure. These abnormalities can be seen as a single finding or in conjunction with many, and with the administration of induction agents, the apneic period, and the transition to PPV, the patient’s hemodynamic status may be exacerbated. With the use of the mnemonic CRASH, we can identify the most seen pre-intubation abnormalities that should be considered .
For a more in-depth dive into the CRASH Mnemonic, consider reading my previous blog: The Physiologic CRASH: Identifying Peri-Intubation Abnormalities.
We must also consider patient factors that are associated with a higher likelihood of cardiovascular collapse [1, pg 26]:
Intubation for respiratory failure
Higher severity of illness (APACHE) score
⚡️ SHOCK INDEX! ⚡️
How Do I Optimize My Patient's Hemodynamics?
It would be negligent if I were to say that optimization doesn’t include “optimization” of anything other than hemodynamics… Because it does. When we reference physiologic optimization, oxygenation, or the prevention of hypoxemia would be included. However, a previous blog I wrote covers this in relative detail, and the purpose of this article is to cover optimization as it applies to hemodynamics. But because I can’t, in my good nature, not hit it at all, here is an image displaying the CRASH variables for pre-oxygenation:
Here is the previous blog written regarding pre-oxygenation: Weapon of Choice During Your RSI: Pre-Oxygenation.
So, how do we do it? How do we optimize our patient’s hemodynamics? To start, it must be mentioned that there is no [1, pg 26-28]:
one-size-fits-all approach regarding hemodynamic resuscitation prior to inserting that tube.
Single induction agent that eliminates concern of the underlying pathophysiology
Vasopressor that can eliminate peri-intubation deterioration
There are a handful of factors that need to be carefully considered, including:
Hemodynamic effects of induction agents
A stepwise hemodynamic strategy with several concepts regarding airway management is found within The Manual of Emergency Airway Management (6th Edition):
1. Repletion of Volume Loss (Dropdown)
Most critically ill patients are volume-depleted, either through fluid loss or blood loss, insensible losses, or fluid shifts. Thus, most patients require some form of fluid resuscitation. In patients who are likely to be volume-responsive, fluid resuscitation should be performed. The type and volume of fluid will be dependent on the underlying pathophysiology and severity. The goal is to increase the circulating stressed volume that exerts a pressure against the vascular walls, and thus contributes to blood pressure, cardiac output, and oxygen delivery. Fluid resuscitation that does not lead to an increase in cardiac output or blood pressure is contributing to unstressed volume, which is volume that is stored in the high capacitance venous system [1, pg 26].
2. Reduction of Unstressed Volume and Vasoplegia (Dropdown)
Any fluid that does not contribute to increased cardiac output is fluid stored as unstressed volume. Additionally, ventilating induction agents convert stressed volume into unstressed volume. Thus, patients not responsive to fluid resuscitation should be started on vasopressor infusions to reduce unstressed volume with vasoconstriction — particularly venoconstriction [1, pg 27].
Patients with an SI ≥ 0.8 are at high risk of developing postintubation hypotension. These patients are at high risk from any myocardial depression or vasodilation and should be started on in-line continuous vasopressors before intubation rather than relying on a bolus-dose vasopressor for rescue after decompensation [1, pg 27].
3. Augmentation of Ventricular Performance (Dropdown)
After fluid resuscitation and vasopressors, the next principle is to determine whether there is any left ventricular or RV dysfunction that will decompensate with induction and PPV. Ventricular contractility that remains poor despite a vasopressor such as norepinephrine may require augmentation with an inotrope such as dobutamine or milrinone. In some instances (e.g., restrictive physiology), the left ventricle may need after-load reduction and inotropic support rather than vasopressors [1, pg 28].
4. Mitigating the Effect of Induction Agents (Dropdown)
All induction agents used for RSI have unfavorable hemodynamic consequences. These need to be balanced with optimizing intubation conditions for the patient to maximize the chances of first-pass success.
At the doses required for RSI, Propofol and Midazolam result in venodilation, reducing both preload and blood pressure.
Etomidate is considered a hemodynamically neutral drug, but recent evidence shows that Etomidate reduces arterial elastance, which can cause hypotension.
Ketamine has indirect sympathomimetic effects, however, is a direct myocardial depressant. Where one patient may respond to the sympathomimetic effect, another may get predominant myocardial depression.
Regardless of the induction agent used, a reduced dose should be used in patients with hemodynamic instability.
5. Protection of the Right Ventricle (Dropdown)
Patients with RV failure should have an RV-focused resuscitation and intubation. The “RV spiral of death” involves decreased RV systolic function leading to RV pressure/volume overload that decreases left ventricular filling, reducing cardiac output and worsening hypotension, which may then reduce RV function further. Intubation is often the final insult that tips the RV over the edge because of the increase in pulmonary vascular resistance that results from any atelectasis, ventilation/perfusion mismatch, hypoxemia, and hypercapnia that comes with apnea. Additionally, the increase in RV after load from PPV can be very deleterious and result in postintubation hypotension or even cardiac arrest. Patients with RV failure may ultimately need pulmonary vasodilators to reduce RV after load. In the ED, the key step is to recognize at-risk patients (e.g., obstructive shock from large pulmonary embolus) and initiate norepinephrine to increase mean arterial pressure, maintain coronary perfusion pressure, and RV contractility.
The treatment for patients with physiologically difficult airways may come from many different sources. However, for myself, my go-to recommendation/source is from the Society of Airway Management’s Consensus Recommendations article in February 2021, published by the International Anesthesia Research Society. In addition to this consensus paper, I utilize the above considerations for stepwise hemodynamic strategies found in the most recent print of The Manual of Emergency Airway Management (staying within my company's guidelines, or course 😏 ).
There are what seems to be a gamut of recommendations, which may be intimidating… But, the recommendations are also pretty intuitive, which makes them easier to recall and understand.
1. Patients should have intravenous access sufficient for rapid fluid administration before intubation.
Two or more IVs are suggested, typically.
2. Patients should be screened for high risk of hemodynamic collapse -- those with a shock index greater than or equal to 0.8 are at high risk.
The higher the shock index, the more likely adverse events are to occur; such as hypotension or cardiac arrest.
3. Hypotensive patients due to obstructive shock secondary to acute or acute-on-chronic RV failure should be managed using RV failure guidelines.
This one is for you POCUS nerds 🤓
4. Fluid-responsive and fluid-tolerant patients should be fluid resuscitated before intubation, or at least during the intubation attempt.
Use appropriate fluids for resuscitation
Standard NS or LR
Bleeders get BLOOD 🩸
5. When possible, vasopressor infusions should be started before intubation in patients who are not volume-responsive or fluid-tolerant.
Norepinephrine is the preferred vasopressor .
6. When vasopressor infusions are not possible or impending arrest is anticipated, bolus-dose vasopressors should be available and used to maintain systemic pressure during and after the intubation, until an infusion can be started.
Epinephrine should be considered as the vasopressor of choice in patients with decreased myocardial function.
7. Hemodynamically neutral induction agents should be used
Ketamine or Etomidate
Reduction of the induction agent dose is reasonable in patients with a high shock index, but SHOULD NOT REPLACE ADEQUATE PRE-INTUBATION RESUSCITATION .
Although I use the term "hemodynamically neutral," be aware that ALL induction agents can cause hypotension; this includes Ketamine and Etomidate 😉
Always expect these agents to cause hypotension -- proceed with caution ⚠️
We frequently see the recommendation to reduce the induction agent dose when a patient presents with hemodynamic instability or a high shock index. This has been "challenged," if you will, in a paper from the NEAR Registry here:
Dr. Jarvis of The EMS Lighthouse Project podcast also covers this paper in detail here:
^^^ I highly recommend listening!
Now, what is the resuscitation end goal? I don't mention how much fluid. I don't mention doses for the drips or the push-dose pressors. I don't mention much about the hemodynamically "neutral" induction agents. What the hell are you to do?! Is there a targeted blood pressure? Is there a targeted SI?
I hate to be "that guy," but this is where you follow your local protocols/guidelines. I could not find a definitive answer to targeting a specific blood pressure or shock index, other than what the "minimums" should be; or what I should say is, when it is absolutely not safe to proceed with induction. I even went as far as asking over 50 or so other medics, nurses, and physicians what their targeted resuscitation goals are (on social media or SMS). And not surprisingly, an overwhelming amount of you gave the golden "SBP < 90, MAP < 65, or SI of 0.9 or higher." That seems to be the consensus... But does that mean we would only aim for those parameters, or should we aim for higher? The answer is... I don't have a definitive answer. I think we can all assume the higher, the better... but I haven't found a perfect source to make that bold claim.
I searched high and low for an answer without luck. However, I will leave you with this bit of info I did find:
1. Per the Manual of Emergency Airway Management (6th Edition), "If the need for intubation is not immediate, then abnormal hemodynamic parameters should be normalized as much as possible prior to intubation."
2. Heffner et al, 2012, reports a study that "demonstrated pre-RSI systolic pressures less than 140 as independently associated with post-intubation hypotension, but SI was not included in this analysis" .
3. In hemorrhagic shock, the patients should be resuscitated with blood products to achieve a SBP above 100mmHg .
4. In a 2020 research article titled, Risk Factors for and Prediction of Post-Intubation Hypotension in Critically Ill Adults: A Multicenter Prospective Cohort Study, they report an increased risk of post-intubation hypotension once SBP fell below 130 mmHg. When a MAP was used rather than SBP, there was a threshold below 95 mmHg that was associated with post-intubation hypotension. Perhaps aiming for a higher perfusion pressure in the critically ill, either via MAP or SBP would prevent post-intubation hypotension and associated poor outcomes . They also report the typical, "this would need to be tested via a future interventional trial."
5. Of the studies I read regarding this topic, most report a high incidence and high likelihood of adverse events occurring at SBP < 90, MAP <65, or a shock index of 0.9 or higher.
6. In an UptoDate.com article, it is mentioned that “The therapeutic target is normalization of the systolic blood pressure, a mean arterial pressure of 65 mmHg, or resolution of clinical signs of poor perfusion.” But it doesn’t report where that statement came from, but it seems appropriate 🤷♀️
The image below is just my "posterboard" for the patients with high shock index requiring resuscitation:
Just a QUICK Word on the Meaning of "Difficult Airway."
Patients are difficult or challenging to intubate for many different reasons. When the airway is anatomically difficult, it becomes easy to identify the reason for the adverse reaction -- the inability to place plastic in the trachea. But in the physiologic difficult airway, even when intubation is successful, the life-threatening complications are thought to be "unpreventable." Buuuuut, there is evidence out there that complications such as hypoxemia, hypotension, and cardiac arrest can be reduced with better pre-intubation optimization .
The term "difficult airway" is typically synonymous with an anatomically difficult airway, and I think most would agree. But in the present day (as of this blog), technological advancements such as video laryngoscopes have absolutely positively increased our ability to safely and appropriately manage patients with an anatomically difficult airway. Attention to the physiologic difficult airway should also be considered when we utilize the term "difficult airway,' as critically ill patients still have a high incidence of life-threatening complications, regardless of how anatomically difficult the airway is.
Jared Patterson, CCP-C, One Rad Medic
Killin' It Since 1989
Committed to Knowledge and Nachos
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