Not many aspects of Emergency Medicine define our specialty better than resuscitation, and few concepts exemplify resuscitation better than shock and intubation. Yet few words together strike greater fear in the minds of savvy resuscitationists. Not because we cannot deftly manage shock, or because we are anything but hardy intubators, but because the swiftest way to transform a living patient into a dying patient or a dying patient into a dead patient is to brazenly intubate someone who is in shock. These are often called "clean kills" for good reason. What are the root causes of endotracheal intubation's (ETI) hemodynamic effects and, most importantly, how do we circumnavigate them? Fundamentally, how do we safely intubate a patient in shock?
Disclaimer: It is not easy to study such a risky procedure of a fragile population, so evidence surrounding the shocked intubation is not as robust as we might wish. Thus, the recommendations offered herein are borne of evidence where it exists, but also expert opinion and some pharmacologic and physiologic common sense.
ETI causes hypotension for myriad reasons, the four major players of which are the 4 Ps:
Poor drug selection & dosing
1. Pre-existing pathology
Successful intubation of the shocked patient begins long before induction drugs are pushed. Just like SEALS prepare for a mission, we must prepare our patients for the hemodynamic (mis)adventure upon which they are about to embark. To that end, the oft quoted "resuscitate before you intubate" mantra must not go neglected. We learn several questionably valid/sensitive mnemonics to anticipate a difficult airway, but sometimes forget the importance of preparing the patient for that airway. Failure to do so makes post-intubation hypotension or PEA arrest all the more likely.
The time allowed for this resuscitation depends on how badly the patient necessitates intubation, but efforts to improve blood pressure and identify/treat the underlying cause of shock must be undertaken whenever possible. To that end (prior to and during intubation), hypovolemic patients should get fluids, hemorrhagic patients should get product, and septic patients should get pressors. Push-dose ino/pressors are a great option in the Air Care setting, but in the ED it is often easier and safer to take the 5-10 minutes to start an ino/pressor drip (even through peripheral access) prior to intubation.
In short, do not underestimate the importance of properly resuscitating a patient prior to intubation whenever possible. Unless you are facing a crash or forced airway, get those fluids, blood products, or ino/pressors going before you intubate.
2. Poor Drug Selection and Dosing
There are two ways in which induction agents enact their hemodynamic effects in shocked patients. The first has to do with the pharmacology of the drug itself. Propofol is a known cardiovascular depressant. Etomidate and ketamine are more benign in this regard (although ketamine also has documented myocardial depression), but none of the three induction players is truly hemodynamically benign in shocked patients. The reason for that is the second and oft-neglected induction path to hypotension: "sympatholysis." This is the phenomenon wherein fully sedating a patient in partially compensated shock inevitably blunts his/her adrenergic drive and impairs the compensatory response. This has been seen with every major induction agent, even our perennial favorite, ketamine (1). The ubiquitousness of sympatholysis among induction agents should not leave us entirely at a loss; it just requires a deeper dive...
Propofol remains a favorite of anesthesiologists and is often viewed negatively because of its notoriously unfavorable hemodynamic properties. Cliff Reid even coined the term "propofol assassins." Indeed, propofol frequently causes hypotension, but in experienced hands at proper doses, it surprisingly can be a viable option. Propofol was studied in shocked pigs with surprising results; at markedly reduced doses, it still achieved sedation during ETI (measured by BIS) in shock states (2). So, at reduced doses that will likely NOT cause sympatholysis, propofol can still achieve sedation in shocked patients. Baltimore Shock Trauma's Division of Anesthesiology uses this as their go-to approach to inducing its many hemodynamically tenuous trauma patients. The problem with propofol is that we in the ED/ICU/Air Care do not regularly use it, and the dose estimations based on shock state are a bit arbitrary at best. Rather than gamble with an arbitrary dosing of an unfamiliar drug and hope it provides loss of awareness without loss of pulses, we are probably wise to choose other options.
Etomidate is the classic induction agent in the US and often touted as hemodynamically benign, but it is unfortunately not reliably so. Etomidate mimics every other agent; at full dose, it often causes sympatholysis and hypotension in the shocked patient. Problematically, unlike propofol, etomidate cannot undergo dose reduction and reliably sedate shocked patients. The same study that found propofol could achieve sedation at reduced doses in shock found that etomidate conversely cannot (3). In fact, more than a standard full dose was required to properly sedate shocked pigs. That is, in patients who are hemodynamically tenuous, a supranormal etomidate induction dose will be required to achieve adequate sedation. While etomidate has few primary cardiodepressant effects, adequate sedation in shocked patients requires more than a full dose, which almost guarantees sympatholysis and near-inevitable hypotension. Ultimately, without even getting into the adrenal suppression debate, etomidate is not a panacea for shock induction,
Ketamine is probably the best option for hemodynamically benign intubations, but not for reasons most people think. Its notorious effects of bolstering BP and HR do exist, but are often offset by sympatholysis and myocardial depression when used at full doses in shocked patients (1). To that end, ketamine is an ideal induction agent for shock when used at a "sub-sympatholytic" dose; the exact dosing is not fully studied but most experts tend to recommend 0.5-1 mg/kg depending on a patient's hemodynamics. Err lower (i.e. 0.5 mg/kg) in the sickest patients. While shocked patient awareness and recall after these nontraditional induction doses of ketamine have not been studied, we can empirically infer that ketamine predictably induces alteration in consciousness at these lower doses. Whether it's a full dissociation, or the sub-dissociated "k-hole" we anecdotally avoid during procedural sedation, probably does not matter because we are giving a paralytic and the patient will be too altered to remember said paralytic. Meanwhile, low-dose ketamine should NOT sympatholyse patients as it might at full doses. We are still in need of RCTs on subsympatholytic ketamine, but the good news is that successful cases of ketamine's hemodynamically benign reduced-dose inductions accumulate as its absolute contraindications continue to fade. At reduced doses in shocked patients, ketamine seems to preserve sedation and sympathetic tone, and it is more predictable and familiar to us than propofol.
Nothing is a reasonable induction agent in the truly shocked, altered patient. Shock unto itself is sedating, so a small subset of our truly moribund patients may require no induction agent. I reserve the paralytic-only approach for peri-arrest patients and/or those with a GCS approaching 3.
Induction Agent Take Home Message: While RCTs are lacking in this area, there are data rejecting dose reduction of etomidate in shock. This leaves one stand-out option for safe induction agents: ketamine at 0.5 - 1 mg/kg. It is familiar to us and at reduced doses can predictably induce loss of awareness while preserving sympathetic tone. In truly obtunded or peri-arrest patients, the induction agent can be omitted entirely.
3. Positive Pressure
The hemodynamic roller coaster of intubation is not over just because you've safely induced the patient and have the tube between the cords. Indeed, there are three major pressure-related contributions to intubation's sum hemodynamic effects, which occur soon after intubation. These are summarized below along with their respective preventive or troubleshooting measures.
Negative to Positive Pressure: First is the transition from spontaneous negative pressure ventilations (NPV) to positive pressure ventilations (PPV), which entails both decreased RV preload and increased RV afterload, a recipe for disaster in an under-resuscitated, shocked patient. We often think of this NPV-to-PPV transition as inevitable, but it is not. In the truly shocked patient who requires intubation but is already on high dose ino/pressors, consider preserving spontaneous ventilations. This can be done by limiting sedation, using a short-acting paralytic, and utilizing a support rather than control ventilator mode. If the patient was intubated for reasons other than ventilatory failure, he/she may tolerate pressure support mode at fairly low positive inspiratory pressures; this will limit the intrathoracic pressure changes classically associated with the ventilator.
Extrinsic PEEP: The negative to positive pressure effects are augmented by extrinsic PEEP set on the ventilator (most default to +5 cm H20). This PEEP further decreases venous return and many of us have seen the effect of "robbing Peter to pay Paul" when increasing PEEP to recruit a shocked patient. Thus, consider minimizing PEEP on shocked patients who are oxygenating well.
Intrinsic PEEP: Finally, the patient's own intrinsic PEEP can further impair venous return. The patients most at risk for this are those with bronchospasm, which will predispose them to air trapping in the distal airways. Keep an eye on intrinsic PEEP by watching the ventilator's flow-time scalar to ensure that the expiration curve completely returns to baseline without evidence of breath stacking. Breath-stacking, air trapping, auto-PEEP, and intrinsic PEEP all mean the same thing and share a common result of hemodynamic decompensation. So it behooves us to watch out for this phenomenon particularly in the shocked and bronchospastic patient.
4. PH Decompensation
So let's say you resuscitate your patient, choose and dose his/her induction agent perfectly, and thoughtfully limit the degree of positive pressure post-intubation. Unfortunately, the post-intubation death spiral may occur several minutes or even hours after, and arises from failing to provide adequate respiratory compensation for a metabolic acidosis. Consequentially, the pH drops, endogenous and exogenous catecholamines become dysfunctional, and circulatory collapse occurs.
To prevent pH decompensation, identify patients at risk for metabolic acidosis and approximate their neural pre-intubation ventilatory rate. Likewise, consider short-acting paralytics in these patients. SIMV is often recommended as the ideal mode for this scenario, since it will provide ventilatory support without mandating a full breath for each of their compensatory spontaneous breaths.
Finally, remember also that any push of bicarbonate will buffer to generate carbon dioxide and can worsen pH if not adequately off-gassed. To that end, any intubated patient not able to increase their own respiratory rate should have their ventilator rate increased if given bicarbonate.
Insofar as Dr. Bill Hinckley has wisely coined the term "Definitive Airway Sans Hypoxia on the 1st Attempt" (DASH-1A). I humbly submit a similar goal in terms of hemodynamics: "Definitive Airway Sans Hypotension on the 1st Attempt." While tongue-in-cheek, it is a somber reminder of the dangers of definitive airway management. If done carelessly in shocked patients, intubation can become an iatrogenic catastrophe. However, performed carefully and with a comprehensive approach, even a shocked patient can be intubated safely:
Resuscitate before you intubate: fluids, products, ino/pressors as needed
Induce with ketamine 0.5-1 mg/kg to avoid sympatholysis, or forego an induction agent if the patient is truly obtunded
Minimize positive pressure and extrinsic PEEP while watching for intrinsic PEEP
Preserve the ventilatory compensation of metabolic acidosis to avoid dropping the pH and causing hemodynamic collapse
Through a deep respect for its perils and a thoughtful deployment of the above strategies, you can successfully circumnavigate the hemodynamic storm clouds of intubation. In doing so, know that you have accomplished one of the greatest challenges of Emergency Medicine and Critical Care: not harming patients in an attempt to save them!
Authored by Christian Renne, MD
posted by Tim Murphy, MD
Miller, Matthew, et al. "Hemodynamic response after rapid sequence induction with ketamine in out-of-hospital patients at risk of shock as defined by the shock index." Annals of emergency medicine 68.2 (2016): 181-188.
Johnson, Ken B., et al. "The Influence of Hemorrhagic Shock on Propofol: A Pharmacokinetic and Pharmacodynamic Analysis." Anesthesiology: The Journal of the American Society of Anesthesiologists 99.2 (2003): 409-420.
Johnson, Ken B., et al. "The Influence of Hemorrhagic Shock on Etomidate: a Pharmacokinetic and Pharmacodynamic Analysis." Anesthesia & Analgesia 96.5 (2003): 1360-1368.