Intubation, Hypotension and Shock


A modified rapid sequence intubation (RSI) approach is usually preferred in shocked patients, including:

  • use of low dose, titrated induction agents to avoid haemodynamic compromise
  • avoidance of apnoea (e.g. via spontaneous breathing or supported ventilation) to avoid exacerbation of coexistent acidaemia
  • appropriate use of IV fluids and/or inotropes/ vasopressors
  • The mantra is “Resuscitate before you intubate!”
  • Richard Levitan has termed this approach “resuscitation sequence intubation” (Levitan, 2015).

“Shock is an anaesthetic” (attributed to Richard Dutton, former Chief Of Anaesthesia at Shock Trauma, Baltimore) so the basic building block of rapid sequence intubation (RSI) is “roc/sux-tube-apology” in a shocked patient with altered mental state

  • Use judicious doses of induction agents to make the procedure is as non-distressing as possible, without compromising safety
  • Remember that the primary objective is to keep the patient alive while achieving intubation



  • Peri-intubation hypotension is associated with increased mortality
  • The most important risk factors for death and complications prior to intubation are (Schwartz et al 1995):
    • haemodynamic instability
    • a requirement for vasopressor agents


  • underlying disease
  • inadequate resuscitation
  • cardio-depressant effects of induction agents
  • decreased venous return due to increased intra-thoracic pressure resulting from positive pressure ventilation, including positive-end expiratory pressure (PEEP)
  • haemodynamic effects of worsening acidosis during apnoea


  • adequately fluid resuscitate prior to, and during, intubation
  • consider using a pressor agent (e.g. adrenaline) prior to intubation to prop up blood pressure before the administration of an induction agent
  • choose an induction agent and a dose that is least likely to exacerbate hypotension (e.g. ketamine)
  • mitigate against high intra-thoracic pressures by avoiding excessive tidal volumes, PEEP, and dynamic hyperinflation when ventilating


Induction agent

  • the dose of any induction agent used may be more important than the choice of the agent — consider using lower doses than usual, regardless of the agent used
  • ketamine is the induction agent of choice in the shock patient (see below)
  • traditionally, many intensivists used fentanyl and midazolam in low doses as their mainstays for the induction of shocked patients; however, onset is very slow in patients with shock (e.g. up to or greater than 5 minutes)
  • even propofol and thiopentone can be used in the shocked patient, but as little as 10% of the usual dose may be all that is needed and onset is slowed — higher doses may lead to profound haemodynamic compromise (Morris et al, 2009)
  • etomidate is not available in Australia, and may be best avoided due to ongoing concerns:
    • it causes adrenal suppression which may be linked to increased mortality in septic patients (though many argue that etomidate is safe)
    • it is unreliable as an induction agent in reduced doses (even in shocked patients)

Neuromuscular blockers

  • use higher doses than usual as the onset for any given dose will be slower
    • e.g. suxamethonium 2mg/kg IV TBW (total body weight), or
    • e.g. rocuronium 1.6 mg/kg IV IBW (ideal body weight) (some centers use up to 2 mg/kg IV IBW)


  • The compounding effect of uncorrected respiratory acidosis from apnea (regardless of the agents used) may be lethal
  • During apnea from RSI, supported ventilation may be necessary for patients with profound metabolic acidosis


  • Ketamine is the least cardio-depressant induction agent available (Morris et al, 2009; Gelissen et al, 1996)
  • Ketamine usually exhibits a stimulatory effect on the cardiovascular system
    • the mechanism is poorly understood but probably involves a centrally mediated sympathetic response and inhibition of noradrenaline re-uptake
  • In the severely shocked patient beware of catecholamine depletion or resistance to further catecholamine effect. The direct effects of ketamine on myocardial depression may outweigh the indirect sympathetic effects and haemodynamic collapse may still occur. This is more likely to occur if:
    • high doses of ketamine, based on dose-dependent negative inotropy observed in vitro (Gelissen et al, 1996), and
    • in patients with a higher shock index (Miller et al, 2016).
  • Consider doses as low as 0.25 to 0.5mg/kg IV IBW, rather than the usual 1-2 mg/kg IV IBW, for RSI of the shock patient
    • be wary that sub-dissociative doses of ketamine may cause agitation or abnormal behaviour, this may require up-titration of the administered ketamine dose to induce dissociation, however most profoundly shocked patients have some degree of decreased level of consciousness
  • Rapid administration of ketamine alone can render the patient apnoeic
    • in the RSI setting, apnea will occur anyway from the administration of paralytics (see the comments above) but has important implications when ketamine is used in other settings such as procedural sedation or delayed sequence intubation (DSI)



  • A phase II multi-centre trial in ICU patients showed that a bundle of therapy, which included fluid loading and early vasopressor use to treat abnormal haemodynamics, reduced life-threatening complications following intubation. This included marked reduction in severe cardiovscular collapse (by nearly 50%). (Jaber et al, 2009).

Slides for the talk “No Apologies: Intubation of the Shocked Patient”, given at EuSEM Congress 2015 in Torino, Italy:

No apologies: intubation of the shocked patient from precordialthump

References and Links


Journal articles

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC


  1. Hi Chris,
    A question re ketamine: you mention that post induction hemodynamic collapse can still occur in these sick patients receiving ketamine, which of course makes sense. You also mention that this may be more likely in patients receiving higher doses and in patients with a higher shock index, citing Miller 2016. That paper does show that hypotension was more likely in those with a higher shock index (again makes perfect sense and not necessarily anything to do with the ketamine), but it was the low shock index group that received a slightly higher mg/kg dose of ketamine (1.4 vs 1.2 mg/kg induction, 2.0 vs 1.7 mg/kg total). Can you point to a reference that shows improved HD parameters when using lower vs higher doses of ketamine? I’ve seen this recommendation of using sub dissociative doses of ketamine for induction during hypotensive intubations on several FOAM sites (EM Crit, REBEL EM) but none of the references compare ketamine dosing strategies to support that statement or even show that using the lower doses is safe/effective. The concern is that people would use partial dissociation dose ketamine in already unstable patients, creating an agitated patient and thereby worsening already difficult intubation conditions. I do not think of ketamine as a titratable sedative like a benzo. If you aren’t crossing the dissociative dose (>1mg/kg) and are above the pain dose (0.15-0.3mg/kg) then you are in the partially dissociated zone, a place no one wants to be. Thoughts? Thanks for the thoughtful post.

    • Hi Meghan

      Really great comment!

      I am not aware of any clinical research showing that hypotension is more frequent or severe in shocked patients with higher doses of ketamine. In the lab, the negative inotropic effects of ketamine are concentration-dependent: https://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949119

      The difference in dosing in the Miller et al, 2016, was minimal, but showed that the high shock index patients had little change in SBP, but were morel likely to become hypotensive – whereas the low shock index patients went the other way and had sustained increases in BP.

      I have also seen two patients intubated one after another using the same dose ketamine. They were both on low dose noradrenaline, and I thought had similar physiology. However, in one patient the noradrenaline doubled post-intubation and the other no longer needed vasopressors after intubation!

      I agree with your concerns about agitation from sub-dissociative doses.

      In practice, my experience (alert!) is that dissociation can occur at lower doses in some patients. If giving lower doses (e.g. 0.5 mg/kg IV), I monitor for response (mental state, breathing, and haemodynamics) and am prepared to give further doses if needed to achieve dissociation. I am yet to encounter a problem with agitation in this setting (touch wood).

      The take homes for me are: come up with a plan based on what you expect and be ready for anything in case you’re wrong.

      In general, with shocked patients I do not want to rush the intubation so I am happy to titrate doses of ketamine to effect while allowing them to continue to spontaneously breathe and pre-oxygenate. In a truly crashing shocked patient, I would use lower dose ketamine (they will almost certainly have reduced level of consciousness anyway) and err on the side of keeping them alive.



  2. Thanks for the reply and the clarification that using sub/partial dissociation dose ketamine for these intubations is based on your clinical experience combined with in vitro data concerns for myocardial depressant effects. I think the confusing statement is this one as it seems to imply (to me at least) that the Miller paper (clinical data) found higher dose ketamine to contribute to HD collapse:

    “In the severely shocked patient beware of catecholamine depletion or resistance to further catecholamine effect. The direct effects of ketamine on myocardial depression may outweigh the indirect sympathetic effects and haemodynamic collapse may still occur. This is more likely to occur at high doses and in patients with a higher shock index (Miller et al, 2016).”

    FOAM is great both for discussing analyzing literature but also for sharing expert clinical opinion when the data isn’t available. It’s just important to make sure we make it explicitly clear when we are discussing the later. Thank you again for the post and all you do for FOAM!

    • I agree Meghan that the sentence could be more clear, and I will clarify.
      The citation relates to higher shock index, which Miller et al’s study supports.

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