From bad to worse: avoiding peri-intubation cardiac arrest

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Intubation in the emergency department (ED) can be a stressful endeavor. We are often presented with patients who have complex anatomy and tenuous physiology. Because of this, it can be hard to look past the critical step of securing the airway. Rapid sequence intubation (RSI) and positive pressure ventilation can dismantle patients’ physiology and contribute to an almost 4% rate of post intubation cardiac arrest (PICA). Is there anything we can do to predict or prevent this? In this podcast, Sam Wood gives us an overview of the literature to help us answer these questions.

Why do patients die when we intubate them?

  • Initiation of positive pressure ventilation increases intrathoracic pressure and decreases venous return

  • With RSI, patients can loss their compensatory endogenous catecholamine surge (“sympatholysis”)

  • Direct effects of induction agents

  • Hypoxia

  • Worsening of acidosis during apneic period of oxygenation

  • Worsening of “high risk” physiologic states like acidosis, bronchospasm

Which patients are at highest risk for PICA?[1-4]

Shock index.jpg

  • Hypoxia and absence of preoxygenation

  • “High risk” physiology: i.e. severe acidosis, hyperkalemia, severe bronchospasm

  • Unstable hemodynamics

    • A shock index (SI) >/= 0.9 significantly increases the risk of PICA. This has been remarkably consistent across multiple studies.

    • SBP<90 has also been shown to be predictive

  • Other risk factors:

    • BMI >25

    • Age >75

    • Nursing shift change

    • Crash versus emergent intubations

What interventions to prevent PICA have been studied?

Intervention bundle graphic 2.jpg

  • Intervention bundle

    • Decreased PICA in the ICU setting from 34% to 21% [5]

      • It is not clear which components made the difference

      • It is unclear how this may help us in the ED as some of these items we scrutinize (eg. Sellick maneuver) and some we already routinely do in the ED (eg. capnography and preoxygenation)

  • Preintubation IV fluids

    • “PREPARE” study [6]

      • Critically ill adults were randomized to receive 500cc IV fluid prior to intubation vs no IV fluid

      • There was no difference in cardiovascular collapse between the two groups

  • Push dose pressors

    • Overall, the data shows that push dose pressors increase blood pressure, improve hemodynamic stability, but do not clearly prevent PICA

    • It is worth noting that push dose pressors are associated with a medication error rate of 10% [7]

    • 30-70% of patients will still need a pressor infusion

  • Induction agent

    • Avoid propofol and benzodiazepines for their potential hypotensive effect

    • Ketamine seems attractive for hemodynamically tenuous patients

    • Interestingly, ketamine’s direct effect on the myocardium is negative inotropy [8], but this is typically offset by an increase in heart rate, arterial pressure, and cardiac output in a patient with an intact autonomic nervous system

      • But what about the patient that might be catecholamine depleted?

        • Study of 112 patients undergoing out of hospital rapid sequence induction with ketamine [9]

          • 26% of high SI patients got hypotensive vs 2% of non-high SI pts

          • This study suggests ketamine may not be as safe as originally thought for catecholamine depleted patients

    • Many sources recommend 0.5 mg/kg (“sub-sympatholytic dose”) of ketamine in the shock patient but there is no specific data to support this

What do we take away from this literature?

  • Calculate a shock index in all patients prior to intubation.

  • If there’s time, resuscitate first: fluids, push dose pressors, or pressor infusion (my preference).

  • There is no clear guidance on what the goal should be for a SI (SI <0.9 seems reasonable).

  • Use ketamine preferentially and at a lower dose (0.5 mg/kg IV)

  • Unfortunately, in a real emergency, the risk factors for cardiac arrest may not be modifiable before intubation (or at all)

Presented at the 2020 Maine Medical Center Winter Symposium

Samantha Wood, MD

Peer reviewed, edited and posted by Jeffrey A. Holmes, MD and Jason Hine, MD

References

1. Heffner AC et al. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation 2013; 84(11): 1500 – 4. [Pubmed]

2. De Jong A, Rolle A, Molinari N, et al. Cardiac arrest and mortality related to intubation procedure in critically ill adult patients: a multicenter cohort study. Crit Care Med. 2018 Apr 1;46(4):532-9.[Pubmed]

3. Wardi G, Villar J, Nguyen T, et al. Factors and outcomes associated with inpatient cardiac arrest following emergent endotracheal intubation. Resuscitation. 2017 Dec;121:76-80. [Full Text]

4. Kim WY et al. actors Associated with the Occurrence of Cardiac Arrest after Emergency Tracheal Intubation in the Emergency Department. Plos One 2014; 9(11): e112779. [Pdf]

5. Jaber S, Jung B, Corne P, et al. An intervention to decrease complications related to endotracheal intubation in the intensive care unit: a prospective, multiple- center study. Intensive Care Med. 2010 Feb;36(2):248–55. [Pdf]

6. Janz DR et al. Effect of a fluid bolus on cardiovascular collapse among critically ill adults undergoing intubation (PREPARE): a randomized controlled trial. Lancet Resp Med 2019 Dec; 7(12): 1039-1047. [Pubmed]

7. http://www.emdocs.net/push-dose-vasopressors-an-update-for-2019/

8. Gellisen HP et al. Inotorpic effects of propofol, thiopental, midazolam, etomidate, and ketamine on isolated human atrial muscle. Anesthesiology 1996; 84:397-403. [Pubmed]

9. Miller M 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. Ann Emerg Med 2016; 16: 181-188. [Pubmed]