Preventing peri- and post-intubation decompensation: Pearls + Pitfalls

Authors: Sara Adibi, MD (@deebs_6, Baylor Scott & White at Centennial), Kathleen Cowling, DO (@ EMdoc911, Central Michigan University School of Medicine), and Michelle McLean, MD (Central Michigan University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC)

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Case Presentation:

A 57 year-old female presents with chest pain and shortness of breath for one week. She has been around multiple family members who have had similar symptoms, but all have recovered from their illnesses while she continues to get worse. Medical history includes diabetes and hypertension, both of which are well controlled with oral medications.

Vitals: BP 108/70, HR 115, Temp 38ºC, RR 26, Sp02 88%.

Her respiratory distress is worsening and now it’s time to intubate. You have a perfect view of her vocal cords and nail the airway using direct laryngoscopy on the first attempt. Just as you are about to high five your attending the monitor begins to alarm and the nurse tells you “Doctor, her pressure is dropping!” Her blood pressure is now 82/58. So, now what?!



Peri- and post-intubation hypotension is associated with increased morbidity and mortality. A paper written by Heffner et al. found post intubation hypotension (systolic blood pressures <90) had a higher in-hospitality mortality of 35% compared to 20% for those that did not. Additionally hypotensive patients had an average stay in the ICU of 9.7 days versus 5.9 days for normotensive patients.

Multiple risk factors were noted including chronic renal disease, respiratory failure, and age, but the strongest association noted was that of a pre-intubation shock index (PSI), defined as HR/SBP, of greater than 0.8 (67% sensitivity and 80% specificity). Thus, it is imperative that emergency physicians be aware of potential complications of Rapid Sequence Intubation (RSI) and develop a plan to manage such complications.



Peri-intubation shock occurs as a result of a variety of mechanisms.

Underlying disease states.

Inadequate resuscitation.

Direct cardiodepressant effects of induction agents. Sedatives also typically reduce catecholamines to varying degrees, which may cause abrupt transient arterial and venous dilatation, and may be more responsible for the hypotension associated with emergent intubation.

Decreased venous return due to positive pressure ventilation.

Hemodynamic effects of worsening acidosis during apnea.



If PSI is greater than 0.8, some measures can be undertaken to prevent or blunt the hypotensive response including…

Adequate fluid resuscitation prior to, and during, RSI.

Consider using a pressor agent prior to intubation to prop up blood pressure before the administration of an induction agent.

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-Administering 0.4 mg of scopolamine a few minutes prior to induction can act as an amnestic agent and the side effect of tachycardia can augment cardiac output as well.

-Choosing an induction agent:

+ Midazolam/fentanyl takes too long to act (3-5 min), so don’t use it for induction!

+ Ketamine is the induction agent of choice in the shock patient. It is the least cardio-depressant induction agent available and usually exhibits a stimulatory effect.

+To prevent further hemodynamic collapse, when dosing RSI medications use half the induction agent and double the paralytic agent.

-Ventilator settings:

+Utilize low tidal volumes, 6ml/kg.

+Monitor plateau pressures to keep less than 30cm H20.


Differential Diagnosis:

There are a few potential causes of post-intubation hypotension and/or cardiac arrest (besides an improperly placed ETT) that require a high index of suspicion by the ER physician.

Tension pneumothorax

Typically pulse oximetry will continue to be abnormal. Signs on physical exam include tracheal deviation and absent breath sounds on side of collapse. Ultrasound (US) can also be used to evaluate for absence of lung sliding. Treatment includes needle decompression followed by placement of chest tube.

Cardiac tamponade

EKG changes may include electrical alternans or low voltage. History may also provide clues (recent penetrating trauma, current malignancy, etc). US can again be used to note a pericardial effusion with signs of RV or RA collapse. Immediate treatment would involve a pericardiocentesis.

Massive pulmonary embolism (PE)

Again pulse oximetry may be abnormal and/or EKG changes may be present. Classically PEs are associated with sinus tachycardia and findings of right heart strain. Treatment would involve considering fibrinolytic administration.



In conclusion, hypotension occurring in the setting of emergent intubation is associated with increased morbidity and mortality, however with adequate preparation and knowledge the Emergency Physician can both prevent and manage these complications.


References / Further Reading:

[1.] Heffner AC. Predictors of the complication of postintubation hypotension during emergency airway management. Journal of Critical Care (2012) 27, 587–593




[5.] Manthous, Constantine A. Avoiding Circulatory Complications during Endotracheal Intubation and Initiation of Positive Pressure Ventilation. J Emerg Med. 2010;38(5):622-631. <>



[8.] Franklin C, Samuel J, Hu TC. Life-threatening hypotension associated with emergency intubation and the initiation of mechanical ventilation. Am J Emerg Med. 1994;12:425-428.

[9.] Heffner AC. The frequency and significance of postintubation hypotension during emergency airway management. Journal of Critical Care (2012) 27, 417.e9–417.e13.

One thought on “Preventing peri- and post-intubation decompensation: Pearls + Pitfalls”

  1. Great article. Anaphylaxis needs to be added to the list of differentials for post-intubation circulatory collapse. If the patient did deteriorate, I would also reconsider the original diagnosis if any doubt existed.

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