Post-Intubation Complications in ED Setting

Authors: Summer Chavez, DO, MPH (EM Resident Physician, Virginia Tech-Carilion) and Timothy Fortuna, DO (EM Attending Physician, Virginia Tech-Carilion) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, SAUSHEC EM, USAF)

It’s a busy Friday night when EMS calls with reports of a 74 year-old female nursing home patient that is altered, hypotensive with a blood pressure of 84/56 and hypoxic on 15 L oxygen by non-rebreather with saturations of 87%. They are three minutes away. You gulp down the rest of your energy drink when a transfer from another hospital comes in, a 62 year-old male with subarachnoid hemorrhage on Coumadin. “You might want to take a look at this,” the nurse remarks as stretcher rolls by. Just then, another call goes out over the intercom – “Zero minute trauma alert by ground.” There’s a high likelihood that all of these patients will need to be intubated. How do these medical conditions affect these patients’ intubations and post-intubation care? What troubleshooting can you do in case of persistent hypoxia after intubation?

Peri-Intubation Hypotension & Cardiac Arrest

Peri-intubation cardiac arrest is defined as cardiac arrest that occurs 60 minutes after starting airway management.1 About two-thirds of post-intubation cardiac arrests happen within 10 minutes.1 Peri-intubation cardiac arrest is more likely in patients that were hypotensive or hypoxic before intubation.1 Furthermore, these patients are 14 times more likely to die in the hospital.1 Before intubating the patient, if they are hypotensive, consider fluid resuscitation or pressors to maintain the patient’s blood pressure. Push dose pressors may help to temporize the gap between pre- and post-intubation.

– Epinephrine is the ideal push dose pressor to use in the emergency department – it increases cardiac output and causes vasoconstriction, leading to an improvement in MAP.2 To create push dose epinephrine, pull up 1 mL of 1:10,000 epinephrine, the same concentration used in cardiac arrest, followed by 9 mL of normal saline in the same syringe.3 10 mcg of epinephrine is now in every 1 mL of solution.3 Mix vigorously. While vasopressors can be given safely in peripheral lines, monitor for infiltration at the IV site.3 Administer 0.5-2 mL (5-20 mcg) of solution every 1-5 minutes as needed for effect.4

– Phenylephrine has pure alpha agonist effects.4 If phenylephrine is not available in premixed syringes, push dose phenylephrine can be created at bedside. Use a 3 mL syringe to pull up 1 mL of phenylephrine in a 10 mg/mL concentration and mix into a 100 mL bag of normal saline.4 There is now 100 mL of phenylephrine at 100 mcg per mL. Phenylephrine is administered at 0.5-2 mL (50-200 mcg) every 1-5 minutes as needed.4 Push dose pressors are useful adjuncts in managing hypotension, but it is also important to discuss why positive pressure ventilation causes hypotension.

Normally when we breathe, air is being pulled into our lungs. When someone is intubated with positive pressure ventilation, air is physically pushed into the lungs. Essentially, preload is decreased, leading to a corresponding decrease in cardiac output and blood pressure. Positive-pressure ventilation reduces the pressure differential for venous return.5 During diastole, it also lowers the transmural pressure causing a drop in ventricular filling.5 Finally, positive pressure ventilation causes the resistance in the pulmonary vasculature to increase, which can cause the right ventricle to dilate and obstruct the left ventricle from filling – ventricular interdependence.5

Post-Intubation Hypoxia

Many times patients are intubated for increased work of breathing, altered mental status, or hypoxia. What do you do when the patient remains hypoxic after intubation or suddenly becomes hypoxic? The underlying problem may be related to displacement of the tube, obstruction, pneumothorax, pulmonary embolism, pulmonary edema, pneumonia, equipment malfunction and stacked breaths6. Scott Weingart discusses the DOPES mnemonic on EmCrit.6

Capnometry is an excellent method for determining tube placement. For patients not in cardiac arrest, the colorimetric CO2 detector has been shown to detect the endotracheal tube in the esophagus in 100% of cases and in 99% of the time, when the tube was in the trachea.5 End-tidal carbon dioxide capnography is becoming increasingly more common in emergency departments across the country. End-tidal PCO2 is a non-invasive marker of arterial PCO2.5 A baseline should be established between the PaCO2 and PETCO2 gradient. This will remain constant unless a process exists that disrupts gas exchange.5 With an increase in the difference between PaCO2 and PETCO2 or sharp fall in end-tidal CO2, think about pulmonary embolism, pneumonia, pulmonary edema, mainstem intubation, excessive tidal volumes. or PEEP causing alveoli to over expand.5

Obstruction, especially a mucus plug, can cause sudden desaturation. To remove a mucus plug, use a suction catheter.6 As mentioned earlier, pneumothorax, pulmonary embolism and pulmonary edema are other causes to think about.6,7 These can be evaluated with physical exam, chest x-ray, or bedside ultrasound. In the event of an equipment failure, disconnect the ventilator and ventilate the patient using a bag-valve mask. This should be the first step.7 Especially in patients with asthma who may be prone to auto-PEEP through breath stacking, disconnecting the ventilator and pushing down on the chest can help to relieve some of the pressure.

D isplacement
O bstruction
P neumothorax

ulmonary embolism

ulmonary edema


E quipment
S tacked breaths


Post-Intubation Sedation & Analgesia

Failing to obtain adequate sedation and pain control after intubating a patient is a common mistake. There are certain combinations of sedation and analgesia that may be more beneficial in particular scenarios. Before describing these clinical settings, let’s briefly review the different medications.


Propofol is a lipophilic anesthetic that is a global CNS depressant.8 The onset of action for a bolus is approximately 30 seconds with a duration of approximately 3-10 minutes depending on the administration.8 For long term use, such as in the ICU, propofol tends to accumulate. Hypotension, as much as a 30% reduction in MAP, can be observed, more so in those who are hypovolemic. For sedation after intubation, start dosing at 5-50 mcg/kg/min IV gtt.5 In the elderly, doses may be reduced by approximately 20%.8


Fentanyl is an anesthetic that acts within the CNS to increase the pain threshold and alter pain perception. When given by IV, the effects are almost immediate, but still takes a few minutes to reach maximum effects.9 One of the benefits of using fentanyl is that it does not cause as much histamine release as morphine, therefore it is less likely to cause hypotension and has few adverse hemodynamic effects.5 Fentanyl lasts about 30 minutes to 1 hour.9 For post-intubation sedation, Fentanyl should be dosed at 1-3 mcg/kg/hr IV gtt.10


Versed (Midazolam) is a benzodiazepine that acts on postsynaptic GABA receptors. By binding at this site, it increases the inhibitory effect of GABA. When given IV, it has an onset of action within 1-5 minutes with a peak effect within 30 to 60 minutes. In patients with renal failure, the drug is more likely to accumulate. In the elderly or chronically ill, reduce the dosages by roughly 20-50%. Induction doses for patients that are unpremedicated: dose at 0.3-0.35 mg/kg; for premedicated patients: dose at 0.05-0.2 mg/kg. Maintenance dosing should start at 20-100 mcg/kg/hr IV gtt.10


Ketamine is a dissociative agent that blocks glutamate through its actions as a NMDA receptor antagonist.11 When given IV, onset of action is 30 seconds with a duration of 1-2 hours.5 One of the side effects of ketamine is hypersalivation. In the past, there were concerns regarding increases in intracranial pressure due to ketamine. The rationale was a sympathetic stimulation could cause ICP to increase, worsening a patient’s condition.12 A review of 10 trials involving intubated ICU patients concluded that ketamine had no harmful effects on patient outcomes including neurologic endpoints and mortality.12,13 Two of the trials in the review involved patients with traumatic brain injury determined there was no difference in cerebral perfusion pressure and daily ICP.12 With this in mind, some authors continue to recommend refraining from using ketamine in patients with HTN and increased ICP.12 Initial bolus for ICU patients is 0.1-0.5 mg/kg with maintenance dosing 0.05-0.4 mg/kg/hour.14 For those with hypotension this may be a good choice. It also produces some bronchodilation and may be useful in cases of bronchospasm, such as asthma or COPD.12

Now that we have briefly reviewed the medications, let’s go over certain combinations of medications:

For the hypotensive medical patient, such as an elderly nursing home patient with sepsis secondary to urinary tract infection, Fentanyl is a good starting point.15 If the patient remains hypotensive after initial fluid resuscitation, start pressors. In the case of the trauma patient that is hypotensive, use of Fentanyl and/or Ketamine is recommended.15 The 62 year-old male with subarachnoid hemorrhage described earlier in the clinical vignette would benefit from Fentanyl and Propofol.15 Propofol is useful in these cases because of its hemodynamic effect of lowering blood pressure. In the case of a patient with delirium tremens requiring intubation, maximize the use of benzodiazepines in the pre-intubation period.15 Propofol and fentanyl are recommended for post-intubation analgesia/sedation.15 Finally, for patients in status epilepticus, fentanyl and propofol, which has anticonvulsant properties, are suitable choices.


  • Maximize resuscitation of the hypotensive patient in the pre-intubation period. Fluids and vasopressors may be necessary. Don’t underestimate the effect of preload in causing hypotension.
  • When evaluating a patient with sudden hypoxia, think about DOPES. Disconnect the ventilator and manually ventilate with a bag-valve-mask. Push on the chest to allow any trapped air to leave. Suction the endotracheal tube. If none of these things resolve the hypoxia, think about the Ps – pulmonary embolism, pneumothorax, pneumonia, pulmonary edema.
  • There are several different medications you can use for post-intubation sedation and analgesia. Think about what the underlying problem is and the hemodynamic effects of the sedative.

References / Further Reading:

  1. Heffner AC, Swords DS, Neale MN, Jones AE. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation 2013;84(11):1500–4.
  2. Herget-Rosenthal S, Saner F, Chawla LS. Approach to Hemodynamic Shock and Vasopressors. Clin J Am Soc Nephrol 2008;3(2):546–53.
  3. William Selde, MD. Push Dose Epinephrine as a Temporizing Measure for Drugs Causing Hypotension [Internet]. JEMS J. Emerg. Med. Serv. 2014 [cited 2016 Apr 4]; Available from:
  4. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med 2015;2(2):131–2.
  5. Marino PL. Marino’s The ICU Book: Print + Ebook with Updates. Fourth, North American Edition edition. LWW; 2013.
  6. Weingart S. Ventilator checklist for the coding asthmatic [Internet]. EMCrit. 2009 [cited 2016 Mar 17]; Available from:
  7. Man versus machine – post-intubation hypoxia [Internet]. LITFL Life Fast Lane Med. Blog. 2010 [cited 2016 Mar 17]; Available from:
  8. Propofol [Internet]. Access Emerg. Med. [cited 2016 Mar 28]; Available from:
  9. Fentanyl [Internet]. Access Emerg. Med. [cited 2016 Mar 28]; Available from:
  10. Sandra Thomasian, Joel Schofer, editors. Emergency Medicine Survival Guide. American Academy of Emergency Medicine Resident and Student Association; 2011.
  11. Midazolam [Internet]. Access Emerg. Med. [cited 2016 Mar 28]; Available from:
  12. Caro, David. Sedation or induction agents for rapid sequence intubation in adults [Internet]. Date. 2016; Available from:
  13. Cohen L, Athaide V, Wickham ME, Doyle-Waters MM, Rose NGW, Hohl CM. The effect of ketamine on intracranial and cerebral perfusion pressure and health outcomes: a systematic review. Ann Emerg Med 2015;65(1):43–51.e2.
  14. Ketamine [Internet]. Access Emerg. Med. [cited 2016 Mar 28]; Available from:
  15. Weingart S. Post-intubation Sedation in the Emergency Department [Internet]. EMCrit. 2010 [cited 2016 Mar 17]; Available from:

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