Post-Intubation Care

Dr. Farrah Nasrollahi

edited by Ilyas Taraki

A Case

65-year-old female with heavy alcohol use and other polysubstance use disorder (primarily heroin), hypertension, hyperlipidemia, with poor medical follow-up and otherwise no known medical issues presents with weakness. Her lactic acid is 4.0. She is ultimately admitted for ALI and severe AKI thought to be secondary to UTI with septicemia and is started on IV fluids and antibiotics. Over the course of the evening, she becomes hypoxic and short of breath and ultimately is intubated.

You've intubated. Now what?

Congratulations — tube in, RSI complete, and CXR/EtCO2/physical exam confirm placement. What now? How will you manage her meds on the vent? Infusion? Pushes?

Consider the patient's age, weight, drug/alcohol use, comorbidities, and renal/hepatic functions.

  1. Pick analgesia. Give a bolus and make sure it's adequate, then start an infusion

  2. Pick sedation if necessary, but be wary

What did she actually receive? Fentanyl and propofol. Was this a good choice for her?

Her Outcome

When I arrived on the unit the next AM, her lactic acid was 7.9. I noticed HR was decreasing: she was 110-120 on arrival but was now in the 40s-50s. Not good!

Looking over her medications, vent settings, volume status, and overall clinical course, it was decided that the propofol should be switched to Versed.

Lactic acid improved!

What did she have?

Propofol Infusion Syndrome (PIS)

Defined as metabolic acidosis with cardiac dysfunction and one or more of the following: rhabdomyolysis, hypertriglyceridemia, or renal failure.

However, intralipid propofol may impair hepatic lactate metabolism leading to lactate accumulation and acidosis.

The disease commonly presents as an otherwise unexplained high anion gap metabolic acidosis, rhabdomyolysis, hyperkalemia, acute kidney injury, elevated liver enzymes, and cardiac dysfunction. Management of overt propofol infusion syndrome requires immediate discontinuation of propofol infusion and supportive management, including hemodialysis, hemodynamic support, and ECMO in refractory cases.

Why this matters: analgesia and sedation choices

PIS aside, how you manage analgesia and sedation on the vent matters:

  • Drug choice

  • Your algorithm for dealing with sedation vs. analgesia

  • How you personalize your practice to the patient

For Sedatives

Current practice favors intermittent bolus doses, daily interruption or dose minimization titrated to light level of sedation (RASS -2 to 0) of continuous infusions [3]. Clinical practice guidelines for the sustained use of sedatives and analgesics in critically ill adults endorse the initial use of intermittent bolus dose, with the initiation of continuous infusions with daily interruption or dose minimization titrated to light level of sedation in patients who require intermittent infusions more often than every two hours [7].

Early Interventions Matter (ED)

  • The SPICE trial: deep early sedation within the first four hours was an independent predictor for delayed extubation and increased mortality. (Shehabi 2012)

  • If you don’t give enough analgesic, you’ll end up unnecessarily giving more sedation

  • Increase in RASS scores, systolic, and diastolic blood pressure in mechanically ventilated patients receiving sedation only when compared to patients also receiving analgesia (Jeitziner 2012)”

  • Not all mechanically ventilated patients require sedatives.

  • A randomized controlled trial of 140 patients: patients in the solo analgesia group had statistically significantly more days without mechanical ventilation and on average shorter ICU length of stays. (Strom 2010)

  • Use of succinylcholine compared to longer acting NM blocking agents for RSI associated with higher likelihood of post RSI sedation. (Lembersky 2019)

Analgesic: Opioids

  • CNS and peripheral tissue

    • Mu- 1 receptor binding: analgesia

    • Mu-2 receptors: respiratory depression, vomiting, constipation, and euphoria

    • Kappa receptor: sedation, miosis, and spinal analgesia

  • Provide mild anxiolysis, but no amnesia

  • PROS:

    • Good for dyspneic and suppresses cough reflex

    • Little cardiovascular effect in euvolemic patients

  • CONS:

    • In hypovolemic patients with reduced cardiac output, decreased venous return, reduced sympathetic tone, and reduction in heart rate can result in hypotension

    • Synergistic effect on hemodynamics (ie. hypotension) and sedation when coupled with benzos

Analgesic/Sedative: Ketamine

  • MOA: NMDA receptor antagonist, phencyclidine derivative

  • Analgesic and sedative

  • PROS:

    • Great for the status asthmaticus (relaxes bronchial smooth muscle)

    • Great for the hypotensive patient

  • CONS:

    • Contraindicated in hypertension, cardiovascular disease, high intracranial pressure (controversial), preeclampsia, glaucoma, seizure (lower seizure threshold) and history of psychosis (altered mood/delirium), laryngospasm

Analgesic/Sedative: Dexmedetomidine

  • MOA: central α2 agonist similar to clonidine, but more specific

  • Analgesia and sedation

  • Lipophilic

  • PROS:

    • Provides sedation and analgesic without respiratory depression

    • Provides lighter sedation, great for delirium and best to use when attempted to extubate

  • CONS:

    • Bradycardia and hypotension if titrated too quickly

    • Extensive hepatic metabolism

Sedative: Benzos

  • MOA: g-aminobutyric acid (GABA) receptor CNS blockade

  • Anxiolytic with sedative and hypnotic effects at increasing doses

  • PROS:

    • Antiepileptic

    • Subtle drug-drug interaction because of above

  • CONS:

    • Propylene glycol toxicity with some

    • Some data suggesting worse outcomes with benzos compared to propofol or dexmedetomidine: delirium, oversedation, delayed extinction and longer time to discharge

    • Have to be mindful in patients with hepatic and renal dysfunction

Sedative: Propofol

  • MOA: Unclear mechanism; GABAergic effects on CNS

  • Lipophilic: onset in seconds/minutes with redistribution to peripheral tissues and a large volume of distribution

  • Powerful anxiolytic and amnestic

  • PROS:

    • Antiepileptic

    • Allows for serial neurologic assessments due to rapidity of action, ease of titration, and lack of active metabolites

    • Preferred in TBI as may decrease cerebral oxygen consumption and reduce ICP

  • CONS:

    • Can cause hypotension, particularly in under-volume-resuscitated patients

    • Lactic acidosis, hypertriglyceridemia, propofol infusion syndrome

Special Case: Bad Liver

56-year-old male with alcohol abuse without known cirrhosis, HTN, DM, HLD with history of DTs and withdrawal seizures. He is being transferred to your ICU for acute liver failure. On arrival, he is confused and becomes more agitated, confused, tachycardic, and hypertensive, and a decision is made to administer medications. What would you try, and why?

Overnight he becomes acutely hypoxic to 70s and develops respiratory distress. A decision is made to intubate him. What would you give, and why?

Opioids and Anesthetics

Opioids are successfully used in patients with liver diseases, and Fentanyl is the drug of choice for these patients. As the average dosage of drug is used, oxygen content of the liver and liver blood flow are not affected [14, 16].

Among the drugs used for induction of anesthesia, propofol is the drug of choice in patients with liver diseases [17]. As a rule, any type of long-acting local anesthetic in patients with cirrhosis should be avoided. Fentanyl from narcotics, lorazepam and oxazepam from sedatives, along with some volatile anesthetic agent such as Sevoflurane or intravenous anesthetics such as propofol are recommended in these patients [18-20].


The ‘LOT’ drugs are those metabolized mostly by conjugation:

  • L – Lorazepam

  • O – Oxazepam

  • T – Temazepam

These do not have active metabolites, and the half-life remains relatively the same even in the setting of liver disease.

The rest of the benzodiazepines are primarily metabolized via hepatic CYP-mediated oxidation. These may have prolonged duration of effect in patients with marked liver impairment, particularly the drugs with active metabolites such as diazepam, clonazepam, and midazolam. Some practitioners like to take advantage of the longer duration of action and active metabolites. Others prefer to have more predictable kinetics in patients with liver disease and stick with the ‘LOT’ options.

Special Case: Bad Kidney

78-year-old female with CKD stage 4 (nearing ESRD), HTN, HLD, and DM2 admitted to the ICU for pneumonia. In your ED she becomes hypoxic and confused and is subsequently intubated. Your colleagues have made you aware she will be boarding in the ED because the ICU has no beds yet. She was intubated with rocuronium and etomidate. Her BPs have been soft despite 2L fluids; MAP is 60. You’re about to place your orders s/p intubation. What are you choosing, and why?

  • Go hard on those opioids

  • Add a pressor

  • Sedation in patients with severe RD shows poorer outcomes

  • Midazolam has delayed metabolism/elimination in renal impairment and should be avoided

  • Dexmedetomidine has been used and is effective

The Current Recommendations

  • Start with picking your analgesic:

    • Opioids, dexmedetomidine, ketamine

  • If you must pick a sedative:

    • Propofol over benzos in cardiac surgery patients, neurosurgical patients, any other cardiac/neuro dysfunction, and hepatic dysfunction

    • Dexmedetomidine over benzos in surgical and medical patients

    • Benzos over propofol/dexmedetomidine in alcohol withdrawal


Barr J, Gilles L, Puntillo K, et al: Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Critical Care Medicine 2013; 41: 263-295 PMID: 23269131

Hoetzel A, Ryan H, Schmidt R. Anesthetic considerations for the patient with liver disease. Curr Opin Anaesthesiol. 2012;25(3):340–7. doi: 10.1097/ACO.0b013e3283532b02.

Keegan MT, Plevak DJ. Preoperative assessment of the patient with liver disease. Am J Gastroenterol. 2005;100(9):2116–27. doi: 10.1111/j.1572-0241.2005.41453.x.

Kiamanesh D, Rumley J, Moitra VK. Monitoring and managing hepatic disease in anaesthesia. Br J Anaesth. 2013;111 Suppl 1:i50–61. doi: 10.1093/bja/aet378.

Kurosawa M, Unno T, Aikawa Y, Yoneda M. Neural regulation of hepatic blood flow in rats: an in vivo study. Neurosci Lett. 2002;321(3):145–8.

Lembersky O, Golz D, Kramer C, Fantegrossi A, Carlson JN, Walls RM, Brown CA 3rd; NEAR Investigators. Factors associated with post-intubation sedation after emergency department intubation: A Report from The National Emergency Airway Registry. Am J Emerg Med. 2020 Mar;38(3):466-470. doi: 10.1016/j.ajem.2019.05.010. Epub 2019 May 6. PMID: 31130369.

Jeitziner MM, Schwendimann R, Hamers JP, et al: Assessment of pain in sedated and mechanically ventilated patients: An observational study. Acta Anaesthesiol Scand 2012; 56: 645-654 PMID: 22404146

Patel S, Kress J: Sedation and Analgesia in the Mechanically Ventilated Patient: Am J Respir Crit Care Med 2012; 185: 486-497 PMID: 22016443

Schwartz RB, Shepherd G. Pharmacologic Adjuncts to Intubation. 6 ed. Elsevier; 2014.

Shehabi Y, Bellomo R, Reade M, et al: Early Intensive Care Sedation Predicts Long-Term Mortality in Ventilated Critically Ill Patients. Am J Respir Crit Care Med 2012; 186: 724-731 PMID: 22859526

Shehabi Y, Chan L, Kadiman S, et al: Sedation Practice in Intensive Care Evaluation (SPICE) Study Group investigators: Sedation depth and long-term mortality in mechanically ventilated critically ill adults: A prospective longitudinal multicenter cohort study. Intensive Care Med 2013; 39: 910-918 PMID: 23344834

Strom T, Martinussen T, Toft P: A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomized trial. The Lancet 2010; 375: 475-480 PMID: 20116842

Vaja R, McNicol L, Sisley I. Anaesthesia for patients with liver disease. (CEACCP). 2009;10(1):15–9. doi: 10.1093/bjaceaccp/mkp040.