Post Intubation Hypotension: The AH SHITE mnemonic

Originally published at R.E.B.E.L. EM on April 20, 2017. Reposted with permission.

Follow Dr. Salim R. Rezaie at @srrezaie

You have just secured the endotracheal tube following an uneventful intubation of a moderately ill  patient in your emergency department. They had a normal pre-intubation blood pressure.  As you are calling the admit in to the ICU the patient’s nurse tells you that the BP is now in the 70’s.


  1. Blindly give a half gallon of saline and stay in your seat.
  2. Get up, walk to the patient’s room, and consider the possible causes of post intubation hypotension.

There is a laundry list of potential pathologies in play, some of which require time critical interventions. Option 2 is the only acceptable option for evaluating a patient with post intubation hypotension.

Here is a  crowd sourced approach that will allow most etiologies of post intubation hypotension to be identified: The AH SHITE mnemonic is something that you can quickly run through en route to the patient’s room, or at the bedside. This is intended as a starting point to the evaluation of the patient with post intubation hypotension.

Treatment of these issues will not be discussed in detail. Thanks to @precordialthump and @pbsherren for helping me  fine tune the list and force the mnemonic.


Patients with profound metabolic acidosis typically have a high minute ventilation, until they become fatigued and then their pH can drop. Post intubation ventilator settings need to provide minute ventilation that approximates pre-intubation levels. One way of ensuring this is to check a pre-intubation ETCO2 and to then aim for this number with a well planned post intubation ventilation strategy. 8cc/kg tidal volume (upper range of ARDSNET vent strategy) and a high RR (30’s) with close attention to post intubation gases is a good start.

Does giving bicarb to profoundly acidotic patients on the vent help?

 Henderson Hasselbalch equation:

H+ + HCO3- <—> H2O + CO2

This equation is an equilibrium, any increase in H+ concentration will tip the equation to the right, and generate more CO2. This will typically cause tachypnea, unless the patient is profoundly fatigued. Adding bicarb will produce more CO2, if the patient is already being ventilated at a maximum minute ventilation this will not be able to be increased, and without removing the CO2 from the system, the pH will not change.

Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations.

  • Anesthesiology. 1990 Jun;72(6):1064-76. PMID: 2161621
  • When isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCO2 increased and pH was unchanged. pH only rises when CO2 is eliminated.
  • If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.

Sodium Bicarbonate for the treatment of Lactic Acidosis.

  • Chest 2000; 117(1): 260 – 7. PMID: 10631227
  • 18 animal studies: no improvement with bicarb
  • 2 human studies, average lactates 7-8mmol/l
  • pH improved by 0.14, and 0.05
  • No improvement in hemodynamic parameters / response to pressors.

Giving bicarb does pose a risk of impaired oxygen delivery via an increased hemoglobin affinity for oxygen. This is seen in studies on healthy volunteers. A downstream effect from this is that lactate concentrations can increase. This has been seen in studies on animals with hypoxic lactic acidosis.


Anaphylaxis to ketamine and etomidate is extremely rare. There are only sporadic case reports of anaphylactoid reactions to each of these agents. Neuromuscular blocking agents are divalent molecules that make it easier for anaphylaxis to occur, even in the setting of no previous exposure. (See REBEL EM post in Anaphylaxis to NMB agents)

Anaphylaxis is more common with rocuronium and succinylcholine than with atracurium.

  • Anesthesiology. 2015 Jan;122(1):39-45. PMID:25405395
  • This was a retrospective, observational cohort study of intraoperative anaphylaxis to NMBDs at two Auckland, NZ hospitals between 2006 and 2012.
  • All cases of suspected perioperative anaphylaxis were referred to the same allergy clinic. These were high grade anaphylaxis events, including profound hypotension, and intraoperative cardiac arrest.
  • 92,858 anesthetic cases involving new exposures to NMB’s. 21 patients with anaphylaxis were confirmed out of 89 patients referred to the allergy clinic.
  • Rates:
    • Sux: 1:2080
    • Roc: 1:2499
    • Atracurium: 1:22451


Consider cardiac tamponade in both traumatic and medical presentations. Penetrating chest trauma should be an obvious trigger to perform bedside cardiac ultrasound. Elderly patients on anticoagulants with minor falls, and end stage renal disease patients may have occult / borderline tamponade that only declares itself after a change to positive pressure ventilation.

Timing of tracheal intubation in traumatic cardiac tamponade: a word of caution.

  • Resuscitation 2009 Feb;80(2):272-4 PMID: 19059695
  • Authors suggest raising the threshold for intubation, and preparing for immediate relief of tamponade after intubation. Consider awake intubation strategy without interrupting spontaneous ventilation. 

Heart: Pulmonary Hypertension

Patients with known severe pulmonary hypertension are a nightmare to intubate. Hypervolemia, hypoxia, and hypercarbia are known to worsen their right heart function. Fluid boluses are unlikely to help an overloaded, distended right ventricle, and may worsen LV impingement.

Pulmonary Hypertension and right ventricular failure in emergency medicine.

  • Annals of Emergency Medicine Dec 2015; 66(6):619-28 PMID:26342901
  • Give norepinephrine, and treating whatever worsened the Pulmonary Hypertension may help.

Stacked breaths / Autopeep

Patients with obstructive lung pathology who are not completely exhaling prior to the next breath being initiated can progressively develop air trapping, this can lead to increased intrathoracic pressure that can decrease venous return overtime, and cause hypotension, and eventual arrest.

Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect.

  • Am Rev Respir Dis. 1982 Jul;126(1):166-70. PMID: 7046541
  • Alveolar pressure can remain positive throughout the ventilatory cycle of intubated patients with airflow obstruction. Abnormally compliant lungs transmit a high fraction of alveolar pressure to intrathoracic vessels so these effects may be exaggerated in patients with chronic obstructive pulmonary disease.
  • Failure to recognize the hemodynamic consequences of auto-PEEP may lead to inappropriate fluid restriction or unnecessary vasopressor therapy.


Hypovolemia from profound shock states such as hemorrhage, sepsis, and anaphylaxis should be reasonably easy to identify. Occult hypovolemia can be unmasked by the physiologic insult that occurs when patients are switched from spontaneous ventilation to positive pressure ventilation. With the increase in intrathoracic pressure that accompanies positive pressure ventilation any patient with low venous pressures / low pre-load may develop hypotension. Adjusting PEEP settings, and giving a bolus of an appropriate resuscitative fluid will help.

Induction Agent

Propofol gets a bad rap for being blamed as the only agent capable of causing post intubation collapse. Any sedative agent that takes away an individual’s conscious drive to survive could potentially result in post intubation collapse; Weingart has described this as the ‘nine inch nails to Bob Marley transformation’. (See intubating the patient in shock from SMACC 2013). Decreasing the dose of sedative, and having pressors / push dose pressors ready could help to mitigate this.

Tension Pneumothorax

Consider tension pneumo in any patient with obstructive lung disease that has increased airway pressures. Rather that blindly needling the chest of these patients, use ultrasound to confirm whether a pneumothorax is present. This will avoid inadvertently causing a pneumothorax in a patient with normal lungs that may have an alternative explanation for their hypotension.


Succinylcholine has a well known set of contraindications due to the risk of succinylcholine associated hyperkalemia. Major burns, crush injuries, and end stage renal disease patients are typically rather obvious. Occult contraindications include those patients with histories of malignant hyperthermia, previous stroke / spinal cord injuries, or those with prolonged ICU stays. Several case reports exist of patients who have had profound hyperkalemia without obvious risk factors. In the absence of an alternative explanation for hypotension, and especially in the setting of any rhythm change consider checking a potassium level, or empirically treating with Calcium.

Cardiac Arrest From Succinylcholine-Induced Hyperkalemia


Anticipate that intubation can worsen underlying physiologic parameters, and can cause some intubation specific causes of hypotension. Anticipating post intubation hypotension and being ready to correct specific causes is an essential part of any intubation.

Transform your mantra for post intubation hypotension evaluation from Resuscitate, Intubate, Panic like #$@#, to Resuscitate, Intubate, Anticipate.

Remember this sage advice from Louis Pasteur: ‘Fortune favors the prepared mind’.  The better you plan your intubation (see Salim’s HOP killer series) the less likely you will be dealing with post intubation hypotension.

Post Peer Reviewed By: Salim Rezaie (Twitter: @srrezaie)


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ECG Pointers: TCA Overdose

Author: Lloyd Tannenbaum, MD (EM Resident Physician, San Antonio, TX) // Edited by:  Jamie Santistevan, MD (@jamie_rae_EMdoc – EM Physician, Presbyterian Hospital, Albuquerque, NM), Manpreet Singh, MD (@MPrizzleER – Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center) and Brit Long (@long_brit  – EM Attending Physician, San Antonio, TX)

Welcome to this edition of ECG Pointers, an emDOCs series designed to give you high yield tips about ECGs to keep your interpretation skills sharp. For a deeper dive on ECGs, we will include links to other great ECG FOAMed!

The Case:

It’s a busy morning shift and you get called into a patient’s room who is actively seizing.  On your way in, the nurse tells you that she has a history of pseudoseizures and warns you not to be fooled.  When you walk in the room, a tech hands you this ECG:

There is sinus tachycardia with a rate of about 110. The QRS duration is prolonged (140ms). There is a wide terminal R wave in lead aVR.

After glancing at the ECG, you look at your patient. She has recovered from her seizure and is sitting comfortably in bed.  Her mom says that she has just increased antidepressant, Amitriptyline.  When you ask to see the bottle, you realize it’s half empty and she had picked it up 5 days ago.  Your patient has been taking about 10 pills a day for the past 5 days!

What are some signs of TCA Overdose on the ECG?[1,2]

  1. Sinus Tachycardia – most frequent dysrhythmia
  2. Widening of the QRS complex
  3. Prolongation of the PR or QT interval
  4. Right bundle branch block
  5. Non-specific intraventricular conduction delay (IVCD)
  6. Brugada pattern
  7. Wide-complex tachycardia (not ventricular tachycardia)
  8. Ventricular tachycardia / fibrillation

What causes these signs? [3]

  • TCAs block the muscarinic (M1) receptors which causes tachycardia
  • TCAs block sodium channels which can cause seizures from blockade of sodium channels in the CNS and ventricular dysthymias from blockade of sodium channels in the heart

Note: Besides anti-muscarinic and sodium channel blockade, TCAs also have an anti-histamine, alpha-1 blockade, GABA-A receptor blockade, potassium channel blockade and amine reuptake inhibition pharmacological effects, which are important to know when treating very sick TCA overdoses.

How wide is too wide? [3]

A QRS duration >100ms is predictive of seizures and QRS >160ms is highly likely to experience a ventricular dysthymia.  The ECG from our patient had a QRS of 144!

What else can I see on the ECG? [3]

A terminal R-wave in AVR is often used to identify a TCA overdose, but what does it mean? Along with QRS prolongation, this finding is not specific to a TCA overdose; rather it is pathognomonic for a sodium channel blockade. You will see a wide R-wave in aVR that is greater than 3mm. This is caused by delayed right ventricular activation from interventricular conduction delays because the right bundle is more sensitive to blockade, causing rightward axis deviation. This produces a deep, slurred S-wave in leads I and AVL, and a large (>3mm) R-wave in lead aVR with a R:S ratio >0.7.

Image obtained from Life in the Fast Lane ( overdose/)

Other drugs that may cause sodium channel blockade include antiarrhythmics (quinidine, procainamide, flecainide) local anesthetics (bupivicaine), antimalarials, propanolol, and carbamazepine.

What are some common TCAs?

  • Amitriptyline
  • Amoxapine
  • Desipramine (Norpramin)
  • Doxepin
  • Imipramine (Tofranil)
  • Nortriptyline (Pamelor)
  • Protriptyline (Vivactil)
  • Trimipramine (Surmontil)

Remember that although TCAs are most commonly used to treat depression, they are also prescribed for anxiety or pain disorders (i.e. neuropathic pain or fibromyalgia).

Now what do you do? [4]

Cardiac toxicity can develop quickly in TCA overdose, so obtaining an ECG early in the clinical course is key. If QRS widening >100ms exists, or in the presence of ventricular dysrhythmias, the patient needs immediate treatment. Give sodium bicarb to overcome the sodium channel blockade! You can give sodium bicarb boluses of 100mEq (1-2 mEq/kg) every 2-5 minutes until the QRS complex narrows. Once the QRS narrows, begin continuous IV infusion of sodium bicarb. You can be quick about making a bicarb drip by putting 3 amps of bicarb (150 meq) into a liter of D5W. Run at a rate of 250 mL/hr in adults.

Fun fact: The mechanism of action that sodium bicarb works to fix a TCA overdose is not completely known. Some studies show that the change in pH from the administration of bicarb is what reverses the toxicity, where as other studies show that it is the sodium overcoming a blockade.

Caveat Emptor: Giving sodium bicarb can cause HYPOkalemia, so watch the patient’s potassium closely!

Case resolution:

The patient was given 2 amps of sodium bicarb and the QRS narrowed right away. The patient was later admitted to the ICU where she made a full recovery.

What are the main ECG pointers for TCA overdose?

  • Cardiac toxicity can develop quickly in TCA overdose, so get an ECG early in the clinical course if suspecting the diagnosis
  • The pattern of ECG findings in TCA overdose includes: tachycardia, prolonged QRS duration, long QT interval, rightward axis deviation and wide R-wave in aVR
  • The wider the QRS complex, the higher risk of seizures (>100ms) and ventricular arrhythmias (>160ms)
  • Treatment is indicated for a QRS complex wider than 100ms and is with sodium bicarbonate

Gimme some more FOAMed:

  • emDOCs ToxCard reviewing TCA poisoning by our Tox Team.
  • Anna Pickens from EM in 5 covers this extensive topic in 5 minute.
  • Life in the Fast Lane has an excellent write up on TCA overdoses and ECG findings.
  • Smith’s ECG Blog has an awesome case of a TCA OD unmasking brugada syndrome.
  • emCrit crew discusses cyclic antidepressant overdose in podcast 98.
  • WikEM overview of TCA OD with a bullet review.
  • EM Cases bring you Crit Cases 1: Massive TCA OD and how to deal with these sick patients.
  • Core EM goes over this topic in fabulous review.


  1. Niemann, JT, Bessen, H, Rothstein, R, and Laks, M. Electrocardiographic Criteria for Tricyclic Antidepressant Cardiotoxicity. Am J Cardiol. 1986; 57: 1154-1159.
  2. Mehta, n, and Alexandrou, N. Tricyclic Antidepressant Overdose and Electrocardiographic Changes. J of Emergency Medicine. 2000. 18(4): 463-464.
  3. Burns, Edward. 13 Apr 2017.
  4. Bruccoleri, RE, Burns, MM. A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening. J Med Toxicol 2016 Mar; 12(1):121-129.

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TOXCard: Loperamide Toxicity

Author: Tim Montrief (@EMinMiami, PGY-1, Emergency Medicine Residency Program, Jackson Memorial Health System) // Edited by: Cynthia Santos, MD (Assistant Professor, Emergency Medicine, Medical Toxicology, Rutgers NJMS), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit)


A 20-year-old man with a past medical history of heroin abuse is brought in to the Emergency Department by EMS complaining of palpitations and syncope. The patient admits to taking up to 100 mg of loperamide per day “for weeks” to attenuate his current withdrawal from heroin. His electrolyte levels are within normal limits, and you get an ECG that shows a QTc interval of 530 ms…


  1. Why is loperamide becoming an emerging drug of abuse? What are the historical, social, and pharmacological factors influencing this?
  2. What is the clinical presentation of a patient with loperamide toxicity? What are the relevant labs and studies to order?
  3. What is the cardiac toxicity of loperamide?
  4. What treatments are available for loperamide toxicity?


  • Loperamide is an inexpensive, widely used nonprescription antidiarrheal that inhibits intestinal peristalsis through its peripheral µ-opioid receptor agonism, as well as calcium channel blockade.1
  • Loperamide abuse is increasing, as patients use it either to experience euphoric effects or to attenuate the effects of opioid withdrawal.2,3
  • The daily maximum recommended dose is 16 mg for the indication of diarrhea treatment. Abuse of loperamide in order to get high or for self-management of withdrawal commonly occurs at very high doses. Average daily dosing of patients presenting with loperamide toxicity has been reported to range from 200-400 mg, with some reports of ingestions exceeding 1000 mg.2,3
  • CYP and P-glycoprotein inhibitors are commonly coingested to increase loperamide plasma concentrations. CYP3A4 and CYP2C8 inhibitors increase the plasma concentration of loperamide by about 2- and 4-fold, respectively, and by over 12-fold when both enzymes are inhibited simultaneously. P-glycoprotein inhibitors also increase the plasma concentration of loperamide by about 2 to 3-fold and can also increase the loperamide CNS concentration by its negative effects on the blood-brain barrier.4
    • For example, some users co-ingest cimetidine and grapefruit juice to inhibit CYP enzymes, or black pepper and quinidine to inhibit P-glycoproteins.2,3
  • At high doses, loperamide blocks cardiac sodium and potassium channels, resulting in prolonged QRS and QT intervals.1

Clinical Presentation and Workup:

  • Clinical presentation: Loperamide toxicity is not characterized by its opioid effects alone. Multiple cases of cardiac toxicity have been published in recent literature, and some have been fatal.5 Signs and symptoms of loperamide toxicity include:
    • Palpitations
    • Nausea and vomiting
    • Anxiety
    • Generalized weakness
    • Presyncope
    • Dyspnea
    • New-onset or recurrent syncope
    • Decreased level of consciousness
    • Seizure-like activity
    • Cardiac arrest
  • Workup: Pay close attention to cardiac effects related to loperamide toxicity.
    • ECG- look for cardiac dysrhythmias, prolonged QRS/QT intervals
    • Electrolytes- look for reverse factors for QT-interval prolongation (such as hypokalemia, hypomagnesemia)
    • Co-ingestions

Cardiac Toxicity:

  • At high doses, loperamide blocks cardiac sodium and potassium channels, resulting in prolonged QRS and QT intervals.6-9
  • Presenting rhythms vary, but include:
    • Ventricular tachycardia/fibrillation
    • Asystole
    • Junctional escape
    • Torsade de pointes


  • The management of loperamide toxicity is largely supportive, centering around the treatment of any drug toxicity, in conjunction with consultation with the local poison control center.4,10
    • Decontamination
    • Enhancing elimination
    • Antidote therapy
    • Supportive care
  • Decontamination
    • Loperamide is likely absorbed by activated charcoal
    • Loperamide levels are reduced nine-fold when activated charcoal is given.
    • In therapeutic doses, loperamide’s peak level is about 5 hours after ingestion. This, in addition to loperamide’s effects on reducing bowel motility means you should consider extending the window of when activated charcoal would be appropriate past the typical ~1 hour.11
  • Enhancing elimination
    • There is no data on whether activated charcoal or whole bowel irrigation would enhance the elimination of loperamide.
    • There is no data on whether loperamide is removed by dialysis, ion trapping, or other methods to enhance elimination of toxins.
  • Antidote therapy
    • Naloxone should be given in the presence of respiratory depression and may require repeated dosing. To prevent the possibility of precipitated opioid withdrawal, the lowest effective dose of naloxone should be used in order to avoid life-threatening complications such as seizures and arrhythmias.5
    • Sodium bicarbonate IV may treat the cardiotoxic effects of loperamide, especially the sodium blockade. If sodium bicarbonate is used, be sure to frequently monitor serum electrolytes.
  • Supportive Care
    • Reverse any electrolyte abnormalities (hypocalcemia, hypokalemia, hypomagnesemia)
    • Cardiac dysrhythmias have all be successfully treated with:
    • Defibrillation
    • Repeated shocks may be required, as one case report required cardioversion more than 15 times.12
    • Magnesium
    • Amiodarone
    • Lidocaine
    • Overdrive pacing
    • VA ECMO is an option for the select patients in cardiovascular shock refractory to all medical therapies.
    • Consideration should be given to managing any underlying opioid use disorder.


  • Loperamide is increasingly used as an inexpensive and legal method for opioid abuse and for self-management of opioid withdrawal.
  • However, multiple cases of fatal cardiac toxicity have been reported.
  • At high doses, loperamide blocks cardiac sodium and potassium channels, resulting in prolonged QRS and QT intervals.
  • Management of loperamide toxicity is largely supportive and should be managed with decontamination, elimination, antidotes, and supportive care in conjunction with consultation with the local poison control center.


  1. Baker DE. Loperamide: a pharmacological review. Rev Gastroenterol Disord. 2007;7(suppl 3):S11-S18
  2. Daniulaityte R , Carlson R , Falck R , et al. “I just wanted to tell you that loperamide WILL WORK”:a web-based study of extra-medical use of loperamide. Drug Alcohol Depend 2013;130:241-44.
  3. Lasoff DR, Koh CH, Corbett B, et al. Loperamide Trends in Abuse and Misuse Over 13 Years: 2002-2015. Pharmacotherapy. 2017;37(2):249-253.
  4. Horn J, Hansten P. Loperamide: Danger of Elevated Plasma Concentrations. Pharmacy Times, published on August 18 2016. Available at:
  5. Wu PE, Juurlink DN. Clinical Review: Loperamide Toxicity. Ann Emerg Med. 2017;70(2):245-252.
  6. Kang J, Compton DR, Vaz RJ, et al. Proarrhythmic mechanisms of the common anti-diarrheal medication loperamide: revelations from the opioid abuse epidemic. Naunyn Schmiedebergs Arch Pharmacol. 2016;389:1133-1137.
  7. Lasoff DR, Schneir A. Ventricular dysrhythmias from loperamide misuse. J Emerg Med. 2016;50:508-509
  8. Bhatti Z, Norsworthy J, Szombathy T. Loperamide metabolite-induced cardiomyopathy and QTc prolongation. Clin Toxicol. 2017.
  9. Mirza M, Attakamvelly S, Dillon A, et al. Potential life threatening cardiac toxicity from an easily accessible over the counter drug. Journal of the American College of Cardiology. 2017;69:2375.
  10. Pharmacy Joe. 88:Treatment of loperamide cardiac toxicity. 2016. Available at:
  11. Juurlink DN. Activated charcoal for acute overdose: a reappraisal. Br J Clin Pharmacol. 2016;81:482-487.
  12. Marraffa JM, Holland MG, Sullivan RW, et al. Cardiac conduction disturbance after loperamide abuse. Clin Toxicol (Phila). 2014;52(9):952-7.

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