Wonder drugs, overdoses, and not understanding sedation…


There seems to be a lot of confusion on sedatives, sedating, and what it means to overdose today…I am tired of explaining it, so here it is so from now on I can just link to it.

So permit me to define some terms first?
Minimal Sedation (Anxiolysis)

  • A drug-induced state during which patients respond normally to verbal commands.
  • Cognitive function and coordination may be impaired.
  • Ventilatory and cardiovascular functions are unaffected.

    Moderate Sedation/ Analgesia (“Conscious Sedation”)

  • A drug-induced depression of consciousness during which

◦ patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation

◦ reflex withdrawal from a painful stimulus is NOT considered a purposeful response

  • No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate.
  • Cardiovascular function is usually maintained.

    Deep Sedation/ Analgesia

  • A drug-induced depression of consciousness during which patients cannot be easily aroused, but

◦ respond purposefully following repeated or painful stimulation.

◦ reflex withdrawal from a painful stimulus is NOT considered a purposeful response

  • The ability to independently maintain ventilatory function may be impaired.

◦ Patients may require assistance in maintaining a patent airway.

◦ Spontaneous ventilation may be inadequate.

  • Cardiovascular function is usually maintained. *credit to the American Society of anesthesiologists for the definitions.

Now in some patients, particularly in the ICU, the term “Profound sedation” is often used. Which seems to be a way of saying general anesthesia without actually using words like TIVA, anesthesia, or “oops, too much or for too long…”

Some textbooks and studies define sedation as separate to analgesia/anesthesia, which is a credible thing to say given that it generally works by different mechanisms, often with different medications, and with different objectives.

However, there is also a school of thought that recognizes that sedation and anesthesia are a continuum, and I find this very credible, because it is not only common to use them together, but the very same medications can reach the exact same effects in the higher (or technically correct, “anesthetic doses”).

Because of all of the similarities, certain terms or phrases I find get confused among providers, particularly the term “sedation.” For about the last 15-20 years, “conscious” sedation, or the more appropriately named “procedural sedation” has become popular. The term “conscious” stems from clinical usage where patients can maintain their own airway, be directed, and generally respond to simple questions.

Anyone assessing these patients for proper depth of sedation, may quickly find that while they are able to be directed or answer simple questions, while maintaining their own airway, they become obtunded enough to answer inappropriate questions appropriately. When checking depth of sedation I have been known to ask “where did you hide the money”, and I have gotten all kinds of wonderful responses from people who could tell me their name, where they are, and generally what is going on. (the best answer was “under the great wall in China”)

The true test of the effectiveness of procedural sedation is whether or not the patient can tolerate the procedure being performed. This makes the definition more unclear. For example, giving a patient a few mg of a benzodiazepine to act as an anxiolytic to tolerate a CT scan or a femoral blood draw is nowhere near the same level of sedation as say… several mg for performing a tracheotomy or reducing an angulated fracture. Both of these do however mean the patient was able to tolerate the procedure to successful completion.

While I used a benzo as an example, it can in actuality be several different types of medications or simply just a high dose of a singular agent.

This has led me to adopt the philosophy of “sedation” actually being part of a continuum, rather than separate from analgesia or anesthesia. Especially since the drugs that can be used for both analgesia and anesthesia are frequently used with sedation or in place of it. Many of the medications are also synergistic so the sedative potentiates analgesia and the analgesic the same for the sedation.

So here is how I explain the continuum.
Way down at the bottom, often not even on my continuum list because it is so mild, is mild sedation. It may or may not require a commonly recognized sedative, and in practice many times a medication with the side effect of sedation will suffice. I primarily like promethazine of the first generation h1 blockers. But your favorite flavor may vary. In more “exteme” mild cases, a low dose benzodiazepine is usually my choice.

Now moving up to the 3 levels I actually consider in the continuum from the practical point:

Analgesia, which is defined as “no pain.” This is most often taught as using escalating medications from NSAIDS, to “middle strength” medications like tramadol, and finally conventional opioids. However, chronic pain vs. acute pain can complicate this. So can modern techniques such as local and regional nerve blocks. But he end game is “no pain” while maintaining all other functions.

Procedural sedation, “no pain, no memory”. This is the middle ground between analgesia and anesthesia. Often since dissociative drugs like ketamine, midazolam, etc. are used, the patient has some level of amnesia of the event. This amnestic medication selection is often done on purpose, especially in children. Generally it makes it so the patient is not afraid of future procedures or will return for follow up. Because it is an increase is dose or medication, and does not meet the 3 requirements for anesthesia, this is the level of sedation most commonly valuable in the acute care setting.

Anesthesia. According to most anesthesia texts, the simple definition is: No pain, no memory, no reaction to stimuli, like a surgeon cutting your abdomen open digging to your aorta. Others describe it as the induction of Coma. Any sedative, opioid, or combination thereof can reach “anesthetic doses”. If procedural sedation was the goal, this may be described as an unintentional overdose. However, I am of the view that this may be both an arbitrary and overly negative description of a purposeful and clinically indicated sedation, based on patient condition and response to lower levels of sedation for performing procedures, pain control, etc. This level of sedation requires support of body functions, like airway, ventilation, respiration, etc. Despite the overly generous definition from the ASA, I have never seen an anesthetized patient sitting in a bed or on a table spontaneously breathing.

For some reason non-anesthesiologists, anesthetists, et al. do not like to use or admit to using this level of “sedation”. However, when looking at the definitions, it may be more common than most think.

I will just interject here, that the use of neuromuscular blockers, was to facilitate and lower the doses of medication required for anesthesia, after all, the purpose of a neuromuscular blocker is “no reaction.”

Now let us analyze the popular emergency procedure of RSI, rapid sequence induction. There are pages upon pages, essentially novels full of debate in print and online about what medications are best and why. But if you take away all of the chaff, what you find is it all comes down to how quickly anesthesia can be reached, and what functions need to be supported.

In case you didn’t get it, RSI requires anesthesia. It is not acceptable for the patient to be in pain, and an analgesic is always indicated. It is not acceptable for a patient to be aware, so a sedative is always indicated. If the patient is not reacting, because a muscular blockade was given, then that patient does not feel pain, has no memory (awareness), and has no reaction, and certainly needs assistance supporting vital functions such as airway, ventilation, and sometimes circulation. That is the very definition of anesthesia. (just a side note, inhaled anesthetics, are a form of drug and delivery model, they are not required to achieve anesthesia, in fact in some types of surgery, total intravenous anesthesia is preferred, aka TIVA)RSI is for all intents and purposes TIVA.

Now it is recommended by both Emergency and Anesthesia societies that anyone administering procedural sedation be capable of supporting life functions in those who either purposefully, because of presentation and reaction, or accidentally, because too much or too fast of medication administration. That seems very prudent, and the fact is emergency providers are extremely skilled in supporting life functions, just the same as anesthesiologists are. I have come to learn where intensive care is not a part of anesthesia, the intensivists is usually even more skilled beyond anesthesia, because of the goals, mentality, and techniques involved (that is a discussion for another time).

When selecting medications for RSI, paramedics, emergency physicians, anesthesiologists, et al, all have their different arguments and preferences. But they all have the same outcome, the same requirements, the same intricacies, only the doses and the timing of the support changes.

A very old but wise anesthesiologist once told me, “Mike, It doesn’t matter what drugs you use, keep it simple, pick 2 or 3 and get really experienced at using them. That is how you become proficient at anesthesia, not knowing every medication and cocktail.”

There are no miracle drugs. There are no safe drugs. Recall the very first lesson of pharmacology:

“Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.” – Paracelsus

In a recent online discussion, there were supporters of the medication ketamine arguing that it was superior because when patients were accidently overdosed by massive amounts, with proper support, they recovered…Except the “overdose” was really from the level of procedural sedation to anesthesia. With the proper support, people wake up from anesthesia will no ill effects every day. That’s the whole point.

People don’t just suddenly get X amount of a drug and decide “ok, I am going to die now I had too much.” That drug creates a physiological effect, which results in decompensation, and in the case of sedatives, opioids, etc. that decompensation can be remedied by proper life support until the medication wears off. The argument one drug is safer than another because of it is simply uneducated or not using the knowledge already attained.

I can’t wait to hear about the next “miracle drug” in emergency medicine, first it was etomidate, now ketamine that is “the safest, bestest”. Maybe we should cut to the chase and get to this already…