Conscious Sedation: Is Your Patient Breathing?

Change in mental status can occur from conscious sedation or opioid administration, hypotension, sepsis, head trauma, acid-base imbalance, alcohol, drugs, or toxins. Change in level of consciousness often affects breathing, sometimes to the point of causing severe hypoxia, arrythmias and cardiac arrest. Let me repeat that. Anything that alters consciousness can alter respiration, which can lead to the vicious cycle of hypoventilation, hypercarbia, and hypoxia. If you don’t recognize inadequate respiration —and treat it— the patient can suffer injury or die. Let’s look at a common clinical example of altered consciousness — conscious sedation.

Everyday, in all of our practices, we purposefully try to alter our patient’s level of consciousness in order to tolerate a procedure. We often take the safety of procedural conscious sedation for granted. After all, we’re only giving a little sedation to make the patient relaxed, calm and more comfortable. Although problems are rare, patients can become hypoxic, hypercarbic, and apneic with conscious sedation, and some have died. The deaths of the celebrities Michael Jackson in 2009, and Joan Rivers in 2014 were related to hypoxia from loss of the airway under deep sedation. Respiratory depression represents the principal potential risk introduced with conscious sedation. If left unrecognized and untreated, it can be the cause of serious complications.

Sleep and Sedation Affect Respiration

To understand why mental status change increases respiratory risk, let’s start with the respiratory effects of sleep.

Janet Smith is a 44 year-old healthy patient who is scheduled for correction of a trigger finger with ambulatory surgery under conscious sedation tomorrow at the surgicenter. She’s worried, so it takes her a long while to fall asleep. When she finally does sleep, her respiratory drive begins to change.

Does oxygen saturation change with normal sleep? For healthy young people between 19-25 years of age, there appears to be no change in oxygen saturation with sleep (1). Other studies looking at a more varied population up to age 64 did find up to an 11% drop in oxygen saturation(2,3,4). Adding a comorbidity such as chronic bronchitis is also associated with saturation drops of about 10%. So the answer seems to depend on age, presence of comorbidities and how ventilation changes with sleep for that particular person due to such things as snoring.

With normal non-REM sleep, PaCO2 rises about 3-7 mmHg as the body’s response to increased CO2, or hypercarbia, is blunted. Tidal volume and respiratory rate decrease. Pharyngeal muscles as well as muscles of the tracheobronchial tree relax, increasing airway resistance and predisposing to potential obstruction, such as snoring.

Although some of us sleep more deeply than others, we usually awaken easily if someone talks to us, or the alarm goes off. If we obstruct our airway and begin to snore, we typically rouse ourselves enough to take a deep breath and turn over. When we don’t easily rouse from sleep induced airway obstruction then we may have sleep apnea. Now, let’s look at how giving sedation to a patient like Janet Smith interferes with her ability to rouse.

Conscious Sedation

When Janet gets to the preop area, she’s nervous and tells her nurse that she didn’t sleep much the night before. Her anesthesia provider gives her 1 mg of midazolam IV to relax her. Her care team then takes her to the OR.

With light conscious sedation she will continue to respond to verbal commands. Cognitive function and coordination may be impaired. She can still carry on a conversation, although she may not remember details of it.  Cardiac and ventilatory function are usually not altered a lot. Like natural sleep, it’s common for the patient’s respiratory rate and tidal volume to decrease slightly. She’ll lie comfortably on the OR bed while we’re attaching her monitors and going through the final safety checks.

Moderate Sedation

Of course, many patients like to nap during their surgical procedure and in this case the anesthesiologist starts a background infusion of propofol at a low rate of 25 mcg/kg/hr to induce a moderate level of conscious sedation while things are being set up. Using this technique, the level of propofol in Janet’s bloodstream builds slowly and she will get progressively sleepier until she’s moderately sedated.

With moderate sedation, a patient still responds to commands, but she might require a tap on the shoulder to rouse and answer a question. She still shouldn’t require any help holding her airway open, but there may be more of a tendency to snore, especially if the patient has a history of snoring. Snoring is a sign of airway obstruction and is a warning sign that the patient needs to be monitored more closely.

Injecting local anesthetic can be a bit painful. As the surgeon gets ready to inject the local anesthetic the anesthesiologist will often give just a little more sedation so that the patient does not remember the injection. This could be more midazolam, or a short acting opioid like fentanyl. However, in this case Janet is given a small bolus of 50 mg of propofol IV. The strategy behind this technique is to temporarily induce a deeper level of sedation during the local anesthetic injection itself. Sedation from a Propofol bolus wears off in a few minutes, allowing Janet’s level of consciousness to return back to the prior moderate level of sedation for the rest of the procedure.

Deep Sedation

With deep sedation the patient is not easily arousable, but will still respond with repeated or painful stimulation. The deeply sedated patient might occasionally require help holding her airway open and spontaneous ventilation might become inadequate. Cardiovascular stability is usually maintained.

Janet tolerates the injection well and appears to be sleeping. However, after the injection is finished, the anesthesiologist notices that Janet is no longer breathing well. Her airway is obstructed. He tips her chin back and lifts her jaw to open her airway and she takes a deep breath. He has to periodically shake her shoulder for the next few minutes to remind her to take deep breaths. After about 2 minutes she starts breathing well again on her own.

Unconsciousness: General Anesthesia

What just happened? It can be easy to take a patient from deep sedation to general anesthesia. With general anesthesia the patient is completely unresponsive and airway support of some type is often required, even when the patient is breathing spontaneously. Cardiovascular changes are common. After the extra Propofol bolus was given, Janet continued to breathe well — as long as she was being stimulated by the pain of the injection. After that stimulus stopped, she slipped into an even deeper plane of sedation. The same scenario can happen postoperatively upon arrival in the recovery room when stimulation ceases (see prior discussion).

Perhaps Janet was just more sensitive to sedatives than some patients. Perhaps it was because she was sleep deprived from her insomnia the night before. Maybe it was the speed with which she got repeated doses of medications in such a short time that added up to too much sedation.

In our case, the anesthesiologist was watching carefully and noticed immediately that he needed to assist Janet’s breathing. Janet’s level of sedation could have eventually become light enough, or her CO2 levels high enough, to allow her to start breathing again on her own. The question is whether she would start breathing again quickly enough — before she became hypoxic or extremely hypercarbic. Prolonged hypoxia and hypercarbia can cause complications, including potential cardiac arrest. And hypoxia and hypercarbia both depress mental status, which, if severe enough can further depress respiration, making complications more likely.

Sedation Is A Continuum

All four stages of sedation are a continuum. At any point with just a little more sedation or a little less stimulation, your patient can stop breathing well. In my job as an anesthesiologist, I see on a daily basis how easy it is to overshoot and cause a patient to become apneic using moderate to deep sedation. And if the patient is frail or sick, or extremely old or young, sometimes even a small dose of sedative or opioid, — one that would normally induce just light sedation — can cause apnea and hypoxia. Sedation, and its effect on respiration, are not just dose related, they depend on the status of the patient receiving that dose and what else is happening to that patient at that time. Be vigilant.

Related Articles

May The Force Be With You

Christine Whitten MD, author

Anyone Can Intubate: A Step By Step Guide
and
Pediatric Airway Management: A Step By Step Guide

Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine WhittenButton link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

Click the cover to preview or purchase book at Amazon.com

References

  1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC459897/pdf/thorax00225-0033.pdf
  2. Gimeno F, Peset R. Changes in oxygen saturation and heart frequency during sleep in young normal subjects. Thorax 1984;39(9):673-675.
  3. Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea and oxygen desaturation in normal subjects. A strong male predominance. N Engl J Med. 1979 Mar 8;300(10):513–517. [PubMed]
  4. Douglas NJ, Calverley PM, Leggett RJ, Brash HM, Flenley DC, Brezinova V. Transient hypoxaemia during sleep in chronic bronchitis and emphysema. Lancet. 1979 Jan 6;1(8106):1–4. [PubMed]

Anatomic Dead Space Affects Hypoventilation

Understanding anatomic dead space is important to recognizing subtle hypoventilation. Hypoventilation from sedation, pain medications, anesthesia in the immediate postoperative period is common. The most obvious sign is slowing of the rate of breathing. A more subtle sign is that tidal volume becomes shallower. Having a tidal volume close to, or smaller than the patient’s dead space can lead to significant hypercarbia, hypoxia, and respiratory failure. This article discusses the concept of dead space and it’s clinical use in recognizing hypoventilation and preventing hypoxia and hypercarbia. Continue reading

Remember That Respiratory Failure Is Not Always Due to Lung Failure

There are many causes of respiratory failure. Some causes of respiratory failure result from disease or damage to the respiratory system. However disease or injury to other organ systems such as the central nervous system, the musculoskeletal system, or the presence of cardiac or septic shock can also cause respiratory dysfunction.

While final diagnosis will certainly affect treatment, assessing and managing the patient’s ability to breathe will not change with diagnosis.  However, once the airway is secure, you then have to diagnose and treat the real problem in order to resolve the respiratory failure.

The Case

In this case, I was an anesthesia resident doing my pediatric rotation at a children’s hospital. It was my turn to be on call for the weekend. At this particular hospital back in 1982, the anesthesia department managed the airway emergencies in the Emergency Department so when I got the page to go to the ED, I ran.

Inside the triage cubicle a 6 year-old girl was clearly unresponsive. She had been sick with fever, nausea, vomiting and diarrhea for several days according to her mother, who was crying in the corner. She hadn’t been able to hold down any food or fluids for over 24 hours. Her temperature was 102F. She was breathing rapidly but very shallowly. We did not as yet have pulse oximetry, but her color was dusky blue. Her blood pressure was 60/40 and her pulse was 150. She looked septic.

I placed an oral airway and assisted her breathing. She didn’t react at all to the oral airway — no gag reflex. We decided to intubate.

My colleagues quickly placed an IV and I decided to intubate without induction agent or muscle relaxant. If she didn’t need those agents then I didn’t want to potentially compromise her status by giving them. Had she reacted at all when I started to perform direct laryngoscopy I would have aborted and changed the plan.

She didn’t respond at all as I slid the endotracheal tube into the trachea.

We gave her two boluses of 20ml/kg of normal saline. Her color improved, her pulse came down to 110 and her blood pressure rose to 80/50, appropriate for her age. But she still hadn’t woken up.

Ten minutes later the first blood test results returned. Her blood glucose was 10, extremely low. We gave her 2 ml/kg of D25W. Within two minutes she woke up and started fighting the endotracheal tube. As her other vital signs looked much improved and she was now awake and protecting her airway, we elected to extubate her.

The child was admitted to the pediatric ward, was treated for gastroenterits and she did well.

Learnings: Hypovolemia and Hypoglycemia Can Cause Respiratory Failure

This was the first experience that I remember seeing in my career that demonstrated that hypovolemic shock and hypoglycemia can cause profound respiratory failure without lung pathology.  It’s important to remember that respiratory failure can result from a variety of other systemic problems, not just dysfunction of the respiratory system.

Table showing the difference multi-system causes of respiratory distress and respiratory failure

Respiratory distress or respiratory failure can come from many causes.

While assisting ventilation and protecting the airway are first priorities to stabilize a patient, treating the cause of the respiratory failure may require more than just ventilation and/or intubation. In fact, treating the cause can sometimes help you avoid the progression of respiratory distress to respiratory failure. If you don’t consider a potential problem or cause, you’re not going to be able to diagnosis it.

May The Force Be With You

Christine Whitten MD
Author of Anyone Can Intubate: a Step by Step Guide, 5th Edition
and
Pediatric Airway Management: a Step by Step Guide

Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine Whitten    Button link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

Please click on the covers to preview at amazon,com

 

 

Communication In A Crisis: A Case of Respiratory Depression In A Child:

When I’m teaching communication in a crisis to my Perioperative/OR nurses, I often recount the story of what happened during one particular child’s recovery years ago. This case, involving a 2 year old child who developed respiratory depression in the recovery room, demonstrates how good communication in a crisis, including the ability to challenge an authority figure, can improve patient safety and allow collaborative teamwork in a crisis management situation. Continue reading

Difference in Manual Ventilation: Self-Inflating Ventilation Bag vs. a Free Flow Inflating Bag

Manual ventilation with a bag-valve-mask device requires a good mask seal against the face in order to generate the pressure to inflate the lungs. But it also requires knowledge of how to effectively use the ventilation device to deliver a breath. This article will discuss the differences in ventilation technique for self-inflating vs free-flow ventilation bags. Understanding those differences is important for successful manual ventilation of your patient. Continue reading

Ventilation Perfusion Mismatch

Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. In other words it depends both on ventilation and perfusion. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered. When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation perfusion mismatch is said to exist.

The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.

Imbalance between perfusion and ventilation is called ventilation perfusion mismatch. This illustration compares shunt, the perfusion of poorly ventilated alveoli; and Physiologic dead space: the ventilation of poor perfused alveoli.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

This article will describe how dead space is different from shunt. It will help you understand how you can use these concepts to care for your patient. Continue reading

Apneic Oxygenation: Increase Your Patient’s Margin Of Safety During Intubation

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. As we saw in a previous blog post, preoxygenation is one of the most important safety measures we can use prior to induction of anesthesia and in preparation for intubation. Adequate preoxygenation can more than double the time to hypoxia during open airway apnea, allowing more time for intubation to occur. However, increasing the time to critical hypoxia from 1 minute to 2 or 3 minutes with preoxygeation, as important as that is, can still be too short if the intubation turns out to be truly challenging. Apneic oxygenation is an easy technique to increase the time to desaturation significantly. However you have to know how to optimally provide it in order to safeguard your patient  Continue reading

Preoxygenation Can More Than Double The Time To Hypoxia During Apnea

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. One of the most important safety measures we use in anesthesia is to preoxygenate our patients prior to induction of anesthesia and in preparation for intubation. This is especially true if we are planning a rapid sequence induction. Adequate preoxygenation can more than double the time to hypoxia during apnea, allowing more time for intubation to occur.

Preoxygenation increases the margin for safety. It treats any pre-existing hypoxemia in the critically ill patient. It also postpones the onset of hypoxia while the patient is apneic during the intubation attempt. This becomes especially important if the intubation attempt becomes difficult and prolonged.

Speed of onset of hypoxia with apnea depends on metabolic rate and on the actual amount of oxygen available in the patient’s functional residual capacity. To see how preoxygenation can effect this let’s review some physiology. Continue reading

Assisting Ventilation With Bag-Valve-Mask

As an anesthesiologist, I often run to emergencies where the patient is not breathing adequately and requires intubation. However, before any intubation, a patient in respiratory distress/failure needs ventilation. Providers who have passed ACLS are often able to ventilate an apneic patient well because they have practiced on the manikin. However, I often see that providers have more difficulty trying to assist ventilation of a patient who is still breathing spontaneously.

The typical inexperienced provider will try to provide large, slow breaths just as they were taught in ACLS. Unfortunately these breaths are often out of synch with the patient’s own breathing. Squeezing the bag while the patient is exhaling means that your inflation pressure must not only overcome the diaphragm, but also reverse the passive outflow of air, the elastic recoil of the lungs, and the rebound of the chest wall combined. The vocal cords may be closed. Ventilating out of synch with the patient won’t be as effective. The breath you deliver will take the path of least resistance to enter the stomach or escape from the mask. It often makes the patient cough.

Even worse,  providers will occasionally hesitate to try to assist a patient’s breathing while waiting for the intubation team because they feel they don’t know how. Delay in improving ventilation can place your patient at higher risk of complication. This is unfortunate because in many ways assisting ventilation is even easier than manually ventilating an apneic patient. Let’s see why. Continue reading

Don’t Withhold Oxygen From That CO2 Retainer

There is often a great deal of confusion about how to manage the care of a patient with COPD because of unwarranted, and incorrect, concern that all patients with COPD are CO2 retainers. This fear of causing CO2 retention sometimes causes providers to withhold or withdraw oxygen inappropriately. Understanding some of the respiratory physiology behind CO2 retention will allow you to make more informed decisions. Let’s start at the beginning. Some of this material comes from my book Anyone Can Intubate, 5th Edition. Continue reading

What’s The Difference Between Oxygen Saturation And PaO2?

I often teach classes for RNs who are orienting to our preoperative and recovery areas. Hypoxemia and hypoxia occur commonly among our perioperative patients so I spend a lot of time on recognizing early signs of respiratory distress such as tachycardia, tachypnea, cyanosis, agitation, and changes in mental status.

Pulse oximetry is one obvious monitoring tool to identify hypoxemia and hypoxia. I find that one frequent area of confusion relates to understanding the important distinction between arterial partial pressure of oxygen (PaO2) and oxygen saturation (O2 sat). I am not alone. Multiple studies have identified this as a knowledge gap. One study of pediatric nurses showed that while 84% of the clinicians felt they had received adequate training, only 40% correctly identified how a pulse oximeter worked, and only 15% had a correct understanding of the oxyhemoglobin dissociation curve. This is such a key concept that we all must take pains to ensure our staff understands how to use this valuable monitoring tool. Some of the material below is from my book Anyone Can Intubate. Continue reading

How Does Hypoventilation Cause Hypoxemia?

I often find that my students sometimes confuse oxygenation and ventilation as the same process. In reality they are really very different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. You must understand the difference to understand how hypoventilation causes hypoxia.

If you hyperventilate with room air, you will lower your arterial carbon dioxide content (PaCO2) significantly, but your oxygen levels won’t change much at all. On the other hand, if  you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Ventilation changes PaCO2. Oxygenation changes PaO2.

Why do we need to understand this? Let’s look at some common examples. Along the way we will painlessly use the Alveolar Gas Equation to explain two common scenarios:

  • how hypoventilation causes hypoxia,
  • why abruptly taking all supplemental oxygen away from a carbon dioxide retainer will hurt them.

Continue reading