The goal of this article is to educate healthcare professionals about issues related to sedating patients for procedural or physiological reasons.
After completing this continuing education course, the learner should be able to:
Combining academic knowledge and practical experience is a challenge that requires critical thinking and teamwork with other members of the healthcare team. A theoretical, policy-based approach may not be appropriate for the fluctuating nuances of patient needs. However, more flexible models focusing on skill and experience depend on the expertise of the practitioner.1 This is just one reason why healthcare professionals—usually nurses or physician assistants—sometimes struggle to perform conscious sedation adequately. The precise, prescribed amount of sedation for two seemingly similar patients could result in comfort and tranquility, pain and trauma, or hypotension and organ damage. Rather than prolonged education about genetic variability in P450 enzyme systems, healthcare professionals are better served by concentrating on effective assessment, intervention, and plan of care to achieve various treatment goals for sedated patients.
Patients who require respiratory assistance via an endotracheal tube or temporary devices such as laryngeal mask airways are considered intubated. These advanced airway devices stimulate gag and other potent reflexes and initially require positive pressure ventilation. Patients receiving positive pressure via a tracheostomy do not require the same level of sedation to achieve adequate ventilation. Patients who require pressure support from specialized masks may not achieve adequate ventilation if heavily sedated, especially without a nasal or oral pharyngeal airway to decrease obstruction.2
Without a firm grasp on normal physiologic parameters, the average nurse may struggle to swiftly and correctly assess problems in ventilation and perfusion. Because trauma patients requiring a chest tube often qualify for conscious sedation, nurses must remember that air between the visceral pleura and the outer parietal pleura—pneumothorax—can worsen if a patient requires positive pressure ventilation through a bag and mask or endotracheal tube.3 Perfusion risks are not absent from scheduled, routine procedures as exsanguination is a rare risk of many procedures, and sedation drugs may decrease blood pressure.
Patients will use muscles of the chest, neck and abdomen when struggling to force air in and out of the lungs, but quickly tire because breathing is far more effective as a mostly passive exchange based on volume and pressure. Intubation prevents respiratory acidosis and subsequent respiratory failure from inadequate carbon dioxide elimination—often a result of excessive sedation. Signs of airway obstruction may be subtle at first. Once intubated, sedation allows the lungs and thoracic muscles to rest and the patient to tolerate mechanical ventilation.3
During normal inspiration, the diaphragm and the external intercostal muscles contract slightly to enlarge the thoracic cavity, decreasing pressure so air will flow into the lungs until atmospheric pressure is reached. The chest and abdomen expand outward and the diaphragm downward. This provides negative pressure ventilation, as opposed to forcing a certain volume and pressure of air into the lungs artificially. At the end of inspiration, when the muscles are relaxed, the elastic lungs and thoracic wall recoil, decreasing in volume to send deoxygenated air out of the lungs. The pressure within the pleural cavity remains negative due to the tendency of alveolar fluid surface tension and elastic lung tissue to pull the lung inward. Also keeping the lungs inflated is the thoracic wall, which pulls away from the lung to enlarge the pleural cavity. Actual separation is prevented by the surface tension of the pleural fluid. All of these opposing forces create the difference between intrapleural and intrapulmonary pressures, which keeps each lung inflated unless lung or thoracic injury obliterates the pressure gradient.4 Because of this interplay, the chest will rise and fall despite medication-induced relaxation of pharyngeal muscles, causing obstruction, and decreased respiratory drive. The classic chin lift and jaw thrust taught in basic life support classes is often a simple remedy to this risk.
Both propofol and the benzodiazepine midazolam depress the central nervous system and cause sedation and amnesia via the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). This does not affect pain receptors, so a completely sedated patient may still require pain medication. Although effects are dose-dependent, propofol is preferred for anesthesia and has a quicker onset and recovery period. Midazolam does not decrease blood pressure, respiratory reflexes or brain activity as much as propofol. Because of this added safety, nurses can “push” midazolam during conscious sedation procedures, rather than just relying on an infusion. Individual variability requiring changes to the infusion rate of midazolam is more pronounced, as is also the case for opioids.5,6
Opioids increase the anesthetic effect of sedation drugs but do not provide amnesia. Their primary action is analgesia due to mu receptor binding in the central nervous system. Synergy is an important concept in pharmacology since multiple drugs acting on different receptors create an effect that is more than additive. Although the nurse may encounter sedation drugs combined with sufentanil or remifentanil infusions for the intubated and sedated patient, the most common opioid for conscious sedation is fentanyl.
|Medication||Route||Time to Effect||Duration||Routine Dosage Equivalent|
|10 mg IV|
10 mg IM
30-60 mg PO
|PO||10-15 min||4-6 hours|
10-20 mg PO
|PO||30-60 min||4-6 hours|
15-30 mg PO
50 micrograms IV
|PO||30-60 min||4-6 hours|
|IM||15 min||3-6 hours|
IV = intravenous
IM = intramuscular
PO = orally
Midazolam and fentanyl is an adequate combination, but propofol and remifentanil have a decreased possibility of awareness. Except for remifentanil, opioids accumulate in the body to cause respiratory depression, constipation and other side effects long after discontinuation. This can complicate subsequent dosing, as can tolerance to initial infusion rates because liver enzymes process opioids more quickly.6 Traditionally, intravenous and inhaled medications are the gold standard to initially bypass the liver, avoiding the variability dependent on the metabolizing ability of hepatic enzymes. Intranasal and buccal administration of fentanyl or dexmedetomidine are rising in popularity.8 Correct doses of oral NSAIDs block COX (often at the injury site) and play an important role in pain control. Antidepressants and the drugs gabapentin and pregabalin, typically reserved for nerve disorders, are also useful adjuncts. Multimodal and preemptive interventions decrease pain and the risk of respiratory depression, constipation, nausea, pruritus and other unfavorable side effects associated with opioids that usually require reversal agents to attenuate. By using lesser amounts of multiple drugs, the risk of complications from any particular approach or class of medications will hopefully decrease.9
Local anesthetics such as lidocaine prevent or relieve pain by binding to receptors on nerve sodium channels to stop nerve conduction. They pass through lipid-soluble nerve membranes but must retain a partially ionic form to be active in the sodium channel. They are manufactured as water-soluble salts but do not work well in acidic environments such as infected wounds. This influence from pH also means that adding sodium bicarbonate to a local anesthetic speeds onset while decreasing the pain of injection. Local anesthetists alter the function of all organs conducting or transmitting nerve impulses, so ACLS algorithms may be needed if an overdose occurs. Plasma concentration depends on dose, absorption, vascularization and other properties of the site injected, and metabolism by the body. Sensory disturbances such as tongue numbness and tinnitus typically precede life-threatening reactions. Large doses can be used with peripheral nerve blocks without the seizures, coma, and eventually respiratory and cardiac failure that could follow the same dose in the bloodstream or spinal cord.6
As opioid tolerance continues to increase in the patient population, options are available to provide simultaneous sedation and analgesia. Ketamine targets the N-methyl-D-aspartate (NMDA) receptor to create a dissociative state, while dexmedetomidine stimulates alpha-2 receptors to provide sedation and suppress the release of pain-stimulating neurotransmitters. As in critically ill patients, parameters such as respiratory rate are no longer valid indicators of pain control. Epidural and regional nerve blocks can play a role in providing analgesia for the sedated and intubated patient, and intravenous acetaminophen and the nonsteroidal anti-inflammatory ketorolac serve as useful adjuncts in select patients. The dysphoric effects of ketamine or the sedative and hypotensive side effects of alpha-2 agonists require adequate patient and healthcare professional education.8
|ANESTHETIC||ONSET (min)||DURATION OF ANESTHESIA (h)||DURATION OF ANALGESIA (h)|
|3% 2-Chloroprocaine (+HCO3)||10-15||1||2|
|3% 2-Chloroprocaine (HCO3 + epinephrine)||10-15||1.5-2||2-3|
|1.5% Mepivacaine (+HCO3)||10-20||2-3||3-5|
|1.5% Mepivacaine (+ HCO3 plus epinephrine)||10-20||2-5||3-8|
|2% Lidocaine (HCO3 + epinephrine)||10-20||2-5||3-8|
|0.5% Bupivacaine or levobupivacaine (+ epinephrine)||15-30||5-15||6-30|
Even if these drugs are rarely used outside surgery or emergency department in some hospitals, nurses in other specialties require a basic knowledge of their duration and effect. Just as the physiologic and pharmacologic effects of volatile anesthesia agents extend into the postoperative period, even short-acting drugs can accumulate and cause side effects much later. Potent induction drugs for intubation may wear off before sedation infusions reach therapeutic levels.
Nurses continually expand their roles as more and more patients require complex sedation and airway management. The number of critically ill patients seeking medical care has increased by a third over the last few decades, but research and education methods preparing nurses to sedate these patients safely are lacking.1 Self-directed learning fails to teach the required skills, and supervision and educational materials insufficiently train nurses how to care for these patients.1
Nurses need training in the clinical environment, as well as preceptorships with experienced practitioners caring for these patients. It takes time to develop confidence when managing sedated and intubated patients. With experience, nurses realize that clear communication with the physician or nurse anesthetist is integral to best practice. Parameters for vital signs and level of sedation differ considerably depending on the situation.1
Without defined goals and written orders for sedation, healthcare professionals must spend even more time carefully titrating infusions. This is especially difficult in emergency departments and other parts of the hospital that accept a wide variety of patients. Visual cues are an important theme for nurses caring for sedated patients, but those cues need to come from vital signs—and occasionally, brain monitoring for awareness.11
Unlike the other drugs mentioned thus far, ketamine is rarely administered as an infusion and makes brain monitoring less accurate. This is because volatile anesthetics and sedation drugs that increase GABA depress cortical activity in the brain, but ketamine increases theta brain wave activity. Observers trying to determine moderate sedation could not correlate their finding with brain monitoring.
The most common monitor to interpret electroencephalogram readings into numeric values related to alertness is the Bispectral Index (BIS) monitor. NeuroSENSE and other competitors use separate algorithms that do not correlate exactly to the values between 40 and 60 representing general anesthesia, especially during propofol infusions.12 The utility of these monitors in the emergency department and intensive care unit may be limited to patients needing constant paralysis, such as in severe respiratory conditions.
The Glasgow Coma Scale, the Richmond Agitation and Sedation Scale, and other instruments provide a fuller picture for nurses to evaluate the level of consciousness for critically ill patients, before, during, and after sedation. Scales provide an objective method to avoid giving too much or subtherapeutic doses of drugs. Both can cause unstable vital signs and iatrogenic harm to the patient. Communication difficulties challenge both nurses and patients, but more accurate sedation and analgesia and improved patient adherence are two additional benefits.2 Of course, assessing sedation and pain in this context is a practical, immediate measure to titrate sedation, not simply documentation to chart.
If sedation is temporarily halted to assess neurological status, some patients can motion with their fingers to indicate pain intensity on a numeric scale. Nurses favor numeric scales unless educated about more reliable alternatives for nonverbal patients.13 Charts that the patient can point to or write on, agreed signals for “yes” and “no” if the patient is unable to nod or speak, and other nonverbal signaling should complement observational pain scales whenever possible to procure the patient’s own report of pain.
Many pain instruments are specifically appropriate for the sedated patient. Most take into account oxygen saturation and other variables that are continuously monitored in patients. One example is the Non-Verbal Pain Scale (NVPS), derived and validated as a more specific, adult version of the Face, Legs, Activity, Cry, Consolability (FLACC) tool. Researchers compared the NVPS to the Behavioral Pain Scale (BPS), which nurse researchers specifically developed to provide nurses with the ability to differentiate noxious from non-noxious stimuli in sedated and mechanically ventilated patients. Observation of the face and upper limbs and respiratory factors such as compliance with the ventilator are the only parameters measured by the BPS. This simplicity is a distinct advantage because one of the purposes of comparing pain scales is to determine whether staff nurses can use the tools as effortlessly and reliably as trained nurse investigators.14
But can’t nurses determine pain needs by observing patient vital signs? Chronic pain rarely causes increased pulse rate and blood pressure like acute pain, and many patients requiring conscious sedation are in acute pain situations. The problem is that respiratory rate and other physiologic parameters in the acute care settings are influenced by disease process and the multiple medications required to keep these patients stable.
NVPS and BPS pain scores do not show objective data to indicate increased pain for the patient. With this in mind, it is essential for nurses to be aware of the preconceived notions about anesthesia and analgesia. Generally, pain scores are low for patients who receive continuous sedation or analgesia, but nurses rarely find a consensus value at which most patients require pharmacologic intervention.14
The amount of time nurses should spend communicating with sedated patients also lacks consensus. In one study, nurses spoke to patients for a maximum of 2 minutes per 3-minute encounter, and the worse the patient scored on sedation and consciousness scales, the less time they spent trying to ascertain their needs.15 Training of perception of communication is one method to improve care for sedated patients. Nurses test much better after receiving education about how communication is perceived. However, quality indicators such as the need for physical restraints and heavy sedation did not change after nurse education, and neither did pain score documentation or the prevalence of ICU-acquired pressure sores.16 Information about receptor sites with pharmacologic action or better ways to assess patients does not improve care by itself. As mentioned earlier, nurses need a combination of education and supervised clinical training to better care for these complex patients. Misplaced caution from lack of knowledge can lead to inadequate sedation. Conversely, misinterpreting movement as justification to administer more anesthesia or analgesia can lead to overdosing the patient.
When a patient is unstable, an induction agent such as etomidate or ketamine and a paralytic drug to facilitate intubation should be considered. Paralytics do not have amnestic or analgesic affects but effects the skeletal muscle receptors for the neurotransmitter acetylcholine. Cardiac and smooth muscle remain unaffected, but the diaphragm is a skeletal muscle, having paralytic effects. Succinylcholine or rocuronium are common paralytics, but they have differing onsets and duration. Like rocuronium, atracurium and cisatracurium can be titrated for long-term use but have the added benefit of reliable elimination independent of kidney and liver function. If the patient is unable to maintain an adequate oxygen saturation, the nurse may need to rely on ACLS skills and ventilate a patient with a bag and mask while waiting for intubation or reintubation.17
Jim is sedating a sick patient for a bronchoscopy. The pulmonologist is struggling, and the patient is coughing and moving quite a bit despite maximum doses of aerosolized lidocaine to numb the airway and an additional five milligrams of midazolam just pushed into the intravenous line. Oxygen delivery is from a simple face mask instead of a nasal cannula with end tidal carbon dioxide monitoring, and oxygen saturation has decreased to 93% for several moments now. The physician asks Jim to give 100 micrograms of fentanyl immediately, so he does. Within moments, the patient stops breathing, despite the stimulation and opened airway from an aggressive jaw thrust.
What indicators are present?
Depending on the exact nature of their pathology, ill patients may take shorter or longer times to exhibit the effects of medications. Familiarity with drug onset and synergistic effects is necessary. Frustration can cause short-sightedness, and the lack of carbon dioxide tracing makes it more difficult to make informed decisions during the fluctuations inherent with stimulating procedures. Also, fixating on 93% as a “safe” value, unlike 92%, could have been an issue. Not questioning the physician’s order and that fact that opioids like fentanyl are supposed to decrease stimulation and respiratory drive is another indication of trouble. Maximum oxygen and a patent airway are useless without ventilation.
Is there reasonable cause to treat this as an emergency? Yes.
What are your next steps?
Typically, immediately giving reversal agents for the midazolam and fentanyl (flumazenil and naloxone, respectively) while breathing for the patient with a bag-mask device is the next step. Current vital signs will deteriorate rapidly, so fixing the problem rather than looking at the monitor is the priority. The presence of backup assistance and the skill set of Jim and the pulmonologist matter, especially if the pulmonologist makes the “point of no return” decision to paralyze the patient for better control of the airway without the risk of laryngospasm. They first should call for backup. Since the problem will not be fixed without oxygen entering the lungs, the pulmonologist may decide to slide an endotracheal tube onto the bronchoscope and immediately intubate the patient.
When it comes to conscious sedation, healthcare professionals may find themselves erring on one side of the sedation continuum more than the other. To provide the best care for a sedated patient, the healthcare professional must understand why the patient is receiving the medications and what the goal is. Pathophysiology and proper understanding of the medication action on the body are crucial for maintaining the safety of the patient.
Is communicating with the patient during conscious sedation a priority, or is the patient on vasopressors and barely able to tolerate any sedation? Has the patient’s cervical spine been cleared, and is he or she at risk of serious injury if writhing about the bed? With education and critical thinking, healthcare professionals can rapidly answer these questions and provide continuity of care throughout a patient’s stay, rather than a shortsighted approach that views the patient’s progress one procedure at a time.