A 66-year-old man with a history of coronary artery disease, chronic renal insufficiency, alcoholic cirrhosis, hypertension, and anxiety is brought to the emergency department after a motor vehicle crash. He has traumatic brain injury (TBI) and rib fractures. After tracheal intubation, he is transferred to the intensive care unit (ICU) for further management. The patient appears agitated and uncomfortable. He is tachycardiac, with a heart rate of 120 bpm; hypertensive with a blood pressure of 188/72 mm Hg; and tachypneic, breathing 38 breaths/min. His home medications include aspirin and clopidogrel.
What is the difference between sedation and analgesia?
It is useful to consider sedation as having three components: anxiolysis (which is indicated for every ICU patient), hypnosis (ie, the induction of sleep, which may be indicated in sicker patients), and amnesia (loss or lack of recall). Sedation is distinct from analgesia, the relief of pain, and sedative agents such as propofol and the benzodiazepines (lorazepam and midazolam) have no analgesic effects. Sedating a patient for agitation induced by pain may further disinhibit their control functions and lead to a paradoxical increase in agitation (see below). Also, although amnesia is essential during general anesthesia in the operating room, the potent anterograde amnesia induced by benzodiazepines—even at subhypnotic doses—results in confusion and disorientation on awakening and may predispose toward ICU delirium. In contrast, propofol provides amnesia only during sleep, so emergence is smoother.
What is the first step in managing this patient’s sedation and analgesia?
The neurointensivist should adopt an “analgesia first” or “A-1” approach to relieve the patient’s pain before administration of sedation.1 This will avoid disinhibiting a patient whose agitation is due to pain, as discussed above. There is evidence that an A-1 approach decreases sedation requirements and time on the ventilator.2–7 ICU patients experience pain and discomfort with procedures such as tracheal intubation, endotracheal tube suctioning, repositioning, and immobility. Failure to treat pain exacerbates endogenous catecholamine activity, which predisposes to myocardial ischemia, hypercoagulability, hypermetabolic states, sleep deprivation, and delirium.8,9
Opioids are the mainstay of pain management in the ICU. Synthetic analgesics such as fentanyl and remifentanil are commonly used and are administered as a bolus or as an infusion to manage pain and facilitate synchronous mechanical ventilation. Fentanyl, a short-acting opioid, has an intravenous onset time of < 1 minute and duration of action of ½ to 1 hour. Duration of analgesia increases with prolonged infusions or repeated dosing. Fentanyl does not have an active metabolite, and its pharmacokinetics is not altered by renal failure. However, uremia potentiates its pharmacodynamic effect, and sensitivity to sedation and respiratory depression is increased. Fentanyl has a high hepatic extraction ratio, and its metabolism is slowed in patients with liver disease (eg, cirrhosis) or hepatic dysfunction (eg, congestive heart failure, shock).10
Remifentanil is an ultrashort-acting opioid and as such may be preferred for patients who require frequent neurologic evaluations. It is metabolized directly in the blood by plasma esterases and has an elimination half-life of 8 to 9 minutes. Described as a “forgiving opioid,” remifentanil is characterized by a rapid onset and offset of action that is independent of liver or renal function.11,12 Infusion of remifentanil has an onset of action of 1 minute11 and rapidly achieves steady-state plasma levels. Its analgesic and sedative effects dissipate within 3 to ...