Sedation and Analgesia in the Cardiac Care Unit
Louis Brusco Jr.
Patients in a cardiac care unit (CCU) experience pain, anxiety, stress and, at times, delirium and altered mental status. Sedation and analgesia of these patients is not only a humane way to treat their discomfort but it also is an integral part of their therapy to allow them to tolerate the various other therapies, treatments, and instrumentation that they are subjected to in the critical care setting. It is also integral in reducing the metabolic response and oxygen demands of the critically ill cardiac patient.
Sedatives and analgesic medications carry with them hemodynamic, respiratory, neurologic, and other side effects, so that proper sedation is a balance between adequacy of sedation and minimizing these other effects. In addition, development of delirium in the cardiac care setting is a complication that dramatically affects the survival and quality of life of patients after they have recovered from their illness. Recently, the implication of the very choice of the agent in the development of delirium has led to a reevaluation of the impact of all sedative/analgesic regimens in the context of their propensity to cause or help delirium.
The desired level of sedation in the cardiac care setting can vary widely between the awake, alert, conversant, oriented, and comfortable patient, and the patient who is in a drug-induced coma and therapeutically paralyzed. The precise level of sedation and the agents used are determined by the indications for sedation, whether they are anxiety, insomnia, agitation, coordination with a mechanical ventilator, prevention of removal of tubes or lines, protection against myocardial ischemia, or the need for amnesia during paralysis. Agents are chosen depending on the relative amounts of the different components of analgesia, anxiolysis, amnesia, sleep, and muscle relaxation that are needed.
Although use of pharmacologic agents is the main way to achieve these goals, it cannot be stressed enough that other measures that reduce even the very need for sedation are tremendously beneficial to patients, their comfort, and the avoidance of confusion and delirium. Such measures include orientation, assurance, and communication from the nursing staff; proper environmental controls such as lighting, temperature, and noise control; assessment and management of sensations such as hunger, thirst, and need to void; providing a variety of stimuli, such as visitors and media; and maintenance of a diurnal variation, with, if possible, a window facing the outside.
EVALUATION OF LEVEL OF SEDATION
One goal of management of critically ill cardiac patients is maintaining an optimal level of pain control and sedation. Unfortunately, pain and anxiety are subjective and somewhat difficult to measure consistently from caregiver to caregiver. More than 50% of patients who were interviewed after their ICU stays rated their pain as moderate to severe, during rest as well as during procedures.1,2 and 3 Thus, the assessment of pain and anxiety must be discussed first before moving on to the pharmacology of the agents.
Although patients in a CCU are monitored with highly sophisticated equipment, technological methods of pain and anxiety such as those using electroenphalography (EEG), cerebral function analyzing monitors (CFAM), lower esophageal contractility, combinations of physiologic variables, or serum concentrations of medications, among others, have all proven to be no more reliable and a lot more complicated and expensive as compared to simple, clinically based scoring systems. Properly designed scoring systems can be used not only to assess and record pain and anxiety but also to allow the bedside nurse to titrate therapy more in a more tightly defined window on their own, meeting regulatory requirements without needing repeated orders from a practitioner who is licensed to prescribe the medications.
The most basic of clinical methods of pain assessment is simply asking the patient to rate their pain on a scale of 0 to 10, with zero being no pain at all and 10 being the worst pain one could imagine. Although simple and widely used, and despite those instructions being given, the very fact that not infrequently some patients will answer “11” shows that when pain is being experienced acutely, the overall severity of the pain seems much greater than some historical control. One step up from a simple number scale is the use of a Visual Analog scale (VAS)—which is simply a line that has the above scale marked off in measured intervals. This scale is highly reliable and valid from patient to patient and caregiver to caregiver.4 It can be further modified to have pictures of happy and unhappy patients or faces on the scale in varying degrees instead of numbers. Unfortunately, it is limited because it ignores qualitative aspects of pain, and many critically ill cardiac patients are not strong enough or awake enough to use such a system.
Measuring sedation and level of consciousness is similarly difficult and requires the assessment of a practitioner observing the patient. The most basic method is to perform a mental status and neurologic exam and report the results. This is not practical on a repeated basis and does not allow the easy determination of changes that would allow titration of medications from time to time. The Glasgow coma scale (GCS) is widely used for the assessment of level of consciousness, but it was designed and validated for patients with neurologic deficits and is not designed for assessment of sedation.
Sedation scales are subjective tools that, in general, measure the patient’s responsiveness to verbal, audio, and/or physical stimuli. The ideal scale would determine the degree of sedation and agitation, be applicable in a variety of patient situations, have a well-defined sedation goal, include behavioral descriptors, be easy to measure and score with minimal training, and be reproducible, reliable, and valid across caregivers. Proper use of such as scale can reduce the duration of mechanical ventilation and also the length of stay in both the CCU and the hospital.5 However, even though this has been known for more than 10 years, the clinical use of scoring systems still remains low.6 It is therefore imperative that every patient care area or unit that sedates critically ill patients chooses a sedation scale that best fits its patients, trains the caregivers in its use, and develops procedures to use that information in the sedation of the patients in the cardiac care area.
One of the most widespread of the currently used sedation scales is the Ramsay sedation scale (RSS), introduced in 1974 and modified slightly since then. The modified scale is shown in Table 29.1. Although it was primarily designed for use during research into sedative agents and was groundbreaking, it was less than ideal for clinical use. Since its debut, many others have been developed for different reasons. Some of the more commonly referenced or clinically used ones include the sedation-agitation scale (SAS—Table 29.2),7 the motor activity assessment scale,8 the Vancouver interactive and calmness scale (VICS),9 the Richmond agitation-sedation scale (RASS; Table 29.3),10 the adaptation to intensive care environment (ATICE) instrument,11 and the Minnesota sedation assessment tool (MSAT).12
A thorough review and comparison of the above scales is beyond the spectrum of this chapter.13 The decision to use one scale or the other is many times a local, multidisciplinary decision. What is important is that a scale is indeed used and that it is performed in a standard and consistent fashion.
ANALGESIC AND SEDATIVE AGENTS
Critically ill cardiac patients are often treated with continuous infusions of potent medications. Some, such as sedative-hypnotics, have sedation as a primary action; whereas others, such as opioids, have a sedative action that is a secondary effect to the primary analgesic effect. Patients require sedatives because of pain, anxiety, delirium, and the desire to keep them from remembering an uncomfortable time in their lives. Most often it is much easier to administer such medications through continuous infusion when patients are on mechanical ventilation. Use of such agents through continuous infusion, however, is associated with prolonged mechanical ventilation and a longer stay in the CCU, whereas daily interruption of sedative treatment has been shown to reduce the duration of mechanical ventilation and CCU duration.14 Thus it is no longer considered acceptable to sedate patients to a deep state but rather to move to a lighter plane of sedation. This is more difficult and requires the use of sedation scales as above, sedation protocols, and the selection of agents that are somewhat easier to titrate and have shorter durations of action than in use previously. It has also been shown that a shift towards more of an analgesicbased sedation instead of a sedative-hypnotic-based regimen is beneficial.15,16 We will therefore review the most commonly used agents in the CCU for sedation.
TABLE 29.1 Modified Ramsay Sedation Scale | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||
Some definitions are needed to help in the classification and description of the various agents. “Analgesic agents” have as their primary mode of action the reduction of patients’ pain. They usually will have the sedation of patients as a side effect, but the sedative effect and the analgesic effect may have different potencies and durations of action. Analgesics can be broadly divided into “opioids,” meaning morphine-like in action, and “nonopioids” that are medications such as nonsteroidal anti-inflammatory agents and acetaminophen.
“Sedative-hypnotics” are medications that have as their primary effect the reversible depression of the central nervous system, inducing sleep, allaying anxiety, and causing amnesia.
Other drugs used in sedation are drugs such as “psychotropic medications,” for example, haloperidol or risperidone that are antipsychotic medications that interfere with neurotransmitters in the brain, which affect the way the cerebral neurons interact with each other.
OPIOIDS
Opioids are the mainstay of analgesic therapy in the CCU patient. Opioid analgesics, such as morphine, act selectively on neurons that transmit and modulate nociception, leaving other sensory modalities and motor functions intact. Opioid receptors are found in the brain, spinal cord, and peripheral tissues. When bound to receptors, opioids produce analgesia, drowsiness, changes in mood, and mental clouding. An important feature of opioid analgesia is that it is not associated with loss of consciousness except at extremely high doses. When given to a patient who is not in pain, the effect will often be described as unpleasant and troubling.
All opioids depress respiratory drive in a dose-dependent manner, and this depression is increased when opioids are given in conjunction with sedative-hypnotic medications. In general, opioids have minimal hemodynamic effects when given to patients who are not volume depleted but can cause hypotension in patients who are volume depleted owing to venodilatation. The primary problems with long-term administration of opioids are tachyphylaxis, dependence, and withdrawal symptoms on discontinuation of long-term continuous infusion. A dosing summary is presented in Table 29.4.
TABLE 29.2 Sedation-Agitation Scale (SAS) | |||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||||||||||||
TABLE 29.3 Richmond Agitation-Sedation Scale | ||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||||
Morphine.
Morphine is the prototypical opioid. It was discovered in 1804 and is the most abundant alkaloid found in opium. It has been sold commercially for almost 200 years and remains a mainstay in the sedation of critically ill cardiac patients, despite the fact that other opioids lack some of the problems associated with morphine, This is primarily because of cost and familiarity factors. The dose required to produce analgesia, as in most opioids, varies and is dependent on factors such as tolerance, tachyphylaxis, and metabolic and excretory ability. Although morphine is metabolized in the liver, 6% to 20% of the
metabolites are morphine-6-glucoronide, a metabolite that is excreted by the kidneys17,18 and although the data are variable, this metabolite is anywhere from half as potent to 20 to 40 times more potent than morphine itself18,19 and can accumulate in case of renal failure. For this reason, the long-acting opioid, hydromorphone, is preferred in renal failure. When given through bolus injection, morphine causes histamine release but this is not a factor when administered through infusion in CCU patients. However, when given by bolus, it was one of the classical treatments for cardiogenic pulmonary edema, as the vasodilation and preload reduction it causes, along with the analgesia, made patients in cardiogenic pulmonary edema much more comfortable.
metabolites are morphine-6-glucoronide, a metabolite that is excreted by the kidneys17,18 and although the data are variable, this metabolite is anywhere from half as potent to 20 to 40 times more potent than morphine itself18,19 and can accumulate in case of renal failure. For this reason, the long-acting opioid, hydromorphone, is preferred in renal failure. When given through bolus injection, morphine causes histamine release but this is not a factor when administered through infusion in CCU patients. However, when given by bolus, it was one of the classical treatments for cardiogenic pulmonary edema, as the vasodilation and preload reduction it causes, along with the analgesia, made patients in cardiogenic pulmonary edema much more comfortable.
TABLE 29.4 Analgesics Used in the CCU | ||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
It is the most hydrophilic opioid and therefore has the longest onset of action. A bolus dose of morphine will act in 5 to 10 minutes and last 2 to 3 hours; after continuous infusion, it does not exhibit prolongations in half-life (known as “context sensitive half-life”) as seen with fentanyl and, to a lesser extent, with sufentanil and alfentanil.20
Usual doses to start morphine through infusion are 0.5 to 2 mg per hour. Bolus doses of morphine can be given at 2 to 4 mg every 1 to 2 hours as a start, but doses can be increased as tolerance develops. It is not unusual to see patients requiring morphine infusions of 15 mg per hour or more.
Hydromorphone.
Hydromorphone, the commonest name for the drug actually called either dihydromorphone or dimorphone, is a semi-synthetic derivative of morphine. It was synthesized and researched in the 1920s. It is slightly more lipophilic than morphine and exhibits superior fat solubility and speed of onset than morphine.21 It is thought to be three to four times stronger than morphine but with a lower risk of chronic dependency. It lacks the renally excreted active metabolites of morphine. It also has a slightly longer duration of action than morphine— approximately 3 to 4 hours. Its duration of action makes it slightly more cumbersome to adjust through continuous infusion; however, because it does not exhibit the context-sensitive half-life prolongation of fentanyl it is sometimes preferable to fentanyl via infusion for long durations of sedation.
Most clinicians will start with hydromorphone at 0.1 to 0.2 mg per hour and titrate as needed. Bolus doses of 0.5 mg given every 2 to 4 hours can be a starting point for intermittent IV dosing.
Fentanyl.
Fentanyl is a fully synthetic opioid that was first developed in 1960 and has served as the parent molecule to the synthetic opioids that have been developed since then— sufentanil, alfentanil, and remifentanil. It is far more potent than morphine—approximately 40 times more potent on a milligram per milligram basis. Similar to other opioids, it works by binding to opioid receptors in the brain, spinal cord and periphery, but its highly lipophilic chemistry causes it to cross the blood-brain barrier very easily, giving it an extremely short onset of action. It does not cause histamine release, and, like other opioids, is neither an arterial vasodilator nor a negative inotrope.22 It can, however, cause venodilatation and hypotension in a patient who is volume depleted. It is a potent blocker of endogenous catecholamines, which can be beneficial (in preventing a patient from becoming hypertensive and/or tachycardic with procedures) and detrimental (causing hypotension in patients whose hemodynamics are dependent on an elevated level of endogenous catecholamines).
Fentanyl is primarily metabolized in the liver to inactive metabolites, but its cessation of action is primarily through redistribution from the brain to the peripheral tissues rather than metabolism of active drug. Therefore, although a single or a few bolus doses have a shorter duration of action than morphine, on the order of 60 to 90 minutes, when given by infusion, even after 2 hours, the time to decrease by 50% concentration goes from 30 minutes for a bolus dose to 120 minutes with the infusion, and the time to decrease by 80% goes from 60 minutes with a bolus to more than 600 minutes with the infusion.20 This “context-sensitive half-life” is due to slow release from the fatty compartments that fentanyl has such an affinity for, and causes a greatly prolonged effect for fentanyl when given by infusion—to an effective half-life much longer than morphine after a few hours of infusion.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
