evidence & practice / critical care

SEDATION

Use of dexmedetomidine infusion

as a sedative drug for patients in the
intensive care unit
Selvaraj N (2017) Use of dexmedetomidine infusion as a sedative drug for patients in the intensive care unit. Nursing Standard.
31, 44, 42-50. Date of submission: 5 November 2015; date of acceptance: 19 August 2016. doi: 10.7748/ns.2017.e10338

Nelson Selvaraj Abstract

Lecturer, adult nursing,
Cardiff University, Cardiff,
Wales
Correspondence
selvarajn1@cardiff.ac.uk
Conflict of interest
None declared
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The administration of sedatives may present several challenges for critical care nurses.
Evidence-based practice requires critical care nurses to remain up to date with developments in
sedation management and ensure safe and effective use of sedative agents in their practice.
Dexmedetomidine is a sedative drug that has been increasingly used in the intensive care
setting in recent years. This article provides an overview of the pharmacological properties
of dexmedetomidine and discusses nurses’ responsibilities in caring for patients receiving
dexmedetomidine infusion.
Keywords
analgesia, analgesic, critical care, dexmedetomidine, intensive care, medicines
management, patient safety, sedation
THE ADMINISTRATION OF effects (Pandharipande et al 2007).
sedatives and analgesics is integral to While there is no single sedative drug or
managing patients who are critically ill combination of agents that have been
(Shehabi et al 2013). Adequate sedation is shown to have these qualities (Schweickert
vital to enhance patient comfort, increase and Kress 2008), there are effective
tolerance of mechanical ventilation, and alternatives to traditional sedative drugs.
reduce the stress response to critical One of these is dexmedetomidine, the use
illness and its associated complications of which has been studied extensively in
(Kollef et al 1998, Sessler and Varney recent years and found to be associated
2008). Conversely, excessive and with reduced incidence of sedation-related
continuous infusion of sedation may be adverse effects (Riker et al 2009).
associated with a risk of accumulation This article provides an overview
and might have serious adverse effects for of the pharmacological properties of
patients, such as cognitive impairment, dexmedetomidine and its sedation
prolonged duration of mechanical efficacy in adult patients in ICU who are
ventilation, increased intensive care unit mechanically ventilated. It also explores
(ICU) and hospital stays (Rowe and nursing implications in relation to the care
Fletcher 2008), post-traumatic stress of patients receiving dexmedetomidine
disorder (Kress et al 2003) and increased infusion in the ICU. It is beyond the scope
mortality (Girard et al 2008). of this article to explore the efficacy of
Therefore, it could be suggested that an dexmedetomidine in relation to other
‘ideal’ sedative drug would have a rapid clinical outcomes such as cost, duration
onset and offset of action, be effective of mechanical ventilation, length of ICU
at providing adequate analgesic-based stay, incidence of delirium and mortality.
sedation, avoid drug accumulation and It is also important to note that dosing
have minimal sedation-related adverse recommendations are based on the

42 / 28 June 2017 / volume 31 number 44 nursingstandard.com

available literature, and there may be
differences in local policies and procedures.
Sedation management practices
Practice in relation to sedation
management in ICUs has changed
considerably over time, especially with
the arrival of new sedative agents and
emerging best practice guidelines (Barr et al
2013, Whitehouse et al 2014). The main
recommendations of the guidelines include
regularly establishing and reviewing the
goal of sedation, and use of a validated
sedation assessment tool, protocols that
provide daily sedation interruption,
and administering an appropriate
sedative agent that provides analgesic-
based sedation. Such approaches have
been shown to reduce the duration of
mechanical ventilation and sedation-
related complications and improve
patient outcomes in relation to mortality
(Girard et al 2008). In addition, substantial
evidence has accumulated that suggests
the choice of sedative agent can have a
significant effect on patient outcomes
such as mortality, duration of mechanical
ventilation, duration of ICU and hospital
stays, and post-traumatic stress disorder
(Skrupky et al 2015).
Sedation management involves a
multidisciplinary approach. Critical
care nurses are becoming increasingly
responsible for initiating and titrating
sedation medications and monitoring
their effects on patients, while
maintaining the sedation at a target
level (Ramoo et al 2016). However,
effective sedation management depends
on factors such as the knowledge,
skills, experience and confidence of the
practitioner who is undertaking the
procedure (Tanios et al 2009). Therefore,
it is important for nurses to understand
clinically-relevant information, such as
dosing, actions and side effects of major
sedative agents, and deliver effective and
evidence-based sedation management in
their clinical practice.
Classification of sedatives
The two major classes of sedative drugs
used to provide sedation in the intensive
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care setting are sedative-hypnotic agents KEY POINT
and opioid analgesics (Table 1) (Trikha Substantial evidence
and Rewari 2008). Most of these drugs are has accumulated that
administered by continuous intravenous suggests the choice of
(IV) infusions, because absorption from sedative agent can have a
the gastrointestinal tract or following significant effect on patient
subcutaneous or intramuscular injection is outcomes such as mortality,
less reliable in patients who are critically duration of mechanical
ill (Trikha and Rewari 2008). It is ventilation, duration of
important to remember that adequate pain ICU and hospital stays,
management must always take precedence and post-traumatic stress
over sedation (Whitehouse et al 2014) disorder (Skrupky et al 2015)
because this can reduce the requirement
for sedation and improve patient outcomes
(Riker and Fraser 2009).
Sedative-hypnotic agents
Benzodiazepines
Benzodiazepines produce sedation,
anxiolysis and amnesia (Gommers and
Bakker 2008), but provide no pain relief.
Depending on the elimination half-life, they
are classified as: short-acting (1-12 hours);
intermediate-acting (12-40 hours); and
long acting (40-250 hours) (Griffin et al
2013). Since benzodiazepines are primarily
metabolised in the liver and excreted
by the kidneys, the metabolites may
accumulate in patients who are critically ill,
especially during renal and hepatic failure
(Whitehouse et al 2014). This can lead
to an increase in the duration of action,
with subsequent difficulty in waking the
patient. Common benzodiazepines used
for sedation in critical care settings include
midazolam, lorazepam and diazepam.
Midazolam is a short-acting
benzodiazepine that can be administered
for sedation in ICU either as an IV
infusion (30-200mcg/kg/hour) or a bolus
dose (30-300 mcg/kg) (British National
Formulary (BNF) 2017). Compared with
other benzodiazepines, it has a rapid onset
of action of 5-10 minutes and the highest
clearance rate of 1-4 hours, rendering it
most suitable as an infusion (Trikha and
Rewari 2008). Despite its high clearance
rate, it produces dose-dependent respiratory
depression (Gommers and Bakker 2008)
and may be associated with the risk of
accumulation, especially with prolonged
periods of infusion (Hogarth and Hall
2004). Larger doses or more prolonged use
volume 31 number 44 / 28 June 2017 / 43
evidence & practice / critical care
of midazolam have also been reported to be
associated with an increased risk of delirium
(Riker and Fraser 2009).
Lorazepam is an intermediate-acting
benzodiazepine with a relatively slow
onset of action of 5-20 minutes (Reade
and Finfer 2014), and has a long
elimination half-life of 10-30 hours
(Whitehouse et al 2014). High-dose or
prolonged use of lorazepam increases the
risk of lactic acidosis and renal tubular
necrosis (Wilson et al 2005). In addition,
similar to midazolam, its prolonged use
has been found to be an independent risk
factor for patients in ICU to ‘transition
into delirium’ (Pandharipande et al
2006). These characteristics mean that it
is more suitable for bolus administration
than infusion (Trikha and Rewari
2008). For sedation, 1-2mg IV bolus
TABLE 1. Common sedative drugs used in the intensive care unit
Drug and mechanism of action Dosing (intravenous)
Sedative-hypnotic agents Midazolam
Benzodiazepines: facilitate sedation (short-acting benzodiazepine)
by binding to gamma aminobutyric Bolus: 30-300mcg/kg
acid (GABA) receptors Continuous infusion: 30-200mcg/kg/
hour
Lorazepam
(intermediate-acting benzodiazepine)
Bolus: 1-2mg
Diazepam
(long-acting benzodiazepine)
Bolus: 10-20mg over 2-4 minutes
immediately before the procedure
Propofol: facilitates sedation by Bolus: 10-20mg
binding to GABA receptors Continuous infusion: 0.3-4mg/kg/hour
Opioid analgesics Morphine
Provide analgesia via mu receptors Loading bolus: 2-5mg
(brain, spinal cord and peripheral Continuous infusion: 1-5mg/hour
tissues)
Fentanyl
Loading bolus: 50-100mcg
Continuous infusion: 20-100mcg/hour
Remifentanil
Bolus: not recommended
Continuous infusion: 0.05-2mcg/kg/min
( Rowe and Fletcher 2008, Trikha and Rewari 2008, Hughes et al 2012, Reade and Finfer 2014, Whitehouse et al 2014, British National Formulary 2017)
44 / 28 June 2017 / volume 31 number 44
of lorazepam will provide moderate
sedation for 4-8 hours (Whitehouse et al
2014).
Diazepam is a long-acting
benzodiazepine with an elimination
half-life of 30-60 hours (Whitehouse et al
2014). Its half-life is significantly increased
by the use of an infusion. In addition, it
can cause extreme pain and irritation at
the injection site (Griffin et al 2013). As
a result of these characteristics, it is used
less often as a sedative for patients in ICU.
However, it may be used occasionally
as an IV bolus to treat acute anxiety or
agitation (Trikha and Rewari 2008).
For sedation during minor surgical and
medical procedures, 10-20mg can be
given intravenously over 2-4 minutes,
immediately before the procedure (BNF
2017).
Onset and duration Common side effects
Onset: 5-10 minutes Respiratory depression, hypotension and
Duration: 1-4 hours delirium.
All benzodiazepines accumulate in patients
with renal and/or hepatic failure.
Onset: 5-20 minutes Respiratory depression, lactic acidosis, renal
Duration: 4-8 hours tubular necrosis, hypotension and pain at the
injection site.
Onset: 1-5 minutes Respiratory depression, hypotension,
Duration: several headache, nausea, constipation, blurred vision,
hours pain at the injection site.
Onset: 1-2 minutes Respiratory depression, hypotension,
Duration: 2-8 minutes bradycardia, hypertriglyceridaemia,
pancreatitis, propofol-infusion syndrome.
Onset: 5-10 minutes Respiratory depression, bronchospasm,
Duration: up to 6 hypotension, nausea, vomiting, pruritis,
hours constipation, urinary retention, hallucination.
Accumulates in renal failure.
Onset: 5-15 minutes Respiratory depression, hypotension, chest
Duration: 30-60 wall rigidity.
minutes Does not accumulate in renal failure.
Onset: 1-3 minutes Hypotension, bradycardia, chest wall rigidity.
Duration: <10 minutes No accumulation in renal and hepatic failure.
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Propofol
Propofol is a widely used IV anaesthetic
agent that has sedative, hypnotic and
anxiolytic properties but no analgesic activity
(Whitehouse et al 2014). It has a rapid onset
of action of 1-2 minutes and a short duration
of action of 2-8 minutes, making it ideal for
short-term sedation (Hughes et al 2012). It
can be given by continuous IV infusion for
the sedation of patients who are ventilated
(usually 0.3-4mg/kg/hour) (BNF 2017), or a
bolus dose of 10-20mg can be used to rapidly
increase the depth of sedation in patients
where hypotension is unlikely to occur
(Whitehouse et al 2014).
Unlike benzodiazepines, hepatic and
renal failure has little effect on the
clearance of propofol (Gommers and
Bakker 2008). The most common side
effects of propofol include hypotension,
bradycardia, respiratory depression and
hypertriglyceridaemia (Hughes et al 2012).
Propofol infusion syndrome is a serious
adverse effect of long-term, high-dose
propofol infusion, and is characterised by
metabolic acidosis, rhabdomyolysis and
hyperkalaemia (Whitehouse et al 2014).
Rhabdomyolysis is a potentially life-
threatening condition that results from the
breakdown of skeletal muscles, with the
leakage of myoglobin into the circulation
(Hohenegger 2012).
Opioid analgesics
Opioids produce various effects, including
analgesia, sedation, respiratory depression,
constipation, urinary retention, nausea
and confusion (Whitehouse et al 2014).
Dose-dependent respiratory depression
is a common side effect of opioids and is
increased when opioids are concomitantly
administered with benzodiazepines
(Gommers and Bakker 2008). Opioids such
as morphine, fentanyl and remifentanil are
commonly used for pain control in ICUs
(Whitehouse et al 2014).
Morphine is a potent analgesic with
sedative and anxiolytic properties. It can be
administered as a loading bolus dose (2-5mg)
or as an IV infusion (1-5mg/hour) (Reade
and Finfer 2014). High-dose morphine
is linked to histamine release, which may
lead to itching, bronchospasm, peripheral
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vasodilation and significant hypotension KEY POINT
(Gommers and Bakker 2008). Nausea and Opioids produce various
vomiting are the most common side effects effects, including analgesia,
observed with morphine administration. sedation, respiratory
Morphine has an onset of action of about depression, constipation,
5-10 minutes and its effect may last up to urinary retention, nausea
six hours (Trikha and Rewari 2008). It and confusion (Whitehouse
is metabolised by the liver and its active et al 2014). Dose-dependent
metabolites accumulate during renal respiratory depression is
failure; hence, it is not a preferred choice a common side effect of
of agent for patients with renal impairment opioids and is increased
(Whitehouse et al 2014). when opioids are
Fentanyl is approximately 100 times more concomitantly administered
potent than morphine (Whitehouse et al with benzodiazepines
2014). Compared to morphine, it has a rapid (Gommers and Bakker
onset of action and short duration of action 2008)
of 30-60 minutes (Trikha and Rewari 2008).
However, compared to morphine, it causes
less histamine release and its metabolites do
not undergo renal elimination; hence, it is a
preferred choice of agent for patients with
renal failure and cardiovascular instability
(Hughes et al 2012). It can be given as a
loading bolus dose (50-100mcg) or as a
continuous IV infusion (20-100mcg/hour)
(Reade and Finfer 2014).
Remifentanil provides analgesic-based
sedation and has a rapid onset of action
of 1-3 minutes (Trikha and Rewari 2008).
It is primarily given as an IV infusion
(0.05-2mcg/kg/min) (Hughes et al 2012)
and, unlike other opioids, is metabolised
by non-specific enzymes in the blood.
Therefore, it does not accumulate during
hepatic and renal impairment (Hughes et al
2012). As a result, it has an elimination
half-life of less than ten minutes, regardless
of the duration of infusion (Rowe and
Fletcher 2008). The rapid offset of
analgesia means that an alternative
analgesic should be administered before
withdrawal of the infusion if pain is likely.
Hypotension and bradycardia are the
most common side effects of remifentanil
infusion (Hughes et al 2012) and therefore
a bolus dose can have serious adverse
effects on the patient’s cardiovascular
stability.
Dexmedetomidine
Mechanism of action
Dexmedetomidine is a sedative drug that
has been increasingly used in ICU in recent
volume 31 number 44 / 28 June 2017 / 45
evidence & practice / critical care
years (Table 2). The US Food and Drug
Administration first approved its use in
1999 for short-term sedation of less than
24 hours in adult patients in ICU who are
mechanically ventilated (Wunsch and Kress
2009). Unlike midazolam and propofol, it
produces sedation and analgesia only by
reducing the sympathetic nervous system
activity and the level of arousal (Gertler et al
2001, Szumita et al 2007). This mechanism
of action produces a normal ‘sleep-like’
cooperative sedation, without suppressing
the respiratory drive. Such characteristics,
together with a concomitant analgesic
property, mean that dexmedetomidine may
facilitate quick weaning from mechanical
ventilation and reduce sedation-related
complications for patients (Kress et al 2003).
TABLE 2. Dexmedetomidine pharmacology profile
Name Dexmedetomidine hydrochloride
Group Selective alpha2-adrenergic agonist
Indications »» Sedation of less than 24 hours for patients in the intensive care
unit (ICU) who are mechanically ventilated
»» Sedation of non-intubated patients before and/or during surgical
and other procedures
Dosage for sedation »» Loading infusion: 1mcg/kg over a period of 10 minutes
in the ICU »» Maintenance infusion: 0.2-0.7mcg/kg/hour, which is adjusted to
achieve the desired sedation outcome
Dose adjustment Consider dose reduction in: patients over 65 years old, hepatic
impairment and concomitant administration with other sedatives and
hypnotics
Compatibility »» Compatible: 0.9% sodium chloride, 5% dextrose, Hartmann’s
solution, 20% mannitol, magnesium sulphate, 0.3% potassium
chloride solution
»» Incompatible: amphotericin B and diazepam
»» Not to co-administer with blood and plasma products as
compatibility has not been established
Side effects Bradycardia, hypotension, dry mouth, nausea, vomiting, hypertension,
atrial fibrillation, agitation, tachycardia, pyrexia, chills, anaemia,
hyperglycaemia, hypoxia, hypocalcaemia, pulmonary oedema,
acidosis, oliguria
Precautions Precaution with loading dose in: patients over 65 years old, patients
with diabetes, hypovolaemia, hypotension, atrioventricular block,
chronic cardiac problems and severe ventricular dysfunction
Clinical Continuous heart rate, blood pressure and oxygen level monitoring is
considerations vital during the bolus dose and throughout the infusion period
(Adapted from Hospira 2013)
46 / 28 June 2017 / volume 31 number 44
Dexmedetomidine has a short
distribution half-life of about six
minutes and an elimination half-life of
approximately two hours (Afonso and Reis
2012). The drug is extensively metabolised
in the liver, with its metabolites being
excreted by the kidneys (Afonso and Reis
2012). However, its clearance is reduced in
patients with low cardiac output status and
hepatic insufficiency (Wunsch and Kress
2009), potentially increasing its duration of
action in those who are critically ill.
Dosing and administration
For sedation of patients in ICU, the
recommended dosing for dexmedetomidine
consists of a loading infusion of 1mcg/kg
over a period of ten minutes, followed by a
continuous infusion of 0.2-0.7mcg/kg/hour
(Hospira 2013). It is prescribed in mcg/
kg/hour not in mcg/kg/minute; therefore
confusing the prescription can result in
a 60-fold overdose (Lam and Alexander
2008). Dose reduction is recommended
for patients over 65 years old and for
those with hepatic impairment (Hospira
2013). Patients may experience transient
hypertension with a loading infusion (Lam
and Alexander 2008). Although its use
beyond 24 hours has been evaluated in
many randomised controlled trials (RCTs)
(Venn et al 2003, Pandharipande et al
2007, Riker et al 2009, Ruokonen et al
2009, Jakob et al 2012), the safety of
prolonged dexmedetomidine infusion
in ICU has yet to be fully established
(Adams et al 2013).
Adverse effects
Dexmedetomidine produces sedation by
decreasing the sympathetic nervous system
activity and could therefore influence
haemodynamic stability in patients
(Pasin et al 2013). Many studies, including
Jakob et al’s (2012) large, multicentre RCT,
demonstrated that the most common side
effects associated with dexmedetomidine
are bradycardia and hypotension
(Riker et al 2009, Ruokonen et al 2009,
Jakob et al 2012). The bradycardic effect
is dose-dependent and is most common
when a loading dose is administered
(Hospira 2013). Afonso and Reis (2012)
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suggested that dexmedetomidine might
cause or worsen first-degree or second-
degree atrioventricular block or lead to
cardiac arrest. These effects are more
pronounced among patients who are
already hypotensive and hypovolaemic
(Pasin et al 2013).
As a result of the unpredictable
haemodynamic effects, many clinicians in
ICU avoid administering the recommended
loading dose of dexmedetomidine (Lam
and Alexander 2008). However, this may
prolong the onset of action and time to
achieve a steady plasma concentration
(Hospira 2013). It has been suggested that
the bradycardic effect of dexmedetomidine
could be beneficial for certain patient
groups, such as high-risk post-operative
cardiac surgical patients, since it may
reduce early post-operative ischaemic
events (Lin et al 2012). However, further
studies are required to confirm this
potential beneficial effect.
Sedation efficacy
Since its approval, the sedation efficacy
of dexmedetomidine has been studied
extensively in the ICU population
(Anger 2013). Many RCTs have been
undertaken to assess the sedation
efficacy of dexmedetomidine, either
with placebo or traditional sedative
drugs such as midazolam or propofol
(Pandharipande et al 2007, Reade et al
2009, Riker et al 2009, Ruokonen et al
2009, Jakob et al 2012). These studies
have not only confirmed the sedation
efficacy of dexmedetomidine, but also
revealed its ability to provide conscious
sedation (in which patients remain awake
but are calm and able to communicate)
and other unique characteristics, such
as its analgesic-sparing property, thus
reducing the requirement for additional
analgesics. In theory, this could enable
much faster weaning of patients
from mechanical ventilation, thereby
reducing the complications associated
with the prolonged use of mechanical
ventilation (Kress et al 2003). As a
result of their unique properties and
associated potential benefits, many
recent clinical guidelines recommend
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the use of non-benzodiazepines such as
dexmedetomidine as a first-line sedative
drug (Barr et al 2013, Whitehouse et al
2014).
Although prescribing guidelines state
that dexmedetomidine infusion could be
titrated to achieve the desired sedation
level (Hospira 2013), its sedation efficacy
has been challenged (Skrupky et al 2015).
In a phase II prospective observational
study, Venn et al (2003) found that
despite using a maximum maintenance
dose of dexmedetomidine of 0.7mcg/
kg/hour, there was a requirement for
additional sedatives to achieve a target
sedation score of 2 or more on the Ramsay
Sedation Scale (Table 3), even at doses of
up to 2.5mcg/kg/hour.
Ruokonen et al’s (2009) phase
III multicentre RCT used twice the
recommended dose of dexmedetomidine
to compare the efficacy of high-dose
dexmedetomidine (>0.7mcg/kg/hour) with
institution-specific standard sedation –
either propofol or midazolam. They found
that patients’ time at the target sedation
level – a Richmond Agitation-Sedation
Scale score of between 0 and -3 – was
similar among the groups, indicating that
dexmedetomidine is not suitable for deep
sedation. Although a subsequent large
multicentre RCT by Jakob et al (2012)
demonstrated that dexmedetomidine was
not inferior to midazolam and propofol
in maintaining sedation at the target level,
the study included only patients with light
to moderate sedation.
TABLE 3. Ramsay Sedation Scale
Score Description
1 Anxious, agitated or restless
2 Cooperative, oriented and tranquil
3 Responsive to commands
4 Asleep, but with brisk response to light glabellar tap or loud auditory stimulus
5 Asleep, sluggish response to glabellar tap or auditory stimulus
6 Asleep, no response
(Adapted from Sessler et al 2008)
volume 31 number 44 / 28 June 2017 / 47
evidence & practice / critical care
KEY POINT Overall, research findings suggest that
Sedation management dexmedetomidine can be an efficacious
is a vital aspect of sedative agent for light to moderate
managing patients sedation. This may present a challenge,
who are critically because deeper sedation is sometimes
ill, and critical care warranted for some patients in ICU,
practitioners, including for example those with severe acute
nurses, are expected to respiratory distress syndrome. Therefore,
incorporate evidence- using dexmedetomidine as a sole agent for
based sedation deep sedation without an adjunct agent is
management into their questionable.
routine practice (Kress
et al 2003) Nursing implications
Sedation management is a vital aspect of
managing patients who are critically ill,
and critical care practitioners, including
nurses, are expected to incorporate
evidence-based sedation management
into their routine practice (Kress et al
2003). The selection of sedative agents
requires a multidisciplinary approach,
and critical care nurses are in a position
to provide valuable input in the selection
of the most appropriate sedative agents
for their patients (Guttormson et al
2010). A thorough clinical assessment
should be undertaken to identify the
clinical needs of patients, specific goals of
sedation, expected duration of sedation
and any particular circumstances that
would favour one agent over another
(Jacobi et al 2002). In addition, other
drug-related factors such as onset of
action, drug accumulation, side effects,
cost-effectiveness and the ability of a
drug to provide analgesic-based sedation
should be considered when selecting
a sedative drug (Pandharipande et al
2007).
Managing patients who are on a
sedative agent such as dexmedetomidine
might present a significant challenge
for many critical care nurses because
of a lack of knowledge of the drug
and uncertainty about the method of
administration. Therefore, it is important
that nurses adhere to the ‘five rights’
of medication use: right patient, right
drug, right dose, right time, and right
route (Grissinger 2010). For the safe
and effective delivery of prescribed
sedation, critical care nurses should also
be familiar with dosing, action, method
48 / 28 June 2017 / volume 31 number 44
of administration, side effects and
contraindications of the drugs.
Dexmedetomidine should be
administered as a diluted IV infusion
using a controlled infusion device,
with the infusion being titrated to a
desired clinical response. Concurrent
administration of dexmedetomidine
with other sedative drugs could increase
the depth of sedation (Wunsch and
Kress 2009); hence, dose adjustment
is warranted. Ongoing assessment
with a valid sedation assessment tool
is important to achieve and maintain
the target sedation score (Kollef et al
1998). Dexmedetomidine should not
be administered with other sedative
agents through the same IV line,
because compatibility has not been fully
established (Hospira 2013).
A loading dose is recommended
but should not be administered
routinely, especially to patients who
are older, hypotensive, hypovolaemic
or have diabetes and/or chronic heart
conditions. This is because of the risk
of bradycardia and hypotension (Anger
2013, Pasin et al 2013). Advice should
be sought from an ICU clinician before
administering a bolus dose to such
patients. Continuous blood pressure,
heart rate and oxygen level monitoring is
vital during the administration of a bolus
dose, throughout the infusion period
and as clinically appropriate following
discontinuation (Hospira 2013). Adverse
cardiovascular events such as bradycardia
and hypotension can be treated with
dose reduction, cessation of therapy and
supportive therapies, including fluid
resuscitation and vasopressors (Anger
2013). When patients are transitioning
from other sedative agents, a loading
dose of dexmedetomidine may not be
required (Hospira 2013).
Critical care nurses should be aware
that, while receiving dexmedetomidine
infusion, patients might remain alert
but calm and be able to communicate
with healthcare professionals. This is
consistent with the Intensive Care Society
guidelines (Whitehouse et al 2014),
which recommend maintaining patients
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at an easily arousable level of sedation.
Dexmedetomidine produces sedation and
analgesia without causing respiratory
depression; therefore, the infusion can
be continued during and even after
extubation (Short 2010). Nurses should
not consider alertness as evidence
of the lack of sedation efficacy of
dexmedetomidine. Since patients remain
awake, they may require periodical
orientation and reassurance to minimise
anxiety and improve cooperation with
the treatment and nursing interventions.
Maintaining an easily arousable level of
sedation would also assist patients to
express their concerns and communicate
their requirement for analgesics.
Several studies have confirmed
the analgesic-sparing property of
dexmedetomidine, and that patients
being administered the medication
have a reduced requirement for
additional analgesia (Herr et al 2003,
Maldonado et al 2009, Abd Aziz et al
2011). However, ongoing pain assessment
and appropriate additional analgesic
interventions remain a crucial aspect of
caring for patients who are critically ill
(Kollef et al 1998). Abrupt discontinuation
of prolonged dexmedetomidine
infusion has been associated with
withdrawal symptoms such as nausea,
vomiting and agitation (Hospira 2013).
Rebound hypertension is also a concern
with discontinuation of prolonged
dexmedetomidine infusion (Jakob et al
2012). While the reason for this is unclear,
slow weaning of dexmedetomidine infusion
with close patient monitoring may be
warranted, and appropriate supportive
therapies should be initiated to manage
withdrawal symptoms promptly.
The quality of communication
between nurses and clinicians in
ICU is known to influence sedation
management (Guttormson et al 2010).
Therefore, the goal of sedation should
be clear and communicated across the
multidisciplinary team to achieve the
desired clinical outcome. Studies have
found that using dexmedetomidine
is associated with improved clinical
outcomes such as reduced duration
nursingstandard.com
of mechanical ventilation, decreased KEY POINT
prevalence of delirium, and improved Several studies have
mortality rates, especially when sedation confirmed the analgesic-
protocols, such as daily sedation sparing property of
interruption, have been incorporated dexmedetomidine, and that
into the daily sedation practice patients being administered
(Pandharipande et al 2007, Riker et al the medication have a
2009, Ruokonen et al 2009, Jakob et al reduced requirement for
2012). additional analgesia (Herr
Sedation protocols were previously et al 2003, Maldonado
shown to reduce sedation-related et al 2009, Abd Aziz et al
complications and improve patient 2011). However, ongoing
outcomes (Kollef et al 1998, Kress et al pain assessment and
2003, Sessler et al 2008). Therefore, appropriate additional
developing an institutional protocol analgesic interventions
for prescribing and administering remain a crucial aspect of
dexmedetomidine is important for its caring for patients who are
safe and effective use. Such a protocol critically ill (Kollef et al 1998)
might reduce variations in practice
between practitioners (Kollef et al 1998)
and assist critical care nurses in effective
decision-making at the patient’s bedside
(White et al 2001).
The Academy of Medical Royal
Colleges (2013) outlined the
responsibilities of those who administer
sedation and indicated the requirement
for formal training in the appropriate
administration of sedative drugs.
Ongoing training and subsequent
supervised practice in the safe and
effective use of dexmedetomidine are
therefore important to improve clinical
outcomes.
Conclusion
Sedation management is an important
aspect of managing patients who are
critically ill. Commonly used sedative
drugs, such as benzodiazepines, are
associated with adverse physical
and psychological outcomes.
Dexmedetomidine is a sedative drug,
which is approved for short-term
sedation of less than 24 hours in adult
patients who are mechanically ventilated.
It can provide analgesic-based sedation
with minimal effect on the respiratory
drive. In selected patients who are
critically ill and require light to moderate
sedation, dexmedetomidine can be a safe
and an effective alternative to traditional
sedative agents.
volume 31 number 44 / 28 June 2017 / 49
evidence & practice / critical care
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