Unit 6: Analgesia, Sedation and Neuromuscular blockage
somatosensory cortex and can be experienced by patients
Analgesia
Pain- Pain is described as an unpleasant sensory and emotional
experience associated with actual or potential tissue damage or
described in terms of such damage.
-
emphasizes the subjective and multidimensional
nature of pain. subjective characteristic implies that
pain is whatever the person experiencing it says it is
and that it exists whenever he or she says it does.
- This definition also suggests that the patient is able to
self-report. However, in the critical care context,
many patients are unable to self-report their pain.
Components of Pain
The experience of pain includes sensory, affective,
cognitive, behavioral, and physiologic components.
The sensory component is the perception of many
characteristics of pain, such as intensity, location, and
quality.
The affective component includes negative emotions such
as unpleasantness, anxiety, fear, and anticipation that may
be associated with the experience of pain.
The cognitive component refers to the interpretation or
the meaning of pain by the person who is experiencing it.
The behavioral component includes the strategies used by
the person to express, avoid, or control pain.
The physiologic component refers to nociception and the
stress response.
Types of Pain
Pain can be acute or chronic, with different sensations
related to the origin of the pain.
1. Acute Pain
Acute pain has a short duration, and it usually corresponds
to the healing process (30 days), but should not exceed 6
months.
It implies tissue damage that is usually from an identifiable
cause.
2. Chronic pain
Chronic pain persists for more than 6 months after the
healing process from the original injury, and it may or may
not be associated with an illness. It develops when the
healing process is incomplete or, as described earlier,
when acute pain is poorly managed.
Both acute and chronic pain can have a nociceptive or neuropathic
origin.
Nociceptive pain arises from activation of nociceptors, and
it can be somatic or visceral.
-Somatic pain involves superficial tissues, such as
the skin, muscles, joints, and bones. Its location is well
defined.
-Visceral pain involves organs such as the heart,
stomach, and liver. Its location is diffuse, and it can be
referred to a different location in the body.
Neuropathic pain arises from a lesion or disease affecting
the somatosensory system.11 The origin of neuropathic
pain may be peripheral or central. Neuralgia and
neuropathy are examples related to peripheral
neuropathic pain, which implies a damage of the
peripheral somatosensory system.
-Central neuropathic pain involves the central
after a cerebral stroke.
-Neuropathic pain can be difficult to manage and
frequently requires a multimodal approach (i.e., the
combinations of several pharmacologic and/or
nonpharmacologic treatments).
Physiology and Anatomy of Pain
Nociception represents the neural processes of encoding
and processing noxious stimuli necessary, but not
sufficient, for pain.
Pain results from the integration of the pain-related
signal into specific cortical areas of the brain associated
with higher mental processes and consciousness. In other
words, pain is the conscious experience that emerges
from nociception.
The pleiotropic effects of pain are due to the complicated
processing of pain from stimulus to cerebral cortex. There
are four described elements of pain processing:
1) Transduction. Noxious stimuli are converted to an
action potential.
-Transduction refers to mechanical (e.g., surgical
incision), thermal (e.g., burn), or chemical (e.g., toxic
substance) stimuli that damage tissues. In critical
care, many nociceptive stimuli exist, including the
patients’ acute illness or condition, invasive
technology used for patients, and multiple
interventions that have to be done for them.
-These stimuli, also called stressors, stimulate
the liberation of many chemical substances, such as
prostaglandins, bradykinin, serotonin, histamine,
glutamate, and substance P. These neurotransmitters
stimulate peripheral nociceptive receptors and
initiate nociceptive transmission.
2) Transmission. Action potentials are conducted via
afferent neurons.
-As a result of transduction, an action potential is
produced and is transmitted by nociceptive nerve fibers in
the spinal cord that reach higher centers of the brain.
3) Modulation- process by which noxious stimuli that
travel from the nociceptive receptors to the CNS may be
enhanced or inhibited.
-Afferent pain signals are altered by efferent
neural inhibition via neurotransmitters, especially in the
dorsal horn of the spinal cord or by augmentation via
neuronal plasticity (eg, central sensitization).
4) Perception. Integration of afferent pain signals in the
cerebral cortex.
-The pain message is transmitted by the
spinothalamic pathways to centers in the brain, where it is
perceived. Pain sensation transmitted by the NS pathway
reaches the thalamus, and the pain sensation transmitted
by the PS pathway reaches brainstem, hypothalamus, and
thalamus.

Strategies for Pain Management
Assessment of Pain
Pain assessment has two major components:
1) non-observable or subjective
The patient’s self-report of pain can also be obtained
by questioning the patient using the mnemonic
PQRSTU:
P: provocative and palliative or aggravating factors
Q: quality
R: region or location, radiation
S: severity and other symptoms
T: timing
U: understanding
2) observable or objective
Behavioral Pain scale
Critical Care Pain Observation Tool
Techniques for appropriate pain management must be
individualized to each patient, starting with an appropriate
assessment of its severity.
If the patient is able to adequately communicate pain, the
following should be assessed: site, onset and timing,
quality, severity, exacerbating and relieving factors,
response to analgesics, and assessment of pain with
movement, breathing, and cough.
-Fluctuations in vital signs should never be used alone but
rather considered as a cue to begin further assessment for
pain.
- Patients who experienced pain during
nociceptive procedures were three times
more likely to have increased behavioral
responses such as facial expressions, muscle
rigidity, and vocalization than patients
without pain.
- Patients who experienced pain during
turning showed significantly more intense
facial expressions (e.g., grimacing), muscle
rigidity, and less compliance with the
ventilator (e.g.,
- fighting the ventilator) compared with
patients without pain.
- Behavioral indicators are strongly
recommended for pain assessment in
nonverbal patients.
-Nurses should observe whether pain is related to any
injury such as breathing (including artificial ventilation) or
movement.
Assessment tools:
 Numerical scales (0-3, 0-10, which
higher numbers indicating worst pain)
 ‘faces’-I originally (pediatric tools, but
adopted for ICU)
 Behavioral tools-was tested mostly in
nonverbal mechanically ventilated
patients with altered levels of
consciousness.
Behavioral Pain Scale- combines
assessment of facial expression, upper
limb movements and compliance with
ventilation so is useful for assessing
pain in ventilated patient.
-Changes in vital signs maybe caused by acute pain, but
can also have other causes. Non-verbal cues can be reliable as verbal
reports of pain. Sudden pain provokes a stress response with
sudden:
 Tachycardia+ shallow breathing
 Hypertension
 Tachypnea
 Vasoconstriction (clammy, pale, peripheries)
 Sweating
Other non-verbal cues include:
 Facial grimacing- clenched teeth, wrinkled
forehead, biting lower lip, wide-open or tightly
shut eyes.
 Position- double up, ‘frozen’, writhing
 Pupil dilatation
Other Strategies:
Electroencephalogram-Continuous electroencephalographic (EEG)
activity is being used more frequently in critical care units, especially
in the brain-injured population, to detect epileptic activity and
ischemia.
Bi-spectral Index- Another innovative technology, the Bi-spectral
Index (BIS), is being explored for its relevance in the pain assessment
process of critically ill, sedated patients.37,68 The primary utility of
the BIS is as an objective measure of sedation levels during surgery
in the operating room or during neuromuscular blocking in the
critical care unit.
Pain Management
Opioids—remain the mainstay of acute pain management.
-Systemic opioids are traditionally the cornerstone of
postoperative and critical care pain management. Opioids'
sites of action affect 3 of 4 pain-processing pathways.
-Opioids act as ligands at G protein-coupled opioid
receptors, namely, the μ (mu), δ (delta), and κ(kappa)
receptors. These receptors are located peripherally, in the
spinal cord dorsal horn as well as at various locations in
the brain.
Opioid receptors are located on primary afferent neurons
and inhibit release of nociceptive substances, decrease
neurotransmitter release in the spinal cord, and activate
descending inhibitory neurons.
Some Opioids used as ICU analgesia:
Morphine- remains the gold standard opioid. It suppresses
impulses from C fibers but not A delta , so relieves dull,
prolonged pain. Its relatively long effect makes bolus
administration feasible, which reduces problems from
accumulation.
Diamorphine ( heroin) is metabolized to morphine.
Fentanyl- twice as lipid- solube as diamorphine, so acts
rapidly.
More potent than morphine, it does not cause
histamine release, so causes less hypotension. Fentanyl
derivatives includes: alfentanil and remifentanil.
Alfentanil- shorter duration (1-2) hours makes continuous
infusion safer; its metabolites are inactive, making it useful
for patients with kidney injury.
Remifentanil- is rapidly metabolized by plasma, so has
few, complications from accumulation but relatively
expensive.
Low dose-ketamine- can be useful for uncontrolled pain
and , unlike most opioids, increases blood pressure.
Pethidine- is rarely used because it is short acting,
produces toxic metabolite known as norphethidine, highly
addictive and provides no greater pain relief than
morphine.
Meperidine. Meperidine (Demerol) is a less potent opioid
with agonist effects similar to those of morphine.
It is considered the weakest of the opioids, and it must be
administered in large doses to be equivalent in action to
morphine. Because the duration of action is short, dosing
is frequent. A major concern with this medication is the
metabolite normeperidine, which is a CNS neurotoxic
agent.
At high doses in patients with kidney failure or liver
dysfunction or in older adult patients, it may induce CNS
toxicity, including irritability, muscle spasticity, tremors,
agitation, and seizures.
Codeine. Codeine has limited use in the management of
severe pain. It is rarely used in the critical care unit. It
provides analgesia for mild to moderate pain. It is usually
compounded
with a nonopioid (e.g., acetaminophen).
To be active, codeine must be metabolized in the liver to
morphine.
Codeine is available only through oral, intramuscular, and
subcutaneous routes, and its absorption can be reduced in
the critical care patient by altered gastrointestinal motility
and decreased tissue perfusion.
Dexmedetomidine
Dexmedetomidine (Precedex) is a short-acting alpha 2
agonist that is indicated for the short-term sedation (<24
hours) of mechanically ventilated patients in the critical
care unit.Its
mechanism of action is unique and differs from those of
other commonly used sedatives in critical care. Indeed,
compared to midazolam (Versed) or lorazepam (Ativan)—
whose hypnotic
effects act mainly on the limbic system and/or the cortex
—the effect of dexmedetomidine is located in the locus
ceruleus section of the brainstem. As a result, patients
receiving dexmedetomidine IV infusions are calm and
sleepy, yet they remain easily arousable.
dexmedetomidine is ideal for mild to moderate sedation,
often referred to as conscious sedation.
Non- Opioids Analgesics
Acetaminophen
Acetaminophen is an analgesic used to treat mild to
moderate pain. It inhibits the synthesis of
neurotransmitter prostaglandins in the CNS, and this is
why it
has no anti-inflammatory properties.
Nonsteroidal Anti-inflammatory Drugs. The use of NSAIDs
in combination with opioids is indicated in the patient with
acute musculoskeletal and soft tissue inflammation.24 The
mechanism of action of NSAIDs is to block the action of
cyclooxygenase (COX, which has two forms: COX-1 and
COX-2), the enzyme that converts arachidonic acid to
prostaglandins.
Preventing and Treating Respiratory Depression
-Respiratory depression is the most life-threatening opioid
side effect. The risk of respiratory depression increases
when other medications with CNS depressant effects (e.g.,
benzodiazepines, antiemetics, neuroleptics,
antihistamines) are concomitantly administered to the
patient.
-it is usually described in terms of decreased respiratory
rate (fewer than 8 or 10 breaths/min), decreased Spo2
levels, or elevated ETCO2 levels.94 A change in the
patient’s level of consciousness or an increase in sedation
normally precedes respiratory depression.
Opioid Reversal.
Critical respiratory depression can be readily reversed with
the administration of the opiate antagonist naloxone.24
The usual dose is 0.4 mg, which is mixed with 10 mL of
normal saline (for a concentration of 0.04 mg/mL).
Naloxone is normally given intravenously very slowly (0.5
mL over 2 minutes) while the patient is carefully
monitored for reversal of the respiratory signs.
Naloxone administration can be discontinued as soon as
the patient is responsive to physical
stimulation and able to take deep breaths.
PCA—Patient Controlled Analgesia
For awake, alert patients with moderate to severe pain—
most commonly postoperative patients—PCA is an
appropriate choice. Before initiatinga PCA order, the
patient must be able to understand how to appropriately
use the PCA apparatus.
To determine the PCA prescription, the following
parameters must be specified:
(1) opioid
(2) incremental (or demand) dose,
 (3) lockout interval,
(4) background infusion rate (if any),
(5) 1- and 4-hour dose limits, and
(6) bolus dose administration (for breakthrough pain).
A reasonable starting prescription in an opioid-naïve
patient would be morphine with an incremental dose of 1
to 2 mg, a lockout of 6 to 10 min, no continuous infusion
rate, a 4-hour maximum dose of 30 mg, and a bolus dose
of 2 to 4 mg every 5 min for 5 doses.
Unsuitable if patient have:
 Impaired psychomotor function
 Muscle weakness
 Visual deficit
 Confusion/ forgetting how to control the
machine
Use observation charts for PCA to assess while on PCA to
include:
 Vital signs (HR, BP, RR, O2 sat)
 Pain
 Nausea
 Sedation level
Sedation-
-usually used to facilitate invasive ventilation and known as
‘chemical restraint’.
Reasons for Sedation
1. Amnesia
2. Ventilator tolerance
3. Anxiety and Fear
4. Patient Safety and Agitation
5. Sleep deprivation
6. Delirium
Drugs for Sedation
Short term Sedation
Midazolam- it can be administered intermittently
in a bolus IV form or as a continuous infusion.
Long term infusions > 24 hours of midazolam are discouraged
because the drug has an active metabolite that may
accumulate in the presence of drugs, renal disease,
liver disease or old age.
Propofol- is an IV general anesthetic designed for
use as a continuous infusion. This drug ideas often
preferred for short term sedation use (<24 hrs) and when a very
rapid offset of effect is desired.
- Is a lipid based and serve as a source of
calories. It should be used cautiously in
those with high triglycerides and the drug is
contraindicated in those with egg allergies.
Frequent change o the containers and
tubing are required to prevent potential
growth of microorganisms.
Dexmedetomidine- is an alpha-2 receptor
agonist that has been approved only for very short-
term use (24hrs) in the ICU setting.
Ketamine- IV general anesthetic that produces
analgesia, anesthesia, and amnesia without loss of
consciousness.
- Contraindicated in patient with elevated
intracranial pressure.
- with bronchodilatory properties make it a
good choice in those with asthma.
Intermediate- Term Sedatives
Lorazepam-most commonly used
benzodiazepine in critical care and be administered
orally and IV as an intermittent bolus or
continuous infusion. When given orally or in
bolus intermittent form, drug effect is intermediate, when
used as a continuous infusion (>24hrs), its effect
is more long term because awakening may take hours to days to
accomplish.
Long Acting Sedatives
Diazepam, a long acting benzodiazine, and
chlordiazepoxide are rarely used in critical
care; however, they may be selected for treatment of
severe alcohol withdrawal.
Goal of Sedation, monitoring, and Management
Goal of sedation administration is important to identify in
order to determine the appropriate and drug.
e.g. if the reason is to decrease pain and increase comfort,
the selection of an analgesic is indicated.
If a patient who is anxious and unable to sleep, the goal is
very different than if the patient is unstable, on a ventilator, and
suffering from profound hypoxemia.- sedation is needed.
Sedation scales
Allow the health-care team to select a level of sedation for
the patient. Descriptors of each level of sedation are provided so
that the sedative maybe adjusted appropriately.
-is done at least hourly and the level of sedation achieved
is recorded.
-it is important for the interdisciplinary team to determine
the level of sedation daily so the infusion rate can be adjusted
accordingly.
Example:
1. Sedation-Agitation Scale
2. Richmond Agitation- Sedation Scale
Complications of Sedation
Oversedation is recognized as a state of unintended patient
unresponsiveness in which the patient resides in a state of
suspended animation resembling general anesthesia. Prolonged
deep sedation is associated with significant complications of
immobility, including pressure ulcers, thromboemboli, gastric ileus,
nosocomial pneumonia, and delayed weaning from mechanical
ventilation.
Delirium- is said to be present in 50% to 80% of critically ill patients.
Patients are especially at risk if they are elderly, have pre-
existing dementia, hx of hypertension, and high severity of illness at
admission.
Coma- is an independent risk factor for the development
of delirium.
SCCM guidelines recommend that routine assessment of
delirium be done with the use of a valid and reliable delirium-
monitoring tool such aa CAM- ICU or Confusion Assessment Method
for ICU or ICDSC- Intensive Care Delirium screening
checklist
When patients are agitated, restless, and pulling
at tubes and lines, they are often identified as
being delirious. In this scenario, delirium may be
described as “ICU psychosis” or “sundowner
syndrome.” However, the delirious patient is not
always agitated, and it is much more difficult to
detect delirium when the patient is physically
calm. Provision of adequate analgesia is an
essential component of delirium prevention.
Neuromuscular Blockade
Pharmacologic neuromuscular blockade (NMB) induces a
state of physical paralysis. NMB is administered to achieve
ventilator synchrony and improve oxygenation when this cannot be
achieved by sedation and analgesia alone.
Because NMB causes a pharmacologic paralysis, the
patient will not be able to respond to verbal or physical stimuli
and additional monitoring methods are required. NMB is never
administered unless adequate analgesia and sedation are also
provided. This is because NMB paralyzes skeletal muscle but
does not alleviate pain or confer sedation. It is vital that measures
are in place to avoid a scenario where a patient who has
received NMB cannot move, yet retains mental awareness.
Blocking release of acetylcholine (a neurotransmitter) at the
neuromuscular junction causes skeletal (but not smooth) muscle
relaxation. Paralyzing agents may be classified as:
o Depolarizing
o Non-depolarizing
Agents:
Succinylcholine is the only depolarizing NMBD available in the
United States—it depolarizes nicotinic acetylcholine receptors and
either desensitizes the receptor, inactivates sodium channels and
prevents propagation of an action potential, or a
combination of both.
Mivacurium- is a rapid acting and has a short duration of action (15
minutes). It may be given as an IV bolus initially but then is
provided by infusion.
Vecuronium- a steroidal-like agent is metabolized by the liver and
excreted renally.
Combination of steroids and vecuronium may
contribute to myopathies.
Pancuronium- is generally given by intermittent IV bolus.
- It is vagolytic and can cause tachycardia; it
maybe contraindicated in patients with
cardiovascular disease and is metabolize by
the liver and is renally excreted.
Monitoring and Management
Peripheral nerve stimulator (PNS)- are devices that deliver series of
electrical stimuli via electrodes to nerves under the skin.
-usually performed on the ulnar nerve at the wrist, with
the temple area of the head is as another potential site for
nerve stimulation. When electrical stimuli are applied for the ulnar
nerve, the thumb abducts and the fingers flex if the
neuromuscular junction is intact.
- use to assess NMB is the train of four.
Four small electrical stimuli are given every half second.
4 twitches= neuromuscular blockade occupies <75% of
receptors
3 twitches= 75 percent blockade
2 twitches= 75-80 percent blockade
1 twitch= 90 percent blockade
0 twitches= 100 percent blockade
Airway Pressure Monitoring
- Use to monitor patient generated
respiratory activity.
- Helpful when initiating NMB and to assess
withdrawal of the drug.
Nursing Management
Nursing Diagnosis
1. Impaired Spontaneous Ventilation r/t acute respiratory
failure. Respiratory muscle fatigue
2. Ineffective airway clearance r/t stasis of secretions,
decreased energy and fatigue, endotracheal intubation
3. Anxiety r/t inability to maintain adequate gas exchange,
inability to breath adequately without support, inability to
communicate verbally or change in health status.
 4. Ineffective Protection related to ventilatory dependency,
positive pressure ventilation, unable to wean off from
ventilator.

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and Management.7th edition. Elsevier Mosby, Missouri.

Buns, Suzanne (2014) AACN Essentials of Critical Care Nursing.3 rd

edition. McGrawHill Education,USA.

Woodrow, Phillip (2014) Intensive Care Unit. 3 rd edition. Routledge,

London.