Sedation & Paralytic Therapy in the ICU
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Transcript Sedation & Paralytic Therapy in the ICU
Sedation & Paralytic Therapy
in the ICU
Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, NP
Education Specialist
LRM Consulting
Nashville, TN
Objectives
Identify the purpose for pain, sedation, &
paralysis management in the ICU
patient
Analyze and compare assessment
methods for determining appropriate
pain, sedation & paralysis management.
Recognize and apply the different
pharmacotherapeutics used in the ICU
for pain, sedation, & paralysis.
Goals of Critical Care
Management
Save the salvageable and relieve suffering
Peaceful & dignified death without prolonging life
Curative therapy should not supplant palliation of
pain
Use of state-of-the-art interventions
Aggressive & fast paced therapy according to need
Quality pain management mandatory for all
patients
Consciousness/Sedation
The Balance of Analgesia, Sedation, and Paralytics to promote comfort
What is Sedation?
Several Clinical Definitions:
process of establishing a state of calm
promoting a sense of well-being
reduction of anxiety and agitation through the
use of pharmacotherapy
Sedation is NOT analgesia
80% of Doctors and 40% of ICU nurses
answered that benzodiazepines provided
analgesia (1990s)
Pathophysiology Response of
Stress and Anxiety
Cardiovascular
Release of systemic epinephrine and
norepinephrine
Elevated HR and BP
Increased cardiac O2 demand
Decrease end-organ perfusion
Endocrine
Release of Cortisol, Glucagon, Glucose
Hyperglycemia
Pathophysiology Response of
Stress and Anxiety
Neurological
Increased response and activation of
peripheral pain fibers
Increased sensation to pain
Release of neurotransmitters in the brain
Pain
Agitation
Delirium
Pathophysiology Response of
Stress and Anxiety
Immune
Increased levels of prostaglandins,
cortisol, glucose, cytokines,
Increase anti-inflammatory response
Decrease wound healing
SIGNIFICANT STRESS IN THE ICU PATIENT OVERALL CAUSES
ORGAN ISCHEMIA AND DECREASED HEALING
Analgesia
Clinical Definition:
The absence of pain through the use of
pharmacotherapy
Acute and chronic pain in the ICU activates
the stress response
Patients with analgesia can still experience
anxiety
PAIN THERAPY - Myth
“One size fits all or
Set and forget therapy.
Its essentially a
maintenance therapy”
Truths
Majority of ICU patents suffer moderate/severe pain
40% are delirious & cannot communicate
50% are either physically/emotionally distressed
10-20% have no hopes of cure --- end-of-life in ICU
Balance between pain relief & maintaining alertness
Multidisciplinary team for multimodal therapies.
Pain in ICU
Repeated episodes of acute pain localized
Surgery/tissue inflammation immobility
catheter/ apparatus discomfort/ nasogastric
& orogastric tubes
endotracheal intubation/ suctioning/ chest
tubes
phlebotomy/vascular access/physiotherapy
routine turning & positioning the patient
Types of pain in ICU
Somatic – most common –localized opiates
Visceral – cramping & colicky anticholinergics
Neuropathic – burning / shooting antidepressants
Mixed type combination therapy
Sustained or chronic pain of varying degrees
Inherent Problems
difficult to differentiate due to lack of
communication
untreated pain affects all body systems
synergistic effect of pain on anxiety,
depression, sleep
all modalities are unpredictable & have
adverse effects
pain therapy to be tailored to individual
needs.
Assessment of pain in ICU
Pain as the 5th vital sign- requires frequent
evaluation
Cognitive impairment/delirium markers
• Behavioral (facial, FACS)
• Physiological (BP, HR, RR)
Creative assessments (teaching hand movements,
blinking
Subjective quantification (numeric/graphic scales –
W-B faces)
Assessment of pain in ICU
Treatment of Pain
treatment of perceived & prevention of
anticipated pain
Opiates – principal agents in ICU
- potent / lack ceiling effects
- mild anxiolytic & sedative
- relieves air hunger & suppresses cough in
respiratory failure
- improved patient – ventilator synchrony
- effective antagonist – naloxone
lack amnesic effects /additional sedatives
required
Treatment of Pain
adjuvant / non-pharmacological / multimodal
therapies
•
Simple Relaxation – must begin preoperatively
•
Jaw relaxation
Progressive muscle relaxation
Simple imagery
Music (either patient – preferred or “easy listening” are
effective in reducing mild to moderate pain
Complex Relaxation – must begin preoperatively
Biofeedback
imagery
Causes of Pain in the ICU?
The Messengers of Pain
• Direct tissue damage stimulates pain fibers
• Local Inflammatory mediators
•
Bradykinin, Prostaglandins, Cytokines
• Tissue Injury
•
•
•
Histamine
Serotonin
TNF
WHY IS THIS IMPORTANT?
Common Analgesic Drugs in the
CVICU
Drug
Dose
Onset
Peak
Duration
Morphine
Renal
1 - 4 mg
5 min
20 min
4 - 5 hrs
Fentanyl
Liver
25 – 100 mcg
1 - 2 min
3 - 5 min
30 - 60 min
Remifentanil
Plasma
.5 – 40
mcg/kg/h
<1 min
<1 min
3 - 10 min
Dilaudid
Liver
.25 – 2 mg
10 - 15 min
15 - 30 min
2 - 3 hrs
Toradol
Liver
15 – 30 mg
Immediate
1 - 3 min
6 - 8 hrs
A Focus on Morphine
First narcotic to be used
Narcotic standard
Relies on good kidney function for excretion
Stimulates mast cells to release histamine
Itching
Rash
Hypotension
Acute Asthma episode
No longer used frequently due to newer drugs
A Focus on Fentanyl
100x stronger then Morphine
Fastest metabolizing narcotic used in the
CVICU
Chest Wall Rigidity
can cause shortness of breath and difficulty
weaning
occurs most often with high IV bolus doses
Decreases BP and HR
A Focus on Remifentanil
Newest synthetic narcotic derived from Fentanyl
Eliminated by plasma esterases
Metabolism not dependent on liver or kidney function
Elimination not dose dependent
Advantages
Organ independent metabolism
Lack of accumulation
Provides analgesia and sedation in ventilated patient
Disadvantages
Expensive
Severe withdrawal
Rebound hyperalgesia
A Focus on Toradol
Is a potent IV/IM NSAID
Decreases sternal incision pain and
inflammation
Like many NSAIDs can be nephrotoxic
Know your patients BNP and Creatinine
Can cause GI bleeding
Usually not given if the patient is…
Age >75
Elevated creatinine
Chest tube bleeding
Low platelets
Sedation in ICU
used in the agitated, ventilated & for
procedure discomfort
to avoid self extubation & removal of
catheters
NM blockade mandates analgesia &
sedation
control of pain before sedation
all have side effects – dose dependent
analgesics are not sedatives/ Sedatives
are not analgesics
Common Sedatives in the ICU
Drug
Dose
Onset
Peak
Duration
Ativan
Liver
.5 - 2mg
5 min.
60-90 min
6 - 8 hrs
Versed
Liver
1 - 2mg
1.5 - 5 min
Rapid
2 - 6 hrs
Propofol
Liver*
Starts at 25
mcg/kg/min
<40 sec.
3-5 min
10 - 15 min
Precedex
Plasma
.2-.7
mcg/kg/hr
(3mcg/kg/hr)
15 - 30 min
30 min
60 - 120 min
Ketamine
2–7
mcg/kg/min
30 s
1 min
5 - 10 min
A Focus on Precedex
Only sedative used that does not cause
respiratory depression
Patients can be weaned and extubated while
on Precedex
Usual titration range 0.2 – 0.7mcg/kg/hr
MD order >0.7mcg/kg/hr
Titrate by 0.1-0.2mcg/kg/hr q30-45min
Can cause SEVERE bradycardia and
hypotension
Very expensive!
A Focus on Ketamine
dissociative anesthetic light sedation &
amnesia
used as an adjunct for patients with
uncontrolled pain or inadequately sedated
rarely used in the CVICU due to myocardial
depressant properties
monitor for hallucinations and vivid dreams
Assessment of Pain and Sedation
Sedation scoring systems
Assess levels to vary according to course
of ICU stay
Observational scales - 4 levels – min,
mod, deep, GA
Addenbrooke sedation scale 0-7 (vocal,
tracheal suction)
Ramsay sedation scale 1-6 (vocal,
glabellar tap)--aim for 3-4
Direct information- ideal to assess
analgesia & sedation
BIS – for deep sedated & paralyzed
RASS ASSESSMENT
+4
+3
+2
+1
0
-1
-2
-3
-4
-5
Combative, violent, danger to self/staff
Very agitated, pulls lines, tubes, aggressive
Agitated frequent non-purposeful movement, fights the vent
Restless / Anxious but not aggressive or vigorous
Alert and calm
Drowsy, not fully alert but can stay awake, eyes open to voice for >10sec
Light sedation, wake and makes eye contact for < 10 sec
Moderate sedation, moves/opens eyes to voice but no eye contact
Deep sedation, no response to voice but moves or opens eyes to physical stimulation
Unarousable, no response to stimuli
BIS monitor
BIS Monitoring
BIS Monitor
BIS monitor utilizes EEG waveforms.
reading is monitored from the patient’s
forehead.
excessive muscle activity can interfere with
EEG detection
Bispectral Index
BIS – an attempt to objectively monitor
patients sedation
processed EEG measurement that
gives a score to help determine the
patient’s response to sedation
useful to help titrate medication
proper sensor placement is key to
accurate monitoring
Sensor Application
Apply sensor on forehead at angle
Circle #1: Centered, 2 inches above nose
Circle #4: Directly above eyebrow
Circle #3: On temple, between corner of eye
and hairline
Press around the edges of each circle to assure adhesion
Press each circle for 5 seconds
BIS Placement
Make sure the forehead is clean and
dry!
Label the sensor with date/time
Replace sensor every 24 hours and
PRN
BIS Monitor
implement BIS monitoring on all patients with
paralytic drips infusing
purpose of BIS monitor is to provide a direct
measurement of the SEDATIVE effects on
the brain.
goal for BIS Monitoring will be 40 – 60.
studies have indicated that this is a safe range
for no memory recall.
BIS Monitoring
Troubleshooting the BIS
If the BIS increases suddenly or is higher
than expected:
Consider:
Is the sedative dose sufficient?
Is there an increase in stimulation?
When was the last analgesic given?
Is the patient adequately paralyzed? TOF?
Is the patient having a seizure
Troubleshooting the BIS
If the BIS decreases suddenly or is lower than
expected:
Consider:
Has there been a decrease in stimulation or
increase in sedation/analgesia?
Is the patient significantly hypothermic?
Has there been a sudden significant drop in BP?
BIS Monitoring
Always consider the overall picture of the
patient
Ex: if nothing significant has changed with
patient and BIS number suddenly reflects very
different readings then fall back to your overall
assessment of the patient
REMEMBER!
Look at the BIG PICTURE!
Do Not Forget
You are treating a patient not just the number
“Sedation Vacation”
Assess for daily awakening
•
Exclusions
Increased ICP
Neuromuscular blockade
Significant ventilation support
CABG, immediate post-op
“Sedation Vacation”
Is patient awake and calm?
•
•
SAS 3 – 4
RASS 0 to -1
If no, restart sedation @ ½ previous
dose
If yes, proceed to spontaneous
breathing trial (SBT)
“Sedation Vacation”
Assess for SBT
•
•
•
•
•
•
Calm & co-operative
Hemodynamically stable
PEEP < 8
FiO2 < 0.60
pH > 7.34
SpO2 > 90%
“Sedation Vacation”
SBT Termination Criteria
•
•
•
•
•
•
•
RR > 35/min for > 5 minutes
SpO2 < 90% for > 2 minutes
New ectopy
HR change 20% from baseline
BP change 20% from baseline
Accessory muscle use
Increased anxiety/diaphoresis
“Sedation Vacation”
Conduct SBT for 1 minute
•
•
•
•
Mode CPAP
PEEP = 0
PS @ least 5 – 10
FiO2 unchanged
Paralytics in the ICU
Paralysis – the loss of voluntary muscular
function due to the administration of a
paralytic
Neuromuscular Blockade Agent (NMB) –
Drugs that obstruct transmission of nerve
impulses to the muscle
Neuromuscular Blockade agents DO NOT
BLOCK THE TRANSMISSION OF PAIN!!!!
Paralytics in the CVICU
Sedation and Analgesics must always be
given FIRST
Must use sedatives with an Amnesic affect
Benzodiazepines (VERSED)
High dose Propofol
Paralytics are always given LAST
Why Do We Paralyze?
Decreases O2 demand
ARDS
Prevent Patient-Ventilator dysynchrony
VDR ventilators
BiVent
Prevents Shivering in hypothermia patients
Shivering increases O2 demand
Raises patients temperature
Open chest
Checklist for chemical paralysis
Must be adequately sedated first before
paralytic administered
Must have anxiolytic drip that has amnesic
properties
Must have analgesic drip infusing
Must have lubrication for eyes/eye bubbles
Common CVICU Paralytics
Drug
Dose
Onset
Peak
Duration
Vecuronium
.08 - .1 mg/kg
1 min
3-5 min
15-25 min
Pancuronium
.04 -.1 mg/kg
30-45 sec
3-4 min
35-65 min
Succinylcholine
.6 mg/kg
30-60 sec
1-2 min
4-10min
Nimbex
3 mcg/kg/min
1-2 min
2-5 min
25-44 min
A Focus on Vecuronium
A non-depolarizing NMB
Will NOT increase K+
Full recovery from paralytic 25-40min
Frequently used in the CVICU for intubation
or as a bolus drug before Nimbex
Rarely used as a drip in the absence of
Nimbex
0.8-1.2mck/kg/min
A Focus on Succinylcholine
A depolarizing NMB
Can increase K+ ~ 0.5-1mEq/L
KNOW YOUR PATIENTS K+ before
administering
Does your patient have any renal disease?
Metabolized by plasma cholinesterase
Very rapid metabolism ~5min
Does not rely on kidney or liver function
A Focus on Nimbex
Is our primary titrating NMB used in the
CVICU
Is also metabolized in the blood
Standard dose is 3mcg/kg/min
Titrate range: 0.5-5mcg/kg/min
Metabolism ~45min
Changes with hypothermia?
Successful Paralysis: How do we
know?
Assessment
Movement
Spontaneous Breaths
Peripheral Nerve Stimulator
Peripheral Nerve Stimulators
Peripheral Nerve
Stimulator – A device
that delivers a determine
electrical current to
create a muscular
contraction
Used to determine the
amount of
neuromuscular blockade
a patient has
An increase in NMB will
show a decrease
response to a peripheral
nerve stimulator at a set
current
Train of Four
Train of Four – 4 consecutive impulses
generated from the peripheral nerve
stimulator resulting in 4 muscular twitches
# of twitches seen = degree of NMB
No blockade – 4 twitches
Total blockade – 0 twitches
GOAL IS 1-2 TWITCHES
Increase drip by 10% if >2 twitches
Decrease drip by 10% if <1 twitch
Train of Four: Facial Nerve
Place one electrode on
the face at the outer
canthus of the eye
(positive/red electrode)
Place the second
electrode 2 cm below
and parallel with the
tragus of the ear
(negative/black
electrode)
Watch and feel for facial
nerve contraction
Train of Four: Ulnar Nerve
Train of Four
Must have 2x baseline TOFs before starting
NMBs
Ulnar nerve is more preferred but facial nerve
is easier to see/assess
Use alcohol pad to wipe clean and dry the
skin before applying electrode
Electrodes must be changed 24 hrs
Possibly inaccurate in hypothermia patients…
Helpful tips for TOF
If checking the thumb – ensure the leads are
placed on the ulnar side of the arm(this is
where the nerve lies)
Be careful with applying maximum MA’s when
leads are placed on the face – this can lead
to burns/scarring
Check your battery
Change your electrodes q24h
Putting it all Together
1. start BIS Monitoring
2. get a Baseline TOF on two locations
3. start Sedation and Analgesic Drips
4. titrate medication up until BIS 40-60
5. bolus paralytic
6. start paralytic drip
7. check TOF q30min until 1-2 twitches
8. monitor TOF and BIS and titrate drips to
endpoints
***** CRUCIAL POINT ******
Prior to the administration of any paralytic
agent - sedation MUST be administered first.
If paralytic will be continued as an infusion,
sedation MUST also be continued.
Sedation MUST be a drug that has amnesic
properties.
Drugs that have amnesic effects
Benzodiazepine class
Examples:
Versed
Propofol (in high doses) dose will be
individual to patient
Intravenous Medicines commonly
used in CVICU
SEDATION
Ativan *
Versed *
Propofol **
Precedex ***
•
•
•
* Amnesic properties
** Amnesic in high
doses only
*** DOES NOT have
amnesic properties
ANALGESIA
Morphine
Fentanyl
Dilaudid
Toradol
Case Study
You are caring for a patient that has an open
chest, they are on a Nimbex, Fentanyl &
Versed gtts:
VS’s:
BP 160/90
HR 128
Vent Settings: SIMV 12, TV 450, PEEP 5, PS 10,
Spontaneous RR 12, 02 saturation 98%, TOF 2/4
Is anything wrong here?
Case Study
Patient has open chest, Nimbex, Fentanyl &
Versed gtts:
VS’s
105/68
HR 80 Paced
Vent settings: SIMV 12, TV 600, PEEP 5, PS 10,
Spontaneous RR 16
TOF 2/4
Is anything wrong here?
Case Study
Patient has open chest, has experienced
excessive blood loss through chest tubes,
Nimbex & Propofol gtts(5 mcg/kg/hr)
VS’s
BP labile 70’s to 100’s systolic
HR 80’s paced
Vent settings: SIMV 12, TV 400, PEEP 5,
PS 5, Spontaneous RR 14, 02 saturation 98%
TOF 0/4
Is anything wrong here?
SCCM task force recommendations
Benzodiazepines most popular for sedation
Short term sedation
• Midazolam <3h (amnesic/ hypotension)
• propofol – infusion syndrome/ pancreatitis
Long term – lorazepam <20h /diazepam>96h (not
for infusion)
Delirium – haloperidol - neuroleptic syndrome/
torsade pointes
Antagonist- flumazenil 0.2mg-1mg (withdrawal
seizures)
ReCap of Key Points
Sedation:
Patient may still experience pain, goal is antianxiety/ – relaxation, goal is usually to give
amnesia
Analgesia:
Used to treat pain, no anti-anxiety properties
Paralytics:
Used to decrease skeletal muscle movement,
imperative that amnesic drugs be used in
combination with analgesic meds, MUST
sedate before paralyzing
ReCap of Key Points
BIS Monitor:
Used to strictly assess patient’s sedation level
Goal is 40-60
Peripheral Nerve Stimulator:
Used to strictly assess patients paralytic state
TOF goal is 1-2/4
Putting it all Together
1. start BIS Monitoring
2. get a Baseline TOF on two locations
3. start Sedation and Analgesic Drips
4. titrate medication up until BIS 40-60
5. bolus paralytic
6. start paralytic drip
7. check TOF q30min until 1-2 twitches
8. monitor TOF and BIS and titrate drips to
endpoints
Final Thoughts
give sedation/analgesia before paralytics
BIS assess for sedation
TOF assess for adequate NMB
If in doubt it never hurts to ask!
References
Gelinas C. Management of pain in cardiac surgery ICU
patients: have we improved over time? Intensive Crit Care
Nurs. 2007;23(5):298-303.
Girard TD, Shintani AK, Jackson JC, et al. Risk factors for
post-traumatic stress disorder symptoms following critical
illness requiring mechanical ventilation: a prospective cohort
study. Crit Care. 2007;11(1):R28.
Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice
guidelines for the sustained use of sedatives and analgesics
in the critically ill adult. Crit Care Med. 2002;30(1):119-141.
Pandharipande PP, Pun BT, Herr DL, et al. Effect of
sedation with dexmedetomidine vs lorazepam on acute
brain dysfunction in mechanically ventilated patients: the
MENDS randomized controlled trial. JAMA.
2007;298(22):2644-2653.