art of sedation in icu
DESCRIPTION
critically ill patients differs from other patients because of their altered Pk/Pd, hence sedation must be titrated to desired responseTRANSCRIPT
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Dr. Surendra FNB-CCMRTIICS KOLKATA
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Hypnosis
± MuscleRelaxation
Analgesia
•Latin word sedare = to calm or to allay fear = sedation
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Conscious sedation•A minimally depressed level of
consciousness induced by the administration of pharmacologic agents in which a patient retains the ability to independently and continuously maintain an open airway and a regular breathing pattern, and to respond appropriately and rationally to physical stimulation and verbal commands
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THE PATIENT IS HERE!
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Chest 2008;133;552-565
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Complications from pain and anxietyStimulation of the autonomic nervous
system and release of humoral factors → increased HR, BP, and myocardial oxygen consumption → myocardial ischemia or infarction
Altered humoral response can lead to
hypercoagulability as a result of increased level of factor VIII, fibrinogen, platelet activity, and inhibition of fibrinolysis
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Cont……..Stress hormones also produce insulin
resistance, increased metabolic rate, and protein catabolism
Immunosuppression with reduction in number and function of lymphocytes and granulocytes
Psychological disturbances - memories of vivid nightmares, hallucinations, and paranoid delusions
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DeliriumDelirium80% of ICU patients have delirium
*may or may not be accompanied by agitation
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Indications and Goals
Facilitate mechanical ventilationCreate anxiolysis, analgesia,
amnesiaDecrease oxygen consumptionReduce dyspneaPrevent patient self-injury“Rest” patient for weaning trialsInduce sleep
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Cont……Create patient unawareness Improve long-term
psychiatric outcomes (?)Permit delivery of efficient
careReduce nursing stressEnsure nursing safetyIncrease family acceptance
of ICU careWeinert, et al. AJCC. 2001; 10:156
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Sedation EvaluationSedation EvaluationShould be integral component of treatment algorithmsprecise dosingreduced sedative and analgesic drug use shorter duration of MVreduced need for vasopressor therapyreduced incidence of over sedation
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Guidelines---SCCM-2013
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scoring system
should be simple, easily performed, noninvasive, and
reproducible.
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Richmond Agitation-Sedation Scale (RASS)Sedation Agitation Scale [SAS]Motor Activity Assessment ScaleRamsay Sedation ScaleAdaptation to the Intensive Care Environment
(ATICE) instrumentMinnesota Sedation Assessment Tool (MSAT). Glasgow coma scale (GCS) – assessment of level of
consciousness
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Richmond agitation sedation scaleScore Term Description
+4 Combative Violent; immediate danger to staff
+3 Very agitated Pulls/ removes tubes, catheters; aggressive
+2 Agitated Frequent non purposeful movement; patient ventilator asynchrony
+1 Restless Anxious or apprehensive
0 Alert and calm
-1 Drowsy Not fully alert but awakens for >10s, with eye contact, to voice
-2 Light sedation Briefly awakens (<10s), with eye contact, to voice
-3 Moderate sedation
Any movement to voice but no eye contact
-4 Deep sedation No response to voice but movement to physical stimulation
-5 Unarousable No response to voice or physical stimulation
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Ramsay sedation scaleAwake1 Anxious and/or agitated2 Cooperative, oriented, and tranquil3 Responds to commandsAsleep4 brisk response to light glabellar
tap or loud auditory stimulus5 Sluggish response to light glabellar
tap or loud auditory stimulus6 No response
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Sedation agitation scale1: Unarousable 2: Very sedated 3: Sedated 4: Calm and cooperative 5: Agitated 6: Very agitated 7: Dangerous agitation
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What is “adequate sedation”?RAAS -0-3SAS – 3-4RAMSAY- 3
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Measurement of Brain ActivityMeasurement of Brain ActivityBispectral index (BIS)Patient state indexCerebral state indexNarcotrend index
•Objective physiologic Objective physiologic parametersparameters
•Numerical displayNumerical display•Near-continuous measurementNear-continuous measurement
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Bispectral indexA practical, processed EEG
parameter that measures the direct effects of sedatives on the brain
.
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BIS range guidelines
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Value of BIS in ICU
Minimize consequencesof over- and
under-sedation
Improve quality of sedation management
Objective sedation assessmentabout a patient’s response to sedation
Optimize clinical and economic
outcomes
Numerical scale correlates to sedation endpoints
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BISProne to artifacts‘Electromyography‘ activity interferes with BIS
measures of sedationConfounding factors that may influence BIS scores
Hypoglycemia / Sleep / temperature / AgeDrugs
aminophylline, epinephrine, and ketamine.Increase variability of BIS in the critically ill ptsCannot be relied upon in circulatory arrest or
hypothermia
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Daily interruption of sedation & analgesia [1B]Allows better assessment of a patient’s
sedative needsReduces drug bioaccumulationReduced incidence of posttraumatic stress
disorderReduced complications of critical illnessMore ventilator-free days and earlier ICU and
hospital discharge, at the expense of a higher incidence of self-extubation
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Sedation therapyNON PHARMACOLOGICAL THERAPY:Good communication with regular
reassurance from nursing staffEnvironmental control such as
humidity, lighting, temperature, and noiseExplanation prior to proceduresManagement of thirst, hunger,
constipation, and full bladder
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Critically ill patients are differentPharmacokinetics of various drugs are
altered including - drug bioavailability, volume of distribution, and clearance.Hepatic dysfunctionDecreased hepatic blood flowRenal dysfunctionAlteration in volume statusPlasma protein binding
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Pharmacologic therapyThe sedative agent should possess the
following qualities:Both sedative and analgesic propertiesMinimal cardiovascular side effectsControllable respiratory side effectsRapid onset/offset of actionNo accumulation in renal/hepatic
dysfunctionInactive metabolitesInexpensiveNo interactions with other ICU drugs
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Pharmacologic therapy
BenzodiazepinesPropofolEtomidateKetamineBarbiturate Short acting opioidsAlpha 2 agonistsInhalational agents
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Benzodiazepines Anxiolytic, anticonvulsant, amnesic,
hypnotic and provide some muscle relaxation
Effects are mediated by depressing the excitability of the limbic system via reversible binding at GABA-benzodiazepine receptor complex
Minimal cardiorespiratory depressant effectThe common drugs in this class are
diazepam, midazolam, and lorazepam
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Pharmacodynamic response Patient-related factors can affect the
BZD responseageconcurrent pathologyprior alcohol useconcurrent therapy with other sedative drugs
Higher volume of distribution and slower clearance in elderly.
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MIDAZOLM LORAZEPAM DIAZEPAM
LOADING DOSE 0.01-0.05 mg/kg 0.02-0.04 mg/kg 0.05-0.2 mg/kg
MAINTANENCE DOSE
0.02-0.1 mg/kg/hr
0.01-0.1 mg/kg/hr
Rarely used
ONSET 1-5 min 5-20 min 2-5 min
DURATION 3-11 hrs 2-6 hrs 2-4 hrs
CARDIAC EFFECTS
Minimal Minimal Present
RESPIRATORY EFFECTS
Important depressant effect
Important depressant effect
Important depressant effect
ANALGESIA None None None
AMNESIA Potent None None
ACTIVE METABOLITES
Yes No Yes
S/E Low BP Low BP, glycol/nephrtoxicity
Low BP, pleibitis
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Propofol The mode of action of propofol is via the GABA
receptorRapid onset of action 1-2 min; metabolized rapidly hepatically and
extrahepatically Recovery within 10 minutes of discontinuation,
can accumulate with prolonged use Ideally infused via a large or central veinProlonged infusions –increase triglyceride and
cholesterol levels A theoretical maximum recommended dose is 4
mg/kg/hour.
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Propofol (contd.)Bolus dose – not recommendedInfusions @25 to 100μg/kg/hrTheoretical maximum dose- 4mg/kg/hrCautious about propofol infusion syndrome
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Propofol: adverse effectsHypotension
Reliable, dose-related Decreased SVR and contractility (CO)
Respiratory depression Apnea with bolus dosing
Synergistic CV and respiratory depression with opioids
Vehicle (soybean emulsion): Hypertriglyceridemia Venoirritation Infection
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Propofol infusion syndromePropofol infusion syndrome is an adverse
drug event associated with high doses (>4 mg/kg per hour or >67 µg/kg per minute) and long-term (>48 hours) use of propofol.
Clinical features:- Cardiomyopathy with acute cardiac failure.- Myopathy.- Metabolic acidosis, K+ - Hepatomegaly.
Inhibition of FFA entry into mitochondria failure of its metabolism.
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Management Supportive treatments addressing the clinical
manifestations The propofol infusion should be discontinued
immediately Alternative sedative should be started Intravenous crystalloid and colloid replacement
and vasopressor and/or inotropic support Cardiac pacing may be used for symptomatic
bradycardia Hemodialysis or continuous renal replacement
therapy to treat the acute renal failure
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KetamineKetamine acts at the N-methyl-D-aspartate
(NMDA) receptorIn subanesthetic doses, sedative and analgesicGenerally not used because of the increase in
blood pressure, intracranial pressure (ICP), and pulse rate
Bronchodilatory properties, sometimes has a role in severe asthma
In the ICU conjunction with a narcoticDose : 5 to 30 μg/kg/min
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Others ETOMIDATE :For maintenance of hypnosis, target
concentration of 300 to 500 ng/mL may be achieved by administration of a two- or three-stage infusion
BARBITURATES: Barbiturates such as Pentothal have been used in the ICU, especially in the management of patients with head injuries and seizure disorders. They cause significant cardiovascular depression and accumulate during infusions, leading to prolonged recovery times.
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Others (contd.) BUTYROPHENONES AND PHENOTHIAZINESAn aggressive dosing regimen of haloperidol may
be useful in a patient with delirium to promote calm, 2 to 10 mg IV every 10 to 15 minutes until the desired response is achieved
VOLATILE AGENTSIsoflurane has been used in concentrations of up
to 0.6% for longterm sedation, with minimal cardiorespiratory side effects and rapid awakening.
Desflurane has been shown to be effective in sedation, with rapid offset of effects.
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Others (contd.)Shorter acting opioidsFentanyl, alfentanyl, remifentanyl
α2 agonistsClonidinedexmedetomidine
Muscle relaxants
Fentanyl
50-100μg
1-2 min
30-60 min
50-350μg/hr
No
No
Loading dose
Onset
Duration
Infusion rate
Active metabolites
Histamine release
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2 AgonistsClonidine
Selectivity: 2:1 250:1
Imidazole derivate 16:1
t1/2 10 hrsAntihypertensive
Dexmedetomidine
Selectivity: 2:1 1620:1
Imidazole derivate 31:1t1/2 2 hrs94% protein boundEliminated by
liver/kidneySedativeOnly available in IV form
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Dexmed.Dexmed. Clinical paradigms
Sedation without
respiratory
deppression
Sympatholyti
csmooth emergence + weaning from mechanical ventilation
Molecular targets + neural substrates1.locus ceruleus2.natural sleep pathways
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Pharmacokinetics Rapid redistribution: 6 minNo accumulation after infusions 12-24 hTypical doses (target plasma levels 0.3-1.2
ng/ml):Onset 5-10 minEt1/2 1.8-3.1 hr1 ug/kg loading dose over 10 min f/b 0.2-0.7
ug/kg/hr infusionLoad only - short proceduresPatients with high sympathetic activity may
need very high doses
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Clonidine Clonidine is synergistic with opioids and
acts at the spinal cord to inhibit nociceptive inputs, thus imparting analgesia
It is contraindicated in hypovolemia and can cause hypotension, bradycardia, and dry mouth
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The Art of Sedation Under sedation:Fighting the ventilator.V/Q mismatch.Accidental extubation.Catheter
displacement.CV stress ischemia.Anxiety, awareness.Post-traumatic stress
disorder.
Over sedation:Tolerance,
tachyphylaxis.Withdrawal
syndrome.Delirium.Prolonged ventilation.CV depression. neuro testing.Sleep disturbance.
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Titration of Sedative Medications
Large variation in dose requirementsAltered PK/PD in critically ill Acute and chronic toleranceDifferences in severity of symptom or behavior
Most drugs are titrated to effectSimilar to hypertensive medications
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How to titrate sedative medications
Identify the target symptom or behavior“Measure” the intensity or severityAgree on the appropriate symptom level for
that patient at that timeRealize that changes will occur
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Propofol
Hypertriglyceridemia
CVS depression
Hypotension
2-agonists
Hypotension
Bradycardia
Benzodiazepines
Hypotension
Respiratory depression
Agitation/ConfusionKetamine
Hypertension
Secretions
Dysphoria
GeneralOver sedation
Delayed awakening/extubation
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Respiratorydepression
ConfusionVasodilation
Gut motilitydepression
Opioids
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WEANING FROM SEDATION
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Hooper. Critical Care Clinics - 25 (July 2009)
Before Assesing daily awakening exclude
Raised ICTNMBVery high PEEP n FiO2CABG- immediate postop
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Results: ABC TrialSAT + SBT = more Ventilator-free days
15 v 12 (p =0.02)Less days in ICU: 9 v 13Less coma but more self-extubationsDecreased risk of dying up to 1 yr
Girard Lancet 371:126 2008
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