Art of sedation in icu

1. Dr. Surendra FNB-CCM RTIICS KOLKATA

2. Hypnosis ± Muscle Relaxation Analgesia •Latin word sedare = to calm or to allay fear = sedation

3. Conscioussedation • A minimally depressed level of consciousness induced by theadministration of pharmacologic agentsin which apatient 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

4. THE PATIENT IS HERE!

5. Chest 2008;133;552-565

6. Complications from pain and anxiety Stimulation of theautonomic nervoussystem and releaseof humoral factors→ increased HR, BP, and myocardial oxygen consumption → myocardial ischemiaor infarction Altered humoral responsecan lead to hypercoagulability asaresult of increased level of factor VIII, fibrinogen, platelet activity, and inhibition of fibrinolysis

7. Cont…….. Stresshormonesalso produceinsulin resistance, increased metabolic rate, and protein catabolism Immunosuppression with reduction in number and function of lymphocytesand granulocytes Psychological disturbances- memoriesof vivid nightmares, hallucinations, and paranoid delusions

8. DeliriumDelirium 80% of ICU patients have delirium *may or may not be accompanied by agitation

9. Indications and Goals Facilitate mechanical ventilation Create anxiolysis, analgesia, amnesia Decrease oxygen consumption Reduce dyspnea Prevent patient self-injury “Rest” patient for weaning trials Induce sleep

10. Cont…… Create patient unawareness Improve long-term psychiatric outcomes (?) Permit delivery of efficient care Reduce nursing stress Ensure nursing safety Increase family acceptance of ICU care Weinert, et al. AJCC. 2001; 10:156

11. Sedation EvaluationSedation Evaluation Should be integral component of treatment algorithms precise dosing reduced sedative and analgesic drug use shorter duration of MV reduced need for vasopressor therapy reduced incidence of over sedation

12. Guidelines---SCCM-2013

13. scoring system should besimple, easily performed, noninvasive, and reproducible.

14. Richmond Agitation-Sedation Scale (RASS) Sedation Agitation Scale [SAS] Motor Activity Assessment Scale Ramsay Sedation Scale Adaptation to the Intensive Care Environment (ATICE) instrument Minnesota Sedation Assessment Tool (MSAT). Glasgow comascale(GCS) – assessment of level of consciousness

16. Richmond agitation sedation scale Score 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

17. Ramsay sedation scale Awake 1 Anxiousand/or agitated 2 Cooperative, oriented, and tranquil 3 Respondsto commands Asleep 4 brisk responseto light glabellar tap or loud auditory stimulus 5 Sluggish responseto light glabellar tap or loud auditory stimulus 6 No response

18. Sedation agitation scale 1: Unarousable 2: Very sedated 3: Sedated 4: Calm and cooperative 5: Agitated 6: Very agitated 7: Dangerousagitation

19. What is “adequate sedation”? RAAS -0-3 SAS – 3-4 RAMSAY- 3

20. Measurement of Brain ActivityMeasurement of Brain Activity Bispectral index (BIS) Patient state index Cerebral state index Narcotrend index •Objective physiologicObjective physiologic parametersparameters •Numerical displayNumerical display •Near-continuous measurementNear-continuous measurement

21. Bispectral index A practical, processed EEG parameter that measuresthedirect effects of sedativeson the brain .

22. BIS range guidelines

23. Value of BIS in ICU Minimize consequences of over- and under-sedation Improve quality of sedation management Objectivesedation assessment about apatient’sresponseto sedation Optimizeclinical and economic outcomes Numerical scale correlates to sedation endpoints

24. BIS Prone to artifacts ‘Electromyography‘ activity interferes with BIS measures of sedation Confounding factors that may influence BIS scores Hypoglycemia / Sleep / temperature / Age Drugs aminophylline, epinephrine, and ketamine. Increase variability of BIS in the critically ill pts Cannot be relied upon in circulatory arrest or

25. Daily interruption of sedation & analgesia [1B] Allows better assessment of a patient’s sedative needs Reduces drug bioaccumulation Reduced incidence of posttraumatic stress disorder Reduced complications of critical illness More ventilator-free days and earlier ICU and hospital discharge, at the expense of a higher incidence of self-extubation

26. Sedation therapy NON PHARMACOLOGICAL THERAPY: Good communicationwith regular reassurancefrom nursing staff Environmental control such ashumidity, lighting, temperature, and noise Explanationprior to procedures Management of thirst, hunger, constipation, and full bladder

27. Critically ill patients are different Pharmacokinetics of various drugs are altered including - drug bioavailability, volume of distribution, and clearance. Hepatic dysfunction Decreased hepatic blood flow Renal dysfunction Alteration in volume status Plasma protein binding

28. Pharmacologic therapy Thesedativeagent should possessthefollowing qualities: Both sedativeand analgesic properties Minimal cardiovascular sideeffects Controllablerespiratory sideeffects Rapid onset/offset of action No accumulation in renal/hepatic dysfunction Inactivemetabolites Inexpensive No interactionswith other ICU drugs

29. Pharmacologic therapy Benzodiazepines Propofol Etomidate Ketamine Barbiturate Short acting opioids Alpha2 agonists Inhalational agents

30. Benzodiazepines Anxiolytic, anticonvulsant, amnesic, hypnotic and providesomemusclerelaxation Effectsaremediated by depressing theexcitability of thelimbic system viareversiblebinding at GABA- benzodiazepinereceptor complex Minimal cardiorespiratory depressant effect Thecommon drugsin thisclassarediazepam, midazolam, and lorazepam

31. Pharmacodynamic response Patient-related factors can affect the BZD response age concurrent pathology prior alcohol use concurrent therapy with other sedative drugs Higher volume of distribution and slower clearance in elderly.

32. 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

33. Propofol Themodeof action of propofol isviatheGABA receptor Rapid onset of action 1-2 min; metabolized rapidly hepatically and extrahepatically Recovery within 10 minutesof discontinuation, can accumulatewith prolonged use Ideally infused viaalargeor central vein Prolonged infusions–increasetriglycerideand cholesterol levels A theoretical maximum recommended doseis4 mg/kg/hour.

34. Propofol (contd.)Bolusdose– not recommended Infusions@25 to 100μg/kg/hr Theoretical maximum dose- 4mg/kg/hr Cautiousabout propofol infusion syndrome

35. Propofol: adverse effects Hypotension  Reliable, dose-related  Decreased SVR and contractility (CO) Respiratory depression  Apneawith bolusdosing Synergistic CV and respiratory depression with opioids Vehicle(soybean emulsion):  Hypertriglyceridemia  Venoirritation  Infection

36. Propofol infusion syndrome Propofol infusion syndromeisan adversedrug event associated with high doses(>4 mg/kg per hour or >67 µg/kg per minute) and long-term (>48 hours) useof propofol. Clinical features: - Cardiomyopathy with acutecardiac failure. - Myopathy. - Metabolic acidosis, K+ - Hepatomegaly. Inhibition of FFA entry into mitochondria failureof itsmetabolism.

37. Management Supportivetreatmentsaddressing theclinical manifestations  Thepropofol infusion should bediscontinued immediately  Alternativesedativeshould bestarted  Intravenouscrystalloid and colloid replacement and vasopressor and/or inotropic support  Cardiac pacing may beused for symptomatic bradycardia  Hemodialysisor continuousrenal replacement therapy to treat theacuterenal failure

38. Ketamine Ketamineactsat theN-methyl-D-aspartate(NMDA) receptor In subanesthetic doses, sedativeand analgesic Generally not used becauseof theincreasein blood pressure, intracranial pressure(ICP), and pulserate Bronchodilatory properties, sometimeshasarolein severeasthma In theICU conjunction with anarcotic Dose: 5 to 30 μg/kg/min

39. Others ETOMIDATE :For maintenanceof hypnosis, target concentration of 300 to 500 ng/mL may beachieved by administration of atwo- or three-stageinfusion BARBITURATES: Barbituratessuch asPentothal havebeen used in theICU, especially in the management of patientswith head injuriesand seizure disorders. They causesignificant cardiovascular depression and accumulateduring infusions, leading to prolonged recovery times.

40. Others (contd.) BUTYROPHENONESAND PHENOTHIAZINES An aggressivedosing regimen of haloperidol may be useful in apatient with delirium to promotecalm, 2 to 10 mg IV every 10 to 15 minutesuntil thedesired responseisachieved VOLATILE AGENTS Isofluranehasbeen used in concentrationsof up to 0.6% for longterm sedation, with minimal cardiorespiratory sideeffectsand rapid awakening. Desfluranehasbeen shown to beeffectivein sedation, with rapid offset of effects.

41. Others (contd.) Shorter acting opioids Fentanyl, alfentanyl, remifentanyl α2 agonists Clonidine dexmedetomidine Musclerelaxants Fentanyl 50-100μg 1-2 min 30-60 min 50-350μg/hr No No Loading dose Onset Duration Infusion rate Active metabolites Histamine release

42. α2 Agonists Clonidine Selectivity: α2:α1 250:1 Imidazolederivate16:1 t1/2 β 10 hrs Antihypertensive Dexmedetomidine Selectivity: α2:α1 1620:1 Imidazolederivate31:1 t1/2 β 2 hrs 94% protein bound Eliminated by liver/kidney Sedative Only availablein IV form

43. Dexmed.Dexmed. Clinical paradigms Sedation without respiratory deppressio n Sympat holytic smooth emergence+ weaning from mechanical ventilation Molecular targets+ neural substrates 1.locusceruleus 2.natural sleep pathways

44. Pharmacokinetics Rapid redistribution: 6 min No accumulation after infusions12-24 h Typical doses(target plasmalevels0.3-1.2 ng/ml): Onset 5-10 min Et1/2 1.8-3.1 hr 1 ug/kg loading doseover 10 min f/b 0.2-0.7 ug/kg/hr infusion Load only - short procedures Patientswith high sympathetic activity may need very high doses

45. Clonidine Clonidine issynergistic with opioidsand actsat the spinal cord to inhibit nociceptiveinputs, thus imparting analgesia It iscontraindicated in hypovolemiaand can cause hypotension, bradycardia, and dry mouth

46. The Art of Sedation Under sedation: Fighting theventilator. 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.

47. Titration of Sedative Medications Large variation in dose requirements Altered PK/PD in critically ill Acute and chronic tolerance Differences in severity of symptom or behavior Most drugs are titrated to effect Similar to hypertensive medications

48. How to titrate sedative medications Identify the target symptom or behavior “Measure” the intensity or severity Agree on the appropriate symptom level for that patient at that time Realize that changes will occur

49. Propofol Hypertriglyceridemia CVSdepression Hypotension α2-agonists Hypotension Bradycardia Benzodiazepines Hypotension Respiratory depression Agitation/Confusion Ketamine Hypertension Secretions Dysphoria General Over sedation Delayed awakening/extubation

50. Respiratory depression ConfusionVasodilation Gut motility depression Opioids

51. WEANING FROM SEDATION

52. Hooper. Critical Care Clinics - 25 (July 2009) Before Assesing daily awakening exclude Raised ICT NMB Very high PEEPn FiO2 CABG- immediate postop

53. Results: ABC Trial SAT + SBT = more Ventilator-free days 15 v 12 (p =0.02) Less days in ICU: 9 v 13 Less coma but more self-extubations Decreased risk of dying up to 1 yr Girard Lancet 371:126 2008

Art of sedation in icu

Art of sedation in icu

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