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Sedation & Paralysis in ICU- DR.RAGHUNATH ALADAKATTI

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  • OUT OF 17 RECEP DESCRIBED IN THE LITERATURE MU: ANALGESIA BECAUSE EUPHORIC EFFECTS AND + REINF Decrease in neurotransimission

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  • 1. Analgesia, Sedation & Neuromuscular Blockade In ICU DR.RAGHUNATH ALADAKATTI APOLLO BGS HOSPITAL MYSORE
  • 2. Objective
    • Why to use?
    • Which one to choose?
    • How to use these drugs?
    • What are the problems?
    • Protocols ?
  • 3. Introduction
    • “ Sedate” – To sooth
    • Nearly all patients in ICU require some kind of “soothing ”
  • 4. Introduction
    • Patient often on mechanical ventilation,
    • Can be extremely upset about their condition and their surroundings;
    • In discomfort from injuries, immobility;
    • indwelling catheters; and emotionally stressed.
  • 5. Why Sedation and Analgesia?
    • Relief from fear and anxiety
    • Relief of pain
    • Reduction of awareness
    • Need for a good nights sleep
    • To cope with technology!!
  • 6. Stress Response to Pain
    • Tachycardia
    • Increased myocardial oxygen consumption
    • Hypercoagulability
    • Immunosuppression
    • Persistent catabolism
  • 7. Stress Response to Pain
    • Sleep deprivation affects up to 50% of ICU patients
    • Agitation occurs at least once in 71% of patients in a medical-surgical ICU
  • 8. Indications
    • Analgesia
    • Anxiety
    • Dyspnea
    • To facilitate care
    • To decrease excess oxygen consumption
    • To achieve amnesia
  • 9. Properties of the ideal sedative
    • Rapid onset of action with rapid recovery
    • No drug accumulation
    • Be easy to titrate
    • No tachyphylaxis or withdrawal symptoms,
    • No hemodynamic instability
    • Inexpensive
    • No single drug has all of these properties
    • Combination of drugs
  • 10. Approach to Sedation & Analgesia
    • Define the problem
    • Identify and treat underlying physiological abnormalities
    • Estimate the duration of treatment required
    • Choose an appropriate drug
  • 11. Approach to Sedation & Analgesia
    • Non Pharmacological therapy
    • Pharmacological therapy
  • 12. Pharmacologic therapy
    • Analgesics
    • Sedatives
    • Neuroleptics
  • 13. Analgesics
    • Opioids
    • NSAIDs
    • Acetaminophen
  • 14. Opioids Naturally Occurring Synthetic Morphine Codiene Fentanyl Pethidine Sufentanil Alfentanil Remifentanil
  • 15. Opioid Receptors
    • µ (mu): OP3a,OP3b
      • Primary action site of all opioids
      • Analgesia,sedation,euphoria,respiratory depression
      • Distribution: CNS and GI
      • Linked to abuse/dependence
    • κ (kappa): OP2a,b,c analgesia, psychotomimesis and dysphoria
    • δ (delta): OP1 analgesia, antitussive, for endogenous peptides
    Decrease in neurotransimission
  • 16. 75 – 200 times as potent as morphine Morphine 3 glucuronide Morphine 6 glucuronide Accumulates in renal failure Can cause hypotension No histamine release Hence useful in hemodynamically unstable patient Norpethidine Agent Half Life Metabolic Pathway Active Metabolites Adverse Effects Intermittent Dose Infusion Dose Range Morphine 3 – 7 hrs Glucuronidation Yes Sedation in renal failure Histamine release 0.01 – 0.15 mg / kg IV 0.07–0.5 mg/kg/hr Codeine 3 Hrs Demethylation and glucuronidation Yes (analgesia, sedation) Lacks potency, histamine release Not recommended Not recommended Fentanyl 1.5–6 hr Oxidation No metaboliteparent drug   accumulates Rigidity with high doses 0.35–1.5 μg/kg i.v. q 0.5–1 hr 0.7–10 μg/kg/hr Pethidine 3 – 4 hrs Demethylation and hydroxylation Yes neuroexcitation, especially in renal insufficiency or high doses Avoid with MAOIs and SSRIs Not recommended Not recommended Remifentanil 3–10 min Plasma esterase None ---- ------ 0.6–15 μg/kg/hr
  • 17. Opioid Side Effects
    • Respiratory depression- dose dependent
    • Hypotension – BZD administered concomitantly
    • Depressed level of consciousness
    • Intestinal hypomotility
  • 18. NSAIDs
    • Nonselective, competitive inhibition of cyclooxygenase, a critical enzyme in the inflammatory cascade .
    • Renal failure especially in hypovoluaemic or septic patients
    •   Risk of gastro-intestinal bleeding.  
    •   Acute bronchospasm.  
  • 19. NSAIDs
    • Ketorolac
    • Half life - 2.4 – 8.6 hrs
    • Metabolized by kidney
    • 15–30 mg i.v. q 6h,
    • Avoid more than 2 days
    • Diclofenac
    • Safest route – rectal
    • 25 – 50 mg q 8h
  • 20. Acetaminophen
    • Role limited to relieve mild pain
    • In combination with an opioid it produces a greater analgesic effect than higher doses of the opioid alone
    • Large doses can cause hepatotoxicity
    • Dosage - less than 2 g per day for patients with a significant history of alcohol intake or poor nutritional status and less than 4 g per day for others
  • 21. Drug Administration Techniques
    • Preventing pain is more effective than treating established pain
    • Drugs administered on an “ as needed ” basis, delivers less than the prescribed dose
    • Administer analgesics on a continuous or scheduled intermittent basis , with supplemental bolus doses as required
  • 22. Benzodiazepines
    • Excellent for relieving anxiety
    • Potent amnestic agents
    • Potent sedatives and Induce hypnosis
  • 23. Benzodiazepines
    • Benzodiazepines enhance the inhibitory effects of the neurotransmitter -aminobutyric acid (GABA) causing generalized depression of the CNS
  • 24. Useful in acute agitation Alpha hydroxy midazolam Not useful in acute agitational states Difficult to titrate continuous infusions Polyethylene glycol Propylene glycol ATN Lactic acidosis Agent Onset of action Half life Metabolic pathway Active Metabolite Adverse effects Intermittent dose Infusion Dose Midazolam 2–5 min 3–11 hr Oxidation Yes prolonged sedation, especially with renal failure 0.02–0.08 mg/kg q 0.5–2 hr 0.04–0.2 mg/kg/hr Lorazepam 5–20 min 8–15 hr Glucuronidation None Solvent-related acidosis, renal failure in high doses 0.02–0.06 mg/kg q 2–6 hr 0.01–0.1 mg/kg/hr Diazepam 2–5 min 20–120 hr Desmethylation and hydroxylation Yes prolonged sedation Phlebitis 0.03–0.1 mg/kg q 0.5–6 hr
  • 25. Benzodiazepines- side effects
    • Dose dependent CNS suppression
    • Dose dependent centrally mediated respiratory depression
    • Cardiovascular minimal depression
  • 26. Context-Sensitive Half-Life
    • The difference between the concentration associated with adequate sedation and the concentration associated with return of an appropriate level of consciousness
    • The effect of lorazepam is shorter-lived than that of midazolam because the concentration “decrement” is less for lorazepam than for midazolam.
    • Pohlman et al: Crit Care Med 1994
  • 27. Benzodiazepine Administration
    • Titrate to a predefined endpoint
    • “ As needed ” doses may be adequate
    • Patients requiring frequent doses may benefit from a continuous infusion
    • Continuous infusions may cause accumulation of parent drug or its active metabolites producing inadvertent over sedation
  • 28. Propofol
    • Intravenous, general anesthetic
    • Rapid onset ( 1 -2 min) and short duration ( 10 – 15 min) of sedation
    • It is rare for the effect to last longer than 60 minutes after the infusion
    • Kinetics unchanged in renal or hepatic dysfunction
  • 29. Propafol
    • Hypnotic agent
    • Potent anxiolytic
    • potent amnestic agent
    • Has no analgesic properties
    • Apnea often occurs after a loading dose of propofol (25% incidence)
    • Significant decreases in blood pressure
  • 30. Propafol
    • Prolonged use (>48 hours) of high doses (>66 μg/kg/min infusion) associated with
    • lactic acidosis
    • bradycardia
    • hypertriglyceridemia (a lipid carrier )
    • Doses >83 μg/kg/min associated with an increased risk of cardiac arrest in adults
    • Propofol infusion syndrome
  • 31. Ketamine
    • Phencyclidine derivative
    • Acts by stimulation of NMDA receptors
    • Profound dissociative state
    • profound analgesia
    • maintain a protective cough reflex
    • Improves BP -Ideal for shock patients
    • Bronchodilator – may be used to treat severe acute asthma
  • 32. Ketamine- side effects
    • Emergence delirium
    • Severe hallucinations
    • Not to be used in high ICP patients
    • Releases catecholamines – can cause tachycardia, hypertension
    • Dose : 25 -50 mg IV bolus followed by 10 – 30 mg /hr infusion
  • 33. Neuroleptics
    • Chlorpromazine
    • Haloperidol
    • result in a state of tranquility, and patients often demonstrate a detached affect
    • No amnesia or analgesia
    • Stabilizes cerebral function by antagonizing dopamine-mediated neurotransmission at the cerebral synapses and basal ganglia
  • 34. Neuroleptics
    • Haloperidol
    • - lesser sedative effect and lower risk of hypotension than chlorpromazine
    • - The half-life is approximately 2 hours
    • - Dosing – 2mg bolus followed by repeated doses (double the previous dose) every 15–20 minutes while agitation persists
    • - no respiratory depression
    • - mild hypotension
  • 35. Adverse Effects of Haloperidol
    • QT prolongation leading to ventricular dysrhythmias, including torsades de pointes
    • Extrapyramidal symptoms
    • Neuroleptic malignant syndrome
  • 36. Monitoring Crit Care 2002, 8:290–298 ©2002 Adequate
  • 37. Ramsay Sedation Score
    • Awake levels:
    • anxious or agitated or both 1
    • co-operative, orientated and tranquil 2
    • responds to commands only 3
    • Asleep levels:
    • brisk response to a light glabellar tap 4 sluggish response to a light glabellar tap 5 no response to loud auditory stimulus 6
    Adequate
  • 38. Complications related to sedative administration
    • critically ill patients exhibit unpredictable alterations in Pk & Pd profiles
    • drug accumulation result in prolongation of mechanical ventilation and ICU length of stay
    • mask the development of intracranial, intrathoracic, or intra-abdominal catastrophes
    • may experience withdrawal symptoms
  • 39. Wake up call
    • daily interruption of continuous sedative infusions
    • reduced the duration of mechanical ventilation and intensive care by 2.5 days and 3.5 days, respectively.
    N Engl J Med 2000;342:1471-7.) DAILY INTERRUPTION OF SEDATIVE INFUSIONS IN CRITICALLY ILL PATIENTS UNDERGOING MECHANICAL VENTILATION
  • 40. Wake up call
    • daily interruption of continuous sedative infusions
    • the number of diagnostic studies to investigate unexplained alterations in mental status was reduced from 27% to 9%, and
    • the total amount of Sedatives administered was decreased.
    N Engl J Med 2000;342:1471-7.) DAILY INTERRUPTION OF SEDATIVE INFUSIONS IN CRITICALLY ILL PATIENTS UNDERGOING MECHANICAL VENTILATION
  • 41. Sedation protocol
    • Mean ventilator time decreased by 2.1 days from 7.4 days before intervention to 5.3 days after.
    • Mean stay decreased by 1.0 day (–0.9 to 2.9 days) from 9.3 days to 8.3 days.
    • No accidental extubations or other incidents were identified.
    Brook et al Guttorm Brattebø
  • 42. Neuromuscular Blockade in ICU
  • 43. Indications
    • Facilitate intubation
    • Facilitate mechanical ventilation
    • Control of ICP
    • Control muscle spasms
    • Decrease oxygen consumption
  • 44. Neuromuscular Agents
    • Depolarizing muscle relaxants
    • Suxamethonium
    • Non depolarizing muscle relaxants
    • - Aminosteroidal Compounds
    • Pancuronium, Pipecuronium, Vecuronium, Rocuronium
    • - Benzylisoquinolinium Drugs
    • Atracurium, Cis atracurium, Dxacurium
  • 45.  
  • 46. Pancuronium
    • Long acting
    • Vagolytic – causes increase in heart rate
    • Active metabolite
    • Prolonged effects in renal failure and cirrhosis
    • Dosage – 0.06 – 0.1mg/KG
  • 47. Vecuronium
    • Intermediate acting
    • Not vagolytic
    • 50% of drug excreted in bile, 35% renally excreted
    • Dose: 0.08 – 0.1 mg/kg, 25 – 30 mins
    • More commonly associated with prolonged blockade after discontinuation
    • Higher risk of prolonged blockade when combined with steroids
  • 48. Rocuronium
    • Intermediate acting
    • Very rapid onset of action
    • Metabolite has only 5 -10% activity of parent compound
    • Dose: 0.6 – 0.1 mg/kg
  • 49. Atracurium
    • Intermediate acting
    • Minimal cardiovascular effects
    • Histamine release at high doses
    • Inactivated by ester hydrolysis and hoffmann degradation
    • Breakdown product Laudonosine associated with CNS excitation, concerns of seziures in patients with hepatic failure
    • Requires continuous infusion 10 – 20 ug/kg/min
  • 50.  
  • 51. Monitoring Neuromuscular Blockade
    • Combination of visual tactile and electronic monitoring
    • skeletal muscle movement and respiratory effort forms the foundation of clinical assessment
    • TOF stimulation most commonly used form of electronic monitoring
  • 52. Complications
    • Prolonged recovery from NMBAs
    • Acute quadriplegic myopathy syndrome (AQMS)
  • 53. Prolonged Recovery From NMBAs
    • More common with steroid-based NMBAs
    • Due to the accumulation of NMBAs or metabolites
    • time to recovery of 50–100% longer than predicted
    • Drug intractions, hypermagnesemia, metabolic acidosis, hepatic or renal failure may be cause
  • 54. Acute Quadriplegic Myopathy Syndrome (AQMS )
    • Devastating complications of NMBA therapy
    • Diffuse weakness that persists long after the NMBA is discontinued
    • Global motor deficit
    • Decreased motor reflexes
    • Higher risk with concurrent administration of steroids, aminoglycosides, cyclosporine
    • Acute asthma
  • 55.  
  • 56. Practice Parameters in Sedation & Analgesia
    • Pain assessment and response to therapy should be performed regularly by using a scale
    • Fentanyl is preferred for a rapid onset of analgesia
    • Fentanyl is preferred for patients with hemodynamic instability or renal insufficiency
    • Morphine preferred for intermittent therapy because of its longer duration of effect
    Jacobi J et al: Crit Care Med; 30, 1 2002
  • 57. Practice Parameters in Sedation & Analgesia
    • Sedation of agitated critically ill patients should be started only after providing adequate analgesia and treating reversible physiological causes
    • Midazolam or diazepam should be used for rapid sedation of acutely agitated patients.
    • Propofol is the preferred sedative when rapid awakening is important
    Jacobi J et al: Crit Care Med; 30, 1 2002
  • 58. Practice Parameters in Sedation & Analgesia
    • Midazolam is recommended for short-term use only, as it produces unpredictable awakening and time to extubation when infusions continue longer than 48–72 hours.
    • Lorazepam is recommended for the sedation of most patients via intermittent i.v. administration or continuous infusion.
    • Ttitrate sedative dose to a defined endpoint with systematic tapering of the dose or daily interruption to minimize prolonged sedative effects.
    Jacobi J et al: Crit Care Med; 30, 1 2002
  • 59. Practice Parameters
    • NMBAs should be used for an adult patient in an ICU to manage ventilation, manage increased ICP, treat muscle spasms, and decrease oxygen consumption only when all other means have been tried without success
    Murray J M et al: Crit Care Med; 30, 1 2002
  • 60. Practice Parameters
    • The majority of patients can be managed effectively with pancuronium.
    • Cisatracurium or atracurium is recommended for patients with significant hepatic or renal disease
    • Patients receiving NMBAs should be assessed both clinically and by TOF monitoring, with a goal of adjusting the degree of neuromuscular blockade to achieve one or two twitches.
    Murray J M et al: Crit Care Med; 30, 1, 2002
  • 61. Thank You