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SEDATIVES & ANALGESICS in ICU

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Improving ICU experience by appropriate use of Sedatives & Analgesics in ICU

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SEDATIVES & ANALGESICS in ICU

  1. 1. PHARMACOTHERAPY of SEDATIVES & ANALGESICS in ICU DR SUBHANKAR PAUL EMERGENCY MEDICINE & CRITICAL CARE Gauhati Medical College & Hospital
  2. 2. “Pain is perfect misery, the worst of evils . . .” John Milton Paradise Lost
  3. 3. CONTENTS • INTRODUCTION • DEFINITIONS • STRESS RESPONSE • PAIN PATHWAY • MODALITIES OF PAIN CONTROL • DRUGS • CONCLUSION
  4. 4. INTRODUCTION • “Contrary to popular perception, our principal function in patient care is not to save lives (since this is impossible on a consistent basis), but to relieve pain and suffering, the patients that experience the greatest pain and suffering are the ones in the ICU” ........................ [Marino] • most patients who are discharged from the ICU remember discomfort and unrelieved pain as a dominant experience during their ICU stay
  5. 5. Stressful Experiences in the ICU (a) unrelieved pain, (b) inadequate sedation, (c) inability to communicate (in intubated patients), (d) difficulty sleeping, and (e) hallucinations and nightmares • The most frequently cited source of stress is painful procedures • Stressful experiences during the ICU stay can have prolonged neuropsychiatric effects INCLUDING post-traumatic stress disorder
  6. 6. STRESS RESPONSE
  7. 7. Stress Response
  8. 8. Pain in Critically Ill Patients • the prevalence of pain is the same in surgical ICUs and medical ICUs • Concept of Hypernociception Critically ill patients experience pain more readily than healthy subjects (hypernociception). For example, the most painful experiences for ICU patients are endotracheal suctioning, and being turned in bed. In addition, 30–50% of critically ill patients experience pain while at rest, without a noxious stimulus. This type of pain typically involves the back and lower extremities
  9. 9. • The heightened pain experience in critically ill patients is attributed to immobility and systemic inflammation. (The rest pain experienced by ICU patients is similar to the myalgias experienced during a systemic infection.) Failure to recognize this heightened nociceptive state is a major source of inadequate pain relief in the ICU. Frequent pain assessments using pain intensity scales (described next) can help to correct problems with inadequate pain control in the ICU
  10. 10. Pain has a number of adverse consequences • provoking anxiety • contributing to lack of sleep • worsening delirium • increasing the stress response • causing respiratory embarrassment due to atelectasis and sputum retention • causing immobility with venous and gut stasis.
  11. 11. Pain pathway Pain pathway
  12. 12. Monitoring Pain • The pain sensation can be described in terms of intensity, duration, location, and quality, but pain intensity is the parameter most often monitored because it reflects the “unpleasantness” of pain. • Pain Intensity Scales • Pain intensity scales are used to determine the need for, and evaluate the effectiveness of, analgesic therapy. There are 6 different pain intensity scales, but only a few are needed to assess pain intensity in most ICU patients
  13. 13. Scale Method Comments Adjective rating scale Easy to administer. Visual analog scale Pain intensity measured in millimeters from one end. Numeric rating scale Can be used in patients with visual, speech, or manual dexterity difficulties. 5-Point global scale Patient rates pain as: A decrease of one point is a large change; other scales allow monitoring of small changes in pain and may be more sensitive. 0 = none 1 = a little 2 = some 3 = a lot 4 = worst possible Verbal quantitative scale The patient is asked to self-report pain on a scale of 0 to 10 without descriptors. Most commonly used scale, easy to administer.
  14. 14. Behavioral Pain Scale (BPS)
  15. 15. Role of Vital Signs ?? • Vital signs (e.g., heart rate) show a poor correlation with patients’ reports of pain intensity (the gold standard), and they can remain unchanged in the presence of pain . As a result, VITAL SIGNS ARE NOT RECOMMENDED FOR PAIN ASSESSMENTS
  16. 16. Modalities of Pain management • a caring and supportive ICU team, whom the patient can trust • warm and comfortable surroundings • attention to pressure areas • bowel and bladder care • adequate hydration and amelioration of thirst (e.g. moistening the mouth) • early tracheostomy where indicated to reduce the discomfort of endotracheal intubation • Analgesics &/or sedatives • Local/Regional Anaesthesia • supplemental treatments such as acupuncture, acupressure, massage and transcutaneous electrical nerve stimulation (TENS).
  17. 17. Drugs OPIOID ANALGESIA NON-OPIOID ANALGESIA Nsaids Drugs for neuropathic pain  Local Anaesthetics
  18. 18. LOCAL ANAESTHETICS – REGIONAL ANALGESIA • femoral nerve block for hip and femur injuries • intercostal or paravertebral nerve blocks or catheters for thoracic and upper abdominal injuries or wounds; • brachial plexus or intravenous regional anaesthesia for isolated upper limb injuries or procedures (e.g. fracture manipulation) • epidural analgesia for thoracic and abdominal pain (e.g. flail chest, pancreatitis • intrapleural analgesia/anaesthesia, applied either via a catheter placed for this purpose or via inter-costal drains
  19. 19. OPIOID ANALGESIA • The natural chemical derivatives of opium are called opiates. Opiates and other substances that produce their effects by stimulating discrete opioid receptors in the central nervous system are called opioids (eg.Morphine/Pethidine/Tramadol) • The term narcotic refers to a general class of drugs that blunt sensation and depress consciousness (i.e., narcotize).
  20. 20. CLASSIFICATION OF OPIOIDS • 1. Natural opium alkaloids: Morphine, Codeine • 2. Semisynthetic opiates: Diacetylmorphine • (Heroin), Pholcodeine. • Many others like—Hydromorphone, Oxymorphone, • Hydrocodone, Oxycodone, are not used in India. • 3. Synthetic opioids: Pethidine (Meperidine), • Fentanyl, Methadone, Dextropropoxyphene, • Tramadol.
  21. 21. Opioid receptor transducer mechanisms
  22. 22. BRAIN periaqueductal gray, locus ceruleus, and the rostral ventral medulla spinal cord interneurons and primary afferent neurons in the dorsal horn Sensory neurons immune cells (recruited to sites of inflammation)
  23. 23. CNS ACTIONS of MORPHINE depressant actions stimulatORY ACtions • CTZ : Nausea and vomiting • Edinger Westphal nucleus of III nerve : miosis , decrease in intraocular tension. • Vagal centre : bradycardia • Certain cortical areas and hippocampal cells : Excitation, Muscular rigidity and Immobility , Convulsions • Analgesia • Sedation • Mood and subjective effects • Respiratory centre • dose dependent DEPRESSION • Cough centre • Temperature regulating centre • vasomotor centre
  24. 24. Neuro-endocrine FSH, LH, ACTH levels are lowered, while prolactin and GH levels are raised Hypothalamic influence on pituitary is reduced CVS Vasodilatation shift of blood from pulmonary to systemic circuit (a) histamine release. (b) depression of vasomotor centre. (c) direct action decreasing tone of blood vessels GIT Constipation Action directly on intestines and in CNS Spasm of pyloric, ileocaecal and anal sphincters. Decrease in all gastrointestinal secretions Central action causing inattention to defecation reflex Biliary tract may cause biliary colic spasm of sphincter of Oddi Urinary bladder urinary urgency and difficulty in micturition Tone of both detrusor and sphincter is increased Bronchi can cause bronchoconstriction releases histamine
  25. 25. Morphine 0.1 milligram/kg IV Onset: 1–2 min (IV) and 10–15 min (IM/SC) 10 milligrams IM Peak effect: 3–5 min (IV) and 15–30 min (IM) 0.3 milligram/kg PO Duration: 1–2 h (IV) and 3–4 h (IM/SC) Meperidine (pethidine) 1.0–1.5 milligrams/kg IV/IM Onset: 5 min (IV) Contraindicated when patient taking a monoamine oxidase inhibitor; neurotoxicity may occur when multiple doses given in the presence of renal failure Peak effect: 5–10 min (IV) Duration: 2–3 h (IV) Fentanyl 1.0 microgram/kg IV Onset: <1 min (IV) High doses can cause chest wallPeak effect: 2–5
  26. 26. Drugs and Dosing Regimens • given intravenously as intermittent bolus doses or continuous infusions • It is important to emphasize that opioid dose requirements can vary widely in individual patients, and that the effective dose of an opioid is determined by each patient’s response, not by the recommended dose range of the drug
  27. 27. Drug EquiAnalges ic Dose (mg) Typical Adult Dose Infusion(dose /kg/hr Onset Peak effect duration Morphine 10 0.03-0.1mg/kg 0.02- 0.07mg/kg/hr 1–2 min (IV) and 10–15 min (IM/SC) 3–5 min (IV) and 15–30 min (IM) 1–2 h (IV) and 3–4 h (IM/SC) Meperidine (pethidine 75mg 1.0–1.5 milligrams/kg IV/IM 5 min (IV) 5–10 min (IV 2–3 h (IV) Fentanyl 200 0.3-1.5 microgram/kg IV 0.7- 10microg/kg/hr <1 min (IV 2–5 min (IV 30–60 minutes (IV) Pentazocine 50 0.5-1mg/kg Buprenorphine 0.3 milligram IV/IM every 6 h 0.01mg/kg/hr Tramadol 350
  28. 28. TRAMADOL MOA centrally acting analgesic relieves pain by opioid as well as additional mechanisms. • affinity for μ opioid receptor is low, while that for κ and δ is very low. • it inhibits reuptake of NA and 5-HT, and thus activates monoaminergic spinal inhibition of pain • Its analgesic action is only partially reversed by the opioid antagonist naloxone.
  29. 29. • Pharmacokinetics : oral bioavailability is good (oral: parenteral dose ratio is 1.4). The t½ is 5 hours and effects last for 4–6 hrs • Dose :Dose: 50–100 mg oral/i.m./slow i.v. infusion (children • 1–2 mg/kg) 4–6 hourly.Injected i.v. 100 mg tramadol is equianalgesic to 10 mg i.m. morphine; • USES ; Tramadol is indicated for mild-to-moderate short-lasting pain due to diagnostic procedures, injury, surgery, etc, as well as for chronic pain including cancer pain, but is not effective in severe pain • Tramadol causes less respiratory depression, sedation, constipation, urinary retention and rise in intrabiliary pressure than morphine
  30. 30. Patient-Controlled Analgesia • For patients who are awake and capable of drug self-administration, patient-controlled analgesia (PCA) can be an effective method of pain control, and may be superior to intermittent opioid dosing. The PCA method uses an electronic infusion pump that can be activated by the patient. When pain is sensed, the patient presses a button connected to the pump to receive a small intravenous bolus of drug. After each bolus, the pump is disabled for a mandatory time period called the “lockout interval,” to prevent overdosing. • When writing orders for PCA, you must specify the initial loading dose (if any), the lockout interval, and the repeat bolus dose. PCA can be used alone or in conjunction with a low-dose opioid infusion
  31. 31. Commonly Used Intravenous Opioids
  32. 32. Adverse Effects of Opioids 1. Respiratory Depression 2. Cardiovascular Effects (decreases in blood pressure and heart rate) 3. Decreased Intestinal Motility (a risk for aspiration pneumonia) 4. Nausea and Vomiting (stimulation of the chemoreceptor trigger zone ) 5. Other smooth muscles • Biliary tract ( spasm of sphincter of Oddi ) • Urinary bladder ( urinary urgency and difficulty in micturition ) • Bronchi (bronchoconstriction mediated by histamine ) • The triad of miosis, hypoventilation, and coma should suggest overdose with an opioid
  33. 33. PRECAUTIONS AND CONTRAINDICATIONS 1. Infants and the elderly are more susceptible to the respiratory depressant action of morphine. 2. It is dangerous in patients with respiratory insufficiency (emphysema, pulmonary fibrosis, cor pulmonale), sudden deaths have occurred. 3. Bronchial asthma: Morphine can precipitate an attack by its histamine releasing action. 4. Head injury: morphine is contraindicated in patients with head injury
  34. 34. PRECAUTIONS AND CONTRAINDICATIONS…… cont 5. Hypotensive states and hypovolaemia exaggerate fall in BP due to morphine. 6. Undiagnosed acute abdominal pain: morphine can aggravate certain conditions, e.g. diverticulitis, biliary colic, pancreatitis. Inflamed Appendix may rupture 7. Elderly male: chances of urinary retention are high. 8. Hypothyroidism, liver and kidney disease patients are more sensitive to morphine 9. Unstable personalities: are liable to continue with its use and become addicted.
  35. 35. NON-OPIOID ANALGESIA NSAIDS DRUGS FOR NEUROPATHIC PAIN
  36. 36. CLASSIFICATION OF NSAIDS
  37. 37. intravenous non-opioid analgesics • acetaminophen, • ketorolac, • Diclofenac sodium
  38. 38. Adverse effects
  39. 39. DRUGS for Neuropathic Pain • recommended drugs for neuropathic pain (e.g., from diabetic are • Gabapentin ( 600 mg every 8 hrs for gabapentin) • Pregabalin (75-150 mg PO OD ) • carbamazepine(100 mg every 6 hours for carbamazepine), • amitryptyline (10-25 mg OD )
  40. 40. Sedation in ICU
  41. 41. ANXIETY IN THE ICU • Anxiety and related disorders (agitation and delirium) are observed in as many as 85% of patients in the ICU • 1. Anxiety is characterized by exaggerated feelings of fear or apprehension that are sustained by internal mechanisms more than external events. • 2. Agitation is a state of anxiety that is accompanied by increased motor activity. • 3. Delirium is an acute confusional state that may, or may not, have agitation as a component. Although delirium is often equated with agitation, there is a hypoactive form of delirium that is characterized by lethargy
  42. 42. Sedation • Sedation is the process of relieving anxiety and establishing a state of calm 1. general supportive measures 2. drug therapy
  43. 43. Monitoring Sedation • The routine use of sedation scales is instrumental in achieving effective sedation • The sedation scales that are most reliable in ICU patients are the the Richmond Agitation-Sedation Scale (RASS) & Sedation- Agitation Scale (SAS)
  44. 44. Richmond Agitation Sedation Scale (RASS)
  45. 45. SEDATIVES in ICU  GABA-A RECEPTOR AGONISTS • Benzodiazepines • Propofol • Barbiturates  MAJOR TRANQUILLISERS  α2-AGONISTS
  46. 46. BENZODIAZEPINES • MOA : BZDs act by enhancing presynaptic/postsynaptic inhibition through a specific BZD receptor which is an integral part of the GABA A receptor–Cl¯ channel complex
  47. 47. BENZODIAZEPINES
  48. 48. ADVERSE EFFECTS • Side effects of hypnotic doses are dizziness, vertigo,ataxia, disorientation, amnesia, prolongation of reaction time— impairment of psychomotor skills • can aggravate sleep apnoea. • BZDs synergise with alcohol and other CNS depressants leading to excessive impairment • Concurrent use with sod. valproate has provoked psychotic symptoms
  49. 49. BENZODIAZEPINES Advantages • dose-dependent amnestic effect that is distinct from the sedative effect. The amnesia extends beyond the sedation period (antegrade amnesia), • anticonvulsant effects • sedatives of choice for drug withdrawal syndromes, including alcohol, opiate, and benzodiazepine withdrawal Disadvantages • (a) drug accumulation with prolonged sedation, and • (b) the apparent tendency for benzodiazepines to promote delirium. • Propylene Glycol Toxicity • Abrupt termination of prolonged benzodiazepine infusions can produce a withdrawal syndrome, characterized by agitation, disorientation, hallucinations, and seizures
  50. 50. PROPOFOL
  51. 51. PROPOFOL CHEMICAL NATURE 2,6diisopropylphenol , Propofol is highly lipophilic, and is suspended in a 10% lipid emulsion to enhance solubility in plasma Commercial Preparation 1% solution in an aqueous solution of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg phosphatide MOA selective modulator OF GABAA-Cl Channel complex DOSE •Propofol dosing is based on ideal rather than actual body weight, •Loading : 5μg/kg/min •Maintenance : 5-50 μg/kg/min •Loading doses are not advised in patients who are hemodynamically unstable (because of the risk of hypotension • no dose adjustment is required for renal failure or moderate hepatic insufficiency ONSET a rapid IV injection (<15 seconds), produces unconsciousness within about 30 seconds DURATION A single intravenous bolus of propofol produces sedation within 1–2 minutes, and the drug effect lasts 5–8 minutes METABOLISM + ELIMINATION Hepatic metabolism ,+ with extrahepatic clearance (pulmonary uptake and firstpass elimination, renal excretion) elimination halftime : 0.5 to 1.5 hours
  52. 52. CNS CEREBRO PROTECTIIVE EFFECT 1. decreases cerebral metabolic rate for oxygen (CMRO2), cerebral blood flow, and intracranial pressure (ICP). DECREASE IOP CVS 1. decreases in systemic blood pressure (relaxation of vascular smooth muscle produced by propofol is primarily due to inhibition of sympathetic vasoconstrictor nerve activity) : exaggerated in hypovolemic patients, elderly patients, and patients with compromised left ventricular function. Adequate hydration before rapid IV administration of propofol is recommended 2. negative inotropic effect : BradycardiaRelated Death RESPI Dosedependent depression of ventilation, with apnea HEPATIC does not normally affect , Prolonged infusions of propofol have been associated with hepatocellular injury RENAL •does not normally affect, •Urinary uric acid excretion is increased (may manifest as cloudy urine when the uric acid crystallizes in the urine under conditions of low pH and temperature ) : no adverse renal effects Prolonged infusions of propofol > excretion of green urine (presence of phenols in the urine.) : does not alter renal function
  53. 53. OTHER EFFECTS (Nonhypnotic Therapeutic Applications) 1. Antiemetic Effects (10 to 15 mg IV) followed by 10 μg/kg/minute More effective than ondansetron in preventing postoperative nausea and vomiting, effective against chemotherapyinduced Nausea and vomiting 2. Antipruritic Effects ((10 mg IV, is effective in the treatment of pruritus associated with neuraxial opioids or cholestasis) 3. Anticonvulsant Activity : 4. Attenuation of Bronchoconstriction 5. Analgesia : does not relieve acute nociceptive pain. 6. Coagulation : does not alter tests of coagulation or platelet function 7. Allergic Reactions (phenyl nucleus and diisopropyl side chain ) 8. potent antioxidant properties resemble endogenous antioxidant vitamin E SIDE EFFECTS respiratory depression and hypotension Anaphylactoid re-actions to propofol are uncommon but can be severe  green urine is observed occasionally from harmless phenolic metabolites lipid emulsion in propofol preparations can promote hypertriglyceridemia Propofol Infusion Syndrome (abrupt onset of bradycardic heart failure, lactic acidosis, rhabdomyolysis, and acute renal failure )
  54. 54. Propofol • Uses • Propofol has sedative and amnestic effects, but no analgesic effects • A single intravenous bolus of propofol produces sedation within 1– 2 minutes, and the drug effect lasts 5–8 minutes • Because of the short duration of action, propofol is given as a continuous infusion. When the infusion is stopped, awakening occurs within 10–15 minutes, even with prolonged infusions • Propofol was originally intended for short-term sedation when rapid awakening is desired (e.g., during brief procedures), but it is being used for longer periods of time in ventilator-dependent patients, to avoid delays in weaning from ventilatory support
  55. 55. • Propofol was originally intended for short-term sedation when rapid awakening is desired (e.g., during brief procedures), but it is being used for longer periods of time in ventilator- dependent patients, to avoid delays in weaning from ventilatory support • Propofol can be useful in neurosurgical patients and patients with head injuries because it reduces intracranial pressure and the rapid arousal allows for frequent evaluations of mental status
  56. 56. Dexmedetomidine • MOA = alpha-2 receptor agonist • has sedative, amnestic, and mild analgesic effects and does not depress ventilation • The most distinguishing feature of dexmedetomidine is the type of the sedation it produces
  57. 57. • Cooperative Sedation • The sedation produced by dexmedetomidine is unique because arousal is maintained, despite deep levels of sedation. Patients can be aroused from sedation without discontinuing the drug infusion, and when awake, patients are able to communicate and follow commands. When arousal is no longer required, the patient is allowed to return to the prior state of sedation • similar to temporary awakening from sleep. In fact, the EEG changes in this type of sedation are similar to the EEG changes in natural sleep
  58. 58. • Delirium • Clinical studies have shown a lower prevalence of delirium in patients who are sedated with dexmedetomidine instead of midazolam and based on these studies, dexmedetomidine is recommended over benzodiazepines for the sedation of patients with ICU-acquired delirium
  59. 59. [MIDEX trial] & propofol [PRODEX trial]) Conclusions: Among ICU patients receiving prolonged mechanical ventilation, dexmedetomidine was not inferior to midazolam and propofol in maintaining light to moderate sedation. Dexmedetomidine reduced duration of mechanical ventilation compared with midazolam and improved patients’ ability to communicate pain compared with midazolam and propofol.
  60. 60. Conclusion In mechanically ventilated ICU patients managed with individualized targeted sedation, use of a dexmedetomidine infusion resulted in more days alive without delirium or coma and more time at the targeted level of sedation than with a lorazepam infusion
  61. 61. Conclusions: From an economic point of view, dexmedetomidine appears to be a preferable option compared with standard sedatives for providing light to moderate ICU sedation exceeding 24 hours. The savings potential results primarily from shorter time to extubation
  62. 62.
  63. 63. Adverse Effects of DEXMEDETOMIDINE • dose-dependent decreases in heart rate, blood pressure, and circulating norepinephrine levels (sympatholytic effect) • Life-threatening bradycardia has been reported, primarily in patients treated with high infusion rates of dexmedetomidine (>0.7 µg/kg/min) together with a loading dose • Patients with cardiac conduction defects should not receive dexmedetomidine, and patients with heart failure or hemodynamic instability should not receive a loading dose of the drug
  64. 64. Haloperidol • MOA : first-generation antipsychotic agent • ACTIONS : • sedative and antipsychotic effects by blocking dopamine receptors in the central nervous system • no respiratory depression, and • hypotension is unusual in the absence of hypovolemia • Because haloperidol has a delayed onset of action, midazolam can be given with the first dose of haloperidol to achieve more rapid sedation
  65. 65. Intravenous Haloperidol for the Agitated Patient
  66. 66. Adverse Effects • (a) extrapyramidal reactions : (e.g., rigidity, spasmodic movements) are dose-related side effects of oral haloperidol therapy, but these reactions are uncommon when haloperidol is given intravenously (for unclear reasons) • (b) ventricular tachycardia : prolongation of the QT interval on the electrocardiogram, which can trigger a polymorphic ventricular tachycardia (torsade de pointes,) reported in up to 3.5% of patients receiving intravenous haloperidol • (c) neuroleptic malignant syndrome : idiosyncratic reaction to neuroleptic agents that consists of hyperpyrexia, severe muscle rigidity, and rhabdomyolysis
  67. 67. NMDA RECEPTOR ANTAGONIST : Ketamine • It produces a sedative state known as ‘dissociative anaesthesia’, with the following characteristics: • mild sedation • amnesia • analgesia • reduced motor activity Limitations: • Hallucinations, and delirium during the recovery/withdrawal Phase • Whole body catatonic state • Sudden shooting of BP
  68. 68. • Uses : LIMITED • sedation in severe asthmatics (for its bronchodilator effect), • In patients following head injury (for its effect at the NMDA receptor) • in patients where analgesia is difficult (e.g. extensive burns) • DOSE • 0.2-0.8 mg/kg IV over 2-3 min • 2-4 mg/kg IM
  69. 69. SEDATION STRATEGIES : Recent Aspects • Goal-directed sedation sedatives are freely adjusted (usually by the bedside nurse) to attain a prescribed level of sedation from a sedation scoring system • Patient-targeted sedation protocols a structured approach to the assessment of patient pain and distress, coupled with an algorithm that directs drug escalation and de-escalation based on the assessments • Daily interruption of sedation daily interruption of both sedative and analgesic infusions until the patient awakens or exhibits distress that mandates resumed drug administration
  70. 70. • Intermittent sedation Involves use of longer-acting sedative agents, typically lorazepam, given by intermittent bolus titrated via a sedation Scoring system • ‘analgosedation’ or analgesia-based sedation • Patient-controlled sedation
  71. 71. THE FUTURE • patient-controlled sedation • target-controlled infusions (TCI) in intensive care • automated/semiautomated sedation delivery systems • melatonergic agents for nocturnal sleep (e.g. ramelteon, valdoxane).
  72. 72. TAKE HOME MESSAGES : Improving the ICU Experience • Critically ill patients experience pain in situations that are not normally painful • Unrelieved pain can be a source of agitation, so make sure that pain is relieved before considering a sedative drug for agitation • When a benzodiazepine is used for prolonged (>48 hrs) sedation, attention to preventing drug accumulation and prolonged sedation can result in a shorter time in the ICU • Consider using dexmedetomidine for sedation, PARTICULARLY in ventilator dependant patients because this drug allows the patient to be aroused while still sedated (more like sleep than a drug-induced stupor) • Finally, communicate with patients (e.g., tell them what you are going to do before doing it), and allow some “down time” for patients to sleep
  73. 73. REFERENCES • Stoelting’s Pharmacology And Physiology In Anesthetic Practice - 5th Edition • Marino's The ICU Book, Fourth Edition - Marino, Paul L • Miller's Anesthesia 8TH EDITION • KD Tripathi - Essentials of Medical Pharmacology, 6th Edition • Tintinalli’s • Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit
  74. 74. THANK YOU

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