PAIN MANAGEMENT IN ICU -final Copy 1

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pain and sedation management in icu is very important to controle the hemidynamics stabe and to facilitate the early recovary and discharge

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PAIN & SEDATION MANAGEMENT IN ICU:

PAIN & SEDATION MANAGEMENT IN ICU DR.S.SREENIVASARAO MD,C.C.P.P.M, ASSIST PROFESSOR, DEPT.OF ANAESTHESIA, S.V.R.R.G.G.H.&S.V.M.C, TIRUPATI

DEFINITION OF PAIN ?:

DEFINITION OF PAIN ?

WHAT IS PAIN………?:

WHAT IS PAIN………? DEFINITION : “ An unpleasant sensory and emotional experience associated with actual or potential damage or described in terms of such damage” - International Association for the Study of Pain, 1979 PAIN IS SUBJECTIVE REACTION TO AN OBJECTIVE STIMULUS WHAT THE PATIENT SAYS – “HURTS”

5th vital sign……..:

5 th vital sign……..

PATHWAYS & PATHOPHYSIOLOGY:

PATHWAYS & PATHOPHYSIOLOGY

PATHOPHYSIOLOGY :

PATHOPHYSIOLOGY Pain: • Involves four physiological processes: - Transduction - Transmission - Modulation - Perception

PowerPoint Presentation:

PAIN PATHWAYS & PATHOPHYSIOLOGY ASCENDING DESCENDING Noxious stimulus Release of inflammatory substances (PG, Hst , Srn , Bdks , Sub.P ) Transduction Transmission Modulation Perception (Generation & electrical impulses) (conduction by nerve fibers) (Modification with spinal corel )

WHY WE ARE WORRIED ABOUT PAIN….?:

WHY WE ARE WORRIED ABOUT PAIN….? 30%-70% of patients are bothered by pain during their ICU stay 50% complain of moderate, severe, or excruciating pain Need to determine the etiology of pain, treat it, and eliminate potential barriers to adequate pain control

FACTORS – PAIN PERCEPTION:

FACTORS – PAIN PERCEPTION FEAR IN STRANGE SURROUNDINGS INABILITY TO REMEMBER OR UNDERSTAMD THE SITUATION ANXIETY & UNCERTAINITY ABOUT ONESELF,ONE’S FAMILY AND ABOUT PRESENT & FUTURE BACKGROUND AGGREVATIONS—NOICE,ALARMS ONGOING ACTIVITY THROUGH OUT THE NIGHT INABILITY TO COMMUNICATE LACK OF SLEEP FATIGUE AFTER SURGERY BOREDOM & LACK OF DISTRACTION

REASONS FOR PAIN IN ICU:

REASONS FOR PAIN IN ICU

REASONS FOR PAIN IN ICU……:

REASONS FOR PAIN IN ICU……

PowerPoint Presentation:

PAIN IN ICU……..

REASONS FOR PAIN IN ICU:

REASONS FOR PAIN IN ICU Primary pathology such as burns,traumatic injuries,fractures,wounds (surgical or traumatic) Complications of original condition or new problems such as bowel perforation,ichemic boel,pancreatitis Other symptoms such as abscesses,skin inflammation,wuond infection Support systems & monitoring— peripheral,central venous line insertions,catheters,drains,regulalar suctioning,dressing changes,phyaiotharapy Tissue hypoxia as a result of low cardiac output,low o2 saturation,fall in hb result in mi Painfull joints,pressure points,pain on changing,position in bed

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY………….?:

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY………….?

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY………….?:

WHAT HAPPENS IF YOU ARE NOT TREATED ADEQUATELY………….?

Management of pain:

Management of pain Assessment  Goal  Therapy

HOW TO ASSESS…….?:

HOW TO ASSESS…….?

Difficulty in pain assessment and management in ICU :

Difficulty in pain assessment and management in ICU  Unable to communicate effectively  Cognitive impairment  Sedation  Paralysis  Mechanical ventilation

HOW TO ASSESS…….?:

HOW TO ASSESS…….?

PowerPoint Presentation:

FASCIAL EXPRESSION Relaxed 1 Partially tightened (brow lowered) 2 Fully tightened (lid closing or tightened, cheek raised) 3 Grimacing (nose wrinkle, upper lip raise) 4 UPPER LIMBS No movement 0 Partially bent 1 Fully bent(fingers flexed),making a fist 2 Permanent retraction(even after stimulus removed) 3 COMPLIANCE WITH VENTILATOR Tolerating movement 0 Coughing ,but tolerating vent most of the times 1 Fighting vent,alarms high pressure,but settles down 2 Unable to controle vent,does not settle down,requires manual ventilation 3 MODIFIED BEHAVIORAL PAIN SCALE Choose the appropriate score from each of the three categories and add together to get the patient’s total score; maximum score is 10.

PAIN ASSESSMENT:

PAIN ASSESSMENT Unparalyzed patient with altered mental status: 0 Painful stimuli necessary to gain attention or solicit movement 1 No grimacing or guarding with spontaneous movement or repositioning 2 Grimacing or guarding with vigorous movement 3 Grimacing or guarding with slight movement, takes greater than 1 min for the patient to relax 4 Grimacing or guarding at rest; not able to relax despite rest

PAIN MAP:

PAIN MAP VAS—7/10 10-6-2012

METHODS OF DRUG ADMINISTRATION:

METHODS OF DRUG ADMINISTRATION

METHODS OF DRUG ADMINISTRATION:

METHODS OF DRUG ADMINISTRATION Oral Intramuscular Intravenous Per rectal-suppositories Subcutaneous-patches Oral Transmucosal-lolly pops Inhalational Nasal spray Regional blocks Epidural

ROLE OF PCA:

ROLE OF PCA

ROLE OF PCA:

ROLE OF PCA From: Rosenburg , Grande, Bernstein. Pain Management and Regional Anesthesia in Trauma . WB Saunders, 2000

DISPOSABLE PCA PUMPS :

DISPOSABLE PCA PUMPS

HOW TO MANAGE……?:

HOW TO MANAGE……? ANALGESIA ONLY ? SEDATION ONLY ? SEDOANALGESIA !!!!!!!!

ANALGESIA:

ANALGESIA

Principles of Sedation and Analgesia :

Principles of Sedation and Analgesia Consider individual patient characteristics when selecting analgesic and sedativemedications – Correct underlying conditions – Considering underlying metabolic/excretion capacities – Considering adverse effects of sedatives/ Analgeiscs

Principles of Sedation and Analgesia:

Principles of Sedation and Analgesia Using an algorithm or guideline to assist the practitioners Tools to assess sedative/pain status Prompting several questions related to patient characteristics When/how to do / what need to do

PowerPoint Presentation:

 Exclusion of treatable causes of discomfort  Exclusion of warning signs  Goal of sedation/ analgesia should be established  Priority of pain management is highlighted  Re-assessment of sedation/ analgesia  Analgesics are not 100% of sedatives, and vice versa

Guideline: Benefit! :

Guideline: Benefit!  Evidence-based; "best practice"  Standardize care  Reduce variability  Reduce complications  Can decrease costs

Principles of Pain Management :

Principles of Pain Management

Principles of Pain Management :

Principles of Pain Management Anticipate pain Recognize pain Ask the patient Look for signs Find the source Quantify pain / Assess the pain Set the goal Treat: Quantify the patient’s perception of pain Correct the cause where possible Give appropriate analgesics regularly as required Remember, most sedative agents do not provide analgesia Reassess………Reassess…………Reassess………… Reassess

SIGNS OF PAIN IN ICU:

SIGNS OF PAIN IN ICU Hypertension Tachycardia Lacrimation Sweating Pupillary dilation

ANALGESIA:

ANALGESIA PHARMACOLOGICAL OPIOIDS NSAIDS LOCAL ANAESTHETICS ALPHA2 AGONISTS NONPHARMACOLOGICAL

Nonpharmacologic Interventions :

Nonpharmacologic Interventions Proper position of the patient Stabilization of fractures Elimination of irritating stimulation Proper positioning of the ventilator tubing to avoid traction on endotracheal tube

OPIOIDS:

OPIOIDS

OPIOIDS:

OPIOIDS Activating opioid receptors in the midbrain & turning on the Descending inhibitory system Activating opiod receptors on the second order pain transmission cells to prevent the Ascending transmission of pain signals Activating opioid receptors at the central terminals of C fibers in the spinal cord Activating opioid receptors in the periphary to inhibit the activation of nociceptors & to inhibit cells that may release inflmmatoy mediators

OPIOIDS:

OPIOIDS BENEFITS Relieve pain or the sensibility to noxious stimuli Sedation trending toward a change in sensorium , especially with more lipid soluble forms including morphine and hydromorphone . RISKS Respiratory depression NO amnesia Pruritus Ileus Urinary retention Histamine release causing venodilation predominantly from morphine Morphine metabolites which accumulate in renal failure can be analgesic and anti-analgesic. Meperidine should be avoided due to neurotoxic metabolites which accumulate, especially in renal failure, but also produces more sensorium changes and less analgesia than other opioids

OPIOID ANALGESICS:

OPIOID ANALGESICS CLASSIFICATION AGONIST AGONIST -ANTAGONIST MORPHINE PENTAZOCINE CODEINE,OXYCODONE BUTORPHANOL DIHYDROCODEINE NALBUPHINE OXYMORPHONE DEZOCINE PETHIDINE ,METHADONE MEPTAZINAL HYDROMORPHONE FENTANYL PARTIAL AGONIST DIAMORPHINE(HEROIN) BUPRENORPHINE TRAMADOL TAPENTADOL ANTAGONIST NALOXONE NALTREXONE

PowerPoint Presentation:

From: Marino. The ICU Book, 2 nd Ed. Lippincott Williams & Wilkins, 1998 .

Methods of Analgesia: PCA :

Methods of Analgesia: PCA

Methods of Analgesia: Epidurals :

Methods of Analgesia: Epidurals

NSAIDS:

NSAIDS

NSAIDS:

NSAIDS Salicylates -Aspirin p-amino phenol derivatives - Paracetamol Propionic acid derivatives- Ibuprofen Acetic acid derivatives- Indomethacin, Diclofenac,Ketorolac Oxicam derivatives- Piroxicam ,Meloxicom Fenamic acid derivatives- Mefeamic acid Cox-2 inhibitors- Celecoxib ,Valdecoxib Sulphonanilides- Nimmesulide Others- Licofelone

RISK STRATAGY WITH NSAID:

RISK STRATAGY WITH NSAID IF ORAL NSAIDS ARE TAKEN FOR 2 MONTHS RISK OF ENDOSCOPIC ULCER IS 1 IN 5 SYMPTAMATIC ULCER IS 1 IN 70 BLEEDING ULCER IS 1 IN 150 DEATH FROM BLEEDING ULCER 1 IN 1300 TEXT BOOK OF PAIN,WALL&MELZACKS,CHAPTER30

PARACETAMOL:

PARACETAMOL Central antinociceptive effect & potential mechanisms for this include inhibition of a CNS COX-2 Inhibition of a central cyclooxygenase ‘COX-3’ that is selectively susceptible toparacetamol , Modulation of inhibitory descending serotinergic pathways Prevent PG production at the cellular transcriptional level, independent of cyclooxygenase activity 1 . Piguet V et al. Eur J Clin Pharmacol 1998;53:321-4. 2. Carlsson KH et al. Pain 1988;32:313-26. 3. Flower RJ et al. Nature 1972;240:410-1. 4. Tjølsen A et al. Eur J Pharmacol 1991;193:193-201. 5. Pélissier T et al. JPET 1996;278:8-14.

PowerPoint Presentation:

PARACETAMOL Activation of opioid receptors

PARACETAMOL METABOLISM:

PARACETAMOL METABOLISM ( N- acetylbenzoiminoquinone ) Metabolism of acetaminophen (Ac) to hepatotoxic metabolites. (GSH, glutathione; GS, glutathione moiety; Ac*, reactive intermediate.)

PowerPoint Presentation:

Paracetamol safety benefits No centrally mediated side-effects 1 (e.g. sedation, constipation, nausea, vomiting, respiratory depression) No effect on platelet aggregation , bleeding , or uric acid excretion 2 No gastrointestinal side effects 3 Good renal 4 and hepatic 5 safety Few contra-indications and drug interactions 1. Lechat P et al. Thérapie 1989;44:337-54. 2. Insel PA. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Goodman & Gilman eds. ,The pharmacological basis of therapeutics. McGraw Hill, 9th edition, 1996:617-57. 3. Singh G. Am J Therapeut 2000;7(2):115-21. 4. Whelton A. Am J Therapeut 2000;7(2):63-74. 5. Whitcomb DC et al. JAMA 1994;272(23):1845-50. .

DOSAGE:

DOSAGE ADULTS- 1GM UP TO 4 TIMES DAILY,MINIMUM INERVAL BETWEEN EACH ADMINISTRATION IS 4 HRS (6HRS IN RENAL,HEPATIC IMPAIREMENT) CHILDREN UPTO 33KG—15MG/KG 4 TIMES A DAY, INTERVAL IS 6 HRS, MAX DAILY DOSE NOT EXCEEDING 60MG/KG IN NEONATES LESS THAN 10 DAYS 7.5MG/KG,4 TIMES A DAY

LOCAL ANAESTHETICS:

LOCAL ANAESTHETICS ACTION—BLOCK THE Na CHANNELS –IMPULSE CONDUCTION ROUTES—ORAL,INFILTRATION,SPINAL,EPIDURAL,SC PATCHES,TOPICAL etc A MAJOR DRAWBACK ANALGESIA TREATMENT IS TACHYPHYLAXIS DRUGS—LIGNOCAINE,BUPIVICAINE TOXIC EFFECTS –CNS & CVS

Serratiopeptidase :

Serratiopeptidase Serratiopeptidase or serrapeptase is a protein ( proteolytic ) enzyme isolated from the non-pathogenic enterobacteria Serratia E15 found in silkworms Swelling caused by inflammation can cause tissue to press against sensitive nerves and cause pain. Serratiopeptidase’s ability to reduce and drain fluid from the inflamed area can reduce swelling and pain. Serratiopeptidase also reduces pain through its ability to block the release of pain-inducing amines from inflamed tissues. Unlike NSAID pain medications, serratiopeptidase does not cause dangerous internal bleeding nor is it addictive like many pain medications

MISCELLANEOUS:

MISCELLANEOUS VASODILATORS - RAYNAUD’S PHENOMENON BUERGERS DISEASE,CRPS etc DRUGS ARE NIFEDIPINE,XANTHINOL NICOTINATE,PENTOXYPHYLLINE MUSCLE RELAXANTS ACUTE MUSCLE SPASM, FIBROMYALGIA,NOCTURNAL LEG CRAMPS DRUGS ARE- TIZANIDINE,BACLOFEN,DANTROLENE,DIAZEPAM

sedation:

sedation

NEED FOR SEDATION:

NEED FOR SEDATION ANXIETY PAIN ACUTE CONFUSIONAL STATE MECHANICAL VENTILATION TREATMENT OF DIAGNOSTIC PROCEDURES PSYCHOLOGICAL RESPONSE TO STRESS

GOALS OF SEDATION:

GOALS OF SEDATION PATIENT COMFORT CONTROLE OF PAIN ANXIOLYSIS AND AMNESIA BLUNTING ADVERSE AUTONOMIC AND HEMODYNAMIC RESPONSES FACILITATE NURSING MANAGEMENT FACILITATATE MECHANICAL VENTILATION AVOID SELF EXTUBATION REDUCE OXYGEN CONSUMPTION

IDEAL SEDATION AGENT:

IDEAL SEDATION AGENT LACK OF RESPIRATORY DEPRESSION ANALGESIA RAPID ONSET, TITRABLE, SHORT ELIMINATION HALF-TIME SEDATION WITH EASE OF ORIENTATION & AROUSABILITY ANXIOLYTIC HEMODYNAMIC STABILITY

CHALLENGES OF ICU SEDATION:

CHALLENGES OF ICU SEDATION ASSESSMENT OF SEDATION ALTERED PHARMACOLOGY TOLERANCE DELAYED EMERGENCE WITHDRAWAL DRUG INTERACTION

Before starting drugs…….:

Before starting drugs……. When patients exhibit signs of anxiety or agitation, the first priority is to identify and treat any underlying physiological disturbances, such as hypoxemia, hypoglycemia, hypotension, pain, and withdrawal from alcohol and other drugs. Sedation of agitated critically ill patients should be started only after providing adequate analgesia and treating reversible physiological causes. (Grade C)

PowerPoint Presentation:

Assessment  Goal  Therapy

ASSESSMENT OF SEDATION:

ASSESSMENT OF SEDATION

An ideal sedation scale :

An ideal sedation scale Good reliability and validity D etermination of the degree of sedation and agitation, B ehavioral descriptors, Applicability R equire minimal training E asy to score For diverse patient population G uide the titration of therapy to a defined sedation endpoint

Subjective methods :

Subjective methods The Ramsay Scale The Glasgow Coma Scale modified by Cook and Palma, GCSC The Sedation Agitation Scale, SAS The Richmond Agitation and Sedation Scale, RASS The Bloomsbury sedation scale the Adaptation to the Intensive Care Environment (ATICE) scale The Avripas sedation scale the Comfort scale for pediatric patients.

Objective methods :

Objective methods Pharmacokinetic methods Physiologic parameters lower oesophageal sphincter contractility measurement heart rate variability measurement Neurophysiologic methods Frontalis muscle electromyograms auditory evoked potentials, AEP Electroencephalography, EEG Bispectral Index, BIS Patient State Index, PSI Entropy Narcotrend

PowerPoint Presentation:

The Ramsay Scale Scale Description 1 Anxious and agitated or restless, or both 2 Cooperative, oriented, and tranquil 3 Response to commands only 4 Brisk response to light glabellar tap or loud auditory stimulus 5 Sluggish response to light glabellar tap or loud auditory stimulus 6 No response to light glabellar tap or loud auditory stimulus

The Riker Sedation-Agitation Scale :

The Riker Sedation-Agitation Scale Score Description Definition 7 Dangerous agitation Pulling at endotracheal tube, trying to strike at staff, thrashing side to side 6 Very agitated Does not calm despite frequent verbal commands, biting ETT 5 Agitated Anxious or mildly agitated, attempting to sit 4 Calm and cooperative Calm, awakens easily, follows commands 3 Sedated Difficult to arouse, awakens to verbal stimuli, follows simple commands 2 Very sedated Arouse to physical stimuli, but does not communicate spontaneously 1 Unarousable Minimal or no response to noxious stimuli

SAS, Sedation-Agitation scale :

SAS, Sedation-Agitation scale Stratification of agitation in more categories than the Ramsay scale

Bloomsbury Sedation Scale :

Bloomsbury Sedation Scale Clinical Status Score agitated and restless 3 awake and uncomfortable 2 aware but calm 1 roused by voice, remains calm 0 roused by movement or stimuli -1 roused by painful stimuli -2 Unrousable -3 natural sleep A Recommendations for dosing sedatives reliability not tested

GCSC, Glasgow Coma Scale modified by Cook and Palma:

GCSC, Glasgow Coma Scale modified by Cook and Palma useful in mechanically ventilated patients Absence of agitation scoring Unuseful to monitor sedation in agitated patients

ATICE, the Adaptation to the Intensive Care Environment scale :

ATICE, the Adaptation to the Intensive Care Environment scale

Avripas sedation scale :

Avripas sedation scale the predetermined standardized sedation goals based on the patient’s weaning classification

Goal :

Goal Mechanical ventilation Pressure support ventilation, CPAP, SIMV good p’t cooperation Ramsay 2, GCSC 13-15, SAS 4, RASS 0 Assisted controlled Ramsay 3, GCSC 8-12, SAS 3, RASS -1~-3 Pressure controlled Ramsay 4-5, GCSC 8-12, SAS 2, RASS -4 Agitation and delirium Ramsay 2-3, SAS 3-4, RASS 0~-2 IICP Ramsay 5, SAS 1, RASS -5

Sedation :

Sedation Causes for Agitation Sedatives

Undersedation :

Undersedation Sedatives Causes for Agitation Agitation & anxiety Pain and discomfort Catheter displacement Inadequate ventilation Hypertension Tachycardia Arrhythmias Myocardial ischemia Wound disruption Patient injury

Oversedation :

Oversedation Causes for Agitation Sedatives Prolonged sedation Delayed emergence Respiratory depression Hypotension Bradycardia Increased protein breakdown Muscle atrophy Venous stasis Pressure injury Loss of patient-staff interaction Increased cost

Choose the Right Drug :

Choose the Right Drug Benzodiazepines Propofol Brbiturates Ketamine  -2 agonists

Sedation Options: Benzodiazepines (Midazolam and Lorazepam) :

Sedation Options: Benzodiazepines ( Midazolam and Lorazepam ) Pharmacokinetics/dynamics Lorazepam : onset 5 - 10 minutes, half-life 10 hours, glucuronidated Midazolam : onset 1 - 2 minutes, half-life 3 hours, metabolized by cytochrome P450, active metabolite (1-OH) accumulates in renal disease Benefits Anxiolytic Amnestic Sedating

Risks :

Risks Delirium NO analgesia Excessive sedation: especially after long-term sustained use Propylene glycol toxicity ( parenteral lorazepam ): significance uncertain - Evaluate when a patient has unexplained acidosis - Particularly problematic in alcoholics (due to doses used) and renal failure Respiratory failure (especially with concurrent opiate use) Withdrawal

Propofol :

Propofol Pharmacology: GABA agonist Pharmacokinetics/dynamics: onset 1 - 2 minutes, terminal half-life 6 hours, duration 10 minutes, hepatic metabolism Benefits Rapid onset and offset and easily titrated Hypnotic and antiemetic Can be used for intractable seizures and elevated intracranial pressure

Risks :

Risks Not reliably amnestic , especially at low doses NO analgesia! Hypotension Hypertriglyceridemia ; lipid source (1.1 kcal/ml) Respiratory depression Propofol Infusion Syndrome - Cardiac failure, rhabdomyolysis , severe metabolic acidosis, and renal failure - Caution should be exercised at doses > 80 mcg/kg/min for more than 48 hours - Particularly problematic when used simultaneously in patient receiving catecholamines and/or steroids

PowerPoint Presentation:

Onset Peaks Duration Propofol 30-60 sec 2-5 min short 3-5  g/kg/min antiemetic 5-20  g/kg/min anxiolytic 20-50  g/kg/min sedative hypnotic >100  g/kg/min anesthetic

Medications for Sedation :

Medications for Sedation Barbiturates Infusion doses are subhypnotic Thiopental: 1-5 mg/min Methohexital : 0.5-2.5 mg/min Prolonged infusion of methohexital is associated with a more rapid recovery than thiopental because the clearance rate of methohexital is 3-4x’s higher, resulting in a shorter elimination half-life

Medications for Sedation :

Medications for Sedation Ketamine Low dose infusions (5-25 mcg/kg/min) effective for sedation in the ICU and for local or regional anesthetic procedures Significantly decreases the opioid analgesic requirement when used for ICU sedation Effective for burn care May need to pretreat with a benzodiazepine

Task Force of the American College of Critical Care Medicine - 1995 :

Task Force of the American College of Critical Care Medicine - 1995 Recommendations: Sedation Midazolam and propofol for short term (<24 hours) Lorazepam for long term Analgesia MSO 4 for most patients Fentanyl for hemodynamically unstable patients

Medications for Sedation: Infusion :

Medications for Sedation: Infusion From: Marino. The ICU Book, 2 nd Ed. Lippincott Williams & Wilkins, 1998.

SEDOANALGESIA:

SEDOANALGESIA

Alpha2 agonists:

Alpha2 agonists

ALPHA 2 RECEPTORS:

ALPHA 2 RECEPTORS A lpha 2A adrenoceptor subtypes appears to couple in an inhibitory fashion to the L-type calcium channel in the locus coeruleus I n the vasculature, the alpha 2B adrenoceptor subtype couples in an excitatory manner to the same effector mechanism . Activation of the receptors in the brain and spinal cord inhibits neuronal firing, causing hypotension, bradycardia , sedation, and analgesia. anesthesiologic viewpoint, neuronal hyperpolarization is a key element in the mechanism of action of α 2 -adrenoceptor agonists

PowerPoint Presentation:

Presynaptic activation of the α 2 adrenoceptor inhibits the release of norepinephrine , terminating the propagation of pain signals Postsynaptic activation of α 2 adrenoceptors in the central nervous system (CNS) inhibits sympathetic activity and thus can decrease blood pressure and heart rate. Combined, these effects can produce analgesia, sedation, and anxiolysis

NECHANISM OF ACTION:

NECHANISM OF ACTION Activation of G 1 -protein-gated potassium channels results in membrane hyperpolarization , decreasing the firing rate of excitable cells in the CNS. Direct regulation of calcium entry through N-type voltage-gated calcium channels ( independent of cAMP and protein phosphorylation & is mediated by G 0 proteins.) results reduction of calcium conductance into cells, thus inhibiting neurotransmitter release These 2 mechanisms represent 2 very different ways of effecting analgesia: ---- in the first, the nerve is prevented from ever firing, and ---- in the second, it cannot propagate its signal to its neighbor.

supraspinal:

supraspinal Highest densities of α 2 receptors has been detected in the locus coeruleus , the predominant noradrenergic nucleus in the brain and an important modulator of vigilance. The hypnotic and sedative effects of α 2 -adrenoceptor activation have been attributed to this site in the CNS The locus coeruleus is also the site of origin for the descending medullospinal noradrenergic pathway, known to be an important modulator of nociceptive neurotransmission. In this region of the brain, α 2 -adrenergic and opioidergic systems have common effector mechanisms, indicating that dexmedetomidine has a supraspinal site of action.

spinal:

spinal It stimulate α 2 receptors directly in the spinal cord, thus inhibiting the firing of nociceptive neurons The substantia gelatinosa of the dorsal horn of the spinal cord contains receptors , When stimulated, inhibit the firing of nociceptive neurons stimulated by peripheral Aδ and C fibers And also inhibit the release of the nociceptive neurotransmitter substance P

PowerPoint Presentation:

In the heart , the dominant action of alpha-2 agonists is a decrease in tachycardia (through block of the cardio-accelerator nerve) and bradycardia (through a vagomimetic action ). In the peripheral vasculature there is both a vasodilatory action via sympatholysis and vasoconstriction mediated through the receptors in the smooth muscle cells . The mechanism for both the anti-shivering and diuretic actions have yet to be firmly established.

Hemodynamic effects:

Hemodynamic effects Combination of effects mediated by: Reduction of central SNS activity (alpha-2a) Reduction of presynaptic NE release (alpha-2a and c) Stimulation of VSM cells (alpha-2b) Stimulation of endothelium Stimulation of central imidazoline receptors Some vagomimetic activity

Effects of Alpha-2 Agonists :

Effects of Alpha-2 Agonists Endocrine  NE release  insulin release  cortisol release  GH release Baroreflexes stay intact (reset) Normal response to vasoactive drugs Attenuates stress response

Effects of Alpha-2 Agonists :

Effects of Alpha-2 Agonists No effect on ICP Reduces IOP No effect on relaxants Prolongs local anesthetic action Decreases metabolism Decreases oxygen consumption

Side Effects:

Side Effects Sinus pause/arrest Orthostatic hypotension/Rebound hypertension on withdrawal Dry mouth Vasoconstriction

Dexmedetomidine:

Dexmedetomidine An intravenous anesthetic agent Selective α 2 receptor agonist. ( 2 : 1 1620:1) Provides -Sedation - Anxiolysis -Analgesia

:

107 Mechanism of Action of Dexmedetomidine NE release decreased SEDATION, SYMPATHOLYSIS Binding on alpha2 receptor ANALGESIA Inhibit Firing rate & Substance P release ANALGESIA

PHARMACOLOGICAL POFILE:

PHARMACOLOGICAL POFILE Rapid redistribution: 6 min Elimination half-life: 2 h Protein binding: 94% Metabolism: biotransformation in liver to inactive metabolites + excreted in urine No accumulation after infusions 12-24 h Pharmacokinetics similar in young adults + elderly

SPECIAL CONSIDERATIONS:

SPECIAL CONSIDERATIONS Hypovolemic patients With other vasodilators or negative chronotropic agents dexmedetomidine have an additive effect With renal or hepatic impairment, metabolites may accumulate and dose reductions may be necessary

Contraindications:

Contraindications In obstetric procedures , cesarean section deliveries, as the safety has not been studied Patients with pre-existent severe bradycardia and related bradydysrhythmias (advanced heart block) Patients with impaired ventricular functions (ejection fraction <30%). Infusion over 24 hours ???

Administration of Dexmeditomidine:

Administration of Dexmeditomidine Loading dose 1µg/kg 0.5ml[50µg] diluted as10ml ×10min. Maintenance 0.3-0.6µg/kg/hr 1.5ml[150µg] diluted in 500ml NS solution conc-0.3µg/ml infusion-16 to32drops/min Recovery 10-12mins after cessation.

SEDOANALGESIA:

SEDOANALGESIA Opioid + Hypnotic Infusion Fentanyl + Midazolam or Propofol Analgesia Amnesia Anxiolysis Hypnosis

PowerPoint Presentation:

Possibility of verbal / nonverbal communication with the critically ill patient No Pain Yes No Assessment with VAS / NRS Exlusion of treatable causes of discomfort OPIOIDS Aim: VAS < 30 / NRS < 3 Assessment with sedation scale Re-assessment after 10-15 minutes Adjustment opioids Re-assessment after 10-15 minutes VAS < 30 / NRS < 3 Re-assessment with VAS / NRS (at least every 4 hours except night) SEDATIVES Aim: short wake-up times Agitation Painful behavior Coma Assessment with sedation scale Exclusion of treatable causes of agitation OPIOIDS, Aim: reduced agitation Behavioral pain scale Assessment with GCS&Sedation scale Consider wake up test Regular assessment (at least every 4 hours Re-assessment after 10-15 minutes Adjustment opioids Re-assessment after 10-15 minutes Re-assessment with sedation scale (at least every 4 hours except night or wake-up test every 24 hours) Ajustment sedatives (and opioids ) yes Decision tree for analgesia and sedation in critically ill patients.

Overview of SCCM Algorithm :

Overview of SCCM Algorithm Jacobi J, Fraser GL, Coursin D, et al. Crit Care Med. 2002;30:119-141.

PowerPoint Presentation:

The Journal of TRAUMA Injury, Infection, and Critical Care Guidelines for Sedation and Analgesia During Mechanical Ventilation General Overview, J Trauma. 2007;63:945–950.

SEDOANALGESIA !!!!!!!!!!:

SEDOANALGESIA !!!!!!!!!! PATIENT IN ICU SEDATION ANALGESIA

THANK YOU ………:

THANK YOU ………

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