ANESTHESIA OVERVIEW

BASICANESTHESIA PRACTICE ANESTHESIA DEFINITION TRADITIONAL LOSS OF SENSATION WITH OR WITHOUT LOSS OF CONSCIOUSNESS MECHANISMS OF ACTION Interaction at cellular receptor site Action Intracellular Cortical depression 1. 2. 3. PAIN Pain is always subjective. Each individual learns the application of the word through experiences related in early life. I.A.S.P. International Association for Study of Pain Pain An unpleasant sensory and emotional experience associated with actual or potential tissue damage or injury, or described in terms of such damage or injury. ETIOLGY OF PAIN 1. 2. 3. 4. HEAT COLD CHEMICAL MECHANICAL TORSION STRETCH CUT PINCH PRICK COMPRESS CRUSH TYPOLOGY OF PAIN 1. 2. 3. Acute Chronic benign Chronic cancer Chronic Pain vs Acute Pain Acute: A Symptom of Injury or Disease Chronic Benign: Pain itself is the disease Chronic Cancer: Actual Tissue destruction Acute Pain A complex constellation of unpleasant sensory, perceptive and emotional experiences and certain associated autonomic psychological, emotional behavioral responses provoked by noxious stimulation. CHRONIC PAIN PAIN THAT PERSIST BEYOND USUAL COURSE OF HEALING (3 - 6 MONTHS) Adverse Effects of Pain 1. 2. 3. 4. Cardiovascular Pulmonary Gastrointestinal Renal 1. 2. 3. 4. Extremities Endocrine CNS Immunologic Adverse Effects of Pain Cardiovascular: Tachycardia, hypertension, increased SVR, increased cardiac work, increased myocardial O2 demand. Pulmonary: Hypoxia, hypercarbia, atelectasis, decreased cough, decreased vital capacity and function residual capacity, V/Q mismatch. Gastrointestinal: Nausea, vomiting, ileus, intolerance for oral intake. Renal: Oliguria, urinary retention. Adverse Effects of Pain Extremities: Skeletal muscle spasm, limited mobility, thromboembolism. Endocrine: Excessive adrenergic activity, vagal inhibition, catabolic metabolism, increased O2 consumption. CNS: Sedation, fatigue, anxiety, and fear cause central sympathetic stimulation. Immunologic: Inhibited cellular immunity, increased risk of infection, ?? impaired wound healing ?? FREE NERVE ENDINGS ARE PRESENT IN ESSENTIALLY ALL BODY TISSUES IN VARYING AMOUNTS IN RESPONSE TO A PAINFUL STIMULUS, SUBSTANCES ARE EXCRETED. ALGOGENIC (substances released by pain) SEROTONIN HISTAMINE BRADYKININS PROSTAGLANDINS NOREPINEPHRINE POTASSIUM ACETLYCHOLINE LEUKOTRIENES SUBSTANCE P29 THE RECEPTORS IN THE FREE NERVE ENDINGS RESPOND TO THE SUBSTANCES BY BECOMING CHARGED ELECTROCHEMICALY RECEPTORS THEN PROPAGATE AN ELECTROCHEMICAL STIMULUS TO DIFFERING NERVE FIBERS NOCICEPTION This electrochemical event that occurs between the site of tissue damage or injury sets off a series of neural transmissions that eventually results in the perception of pain……Collectively this known as nociception NERVE FIBER PAIN CLASSIFICATION A FIBER……..SHARP-STABBING-LOCAL “ FIRST PAIN” B FIBER....PHYSIOLOGIAL REACTION C FIBER....DULL-ACHE-BURN-THROB NONLOCALIZED-RADIATE “SECOND PAIN” NERVE FIBER CLASSIFCATION TYPE A a A alpha A beta A delta A gamma FUNCTION myelinated motor myelinated touch-pressure myelinated touch-pressure myelinated pain-temperature myelinated proprioception A Delta 1. 2. 3. 4. 5. 1 - 4 micrometers diameter Myelinated, Rapid conduction Sharp, localized Heat, cold “First pain” NERVE FIBER CLASSIFCATION TYPE B myelinated C non-myelinated FUNCTION preganglionic autonomic pain-temperature C Fibers 1. 2. 3. 4. Small Slow Conduction Unmyelinated Postganglionic autonomic C Fibers 1. 2. 3. 4. Dull pain, burning, Aching throbbing Nonlocalized - radiating - diffused Temperature,Touch,Mechanical “Second pain” Gate Theory Balance between A delta and C fibers to dorsal horn determines the intensity of the stimulus that is passed to higher brain center Area of High Nociceptor Concentration 1. 2. 3. 4. 5. 6. 7. Mucosal membranes Periosteum Deep fascia Ligaments Joint capsules Cornea Subcutaneous tissue Areas of Moderate Nociceptor Concentration 1. 2. 3. Skeletal muscle Cardiac muscle Smooth muscle Areas of Minimal Nociceptor Concentration 1. 2. 3. Bone Cartilage Marrow Physiologic Processes of Nociception 1. 2. 3. 4. 5. Detection Transduction Transmission Modulation Perception Detection 1. “First pain” “Second pain” 2. TRANSDUCTION NOXIOUS STIMULI TRANSLATED INTO ELECTRICAL FIRING AT THE SENSORY NERVE ENDINGS TRANSMISSION 1. 2. 3. 4. PROPAGATION OF IMPULSE TRAVELS VIA NEURAL PATHWAYS. SENSORY AFFERENT NEURONS PROJECT INTO THE SPINAL CORD ASCENDING NEURONS RELAY TO BRAINSTEM AND THALAMUS THALAMUS RELAYS TO CEREBRAL CORTEX MODULATION INTRINIC PAIN MODIFICATION 1.DIFFERENT IN INDIVIDUALS 2.DEPENDS ON..... PAST EXPERIENCES CULTURE PSYCHIC MODULATION-CONT 1. 2. 3. 4. 5. 6. 7. STIMULUS PRODUCED ANALGESIA NEUROENDOCRINE ANALGESIA CNS/PNS ANALGESIA OPIOID ANALGESIA SITUATION PATHOLOGY PHYSIOLOGY Modulation – Excitatory Substances 1. Peripheral Prostaglandins, bradykinins, histamine, K, substance P, serotonin (5HT2) 2. Spinal Glutamate, aspartate, amino acids, substance P, norepinephrine (alpha 1) Modulation - Inhibitory Supraspinal – Endorphins, enkephalins, dynorphins, norepinephrine (alpha 2), GABA, somatostatin (5HT1), neurotensin First Neuron Pain Peripheral afferent fibers to dorsal horn Second Neuron Pain Dorsal horn to thalamic Third Neuron Pain Thalamus to cortex IDEAL ANESTHETIC 1. SEDATION - HYPNOSIS 2. AMNESIA 3. ANALGESIA 4. MUSCLE RELAXATION 5. OBTUND REFLEXES 6. PHYSIOLOGICAL STABILITY 7. REVERSIBLE 8. ANTIEMETIC IDEAL COMPONENTS 1. 2. 3. 4. 5. 6. 7. Block SENSORY feeling Immobilize MOTOR responses Obtund REFLEXES wipe out MEMORY Control VC and CTZ Not permanent Cause sense of well-being DELIVERY METHODS 1. REGIONAL ( conduction) 2. INTRAVENOUS (systemic) 3. INHALATION (ventilatory) REGIONAL ANESTHESIA SEGMENTAL LOSS OF SENSATION BY BLOCKING NERVE CONDUCTION REGIONAL 1. SPINAL 2. EPIDURAL 4. INTRAVENOUS ( BIER ) 5. AXILLARY (INFILTRATION) 6. RETROBULBAR REGIONAL 1. 2. 3. PAIN RELIEF DIAGNOSTIC THERAPEUTIC LOCAL ANESTHETICS AMIDES  BUPIVACAINE  LIDOCAINE  ROPIVACAINE  MEPIVACAINE  PRILOCAINE MAX / DOSE 2 MG/KG 7 MG/KG 4 MG/KG 7 MG/KG 6MG/KG LOCAL ANESTHETICS ESTERS CHLOROPROCAINE COCAINE NOVOCAINE TETRACAINE MAX /DOSE 20 MG/KG 3 MG/KG 12 MG/KG 3 MG/KG REGIONAL ADDITIVES MUSCLE RELAXANTS NARCOTICS NON-STEROIDAL ANALGESICS GENERAL ANESTHESIA INDUCTION AGENTS INHALATION GASES INTRAVENOUS AGENTS BARBITURATES OPIOIDS BENZODIAZEPINES DIISOPROPYLPHENOL IMIDAZOLE INHALATION AGENTS 1. 2. 3. 4. 5. 6. NITROUS OXIDE HALOTHANE ETHRANE FORANE SUPRANE ULTANE MAC MINIMUM ALVELOAR CONCENTREATION 50% of the population will be anesthetized...and won’t move upon skin incision...or won’t jump with a clamp on their tail!!!!!!!!!!! MAC 1. 2. 3. 4. 5. 6. 7. MAC- INDUCTION MAC - INTUBATION MAC - INCISION MAC- MAINTENANCE MAC - AMNESIA MAC-BAR MAC-AWAKE UPTAKE AND DISTRIBUTION Blood:Gas Coefficient Solubility Higher Concentration to Lower INTRAVENOUS AGENTS 1. 2. 3. 4. 5. 6. 7. DISSOCIATIVE DRUGS BARBITUATES DIISOPROPYLPHENOL IMIDAZOLE TRANQUILZERS NARCOTICS NEUROLEPTICS (4 & 5 COMBINED) DISSOCIATIVE 1. 2. KETAMINE ARYLCYCLOHEXYLAMINE LSD PHENCYCLIDINE BARBITURATES 1. 2. THIOPENTHAL - PENTOTHAL METHOHEXITAL - BREVITAL DIISOPROPYLPHENOL  PROPOFOL IMIDAZOLE  ETOMIDATE BENZODIAZEPINES (TRANQUILIZERS) ATIVAN - LORAZEPAM  VERSED - MIDAZOPAM  VALIUM - DIAZEPAM  VISTARIL - HYDROXYZINE  Benzodiazepines 1. 2. 3. 4. 5. 6. Sedation Anxiolytic - anti anxiety Anticonvulsant Indirect muscle relaxation GABA Amnesia (No analgesia) Benzodiazepines Adverse Effects 1. CNS Increased sedation, ataxia,confusion, dizziness 2. Paradoxical excitation age extremes, agitation, anxiety, hallucinations 3. Respiratory depression Benzodiazepines Adverse Effects 1. 2. 3. 4. 5. Cardiovascular - P, BP Propylene glycol - rapid IV push Constipation Blurred vision Hiccups Benzodiazepine Reversal 1. 2. Romazicon - 0.2 mg up to 1 mg every 1 min. Withdrawal - seizures OPIOIDS MORPHINE  DEMEROL  FENTANYL  SUFENTA  ALFENTANIL  REMIFENTANIL  NON-STEROIDALS (TORADOL)  Opiate Receptor Functions  (mu) (kappa) (sigma) (delta) (epsilon) Supraspinal analgesia;  Respiratory depression;  Euphoria ,Physical dependence Analgesia, Sedation Dysphoria,Hallucinations Unknown Unknown Classification of Opioid Agonists and Antagonists Agonists Morphine Demerol Sufenta Alfenta Codeine Fentanyl Remifentanil Agonist-Antagonists Talwin Stadol Nubain Antagonists Narcan Naltrexone Opioid Adverse Effects 1. 2. 3. 4. Cardiovascular Respiratory GI GU NEUROLEPTIC COMBINATION OF NARCOTIC AND TRANQUILIZER ORIGINALLY..LYTIC COCKTAIL  2nd GENERATION...INNOVAR  3rd.GENERATION....PROPOFOL ..NARCOTIC..VERSED  ANTIEMETIC H1 BLOCKERS PHENOTHIAZINES BUTYROPHENONES H2 BLOCKERS 5-HT ANTAGONIST ONDANSETRON-ZOFRAN GRANISETRON –KYTRIL DOLISETRON - ANZEMET AMNESTICS 1. 2. 3. 4. SCOPALOMINE PROPOFOL VERSED NITROUS OXIDE MUSCLE RELAXANTS DEPOLORIZER (SHORT -ACTING) SUCCINYLCHOLINE NON-DEPOLORIZER (LONG - ACTING) MIVACURIUM CURARINE ROCURONIUM RAPALON PANCURONIUM VECURONIUM ATRACURIUM REVERSALS    NARCOTIC NARCAN BENZODIAZAMINE ROMAZICON MUSCLE RELAXANTS PYRIDOSTIGMINE PROSTIGMIN EDROPHONIUM PHYSOSTIGMINE T.I.V.A. TOTAL INTRAVENOUS ANESTHESIA 1. INDUCTION AGENT 2. TRANQUILER 3. AMNESTIC 4. ANALGESIC 5. MUSCLE RELAXANT BALANCED JUST ENOUGH OF ALL PHASES OF ANESTHESIA  INDUCTION MAINTENANCE EMERGENCE   INDUCTION  ANS SYMPATHETIC PARASYMPATHETIC  CARDIOVASCULAR BLOOD PRESSURE BLOOD VOLUME •BLOOD VOLUME ESTIMATING ALLOWABLE BLOOD LOSS (EABL) EABL = (HCTs -HCTa ) X EBV HCTs s = starting a = allowed Estimated Blood Volume PREMATURE INFANT CHILD MEN WOMEN 100 90 80 70 60 IDEAL WEIGHT=ht. in cm-100=kg 5 ft.=100 # +5# per in. F 5 ft.=100# + 7# per in. M OBESE CALCULATION IDE AL WEIGHT 5FT.=100 # FEMALE = 1 in = 5 # MALE = 1 in = 7.5 # OBESE WT. ADD TO IDEAL WEIGHT INDUCTION POSITION CHANGES PULSE RATE ARRYTHMIAS RENAL -1 CC/KG/HR TEMPERATURE ACID/BASE BALANCE RESPIRATORY RESPIRATION CALCULATIONS RESPIRATORY Vd Vt POX RMV ETCO2 PCO2 desired X RMVhave=PCO2 perfect PCO2 got RMVwant FLUID MANAGEMENT   FLUID THERAPY a) CRYSTALLOID b) COLLOID FLUID THERAPY a)NPO b) MAINTENANCE c) 3rd. SPACE LOSSES d) EBL 3:1 or 1:1 EPINEPHRINE DILUTION A)1:200,000= 5 mcg/ml=0.15 ml of 1:1000 in 30 cc’s of solution B)1:100,000=10 mcg/ml=0.30 ml of 1:1000 in 30 cc’s of solution C)1:300,000 = 3 mcg/ml=0.1 ml of 1:1000 in 30 cc’s of solution EPINEPHRINE 1. 2. CHILDREN.......10 MCG/KG ADULTS... HALOTHANE 1 MCG/KG ENFLURANE 3 MCG/KG DESFLURANE ? MCG/KG SEVOFLURANE ? MCG/KG MONITORED ANESTHESIA CARE 1. 2. 3. 4. 5. HISTORY/ PHYSICAL REQUIRED USUAL STANDARDS OF CARE COST OF SERVICE ALTERNATIVE CASE PLAN USUALLY THE SICKEST MONITORED ANESTHESIA CARE SEDATION-HYNOSIS ANALGESIA AMNESIA PHYSIOLOGICAL STABILITY REVERSIBLE http://www2.kumc.edu/instruction/sah/NurseAnesthesia/nura833/conscious.htm SIGNS - STAGES 1. 2. 3. 4. ANALGESIA EXCITEMENT SURGICAL MEDULLARY DEPRESSION KEY TERMS SECOND GAS EFFECT DIFFUSION HYPOXIA VENTILATORY RESPONSE TO CO2 HYPOXIA PULMONARY VASOCONSTRICTION PROTEIN BINDING IONIZATION PRETREATMENT - PRIMINING PREANESTHETIC VISIT 1. 2. 3. 4. 5. Patient education History & physical Surgeons or patient choice Informed consent Care Plan development PREANESTHETIC WORK-UP REVIEW: 1. CHART 2. LAB VALUES 3. EKG 4. X-RAYS PREANESTHETIC WORK-UP SYSTEMS REVIEW NEURO-MUSCULAR STATUS AIRWAY CARDIOPULMONARY RENAL ENDOCINE GASTROINTESTINAL ALLERGIES DRUG HISTORY History and Physical 1. 2. 3. 4. 5. AIRWAY……special needs SUBSTANCE ABUSE…withdrawal DIABETES…tight control REFLUX……..pretreat CARDIOVASCULAR…Goldman… pretreatment need, blood dyscrasia History and Physical 1. 2. 3. 4. 5. 6. 7. Malignant Hyperthermia Myo-neural problems Renal Liver….Enzymes..metabolism Gastrointestinal…electrolytes Endocrine……thyroid, steroids Herbal intake History and Physical Electrocardiogram         Atrial fib-flutter 1-2-3 ° Block AV disassociation PVCs-PACs ST segment…ischemia QT Interval Tall p….deep q W.P.W ANESTHESIA CARE PLAN INFORMED CONSENT