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Larynx: (Vagus) Pulmonary Lung Compliance Chest Wall ComplianCO has a 200-250 X greater affinity for HgB than O2 Motor: External Superior Laryngeal = Cricothyroid Peds ↓  (d/t  ↓  #  alveoli...

Larynx: (Vagus) Pulmonary Lung Compliance Chest Wall ComplianCO has a 200-250 X greater affinity for HgB than O2 Motor: External Superior Laryngeal = Cricothyroid Peds ↓  (d/t  ↓  #  alveoli) ↑ (stim of SLN = laryngospasm) Geri ↑ ↓ Recurrent Laryngeal = everything else 4 ways CO2 is carried in Blood: Sensory: Internal Superior Laryngeal = Above Vocal Cords & Cords V/Q Alveolar V/Q = 4/5 = 0.8 [MV/CO] 1. Physically dissolved (5%) Recurrent Laryngeal = Below Vocal cords PaO2 size V/Q = 10/0 = ∞ = dead space 2. Carbonic Acid (Theta >Alpha >Beta Allodynia: perception of an ordinarily non-painful stimulus 4.  ↑  Skin  Tem   Frequency: Beta > Alpha > Theta > Delta as pain 5. Anhydrosis (lack of sweating on face) Hyperpathia is a combined disorder consisting of hyperesthesia, 6. Nasal Congestion Gamma: high-order activity like problem solving (> 25yo) allodynia, and hyperalgesia Mu: beta wave variant- seen over motor areas- amplitude ½ of beta Bier Block Lambda: awake patient that is staring, reading or looking @ objects Neurochemical mechanisms of pain involve different NT: Minimum tourniquet time = 15-20 mins or 20-40 Sub P, Bradykinins & serotonin released → arachononic acid Lidocaine 0.5% or Prilocaine 0. 5% -40 – 50ml GA:    ↓  high  frequency  in  Beta  waves released = thromboxane, prostaglandins & leukotrines No bupivacaine- ♥  tox  or  chloroprocaine- thrombophlebitis ↑  low  frequency  in  delta  &  theta  waves 300 torr or 2.5 times the SBP Preganglionic Parasympathetic Nerves originate: Contraindicated: severe crush injuries, uncontrolled hypertension Surgical stimulation  or  light  anesthesia:  ↑  high frequency, low voltage Cranial nerves III, VII, IX, & X 3,7,9,10 craniosacral Raynaud's disease PVD, Homozygous sickle cell activity Sacral segments S2-S4 Right Hand: Pronated Supinated Cerebral compromise & deep anesthesia: low frequency, high voltage Weak Acids: (Thiopental, other barbit, [+ Charge/ Na+, Mg++], activity Proton Donor 1 = Ulnar 2 Acid + Acid = unionized 2 = Median 1 2 Sevo & Enflurane: can accentuate epileptic activity 3 = Radial - - Isoelectric 1.5-2.0 MAC Weak Base: (LA, ketamine, opiods, benzos) [- Charge/ Cl , SO4 ] 3 1 3 Barbiturates, etomidate, and propofol = burst suppression Proton Acceptor Nerves that Flex the Forearm: Ketamine, opioids and etomidate- do not produce a Δ in latency & Base + Base = unionized Musculocutaneous amplitude Radial Ionized = H2O soluble Spinal Cord: Non-Ionized – lipid soluble (crosses BBB) The Radial Nerve innervates Sensory – Afferent – Dorsal Horn S.A.D -Posterior Potency = lipid solubility Extension @ elbow, supination of FA, extension of wrist & fingers Motor – Efferent – Ventral Horn Anterior Duration = protein binding & solubility Damage = inability to ABDUCT thumb & wrist drop MMEP: Peripheral- popliteal, Central- anterior Speed of Onset = pKa Preganglionic SNS – Intermediolateral Horn Fetus  pH  <  maternal  pH  =  ↑  ion  trapping   The median nerve innervates: Pronation of FA, flexion of wrist Dorsal-Lemniscal (Sensory): Damage ↓amplitude mcg/ml S/S of Lidocaine Toxicity To thumb, index finger, middle finger & lateral ring finger SSEP Monitoring (posterior spinal arteries) ↑  latency 3 Circumoral Numbness(non CNS- d/t extracellular extravasation) Innervates the medial aspects of FA Touch, pressure, vibration 4 Lightheadedness Pronator teres 6 Visual Disturbances Flexor carpi radialis Dorsal (posterior) cord – Cuneatus & Gracilis tracts 8 Muscular Twitching Palmaris longus Ascend ipsilateral side 10 Unconsciousness Flexor digitorum superficialis Decussate @ brainstem to contralateral thalamus & sensory 12 Convulsions Damage = inability to ADDUCT thumb & Ape Hand cortex 15 Coma Also goes to RAS where it percolates to sensory cortex 20 Respiratory Arrest Somewhat sensitive The ulnar nerve innervates: 26 Card iovascular Collapse (widen QT precedes) Flexion of wrist, adduction of all fingers Tibial – electrodes midline scalp, Ulnar- electrodes lateral The little finger & medial ring finger (C8) Blood flow highest to lowest- loss of LA d/t vascular reabsorb In the forearm: Visual evoked potential- CN II- very sensitive to IA In Intravenous Flexor carpi ulnaris BAEP – CN VIII- barely sensitive (altered most by temp) Time Tracheal Medial ½ of flexor digitorum profundus Ketamine,  etomidate,  &  opioids,  barbs,  propofol  =  no  Δ  in  latency  or   I Intercostal And in the hand: amplitude in SSEP Can Caudal Palmaris brevis muscle Please Paracervical Abductor digiti minimi Ascending Pain (Anterolateral): Everyone Epidural Flexor digiti minimi Lateral Spinothalamic Tract (neopalatine) But Brachial Plexus Damage = Claw hand A- Fibers – Myelinated,  Fast  “first”  Pain  &  temp Susie & Spinal Innervates the adductor pollicis of the thumb Rexed’s  lamina  I  &  V, dorsal horn Sally Subcutaneous Neurotransmitter - glutamate Musculocutaneious C Fibers – Unmyelinated,  Slow  “dull”  Pain  &  temp Brachial Plexus: Flexion @ elbow Rexed’s  lamina  II (substantia gelatinosa) & III, dors Neurotransmitter – substance P Musculocutaneous Nerve Median Nerve Nerves of Lower Extremity Interneurons go from II & III to V Axillary Artery Femoral Sciatic Epidural steroids Ulnar Nerve Both fibers ascend or descend in the tract of Lissauer 1-3 segmnt Saphenous Common Peroneal Tibial Both fibers decussate and ascend on the contralateral side. Radial Nerve Deep peroneal superficial peroneal Sural Five factors that alter the latency and/or amplitude of SSEP: Right Foot: 4 1. Cerebral perfusion 20 hypotension, PaCO2, ICP “Robert  Taylor  Drinks  Cold  Beer”  =  Root,  Trunk,  Division,  Cord,  Branch 2. Cerebral hypoxia 1 = Tibial Sciatic R T D C R 3. Hypothermia (MOST) C5 superior lateral musclecutanous 2 = Sural 4. Hyperthermia C6 median 3 = Saphenous Femoral 5 5 2 3 2 5. Hemodilution; Hct < 15% C7 middle posterior axillary 4 = Deep Peroneal Sciatic C8 radial 5 = Superficial Peroneal Descending Pain (Dorsolateral): T1 inferior medial ulnar& median 3 Dorsolateral Funiculus – modulates pain (spinal analgesia) Four Approaches: supraclavicular, infraclavicular, axillary, top of foot 1 Originate in the periventricular and periaqueductal gray areas and interscalene Bottom of foot terminate on enkephalin-releasing interneurons in Rexed’s  lamina  II from hee (substantia gelatinosa). This inhibits the release of substance P. Axillary: for forearm & wrist, safest, miss the muscultaneous Functions of nerves of ankle & Foot (Presynaptic inhibition) 30-40ml, musculocutaneous = 3-5 mL of LA into coracobrachialis muscle. 1.Saphenous = anteromedial foot, medial anterior calf and the Periventricular Gray Substantia Enkephalin Substance Supraclavicular = greatest risk of pneumo, most compact 40ml dorsum of the foot Periaqueductal Gray Gelatinosa Interneurons P Less likely to miss the peripheral or proximal branches 2. Deep peroneal nerve= toe extension & sensation to medial ½ All via nucleus magnus raphe in the pons and then descending via Interscalene = shoulder surgery, miss of ulnar nerve & targets 3. Superficial peronal nerve = sensation superficially to dorsum of the dorsolateral funiculus TRUNKS, no hand 40 ml foot & all 5 toes 4. posterior tibial – sensation to heel, medial sole & lateral sole Isobaric = CSF High Spinal: 5. Sural – sensation to lateral foot Hyperbaric = Dextrose solution C8 = numbness @ little & ring finger Hypobaric = sterile H2O C7 = numbness @ middle fingers Flexion of foot= medial plantar & lateral plantar - tibial C6 = numbness @ thumb & index finger Extension – peroneal nerve Epidural 1-2ml of LA per segment for epidural block Blocks for SAB: Superficial  :  saphenous,  superficial  peroneal,  sura    “S’s” 13cm needle Sympathetic = 2-6 dermatomes higher than sensory 17 or 18 gauge needles Motor = 2 dermatomes lower than sensory Femoral Nerve ~ 5cm from skin to epidural space (up to 8cm obese) Progression of blockade: Autonomic>sensory>motor L2, L3, L4 Anterior thigh & knee Batson's plexus in the epidural space communicates with the 1. Temperature sensation Anterior muscles of the thigh azygous system- important during times of engorgement which 2. Proprioception (kinesthetic sense) NAVEL (nerve, artery, vein, empty space, and lymphatics can cause engorgement of the vessels during instances of 3. Motor function increased abdominal pressure 4. Sharp pain Obturator nerve 5. Light touch Provides sensation to the medial aspect of the thigh and motor Caudal innervation to the adductor muscles located in the medial thigh Sacrococcygeal membrane (injected into epidural space) Type    B  >  Type  Aδ  =  Type  C  >  Aβ  >  Aα Anatomical landmarks: 2 sacral cornua, the coccyx, and the C type = more resistant to blockade than A & B fibers On or above knee surgeries: Femoral, Sciatic, Lateral Femoral, posterior superior iliac spines cutaneous obturator Sensitivity: large mylenated > smaller mylenated > unmylenated Complications: pain at site #1, urinary retention, infection Dosages: (Adult) Childrens Sciatic S5-L2: 15-25ml 0.5-1.0ml/kg of 0.125-0.25 SAB additives L4, L5, and S1-S3 S5-T10: 35ml bupivicaine Epinephrine 0.2 to 0.3 mg sciatic nerve innervates the muscles of the back of the thigh (biceps premature infant: chloroprocaine 1mlg/kg bolus & 0.3ml/kg Clonidine 75 to 100 mcg femoris, semitendinosis, semimembranosus, and adductor magnus). phenylephrine 2 to 5 mg 1mcg/kg clonidine As the sciatic nerve continues, it innervates the muscles of the lower prolong the duration w/o resulting significant ♥  changes leg and foot Caudal Dose Bupivacaine: Popiteal Block = sciatic Epidural Steroid Injection 0.5-1.0 mg/kg Epidural steroid injections provide relief from acute radicular pain Infant test dose = 0.5 mcg/kg epinephrine Nerve Injuries when  the  nerve  root(s)  exhibits:  edema,  inflammation  and  ↑  levels Max dose is 3mg/kg – (bupivacaine) Primary mechanisms responsible: peripheral nerve injury of phospholipase A2 expression are transection, compression, stretch, and kinking Needles Face mask ventilation – CN 5 & 7 (facial & tongue numbness) Affects unmylenated C fibers Cutting: Quinke, Pitkin LMA – SLN or RLN Non-Cutting: Whitacre, Spotte, Greene Intubation – RLN, SLN, CN 10, CN 12 SAB 24-27G Cervical @ C6-C7 & C7-T1 d/t the largest interlaminar distances Epidural- 18 to 16G Toughy Ulnar nerve Lumbar sympathetic block @ L2 Nerve Blocks – 23G Is the most commonly injured peripheral nerve in patients undergoing anesthesia Methylprenisone 40-120mg & triamcinolone diacetate 40-80mg Passage of Needle More common in those with BMI > 38 & men Skin Subcutanous tissue Procedures & Level of Block: Brachial Plexus Supraspinous ligament will not pass through on paramedian TURP – T 10 C-Section T4 Placement of shoulder braces = acromion ESWL- T4-6 Testicles- T10 Interspinous ligament approach (paraspinous muscle) Extreme flexion at the thigh can result in injury to the sciatic, Urinary bladder- S2-S4 Tourniquet- T8 Ligamentum flavum obturator, and femoral nerves. Lower abd – T6 Upper abd- T4 Epidural Space Dura Kidney – T10-L1 Cysto- T8-T10 Radial Nerve Subarachnoid Uterine – T8-T10 hysteroscopy- T10 Damaged = loss of the ability to supinate the extended forearm, wrist Hip Arthroplasty- T10 drop, abduct thumb, extend the metacarphophalaneal joints Dermatome Landmarks C1- Completely Motor Conditions that Increased height of spinal block Common Peroneal nerve. C4- Clavicle T10- umbilicus ↑ abdominal pressure or engorgement of epidural veins: Most commonly injured nerve of lower extremity pregnancy, ascites, abdominal tumors, kyphoscoliosis, T4- Nipples L4-L5-Tibia Most common injured nerve during lateral position ↑ age =    ↓  CSF volume & increase height of spinal blockade T6- Xiphoid S2-S5-Perineium 3 issues with common peroneal nerve injury Loss of dorsiflexion of the foot is consistent with injury to the The tip of the 12th rib corresponds with L1 Complications Foot drop and inability to evert foot The origin of the scapular spine corresponds with T3 Infection: streptococci- spinal , staphylococcus- epidural The most protuberant cervical vertebra is at the level of C7 Failure of block Pudendal nerves The tip of the scapula corresponds with T7 Backache #1 Fracture table level of the posterior superior iliac spine S2 Spinal Headache #2 quicker onset = greater dural damage- harder to treat Sciatic SAB vs. Epidural usually the next day Protect w/ pillow under knees SAB segmental spread is 10 d/t: mg, baricity, positions of LA ↑  Women > men & Young > old Injured when patient rotated to semi supine (hips) Tx: bed rest, caffeine, fluids, epidural blood patch (max 20ml) Epidural spread is d/t volume of LA Neurologic dysfunction allergic reaction Saphenous anterior spinal artery syndrome trauma Neuroaxial Opioids Inside of knee (litho with strap medially) drug toxicity infection hematoma 1. Hydrophilic: Morphine Numbness & tingling along medial aspect of the calves total spinal blockade – s/s = dyspnea, resp arrest, HoTN Slow onset & prolonged DOA Intrathecal – 0 early respiratory depression Femoral Arachnoiditis: inflammatory disorder of arachnoid mater + late resp depression d/t rostral spread (6-12 hrs) Decreased sensation LATERAL thigh which surrounds the spinal cord and cauda equina. Epidural – + early respiratory depression after 2 hours caused by exposure of the arachnoid membrane to povidone iodine + late resp depression d/t rostral spread (6-12 hrs) Foot drop: Sciatic (lumbosacral, common peroneal), anterior tibial 2. Lipophilic: Fentanyl, Sufentanil, Alfentanil solution, vasoconstrictors, LA, blood, and contrast media. Hip vag delivery lateral decub feet plantar flex Fast onset & short DOA Intrathecal - + early resp depression (2 hrs) Cauda equina syndrome: Complications of retrobulbar block 0 late respiratory depression s/s:lower back pain, sciatica, motor & sensory loss, & bladder & Stimulation of the oculocardiac reflex, retrobulbar hemorrhage, bowel dysfunction Epidural- + early resp depression (2 hrs) circumorbital hematoma, penetration of the globe, optic nerve trauma, d/t trauma, lumbar disc disease, ankylosing spondylitis, tumors, or 0 late respiratory depression optic nerve sheath injection, extraocular muscle injury, intra-arterial abscesses in the lumbar area. It has also been associated with injection prolonged exposure of the cauda equina to high doses or high Four common side effects of intrathecal opiods: 1. Pruritus (most common) concentrations of LA that cause direct neurotoxicity. Transtracheal 2. Urinary retention Blocking of RLN through cricothyroid membrane w/4% lido TNS: transient radicular irritation, pain in the lower back or 3. N & V Absorbed across mucous membranes (sim to sublingual) buttocks that may radiate to one or both legs after a spinal 4. Respiratory depression anesthetic Regional Common side effects of epidural opioids: Mepivicaine & lidocaine implicated & lasts ~ 1 week High points in spinal canal: High = C3 & L3 Low= T6 & S2 1.urinary retention (bup/morphine) Widest point in space: L2 2. pruritus (morphine) Absolute Contraindications to Regional Anesthesia Biggest vertebral opening: L5-S1 1.Infection @ site 2. Coagulopathy 3.weakness of hands & HoTn Blood supply to SC – single anterior spinal, paired posterior 3. Marked hypovolemia 4. True allergy to LA Site of action: nerve root (epidural space), nerve rootlets(spinal), 5. Pt. refusal/inability to cooperate 6. Severe Stenosis C8-T1 = Stellate Ganglion- if  blocked  =  Horner’s  syndrome spinal cord 7.  ↑  ICP 8. Abruption placentae Horner’s  syndrome- ipsilateral miosis, ptosis, enopthalamos, Apnea d/t Hypoperfusion of resp centers in medulla flushing,  ↑  skin  temp,  anhydrosis,  nasal  congestion CSF (+) Epidural (-) Relative Contraindications to Regional Anesthesia Motor Blockade with LA Tests: Sensitivity: 1.Preexisting neurological dz 2. Back disorder (Ankylosis) Minimal: lidocaine 1%, Mepivicaine 1%, Bupivacaine 0.25% SnNOut 3. Heart Disease 4. Surgery above umbilicus Dense: chloro 3% (most), lidocaine %, mepiviaince 2-3%, Sensitivity, Negative, Out 5. Failure to obtain free flow 6. Sepsis etidocaine 1.5%, prilocaine 3% 7. Mobitz type I or II 8. 3rd degree w/o paceer Specificity: Four anticholinesterases prolong esters: ↓  plasma  pseudocholinesterase SpPIn Risk & Complications of Regional Anesthesia 1. Echothiophate (irreversible) Specificity, Positive, In 1.infections 2. HoTN 3.Urinary retention 2. Neostigmine 4.inadequate analgesia 5. Intravascular injection 3. Pyridostigmine Volatile Anesthetics: 6. High spinal 7.PDPH 8. Back pain 4. Edrophonium VP Bld:Gas Oil:Gas FA/FI MAC.70 N2O 9.N/V 10. pain on injection N2O 0.47 1.4.99 104 Four conditions that plasma cholinesterase: Sally Sevo 170 0.65 53.4.85 2.1 0.66 Parturient & LA 1. Pregnancy Eats Ethr 175 1.9 98.5.65 1.68 0.60 SAB  &  Epidural  =  ↑  spread  &  Depth 2. Liver disease (cirrhosis) Ice cre Iso 239 1.4 90.8.73 1.15 0.50 Related  to  ↓  thoracolumbar  CSF  volume  &  ↑  neural  sensitivity 3. First six months of life Hot Halo 243 2.3 224.58 0.74 0.29 Hormonal progesterone  in  CSF  may  ↑  segmental  spread 4. Atypical plasma cholinesterase Days Des 669 0.42 18.7.91 6.3 2.83 Bupivacaine 0.25-0.5% = good sensory but minimal motor Volatile anesthetics, propranolol, and cimetidine decrease Note! There may be additive effects between the cardiac Anticoagulants hepatic clearance of amides. (They inhibit Cytochrome P-450) depression associated with Enflurane (or for that matter Halothane) NSAID, ASA, sub-q or mini dose heparin- No issues and beta-adrenergic antagonists (i.e. Esmolol) IV heparin – need nml PTT before regional Avoid Beta-blockers with amide LAs: Hold 1 hr after placement Labetalol & Propranolol Small Vd = fast elimination Cathetars removed 2-4/hr AFTER last heparin dose Also: Heparinization 1 hr after catheter removal Digitalis & Ca++ channel blockers potency = lipid solubility = MAC LMWH- first dose 24 hrs post op (2x daily dosing) 6-8 hs post op (daily dose) Bretyllium is used to treat cardiac toxicity by amides. Oil/gas: measurement of solubility First dose 2 hours after catheter removal Three reasons to add epinephrine to LA: Warfin- stop 4 days before surgery & INR < 1.5 1. Prolong the duration of anesthesia Blood Solubility = speed of uptake Fibrinolytic or thrombolytic – 10 days 2. Systemic toxicity by rate of absorption Ticlodipine – 14 days 3. Permit use of larger amounts of LA Inhalation agents: solubility = speed of inhalation induction Clopidorgrel- 7 days ↓  solubility  =  ↑  speed  of  inhalation  induction GPIIb/IIIA – hold for 4 weeks post operative 1% = 10 mg/ml Epinephrine = 1:200,000 = 5 mcg/ml Volatile = CBF, CMR ↑  potency  of  LA: Concentration = Amt/Vol C=A/V Ketamine/N2O = CBF, CMR ↑  potency  =  ↑  protein  binding,  ↑  DOA,  ↑  affinity  for  Na  channels,  ↑   Amt = Conct X Vol IV anesth = CBF, CMR tendency of cardiac toxicity % = gm/100 ml Vapor pressure of liquid dependent on SOLEY on temperature ↑  #  of  carbons,  +  Halide,  +  ester  linkage,  large  alkyl  on  tertiary  amide Max Dose Epinephrine: Subcutaneous or Submucosal infiltration: Wrong Agent in Vaporizer : Bier Block: 2-3 mcg/kg for adults High Low High Method of anesthetizing a limb by IV injection while blood flow to or 1 mcg/kg on Halothane Low High Low extremity is occluded by a tourniquet Minimum: 15-20  mins  (don’t  release  before- local in systemic) 3 mcg/kg for children Percentage of volatiles metabolized: Max: 40-65 min (usually d/t tourniquet pain) or 1.5 mcg/kg on Halothane Halothane 15-20% With local anesthetic: Enflurane 2.4% Local anesthetics: 200-250 mcg Isoflurane 0.2% Cmin: minimum concentration of LA to produce conduction block or 3-5 mcg/kg Adults Desflurane 0.02% MOA: non-ionized LA crosses membrane and ionized binds to Sevoflurane 3.0% receptor to produce effect. (Ca controls Na permeability) *Do not inject epi:in/around end arteries- fingers, toes, ears, penis, Block rapidly firing nerves > idle nerves nose Cardiovascular Side Effects: Autonomic > perception of pain/touch/temp > motor > proprioception Sux = HR, Histamine + Na+ Bicarb =↑  speed  of  onset,  intensity  of  block,↓  pain,  ↑  DOA EMLA Cream: Mivacurium = Histamine +  Dextran  =  ↑  DOA 2.5% Lidocaine, 2.5% Prilocaine Atracurium = Histamine +  hyaluronidase  =  ↑  spread  of  the  LA  into  the  tissue. Biggest barrier = stratum corneum D-Tubocurarine = Histamine, HR, BP, ganglionic blockade Psoriasis or  broken  skin  =  ↑  onset &  ↓  duration  (↑  toxicity) Ester local anesthetics are eliminated by plasma pseudocholinesterase Contact time at least one hour under an occlusive dressing Metocurine = Histamine, HR, BP, ganglionic blockade except cocaine, which is eliminated by hepatic metabolism. Reaches a depth of analgesia of about 3-5 mm, Pancuronium = HR, BP Metabolism: chloroprocaine > procaine > Tetracaine DOA = 1-2 hours. Gallamine = HR, BP ↑  likely hood of allergic reactions d/t para-aminobenzoic acid ESTER Max Dose (mgkg) Duration Benzocaine Na Agent Renal Biliary Metabolism Tetracaine is hydrolyzed much more slowly by plasma cholinesterase Chloroprocaine 12 (800) 0.5-1 Succinylcholine Neglig Neglig Primary and is highly protein bound. Therefore it is the most toxic ester local Cocaine 3 (200) Atracurium Neg Neg Primary anesthetic. Procaine is the least potent ester. Procaine 12 (800) Mivacurium Neg Neg Primary Tetracaine 3 (200) 1.5-6 Cisatracurium Neg Neg Primary Cocaine is an ester of benzoic acid and is the only local anesthetic AMIDE Vecuronium Second-20% Primary Second that produces vasoconstriction. It is also the only naturally-occurring Bupivicaine 3 (175) 1.5-8 Rocuronium Second Primary Second local. Blocks  epi  uptake:  caution  in  use  of  tricyclics,  MAO’s,   Lidocaine 4.5, 7 w/epi (500,700) 0.75-2 catecholamine metabolism blockers. The max dose is 1.5 Mepivicane 4.5, 7 w/epi (300,500) 1-2 mg/kg Prilocaine 8 (400) 0.5-1 Cocaine & ropivicaine = constriction Ropivicaine 3 (300) 1.5-8 Brain uptake of anesthetics depends on: Manifestations of hypersensitivity reactions include: 1. Blood solubility Amide local anesthetics are metabolized by hepatic metabolism. 1. Localized edema 2. Cardiac output Metabolism: prilocaine >etidocaine > lido > Mepivicaine >Bup 2. Urticaria 3. Alveolar ventilation Prilocaine is the least toxic amide LA. 3. Bronchospasm 4. Inspired concentration 4. Anaphylaxis Prilocaine is metabolized to orthotoluidine. Orthotoluidine is an Three ways to speed of equilibrium: oxidizing agent capable of converting hemoglobin to methemoglobin. Cardiac Toxicity: 1. Inspired anesthetic concentration Hypoxia, hypercarbia, and acidosis 2. Second gas effect Bupivacaine is highly lipid soluble and dissociation form sodium Tx: Fluid bolus, rest, pain meds, caffeine, blood patch (10-30cc) 3. Alveolar ventilation channels are slow. Cardiac toxicity is high. TNS: Transient Neurological Symptoms Two most important factors for alveolar partial pressure: Mepivicaine, etidocaine, & bupivacaine = no enhancement w/epi Lidocaine spinals 1. Inspired concentration Risk Factors: lithotomy, outpatient, knee arthroscopy 2. Blood solubility Tetracaine, Etidocaine, and Bupivacaine are about equipotent & most Tx: NSAIDs—d/t sensory nature toxic LAs. Etidocaine causes seizures at a lower plasma Partial pressures concentration. Etidocaine & Bupivacaine have lowest maximal dose Lipid Rescue: Inspired>Alveolar>Arterial blood>Brain ranges. 20% Intralipid Note! This order is reversed during emergence when gas is turned 1.2 to 2 ml/kg and then an infusion off. Monoethylglycinexylidide: an active metabolite of Lidocaine that 0.25/ml/kg/min for 30-60 mins contributes to toxicity even when lidocaine plasma levels are low The Meyer-Overton Theory explains that the anesthetic potency Benzocaine: of anesthetic agents directly correlates with their lipid solubilities. Ester, Weak ACID May cause methemoglobinia MAC is  the  “Minimum  Alveolar  Concentration”  of  anesthetic  at  one   Enflurane and Desflurane most depress ventilation. Halothane To figure out ½ Lies and amounts excreted atmosphere that produces immobility in 50% of patients exposed to a least depresses ventilation. Time ½ Life Amount of Drug noxious stimulus. MAC is inversely proportional to potency. 0 0 0 Sevoflurane is most degraded by soda lime and Desflurane least. 1 50 (1/2) 50% MAC ED50 of non-inhalational drugs. 1.3 MAC ED95 2 25 (1/4) 75% Isoflurane facilitates CSF absorption = favorable effect on CSF 3 12.5 (1/8) 87.5% There is approximately 1% in MAC for every 1% of N2O delivery. 4 6.25 93.8% Decrease response to CO2 ventilatory drive 5 3.125 (1/32) 96.9% Highest Mac 6mos-12mos 6 1.562 (1/64) 98.4% Fluoride: des =6, iso= 5 sevo=7 7 0.782 (1/128) 99.2% Seven factors that MAC: 1. Increasing age Steady-state Point at which the plasma concentration of a drug is in Second messengers: 2. Hypothermia Molecules that relay signals from receptors on the cell surface to 3. CNS depressants equilibrium with all other tissues is the body target molecules inside the cell 4. Acute ethanol intoxication Receptors & Drugs cAMP, cGMP, IP3, calcium 5. Alpha-2 agonists (Clonidine) 6. Pregnancy Agonist: affinity and efficacy Antagonist: affinity for a receptor but lacks efficacy (cannot Proteins 7. Levels of CNS neurotransmitters Albumin = acid produce  conformation  Δ) Competitive:  can  be  overcome  by  ↑  concentrations  of  agonist Alpha-1 acid glycoprotein & Beta-globulins = Base Three factors that MAC: 1. Hyperthermia Non-Competitive:  antagonism  can’t be  overcome  by  ↑  concern Partial Agonist: bind with the receptor and has some efficacy, but GABA is the major inhibitory transmitter of the CNS. It opens Cl- 2. Hypernatremia ion channels. It hyperpolarizes neurons inhibiting action potential 3. Levels of CNS neurotransmitters it cannot elicit the maximal tissue response Inverse Agonist: but results in the opposite reaction of an agonist production. Volatile anesthetics are metabolized in the liver by cytochrome P-450 Barbiturates, benzodiazepines, propofol, and etomidate work in hepatic microsomes. Zero Order Kinetics Constant AMOUNT of drug over a constant time primarily on the GABA receptor. Opens Cl- channel- hyperpolarization An oxidative trifluoroacetyl metabolite of Halothane is thought to be ASA, phenytoin, ASA responsible for acute hepatotoxicity in susceptible individuals. Current research also indicates that inhaled anesthetics also work Reductive liver metabolism occurs with Halothane in the presence of First Order Kinetics on GABA receptors. hypoxia. Thymol is the preservative in Halothane. Constant FRACTION eliminated per time 1 compartment = albumin 2 compartments = most other drugs Barbiturates Fluoride is the most clinically important metabolite of Enflurane. Prolong the attachment of GABA to its receptor. Vd = Q/Cpt=0 Q = quantity of drug injected Cpt=o = plasma concentration @ time=0 They work in the reticular activating system (RAS). Inorganic fluoride and chloride are common metabolites of Halothane Draw line back from elimination phase to t = 0 Sodium Thiopental (acid) is 72-86% bound to albumin. It reduces and Enflurane. the sensitivity of the central respiratory center to CO2.  It’s  onset  is   within 10-15  seconds.  It’s  elimination  half-time is 11.6 hours. N2O is the only inhalational agent without a halogen. Metabolized by redistribution dependent on CO. α  phase=  distribution Acceptable levels in the OR: ↓  CMRO2 &  ↓CBF (2nd ↑  cerebral  resistance) N2O & Volatile together: Inverse Steal β  =  elimination  phase   N2O = 25 ppm Reconstitute w/ Sterile Saline (NO LR-precipitate) Volatile = 0.5 ppm Hyperalgesia Dose response curve: Volatile alone: S/S of intra-arterial Thiopental injection: Potency: determined by the binding affinity of receptors for the Volatile = 2 ppm 1. Arterial vasospasm with intense pain down the arm drugs as well as the efficiency of coupling of binding to response Slope: relationship between dose and effect 2. Blanching of the skin with loss of distal pulses N2O is metabolized to N2 in the intestine by reductive anaerobic 3. Eventual cyanosis and possibly gangrene Efficacy: maximum drug effect metabolism. Phase I biotransformation: Intra-arterial injection is treated with Phenoxybenzamine Six contraindications to the use of N2O: (Dibenzyline). Alter the molecular structure of a drug by modifying an existing 1. Venous air embolism functional group of a drug. 2. Malignant hyperthermia pH of Barbiturates is > 9.0, pH of 10-11 is often cited. 1. Oxidation 3. Ear surgery (middle ear) 2. Reduction 4. Closed pneumothorax Barbiturates are contraindicated in status asthmaticus and 3. Hydrolysis 5. Potential pneumocephalus porphyria. -Cytochrome P450 participates in most oxidation and some 6. Bowel obstruction reduction. Methohexital is associated with a higher incidence of hiccups than Four adverse side-effect of N2O: other non-opioid induction drugs. Phase II biotransformation: 1. Aplastic anemia Consists of a coupling or conjugation of a variety of endogenous 2. Congenital anomalies Benzos: (base) compounds to polar chemical groups of the drug. 3. Spontaneous abortion Sedative: effects: the cortex 4. CNS toxicity amnesia: forebrain and hippocampus Biotransformation often makes drugs more water soluble and inactive for excretion in the urine or bile. anxiolytic effects: ↓  methionine synthetase- B12 deficiency = no N2O amygdala, hippocampus, & limbic system. N2O decreases BP and CO when added to high dose opioids. ↓swallowing  reflex  &  upper  airway  reflexes Six groups of drugs metabolized by Cytochrome P450: N2O PVR and PA blood pressure due to mild sympathomimetic 1. Barbiturates ↓CMRO2 &  ↓CBF effects. It will support fire, but is neither flammable nor explosive. 2. Opioids Flumazenil- competitive antagonist of benzos 3. Benzodiazepines ↑  CBF  &  ↑CMRO2 4.  Amide  LA’s Three renal changes associated with volatile anesthetics: 5. Tricyclic antidepressants Propofol (acid) 1. RBF 6. Antihistamines weak acid 2. GFR 2,6 diisoprorylphenol 3. UO Quantal Dose Response: ↓  SVR  =  ↓BP Therapeutic Index = LD50/ED50 Liver metabolism 70% & lung metabolism 30% Halothane least potentiates NDMRs. ED50 is the dose of drug that is effective in 50% of patients. *Caution with soybean & egg allergy TD50 dose that produce toxic effect in 50% of animals Isoflurane and Desflurane most SVR, Halothane has little effect on LD50 death to 50% Etomidate: (base) SVR. Maintains CV stability the best. Elimination half-time (T ½) = time taken for the plasma It directly depresses the adrenal cortex. Halothane and Enflurane produce the greatest myocardial depression. concentration to fall by one-half. T ½ is directly related to Vd and It cerebral blood flow, ICP, & CMRO2 inversely related to Clearance (Cl). Halothane and Sevoflurane most depress the baroreceptor reflex. Venous thrombosis and phlebitis are most likely after etomidate, (There is no increase in HR despite decreases in BP) Cl = Vd/ T ½ diazepam, and lorazepam. ↑  Vd=  ↑  T1/2                                                        Small  Vd=↓  T1/2 Isoflurane depresses the temperature-regulating center in the Fast CL=short T1/2 Slow CL= Long T1/2 Four potential problems during recovery from etomidate: hypothalamus. 1. Suppression of adrenocortical response to stress 2. N & V Isoflurane, Desflurane, and Sevoflurane decrease cerebral metabolic 3. Plasma cortisol concentration rate. 4. Depressed immune response N2O alone increases cerebral blood flow & ICP. Ketamine: (base) Agonist-antagonist opioids 9. Skeletal muscle rigidity Causes dissociation between the thalamocortical and limbic systems Kappa: provide analgesia 10. Myoglobinuria by antagonistic actions on the NMDA receptors. Mu: reverse respiratory depression 11. Hypoxemia Dysphoria is cause by misperception and/or misinterpretation of Naltrexone, naloxone, nalbuphine auditory and visual stimuli by stimulating the kappa receptor, The earliest sign of MH is ETCO2 antagonizing the muscarinic receptor, and stimulating the sigma Muscle Paralyzation Temperature may increase 1-2 C0 every 5 minutes. receptor. Eye muscles → extremities→trunk→abd muscles→ diaphragm. Succinylcholine and volatile agents are triggering agents Recovery is restored in reverse order Masseter muscle rigidity is an early sign of MH. ♥  Effects:  ↑  MAP,  CI,  PAP,  CVP,  HR Ketamine produces bronchodilitation Facial muscle = diaphragm -1% of children experience masseter muscle rigidity after ↑  airway  secretions- give glyco Abductor pollis = readiness for intubation halothane and succinylcholine administration. CPK > 20,000 Analgesia Recovery from NMB = ulnar nerve confirms the diagnosis after masseter muscle rigidity following ↓  emergence  delirium  in  kids   & higher bioavailability in kids halothane and succinylcholine administration. MOA NMB: - Halothane-caffeine contracture test is the standard diagnostic test Opioids: (bases) Site of action is the motor end plate- nicotinic receptors for MH, but it has too many false positives. Shortest elimination ½ life ALL MR resemble acetylcholine Remi < Alfent < MSO4 remifent > fent > alfent > MSO4 > Meperidine 2. Metocurarine 3. Administer Dantrolene 3. Atracurium 4. Treat acidosis with NaHCO3 (1-2 mmoles/kg) Morphine: 4. Mivacurium 5. Body temp to 38 C0 26-36% is protein bound in the adult 6. Replace anesthesia circuit and CO2 absorber Less is protein bound in the neonate 20 alpha-1 acid glycoprotein. Mivacurium is metabolized by plasma cholinesterase. 25% 7. Monitor ETCO2 & ABGs Metabolite: morphine-6-glucuronide- prolonged in RF & crosses BBB spontaneous recovery is reached in 13 minutes in adults and 7 8. Treat hyperkalemia and dysrhythmias if necessary by mass action minutes in children. Atracurium is eliminated by ester hydrolysis and Hoffman Dantrolene: binds to the ryanodine-1 channel and inhibits the Meperidine (Demerol) elimination; Cisatracurium is only eliminated by Hoffman calcium channel in the sarcoplasmic reticulum. Decreasing the myocardial contractility and HR elimination. release of Ca++ from the sarcoplasmic reticulum in skeletal muscle ↓  shivering  - Kappa receptors and causes skeletal muscle to relax. The initial dose is 2.5 mg/kg ↓  sz  threshold  (↑  having  a  sz)    d/t  Normeperidine Hoffman elimination is temperature and pH dependent. The rate followed by 1-2 mg/kg boluses to a maximum dose of 10 mg/kg. It should be avoided with MAO inhibitors & Imipramine of metabolism is slowed by acidosis or temperature. The therapeutic blood level is 2.5 mcg/ml. Vials of Dantrolene contain 20 mg and each is mixed with 60 ml of sterile distilled Adverse S/S of MAO inhibitors & Demerol: Laudanosine is a lipid-soluble metabolite of atracurium that can H2O. 1. Hyperpyrexia ♥  Effects: cause CNS stimulation in high concentrations. It should be repeated every 10-15 hours for three days. 2. HTN ↓  HR,   3. Hypotension ↓SVR Four MRs that use renal excretion least: Five complications include: 4. Respiratory depression ↓  venous  retur 1. Succinylcholine 1. Reoccurrence 5. Skeletal muscle rigidity ↓  BP 2. Atracurium 2. DIC 6. Seizures 3. Cisatracurium 3. Myoglobinuric renal failure 7. Coma 4. Mivacurium 4. Skeletal muscle weakness 5. Electrolyte abnormalities Most clinically used opioids are relatively selective for Mu receptors. Three NDMRs not significantly excreted by kidneys: 1. Atracurium Gastric lavage is the best method to Temp with MH. Lamina II- substania gelatinous of SC 2. Cisatracurium Procainamide, 15 mg/kg is the best antiarrhythmic for MH. PAG & periventricular area in brain stem = spinal analgesia 3. Mivacurium The incidence of MH in children is 1:15,000 Spinal analgesia is mediated primarily by Mu-2 receptors, but also Pipecurium is primarily eliminated by renal (70%) and The incidence in adults is 1:50,000 by kappa and delta receptors. Besides the substania gelatinosa secondarily by biliary (20%). The mortality rate is 10% (Rexed’s  lamina  II),  the  periaqueductal and periventricular gray areas Rocuronium undergoes  no  metabolism,  eliminated  w/  no  Δ   are important sites of spinal analgesia. Neuroleptic malignant syndrome can mimic MH, but the onset Supraspinal analgesia is primarily mediated by Mu-1 receptors, but What can augment NMB: and recovery are different. Patients treated with antipsychotic also by kappa and delta receptors. 1. Hypermagnesium drugs such as Haldol, prolixin, or thorazine are susceptible to 2. Hypocalcemia neuroleptic malignant syndrome. Fever is the cardinal sign Mu-1 receptors produce: 3. Hypokalemia (low abuse potential) (Supraspinal analgesia) 4. VA : des > sevoflurane > iso > N2O/fentanyl Anticholinergic: 1. Euphoria 5. Hypothermia 1. Atropine, - most  ↑  HR 2. Miosis 2. Scopolamine- most sedative 3. Bradycardia Eleven possible complications of Succinylcholine 3. Glycopyrrolate - does not cross BBB d/t being a quaternary 4. Hypothermia administration: Combine reversibly w/ muscarinic cholinergic receptors prevent 5. Urinary retention 1. Hyperkalemia acetylcholine from binding to the receptor. 6. Pruritus 2. Bradycardia (Succinylmonocholine-metabolite  @  ♥  SA  Node) Sedative effect: Scopolamine > atropine > 0 glycopyrrolate 3. HR and/or BP Antisialogogues effect: Scopolamine > glycol > atropine Mu-2 receptors produce: 4. Skeletal muscle myalgia HR: Atropine > glycopyrrolate >scopolamine - < PR interval (high abuse potential) (Spinal analgesia) 5. Allergic reaction Infants & elderly little effect on HR 1. Respiratory depression 6. Triggering of MH Bronchodilatory effects: Ipratropium 2. Marked constipation 7. Sustained masseter muscle contraction Do not use scopolamine in GLAUCOMA 3. Physical dependence 8. Myoglobinuria 9. IOP (NOT prevented with defasculating dose) Gastric Effects: ↓gastric secretions, ↓ peristalsis and intestinal Kappa receptors produce: 10. Intragastric Pressure (prevented with defasiculating dose) motility, ↑ gastric emptying time, & ↓  lower esophageal sphincter (Spinal [Kappa-1] and Supraspinal [Kappa-3] analgesia) 11. ICP (prevented with defasiculating dose) tone. 1. Sedation Five conditions that accentuate succinylcholine-induced Central anticholinergic syndrome: 2. Dysphoria hyperkalemia: Scopolamine & atropine both cross the blood-brain barrier and 1. Unhealed third-degree burns block muscarinic cholinergic receptors in the CNS, producing Four Ventilatory effects of opioids: 2. Denervation of skeletal muscle restlessness, hallucinations, somnolence, and potentially, 1. Breathing rate 3. Severe skeletal muscle trauma unconsciousness. Predisposed patients: Tricyclic antidepressants 2. Minute ventilation 4.  Upper  motor  neuron  injury  (head  injury,  Parkinson’s,  CVA) (like amitriptyline), antipsychotics, and antihistamines 0 3. Response to CO2 2 brainstem depression 5. Muscular dystrophy (antimuscarinic characteristics) 4. Arterial CO2 tension 6. Renal Failure w/ hyperkalemia Tx: physostigmine 7. Severe Sepsis Naloxone, Nitroglycerine, and Glucagon can reverse opioid-induced 8. Duchennes Xanthines: sphincter of Oddi spasm. 9. Guillian Barre Aminophylline & theophylline cause release of norepinephrine from sympathetic postganglionic Alfentanil is eliminated faster than all other opioids (except Eleven clinical manifestations of Malignant Hyperthermia: neurons and should be avoided with Halothane. Remifentanil) because it has a small Vd. The elimination ½ time is 1. Hypercarbia 10-30 minutes. 2. Tachycardia Halothane should be avoided with patients intoxicated with 3. Tachypnea cocaine or using imipramine, because they both block reuptake of Remifentanil is metabolized by blood and tissue nonspecific esterases. 4. Hyperthermia norepinephrine. Has glycine buffer- DO NOT use in neuroaxial. 5. Hypertension 6. Cardiac dysrhythmias Calcium channel blockers and volatile agents act synergistically 7. Acidosis (metabolic) 8. Hyperkalemia Chemotherapy Medications and Site of Toxicity One  PRBC  =  ↑  Hct  3-4% 1g/dl Sickle Cell Disease: Bleomyocin – Lungs doxorubicin -Heart 1cc/kg  PRBC=  ↑  Hct  1% A hereditary hemolytic anemia resulting from the formation of an Cisplatin- Kidneys cyclophophains, streptozocin, 1  unit  plts  =  ↑  5,000-10,000 mm3 abnormal hemoglobin (Hb S). Red cell survival is reduced to 10-15 Methotrexate-Liver Massive transfusion = 1 complete blood volume in 24 hours days, compared with up to 120 days in normal individuals. Immunosuppressive PRBC Sickling occurs only under extreme hypoxemia or in low-flow 3 major risks- 1. Infection 2.malignency 3. Progressive vascular dz Universal Donor = O Universal recipient = AB states. Calciumium inhibitors = cyclosporines & tacrolines Platelets The goal of exchange transfusions is to decrease blood viscosity S/E: HTN, hyperlipidemia, ischemic valve dz, DM, neuropathy, CNS Universal Donor= AB Universal Recipient=O and achieve a Hct of 35-40% with 40-50% normal hemoglobin (Hg effects A1). Avoid hypo- and hyperthermia, acidosis, and even mild Coumadin drugs competitively inhibit vitamin K so synthesis of degrees of hypoxemia, hypotension, or hypovolemia. Generous Calcium Channel Blockers work: Vitamin K-dependent factors (II, VII, IX, and X) is diminished. hydration and a relatively high (>50%) FiO 2 are desirable. Many Phase 2, plateau phase of ventricular action potential avoid the use of tourniquets. Phase 4 of the pacemaker action potential Cryoprecipitate is the fraction of plasma that precipitates when FFP is thawed at 40 C.  (The  drug  of  choice  for  Von  Willebrand’s   Acute chest syndrome – dyspnea, chest pain, hypoxemia Drugs to avoid with MAO inhibitors: disease) 1. Tricyclic antidepressants (imipramine) Cryoprecipitate contains factors I, VIII, XIII Normal hemoglobin (Hemoglobin A) has: 2. Opioids (especially Demerol) 2 beta globin chains 3. Indirect acting sympathomimetics (ephedrine) Aprotinin inhibits plasmin and therefore inhibits the breakdown & 2 alpha globin chains 4. Fluoxetine of fibrin. Sickle Cell Anemia is a mutation of the beta globin chains – Digoxin: (Digitalis) FFP glutamic acid instead of valine -Enhances myocardial contractility, HR, & slows impulse 10-15mg/kg propagation through the AV node. Contains all clotting factors but plts Four diseases associated with thrombocytopenia: -Used to treat CHF & SVT Uses: isolated coagulation factor deficiencies, reversal of 1. Chemotherapy or unrecognized cancer + + ++ -Inhibits the Na -K pump causing intracellular Ca accumulation. Coumadin, liver dz- reverse coagulation issues, after massive 2. Liver disease and splenomegaly -Work by decreasing Phase 4 depolarization of the SA node transfusion and still bleeding 3. DIC -Hypokalemia, hypercalcemia, and hypomagnesemia increase the 4. Pre-eclampsia likelihood of digitalis toxicity. Max Allowable EBL:( 20% EBV) -Hyperventilation should be avoided because it creates a relative Porphyria hypokalemia. Hypokalemia causes binding of digitalis to myocardial Hct - aHct Hct = 3 x Hbg Metabolic d/o affecting biosynthesis of heme = thick blood cells, resulting in an excessive drug effect. MABL= EBV X Hct Signs & Symptoms -Eliminated primarily by the kidneys, 35% daily 1. Acute abdominal pain, N & V 2. Neurotoxicity: confusion, SIADH, difficulty swallowing, HTN Three side effects of tricyclic antidepressants: PRBC replacement: Hct of PRBC = 75 & tachycardia (Amitriptyline) 3. Sensory & motor neuropathies 1. Anticholinergic effects (dry mouth, blurred vision, tachycardia) PRBC (ml) = (Blood loss – MABL) x desired Hct 2. Orthostatic hypotension Hct of PRBC AVOID Triggering Agents: KEPT MAN 3. Sedation Barbs Benzos Ketamine Etomidate Estimated Blood Volume (EBV): Total Body Water (TBW): Nifedipine Ketorolac Enflurane Sulfamides Tricyclic antidepressants interact with: Premie (< term) 95 ml/kg Adult 60% = 42L Phenytoin Hydralazine mepivicaine lidocaine 1. Anticholinergics (atropine, scopolamine) Term 90 Neonate 80% GA- no regional 2. Sympathomimetics (ephedrine) Infant (< 6 wks) 80 Premie 90% 3. Inhaled anesthetics ( dysrhythmias) Toddler (6 wks-2yrs) 75 Hemophilia : x-lined recessive 4. Antihypertensives (rebound HTN) Child (2 yrs-12yrs) 72 ICF: 60-66% 25-28L A- Factor VIII Deficiency 5. Opioids ( analgesia & respiratory depression) Men 70-75 ECF: 33-40% 14-17L B- Factor IX Deficiency Women 65 Interstitial fluid 80% Prolonged PTT & normal PT Anaphylactic Reaction: (Type I hypersensitivity reaction) Plasma water 20% Tx: Factor Concentrates Antibody Ig E (immunoglobulin E) is produced in response to an Fluid replacement: antigen (foreign protein). Upon a second exposure to the antigen, Ig E 4 ml/kg first 10 kg (1-10kg) Polycythemia: on the surface of mast cells and basophils triggers the release of 2 ml/kg second 10 kg (10-20) Abnormal  ↑  Hct   can develop AVWD mediators including histamine. This causes bronchoconstriction, upper 1 ml/kg remainder (20+) 50-60% Hct = HA Ideal Hct = 33-36 airway edema, vasodilation, increased capillary permeability, and Short cut: Add 40 to your total Kg (if >20) Tx: phlebotomy, avoid dehydration urticaria. Life-threatening. Fluids: Heat Loss: Anaphylactoid Reactions do not involve Ig E. Foreign substances LR: pH 6.5 - contains K 4, Na 130,lactate 28– hypo (osm 273) Radiation 40%>Convection 32%>Evaporation 28%>Conduction (i.e. drugs, hetastarch) directly stimulate the emptying of mast cells Too much = metabolic alkalosis and basophils. NS: Na = 154 meq/L = Isotonic (osmol = 308) For each 10 C in body temperature, Too much= hyperchorlemic acidosis Basal metabolic rate > 7% Anaphylactic and Anaphylactoid reaction = same S&S D5: Hypotonic (osmolality 252 mOsm) 5% Albumin- colloid osmotic pressure of 20mmHg The center for Heat Loss is located in the anterior (preoptic) Top 5 Causative of Anaphylactic Reactions Normosol- No Ca++ (osmol 294) hypothalamus and the Heat Gain center is located in the posterior NMB 60% Hespan: 6% hydroxyethyl starch in NS =/>  20ml/kg/day  =  ↑   hypothalamus. Latex 17% serum amalayse levels Abx 15% Hextend- 6% hydroxyethy starch in solution w/ electrolytes, Great decrease of core temp occurs in 1st hour of surgery Colloids 4% glucose and lactate Hypnotics 3-4% Operating room temp #1 critical factor min OR temp 21C Isotonic: ~ 285 mOsm/L- effective osmolality close to body fluid Latex Allergy CELLS DO NOT SWELL OR SHRINK Hypothermia 1.multiple surgical procedures Hypotonic ~ 305 mOsm/L -- ↓  cells  shrink   blood viscosity, left shift of oxyhemoglobin dissociation curve, 3 atopic people w/ hx of multiple allergies + impaired coagulation, and thrombocytopenia 4. food allergies: bananas, avocados, chestnuts, stone fruit P osm= 2 x plasma [Na ] drug elimination 20 hepatic blood flow and metabolism. Renal blood flow and clearance slow renal excretion of drugs. Coagulation: Dextran 40: Intrinsic Path = XII, XI, IX, VIII (12,11,9,8) Improves blood flow through the microcirculation presumably by Eight Physiologic effects of Hypothermia: Extrinsic = III, VII (3,7)