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Date Created: 01/15/15
GENERAL ANESTHESIA Stages of Anesthesia 1. Analgesia early pain relief w/o amnesia (unconsciousness); late analgesia + amnesia 2. Excitement – no memory, not responsive, but hyperactive, vomiting risk 3. Surgical anesthesideep unconsciousness, unresponsive to pain 4. Medullary depressio– ventilation, eventually depresses CV system, can lead to death Potency also Minimum Alveolar Measure of potency. Alveolar concentration (%) of inhaled Concentration (MAC) agent that produces immobility to skin incision (human) or tail determined by lipid solubility clamp (mouse) in 50% of subjects. Represents partial pressure of(to pass BBB) anesthetic in CNS MAC = potency (need less) MAC by 25% per MAC w/ body temp – use less if cold in body temp MAC w/ age – use less w/ elderly Nitrous Oxide MAC > 100% so not potent Nitrous oxide >> Desflurane > Sevoflurane > Isoflurane enough to maintain High MAC – fast induction Low MAC anesthesia LEAST potent MOST potent Speed of Induction 1. Uptake: Alveolar partial pressure = Brain partial pressure [ ] is NOT a good marker of induction b/c has to dissolve alveolar partial pressure: from alveolus blood then [ ] going in = need less back to brain minute ventilation solubilityblood releases drug to brain more ea uptake by blood/ CO – blood doesn’t move drug away, stays in lungs blood solubility = need Alveolarvenous difference tissue uptake more raises venous Partial P alveolar [ ] more rapidly 2. Distribution – elimination by exhalation; less soluble Drugs w/ lipid eliminated more rapidly; exposure time = eliminatisolubility = potency = time due to accumulation in less perfused tissue (musc1/MAC fat, skin); elimination affected by CO + minute ventilation Pulmonary Effects of Inhaled Anesthetics Minut Apneic Broncho Airway Agent TV RR e Threshol dilation Irritabilit Vent. d y All inhaled anesthetics Nitrous Oxide bronchodilate Sevoflurane Desflurane Narcotics apneic Isoflurane threshold (stop breathing sooner) Apneic threshold : pCO at which apnea occurs 2 Sevoflurane + 2 O – induction in child (no iv) Ether ventricular funx so not Cardiovascular Effects of Inhaled Anesthetics used anymore Myocardial Coronary All inhaled anesthetics Agent BP Function SVR HR Vasodilation depress CV funx + cause Nitrous Oxide coronary vasodilation Sevoflurane Desflurane N 2 SVR (only drug to SVR) Isoflurane cerebral blood flow ( ICP) > in metabolic rate (can brain During MI/reperfusion injury – inhaled anesthetics blood flow heart, myocardial O 2emand, excessive intracellular Ca by partially inhibiting Ca 2+ channels during reperfusion ANESTHESIA I.V. Nonopiod General Anesthetics Side Agent BP CO HR ICP Effects Antiemetic Propofol Pain on injection Euphoria Infx/sepsis ++++Analgesic Ketamine Salivation (obstruction) Emergency rxn Pain on injection ? cortisol suppression Etomidate N/V Myoclonus + Nonionized faster Local Anesthetics Reversible conduction blockade of impulses by blocking Na channel conductance No. onized form diffuses into neuron onset than ionized + ionized blocks Na channel from intracellular cell. Delayed onset w/ pH due to shifting to ionized form. Max Dose Duration Seizure b/f cardiac Drug Onset (w/ Epi) (w/Epi) arrest/coma Lidocaine for surgery then bupivacaine for LIdocaine Rapid 4.5 (7) mg/kg 120 min (240) yes postop longer pain BupIvacaine Slow 2.5 (3) mg/kg 8 hr yes or no control(longer duration of action b/c protein binding) Adjuvants: toxicity of local anesthetic: Bupivacaine causes Bicarbonate Speeds onset of local anesthetic by pH to shift equilibriresuscitation resistant unionized form. +0.1 cc bicarb for every 10 cc bupivacaine cardiac arrest Local vasoconstriction prevents local anesthetic washout = Epi duration of action CNS blockade only (no mu R in PNS); allows to lower [ ] local Epi beyond ankles Opiods or toes anesthetic (vasoconstriction Hyaluronidase penetration of local anesthetic (e.g. optic nerve surgery) causes necrosis of fingers/toes) Allergic Class Drug Metabolism Rxn? Vasodilation CV Toxicity CNS Toxicity LIdocaine BupIvacaine Bradycardia, MepIvacaine Yes except vfib, Amide PrIlocaine Liver No bupivicaine (no asystole Progression: EtIdocaine effect) DIbucaine (neg. Tongue ionotropy) numbness Tetracaine Plasma Lightheadedness Procaine Yes Hypotension Double vision Ester Chloroprocain cholinesteras (PABA Yes Benzocaine e metabolite) (vasodilation Muscle twitching ) Unconsciousness No Arrhythmias Coma Ester Cocaine Liver No (vasoconstricts w/o ) hypotension ANESTHESIA Regional Anesthesia 1. Topical – lidocaine, benzocaine spray or cream 2. Local 3. i.v. regional (Bier block) – mainly upper extremity, alternating tourniquets to keep anesthetic locally 4. Peripheral nerve block 5. Spinal anesthesia 6. Epidural anesthesia 7. Caudal block – pediatrics Pass through ligamentum flavum into epidural space Epidural – L1L2 Caudal block – < S2 Spinal Analgesia Local anesthetic applied intrathecally (into CSF); as if SC transection (loss of sensory, motor, proprioception). Apply below L2 (where SC ends). Can spread up, so go lower to prevent BP drop/chest wall paralysis. Epidural Local anesthetic crosses dura + hits nerve roots causing band like analgesia. Can go as high as T10/T11 for abdomen, L1/L2 for pelvic surgery, T57 for lobectomy. Can block cardiac accelerators if Afib or Vfib at T2T4. Epidurals allow in narcotic dose (less confusion, better pain control), gets out of bed sooner, faster return of bowel control due to faster return PSNS, less DVT/PE risk (moving around sooner). Caudal Block Used in pediatrics instead of epidural for peritoneal or urologic Surgery. Below S2 ANESTHESIA NMJ Blockade ACh responsible for analgesia (SC), arousal/attention (RAS), SNS – thoracolumbar cognition (lost in AD). ACh at all preganglionic synapses, all PSNS – cervicosacral PSNS postganglionic synapses, SNS postganglionic sweat glands (muscarinic Rs), somatic motor neurons. NMJ Blockers 1. Intubation 2. Muscle relaxation for intraabdominal, orthopedic, laproscopic, delicate (eye) surgeries Botox used for tx tension Botulinum Toxin Produced by Clostridium botulinum found in raw honey, imported meats. Degrades synaptobrevin preventing ACh migraine, spasticity vesicles from fusing w/ presynaptic membrane. “Floppy” (dystonia), cosmetic (flaccid) baby. Treat w/ antitoxin + supportive care. NMJ Blockers by Duration of Action NDMBs Duration Metabolism Notes Short acting duration if atypical Mivacurium (< 20 min) Pseudocholinesterase pseudocholinesterase Rocuronium Intermediate Roc/Ver – hepatic/biliary, some renal Cisatracurium acting Cis – Hoffman eliminati(pH/temp dependent Use Cis if renal/liver dz Vecuronium (< 90 min) enzymatic degredation, NOT organ dependent) Pan used in long cases + Pancuronium Long acting peds; inhibits vagal = Pipecuronim (60120 min) Renal clearance HR (peds tend to get Doxacurium bradycardic) LOCAL ANESTHETICS Drug Classification Main Clinical App Pharmacodynamics Side Effects/ADR Ester local 1. Topical anesthetic Unique property of vasoconstriction. 1. Toxic anesthetic Metabolized by liver (vs. other ester 2. Addictive Cocaine anesthetics). First local anesthetic Inhibits NE reuptake PNS + CNS nerve block Lidocaine is most widely used local 1. Systemic toxicity: Rapid CV anesthetic. Cocaine derivative. depression, hypotension * give w/ Epi to enhance Blocks membrane depolarization by (vasodilation), bradycardia, V + local block at lower [ ] + reversibly blocking Na fib, asystoles. Reversed by bleeding conductance. Unionized (B) form is intralipid antidote transported INSIDE cell reionizes 2. Progressive CNS toxicity (BH) blocks intracellular side of dizziness, tinnitus, metallic LIdocaine + BupIvacaine AmIde local Na channel. Delayed onset w/ pH taste, double vision, tongue MepIvacaine anesthetic (abscess) by shifting toward ionized numbness, seizures, coma, form (BH) – use more anesthetic. respiratory arrest. PrIlocaine + Blocks C pain fibers (unmyelinated) 2. Allergic rxn less likely than EtIdocaine Reversible Na DIbucaine channel blocker + mediumsized Adelta (myelinated) esters w/o blocking pressure, vibration. Order of blockade: small myelinated > small unmyelinated > large myelinated > large unmyelinated fibers. Order of loss: pain (lose first) > temp > touch > pressure (lose last). Liver metabolism. 1. Benzocaine for mucous Same action as above. Metabolized 1. Hypersensitivity rxn (due membranes by pseudocholinesterase + excreted to Tetracaine Procaine 2. PNS + CNS nerve block in urine (except cocaine; liver PABA) Chloroprocain Ester local metab). PABA metabolite causes 2. Systemic toxicity of CV + allergic rxn CNS (see above) Cocaine anesthetic 3. Tissue infarct Benzocaine 4. Benzocaine – methemoglobinemia 5. Chloroprocaine – back pain ANESTHESIA PHARMACOLOGY GENERAL ANESTHESIA Drug Classification Main Clinical App Pharmacodynamics Side Effects/ADR INHALED ANESTHETICS 1. Anesthesia induction Not sole anesthetic b/c low potency 1. Causes bowel enlargement, 2. w/ sevoflurane – sole (high MAC/100% MAC). Use at inner ear, pneumothoraces, induction in child high [ ]. Bronchodilate. Coronary air emboli (less soluble than Nitrous Oxide vasodilation but SVR. NO so enters air spaces (N2O) Inhaled anesthetic faster than NO can leave). 2.Apnea 3. CV depression 4. ICP 5. GFR 1. Anesthesia induction Isoflurane most potent/low MAC > 1. Apnea 2. Sevoflurane + N2O – sole Sevoflurane > Desflurane. 2. Respiratory depression induction in child Bronchodilation + coronary 3. CV depression Isoflurane Inhaled anesthetic Sevoflurane 3. MI/reperfusion injury vasodilation (w/ SVR). 4. ICP – cerebral flow GABAA agonist 4. Uterine relaxation Prevention of uterine contraction can 5. GFR/nephrotoxicity Desflurane lead to postpartum bleeding 6. Postpartum bleeding 7. Rare malignant hyperthermia IV ANESTHETICS Propofol Rapid i.v. Rapid induction + short Most frequently used i.v. anesthetic. 1. Pain on injection i.v. anesthetic proceudres Causes hypnosis via GABAA 2. Euphoria 1. Induction (bolus) agonist; DA NcA (abuse), 5HT 3. Infection/sepsis risk (due to 2. Maintenance (infusion) in area postrema (antiemetic). intralipid solvent as growth 3. Short or outpt cases ICP, BP, CO, HR medium) 4. Neurosurgical cases 4. Abuse potential (MJ O.D.) 5. Ophthalmo cases 5. Apnea + CV depression * less postop nausea than * Requires good CV funx thiopental * Minimal analgesia * Antiemetic 1. +++Analgesia + amnesia NMDAR inhibitor induces 1. Combativeness though Phencyclidine 2. Trauma w/ hypovolemia dissociative anesthesia (profound unconscious, hallucinations, or shock ( CO) unconsciousness + amnesia but eyes nightmares (PCP) analog 3. Peds (esp. congential R remain open + pt combative). 2. ICP ( cerebral perfusion) Ketamine L shunt) Activates SNS causing CO, i.v. anesthetic 3. salivation – possible i.v., i.m. SVR, BP (used in MVA/trauma). airway obstruction in ICP. children NMDAR 4. Psych rxn upon awakening antagonist (nightmares, illusion) attenuated by benzos 1. Induction (bolus) GABA agonism results in hypnosis, 1. Severe pain on injection 2. Cardiac + vascular cases – sedation, unconsciousness. ICP/O 2 by prelidocaine injection i.v. anesthetic no SNS/hemodynamics 2. ? Cortisol suppression Etomidate demand but net cerebral O 2upply i.v., infusion GABA agonist 3. Heart + lung transplant demand ratio. Minimal CV or 3. N/V in 50% 4. Neurosurgery ( ICP, respiratory changes. Imidazole 4. Myoclonus + hiccups (most) 2 demand) derivative. Cleared by liver. 5. Brief periods apnea 1. Brief (< 24h) sedation Recently approved. Minimal effect Selective 2 Dexmedetomidine agonist postop ICU pts on respiration. BP, HR, CO. Anesthesia induction + short Faciliatate GABAA action by 1. Contraindicated in porphyria surgical procedures duration of Cl channel opening, thus 2. cerebral blood flow neuron firing. BarbiDURATe = Thiopental Barbiturate DURATion. High potency, high lipid GABAA agonist solubility, rapid entry into brain. Effects terminated by rapid redistribution into tissue + fat. cerebral blood flow. Endoscopy in combo w/ Facilitate GABAA action by 1. Severe postop respiratory gaseous anesthetics + depression frequency of Cl channel opening. Midazolam Benzodiazepine narcotics REM sleep. Causes amnesia + 2. BP – treat O.D. w/ muscle relaxation (general flumazenil anesthesia) 3. Amnesia MALIGNANT HYPERTHEMIA DRUGS 1 Malignant hyperthermia Prevents release of Ca from Skeletal muscle weakness 2. Neuroleptic malignant sarcoplasmic reticulum of skeletal (little – no effect on cardiac or Peripheral skeletal muscle syndrome – antipsychotic muscle. Malignant hyperthermia is smooth muscle) Dantrolene relaxant ADR caused by concomitant use of inhaled 3. UMN disoder anesthetics (except N 2) + SR CCB succinylcholine in genetically predisposed ANESTHESIA PHARMACOLOGY (continued) NMJ BLOCKERS Drug Classification Main Clinical App Pharmacodynamics Side Effects/ADR 1. Rapid intubation – esp. if ACh agonist binds 2 1. Hyperkalemia (esp. burns, aspiration risk subunits of nicotinic ACh R. NMJ disorders, renal failure) 2. Muscle relaxation for Rapid depolarization causes 2. Malignant hyperthermia short procedures(biopsies) fasciculations followed by 3. Myalgias ~ due to flaccid paralysis lasting fasciculations 5min1h. Reversal due to 4. ICP, ophthalmic P, Succinylcholine Depolarizing degredation by intragastric P NMJ Blocker pseudocholinesterase in 5. Prolonged paralysis if blood (not AChE at NMJ). atypical pseudocholinesterase Depolarization releases K (10h) from cells (hyperkalemia) 6. Hypercalcemia made worse if burn or ALS (not using muscle so ACh R around NMJ). Aminosteroids: Nondepolarizing 1. Paralysis (esp. in ALS, Competitive antagonist of 1. Anaphylaxis Rocuronium NMJ Blockers burns, longer cases) nicotinic R (binds subunit). 2. Histamine release (atra, pan, Pancuronium Quarternary ammonium miva; NOT cis) – Vercuronium Nicotinic R Reverse w/ neostigmine similar strx to ACh. Reversal bronchospasm, flushing, competitive (AChEi) due to slow release from hypotension, peripheral Curare Derivatives: antagonist NMJ + hepatic/biliary +/ vasodilation dTubocurare renal metabolism (slower (avoid in asthmatics, sepsis) Atracurium than succinylcholine). Cisatracurium 1. NMJ blockade reversal Inhibition of AChE = ACh. 1. Cholinergic crisis at (given in combo w/ Peak effect in 10 min, lasts > muscarinic Rs = SLUDGE glycopyrrolate) 1h. Never give Salivation + Sweating (wet) succinylcholine after Lacrimation reversal b/c AChE also Urination (incontinence) Neostigmine Reversible AChE inhibit pseudocholiesterase. Defication (diarrhea) inhibitor Prevent cholinergic crisis w/ GI hypermotility/Emesis antimuscarinic Bradycardia (glycopyrrolate, atropine) Prevent w/ glycopyrrolate or Atropine (antimuscarinics) 2. muscle weakness at high doses 1. Myasthenia Gravis Dx Rapid onset in 12 min. Test muscarinic effects –bradycardia, (given in combo w/ dose is given to suspected urethral construction, sweat, Fast acting atropine) myasthenia gravis pt, if saliva, bronchial constriction Endrophonium reversible AChE 2. Reverse action of inhibitor strength improves = +dx. nondepolarizing NMJ blockers 1. Treatment of Myasthenia Competitive inhibitor at ACh Cholinergic crisis – bradycardia, Gravis (given in combo binding site potentiates ACh urethral construction, sweat, Pyridostigmine Reversible AChE w/ glycopyrrolate) action at NMJ (nicotinic Rs) saliva, bronchial constriction (reverse inhibitor 2. Reverse action of + GI (muscarinic Rs) w/ pralidoxime) nondepolarizing NMJ blockers 1. CNS antiACh toxicity Only AChE inhibitor that Physostigmine/Antiliriu Reversible AChE 2. Reverse effects volatile crosses BBB. Given if slow m inhibitor anesthetic to awaken (elderly) to help w/ 3. AD attention/arousal. Irreversible 1. IOP by inducing miosis Treat organophosphate poisining Organophosphates AChE inhibitor * pesticide exposure acutely w/ atropine; definitive tx = pralidoxime 1. Bradycardia (ACLS) – Atropine – fast onset, crosses atropine BBB; glycopyrrolate – 2. Surgery induced intermediate onset, does NOT Atropine AntiACh bradychardia (PSNS cross BBB. Glycopyrrolate Antimuscarinic activatio glycopyrrolate 3. Cholinergic crisis prophylaxis b/f reversal agent 1. NMJ blockade reversal Available only in Europe. Aminosteroid Binds Rocuronium > other Sugammadex inhibitor aminosteroid NMJ blockers causing release from nAChR. FLUIDS Total Fluids TOTAL FLUIDS Maintenance Deficits Ongoing Losses Water Salt Water Salt Water Salt + + 100+50+20 cc/day 3 mEq/kg/day Most pts 10% down, so cc for cc replacement Measure Na /K of replace 10% body water lost fluid = hang bag Main Line (1g = 1 cc) of same [ ] Piggyback so can with losses Dehydration 2 WAYS TO CATEGORIZE + [Na ] Degree Hypo Iso Hyper Na 130150 Na > 150 Mild Moderate Severe Na < 130 *most common 35% 710% > 12% Correct over 24 hours Correct over 48 hours ~5% ~10% ~15+% ½ deficit in first 8 hours Weight weight by 5% by 10% by 15% then give rest over next 16 h Regular urine urine 01 urine Urine output output output output or slight in 13x over last over last 1218 volume/frequency 1218 hours hours Tachy Vital No change Tachy Signs Normotensive BP Sick + AMS Sunken fontanel Dry mucous Sunken eyes Mildly dry membranes Physical mucous Nl turgor Dry MM Exam Cap refill < 2 (parched) membranes skin turgor sec Cap refill > 3.5 Two Phases of Rehydration sec Treatmen Outpatient Admit to Admit to ICU t rehydration floor 1. Emergency Phase: Restore or maintain intravascular compartment for adequate perfusion Completed when peeing Same for every patient 20 cc/kg NS/lactated ringers (or any colloid) q2030 minutes until peeing check BUN/Cr after 2 bolus 2. Repletion Phase: Gradually fine tune fluids + electrolyte balance Correct hyponatermia/isonatremia over 24 hours Correct hypernatremia over 48 hours FLUIDS continued Fluid Preps NS = 154 mEq NaCl + 1L H O 2 ½ NS = 77 mEq NaCl + 1L H O 2 ¼ NS = 38 mEq NaCl + 1L H O 2 D5W = 5% dextrose = 50g dextrose + 1L H O (52 in 100 cc) + Don’t give lactated ringers if renal failure b/c high K (4 mEq/L) Lactated ringers better for significant acidosis b/c lactate bicarb in liver (better buffer) Maintenance Fluids Maintenance fluid (INS) = patinet’s usual daily loses (OUTS) Account for sensible (urine) + insensible (respiration, skin, stool, fever) losses Fever: for 1ºC > 38.0 = 10% rate If urine output = fluids If RR = fluids 100/50/20 RULE: First 10 kg = 100 cc/kg/day 2 10 kg = 50 cc/kg/day wt > 20 kg = 20 cc/kg/day + Maintenance Na = 3 mEq/kg/day e.g., 8 kg patient = 800 cc/day 12 kg patient = 1100 cc/day 25 kg patient = 10(100) + 10(50) + 5(20) = 1600 c/day Adult standard = D5W 1/2NS + 20 KCl @ 100125 cc/hr 70 kg maintenance = 10(100) + 10(50) + 50(20) = 2500 cc/24h 2500 cc/24 hours = 100 cc/hr Na = (3 mEq/kg/d)(70kg) = 210 mEq/day _2500 cc/d_ = _1L_ 210 mEq/d x x = 80 mEq NS = ~1/2NS Deficits Most patients 10% down (moderate dehydration) Fluid replacement at 1g deficit = 1cc replacement e.g., 8 kg at presenting weight with moderate dehydration (tachy) = 800g give 1cc/g = give 800 cc Na deficit in moderate dehydration Hyponatremic Dehydration 15 mEq/kg Give over 24 hours < 130 Isonatremic Dehydration 10 mEq/kg Give over 24 hours 130150 Hypernatremic Dehydration Deficit = 5 mEq/kg Give over 48 hours > 150 + If clinically dry (> 10% total body water loss) = ALL patients are total body Na depleted (doesn’t matter if hyper/iso/hyponatremic). Only exception is DI. Ongoing Losses Volume IN = Volume OUT cc for cc replacement over the following shift so never more than 1 shift behind For salt, measure electrolyte output (Na + K only) & hang bag with that [ ] + + e.g., patient stooling out with 82 mEq/L Na + 12 mEq/L K in stool Use ½ NS + 10 KCl in D5W at rate of previous loss to approximate the loss FLUIDS continued + + Four Rules of K 1. No K unless kidneys are working 2. Once K is added, add enough to account for predicted shifts in serum K based + upon predicted change in serum pH e.g. for diarrhea + dehydration metabolic acidosis (lose bicarb in stool + perfusion; as correct dehydration lactic acidosis so bicarb = K goes INTO cells so serum K 3. Forms: KCl KPO 4good for low phosphate states like DKA/low ATP states) Kacetate (good for very acidodic b/c acetate bicarb by liver) + 4. How much K ? If serum K normal + no anticipated shifts 20 mEq + If serum K high don’t give + If serum K low 30–40 mEq Sample Problems e.g. 8 kg baby moderate dehydration (tachy but normal BP) = 10% total body water. Presenting Na = 134 Maintenance water = (8kg)(100cc) = 800 cc/24hr Maintenance salt = (3 mEq/kg/day)(8kg) = 24 mEq/24hr Deficit water = by 10% and 1g = 1cc so = 800 cc total Deficit salt (isonatremic) = (10 mEq/kg)(8kg) = 80 mEq total e.g. 12 kg baby moderate dehydration = 10% total body water. Presenting Na = 122 Maintenance water = (10kg)(100cc) + (2kg)(50cc) = 1100 cc/24hr Maintenance salt = (3 mEq/kg/day)(12kg) = 36 mEq/24hr Deficit water = by 10% and 1g = 1cc so = 1200 cc total Deficit salt (hyponatremic) = (15 mEq/kg)(12kg) = 180 mEq total e.g. 5 kg baby with N/V/D x 3d with 1x diaper overnight, tachycardia, elevated RR (metabolic acidosis with compensatory respiratory alkalosis), normal BP, no tears, dry mouth, normal cap refill (moderate – severe dehydration); Na 138, K 3.9 Phase 1 = give emergency fluids = (20 cc/kg)(5 kg) = 100 cc NS over 30 minutes; if no pee repeat Phase 2 = replete over 24 hours b/c isonatremic dehydration Maintenance water = (5kg)(100cc) = 500 cc/24hr = rate of 20 cc/hr Maintenance salt = (3 mEq/kg/day)(5kg) = 15 mEq/24hr Deficit water = by 10% and 1g = 1cc so = 500 cc total (but already gave 200 cc in emergency phase so only give 300 of this). Give ½ (150 cc) in 8 hours = 20 cc/hr 2 ½ (150 cc) over next 16 hours = 10 cc/hr Deficit salt (isonatremic) = (10 mEq/kg)(5kg) = 50 mEq total (but already gave (0.2L)(130mEq/L) = 26mEq given so 5026 = 24 mEq Na left to give In total, give 800 cc/24 hours + 40 mEq Na in 24 hours 20 cc/hr maintenance + 20 cc/hr deficit = 40 cc/hr x 8 hours 20 cc/hr maintenance + 10 cc/hr deficit = 30 cc/hr x next 16 hours _40mEq_ = __x__ 800 cc 1000cc x = 50 mEq D5W + 50 mEq NaCl/L + 30 Kacetate (b/c acidodic) = D5W 1/2NS + 30 Kacetate HEMATOLOGY ANATOMY Hematopoiesis hSC ood Macrophages Histiocytes Kupfer cells Microglia 3 Peripheral Blood Smear Total WBC = 5,000–10,000/mm (Normal Values) % Absolute Count 3 Neutrophils 50–70% 2,000–7,000/mm 3 Lymphocytes 20–40% 1,000–4,000/mm Monocytes 1–6% 50–600/mm 3 3 Eosinophils 1–5% 50–500/mm3 Basophils 0–2% 0–100/mm HEMATOLOGY – ANATOMY (continued) Erythropoiesis Fetal period 3–6 weeks: Yolk sac (early precursors) 6–10 weeks: Liver (main site weeks 9–24) + spleen (blood, nodes, thymus) 10–11 weeks: Bone marrow (main stie > 24 weeks) 2 weeks postpartum: All in bone marrow Adult Pronormoblast Basophilic Polychromatophilic Orthochromic Reticulocyte Mature (RBC) normoblast normoblast normoblast larger than Erythrocyte (blue cyto = (larger than (2+nk cyto = ribosomes for RBC; has RNA Fe of Hgb; no Hg production but no nucleus) nucleus, no mitochondria) Eryth = red Erythrocytes Anucleate, biconcave large surface area: volume ratio easy gas exchange (O +2CO ). E2ergy from glucose only – 90% anaerobically degraded to Erythrocytosis = polycythemia = # RBCs lactate; 10% by HMP shunt. Live for 120d. Membrane contains chloridebicarb antiport Anisocytosis = varying sizes important to “physiologic chloride shift” which Poikilocytosis = varying shapes allows the RBC to transport CO from the 2 Reticulocyte = immature RBC periphery to the lungs for elimination Platelets Small cytoplasmic fragment derived from Thrombocytopenia or platelet (thrombocytes) megakaryocttes. Involved in 1º hemostasis. When dysfunction results in petechiae (small capillary hemorrhage) activated by endothelial injury, aggregates w/ other platelets + interacts w/ fibrinogen to form a platelet (hemostatic) plug. Contains dense granules (ADP, Lifespan 57 days 2+ Ca ) + granules (vWF, fibrinogen). Approximate ½ of platelet pool is stored in spleen. Leuk = white Leukocytes Types: granulocytes (basophils, eosinophils, neutrophils) and mononuclear cells (monocytes, Nl – 4,000 – 10,000/uL lymphocytes). Responsible for immune response. Basophilic – staining readily w/ basic stains (dark blue granules) Basophils Mediate allergic reaction. < 1% of all leukocytes. Bilobate nucleus. Densely basophilic granules containing heparin (anticoagulant), histamine (vasodilator), and other vasoactive amine, and leukotrienes (LTD4). Found in blood. HEMATOLOGY ANATOMY (continued) Mast Cells Mediates allergic reaction. Degranulation – Involved in Type I hypersensitivity histamine, heparin, eosinophil chemotactic reactions factors. Can bind IgE to membrane. Mast cells Cromolyn sodium prevents mast resemble basophils structurally + funcationally but are not the same cell type. Found in tissue. cell degranulation (used to treat asthma) Eosinophils 16% of all leukocytes. Bilobate nucleus. Pakced w/ Eosin = a dye large eosinophilic granules of uniform size. Defends Causes of eosinophilia = against helminthic + protozoan infection (major basic protein). Highly phagocytic for AgAb complexes. NAACP Produces histaminase + arylsulfatase (help limit Neoplastic Asthma reaction following mast cell degranulation). Allergic processes Collagen vascular disease Parasites (invasive) Neutrophils Acute inflammatory response. 4075% of WBCs. Normal = 25 segments Phagocytic. Multilobed nucleus. Hypersegmented ( > 5 Large, spherical azurophilic granules (lysosomes) contain hydrolytic enzymes, lysozyme, segments) polys (bands, myeloperoxidase, lactoferrin. stabs) are seen in Vit B12folate deficiency Mono = one (nucleus) Monocytes 210% of WBCs. Large, kidneyshaped nucleus. Extensive “frosted glass” cytoplasm. Differentiates into macrophages in tissues. Macrophages Phagocytoses bacteria, cell debris, senesce
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