CONTENTSContributingAuthors ixPre/iKe xiiipREOpERATIVE pATIENT EVA! UATION 1_1{esse M. EhrenfeldPHARMACOLOGY'INHALATIONALAMESIHFTICS 2A_ lDavid LParris and SamuelC.SeidenPHARMACOLOGY' INTRAVENOUSANESTHETICS AND ANALGESICS 2B.5W OOl/e l ( SeidenpHARMACOI cay I DCAI ANESTHETICS K _l aJenna Honsen andSamuel C. SeidenPHARMACOLOGY' NEUROMUSCULARBLOCKING DRUGS AND REVERSAL AGENTS 20.22Jenna Hansen and Samuel C.SeidenPHARMACOLOGY: VASOACTIVE. AUTONOMICAND CARDIOVASClJI Aft DRLlGS 2E_2SSqmuel C SeidenI ENCOUNTERED DRUGS IN ANESTHESIA 2E_38Samuel C.Seiden andStephen FinkPHARMACal cay ANTIBIOTICS ANDHERBALMEllli:lNES lG:.l2Richard D. Urman and Jesse M. EhrenfeldANESTHESIA EQUIPMENT 3- 1(ennifer Bartlett 4.1TQwn BhgNgANESTHESIA TECHNIQUES 5- 1Benjamin UngerREGIONAl ANESTHESIA 6-1I'ereLIImPERIOPERATIVE MONITORING 7. 1Fronds X Djllon8. 1FrondS X DjllonFLUIDS, ELECTROLYTES, &TRANSFUSIONIHERAPY 9.'Aranva BagchiCOMMON INTRAOPERATive PROBLEMS 10. 'Randy Fayne11 .' l.hlKa; MouhesAcUTe PAIN MANAGEMENT 12.'No'in; Vadivelu and Christian Whitney 13-1Piyush MathurCOMPliCATIONS OF ANESTHESIA 14-1Michael W Sanford and David A.NakataTRAUMA, BURN,AND CRITICAL CAREMANAGEMENT 1 5_1DanielW JohnsonANESTHESIA FOR CARDIAC SURGERY 16. 'AmandaRheeand Unda Shore-LessersonANES.IH.ESIAEO.R.IHO..RAc.u:...s.uRGERY 17. ''Gnochon M. AnagnostouANESTHESIA FOR GENERAL ANDABDOMINAl SURGERY 18_1Moged ArgoliousANESTHESIA FOR VASClII AB SURGERY 19. 'ANESTHESIA FOR NEUROLOC:;IC SURC:;ERY,NEURORADIOLOC:;Y, AND ECT 20-1'oshun H. AtkinsANESTHESIA FOR DIDI dRYNGO! ooy(ENT) AND OPHTHALMOLOGY 21-1'oshunH. Atkins&EN.A.! SYSTEM AND..ANESIHESIA....EORURO! OGIC SURGERY 22-1Christine fin e rANESTHESIA FOR ORTHOPEDIC SURGERY 23.1Robert Hsiung and Peter WuANESTHESIA FOR ENDOCRINE SURGERY 24-1Matvey &bylevANESTHESIA FOR OBSTETRIC AND Paloma ToledoPEDIATRIC ANESTHESIAThamas M RomaoeW26_1AMBULATORYAIIIESIHESIA 2{,..1Ursula GalwayANESTHESiA FOR AESTHETiC SURGERY &SURGERY OUTSIDE OFTHE OpERATINGROOM 28. 1Ruchir Guptaand Padmo SurampudiMANAGEMENT OF CHRONIC PAIN 29_1Nalini Vadivelu and Christian WhitneyORGAN TRANSPLANTATION 30. 1Amoocln Rhee ood Mark AhelANESTHESIA FORTHE ELDERLyRaymond C.RoyECG INTERPRETATIONAmanda Rheeand Linda Shore-LessersonETHICAl ISSUES IN ANESTHESIAJesse M. Ehrenfeld and Richard D. Ull71anEMERGENCY AI GORITHMSTracy Palumbo Davich31.132_133. 134 1COMMON MEDICAl PHRASES IN SPANISH 35_1Solomon MayaNORMAL LABORATORY VALUES 36.1MarkA. HoeftAppENDIX A.1A: Formulae and Quick ReferenceB.:An.e.stb.esia....MachioeOR ChedmutRe.ClllIlm..e.QdotioasC: SettingUpThe OR For AnAnesthesia CaseD: Mana!?ement orMalignant HYPerlhermiaAcquisitions Editor: lisc MeAliSlerManaging Editor: Mal !eT. DemoskiProject Manager : Bridgett DaughertySenior Manufact ur ing Manager: Benjamin RiveraSenior Mar ket ing Manager: Angela PanettaC"'ative Director: Doug Sm""kProduction Serv",e : ApUlrl, Inc. 200 9 by Lip pinco tt WiIli a m s &Wilkin s, a W o lte rs Kluwe r bu si nes sB OW alnut StreetPhil ad "l phi a, PA 19106 US ALWW.co mAll rights r"' e..... ed. Tnis book is protected by copyright. No part of th is book may bereproduced in any form by any means. including pnotocopying.or uti lized by any infor -mat ion storage and ret rieval sy5tem without wr itten perm ission from tne copyrightow ner. exce pt for br ief quo tations embod ied in crit ical art icles and reviews. Materialsappeari ng in tn i. book pre pared by indr.iduals as p.rt 01 thei r official dutie' as U.S. gov-ernment employee, are not cover ed by the above-me nt ioned copyright .Primed in ChinaLibrary of Congre ss Catalogi ng-in-Pu bl ication DataPocket anesthes ia I [ed ited by] Richar d D. Urman, Jesse M. Ehrenfeld.p. ; cm.Includes bibliograp hical refere nces and index.ISBN 1l: 9780-78179584 -5 (alk. paper)ISBN 10, 078 17-9584-2 (alk. paper)1. Anen nesiology---Handbooks, manuals. etc. 2. Anenhe,O>--Handbooks, m"nual" etc.I. Urman, Richard Q II, Ehre nfeld. Jesse M[DNLM: 1. Anen he, ia- l-'h ndbooks. 1 Anesthet "'s-Handbooks. WO 231 P7192009]RD82.2.P62520096 17.9'6--dc222009008498Ca re h"s been taken to confirm t he .ccur"er of the informauoo present ed "nd to describ e genera lly "cc ept ed pract ices. How"""r, the authors, edito rs, "nd arenot responsible for errors or omissions or for any con seq uences from application oft he ioformatio n in t his book and make no watT:Imy. expre"ed or implied, wit h re' pectto the currency, complete ness. or accuracy of the contents 01the publication. Applicanon of the information in a parti cular situation remains t he profess ional respo nSibilityof the pract itioner.The authors, ed itors , "I' d h:r;e exerted every effort to ensure th"t drugselect ion and dcsage set lo rth in this text are in accordance With current recommen-dations and practice at t he t ime 01 publicat ion. However, in view of ongOing resea rch,ch" ng." in gov"r nment r"gub t ion. , "I'd the con55)BUN/Cr/Gluc >65ECG(M>45; F>55)BUN/Cr/Gluc >65CXRECG/CBC/CXRElectrolytes/BUN/Cr/GlucMod. Risk*ECG (M>45;F>55)BUN/Cr/Gluc >65CBC>65ECG(M;45; F;SS)BUN/Cr/Gluc >65CXR/CBCECG/CBC/CXRElectrolytes/BUN/Cr/GlucH I g h J ~ i ~ ~ ~ECG/CXRICBC/BUN/Cr/Gluc>65Blood bankT+SECG/CXRlCBCBUN/Cr/Gluc >65Blood bankT+SECG/CBC/CXRElectrolytes/BUN/Cr/GlucBloodbankJ-tS*Seetable belowon page1-4:"Predictorsof Increased Cardiovascular Risk," for low-/mod-/high-riskcategories.INFECTIVE ENDOCARDITIS (IE) ANTIBIOTIC PROPHYLAXISBased on risk of developing IE& severity of outcome if IEwere to occurHighest-risk patients (those requiring prophylaxis) include those with: Prosthetic cardiac valve Previous infectiveendocarditis Congenital heart disease (CHD) (Unrepaired cyanotic CHD, completely repairedCHD with prosthetic device) Repaired CHD with residual defect at site Previous cardiac transplantation with subsequent cardiac valvulopathy.Note: Current guidelines no longer include pts with common valvularlesions (bicus-pid aortic valve,acquired aortic/mitral valve dz, mitral valve prolapse, hypertrophiccardiomyopathy)gCefazolin 2 g IV/1MCeftriaxone1 g IV/I MSource:Adapted fromWilsonW, et al. Prevention of Infective Endocarditis. Circulation 2007;116(15):1736-1754.Figure 1-2 Perioperative risk-assessment algorithm. (From Fleisher LA, et al.ACC/AHA 2007 Perioperative Guidelines.] AmCall Cardiol 2007;50(17):1707-1732,with permission.)Perioperative surveillanceand postoperative riskstratification and risk factormanagement1 or 2 clinicalrisk factors:j:: No clinicalrisk factorsforcardiactesting,symptomatic/unstable angina)Symptomatic valvular dzDecompensated CHF (pulmonaryedema/peripheral edema, PND)Source:Adaptedfrom Eagle KA,et aI.ACC/AHA Guidelines Updatefor PerioperativeCardiovascular Eval-uationfor NoncardiacSurgery-Executive Summary. JAmColi Cardiol 2002;39:542-55lPERIOPERATIVE BETA-BLOCKER THERAPY (NONCARDIAC SURGERY) Perioperative may-i cardiac events &mortality(controversial, as recentdatasuggests may t morbidity) Pts already on therapy should be continued Consider initiation of therapy in: Pts who have an indicationfor Major vascular surgeryPHARMACOLOGY: INHALATIONALANESTHETICSDAVID L. PARRIS SAMUEL C. SEIDENPotent inhalational agents: mechanism of action still undetermined. Theorized mem-brane disruption or decreased membrane conductance, GABAA receptor action. Anes-thetic binding might significantly modify membrane structure.Partition Coefficients Express relative solubility of anesthetic gas at equilibrium Lower partition coefficients imply low solubility, slower solution/tissue uptake, butrapidinduction (e.g. desflurane) Higher partition coefficients imply high solubility, prolonged induction (e.g., halothane) Tissue:blood partition coefficient =time for equilibrium of tissue (brain, fat, mus-cle) with arterial bloodMAC: minimum alveolar concentration.Source:Adaptedfrom MorganG, Mikhail M,MurrayM.Clinical Anesthesiology 4th ed. McGraw-Hili Medical:NewYork,NY:2005.FACTORS AFFECTING ANESTHETIC UPTAKE Agent levels in the brain depend on agent levels in the alveolus. Goal is to achieve rise in Fa (alveolar anesthetic concentration)/Fi (inspiredanesthetic concentration). t Fa/Fi ---",t speed of induction.Factors that t FalFi Low solubility in the blood; anesthetic potency correlates with lipid solubility. Potency: halothane > isoflurane > sevoflurane > desflurane > N20. Uptake and solu-bility are inversely proportional to induction time-Le., the lower the partition coeffi-cient, the less soluble the agent and therefore the faster the rise in partial pressure. High alveolar ventilation and alveolar blood flow. High Fi. High fresh gas flow rates. The difference in- partial pressure between alveolar gas and venous blood. Anesthetic uptake is directly proportional to cardiac output as a function of alveo-lar blood flow. Low-flow states (e.g., sepsis, sympathetic blockers, CHF) reduce uptakeand t induction time because of the rapid rise of Fa. High CO ---",t rate of anestheticremoval from alveolus ---",t rate of induction.Concentration Effect Increasing the inspired concentration of a gas results in a disproportionate increasein the alveolar concentration. Most clinicallysignificant with N20, as can be used at much higher inspired concen-trations than volatile anesthetics.Second Gas Effect The ability of a large-volume uptake of one gas (first gas) to accelerate the uptake ofa coadministered gas (second gas). Example: N20 accelerates uptake of both volatile anesthetic and oxygen, althoughthis is probably not clinicallysignificant.The faster the alveolar/brain concentrationreaches inspired concentration of agent, the faster the induction.Other Factors Affecting Anesthetic Uptake Tissue uptake (tissue/blood partition coefficient for fat vs muscle vs brain) Intracardiac shunts (R-to-L shunt ---",t rate of induction) Pediatric pts ---'" faster induction due to t alveolar ventilation, t FRe, t %of blood flow tobrainELIMINATION/RECOVERY Reduction of anesthetic in brain tissue is by biotransformation (P-450),transcutaneous loss, or exhalation, with exhalation being the most significant. Recovery expedited by high fresh gas flows, elimination of rebreathing, low absorptionby the circuit, decreased solubility, high cerebral blood flow and increased ventilation.DIFFUSION HYPOXIA As anesthetic diffuses out of the blood and enters the alveolus, it displaces and re-duces the concentration of inspired oxygen and CO2, With rapid-offset agents such as N20 , where the concentration is high and bloodsolubility low, the diffusion of alveolar O2 can lead to hypoxia.. Administer high-flow 100% oxygen for 5 to 10 min after discontinuation of N20 toprevent significant hypoxia.MINIMUM ALVEOLAR CONCENTRATION (MAC) The MAC of an inhaled anesthetic is the alveolar concentration at which 50% of pa-tients will not move in response to a standardized stimulus (e.g., surgical incision). Developed to compare potency of agents. MAC values are roughly additive (i.e., 0.5 MAC of N20 plus 0.5 MAC of sevoflurane= 1.0 MAC). At MAC 1.3, 95% of patients will not move in response to surgical stimulus. MAC-BAR (1.5-2.0 MAC): Concentration required to block autonomic reflexes tonociceptive stimuli. MAC-Aware: Concentration at which 50% of patients will not be forming long-termmemory. MAC-Awake (0.3-0.5 MAC): concentration required to block voluntary reflexes andcontrol perceptive awareness (i.e., opening eyes on command). MAC greatest at 1 year of age and reduced by 6% per decade of life.MACVARIABILITYElderly ptsBenzodiazepinesIntravenous anestheticsOpiatesPregnancyA,::.. ........,.. ; ~ . . . . . useHypothermiaIncreased altitudeHyponatremiaSevere hypotensionAcidosis, hypoxiaChronic alcohol abuseVery young age (closer to 1 year of age)Increased temperature (>42C)Decreased altitudeDrugs: MAOls,TCAs, cocaine, acute amphetamine useBENEFITS OF INHALATIONAL ANESTHETICSNonflammable; reusable (via circle system); hypnotic; overall low degree of respiratorydepression vs intravenous agents, potent bronchodilatorsSIDE EFFECTS OF VOLATILE ANESTHETICS Hypotension 2 to vasodilation &myocardial depression Potentiates neuromuscular blockade During spontaneous ventilation ~ . . j , RR & ..j, T\I, hypercarbia, ..j, ventilatory response tohypoxemia Inhibitor of hypoxic pulmonary vasoconstriction (HPV) May trigger malignant myperthermia (MH) (see Appendix D)INHALATIONAL ANESTHETICS, SPECIFIC COMMENTSNitrous Oxide (N20) Key features: MAC 105%; rapid onset/offset of action. Low solubility. Incompleteanesthetic, as 1 MAC requires a hypoxic gas mixture. Has analgesic properties. Disadvantages: Can rapidly diffuse into and expand air-containing cavities; ~ avoidin air embolism, pneumothorax, intestinal obstruction, intracranial air, pulmonary hy-pertension, some open eye procedures. Prolonged exposure -+ in bone marrow depression; inhibits Bn-dependent enzymes,methionine synthetase (myelin formation), thymidylate synthetase (DNA synthesis). Possible teratogen. Supports combustion (although itself not flammable). May increase PONV risk. Decreases myocardial contractility, increases PVR in patients with preexisting pul-monary hypertension. Interactions: Potentiates neuromuscular blockade (less then volatiles). Use with epi-nephrine may increase incidence of arrhythmias as N20 increases endogenous cate-cholamine levels.Isoflurane (Forane)Key features: MAC 1.2%; inexpensive; slow onset/offset of action, pungent, causestachycardia. Versatile use. Disadvantages: Potential coronary steal effect due to coronary artery dilation.Desflurane (Suprane) Key features: MAC 6.0%; most rapid onset/offset of action; very pungent. Disadvantages: Produces carbon monoxide in desiccated absorbent barium hydrox-ide lime (Baralyme) and also in sodium and potassium hydroxide. 'High vapor pressure requires an electrically heated vaporizer (eliminates substantialvariation of delivered concentrations owing to fluctuations in ambient temperature). Pungency may be irritant in patients prone to bronchospasm. Rapid increase or high MAC (>1.25) may cause significant sympathetic stimulation.Sevoflurane (Ultane) Key features: MAC 2.0%; expensive, less pungent than desflurane: Best for inhala-tional induction. Fast onset/offset of action. Causes less tachycardia than desfluraneor isoflurane (does not sensitize myocardium to catecholamines). Disadvantages: Compound A, a nephrotoxic by-product, produced when sevoflu-rane is degraded in barium lime and to a lesser extent soda lime, especially with low-flow anesthesia of less than 2 L/min over several hours. Toxicity demonstrated only in animal models; 5% metabolized with increased serumfluoride levels-questionable renal toxin. In theory, avoid in renal failure.Halothane Key features: MAC 0.75%; low pungency (ideal for gas induction) Toxicity: Postoperative hepatic dysfunction (halothane hepatitis) 1:35,000 Contra indications: Liver dysfunction on prior halothane administration. Pre-existingt ICP. Severe cardiac disease (due to negative inotropic effect). Interactions: Myocardial depression potentiated by l3-blockers/Ca-blockers; tricyclicantidepressants, MAOi's, aminophylline + halothane -+ arrhythmiasSVR, systemicvascularresistance;NM,neuromuscular; RR,respiratory rate;TY, tidal volume;ICP, intracra-nialpressure;CMR02, cerebral metabolicrequirement of oxygen(oxygenconsumption); GFR,glomerularfiltrationrate; RBF, renal blood flow;HBF, hepatic blood flow.*Keyfeatures shown in bold and italics.Source: Adaptedfrom Morgan G, Mikhail M,MurrayM.Clinical Anesthesiology 4th ed. McGraw HillMedical:NewYork, NY:2005.Heliox (Helium-Oxygen Combination) Common mixtures: 70%/30% and 80%/20% helium-oxygen 80%/20%: Density 1/3 of air/oxygen mixture ~ reduced density helps I airway resist-ance by promoting laminar flow Reduces airway resistance ~ used to treat upper airway obstruction, asthma, COPD Can help I pressures needed to ventilate pts with small-diameter ETTsanddecreases work of breathing~ Nitric Oxide (NO) Inhaled NO/02 blends are used to promote capillary and pulmonary dilation to treatpulmonary hypertension.Oxidative reaction of NO with oxyhemoglobin ~ nitrate.. Selective relaxation of pulmonary vasculature and improved arterial oxygenation. Little systemic hemodynamic effects. Adult clinical outcomes do not show clear benefit.Adapted from Stoelting,Miller. Basics ofAnesthesia, 5th ed. 2006 p99.*Infusion of etomidate is only recommended for short procedures due to risk of adrenal suppression.**Note dexmedetomidine is dosed meg/kg/h.Z-ISmZ0CV)zmV)-I::I:m-InV)(/)3:Cmr(1(/)mamZ- II'Opiate Pharmacokinetics:Clearanceis primarily hepatic,although differences in lipid solubility affectpharrnacoki-netic variability.Benefits:Analgesia and sedation (dose-dependent); reduces MAC; amnesticwith largedoses(unreliable); coughsuppression.Sedation:0.5-1 mcg/kgload (35-70 mcg)infusedover 30-60 sec; 0.025-0.2mcg/kg/min maintMaybolus 1 meg/kgwhenchanging infusionratesFentanyl (Sublimaze IV;Fentora Buccal;Actiq Lozenge; Duragesic/lonsysTransdermal)Dose: (70-kg pt)Intubation:1.5-3 mcg/kg(100-200 mcg)Intrathecal:25 mcgEpidural: Epidural PCA (PCEA): 10-30mcgq1Omin; epidural infusion: 5-10mcg/mL local anestheticPost op: 0.5-1.5 kg (35-105 mcg)Sedation/analgesia: 0.5 mcg/kg(load);0.01-0.04 mcg/kg/min (maint)GA (sole agent) Induction:50-150mcg/kg; Maint: 0.1-5 mcg/kg/hVeryhighdose (150 mcg/kg) is usedrarely,e.g.,open heart surgeryGA adjunct: Loadingdose: 2-50 mcg/kg;Maint: 0.03-0.1 kg/minClearance: Liverand intestinal mucosa by CYP-450 3A4;metabolite: Norfentanyl(active)Comments: Highlipidsolubilitycauses rapid redistribution to inactivesites (fat,skeletal muscle);therefore, quick onset and quick redistribution below therapeuticindex. Comparative potency (to morphine): x75-x125Remifentanil (Ultiva)Dose: (70-kg pt)Induction: 1-3 mcg/kgover 1 min(70-270 mcg)GAAdjunct:Loading dose: 0.5-2 mcg/kg(35-140 mcg);bolus 0.5-1 mcg/kg;Maint: 0.05-2 mcg/kg/minClearance: Rapidmetabolismof ester linkage by nonspecificblood and tissueesterases (NOT plasmacholinesterase); carboxylicacid metabolite (inactive)Comments: Contains glycine, therefore contraindicated for epidural/intrathecaladmin-istration. Do not administer concomitantlywith blood as esterases maymetabolize.GA (major proc): 8-30 mcg/kg(560-2100); bolus 10-50 mcg;Maint:0.5-2.5 mcg/kg/hrSedation: Load:0.1-0.5 mcg/kg(7-35mcg);Maint: 0.005-0.01 mcg/kg/minEpidural: 10-15 mcg/10mLof 0.125%bupivacaineMinor proc: Load20 meg/kg; bolus 3-5mcg/kgqS-20 minto max8-40 mcg/kg; or 0.5-1 mcg/kg/minMajor proc: Load 20-50 mcg/kg; Maint5-15 mcg/kgqS-20min to max75 mcg/kgSufentanil (Sufenta, IV, intransal)Dose: (70 kg pt)GA (minor proc) Ind:1-2 mcg/kg(70-140), bolus: 10-25 mcgGA (moderate proc): Ind:2-8 mcg/kg(70-560), bolus: 10-50 mcg;Maint:0.3-1.5 mcg/kg/hrClearance: Liverand small intestineComments: Produces hypnosisat doses ;:::8 mcg/kgAlfentanil (Alfenta). Dose: (70 kg pt)Intubation:20-50 mcg/kg(1400-3500)Induction:130-245 mcg/kg(9.1-17.1 mg)Infusion: Load50-75 mcg/kg; Maint: 0.5-3mcg/kg/minMAC: 3-5 mcg/kgIVqS-20min or 0.25-1mcg/kg/min IVfor maintenance;start:3-8 mcg/kgIVx1 for sedated, respon-sive,spontaneously breathing pts; usualtotal dose = 3-40 mcg/kgClearance: LiverComments: May increase ICP. Not recommendedfor children75. May skip dose titration if immediateonset desired.Mechanism: Opiate agonist and plus inhibitionof norepinephrine and serotonin reup-take. Not completely antagonized by naloxone. Codeine analog.Clearance: Liver; adjust dose in elderly,renal, and pts with hepatic disease.1-2 tabs q4-6h prn Dose: 1=ftabq4l1 prn5-10 mgq2-6h10 mgq8-12h1-2 PO q4-6h basedon APAP dose*1 PO q6h prn5-10 mgq2-6h10-30 q3-4h15=jOq8=12h15-30 q8-12hf6=30mgq4h prnHC 5 mg+ APAP 500mgHe7.5 mg" ... 650mg Morphine sustainedreleaseMorphine sustainedrelease PercodanOxyFastMorphine-containingMorphineOramorph SRMSContin-Roxanol Brand Name Generic Adult Starting DoseHydrocodone (HC) containing + acetaminophen (APAP)*Norco HC 10 mg + APAP 325mgLortab2.5i5oo HC 2.5mg + APAP 500mg 5/500,Zydone,Anexia5/500,Hydrocet Vicodin ES,Anexia7.5/650Lortab 10/500,Vicodin HP Dose: 1-2 tab q4h prn HC2.5mg+APAP 120mg/5 mLHydrocodone(HC5:tAspirin"'or"lbuprofen HC Vicoprofen 200mg Roxicodone OxycodoneOxyContin Oxycodone (sustain release)Percocet OxycodoneiAPAPf5:5,i.5,10/325; 7.5/500; 10/650 20rng/mLAdult Starting Dose3 ~ 0 mgcodeine q4h*2 q4h15-60 mgq4h prn1-2 caps q4h prn,max6/d1-2 caps qid'6 mgq3-4100mgq3h4 mgq6-8h10 mgq8-12h25mgqAMAPAP 300mg + codeine 15, 30,60mgCodeine sulfateAPAP 325,codeine 30, butalbital50, caffeine 40Carisoprodol 200mg,ASA 325mg,codeine 16 mgDihydrocodeine 16 mg,aspirin356.4mg,caffeine 30mgHydromorphoneMeperidineLevorphanolMethadoneTramadolOtherDilaudidDemerolLevoDromoranDolophineUltram 'Common. Oral Opiates (Continued). ...Brand Name GenericCodeine-containingTylenol #2, #3, #4FioricetiFiorinal withcodeineSomawith codeineSynalgos-DC*CAUTION: Do not exceed maximum dailydose for APAP: 4 g/d healthyadults;2 g/d if hepaticdiseaseCOMMON BENZODIAZEPINES IN ANESTHESIA, SPECIFIC COMMENTSMidazolam (Versed)Metabolites: 1-0H-midazolam (inactive)Comments: Highest lipidsolubilityof benzodiazepines.Increased lipidsolubilityafterentering physiologic pH. Short-context sensitive half-timemakes suitable for infusion.Approximatelydouble affinity for gamma subunit of GABAareceptor explainsgreater potency of midazolam.Diazepam (Valium)Metabolites: Desmethyldiazepam (active),oxazepam (active)Comments: Poor water solubility-propylene glycol solvent causes pain on injectionLorazepam (Ativan)Metabolites: Lorazepamglucuronide (inactive)Comments: Infusion not recommended(Librium) q6h(continued)Source.AdaptedfromAttia RR,GrogonoAW,Domer FR,eds. Psychotropic Agents inPractical Anethetic Phar-macology, 2nd ed. Norwalk,CT:Appleton-Century-Crofts, 1987:149-169.ANTAGONISTS FOR ANALGESICS AND INTRAVENOUS ANESTHETICSNaloxone (Narcan)Indications: (1) opiate overdose; (2) reversal of opiate respiratory depression; (3)treatment of opiate-induced pruritus.Dose: Adult: (1) 0.4-2 mg IVq2-3min prn; (2) 0.04 to 0.4 mg doses 1\1, titrated q2-3min.Infusion: Load 5 meg/kg, infusion 2.5-160 mcg/kg/hr; Peds: (1) Birth to S yr: S yr or >20 kg: 2 mg/dose q2-3min prn; infusion sameas adult. (2) 1-10 meg/kg IVtitrated q2-3min (up to 0.4 mg).Mechanism: Competitive inhibition of opioid receptorsClearance: Hepatic metabolism (95%); primarily renal elimination.Comments: Maycause hypertension, dysrhythmias, rare pulmonary edema, delirium,reversal of analgesia, or withdrawal syndrome (in opioid-dependent patients). Renar-cotization may occur because antagonist has short duration. Caution in hepatic fail-ure and chronic cardiac disease.Methylnaltrexone (Relistor)Dose: 150mg/24 hrUsual Daily Dose(Adults)600-1800 mg/24h400, 600,800mg;800-2400 mg100,200mgbid,200mgqd325---1000mgPO/PRq4-6h500mgbid,up to1500mg/24 hr10,20 mgqd100mgtid up to600mg/24hr7.5-15 mg50-100 mgtid-qid'2S0'rngqidBrandNameDayproTolectinEtodolacMedicationOxaprozinTolmetinTolmetinSulindacDiclofenacToradolFenamatesMedofenamate MeclomenMefenamic'acid PonstelE.nolic Acid DerivativesPiroxicam Feldene ButazolidinAcetic Acid DerivativesIndomethacin Indocin,Indocin SRIndocin SRSee aboveClinorilVoltaren,ArthrotecLodinep-Aminopheno/sAcetaminophen MultipleMeloxicam MobicNaphthylkanonesNabumetone RelafenNonSteroidal Anti-inflammatoryMedications, Serum MaximumHalf-Life ' Daily Dose(hr) (mg)40-50 18001 1800C::OX.2SeleC:tiveNSAIOSCelecoxib CelebrexSource: Adapted fromWarfieldC, Fausett H. Manual ofPain Management, 2nd ed. Philadelphia: LippincottWilliams&Wilkins,2002.*AvoidPRacetaminophenin pts with cancer,immunosuppressedneutropenic pts, etc.**Riskfor Reye'ssyndrome if concurrent influenza, viral illness.Source: Adapted from Berde C, MasekB.Painin children.InWall PO,Melzack R,eds. Textbook ofPain.Edinburgh: ChurchillLivingstone, 1999.NONSELECTIVE COX INHIBITORSAcetaminophen (Tylenol, Paracetamol)Dose: q4-6h PO, PRo Adults: max 4 g/d or 2 g/d in pts with hepatic diseaseMechanism: Not true NSAID as lacks significant anti-inflammatoryeffectClearance: LiverComments: Does not produce GI irritation, affect platelet aggregation. Doescontribute to nephrotoxicity, Single dose>15g leads to hepatic necrosis due toformation of N-acetyl-p-benzoquinone (scavenged by antioxidant glutathione). Toxic-ity occurs due to depletion of glutathione. Acetylcysteine may substitute forglutathione and prevent hepatotoxicity if administered within 8 hr of ingestion. Intra-venous form in clinical trials in U.S. (available in Europe).Propionic Acids (Ibuprofen, Naproxen, Fenoprofen, Ketoprofen, Diclofenac)Comments: Alter platelet function, but duration of COX inhibition varies with spe-cific drugs. Naproxen may be dosed twice daily owing to longer half-life. May exacer-bate renal disease. Extensive protein binding leads to adverse drug effects (e.g., re-duce dosing of warfarin because of extensive displacement from protein binding sitesand effects on platelet function). Ibuprofen has less protein binding than other propi-onic acids.PYRROLOPYRROLE (e.g., KETOROLAC)Ketorolac (Toradol)Dose: Adult: >50 kg: bolus 30-60 mg IV/1M, then 15-30 mg q6h, max 120 mg/d for pts65 yr/o or with renal disease; 8. A significant metabolite, PABA(para-amino benzoic acid), can cause an allergic reaction. Amides(lidocaine [Xylocaine], bupivacaine [Marcaine], mepivacaine [Carbocaine], eti-docaine [Duranest]) They undergo metabolism by hepatic microsomal enzymes. The pKa is usu intercostal > caudal> epidural > brachial plexus > subcutaneousToxicity mainly affects CV system and CNS. CNS is more sensitive and usually affectedfirst. Signs of local anesthetic toxicity with increasing plasma concentrations include:Light-headedness ~ circumoral numbness ~ facial tingling ~ tinnitus ~ slurred speech~ seizures ~ unconsciousness ~ respiratory arrest ~ cardiovasculardepression ~ circulatory arrest CNS toxicity: t with hypercarbia & acidosis (..J, seizure threshold). LA potency, totaldose, and rate of injection. CV toxicity: HTN, tHR, myocardial depression, hypotension, dysrhythmias. ECG L\s: tPR, tQRS. LA toxicity treatment: Stop injecting LA;get help;maintain airway (intubate if necessary); give 100% oxy-gen and consider hyperventilation in presence of metabolic acidosis; treat seizures(benzodiazepines, propofol, thiopental in small doses). If cardiac arrest with LAtoxicity: CPR and treatment of arrhythmias with standardprotocols. Consider cardiopulmonary bypass or treatment with lipid emulsion: Lipid emulsion: Intralipid 20%, 1.5 mL/kg over 1 min (-100 mL in 70-kg pt):Start intralipid infusion at 0.25 mL/kg/min (17.5 mL/min for 70-kg pt): Repeatbolus (1.5 mL/kg) x2 at 5-min intervals; after 15 min, increase infusion to 0.5mL/kg/min (35 mL/min for 70-kg pt) if circulation not restored. Continue CPR throughout intralipid infusion. Recovery from LA-induced cardiacarrest may take as long as 1 hr. EMLA cream-eutectic mixture of lidocaine and prilocaine ~ used for dermal anes-thesia. Onset -45-60 min, duration -2 hr. Risks/contraindications: LAtoxicity possible, including methemoglobinemia. Avoid in G6PD deficiency. Avoid with history of amide allergy. Methemoglobinemia (normal hemoglobin oxidized to methemoglobin)Causes: LAs (benzocaine, prilocaine), antibiotics (dapsone, trimethoprim), nitratesSymptoms and signs: SOB, cyanosis, MSL\s,loss of consciousness; if >50% met-Hb ~dysrhythmias, seizures, coma, and death.Dx: Blood is "chocolate-brown" color.ABG analysis will typically reveal normal P02 +1- metabolic acidosis.Use co-oximetry and measure met-Hb level.Tx: Supplemental oxygen.1% methylene blue 1-2 mg/kgIV(restores iron in Hb to its normal reduced0rcarrying state)Ascorbic acid. Cocaine PharmacologyEster LA, a vasoconstrictor (others are vasodilators)CNS stimulant ~ t release &..J, reuptake of epi, norepi, dopamine, serotoninUsed as topical anesthetic (sinus surgery, awake nasal fiberoptic)Side effects: HTN, tachycardia, arrhythmias, cardiomyopathy, coronary ischemia,stroke, cerebral &pulmonary edema, seizures, hyperthermia, myoglobinuria, renal fail-'-" ure, hallucinations, platelet dysfxANESTHETIC CONSIDERATIONS IN COCAINE ABUSECocaine use ~ depletion of catecholamines (use direct-acting sympathomimetics)Consider: selective ~ 1 antagonists (esmolol) for HR controldirect vasodilator (nitroprusside, nitroglycerin) for HTNa balanced anesthetic technique to blunt sympathetic stimulationregional anesthesia if can correct coagulopathy & hypovolemia'-" Use caution with inhalational agents (can worsen myocardial depression, may have trequirements to ..J, effects of high systemic catecholamines)PHARMACOLOGY: NEUROMUSCULARBLOCKING DRUGS AND REVERSALAGENTSJENNAHANSEN SAMUEL C. SEIDENMECHANISMNeuromuscular blocking drugs (NMBDs) work at the postsynaptic nicotinic cholinergic. receptor of the neuromuscular junction (NMJ) ~ stop conduction of nerve impulses ~leading to skeletal muscle paralysis. Nondepolarizing NMBDs (Pancuronium, Rocuronium, Vecuronium, Atracurium,Cisatracurium) Interfere with the actions of acetylcholine (Ach) at the NMJ,which keeps ionchannels closed so no depolarization can occur. Because NMBDs compete with Ach for receptor binding, they are considered an-tagonists or competitive blockers. NMBD action can be overcome by increasing ACh in the synaptic cleft (the mech-anism behind reversal of neuromuscular blockade with acetylcholinesteraseinhibitors). Depolarizing NMBDs (Succinylcholine) MimicACh by binding to the a-subunit of the nicotinic cholinergic receptor keep-ing the ion channel open. Cause prolonged depolarization which initially manifests as diffuse muscle contrac-tions known as fasciculations. The depolarized, occupied membrane cannot react to further release of Ach,thereafter causing muscle paralysis.Aminosteroids (Pancuronium, Rocuronium,Vecuronium) Pancuronium-Iong-acting (duration of action, ::;90 min.) Clinical Considerations Tachycardia, tBp, tCO. Elimination is mostly renal (increased duration in renal disease, neonates, elderly). Rocuronium-intermediate-acting duration of action ::;35 min when dosing at0.6 mg/kg. More rapid onset than other nondepolarizers if 1.2-mg/kg dose is used(however, this may prolong duration of action). Clinical Considerations Used in rapid sequence intubation instead of succinylcholine. Does not release histamine or cause cardiovascular effects. Biliary and renal excretion. May promote muscarinic block. Vecuronium-intermediate acting (duration of action ::;35 min.) Clinical Considerations Does not release histamine or cause cardiovascular effects. Biliary elimination; renal excretion of metabolites. Increased duration in hepatic disease, esp with repeated dosing.Benzylisoquinolines (Atracurium, Cisatracurium) Atracurium-intermediate acting (duration of action ::;35 min.) Clinical Considerations Metabolism is independent of liver and kidney function or plasma cholinesteraseactivity Cleared by hydrolysis via nonspecific plasma esterases and Hofmann elimination(nonenzymatic spontaneous degradation at normal pH and temperature) to themetabolite laudanosine. Laudanosine can cause CNS stimulation/seizures at high concentrations (worsein pts with renal failure). Dose-dependent release of histamine -+ hypotension. Cisatracurium-intermediate acting (duration of action ::;35 min.) Clinical Considerations Metabolism independent of liver, kidney, or plasma cholinesterase function. Useful in patients with renal failure. Cleared mainly by Hofmann elimination to the metabolite laudanosine, but con-centrations of laudanosine are less than with atracurium. Cisatracurium does not release histamine.Succinylcholine (SCh)Only depolarizing drug available, used for its rapid onset and short duration (seetable on next page).Dose of 0.5-1.5 mg/kg: onset ~ 30 sec, paralysis for 5-10 min.Rapidly hydrolyzed by plasma cholinesterase (pseudocholinesterase).Length of blockade is determined both by the amount of SCh that reaches the NMJand the rate of diffusion of SCh away from the NMJ into the plasma (there is nopseudocholinesterase at the motor plate). Patients with a genetic defect causing atypical plasma cholinesterase(pseudocholinesterase deficiency) may demonstrate marked prolonged paralysisafter a standard intubating dose of SCh. Diagnosis: Determine dibucaine number ( ~ 2 0 % in affected homozygotes). Dibucaine number indicates the quality but not the quantity of plasmacholinesterase ~ if pt has decreased levels of plasma cholinesterase due to liverdisease, pregnancy, burns, etc, the dibucaine number would be normal ( ~ 8 0 % ) .Prolonged effect also seen in:1. Severe liver disease2. Echothiophate use in glaucoma pts (binds irreversibly to cholinesterase)3. Organophosphate poisoning (irreversibly bind to cholinesterase)4. Anticholinesterase use (inhibition of pseudocholinesterase may occur)5. Lithium, magnesiumIndications-used for rapid sequence induction when aspiration is a risk (Le.,fullstomach, trauma, diabetes mellitus, hiatal hernia, obesity, pregnancy)Contraindicated in malignant hyperthermia susceptible pts (SCh = known MH trig-ger)Use caution in pt's with open eye injury, elevated ICp, extrajunctional receptor prolif-eration (burn pts ~ probably safe if given 6 mo of injury; spinal cordtransection pts ~ probably safe if given Pharyngeal > Masseter > Adductor pollicis > Abdominal rectus >Orbicularis oculi > Diaphram > Vocal CordFigure 20-2 Speed of Onset & Recovery of Neuromuscular BlockadeFastest Onset Slowest OnsetLarynx> Diaphram > Orbicularis oculi> Adductor pollicisFastest Recovery Slowest RecoveryLarynx> Orbicularis oculi = Diaphram > Adductor pollicis-*Durationprolonged in renal failure; maycause bradycardia,hypotension, CNSstimulationor depression;GI cramps or cholinergiccrisis;because of differencein onset times,administerglycopyrrolate several minutesin advance.**Durationprolongedin renal failure;maycause bradycardia,hypotension,CNS stimulationor depression,GI cramps,or cholinergiccrisis.***Duration prolonged in renal failure; does not significantly cross the blood-brain barrier; not recommendedfor use with atropine becauseof the differencesin onset times;therapy for myasthenia gravis.Sugammadex (Proposed Trade Name: Bridion) A new agent designed specifically to reverse the effects of rocuronium and vecuro-nium (not currently FDA approved.) Binds to rocuronium and vecuronium encapsulates it, rendering it incapable of bind-ing at the NMJ. Advantages: Can be given at any time after administration of rocuronium, thereby resulting infast recovery of neuromuscular blockade. Mechanism does not rely on acetylcholinesterase inhibition and therefore it doesnot have undesirable cardiac effects. . Studied dosing 2-8 mg/kg.ANTICHOLINERGIC AGENTSBlock peripheral muscarinic effects of cholinergic agents.Atropine Give 0.6-1.2 mg IVfor each 0.5-2.5 mg neostigmine, 10-20 mg pyridostigmine, or10-20 mg edrophonium dose.Central anticholinergic syndrome: Occurs with administration of atropine or scopolamine (both cross blood-brainbarrier). Manifested as delirium or somnolence. Elderly pts more susceptible. Responds to treatment with physostigmine.GIycopyrrolate Give 0.2 mg IVfor each 1 mg neostigmine or 5 mg pyridostigmine dose.Scopolamine Anticholinergic dose: 0.3-0.6 mg IM/IV/SCtid-qid prn. Antisialagogue dose: 0.2-0.6 mg 1M x1; give 0.5-1 hr prior to anesthesia. Amnesia dose: 0.32-0.65 mg IM/IV/SCtid-qid prn. Sedation dose: 0.6 mg IM/IV/SCtid-qid prn. Antiemetic, transdermal administration, see page 2F-38.PHARMACOLOGY: VASOACTIVE,AUTONOMIC ANDCARDIOVASCULAR DRUGS.DruS! Direct Indirect (Arterial) (Venous) a-2 B-1 B-2+++++++++++++++++++++++,0+++++o++++ooplnephrine,nineohrine,:pnephrine,:phedrine)opamine,Dopamine,Dobutarni+++++++++++++++++++++++++++++++++++++++++++++o++++++ 0-o+ ++++ +++++++ ++++++ ?++++++++ ?++++ ?? 0o 0++++ ++++++++ ++++++++ +++++++ ++o agoni+++ ++++++++++ +++++++ +++++++ +++++Source:Adaptedfrom CusickJ.Anesthesiaand criticalcare reference sheet, 2007.www.accrs.comEpinephrine dose/response (mcg/kg/min): (1) 0.01-0.03 (2) 0.03-0.15 (3) 0.015-0.5;Dopaminedose/response (mcg/kg/min): (1) 0.5-3 (2) 3-10 (3) 10-20( ( ( (HR,heart rate; MAP, mean arterial pressure; SYR, systemic vascular resistance;PYR, peripheral vascular resistance;RBF, renal blood flow.Epinephrinedose/response (mcg/kg/min): (1)0.01-0.03 (2) 0.03-0.15 (3)0.015-0.5; Dopaminedose/response (mcg/kg/min): (1) 0.5-3 (2) 3-10 (3) 10-20Source:Adapted from CusickJ. Anesthesiaand critical care reference sheet, 2007. www.accrs.com-(~-HR,heart rate; MAp, mean arterial pressure; SVR, systemic vascular resistance;PVR, peripheral vascular resistance;RBF, renal blood flow.Source:Adapted from Cusick J. Anesthesiaand critical care reference sheet, 2007.www.accrs.comADRENERGIC AGONISTSGeneral comments: Act on alpha, beta, or dopaminergic receptors (see Table 2E-2).May cause hypertension, arrhythmias, myocardial ischemia, and tissue necrosis withextravasation (treat with phentolamine).Dobutamine (Dobutrex)Indications: Heart failureDose: Infusion prep: 500 mg in 250 mL D5W or NS = 2000 mcg/mL (2 mg/mL)Adult: 2 meg/kg/min, titrate 2-20 meg/kg/min, max 40 meg/kg/min; Peds: 5-20meg/kg/minMechanism: f)1-Adrenergic agonistClearance: Hepatic metabolism. Renal eliminationDuration: < 10 minComments: Less tachyarrhythmias than with dopamine. Can increase ventricular ratein atrial fibrillation. Do not mix with sodium bicarbonate. Lowers CVP and wedgepressure, but little change on pulmonary vascular resistance.Dopamine (Intropin)Indications: (1) Hypotension, heart failure; (2) oliguriaDose: Infusion prep: 400 mg in 250 mL D5W = 1600 mcg/mL;(1) infusion at 1-20 meg/kg/min IVtitrate to effect; (2) Infusion at 0.5-3 meg/kg/min IVMechanism: Dopaminergic; (X- and f)-adrenergic agonistClearance: MAO/COMT metabolismDuration: < 10 minComments: Contraindicated in pts with pheochromocytoma or ventricular fibrilla-tion. Improved renal blood flow (controversial) primarily at lower doses. Beta activitypredominates at doses 20% of patients. Reduce dose in hepatic insufficiency.Recommend discontinuing 7 d prior to neuraxial anesthesia.Dalteparin (Fragmin)Indications: (1) DVT prophylaxis; (2) DVT tx; (3) ACSDose: (1) 2500-5000 U SC qd; (2) 100 U/kg SC bid or 200 U/kg SC qd; (3) 120 U/kgSC to max 10,000 U SC q12h x 5-8 d combined with aspirin therapyMechanism: Anticoagulant via factor Xa and lIa inhibition.Metabolism: Hepatic with renal eliminationComments: As effective as unfractionated heparin with more predictable dose-response relationship. Occurrence of hematoma with neuraxial anesthesia, especiallywith indwelling catheters, has been reported. Incidence of thrombocytopenia rare.Not studied in children.",-,.'Eptifibatide (Integrilin)Indications: Prevents thrombus formation after PCI and treatment of patients withACSDose: Bolus 180 mcg/kg, then 2 mcg/kg/mininfusion and repeat bolus of 180 mcg/kg10 min after 1st bolus.Mechanism: Prevents platelet adhesion and aggregation by reversible inhibition of gly-coprotein Ilb/llla, fibrinogen, and von Willebrand factor.Clearance: Platelet function recovers within 4 to 8 hr after discontinuation of infu-sion.Comments: Bleeding complications and thrombocytopenia are common side effects.Contraindicated in bleeding diathesis, severe uncontrolled HTN, severe bleedingwithin preceding 6 wk, renal dialysis dependency, CVA within last 30 d. Decrease in-fusion to 1 mcg/kgin pts with creatinine clearance 10 kg, 100 U/mL for line flushing, 1 U/mLfor arterial lines; Infants/neonates: (1) Load: 50-75 U/kg IVover 10 min; Maintenance:28 U/kg/hr (range 15-35 U/kg).Titrate to ACT. (5) 150 mg have been associated with an increased incidence ofintracranial hemorrhage. Contraindicated with active internal bleeding, history ofhemorrhagic stroke, intracranial neoplasm, aneurysm, or recent (within 2 mo) in-tracranial or intraspinal surgery, or trauma. Should be used with caution in pts whohave received chest compressions and in pts who are currently receiving heparin,warfarin, or anti platelet drugs.VitaminJK (Phytonadione,AquaMEPHYTON)Dose: Adult: 2.5-10 mg 1M/SCIor 5-25 mg/d PO, or 1-10 mg IVat esl mg/min (withcaution). If international normalized ratio (INR) time is not improved 8 hr after initialdose, repeat prn.Mechanism: Vitamin Kis required for synthesis of clotting factors II,VII, IX, X.Clearance: Hepatic metabolismComments: Indicated for deficiency of vitamin K-dependent clotting factors, re-versal of warfarin anticoagulation. Excessive doses can make pt refractory to fur-ther oral anticoagulation. May fail with hepatocellular disease. Rapid IV bolus cancause profound hypotension, fever, diaphoresis, bronchospasm, anaphylaxis, andpain at injection site. Crosses the placenta. Reserve IVadministration for emer-gency use.Warfarin (Coumadin)Dose: Load: 5 mg PO x 2-5 d; Maintenance: 2-10 mg PO, titrated to prothrombin time(INR should be 2 to 3, based on indication).Mechanism: Interferes with utilization of vitamin K by the liver and inhibits synthesisof factors II,VII,IX, X, proteins C &S, prothrombin.Clearance: Hepatic metabolism; renal elimination.Comments: Indication for anticoagulation. Contraindicated in severe renal or hepaticdisease, GI ulcers, neurosurgical procedures, malignant HTN, pregnancy (teratogenic).Multiple drug interactions causing potentiation/antagonism. Crosses the placenta.Thrombostatic only, no lysis of existing thrombus.DIURETICSAcetazolamide (Diamox)Indications: (1) Secondary metabolic alkalosis; (2) Increased ICPDose: (1) 3-5 mg/kg/dose q6h x 4 doses; (2) 20 mg/kg/24 hr div q8h; Max 100mg/kg/24 hr to max 2 g/24 hrMechanism: Carbonic anhydrase inhibitor, increases HC03 excretionMetabolism: Renal clearance, unchangedComments: Indicated for respiratory acidosis with metabolic alkalosis, increased ICP,lOP. Contraindicated in hepatic failure, renal failure. Rare reaction in pts with sulfaallergy.Bumetanide (Bumex)Indications: Edema, HTN, intracranial HTN.Dose: 0.5-1.0 mg rv, repeated to a maximum of 10 mg/d. PO also available.Mechanism: Loop diuretic; inhibits Na + and CI- reabsorption in ascending limb ofloop of Henle and increases K+ excretion.Clearance: Hepatic metabolism; 81% renal excretion (45% unchanged).C:::omments: May cause electrolyte imbalance (especially hyponatremia, hypokalemia),dehydration, ototoxicity (in animal studies with higher dosing), and rarely thrombocy-topenia. Patients who are allergic to sulfonamides may show hypersensitivity tobumetanide. Effective in renal insufficiency but contraindicated in anuria; andbumetanide should be discontinued if renal function worsens during therapy. Dose of1 mg bumetanide approximately equal to 40 mg furosemide. Oral and IVIIM havesimilar bioavailability.Chlorothiazide (Diuril)(hydrochlorothiazide for PO dosing)Dose: Adult: 100-500 mg IVat 50-100 mg/min in 1-2 doses; max 2 g/24 hr. 500 mg-2g/d PO. Peds: 4 mg/kg/d IVdiv q12h, 20 mg/kg/d PO div q12h. Infant 2 yr/o: 0.25-0.5 mL of 2.25% solution in 2.5-3.5 mL of NS q4hprn; epidural)(often by up to two dermatomes, with degree of blockade determined by block height) Infection Hematoma CardiovascularSympathectomy (spinal> epidural) --+ loss of vascular tone --+ hypotension & reflextachycardiaSupra-T4 levels block cardioaccelerator fibers (T1-T4) --+ paradoxical bradycardia --+decreased CO & further hypotension; large volumes of local anesthetic used forepidurals --+ higher systemic absorption --+direct cardiac depressant effects PulmonaryImpaired cough reflex, high blockade .J, use of accessory resp muscles (intercostals)--+ use caution in pts with limited pulmonary reserveInspiratory fx preserved (unless respiratory centers (C3-CS) blocked)PFTchanges:.J, or unchangedVC,.J, ERV,.J, expiratory flow rate GISympathectomy --+ hyperperistalsis (get unopposed parasympathetics) --+ NN GUSacral blockade --+atonic bladder (consider catheterization); renal blood flow usuallymaintainedContraindications to Placing a Neuraxial Block Absolute, Refusal/inability to cooperate, local infection,coagulopathy,severe hypovolemia, sepsis, severe cardiac disease (aortic/mitral stenosis), t ICP RelativePrior back surgery, neurologic disease (MS), infection distal to needle insertion siteSource:Adaptedfrom RegAnesth Pain Med2003;28:172-197.Patient Positioning for Block Placement Goal for optimal positioning:widen intervertebral spaces--+ Knees flexed towards abdomen, chin flexed to chest, shoulders relaxed Sitting position-easier to identifymidline,can create saddle block if using hyperbaricsolutions Lateral decubitus position-use if patient unable to sit--+Can preferentially block 1 side (if using hypo- or hyperbaric solutions) Prone jackknifeposition-good for perirectal surgery (if using hypobaric solution) Pruritus Hypotension Urinary retention Transient neurologic symptoms (TNS)-more common with ambulatory proce-dures, lithotomyposition,lidocaine spinals. Symptoms: Delayed onset of radicular painin lower back,buttocks, posterior thighs (can last up to 7 d)Symptoms: Bowel/bladderneurosurgical consult Postspinal headache-(see postdural puncture headache below) High/total spinal-supracervical blockadecan cause cardiovascular collapse,apnea,loss of consciousness; supportive treatment/intubation maybe necessary c:ornpliC:Clti()Jls Postdural puncture headache (PDPH)-from inadvertent dural puncture (wettap); usually self-limited 7 d). Initial management: hydration,caffeine (500 mg),NSAIDs, abdominal binders.Epidural blood patches >90%effective for persistent PDPH Spinal cord injury-can occur ifwet tap occurs at levelabove where spinalcord ends Local anesthetic toxicity-dizziness, tinnitus,CNS excitation,seizures,cardiacarrest can occur from systemicabsorption of local anesthetic.Treatment is supportive.Consider 20%intralipid emulsionsfor refractory cardiacarrestSPINAL ANESTHESIA Rapid& reliable onset of lower body anesthesia by injectinglocal anesthetic into theintrathecal space Blocksspinal cord fibers and nerve rootlets Usuallysingle-shot,although continuous catheters can be used Consider volume loading(500-1000 mLfluid) to avoideffects of rapid sympathectomy Needles: Smallgauge (>24 G), pencil point needles (Sprotte,Whitacre) reduce risk of PDPH-+ Often require introducer (19 G) to penetrate superficialtissue Largegauge 22 G), cutting (Quincke, Greene) needles-+ Used in difficultspinals to penetrate fibrotic, calcifiedligaments Introduce needle (midlineor paramedian technique) at L2-L5 interspaces until dural"pop" felt or if CSFflows freely when stylet removed Taylor approach:Spinal performed at L5-S1 by insertingneedle 1 cm medial& caudaltoipsilateral posterior superior iliac spine&directingit cephalomedially toward the midlineLocal solution in to mixingdextrose or sterile water results in hyperbaricor hypobaricsolutions (respectively) Isobaric(density= CSF)-get blockat level where medicationis injected Hyperbaric(density>CSF)-get spread of medicationwithgravityin intrathecal space Hypobaric(density 150 mL/70 kg/min Hypothermia, liver dz, liver transplantation, & hyperventilation t risk Monitor ionized calcium during rapid transfusions Treat hypocalcemia with Ca gluconate (30 mg/kg) or Ca carbonate (10 mg/kg) Hyperkalemia-unlikely at transfusion rates 100 mg/dL for pts with severe bleeding/massive transfusion Fibrin degradation products (FDP)-made by action of plasmin on fibrinogen t In DIC, 1 fibrinolysis, & severe liver dz (due to impaired clearance) Influence clotting by interfering with fibrin monomer polymerization & by impair-ing platelet function D-dimer-specific fragment produced when plasmin digests cross-linked fibrin tin DIC, pulmonary embolism & in the immediate postop period( t (TEG)ngthof blood clot over entire period of clotting& fibrinolysis:em, platelet function,& fibrinolysis( Thrombol Viscoelastic test that characterizes formation & stre Assesses coagulation syst

agents1t Clinically insignificant increase:tt: Possibly clinically significant increase,m:Clinically significant increase(-Source:Adaptedfrom Nutescu EA,et al. Cleve C1in JMed 2005;72(Suppl 1):S2-S6.*Initial step should be immediatedlc of anticoag.Decisionto dialyzeshould take into account time foranticoag.to be metabolized(noting renal/liverinsufficiency) wlo dialysis vs. potential sequelae of bleedingwhilewaiting. K,kidney; L,liver;RES, reticuloendothelialsystem.Platelet InhibitorsAspirin Irreversibly inactivates cyclooxygenase (COX) enzyme Get suppression of prostaglandin &thromboxane productionIbuprofen NSAID that reversibly inhibits cyclooxygenaseClopidogrel Irreversible blockade of adenosine diphosphate (ADP) receptor on platelet cell mem-branesAbciximab Platelet aggregation inhibitor (inhibits glycoprotein lib/Ilia)Dipyridamole Inhibits platelet adhesionBleeding Disorders (Coagulopathies) Classic hemophilia (hemophilia A,faetorVIII deficiency) X-linked recessive trait, 1:5,000 livemale births Prolonged PTT but normal PT & normal platelet function Bleedingepisodes related to level of factor VIII activity < 1%spontaneous bleeds 1-5% bleedingafter minor trauma >5% infrequent bleeding Treatment: Factor VIII replacement (cryoprecipitate, lyophilized or recombinantfactor VIII) Activitylevels of 20-40% recommended prior to surgery Half-lifeoffactorVIII=8-12hr . 20%of pts will eventuallydevelop factorVIUantibodies Treated with high-dose factor VIII, activated factor IX,or plasmapheresis Highincidence of hepatitis & HIV(givenexposure to blood products) Christmas disease (hemophilia B,faetor IX deficiency) Sex linked,occurring almost exclusively in males, incidence 1:100,000 Presentation similar to hemophiliaA Treatment: Factor IXconcentrates, rFVllia or FFP For surgical hemostasis ~ factor IXactivity levelsof 50-80% required Half-life of factor IX = 24 hr vonWillebrand disease (vWD) Abnormalities of vonWillebrand factor (vWF) Glycoprotein produced by megakaryocytes & endothelial cells vWF stabilizesfactor VIII & forms cross-linksbetween platelets & endothelial cells vWD is classified as type 1 (classic),type 2 (variant) &type 3 (severe) Type 1 vWD = autosomal dominant inherited Most common inherited bleeding disorder, prevalence = 1% Pts present with variable bleedingtendency; epistaxis often presenting feature Most common laboratory finding= prolonged bleedingtime Treatment: Desmopressin (0.2 mcg/kgin 50 mLsaline over 30 min) or cryoprecipi-tate; desmopressin has half-life = 8-12 hrHeparin-Induced Thrombocytopenia (HIT)Source:Adaptedfrom Pocket Medicine, 3rd ed. Philadelphia: LippincottWilliams&Wilkins,2008. Type II HIT= immune-mediated thrombocytopenia triggered by IgGantibodiesagainst heparin platelet factor 4 (PF4) complexes (PF4antibodies) Bound antibody ~ stimulates platelet activation ~ thrombocytopenia, platelet ag-~ gregation, & thrombosis Manymore pts develop antibody than the syndrome 50%of cardiac surgery pts exposed to heparin developed PF4 Ab's Only 1%go on to clinical HIT Riskreduced with the use of low-molecular-weight heparin Riskeliminated with use of fondaparinux or direct thrombin inhibitors(Iepirudin,argatroban) Type II HITtreatment: Stop all heparin exposure, includingheparin flushes Start alternative anticoagulation Argatroban (1-2 mcg/kg/min) Lepirudin(0.4 mg/kgbolus, then infuse at 0.15 mg/kg) In absence of alternate anticoagulation,40%of pts will develop thrombotic compli-cations, with resultant amputation in 10-20% & death in 30-50% Oral anticoagulation: Do not start until platelet count is > 100,000/f.1L Warfarin should overlap direct thrombin inhibitors (as warfarin reduces proteinC levels before prothrombin, causing transient hypercoagulable state) Optimal duration of therapy unknown, consider >6 weeksDisseminated Intravascular Coagulation (Ole)Consequence of abnormal, diffuse activation of the coagulation &fibrinolytic systems Trauma Obstetric (e.g., amnioticfluid embolism) Hemolytic transfusion reaction Extensive burns Malignancy Liver disease Retained dead fetus Intra-aortic balloon pump Peritoneovenous shunt Aortic dissection/aneurysm Pathogenesis, Excessive deposition of fibrin throughout microvasculature & consumption of co- agulation factors Widespread platelet activation & fibrinolysis Clinical features Petechiae, ecchymoses, oozing from surgical sites Diffuse thrombosis ---+ life-threatening ischemia of vital organs Laboratory features Elevated D-dimers, PT,& PTT levels Serial measurements reveal a fallingfibrinogen level & platelet count FOPs elevated (but nonspecific) Peripheral blood smears ---+ schistocytes (from microvascular RBC trauma) Treatment Recognition & treatment of underlying cause of DIC FFPor cryoprecipitate to keep fibrinogen >50 mg/dL & replace clotting factors Platelets should be kept >25,00Q-50,000/f.1L Consider heparin for pts with predominantly thrombotic DIC Inhibitors of fibrinolysis (aminocaproic acid, aprotinin) not recommendedVitamin K Deficiency: Vitamin K is needed by the liver to make prothrombin (factor II);factors VII, IX, X;protein C; protein S. Deficiency can lead to coagulopathy and i PTIINR. Treatment:Vitamin K 2.5-10 mg SC/IM/PO or 1-10 mg IVat ~ 1 mg/minSickle Cell Disease (also see Chapter 29, "Chronic Pain') Abnl hemoglobin (HbS) results in sickling ---+ chronic hemolysis, vasocclusive crises End-organ effects: Renal & pulm. infarction, liver cirrhosis, CVAs, bone ischemiaCOMMON INTRAOPERATIVEPROBLEMSRANDY FAYNEHYPOXEMIA: Pa02 IJ), chylothorax (L1J or LSC) Hemothorax, infection,sepsis (Fern> SC > Ij),Thrombophlebitis (Fern > SC > Ij) Nerve injury (Horner syndrome, brachial plexus lesions), air embolismUltrasound-Guided Central Line PlacementInsertion of central lines with USguidance may provide enhanced safetyINSERTION OF A PULMONARY ARTERY CATHETER (PAC) (also see Chapter 7,on perioperative monitoring)Indications Management of complicated myocardial infarction (ventricular failure, cardiogenicshock) Assessment of resp. distress (cardiogenic vs. noncardiogenic pulm edema, 1 vs. rpulm HTN) Assessment of shock Assessment of fluid requirements in criticallyill (hemorrhage, sepsis, acute renal fail-ure, burns) Postop management of cardiac pts Need for heart rate pacingContraindications Tricuspidor pulmonary valvemechanical prosthesis Right heart mass (thrombus and/or tumor) Tricuspidor pulmonary valveendocarditisTechnique Central venous access as described above Positioning: FloatingPAcatheter easier in flat or slightlyreverse Trendelenburg incontrast to central lineplacement (Trendelenburg) Aseptic technique: Sterile gown, face mask,gloves,skin disinfection,&whole-bodydrape PACsetup Calibrate ("zero") PAC,check PACfor damage,test balloon inflation/deflation Connect all lumens to stopcocks, flush to eliminate air bubbles Check PACtip frequency response by touching tip PACthreaded through sterile sleeve prior to insertion into cannula PACinserted percutaneously into major vein (lJ,SC, femoral) via an introducersheath RIJ: Shortest & straightest path LSC:Acuteangle to enter SVC(compared to RSCor L1J) Femoral veins: Distant sites, difficult if R-sided cardiac chambers enlarged (often~ u o r o s c o p i c guidance necessary) Insert into introducer maintaining preformed curve (Rljapproach: Concave-cephalad) Once PACenters RY, a clockwise quarter turn moves tip anteriorly (allows easier"-.,..- . passage intoPA) After inserting PACto 20-cm mark (30-cm mark if femoral route used), inflateballoon with air (1-1.5 mL) Always inflate balloon before advancing & always deflate balloon beforewithdrawal While advancing, waveforms will be observed (distal lumen pressure monitoring): RA"'" 25 cm (Rlj) RV "'" 30 cm (t systolic pressure than RA,absence of dicrotic notch) PA"'" 40 cm (t diastolic pressure.J systolic pressure) PCWP "'" 45 cm (some damping& ,t.. pressure with occlusion of PA) Obtaining pulmonary capillarywedge pressure Disconnect breathing circuit Determine volume of air in balloon required to obtain a PCWP waveform(volume < half balloon max.may indicate tip too fardistal) Read PCWP (correlates with LVEDP =4-15 mmHg is normal) Reconnect breathing circuit, deflate balloon, observe PAwaveform return PAdiastolic pressure usually correlates well with PCWP pressure(should be usedas parameter to assess left ventricular filling) Withdraw PAC slightly (1-2 cm) to prevent PA rupture from distal tip migration Secure catheter sleeve once PCWP obtained(assure PCWP pattern is reproducible before removing sterile field) Troubleshooting a coiled/knotted catheter: Prevention: Withdraw PAC slowly to ..t- risk of knotting catheter upon itself Use fluoroscopy if necessary to remove a knot Remove PAC & introducer as one unit if unable to release a knot Obtain a CXR to check PAC positionComplication: PA Perforation Predisposed when no wedge pattern evident after deep insertion Circumstances that predispose to PAperforation:papillary muscle ischemia, mitral stenosis or regurgitation, pulm. HTN, intrapulmonaryshunting, LV failure Caution if no definitive wedge pattern is observed'(repeated attemptsto advance PAC mayleadto PA perforation) Coiling or actual false-negative wedging may occur & predispose to PA ruptureDECOMPRESSION OF A PNEUMOTHORAX (Needle Thoracostomy)Indication Tension pneumothorax (symptoms: Hypotension, ..t- Sp02, ..t- breath sounds & tympanicto percussion on affected site; deviated trachea & mediastinum on CXR)Technique Insert large bore cannula or needle into 2nd intercostal space on midclavicular line Release pressure in pleural cavity(converts tension pneumothorax ~ simple pneumothorax) Subsequent chest tube insertion usually required to treat pneumothoraxComplications Lung laceration (esp. if no tension pneumothorax present) Reaccumulation of air in pleural space(maybe undetected if needle thoracostomy becomes dislodged)INSERTION OF A NASOGASTRIC TUBE (NGT)Indication Decompression &emptying of stomach (after RSI, prior to laparoscopy, GIsurgery) Aspiration of gastric fluid (lavage to detect intragastric blood in setting of GI bleed) Tube feeding Drug administrationContraindications Base of skull fractures, severe facial fractures (esp to nasal bones) Obstructed esophagus or airwayTechnique Measure tube length (tip of pt's nose to ear & down to xyphoid process)Lubricate end of plastic tube being inserted into anterior nares Advance tube through nasal cavity & into throat Pass pharynx rapidly with gentle continuous pressure to go into stomach(if pt awake, encourage patient swallowing)(if pt asleep, consider use of largyngoscope to visualize entryintoesophagus) Confirm placement by CXR (safest), aspiration or injecting air (stomach auscultation)Complications Malplacement (endotracheal, intracranial) Esophageal perforation Pulmonary aspiration, pneumothorax Nose erosion/bleeding, sinusitis, sore throatACUTE PAIN MANAGEMENTNALINI VADIVELU CHRISTIAN WHITNEYNormal Pain Mechanisms & Pain Pathways Pain pathways from periphery: Start in peripheral nociceptors ~ end in brain Nociceptors present in skin, mucosa, muscles, & joints Stimulated by mechanical, chemical, thermal stimuli Inflammatory agents (bradykinins, cytokines, prostanoids) can sensitize nociceptors Somatic pain = musculoskeletal pain; arranged in dermatomes Visceral pain = pain from organs (bladder, bowel, ovaries)Neuropathic PainDefinition: Pain caused by a lesion/dysfunction of the nervous system Due to pathological change in pain pathways (peripheral or central) Subtypes: Inflammatory or noninflammatory Inflammatory pain includes cancer pain, complex regional pain syndrome, herpeszoster neuritis (shingles) Noninflammatory pain includes postherpetic neuralgia, stump pain, trigeminal neu-ralgia Usually develops after partial injury Uninjured 10sensory neurons can change phenotypePain Assessment Pain description: Throbbing, burning, dull, aching, crushing, shooting Timing:When pain started, duration, onset (sudden/gradual), exacerbating or relievingfactors, diurnal variation, accompanying signs, frequency Localization and radiation of painPain Measurement Numerical rating scale: Pt marks 1-10 line intensity of pain(0 = no pain, 10 = worst pain imaginable) "Faces" rating scale: Mostly utilized with children pioid DosageTable for a 70-KgAdultAdults 1-2 tabs PO q4-6hBased on hydrocodone contentAdult (5 mg) 1-2 tab q4-6hAdult (7.5,10 mg) 1 tab q4-6hAdult:2.5-10 mgPO q3-4h5-30 mg PO q4rh prn10-160 mg PO q12h50-100 mg PO q4-6hIndication: Chronic painthat requires continuous opioids;use only in pts alreadyon opioidtherapyEquivalence: 25 mcgq72h = 50 mgoral morphine q24hDrug Oral Parenteral Half-lifeCodeine 200 mg 120 mg1M 3 hrMorphine 30-60 mg 10 mg1M/IV 1.5-2 hrHydromorphone 7.5 mg 1.5 mg1M/IV 2-3 hrMeperidine 300 mg 75 mg1M/IV 3-4 hrFentanyl N/A 0.1 mg1M/IV 1.5-6 hrOxycodone 20 mg N/A N/AMethadone 10-20 mg 10 mg1M/IV 15-40 hrOxymorphone N/A 1 mg 1M/IVLevorphanol 4 mg 2 mg1M/IVHydrocodone 30 mg N/APropoxyphene 130 mg N/A 12 hr(Darvon)Propoxyphenenapsylate 12 hr(Darvon-N)Fentanyl patch (duragesic)12/25/50/75/100mcgq72hr[)rugCodeine/acetaminophen*Tylenol #2 (15 mg/300mg)Tylenol #3 (30 mg/300mg)Tylenol #5 (60 mg/300mg)Hydrocodone/acetaminophen*Norco (5, 7.5, 10 mg/325mg)Vicodin (5/500,7.5/750)MethadoneDolophine(5, 10 mg)Oxycodone/acetaminophen*Percocet (2.5,5,7.5, 10/325;7.5/500;10/650)Oxycodone (OxyContin)Oxycodone extended releaseTramadol (Ultram)*Maxacetaminophen dose = 4 g/day inadults. Largepercentage of populationlackenzymeto convertingcodeine ---+ morphine (accounts for variability to analgesiceffects)Source:Adaptedfrom Ezekiel MR. Handbook ofAnesthesiology, 2008 ed. Indianapolis, IN: CCS Publishing,2008.MULTIMODAL ApPROACH TO PAIN CONTROL: (see Chapter 27,on ambulatory anesthesia)Analgesic Delivery Systems PO"'-_ Not optimal for immediate postop pain (delayed time to peak effect) Opioids commonly combined with COX inhibitorsSC/IM Less desirable routes (pain on injection &erratic absorption) Cyclical period of sedation ~ analgesia ~ inadequate analgesiacommon Intravenous administration Requires close respiratory monitoring Common in in PACU, ICU, &specializedunits Patient-controlled analgesia (PCA) Allows pt to self-administer opioids with button push Physicianspecifies dose, minimum time period between doses (lockout), basalinfusion rate, max delivered dosePedi AdultLockout Infusion PediOpioid (min) (mglhr) InfusionMorphine 'qi-..3h 0-10 15-20mcg/kg/hFentanyl 0.015- 3-15 q1-2h 0-0.1 2-40.05 mgoio.1 mcg/kg/hSufentanil 0.003- 3-100.015 mgHydromorptlone 6=10 10-20 q3-4h 0:-:0..5 3-4mcg/kg mcg/kg/hMeperidine 5-15 mg 5-15 0-30Methadone 10 mcg/kg 10 mcg/kg 10-15 q10-15h 20 20mcg/kg mcg/kgNeuroaxial Analgesia Intrathecal or epidural routes; effectivefor postop painafter abd, pelvic, thoracic, &orthopedic surgeries of lower extremity Opioid infusionsoften combined with local anesthetics(bupivacaine, lidocaine, ropivacaine) Clonidine & buprenorphine also used epidurallyEpidural Opioids Site of action = pre- & postsynaptic receptors in doral horn substantia gelatinosa Opioid drugs enter CSFat rate dependent on physicochemical properties Molecularweight, pKa, oil:water solubility Direct transport via spinal cord blood supplycan occur Diffusion through dural cuff regions to spinal cord can occur Lipid soluble opioids (sufentanil, fentanyl) enter spinal cord faster Also eliminatedfaster by vascular uptake, leadingto a short duration of action Morphine= water-soluble opioid (slower action onset, longer duration of action)Solution1/16%(0.0625%) Bupivicaine + 1 mcg/mL fentanyl1 -j-"2mcg/mLepi ,Smcg/mLtlydromorptlone-j-2mcg/mCEpii Clonidine.5mcglmC+ropivacaineO.2%1/5%(0.2%) Bupivicaine :t dilaudid 0.01 or 0.02 mg/mL1iS%(O.12.5%)Bupivicaine:tdilaudidO.61or 0.02"mg/mL1i16%(0.662.5%yBupivicaine:tdiiaudid0:01orO:02mg/mLEpidural Clonidine Dose = 3-5 mcg/kg; can be added to epidural mix (local or opioid) Prolongs duration of epidural local anesthetic by = 50% J.. Epidural opioid requirements = 30% Side effects: Severe bradycardia (if used>1 mcg/kg/hr)Rate 0.1-0.2 0.3-0.5mcg/kg/h Epidural Placement Levels Thoracotomy T4-T6 Upper abdomen T8 Lower abdomen T10-T12 Lower extremity/pelvis L2-L4Signs of an Inadequate Epidural Pain at rest &with movement (pain score >5) Tachycardia t Respiratory rate For thoracic &abd cases~ Inability to breath deeply, cough, use incentive spirometerTesting of Epidurals 2% lidocaine with 1:200,000 epinephrine or0.25% bupivacaine with 1: 200,000 epinephrine Give 3 mL of either via epidural ~ check BP, motor block & pain relief May repeat 3 mL after 3-5 min Consider replacing epidural if no pain relief after 8 mL of test dose over 10 min"Splitting" Epidural with IV peA Technique: Add IVpeA in addition to epidural infusion(must simultaneously remove opioids from epidural infusion) May be necessary for Pt with opioid dependence Incomplete incisional coverage from epidural Upper &lower body surgeries (trauma victims) Large surgical incision Lower level epidural catheter placementIntrathecal Opioids Act on substantia gelatinosa of the spinal cord Potent analgesia due to central localization of receptors Side effects are mediated by mu receptors (in brain & brain stem)Mixed Agonists/Antagonists Block effects of high doses of morphine-like drugs By competing with morphine-like drugs to bind to mu opioid receptor Produce partial agonist effects at K (kappa) and/or 0 (delta) opioid receptorstomorphine discontinuationcan causeopioidwithdrawalrespiratorydepressionthanmorphinePACU MANAGEMENT ANDDISCHARGEPIYUSH MATHURCOMMON POSTOPERATIVE PROBLEMSHYPOTENSIONcontractility Cardiac tamponade Congestive heart failure Anaphylaxis/anaphylactoidreaction Pneumothorax Adrenal insufficiency/severehypothyroidismarrhythmias Drugs/anesthesia (spinal/epidural) Error in measurement (inappropriate cuffsize, machine malfunction).... Pulmonary embolismSource:Adaptedfrom Keith,RD,et al. Cardiovascularevents in postanesthesia care unit:Contribution ofrisk factors. Anesthesiology 1996;84:772.Initial Diagnosis & Management1. Examine & stabilize-check Airway, Breathing & Circulation2. Fluid resuscitate-obtain adequate venous access3. Review data-patient history, anesthesia record, surgical procedure, estimated bloodloss, PACU data4. Consider laboratory studies ABG-assess oxygenation & acid-base status CBC-assess hemoglobin & platelet level (also consider coagulation studies) ECG-assess for arrhythmias (also consider cardiac enzymes) CXR-rule out pneumothorax/hemothorax/cardiomegaly Blood cultures-esp. if sepsis suspected Transthoracicltransesophageal echo-assess cardiac contractility, LV/RV function,LVfilling,IVC collapse, valvular abnl5. Consider invasive monitoring-arterial Bp,CVp, pulmonary artery catheter6. Initiate pressor/inotropic support-phenylephrine, norepinephrine, dopamine7. Obtain consultations as needed-eardiology, ICU, surgeryManagement of Specific ConditionsHypovolemiaDiagnosis: Tachycardia, hypotension, low CVP/PCWP, respiratory variation in arterialwaveform, IVC collapse/underfilled LVon echoTreatment: Fluid resuscitation, assess for causes (ongoing bleeding, diuresis, high NGoutput)BleedingDiagnosis:Treatment:Tachycardia, anemia, hypovolemia, sanguinous drain outputFluid resuscitation, blood transfusion, correct coagulopathy &thrombocy-topenia, treat hypothermia, consider return to ORSepsisDiagnosis: Fever, leukocytosis, tachycardia, hypovolemia, lactic acidosisTreatment: Fluid resuscitation, obtain blood/specific cultures, initiate broad-spectrumantibioticsMyocardial Infarction/IschemiaDiagnosis: 12-lead ECG, TTE/TEE, cardiac enzymes, cardiology consultTreatment: Cautious fluid resuscitation, aspirin, discuss with cardiologist & surgeonrole of heparinization/cardiac cath/antiplatelet agents; considerinotropiclvasopressor/IABP support; may initiate dluresis/Bcblockadeonce BP stabilizedArrhythmiasDiagnosis:Treatment:12-lead ECG, cardiac enzymes, check electrolytes, ABGTreat the cause, follow ACLS protocol Tachyarrhythmia: Electrical/chemical cardioversion, correct electrolytes,cardiology consultation, maintenance antiarrhythmics. Bradyarrythmia: Atropine/epinephrine/dopamine, transcutaneoustransvenous pacing, cardiology consultDrugsTreatment: Stop the drug, administer antagonist agent (e.g., naloxone for morphine)Pulmonary EmbolismDiagnosis: ECG~ sinus tach/S,Q3T3; ultrasound (US) of lower ext; D-dimer nothelpfulTTE/TEE ~ rule out central pulmembolism/assess RV dysfxV/Qscan/CT chest pulmangiogramwhen stableTreatment: Cautious fluid resuscitation, invasive monitoring, inotropes/pressorsConsider thromboembolectomy/catheter directed thrombolysis/anticoag-ulation/IVCfilter placementCongestive Heart FailureDiagnosis: Bibasilar crackles, frothy sputum on examChest x-ray ~ cephalization of blood vessels, pulmonary edema, TcardiacshadowInvasive hemodynamic monitoringshows ~ cardiacoutput, t filling pressuresTreatment: Supplemental 02, diuresis, digoxin/inotropic supportAnaphylaxisDiQ,gnosis: Tachycardia, vasodilatory shock ( ~ SVR, t cardiac output)Check serum tryptase &eosinophil count, consult allergyTreatment: Remove causative agent, fluid resuscitation, diphenhydramine, steroids, ep-inephrinePericardialTamponadeCauses: Postcardiac surgery bleeding,trauma, dissecting thoracic aneurysm, pro-cedure related (e.g.,sIp CVP placement, coronary cath)Diagnosis: Beck'striad: Hypotension, jugular venous distension, muffledheart sounds Pulsus paradoxus: ~ of > 10 mmHg in systolic bp with inspiration ECG: Nonspecific ST-segmentchanges, low-voltage QRS Chest x-ray: Enlargedcardiac shadow Echo: Diagnostic & mayassist in therapeuticpericardiocentesisTreatment: Fluidresuscitation, pericardiocentesis, surgical repair of bleedingsitePneumothoraxDiagnosis: ~ Breath sounds, ~ lung markings on chest x-rayTreatment: Needle decompression/chest tube placement, surgery consultErrors in MeasurementDiagnosis: Inappropriate BPcuff size, incorrect transducer level,poor arterial wave-form (under/overdamped), machine malfunctionTreatment: Place appropriate size BPcuff,manual measurement, check a-line wave-form, zero transducer at appropriate level,check equipmentEndocrine Disorders: Adrenal InsufficiencyDiagnosis: ACTH stim test; random cortisol levels nonspecific& unhelpfulTreatment: Fluids, administer hydrocortisone, endocrinology consultEndocrine Disorders: Severe HypothyroidismDiagnosis: Hypothermia, bradycardia, highTSH level,low free T3 & T4 levelsTreatment: Fluidresuscitation, levothyroxine administration, endocrinology consultBleedingCommon Causes1. Surgical bleeding2. Coagulopathy3. ThrombocytopeniaDiagnosis Bleedingmay be obvious or occult Important to examine surgical drains/surgical site Signsof hypovolemia(tachycardia,tachypnea, ~ urine output) maysuggest bleedingManagement Consult surgeon, place large-bore IVs & initiate fluid resuscitation Send CBC, PT; PTT,INR,& fibrinogen & request blood cross-match Transfuse: PRBCsbased on hemoglobin level,pt's condition & coexisting diseaseFFPto correct coagulopathyCryoprecipitate if evidence of hypofibrinogenemiaPlatelets if level 0.5 mLlkg/hr4. Maintain central venous oxygen saturation >70%Steroids in Sepsis Hydrocortisone-no improved survival/reversal of shock in pts with septic shockeither overall or in pts who did not have a response to corticotropin~ Hydrocortisone hastened reversal of shock in pts in whom shock was reversed(N Engl JMed 2008;358(2):111-124) Earlier study showed pts in septic shock may benefit from hydrocortisone 50 mg IVq6hr &fludrocortisone 50 mcg enterally dailyUAMA 2002;288:862-871) Subsequent large trials have not confirmed this benefit~ Recommend: Consider steroids for refractory septic shock not responsive to va-sopressorsMarkers of Resuscitation in SepsisContinuous central or mixed venous oxygen saturation monitoringInadequate tissue perfusion ~ rise in oxygen extraction~ Lower than normal O2level in blood returning to right heartLacticacid level or base deficitRecombinant Activated Protein C (Xigris) May.,J.. mortality in pts with severe sepsis at high risk of death (t APACHE IIscore) Common adverse reaction = bleeding Dosing= 24 mcg/kg/hIVcontinuous infusionfor 96 hr Contraindications:Active bleeding,hemorrhagic stroke within 3 mo, severe headtraumalintracranial surgery/intraspinal surgery within 2 mo, intracranial neoplasm ormass lesion, evidence of cerebral herniation, presence of an epidural or spinalcatheter, or trauma with risk of life-threatening bleedingMANAGEMENT OF SEPSISSurviving sepsis campaign:IntI.Guidelines for Management of Severe Sepsis &SepticShock, 2008. (Tablesreproduced with permission from Crit Care Med2008;36(1):296-327.)qualitycriteria, presented in parentheses after each guideline. Indicates a strong recommendationor "we recommend"a Indicatesa weak recommendation,or "we suggest"Initial resuscitation (first 6 hours) Begin resuscitationimmediately in patients with hypotensionor elevatedserum lactate>4 mmoUL; do not delaypendingICUadmission (1C) Resuscitation goals:(1C)CVP8-12 mmHtMeanarterial pressure ::::65 mm HgUrine output ::::0.5 mL.kg-1.hr-1Central venous (superior vena cava)oxygensaturation ::::70%, or mixedvenous ::::65%a Ifvenous oxygensaturation target is not achieved(2C)Consider further fluidTransfuse packed red blood cells if required to hematocrit of ::::30% and/orStart dobutamine infusion maximum 20 /-Lg.kg-1.min-1Diagnosis Obtain appropriate cultures before starting antibioticsprovidedthis does not signifi-cantlydelayantimicrobial administration(1C)Obtain two or more BCsOne or more BCsshould be percutaneousOne BCfrom each vascularaccess device in place >48 hrsCulture other sites as clinically indicated Perform studies promptlyto confirmand sampleanysource of infection; ifsafe to do Begin intravenousantibioticsas earlyas possibleand always withinthe first hour ofrecognizing severe sepsis (1D) and septic shock (1B) Broad-spectrum: One or more agents activeagainst likely bacterial/fungal pathogensand with good penetration into presumed source (1B) Reassessantimicrobial regimendailyto optimize efficacy, prevent resistance,avoidtoxi-city& minimize costs (1C)a Consider combinationtherapy in Pseudomonas infections (20)a Consider combinationempirictherapy in neutropenic patients (20)a Combinationtherapy ::;3-5 daysand de-escalationfollowing susceptibilities (20) Duration of therapy typically limitedto 7-10 days: Longer if response slowor there arundrainable foci of infectionor immunologic deficiencies (1D) Stop antimicrobial therapy if cause is found to be noninfectious (1D)Source identification andcontrol A specific anatomic site of infectionshould be establishedas rapidly as possible(1C)and withinfirst 6 hrs of presentation (1D) Formally evaluatepatient for a focus of infectionamenableto source control measures(e.g.,abscess drainage,tissue debridement) (1C) Implementsource control measures as soon as possiblefollowing successful initial re-suscitation(1C) (exception:Infectedpancreaticnecrosis,where surgical intervention isbest delayed) (2B) Choose source control measure with maximum efficacy and minimal physiologic upset(10) Removeintravascular access devicesif potentially infected(1C)GRADE, Grades of Recommendation,Assessment, Development and Evaluation: ICU,intensivecare unit;CYP, central venous pressure; BC,blood culture.aA higher target CYPof 12-15 mm Hg is recommended in the presence of mechanical ventilationorpreexistingdecreased ventricular compliance. Fluid-resuscitate usingcrystalloids or colloids (1B) Target a CVPof 2:8mm Hg (2:12mm Hg if mechanically ventilated)(1C) Use a fluid challenge technique whileassociatedwith a hemodynamic improvement(1D) Givefluid challenges of 1000 mLof crystalloidsor 300-500 mLof colloidsover30 min.More rapidand larger volumesmaybe required in sepsis-induced tissue hypop-erfusion (1D) Rate of fluid administrationshould be reduced ifcardiacfilling pressures increasewithout concurrent hemodynamic improvement (1D)Vasopressors Maintain MAP 2:65mm Hg (1C) Norepinephrine and dopaminecentrallyadministeredare the initial vasopressors ofchoice (1C)o Epinephrine, phenylephrine, or vasopressinshould not be administered as the initialvasopressor in septic shock (2C).Vasopressin 0.03 units/minmaybe subsequentlyaddedto norepinephrine with anticipationof an effect equivalentto norepinephrinealone.o Use epinephrineas the first alternativeagent in septic shock when blood pressure ispoorly responsiveto norepinephrineor dopamine (2B) Do not use low-dose dopaminefor renal protection (1A) In patients requiringvasopressors, insert an arterial catheter as soon as practical (1D)Inotropic therapy Use dobutamine in patients with myocardial dysfunction as supported by elevated car-diacfilling pressures and lowcardiacoutput (1C) Do not increase cardiacindexto predetermined supranormal levels (1B)Steroidso Consider intravenoushydrocortisone for adult septic shock when hypotensionresponds poorly to adequate fluid resuscitationand vasopressors (2C)o ACTHstimulationtest is not recommended to identify the subset of adults with septicshock who should receive hydrocortisone (2B)o Hydrocortisone is preferred to dexamethasone (2B)o Fludrocortisone (50 f-Lg orallyonce a day) maybe included if an alternativeto hydro-cortisone is beingused that lackssignificant mineralocorticoidactivity. Fludrocortisoneif optional if hydrocortisone is used (2C)o Steroid therapy maybe weaned once vasopressors are no longer required (2D) Hydrocortisone dose should be ~ 3 0 0 mg/day (1A) Do not use corticosteroids to treat sepsis in the absence of shock unlessthe patient'sendocrine or corticosteroid history warrants it (1D)Recombinant human activated protein Co Consider rhAPCin adult patients with sepsis-induced organ dysfunction with clinicalassessment of highrisk of death (typically APACHE II2:25or multipleorgan failure) ifthere are no contraindications(2B,2C for postoperative patients) Adult patients with severe sepsis and low risk of death (typically, APACHE II0.6 = severe) Acute MR: t pulmonary pressure & pulmonary congestion Chronic MR: t LA size &complianceClinicalfeatures Apical holosystolic murmur radiatingto axillaTreatment Medical therapy; mitral valve repair/replacementAnesthetic management MaintainHR normal or high Avoid myocardial depression Avoidt SVR(can worsen regurgitation) Initiate prophylaxisagainst endocarditis PAcatheter v-waves increase as regurgitant fraction increasesAortic StenosisCauses: Bicuspid AY, rheumatic fever,senile degenerative diseaseRiskfactors: Malegender, hypercholesterolemia, smokingPathophysiology Blood flow across valve is obstructed during systole Concentric LV hypertrophy Dependence on atrial kickto fill stiff ventricle Develop fixed stroke volume Compression of subendocardial vessels ~ ischemiaSymptoms & severity Angina-median survival 5 years Syncope-median survival 3 years Congestive heart failure-median survival 2 yearsClinical features Harsh, holosystolic, crescendo-decrescendo murmurClassification Mild = valvearea 50% incidence of concomitantCAD Procedure times often long (on uncomfortable fluoroscopy bed) usuallybest toavoid long infusions/largedoses of midazolam/propofol (problem ofconfusion/disori-entation) . Alwaysbe prepared for conversion to open procedure Regionaltechniques may..l.- incidence of hypercoagulability &perioperative vesselclot formation (esp for lower extremity procedures)Endovascular Safety Concerns Perioperative 13-blockade: Current ACC guidelines- recommend perioperative13-blockade in vascular pts found to have myocardial ischemia on pre-op testing(less strong evidence forpts with low/intermediate cardiac risk) Transfusiontriggers: Evidencesuggests vascular pts allowed to bleed below a hemo-globin level of 10 mg/dLhave t incidence of periop myocardial ischemia-, Regionalanesthesia &anticoagulation (see Chapter 6, on Regional Anesthesia)Contrast-induced Nephropathy (CIN) ARFafter ischemia or contrast thought 2 to acute tubular necrosis from Free-radical formation, which is promoted in acidic environment (e.g., renalmedulla) Contrast-related I in renal blood flow Atheroembolism Tips to Avoid CINMaintain plasmavolume, good urine output NaHC03 may be protective: 05 NaHC03 154 mEq/L(from pharmacy) Load: 3 mLlkgover 1 hr,given 1 hr before contrast Maintenance: 1 mLlkg/hr until 6 hr after procedure Use 110 kg max weight for calculations If bolus leads to significantHTN -+ stop bolus, diurese before injectingcontrast,then resume infusion N-acetylcysteine (free-radical scavenger) 600 mg PO bid starting day before surgery and through day of surgery RiskFactors Patient factors: Renal dz, diabetes, CHF,t age, anemia, LV dysfx Nonpatient factors: t Osmolar or ionic contrast, contrast viscosity&volumePeripheral Vascular Surgery Preop risk: Patients often have significant comorbidities (t risk of associated CAD) Procedures: Bypassgrafts (fern-pop,ilio-fem,etc.), embolectomy, pseudoaneurysmrepair Monitoring:Invasive monitors per pt condition (hemodynamics often labile)(place A-line in sideopposite surgery) Anesthetic General anesthesia/regional/MAC Epidural& GA -+ associated with comparable rates of cardiac morbidity Continuous epidural/spinal ..l.- Incidence of postop vascular graft clotting (Anesthesiology 1993:79:422) Continuous lumbar epidural catheter commonly used (occ spinal) Awake pts can notify personnel of acute MIsymptoms (chest pain) Helpfulfor postop pain control Intraop heparin after epidural placement does not t risk of epidural hematoma Epiduralassociated with ..l.- incidence of reoperation for inadequate tissue perfu-sion (compared to GA) (Anesthesiology 1993;79[3]:422-434)ANESTHESIA FOR NEUROLOGICSURGERY, NEURORADIOLOGY,AND ECTJOSHUA H. ATKINSHypocarbia: CBF ,1., CMR ++CO2response byinhaled potent agents, preserved byIVagentsC02 response curve inpresence ofchronic hypercapnea Profound hypoxia (Pa02 ICP) Goal of CPP >60 mm Hg in normal pts Higher pressures needed to achieve adequate tissue 02 delivery in pts with exist-ing brain pathology/elevated ICP (>70 mm Hg) Cerebral blood flow in healthy pts is autoregulated (MAP 50-150 mm Hg) Global cerebral blood flow mU100 g brain/min to gray matter) In chronic HTN autoregulation curve shifts to right-, Modest hypotension may result in hypoperfusion &ischemia Extreme hypertension large increases in CBF & ICP Brain edema, hyperemia, &tissue injury from disruption of BBB Blood flow changes with cerebral metabolic rate Brain 02 delivery closely approximates demand of 02 extracted at 1st pass) Blood flow less than 15 mL/100 g/min ischemia detectable by EEG Anesthetics, temp, arterial P02&Pco-, and pathophysiologic states influence rela-tionship between autoregulation of CBF (see table below) Displacement of brain tissue by surgical instruments impairs local perfusion Global brain physiology differs from that occurring at regional/cellular level (e.g.,mitochondria)'--'Intracranial Pressure (ICP)ICP = cranial (closed space) pressure on brain, CSF,& blood components Brain components: brain mass/cells (80%); blood (10%); CSF (10%) Normal range: 0-10 mm Hg; CSF: 150 mL normal volume; 450 mUd Increased