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ANESTHESIA PLAN OF CAREAge: 64 Sex: F Ht: 65” Wt: 90kg ASA: 3 Proposed Procedure: Consent signed for Sx: Y Anes: Y Left carotid endarterectomy Pre-Procedure VS:BP: LUE 123/69 RUE 112/66 HR: 59 RR: 16 Temp: 36.5 C Spo2: 99%NPO Status: 10 hrs Allergies: NKDA, No food allergiesCurrent Medications:Prilosec 20 mg PO dailyAtenolol 100 mg PO dailyAspirin 81 mg PO daily-last dose 7 days agoLipitor 20 mg PO dailyPrevious Anesthetics/Surgeries: TAH-10 yrs ago, Appendectomy-45 yrs ago, Colonoscopy-5yrs agoAny Pt/Family Anesthetic Complications: pt has a hx of PONV, no family hx of complicationsAirway Assessment:MP Class: 2 TMD: WNL Cervical Mobility: NML Teeth: NML SYSTEMS:Respiratory:Smoker-1 ppd x 40 yrs, denies SOB or asthma symptomsCardiovascular:CAD, HTN, PVD, Hypercholesterolemia, Carotid Doppler studies show Lt carotid 95% occluded, Rt carotid 85% occluded, ECHO-73% EF, 4 METs-able to do light housework and walks 4 blocks per day.Hepato/Gastrointestinal:GERDNeuro/Musculoskeletal:(-) Hx, Hand grips strong and equal, moves BLE symmetrically, facial symmetry normal, denies any new visual deficits, able to stick tongue out to midline and move it laterally.Renal:(-) HxEndocrine:(-) HxReproductive:Previous TAHDiagnostics StudiesEKG: Sinus Brady-rate 55CXR: No acute findingsLabs: Hgb 14 Hct 40.7 WBC 6.6 Plt 221 Pt 10.7 INR 1.1 BUN 14 Cr 0.8Na 141 K 3.7 Gluc 102 Type and ScreenPROBLEM LIST/ANESTHETIC CONSIDERATIONSSurgical Procedure: Carotid EndarterectomyCarotid endarterectomy is indicated for severe atherosclerotic occlusive disease involving internal carotid arteries at the common carotid bifurcation which is a common cause of thromboembolitic or hemodynamic stroke and TIAs. The surgery involves opening the carotid artery and the proximal internal carotid artery, removing plaque from inside the artery, and repairing the vessel wall. Opening the carotid artery requires temporary occlusion of the proximal common carotid, distal internal carotid, external carotid, and usually its first branch, the superior thyroid artery. The entire procedure can be performed under continual occlusion of these vessels if the collateral flow to area supplied by the occluded internal carotid is deemed adequate (on the basis of Intraop EEG monitoring, internal carotid artery back-bleeding, stump pressures, CBF studies, or angiography). Alternatively, an internal shunt between the proximal common carotid artery and distal internal carotid artery can be placed after the opening of the carotid artery for use during the endarterectomy. Often a synthetic graft (Dacron patch) or occasionally a vein graft is needed to reconstruct the arteriotomy site and increase the luminal plications: circulatory instability, MI, Stroke, loss of carotid body chemoreceptor function, acute respiratory insufficiency secondary to hematoma and tracheal deviation, tension pneumothorax. Position: supine Surgical time: 2-3hrs EBL: 50-150mlPhysiology/Anesthetic considerations:The internal carotid arteries supply the ocular globe by way of the ophthalmic artery, and the cerebral hemispheres from the middle and anterior cerebral arteries. The external carotid arteries supply the neck, face, scalp, oral and nasal cavities, and the meninges. There are numerous vascular and nerve structures in close proximity to the carotid surgical site including the Glossopharyngeal (IX) and Vagus (X) nerves. When the surgeon is working in the area of the carotid bifurcation, severe bradycardia can occur secondary to stimulation. Treatment for the bradycardia would be to have the surgeon stop stimulation, administer Atropine if necessary, and have the surgeon localize the area before returning to work in that area. Full anticoagulation with heparin (5,000-10,000 units IV) is administered just prior to arterial occlusion. During occlusion, the patient is relying on the circle of Willis and the contralateral carotid for perfusion or a shunt if placed. Mild hypertension (MAP 90-110) is to be maintained during the internal carotid artery occlusion to ensure cerebral perfusion. In the patient undergoing an awake carotid, the patient may be asked to speak or follow commands such as squeezing their hands to ensure adequate blood flow. In the asleep patient, EEG, SSEP, or cerebral oximetry may be used. Approximately 10 minutes after the repair and reopening of the carotid arteries, the surgeon may ask for reversal of the Heparin with Protamine (0.5mg per 100 units of Heparin IV slowly over at least 10 min-slower rate if hypotension occurs). During closing, maintain MAP as close to patients preop as possible, but take care to avoid high pressures on the new carotid graft and suture line. Positioning Concerns: supineThe patient is positioned supine with arms tucked at sides. Elbows should be kept off table edge to prevent ulnar nerve damage and hands should be kept parallel to trunk. Be aware that flexion and extension of neck will effect Ett position. Legs should be flat, uncrossed and heels should be padded. Patients face and eyes should be padded to avoid injury from surgeon leaning or placing instruments in that area. Physiologic changes that occur due to the supine position are an initial transient increase in VR, HR, contractility, CO, and BP. This is followed by a compensatory response that decreases sympathetic outflow leading to a decrease in HR and vasodilation. The compensatory response is attenuated by induction of general anesthesia. FRC and TLC are significantly decreased by the supine position, general anesthesia, and neuromuscular blocking agents.Current Medications/Anesthetic Considerations:Prilosec-proton pump inhibitor used for GERD, gastric ulcer/prophylaxis, H. pylori infection, hypersecretory conditionsAdverse effects: blood dyscrasias, hepatic impairment, Stevens-Johnson syndrome, interstitial nephritis, hypomagnesemia, fractures, H/A, diarrhea, constipationDrug interactions: when combined with any diuretic may increase risk of hypomagnesemia.When combined with Diazepam may increase Diazepam levels, prolong effects, and increase CNS depression and psychomotor impairment.Atenolol-selective beta1 blocker used in the treatment of HTN, angina, and cardiovascular event protection.Adverse effects: CHF, heart block, severe bradycardia, arrhythmias, Raynaud phenomenon, bronchospasm, hypersensitivity reaction, lupus, hypotension, fatigue, dizziness, depression, dyspnea, leg pain, bronchospasm, lethargy, diarrhea, nausea, vertigo, drowsiness. Drug interactions: when combined with Clonidine, may increase the risk of severe rebound HTN on alpha 2 agonist withdrawal. When combined with Cimetidine, Alfentanil, or Dexmedetomidine may increase the risk of bradycardia and hypotension. When combined with insulins or hypoglycemics, may prolong/mask hypoglycemia. When combined with Ephedrine, may decrease vasopressor effects. When combined with beta 2 agonists, may decrease bronchodilating effects. When combined with cholinesterase inhibitors, may alter cardiac conduction, increase risk of bradycardia/AV block and may increase the risk of bronchospasm. Aspirin-prevention of plt aggregation, reduces pain, fever, and inflammation-no antidote-binds with plts, requires excretion with plts (8-10 days)Adverse effects: anaphylactic/anaphylactoid reactions, angioedema, bronchospasm, bleeding, GI ulcer/perforation, DIC, pancytopenia, thrombocytopenia, agranulocytosis, aplastic anemia, nephrotoxicity, hepatotoxicity, Reye syndrome, dyspepsia, N/V, abdominal pain, rash, tinnitus, dizziness, hyperuricemia, ecchymosis, constipation, diarrhea. Drug interactions: when combined with NSAIDs corticosteroids, SSRIs, Verapamil, or Neostigmine may increase the risk of GI bleeding, Ibuprofen may inhibit the cardioprotective effect of low-dose aspirin. When combined with ARBs, ACE inhibitors, may decrease antihypertensive effect. When combined with diuretics may decrease antihypertensive, diuretic, and natriuretic effects and increase the risk of ototoxicity.Lipitor-statin/dyslipidemiaAdverse effects: myalgia elevated CK, rhabdomyolysis, acute renal failure, hepatotoxicity, interstitial lung dz, angioedema, myopathy, tendon rupture, pancreatitis, hypersensitivity reaction, anaphylaxis, lupus, vasculitis, thrombocytopenia, leukopenia, hemolytic anemia, photosensitivity, Stevens-Johnson syndrome, H/A, rash, abdominal pain, back pain, flu-like symptoms, pharyngitis.Drug interactions: when combined with Diltiazem, azole antifungals, Amiodarone, Clarithromycins, or erythromycins, may increase statin levels and risk of myopathy and rhabdomyolysis. Co-morbidities: Smoking Hx:Cigarette smoking has effects on every organ system. It is the single most important risk factor for the development of COPD. Patients who have smoked more than 60 pack years, have double the risk of any pulmonary complication, and triple the risk of pneumonia. It is also a risk factor for the development of cardiovascular disease. Carbon monoxide decreases oxygen delivery and increases the work of the myocardium. Smoking releases catecholamines and causes coronary vasoconstriction. It causes mucous hypersecretion, reduces the activity of mucocilia of the airways and results in hyperreactive airways. It also causes decreased pulmonary immune function. Smoking delays wound healing. Preoperatively, the patient should be counseled not to smoke for at least 24 hours prior to and after surgery and on smoking cessation. Soon after a patient quits smoking, carbon monoxide levels decrease which improves oxygen delivery. Cyanide levels decrease which benefits oxidative metabolism and lower nicotine levels decrease vasoconstrictive effects of smoking. There is also a decrease in many of the toxins from cigarette smoke that cause delayed wound healing. The patient should be assessed for undiagnosed lung disease and cardiovascular disease associated with smoking. Consider getting a chest x-ray, ECG, and pulmonary function testing. Auscultate the lungs and treat wheezing as needed with beta agonists such as Albuterol.CAD:Preop considerations: Determine the extent of CAD and any previous interventions as well as current stability of the disease process. Review medication therapy and note any drugs which may increase risk of bleeding or contraindicate a particular anesthetic technique. Risk stratification should be determined to optimally manage the patient and lessen the risk of perioperative cardiac events. This patient is on a regimen of Metoprolol, Aspirin, Plavix, and Lovanza. It is recommended that the patient continue with her Metoprolol and Aspirin therapy on the day of surgery and that her glucose be kept under tight control. Plavix should be stopped 5 days prior to surgery. Anxiety should be reduced thorough explanation of the anesthetic and with Anxiolytics such as Versed.Intraop considerations: IV induction is acceptable but Ketamine should be avoided because it causes increase in HR and BP thereby increasing myocardial oxygen requirements. Direct laryngoscopy should be of short duration (<15 sec) to minimize the magnitude and duration of circulatory changes associated with laryngoscopy. Laryngotracheal Lidocaine, IV Lidocaine, Esmolol, and Fentanyl can be used to blunt the effects of tracheal intubation. Volatile anesthetics are useful because they decrease myocardial oxygen requirements and precondition the myocardium to tolerate ischemic events. Opioids are useful in preventing/treating tachycardia and hypertension associated with surgical pain response. Muscle relaxants with little or no effect on HR and BP are Vecuronium, Rocuronium, and Cisatracurium. Reversal of neuromuscular blockade with Neostigmine can be safely accomplished. Robinul is preferred over Atropine because it has less of a chronotropic effect. Intraop goals are to prevent MI by optimizing myocardial oxygen supply and reducing oxygen demand and to monitor closely for ischemia and treat promptly any ischemia that develops. It is important to avoid persistent and excessive changes in HR and BP (keep within 20% of pt’s preop HR and BP). Anemia, tachycardia, diastolic hypotension, hypocapnia, and hypoxemia cause decreased oxygen delivery. SNS stimulation, tachycardia, HTN, increased contractility, and increases in preload and afterload cause increases in myocardial oxygen demand. Avoid hyperventilation because hypocapnia causes coronary artery vasoconstriction. Avoid hypothermia because this will predispose the patient to shivering on emergence leading to abrupt and dramatic increases in myocardial oxygen requirements. Have uppers and downers readily available. Close monitoring of the ECG is important and treatment of myocardial ischemia should be instituted when there is a 1-mm ST segment change. Persistent increase in HR should be treated with Esmolol. NTG is a better choice when the BP is normal to modestly elevated. Hypotension should be treated with sympathomimetic drugs to restore coronary perfusion pressure. Fluid infusion can also be helpful.Emergence Considerations: The timing of weaning and extubation requires careful consideration. A smooth emergence is key in preventing significant hemodynamic changes. Early extubation is possible and desirable as long as criteria are met. Hypertension:Preoperatively determine the adequacy of blood pressure control, review pharmacology of patient’s antihypertensives pt, evaluate for evidence of end-organ damage (angina, LVH, CHF, Cerebrovascular disease, stroke, PVD, renal insufficiency), and continue antihypertensives. Rebound hypertension may occur with certain drugs like Beta blockers and Clonidine if stopped abruptly. ACE inhibitors are not usually associated with rebound hypertension. The patient should be made normotensive preoperatively for elective surgery to decrease the incidence of perioperative hypertensive episodes and postoperative cardiac complications. If end-organ damage is exhibited and can be improved or optimized prior to elective surgery, postponement of surgery is justified. Renal insufficiency secondary to chronic hypertension is a marker of widespread disease. It is not uncommon for patients to present with elevated BP secondary to anxiety (white coat syndrome) but these patients are likely to have exaggerated responses to direct laryngoscopy, perioperative ischemia, and to require antihypertensive therapy intraoperatively. In patients with chronic hypertension, consider need for invasive monitoring based on the complexity of the surgery. During induction, anticipate exaggerated BP response to anesthetic drugs, limit duration of laryngoscopy to <15 seconds, administer balanced anesthetic to blunt hypertensive responses. Direct laryngoscopy and tracheal intubation may result in significant hypertension despite normotension preoperatively. Myocardial ischemia is more likely to occur during times of hypertension and tachycardia. Monitor closely for myocardial ischemia. The goal of maintenance is to minimize fluctuations in BP. The most likely intraoperative BP change is hypertension associated with pain stimulus. In this case, the anesthetic should be deepened by narcotic or increasing the volatile agent. All volatiles produce dose dependent decreases in BP. There is no evidence that one particular muscle relaxant is more beneficial than another in hypertensive patients. Pancuronium can modestly increase BP in all patients but this in not exaggerated in the hypertensive patient. Exaggerated hypotensive responses may be seen with blood loss, positive pressure ventilation, or sudden changes in body position secondary to some antihypertensive drugs effect on autonomic system function. In this case, vasopressors such as Ephedrine and Phenylephrine usually provide reliable appropriate responses. Also lightening the anesthetic should be considered. Intraoperative hypotension in patients on ACE inhibitors is often responsive to IVFs, sympathomimetics, or vasopressin. During the postoperative period, anticipate periods of systemic hypertension and treat promptly to decrease risk of myocardial ischemia, cardiac dysrhythmias, CHF, stroke, and bleeding. Maintain monitoring of end-organ function.PVD:Chronic PVD is most often due to atherosclerosis and acute PVD is usually caused by arterial embolism. Vasculitis is also a cause of compromised peripheral flow. The incidence of atherosclerosis increases with age (70% of people >75yrs old have it). Patients with PVD have a 3-5 times greater chance of having cardiovascular ischemic events. Risk factors for PVD include: DM, HTN, tobacco use, dyslipidemia, and a family history of premature atherosclerosis. Signs and symptoms of PVD are: intermittent claudication, extremity pain with rest, decreased or absent pulses, bruits of the abdomen, pelvis, or inguinal area, atrophy of the extremity, hair loss, coolness, pallor, cyanosis, and dependent rubor. Treatment includes: exercise programs, smoking cessation programs, lipid-lowering therapy, tight control of DM, antihypertensive therapy, revascularization procedures, and bypass procedures. GERD: In a healthy person, the lower esophageal sphincter (LES) opens with swallowing and closes afterward to prevent gastric acid from the stomach from refluxing upward into the esophagus. During times between swallowing, the LES exerts enough pressure (approximately 29 mm Hg) to prevent reflux. In a patient with GERD, there is inappropriate relaxation and weakness of the LES leading to a pressure of only approximately 13mm Hg which allows gastric acid to rise up into the esophagus causing irritation. Reflux into the pharynx, larynx, and tracheobronchial tree can lead to chronic cough, pharyngitis, laryngitis, bronchitis, and pneumonia. During anesthesia, there are many factors that contribute to the likelihood of reflux of gastric contents and aspiration. Some of these factors are: urgency of surgery, airway problems, inadequate depth of anesthesia, use of lithotomy position, autonomic neuropathy, IDDM, pregnancy, depressed consciousness with loss of airway reflexes, increased acuity of illness, obesity, and increased intra-abdominal pressure. Medication often administered during anesthesia that cause decreased LES tone are: Atropine, Glycopyrrolate, Dopamine, Nipride, Thiopental, Tricyclic antidepressants, Beta adrenergic stimulants, Opioids, and Propofol. Medications that improve LES tone are: Metoclopromide, Edrophonium, Neostigmine, Succinylcholine, Pancuronium, Metoprolol, Alpha-adrenergic stimulants, and Antacids. Prophylactic treatment can include Cimetidine, Rantidine, Famotidine, or Nizatidine to decrease gastric acid secretion and increase gastric pH. This effect in Cimetidine takes up to 1.5 hrs to work and only lasts 3 hours. Rantidine is 4-6 times more potent and has fewer side effects. Famotidine and Nizatidine can be given IV and have a longer duration. Protein pump inhibitors can also be effective, but must be given orally the night before and morning of surgery. In patients who are diabetic, morbidly obese, or pregnant, Sodium Citrate, an oral nonparticulate antacid that increases gastric pH should be considered. If given, a gastrokinetic agent such as IV Metoclopramide should also be administered. For induction of general anesthesia, cricoid pressure application is recommended to compress the lumen of the pharynx between the cricoid and cervical vertebrae to prevent reflux. The force applied should be sufficient to prevent aspiration but not cause airway obstruction (approximately 6-8 lbs of pressure) and should be held from the beginning of induction until endotracheal tube placement is confirmed and the balloon is inflated. Endotracheal intubation with a cuffed tube is the gold standard for protection of the airway from aspiration. Antibiotic Prophylaxis:Cefazolin 1 gm IVPB Side effects-diarrhea, N/V, rash, urticaria, anaphylaxisBlood/Fluid Loss:Administer hourly maintenance and replace NPO deficit, UOP, blood loss, and third space loss.Monitor for adequate perfusion-UOP, cap refill, MAP, skin color.Labs prn to ensure stable Hgb/Hct.Risk of Hypothermia:Continuously monitor temp (esophageal probe distal 1/3) or skin temp if regional used.Warm blankets preop, fluid warmer, bair huggerPONV:Zofran 4 mg IV 30 min prior to emergence (5HT3 Serotonin blocker)Scopalamine patch preop (antimuscarinic)Metoclopramide 10 mg IV (Dopamine blocker-avoid use in Parkinison’s)Benadryl 12.5-25 mg IV (Histamine blocker) PLAN OF ANESTHESIAPosition: supine IVs/lines: 2 lg bore IVs, AlineMonitors/Special Equipment: Pulse ox, NIBP, ECG-5 lead, ETCO2, PNS, BIS, Precordial and Esophageal stethoscopes, Bair hugger, Hotline, arterial line transducer and kit, size 7.0mm Ett, Mac 3 blade, oral and nasal airways, lube, and tongue blade. Have Bougie in room, and emergency airway cart and Storz available. Phenylephrine gtt and syringe, Ephedrine syringe, Nipride gtt, NTG gtt, Esmolol, Atropine, Robinul, Heparin, and Protamine should be readily available.BP control: Maintain MAP at or slightly above the patient’s highest recorded resting pressure while awake. Phenylephrine (pure alpha agonist) is ideal to support the BP because it has minimal dysrhythmogenic potential. V4 or V5 lead will indicate if hypotension is causing ischemia. Administration of simultaneous NTG (0.2-0.4 mcg/kg/min) may improve coronary flow during periods of induced hypertension. If hypertensive episodes occur during surgery, infusions of esmolol +/- NTG/SNP work well to control BP.PLAN ARegional: Deep and/or superficial cervical plexus block with sedationVersed 1-2mg (anxiolytic) may be given preoperatively. Just prior to the block, Fentanyl 25mcg and Propofol 10-30 mg may be titrated to allow patient to remain still during the block while maintaining their airway. A Precedex gtt should be started at 0.4 mcg/kg/min and can be titrated to up to 1 mcg/kg/min to keep patient in a state in which they can be aroused easily and follow commands/answer questions, but yet comfortable enough to tolerate lying still. Deep Cervical Plexus Block:Position the neck slightly extended with the head turned away from the side to be blocked. Draw a line between the tip of the mastoid process and Chassagnac’s tubercle (C6 the most easily palpable transverse process). Draw a second line parallel and 1 cm posterior to the first line. Next, locate the C4 process by first finding C2 1-2 cm caudal to the mastoid process then running the fingers down to C3 then C4. At the C4 transverse process, insert a 22g 5 cm needle immediately over the process until it contacts the process at ~1.5-3cm deep. If paresthesia is obtained, inject 10-12 ml of local anesthetic. If a paresthesia is not obtained, the needle should be obtained and “walked” down in a step wise antero-posterior fashion. Risks/Adverse Effects: There is often at least a phrenic nerve block. There is a risk of puncture of the vertebral artery as it is in close proximity to the landmarks.Superficial Cervical Plexus Block:This block relies on the volume of the local anesthetic for effectiveness. A 22g 4 cm needle is inserted SQ posterior and immediately deep to the sternocleidomastoid muscle and 5ml of local anesthetic is injected. The needle is then redirected superiorly and inferiorly along the posterior border of the sternocleidomastoid and 5ml is injected along each of these sites. Be aware that the EJ overlies the block site. There is a risk of intravascular injection via the IJ if the needle is too deep. PLAN BTechnique: GETA (muscle relaxant not necessary because SSEP, EEG, or Cerebral oximetry may be performed to assess CBF)INDUCTIONSequence: Apply monitors, preoxygenate with 8L 02 by FM x 3-5 min. Get airway equipment to bedside (suction, laryngoscope with Mac 3 blade, size 7.0mm Ett styleted, oral airway and tongue blade.Meds/Doses:Versed 2 mg IV (anxiolytic-use if not oversedated by previous dose)Fentanyl 50-100 mcg IV (opioid to blunt effects of laryngoscopy)Lidocaine 90mg IV (1mg/kg, prevents burning from Etomidate, blunts effects of laryngoscopy)*Have pt take 4-8 VC breaths and place in sniffing position.Etomidate 20 mg IV (0.2-0.3mg/kg-GABAmimetic induction agent)Airway Management:Once Etomidate causes unconsciousness (no response when calling pt’s name and loss of lash reflex), place tape over closed eyes and assure ability to mask ventilate repositioning and placing oral airway as needed. Assess baseline neuromuscular status with PNS TOF. Administer Succinylcholine 80mg IV (DMR). Verify paralysis with PNS. Intubate and verify placement (visualize tube through cords, condensation, BBS, EtCO2) and secure Ett.MAINTENANCEAgents:*Volatiles impair autoregulation therefore, maintaining a MAP slightly greatly than the pt’s normal is more likely to maintain cerebral perfusion.Sevoflurane (MAC 2%)-agent of choice (up to 1% in combination with N20 50% will not interfere with EEG or EP monitoring)Isoflurane (MAC 1.15%)-0.6% with N20 50% will not interfere with EEG or EP monitoring.Desflurane (MAC 5.8%)Opioids: Fentanyl 50 mcg prn S/S of pain (increased HR and BP)NMB: Once TOF 4/4 (return to baseline from Succinylcholine dose), if surgeon requests muscle relaxation, give Cisatracurium (Nimbex) 0.02mg/kg (2.3 mg) for. Onset 2-4 min Duration 40-75 min Metabolism is Hofmann elimination 77% and non-specific esterase hydrolysis 23%.Alternate: Rocuronium (Zemuron) 0.6 mg/kg (actual body weight) initially and repeat for TOF 2+ and ongoing sx. Onset: 1-3 min Duration: 30-60min. Metabolism: undergoes no metabolism and is eliminated primarily by the liver and slightly by the kidneys. Vent: Volume Control, keep PIP < 30 cm H20, TV 6-10 ml/kg (650), Rate 8-10 (10), I:E ratio 1:2. Maintain EtCO2 30-40).BP Maintenance:Fluid Requirements:Maintenance: 90kg + 40ml= 130mlNPO deficit: 10 hrs X 130ml=1300ml3rd space loss: 1ml/kg/hrEBV: 65ml/kg X 90kg=5850mlABL: 3{(5850ml X .40)-(5850ml X .30)}=1755 ml*It significant blood loss replace with colloid or PRBCs (ratio 1:1). Otherwise replace with crystalloid 3:1.Hr: Maint: NPO deficit: 3rd sp: EBL: Total: 1 130ml 650ml 90ml (50ml) 150ml =1020ml2 130ml 325ml 90ml =545ml3 130ml 325ml 90ml =545ml 2110 ml*Note total carotid occlusion time after cross-clamps removed. EMERGENCESequence:Wean pt off any vasopressors because HTN is likely with wake up. The need to control HTN with Nipride or NTG and/or Esmolol is likely during the emergence phase. Titrate volatiles down, increase FGF. Assess NM status with PNS. Administer reversal when TOF >1/4. Administer Lidocaine 90 mg IV to prevent coughing/bucking. Change ventilator to bag mode to assess pt effort and supplement prn. When awake extubation criteria met (able to open eyes, lift head off bed > 5sec, sustained hand grips, TV 5ml/kg or more, adequate Spo2 and RR) suction oropharynx, untape Ett, deflate cuff, extubate with + pressure. Apply O2 8L by FM.Reversal Agents: Neostigmine 4mg IV (0.04-0.07mg/kg)-AntiachesteraseGlycopyrrolate (Robinul) 0.8mg IV (0.01mg/kg)-AnticholinergicPOST-OPERATIVE CAREAirway: Monitor for S/S of laryngospasm. Ensure intact airway and adequate RR/TV/Spo2. Obeserve for hematoma leading to tracheal deviation.VS: Ensure VSS-tx as needed. Assess pain level. Pt may have phantom pain.Neuro Status: Assess neuro status and ensure back to baseline before pt leaves O.R.Postop Pain Control: Dilaudid 0.5 mg IV for pain if respiratory status adequate. Report to PACU RN and ensure comfortable with pt status.REFERENCESBrown, D Atlas of Regional Anesthesia. 2nd ed. Philadelphia, PA: WB Saunders; 1999.ePocrates (ePocrates Rx) [computer program]. ePocrates, Inc; Ver 1.335/2011.Jaffe, RA, Samuels, SI Anesthesiologists Manual of Surgical Procedures. 4th ed. St Louis, MO: Elsevier Saunders; 2010.Miller, RD, Eriksson, et al Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010.Nagelhout, JJ, Plaus, KL Handbook of Nurse Anesthesia. 4th ed. St Louis, MO: Elsevier Saunders; 2010. ................
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