Download ANESTHESIA PLAN OF CARE Age: 64 Sex: F Ht: 65” Wt: 90kg ASA

ANESTHESIA PLAN OF CARE
Age: 64
Ht: 65”
Sex: F
Proposed Procedure:
Wt: 90kg
Consent signed for Sx: Y
ASA: 3
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 allergies
Current Medications:
Prilosec 20 mg PO daily
Atenolol 100 mg PO daily
Aspirin 81 mg PO daily-last dose 7 days ago
Lipitor 20 mg PO daily
Previous Anesthetics/Surgeries: TAH-10 yrs ago, Appendectomy-45 yrs ago, Colonoscopy-5yrs ago
Any Pt/Family Anesthetic Complications: pt has a hx of PONV, no family hx of complications
Airway Assessment:
MP Class: 2
Cervical Mobility:
TMD: WNL
NML
Teeth: NML
SYSTEMS:
Respiratory:
Smoker-1 ppd x 40 yrs, denies SOB or asthma symptoms
Cardiovascular:
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:
GERD
Neuro/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:
(-) Hx
Endocrine:
(-) Hx
Reproductive:
Previous TAH
Diagnostics Studies
EKG: Sinus Brady-rate 55
CXR: No acute findings
Labs: Hgb 14
Na 141
K 3.7
Hct 40.7
Gluc 102
WBC 6.6
Plt 221
Pt 10.7
INR 1.1
BUN 14
Cr 0.8
Type and Screen
PROBLEM LIST/ANESTHETIC CONSIDERATIONS
Surgical Procedure: Carotid Endarterectomy
Carotid 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 backbleeding, 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 diameter.
Complications: 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: 50-150ml
Physiology/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: supine
The 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 conditions
Adverse effects: blood dyscrasias, hepatic impairment, Stevens-Johnson syndrome, interstitial nephritis,
hypomagnesemia, fractures, H/A, diarrhea, constipation
Drug 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/dyslipidemia
Adverse 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, anaphylaxis
Blood/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 hugger
PONV:
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 ANESTHESIA
Position: supine
IVs/lines: 2 lg bore IVs, Aline
Monitors/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 A
Regional: Deep and/or superficial cervical plexus block with sedation
Versed 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 B
Technique: GETA (muscle relaxant not necessary because SSEP, EEG, or Cerebral oximetry may be
performed to assess CBF)
INDUCTION
Sequence: 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.
MAINTENANCE
Agents:
*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= 130ml
NPO deficit: 10 hrs X 130ml=1300ml
3rd space loss: 1ml/kg/hr
EBV: 65ml/kg X 90kg=5850ml
ABL: 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 =1020ml
2
130ml
325ml
90ml
=545ml
3
130ml
325ml
90ml
=545ml
2110 ml
*Note total carotid occlusion time after cross-clamps removed.
EMERGENCE
Sequence:
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)-Antiachesterase
Glycopyrrolate (Robinul) 0.8mg IV (0.01mg/kg)-Anticholinergic
POST-OPERATIVE CARE
Airway: 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.
REFERENCES
Brown, 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.