AKT-1 Flashcards

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Complication of Cricoid Pressure
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i.e. Sellick manoeuvre Complications: 1) N/V 2) Esophageal rupture 3) Difficult tracheal and mask intubation 4) minimal hemodynamic changes 5) complete AW obs 6) fracture of cricoid cartillage
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Contraindications of LMA
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1) small oral opening 2) "full stomach" (i.e. not npo, morbidly obese, trauma, GERD, intestinal obs) 3) dec lung compliance 4) not profoundly anesthetized 5) oropharyngeal growth/trauma
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Extubation Criteria
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1) Oxygenation: SaO2 > 92%, PaO2 > 60 mm Hg 2) Ventillation: Vt> 5ml/kg, RR >7, ETCo2 < 50, PaCO2 0.9. Sustained 5-sec head lift or hand grasp 5) Neuro - follows verbal commands, intact cough/gag 6) Acid/Base - pH > 7.25 7) Normal metabolic - electrolytes, volume status 8) Normothermic 9) Other - aspiration risk, airway edema, Awake versus Deep (recall stage 1 - analgesia stage 2 - excitement stage 3 - surgical anesthesia stage 4 - medullary paralysis)
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Confirming endotracheal intubation
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continuous waveform capnography along with clinical assessment is the most reliable method of confirming and monitoring correct placement of an ET tube
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Rapid sequence induction
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http://image.slidesharecdn.com/13-enpediatricresuscitation-120507075455-phpapp02/95/emergency-lectures-pediatric-resuscitation-49-728.jpg?cb=1336377382 Indications: - ileus/obs - delayed gastric emptying (pain, trauma, opioids, ETOH, vagotomy) - incompetent LES, hiatus hernia, GERD - altered LOC - neurological/NM dz - pregnancy - difficult AW Contraindications: - total AW obs - loss of facial/oropharyngeal landmarks - anticipated difficult intubation (lemon, 332)
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Head position for tracheal intubation
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head should be 10 cm above table with extension of the atlanto-occipital joint to be in the sniffing position
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Difficult Airway Mangement
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http://www.ebmedicine.net/media_library/aboutUs/Clinical%20Pathway%20Management%20Of%20The%20Difficult%20Airway.JPG
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Position of Endotracheal tube
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tip should be approximately 5 cm above the carina
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CPR, Interruption of cardiac compressions
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Primarily - Pauses for establishing ETT (ventillation) Secondary - rhythm checks, shocks
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Therapeutic hypothermia and cardiac arrest
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only useful for VT/VF
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Cardiac arrest, blood gas changes
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Metabolic Acidemia - Lactic Acidosis Respiratory Acidemia/Alkalosis - depending on ventilation Low HCO3- Low PaO2 Neg BE (quantify degree of MA) Hyperkalemia (from acidosis) Hyperglcemia (stress response)
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Postobstructive pulmonary edema
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Obstruction then patient takes a large breath (e.g. closed APL, patient bitting on the ETT)
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Postoperative urinary retention
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The risk of retention is especially high after anorectal surgery, hernia repair, and orthopedic surgery and increases with advancing age. - >750 mL fluids - Long duration of surgery - Spinal anes with (long acting LA, high dose LA, high dose Opioids, hydrophilic opioids like morphine)
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Risk factors for PONV
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Patient: - Female - non smoker - h/o motion sickness Anesthesia: - inhaled anesthestic -N2O - intra and postop opioids Surgery: -duration > 30 min increases risk to 60% - types (celioscopy, ENT, Neuro, breast, strabismus, laparotomy/laproscopic, plastic surgery)
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TOF and pharyngeal muscle strength
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TOF >0.9 return of pharyngeal muscle strength. Abductor pollicis (AP) last to return orbicularis oculi (OO) is a beter predictor of the onset of NMB at the vocal cords than AP. Laryngeal adductor muscles and OO block have similar onset times. The onset time at the OO is shorter than the AP. The OO is thought to better reflect the diaghram and laryngeal muscles than AP.
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Nausea during spinal blocks
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Increased vagal activity after sympathetic block causes increased peristalsis of the gastrointestinal tract, which leads to nausea. More common in high blocks
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Contraindications to spinal anesthesia
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Absolute: - patient refusal - local anesthetic allergy - insurmountable technical difficulties - active infx at site of cannulation Relative: - bleeding diathesis (e.g. INR >1.2 or platelets < 80) - thrombophillia - continuing anticoag - hypovolemia - severe AS/MS - neurologic condition - raised ICP - previous back surgery at point of cannulation
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Back pain after spinal anesthesia
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The frequency of backache is approximately similar after spinal or general anaesthesia. Localised trauma to the intervertebral disk or excessive stretching of associated ligaments after loss of lumber lordosis due to relaxation of paraspinal muscles are supposed to be the causative factors. The pain is usually mild and self limiting although it may last for several weeks. Nonsteroidal anti-inflammatory agents and warm or cold compresses are sufficient for backache. Although backache is usually benign, it may be an indication of more serious complications like epidural abscess, spinal hematoma or syndrome of transient neurologic symptoms.
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Treatment of bupivacaine cardiotoxicity
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Treat seizures with GABA agonists. Treat convulsions with paralytics and airway management. Vasopressors may be indicated, although in some animal models they have been shown to promote CNS toxicity (still, on that basis they should not be withheld in the setting of cardiovascular collapse). Total cardiovascular collapse may be treated with CPR plus 1.5-4 mL/kg bolus of 20% lipid solution followed by 0.25-0.5 mL/kg/min for 10-60 minutes.
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Determinant of epidural spread
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Age - older is faster Pregnancy - engorgement of epidural vv by inc intraabdo pressure Positioning - later decub and trendelenburg faster Needle direction and catheter position Volume of LA Concentration of LA Addition of NaHCO3 - increased nonionized fraction of LA and thus better penetration alpha2-agonists and opioids pKa of the anesthetic ****
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Respiratory effects of spinal block
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Neuraxial blockade plays a very minor role in altering pulmonary function. Even with high thoracic levels of blockade, tidal volume is unchanged. There is a slight decrease in vital capacity. This is the result of relaxation of the abdominal muscles during exhalation. The phrenic nerve is innervated by C3-C5 and is responsible for the diaphragm. The phrenic nerve is extremely hard to block, even with a high spinal. In fact, apnea associated with a high spinal is thought to be related to brainstem hypoperfusion and not blockade of the phrenic nerve. This is based on the fact that spontaneous respiration resumes after hemodynamic resuscitation has occurred.
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Local anesthetic test doses
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Traditional Test Doses: - lidocaine: 1.5% w/ epinephrine - bupivacaine 0.25% w/ epi - 2-chloroprocaine w/ epi What is a positive test dose? Increase in HR by 10 beats is usually taken as an IV injection IT injection is usually evidenced by unusual sx by the pt: tinnitus, dysgeusia (odd taste in mouth), periororal numbness/tingling NOT THERE IS CONTROVERSY OVER THIS TECHNIQUE
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Intravscular injection of test dose
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- Drowsiness - Perioral/tongue parasthesia - tinnitus, auditory hallucination - muscular spasm - seizures - coma - respiratory arrest - cardiac arrest
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Treatment of post-spinal headache
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- Supine - NSAIDS - Methylxanthine derivatives (e.g. caffeine) - epidural blood patch
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Intermediate Cardiac Risk Procedures
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High (>5%): VASCULAR!!! --> peripheral/aorta Intermediate (1-5%): - intraperitoneal/intrathoracic - Carotid endartectomy - H and N - Ortho - Prostate Low (<1%): - Endoscopic - Superficial - Cataract - Breast - Ambulatory
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Airway Exam
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a. Patency of nares, deviated septum, etc b. Mouth opening > 3 large finger breaths (> 3 cm) c. Teeth (prominent upper incisors, severe overbite, edentuous) d. High arched palate e. Prognathism (ability to protrude lower jaw beyond upper incisors) f. TMJ movement g. TMD > 6 cm (3 FB) h. ROM neck i. Stridor? (stenosis, angioedema, burns, obs) j. Mallampatti k. Neck circ (OSA, Obesity) --> 17 inches M, 16 FM l. Beard
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Risk of deep vein thrombosis
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Patient-related risk factors for VTE include age older than 40 years, malignancy, estrogen use, immobilization, varicose veins, severe cardiopulmonary disease (prior MI, congestive heart failure, chronic obstructive pulmonary disease), prior stroke, paralysis or spinal cord injury, prior VTE events, hyperviscosity syndromes (polycythemia vera or malignancy related), and major vascular injury. Highest risk surgeries --> major ortho High risk surgeries --> general and emergency, major gyne, neuro, urological
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Preop evaluation of asthma
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Determine if controlled or uncontrolled: no nocturnal symptoms, SABA <= 2x/week, symptoms <= 2x/week, no significant activity limitations, no hospitalizations, FEV1 N
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Preoperative vitamins
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All good except vitamin E (bleeding risk) Good preop med list: http://med.umich.edu/preopclinic/guidelines/meds_to_stop1.pdf
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Functional capacity and metabolic equivalents (METS)
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3.5 ml/kg/min = 1 MET
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ASA Physical Status Classification
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1. Healthy person. 2. Mild systemic disease. 3. Severe systemic disease. 4. Severe systemic disease that is a constant threat to life. 5. A moribund person who is not expected to survive without the operation. 6. A declared brain-dead person whose organs are being removed for donor purposes.
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Epinephrine reactions and local anesthesia
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Epinephrine causes vasoconstriction. Epinephrine may cause: cardiac palpatations
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Pre-op cardiac assessment
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https://www.google.com/search?q=preoperative%20cardiac%20evaluation%20ppt&rct=j ppt then algorithm
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Lab tests in healthy patients
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Routine laboratory tests in patients who are apparently healthy on clinical examination and history are not beneficial or cost effective http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464262/table/T1/
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Preoperative ACE-Inhibitors
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Hold day of surgery. Hypotension can be refractory to traditional interventions such as administration of a fluid bolus, ephedrine, or phenylephrine. Vasopressin and methylene blue have been found to be effective treatments for ACE inhibitor-associated refractory hypotension
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Continuation of Preop Drugs
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http://med.umich.edu/preopclinic/guidelines/meds_to_stop1.pdf
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Treatment of Warfarin Anticoagulation
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Warfarin hold for 5 days Aspirin hold for 7 days (caution with stented px's) Plavix hold for 7 days (caution with stented px's) Do not discontinue either aspirin or clopidogrel in patients with coronary stents unless given specific permission to do so by the cardiologist who prescribed these medications.
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Capnogram and Pulmonary Embolus
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Exponential decrease in the capnograph's amplitude
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Failure of piped O2 -- effects
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The low pressure or oxygen supply failure alarm will go off when there is a significant increase or decrease of the O2 supply pressure. This occurs when there is a sudden loss of cylinder or pipeline pressure or when the anesthesia machine is turned on or off.
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Circuit valve malfunction
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Work through the circuit from gas inlet to patient
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Pulse oximeter artifacts
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Motion artifact can show lower values Nail polish (black, blue, green) Venous congestion Low peripheral perfusion
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Color coding of gas cylinders
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USA: Green - O2 (E cylinder = 660, H Cylinder 7000, 2000 psi) Yellow - Air (E cylinder = 660, H Cylinder 7000, 2000 psi) Blue - N2O (E cyl = 1590, H cyl 15,900, 745 psi, liquid) Black - N2 (E cyl = 660, H cyl 7000, 2000 psi) International (same E cyl, H cyl, pressures and forms) White - O2 (660, 7K, 2K) White and Black - Air (660, 7K, 2K) Blue - N2O (1590, 15,900, 745) Black - N2 (660, 7K, 2K)
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Scavenging system failure
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capnograph does not return to baseline there may be leak
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E cylinder/ oxygen pressure/ volume relationship
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O2 (E cylinder = 660, H Cylinder 7000, 2000 psi) Same for all gases except N2O (1590, 15,900, 745 psig)
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Inspired oxygen monitoring
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The unidirectional valves in the inspiratory and expiratory limb of a breathing circle system prevent rebreathing. Inspection of the valve leaflets during ventilation ran detect some valve malfunc6ons. Difficult to see are malfunctions caused by a warped valve disc. Spirometry in the circle system helps monitor valve function. If the inspiratory valve becomes incompetent, some of the expired volume returns into the inspiratory limb of the breathing circle; the expired tidal volume, therefore, is reduced
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ASA monitoring standards
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ASA monitoring standards (what is essential) a. Qualified Anesthesia Personnel b. Oxygenation (SpO2) c. Ventilation (ETCO2) d. Circulation (ECG, BP) e. Temperature shall be continually evaluated. f. Agent specific monitor (i.e. anesthetic gas monitor)
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Desflurane vaporizer
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Desflurane's unique characteristics (high volatility/moderate potency) require the use of a special vaporizer for proper utilization of this gas. Desflurane vaporizers are heated to 39 degrees C, which increases the vapor pressure in the sump to 1300mmHg, preventing the possibility of boiling in warm OR rooms. Providing an external heat source compensates for the significant heat loss associated with desflurane vaporization. And unlike stand variable bypass vaporizers that pass fresh gas through the vaporizing chamber, desflurane vaporizers add agent directly to the gas stream.
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Anesthesia vaporizers and principles of operation http://www.howequipmentworks.com/vaporisers/
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All vaporizers (except Des which use Tec 6) use: Variable bypass- Fresh gas flow from the flowmeters enters the inlet of any vaporizer which is on. The concentration control dial setting splits this stream into bypass gas (which does not enter the vaporizing chamber), and carrier gas (also called chamber flow, which flows over the liquid agent). So some of the carrier gas flows freely and some is mixed with the inhalation anesthetic. Flow over- Carrier gas flows over the surface of the liquid volatile agent in the vaporizing chamber, as opposed to bubbling up through it (as in the older copper kettle and Vernitrol)
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NIBP function http://www.infiniti.se/upload/Bruksanvisningar/CAS/NIBP%20Simulator%20White%20Paper%20II%20Oct07.pdf
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- Cuff pressure is increased to completely occlude the artery - pressure is decreased and there is a increase amplitude of the oscillating flow - sBP is found to be about 25-50% of MAP - maximum amplitude is determined = MAP - MAP = DP + 1/3 [SP-DP] --> dBP is calculated
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Abnormal capnograph patterns
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Encyclopedia http://www.capnography.com/new/capnograhs/en-chinaal
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Basal Oxygen Consumption
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1 Metabolic equivalent = 3.5 mL O2/kg/min
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O2 saturation/ PAO2 relationship
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PaO2 (mmHg) O2 sat 27 50 40 75 60 90 100 98 Right shift with "running man" (inc temp, dec pH, inc 2-3 DPG) --> reduced O2 affinity so O2 is released easier Arterial O2 Content=SaO2 x 1.34 x Hb + 0.003(PaO2) 1.34=ml O2/gram Hb
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CO2 measurement -- ET vs arterial line
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P(arterial - end tidal)CO2 gradient N= 2 to 5 Acute Decrease in Perfusion (i.e. dead space) = 22 (results in large drop in ETCO2 --> e.g. PE, dec in CO) Acute Decrease in Ventilation (i.e. shunt) = 6 (results in normal ETCO2 but inc in PIP --> alveoli to collapse or fill with fluid, such as periods of shallow breathing, bronchial intubation, or increased bronchial and alveolar secretions that cause mucus plugging, or atelectasis)
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Oxyhemoglobin dissociation
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PaO2 (mmHg) O2 sat 27 50 40 75 60 90 100 98 Right shift with "running man" (inc temp, dec pH, inc 2-3 DPG) --> reduced O2 affinity so O2 is released easier Arterial O2 Content=SaO2 x 1.34 x Hb + 0.003(PaO2) 1.34=ml O2/gram Hb
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Calculation of blood volume
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Calculation of blood volume (ml/kg) a. Women 65 b. Men 75 c. Infants 80 d. Neonates 85 e. Premature neonates 96 TOTAL BODY WATER: Elderly - 45% Men - 50% Women 60% Infant 70% 2/3 --> ICF 1/3 --> ECF --> then 3/4 is ISF and 1/4 is IVF
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Interpretation of blood gases
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Acidemia: Metabolic --> low HCO3 Resp --> high PaCO2 Alkalosis: Metabolic --> high HCO3 Resp --> low PaCO2
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Correction for Acid/Base
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"1 for 1, 10 for 7, 1, 4, 2, 5" 1:1 Metabolic acidosis 10:7 Metabolic Alkalosis (inc 10 HCO3, inc 7 PaCO2) 1:10 Acute Resp Acidosis 4:10 Chronic Resp Acidosis 2:10 Acute Resp Alkalosis 5:10 Chronic Resp Alkalosis for every 10 inc PaCO2, pH dec 0.08
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Metabolic Acidosis
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AG (Na - Cl - HCO3) --> greater 10; falls 2.5 for 1 fall albumin CATMUDPILES: C- CO, Cyanide, Congenital HF A- Aminoglycosides T- Theophyline, Toluene M-Methanol U- Uremia D- DKA, starvation acidosis P- Paracetamol (tylenol), paraldehyde I- Iron, isoniazide, inborn errors of metabolism L- Lactic acidosis E- Ethanol, Ethylene glycol S- Salicylates (ASA)
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Non-AG Metabolic Acidosis
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USEDCARS Ureterosigmoidostomy Saline (large volumes) Early Renal Failure (impaired HCO3 generation) Diarrhea (GI loss of HCO3) Carbonic Anhydrase inhibitors (renal H+ retention) Amino Acids (arginine, lysine) RTA Supplements (TPN - excess chloride vs acetate)
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Metabolic Alkalosis
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Saline-Responsive: - Volume Depletion (NGT, Vomiting, villous adenoma) - Diuretics/"contraction alkalosis" (diuresis --> loss of HCO3 poor fluid --> extracellular fluid "contract" around fixed HCO3 --> inc [HCO3] -Posthypercapnea (recent resp acidosis, kidneys not completely readjusted) Saline-Resistant (excess steroid) -HTN --> hyperaldosteronism, cushings, liddle's, exogenous minercorticoid) -Normotensive --> hypokalemia (severe), Milk alkali syndrome (exogenous alkali), Barter's/Gittleman's
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Respiratory Acidosis
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"Won't Breath or Can't Breath" Won't: -CNS depression --> sedatives, head injury, infarct, infx, hypothyroid, severe metabolic alkalosis Can't - Neuromuscular Dz - Parenchymal/AW dz --> PNA, CHF, Restrictive Lung Dz, ILD, COPD, Asthma - Thoracic abnrm --> kyphosis/scoliosis, flail chest, obese, effusion, fibrosis, PTX
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Respiratory Alkalosis
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Hyperventillation Primary: - pain, fever, CNS, ASA, progesterone, Beta agonists, pregnancy, sepsis, liver failure, excessive ventillation Secondary: -asthma, PNA, PE, Restrictive Lung Dz, CHF (early)
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Ventilation assessment during anesthesia
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- Adequacy --> clinical signs plus ETCO2 - Assessment of ETT/LMA placement - Detection of circuit integrity - Depth of Anesthesia
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Denitrogenation and Functional residual capacity good picture to include https://drkamaldeep.files.wordpress.com/2013/06/image_thumb.png?w=784&h=475
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Effective preoxygenation/denitrogenation with 100% oxygen increases the oxygen content of gas in the patient's functional residual capacity (FRC) from 21% towards 100% which should theoretically produce a proportionate increase in the safe apnoea time Average time is approximately 3 minutes of TV with 100% O2 OR 8 vital capacity breaths
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Paradoxical respiration
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There is also dyssynchrony between rib cage and abdomen, causing a "seesaw" type motion. Blunt injury (diaphragmatic injury/paralysis) Flail chest Pneumothorax High AW obstruction (e.g. tracheal obstruction)
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Effects of defasciculation dose
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Fasciculations: - Associated with increased ICP, IOP, IGP - ICP only clinically important - Cause and Effect - unknown - If needed pre-treat with Lidocaine, and a defasciculating dose of a non-depolarizing neuromuscular blocker - - Rocuronium 0.06 mg/kg
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Atracurium dose, metabolism, and SEs
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0.5 mg/kg 3 min onset 45 min duration Ester hydrolysis and Hoffman Elimination Hypotension/Tachycardia/Bronchospasm (Re: histamine)
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Cisatracurium dose, metabolism, and SEs
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0.15-0.2 mg/kg 3-7 mins onset (dose dependent) 45-60 min duration Hoffman Elimination Side Effects are minimal (minimal histamine release)
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Pancuronium dose, metabolism, and SEs
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0.1 mg/kg 4 min onset 100 min duration Primarily hepatic metab and RENAL excretion - HTN/Tachycardia (vagal block and sympathetic stimulation) - AV blockade - Possible allergic rxn if allergic to bromides Pancuronium, Doxacurium, vercuronium and pipecuronium partial excretion by kidneys thus renal failure may lead to prolonged blockade
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Vecuronium dose, metabolism, and SEs
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0.1 mg/kg 2.5 min onset 45 min duration Hepatic Metabolism --> prolonged blockade with infusion in ICU (3-hydroxy metabolite). Some Renal involvement Primary SEs LIVER FAILURE (80% hepatobil metab/exc) Prolonged blockade with infusion
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Rocuronium dose, metabolism, and SEs
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0.6-1.3 mg/kg 1.5 min onset 30-45 min duration Hepatic exc/metab Slight vagolytic properties
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Succinylcholine dose, metabolim, and SEs
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1-2 mg/kg 30-60 sec onset 5-10 min duration metabolized by pseudocholinesterase Beware of situation of high K+ (inc about 0.5 meq) - burns after 24 hours to 6 months - rhabdo/quads/immobility - risk of elevated ICP - MH - Histamine release - Sinus bradycardia
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Anesthesthetic agents and bronchodilators
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Most volatile anaesthetic drugs are bronchodilators and can be effective under anaesthesia. Ketamine is also a bronchodilator. Halothane, isoflurane, enflurane, sevoflurane, ether (nitrous oxide) NOT DES!!!!
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Risk factors for latex allergy
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skin symptoms with latex glove use (hives, rash, itching) history of atopy and a history of allergy to certain fruits ***bananas, avocados, kiwis***
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Recovery after general anesthesia
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- Reverse the NMB with anticholinesterase (e.g. neostigmine 0.04-0.08 mg/kg) in conjunction with anticholinergic (e.g. 0.2-1 mg) - Turn off anesthetic (volatile or intravenous) - Ensure adequate reversal - Post operative analgesia (narcotics, adjuncts, regional) - PONV prevention - Remove airway
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Blood/gas partition coefficient the volatiles
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N2O - 0.47 Halothane - 2.4 Isoflurane - 1.4 Desflurane - 0.42 Sevoflurane - 0.65
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MAC values of the volatiles
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N2O - 105 Halothane - 0.75 Isoflurane - 1.2 Desflurane - 6 Sevoflurane - 2
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Side effects of desflurane.
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Note fastest wake up with lowest B/G partition coefficient CV - dec BP, dec SVR, stable HR, stable CO Resp - dec TV, inc RR Cerebral - inc BF, inc ICP, dec metabolic rate, dec seizures Renal - dec BF, dec GFR, dec U/O Hepatic - dec
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Solubility of agent and speed of induction
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lower the solubility the faster the induction and emergence Blood/gas partition coefficient N2O - 0.47 Halothane - 2.4 Isoflurane - 1.4 Desflurane - 0.42 Sevoflurane - 0.65
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Succinylcholine and recent stroke
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Contraindicated because are at increased risk of severe hyperkalemia
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Adverse effects ondansetron
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• 5-HT3 serotonin antagonist Adverse effects: Constipation, dizziness, and headache. QT PROLONGATION
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Neuromuscular blocking drugs in renal failure
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Paralytics in Setting of Renal Failure - Rocuronium: t 1/2 increased 37%, may not translate into increased duration - Vecuronium: t 1/2 increased 24-56%, duration longer and more variable - Pancuronium: t 1/2 increased 97%, prolonged duration of action
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Potency of inhalation anesthetics
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Potency measured in Minimum Alveolar Concentration MAC = alveolar concentration at which 50% of patients will not move in response to standard surgical stimulus 1.3 MAC --> 95% of patients will not move to surgical stim MAC-BAR (blocks adrenergic response to nociceptive stim) --> 1.5 to 2 MAC MAC-Aware --> 0.5 MAC MAC-Awake --> 0.15 to 0.5 MAC
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Factors enhancing inhalation induction (Dec MAC thus Inc Potency)
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Acidosis Acute alcohol use Advanced Age Anemia Altitude Benzos IV anesthetics Hypotension Hypothermia Hypoxia Opiates Pregnancy
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Factors that increase MAC (decrease potency)
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Chronic ETOH Very young age (max MAC at 1 yoa) Increased temperature (>42 degrees) Decreased Altitude Drugs: MAOIs, TCAs, Cocaine, acute amphetamines
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Pattern of residual neuromuscular blockade (TOF <0.9 is now considered as residual neuromuscular blockade)
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Upper airway pharyngeal and esophageal muscles: -Increased risk of aspiration - Increased risk of airway obstruction Laryngeal muscles: - Increased risk of aspiration - Impaired phonation - Impaired cough Respiratory muscles - Impaired ventilation and oxygenation Other: - Generalized weakness - Visual disturbances - Patient distress - Prolonged Vent Weaning
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Ester vs Amide Local Anesthetics
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Amides ("i") --> Liver Metabolized: - Etidocaine; rapid, 2.5 (4), 4 hours (8 h) - Mepivacaine; rapid, 5 (7), 3 hours (6 h) - Lidocaine; rapid, 4.5 (7.5), 2 hours (4 h) - Bupivacaine; slow, 2.5 (3), 4 hours (8 h) - Ropivacaine; medium, 2.5, 3 hours (6 h) - Prilocaine; medium, 5 (7.5), 1.5 hours (6 h) Esters --> Plasma Metabolized: - Cocaine - Tetracaine; slow, 1.5 (2.5), 3 hours (10 h) - Procaine; slow, 8 (10), 45 min (90 min) - Chloroprocaine; rapid, 10 (15), 30 min (90 min) - Benzocaine
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Interaction of inhalational anesthetic and neuromuscular blockade
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Neuromuscular Nondepolarizing Blockade N20 - ↑ Halothane - ↑↑ Isoflurane- ↑↑↑ Desflurane - ↑↑↑ Sevoflurane - ↑↑
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Sevoflurane metabolism
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Hepatic (P-450). Not to the same extent as Halothane (worried about halothane hepatitis in 1/35,000) but still something to keep in mind
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Post-op nausea and induction drugs
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Anesthetic Factors: Duration of surgery Adequate hydration Volatiles Opioids
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Adverse effects of antiemetics
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5-HT3 Receptor Antagonists (Ondansetron, Dolasetron, other "trons") --> QTc prolongation, H/A, Constipation, Dizziness Corticosteroids --> infx, blood glucose Butyrophenones (droperidol) --> QTc prolongation. Haloperidol --> QTc prolongation, extrapyramidal signs Antihistamines --> drowsiness Anticholinergics (e.g. scolpamine) --> visual disturbances, dry mouth, and dizziness Phenothiazines (e.g. metaclopramide) --> Contraindications: pheochromocytoma (can cause catecholamine surge), Parkinsons, hyperprolacinemia Adverse effects: Fatigue, Diarrhea, abdominal cramping, Restlessness NMS, Tardive Dyskinesia, focal dystonia, Depression
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Succinylcholine after neostigmine
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depolarizing relaxant (sux) after reversal, which would prolong it's duration because of the pseudocholinesterase inhibition of neostigmine.
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Definition of time constant
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time constant of volatile (τ) = volume/flow Definition (circuit): volume of the circuit divided by the fresh gas flow rate Definition (lungs): volume of the lungs (FRC) divided by minute ventilation Meaning: it takes three time constants for 95% of a concentration change to be achieved
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Laryngospasm and desflurane
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Pungency and AW irritation can produce: salivation breath holding coughing laryngospasm
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First-order kinetics
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First Order Kinetics: Elimination of the Drug is directly proportional to its plasma concentration. t1/2 (1) --> 50% t1/2 (2) --> 25% t1/2 (3) --> 12.5% t1/2 (4) --> 6.25% t1/2 (5) --> 3.125
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Phenylephrine heart rate effect
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alpha 1 agonist Phenylephrine often causes a reflex bradycardia (baroreceptors).
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Tachycardia with muscle relaxants
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Pancuronium --> significant vagal blockade Rocuronium --> mild vagal blockade Atracurium --> histamine release
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Methoclopramide mechanism of action
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Dopamine (D1) antagonist --> prokinetic
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Succinylcholine train-of-four
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A depolarized post-junctional membrane (resulting in inactivation of Na channels) causes the postjunctional membrane to become unresponsive to ACh released by motor neurons. --> "Phase I block" & produces a characteristic reduction in contractile response (***with no fade***) during a train of four stimuli. After 60 sec a flaccid paralysis develops due to the development of a desensitized state where the membrane becomes repolarized, but insensitive to ACh (due to receptor desensitization). --> "Phase II block" and responds to a train of four stimuli ***with a "fade"*** (like NDNMB)
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Vapor pressure of Volatile Anesthetics
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N20 - Halothane - 243 Isoflurane - 248 Desflurane - ***669**** Sevoflurane - 157
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Vasoactive drugs
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http://www.aaemrsa.org/UserFiles/HelpfulDocVasopressorsTable3.JPG
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Rocuronium elimation
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Rocuronium undergoes no metabolism and is eliminated primarily by the liver and slightly by the kidneys.
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Tachycardia treatment
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- Ensure adequate oxygenation and ventilation - Verify ECG leads - Assess BP (treat accordingly) - Consider Arterial line placement - Assess volume status - Assess depth of anesthesia - Determine if pain involved - Treat underlying cause --> ddx: pain, light, hypovolemia, hypercapnia, hypoxia, acidosis, drugs, electrolytes (hypomag, hypokal, hypoglycemia), myocardial ischemia, endocrine (pheo, hyperthyroid, carcinoid, adrenal crisis), bladder distension
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Differentiate between ropivacaine and bupivacaine
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Both Amides - Bupivacaine; slow, 2.5 (3), 4 hours (8 h) - Ropivacaine; medium, 2.5, 3 hours (6 h)
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Side effects of succinylcholine
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CV - variable HR, BP Fasiculations Hyperkalemia (know high risk groups) Myalgia Increased intragastric pressure Increased IOP Masseter Muscle Rigidity MH Histamine release (mild)
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Sodium bicarbonate effects
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- Useful for Metabolic Acidosis if pH but not if high anion gap - Emergency treatment of hyperkalemia - Alkalinisation of local anesthetics: 1) Firstly, the higher pH of the solution may result in less stinging pain being experienced by the patient 2) Secondly, after injection, the pH of the injected solution may more quickly approach that of the normal tissue pH. The faster formation of a mixture with charged and uncharged forms may then result in ***more rapid drug diffusion and a quicker onset of nerve blocking***
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Characteristics of ephedrine
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alpha 1, beta 1, mild beta 2 agonist Indirect effect by NE release at sympathetic nerve endings inc HR, inc BP, inc CO avoid in patients taking MAOi or with closed angle glucoma
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ARB Refractory Hypotension Therapy
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similar mechanism as ACEi refractory hypotension
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Laparoscopy: Hemodynamic Changes
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3 factors: increased intraabdominal pressure, pressurized with CO2, Trendelenburg positioning CVS - Decreased preload, CO (+/- contractility in ICM) - Inc venous pressure secondary to increased intrathoracic pressure - Increased thoracic pressures (PAP, CVP, PCWP) - Increased afterload (SVR, PVR, MAP) - No change/increased HR - Increased SNS
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Fasting Guidelines
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Clear liquids - 2 hours Breast milk - 4 hours Nonhuman milk/light meal - 6 hours Regular meal - 8 hours
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Positioning Injury
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Lithotomy - common peroneal nerve and sometimes sciatic nerve injury Supine - caution with brachial plexus when arms outstretched Caution with ulnar nerve when elbows secured Closed Claims (ulnar nerve 28%, brachial plexus 20%, lumbosacral nerve roots 16%, and spinal cord 13%)
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Intraoperative awareness
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Insufficient Anesthesia (MAC Aware - 0.3 MAC) Risk Factors: - Routine use of NMB (double incidence from .1% to .18%) - TIVA - Light anesthesia for sake of turnover - Hemodynamic instability - Procedures: Obstetric / Cardiac / Trauma - Patient Age - History of difficult airway - Limited cardiac reserve - History of substance abuse (chronic ETOH, anxiolytics, cocaine)
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Treatment of postanesthetic hypercarbia
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Treatment includes identification and management of the cause of the hypoventilation, supplemental oxygen administration, verbal and tactile stimulation, deep breathing exercises, repositioning, and cautious use of analgesics or sedatives. Oxygen saturation monitoring is necessary, and capnographic monitoring may be appropriate for patients at risk May need reversal of causitive Rx (e.g. narcan, flumazenil)
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Flumazenil: indications
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benzodiazepine overdose --> competitive antagonist at the benzodiazepine site on the GABAa receptor most appropriate if patients were benzo naive Flumazenil has numerous contraindications: - benzodiazepine dependence - coingestion of seizure threshold lowering or arrhythmia causing agents such as tricyclic antidepressants - tachycardia - QRS prolongation - anticholinergic symptoms (i.e. tricyclic antidepressant has been ingested) - seizure history
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MH Triggers
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Sux and all inhaled anesthetics (except N2O). Presentation: - elevated ETCO2 - Tachycardia - Tachypnea - hyperthermia
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Pneumoperitoneum effects
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Cardiac Resp CO2 absorption Renal Trochar insertion risk
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Epinephrine Calculations
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CONC DOSAGE EQUIVALENCE PERCENT 1:1,000 1mg/mL 0.1% 1:10,000 0.1mg/mL 0.01% 1:100,000 0.01mg/mL 0.001% 1:200,000 0.005mg/mL 0.0005%
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Calculating time remaining in E Cylinders
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T (min) = Remaining volume (L) / flow rate (L/min) --> determine remaining volume when given psig with cross multiplication of ratio to psi and known volume of E cylinder For O2 tanks you need a conversion: E cylinders --> T (min) = 0.28 x psig/ FR. OR --> T(hr) = psig/200 FR. H cylinder --> T(min) = 3.14 x psig / FR
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