GW Anesthesia Exam – Jen – Flashcards
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What two things do you look for in a family hx preop?
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1. Pseudocholinesterase deficiency 2. H/o malignant hyperthermia
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Which meds should be stopped prior to DOS? On DOS?
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- Pre-DOS: ace/arb, diuretics (if not for CHF) - DOS: oral DM meds, decrease insulin - Stop NSAIDs days before surgery
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Why should beta and alpha 2 blockers not be stopped preop?
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Can cause rebound HTN
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What are s/e of surgery on ace/arbs?
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Prolonged and resistant HoTN
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What do you have to consider when stopping antiplatelet meds preop?
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- Type of anesthesia (stop meds for spinal or epidural) - CV dz rfs
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How does placement of a BMS or DES make a difference in terms of when to plan for surgery?
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- BMS: delay 6 wks after placement - DES: delay 12 mo after placement
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- What does MET stand for? - What does it mean? - What is 1 MET equivalent to?
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- MET: metabolic equivalent of task - A physiologic measure expressing the energy cost of physical activities; defined as the ratio of metabolic rate during a specific physical activity to a reference metabolic rate - 1 MET = the resting metabolic rate during quiet sitting
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How do METs relate to surgery?
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Asx pts with functional status > 4 METS (walk 2 flights) are ok for surgery
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Which RFs would you examine in someone with a low functional capacity for preop workup? (5)
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- Renal dz - Heart failure - Ischemic heart dz - CVD - DM
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Define ASA levels
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ASA 1 - no systemic dz ASA 2 - mild systemic dz with minimal fx limitations (well controlled) ASA 3 - systemic dz with fx limitations (uncontrolled) ASA 4 - severe systemic dz that is constant threat to life ASA 5 - not expected to survive without surgery ASA 6 - brain dead E - emergency surgery
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Preop, when do you order - Hct? - Coags? - Chemistries? - EKG? - CXR?
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- Hct: likelihood of symptomatic anemia or high EBL - Coags: Liver dz, coag dzr, malnutrition, malabsorption, pt on anticoags - Chemistries: anything that affects renal, liver, vasc - EKG: male >45, female >55, based on PMH - CXR: surgery related to thorax, COPD, pna
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What meds are used in monitored anesthesia care (local anesthesia together with sedation and analgesia)?
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Propofol, fentanyl, midazolam, dexmedetamidine
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Sequence of airway management (7) *What is the most important step of airway management?
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1. Monitor 2. Preoxygenate 3. VSS 4. Induce 5. Mask Ventilate* 6. Paralyze 7. Intubate (listen/look)
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How long does preoxygenating last? - Benefits? - How long does it take to desat below 90 on RA vs. O2? - How does this affect CO2?
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- Lasts 3 minutes, 100% O2 - Gives pt additional oxygen reserve so that if intubation fails, they will have time to be awakened and breath on own - 2mins on RA vs. 5 mins on O2 - Alveolar CO2 increases during apnea independent of preoxygenation
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What 3 signs show that your ETT is in the trachea?
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ETCO2, misting in mask, chest rise
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Tx of bronchospasm vs. laryngospasm
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- Bronchospasm: propofol, albuterol, epi, gas - Laryngospasm: propofol, lido, LMA, succs, positive pressure
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Oral vs. Nasal airways - Do they change delivered O2 concentration?
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- Oral: follows tongue, pulling it away from epiglottis and away from posterior pharynx - Nasal: extends to above epiglottis - Nope
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Rapid sequence intubation - Purpose - Chain of events
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- Purpose: rapid induction and intubation to minimize aspiration risk - Preoxygenate, IV induction, paralyze, Sellick maneuver, ETT tube intubation - NO mask ventilation
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Why do you avoid mask ventilation with rapid sequence intubation?
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To prevent insufflation of gas into the patient's stomach
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Indications for rapid sequence induction [6(5)]
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LT PoNGS L: decreased LES tone (obese, pregnant) T: trauma GCS <6 Po: unknown NPO status N: neurological deficit G: gastroparesis (MS, ALS, DM, uremia, CKD) S: SBO
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C/i to Sellick Maneuver
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Injury (to c spine or trachea) or active vomiting
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When do you release cricoid pressure in rapid sequence induction?
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Only after placement in lungs is confirmed
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Complications of rapid sequence induction (4)
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- Cricoid fracture - Esophageal rupture - Failure of intubation - Profound HoTN
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Miller blade vs. Mac
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Miller is straight and goes right under epiglottis, Mac is curved and goes to vallecula
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Dire consequence of laryngospasm and tx
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Pulmonary edema, tx with diuretics, positive pressure and oxygenation
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Steps in extubation
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- Give Achesterase inhibitor (neostigmine) and anti-muscarinic (glycopyrrolate) - Decrease gas - Decrease vent rate so that CO2 gets retained and medullary centers are stimulated by increased CO2 to begin spontaneous breathing
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LMA - Does it protect the airway from aspiration? - PPV and tidal volume - When is it used and why?
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- No - PPV: 20cm pressure and 8cc/kg tidal volume - Used for short surgeries, asthmatics because doesn't require full sedation and doesn't encourage bronchospasm as much as a ETT
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C/i to LMAs
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Obstruction -- Airway: increased resistance, decreased compliance, glottic obstruction, unable to open mouth -- Intestinal: hernia, SBO Aspiration risk -- GERD -- Not NPO -- Gastroparesis
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Complications of LMAs
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- Aspiration/GERD - Spasm, cough, sore throat, hoarseness - Nerve injury (recurrent laryngeal or hypoglossal)
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Med used for awake intubation and MOA
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Ketamine -- blocks NMDA receptors
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How do you calculate preop deficit?
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Preop deficit = maintenance fluid x hours NPO
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How do you calculate maintenance replacement with crystalloids? How fast do you give it?
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60 cc/kg/hr + 1cc/kg/hr(wt - 60) - Give 50% in 1 hr and 25% at 2 and 3 hrs
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How much fluid do you lose to 3rd spacing in major, moderate, and minor?
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Major - 10cc/kg/hr Moderate - 8cc/kg/hr Minor - 6cc/kg/hr
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How to replace fluids for EBL?
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- Replace 3cc crystalloid for 1 cc blood loss - Replace 1 cc colloid for 1 cc blood loss
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How much of blood volume is lost when BP is affected? Which vital sign is the most sensitive marker of blood loss?
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- 30% - HR
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How do you calculate redistributive/evaporative surgical losses?
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- Depends on degree of tissue trauma - Minor surgery: 4cc/kg/h - Moderate surg: 6cc/kg/h - Major surg: 8cc/kg/h
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How well do crystalloids stay in the intravascular space? How do LR and NS affect pH of body?
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- Don't stay in intravascular space well, so they can cause interstitial edema d/t dilution of plasma proteins and therefore decreased oncotic pressure - LR causes metabolic alkalosis d/t bicarb made from lactate - NS causes hyperchloremic metabolic acidosis
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How well do colloids stay in the intravascular space? S/es of colloids?
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- More likely than crystalloids to stay in intravascular space - S/e: hypersensitivity rxn and bleeding dzrs d/t reduction in platelet aggregation
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How do you calculate MAP? - What are the determinants of myocardial oxygen and delivery?
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MAP = CO x SV - SVR, HR, SV, intravascular volume
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What are the 4 phases of pharmacokinetics? What's pharmacodynamics?
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- ADME: absorption, distribution, metabolism, excretion - What the body Does to the Drug
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What is hypoxic pulmonary vasoconstriction and how is it affected by inhaled anesthesia meds?
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- Hypoxic pulmonary vasoconstriction is when the lung constricts arterioles to shunt blood to alveoli with more oxygen in a hypoxic setting - Inhaled gases decrease this reflex
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How do inhaled anesthesia meds affect airway resistance? Vascular resistance?
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- Decrease airway resistance by causing bronchiole relaxation - Decrease vascular resistance
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Inhaled anesthetics - Desflurane - Sevoflurane - Isoflurane - Enflurane - Methoxyflurane
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- Desflurane: shortest acting, bad smell, sympathetic stimulator, hepatotoxic, CO - Sevoflurane: good smell (peds), fluoride, compound A, most bronchodilation (so good for lung path), nephrotoxic - Isoflurane: longest acting, bronchodilation (good for intubation past OR) - Enflurane: seizure risk - Methoxyflurane: nephrotoxic
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How does MAC change with temperature?
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Decreases.
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What affects speed of induction with inhalants?
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- Increased by: increased concentration, higher flow of air, increased minute ventilation - Decreased by: increased CO, high lipid solubility
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What affects MAC (5/3)?
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- Decreased by: old age, pregnancy/prematurity, hyponatremia/hypothermia, opiods/acute etoh, barbs/a2 antag/ccbs - Increased by: hyperthermia, chronic etoh, CNS stimulants
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Pros/Cons of using NO
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- Pros: less HoTN, decreases MAC of other agents - Cons: need to use with other agents because it competes with O2 and can cause hypoxia, s/e n/v, gas expansion (bad for laparoscopic cases), bowel distension
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Nitrous Oxide - Indication - Speed - Pros (2) - Cons (5)
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- ANALGESIA - fastest on/off - less CVS/Resp effects - N/V, low potency, sympathetic stimulation (bad for CAD), BM toxicity
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Propofol - Dose - MOA - Indications - S/es and tx/why - Which surgeries is it good for? - Allergy
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- 1.5-2.5 mg/kg - MOA: activates GABA - Indications: hypnosis, amnesia (NO analgesia) - Antipruritic, antiemetic; HoTN d/t increase in SVR so give phenylephrine because it's an alpha agonist. Burns on injection - Good for neurosurgery because decreases CBF - Allergy: contains egg lecithin, soy bean *NEVER associated with Malignant Hyperthermia*
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Etomidate - How fast is it? - s/e - What surgeries is it good for and why?
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Short-acting IV anaesthetic agent for the induction of general anaesthesia and sedation for short procedures - Fast on/offset - S/e: adrenal suppression - Good for neurosurgery because decreases CBF (good for cases with increased ICP), and cardiac cases because CVS sparing
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What are 4 qualities of the perfect anesthestic drug?
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Amnesia, analgesia, hypnosis, muscle paralysis.
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Which drugs act on GABA and how does that work?
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- Thiopental, propofol, etomidate, volatile anesthetics, Midazolam - Increase GABA so chloride channels open and hyperpolarize neurons
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Which drugs act on the NMDA receptors and how does that work?
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Ketamine prevents excitatory neurotransmiters from interacting with NDMA receptors
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What's a therapeutic index?
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TI = LD50/ED50
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Midazolam - MOA - Indications - S/e
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- MOA: increases GABA - Amnesia and anxiolysis - S/e: respiratory depression
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Fentanyl - MOA - Indications - S/e - How soluble is it relative to morphine? - Where is it absorbed?
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- MOA: opioid so acts as a mu 1/2 agonist - Analgesia - s/e: mu 2 causes hypoventilation, bradycardia, physical dependence, HoTN d/t depression of sympathetic tone (that's why you give epi) - Much more lipid soluble, so redistributes rapidly after initial distribution - 75% absorbed in lung (first pass phenomenon), so duration of drug is determined by distribution to lung
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Lidocaine - MOA - Indications
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- MOA: local anesthetic, binds sodium channels intercellulary - Indications: analgesia, antiarrhythmic
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Morphine - SE
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- Hist release -> pruritis, Hypotension - Low lipid sol & high ionized , prolonged time to peak, less likely respiratory failure but more stacking on PCA
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Central Sensitization - def - relief
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- pain receptors just firing continually - wind up phenomenon with chronic pain - KETAMINE: can cut off these signals
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What's the Henderson-Hendelbach equation?
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pH = pKa + log (unionized/ionized)
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Local Anesthetics - dosage based on what - MOA - relation to vascularity - value of bicarb
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- lean body weight - Block Na channels from within using the Non-ionic form, bind open Na channels, most effective when more non-ionic form - More vasc -> higher tox potential and shorter duration - raises pH to increase anionic form
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Why use epinephrine with Local Anesthetics?
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1. Test if vascular access --> rise in HR/BP 2. Local vasoconstriction --> less tox & increased duration
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s/e of Succs
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Myalgias, bradycardia, arrhythmia, hyperkalemia in high risk pts, increases ICP/IOP/intragastric pressure/LES tone
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Succinylcholine - MOA - Indications - Reversal - C/i
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- MOA: depolarizing NMBD that mimics Ach, causing sustained depolarization --> K release - Indications: Paralysis - No reversal needed because it's metabolized by pseudocholinesterase - C/i: hyperkalemia (don't give to pt with K >5.5), burns/MS/ALS/anything with increased cellular enzymes (bedbound), stroke, patients with spinal cord transection, MH trigger
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Homozygous vs. heterozygous MH pts
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- 8hr half life in homozygous pts - 20 min half life in heterozygous pts - Gene related to pseudocholinesterase
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Non-depolarizing NMBDs - MOA - C/i - Reversal
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- MOA: competitive inhibition of ach - C/i: none - Reversal: neostigmine (Achesterase inhibitor) and glycopyrrolate (anti-muscarinic)
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Ketamine - MOA - Indications - What is the TI (low/high)? - What surgeries is it bad for? - S/e & who not good for - What clinical pictures is it good for?
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- MOA: blocks NMDA channels - Indications: analgesia and amnesia (dissociative state) - TI is high - NO NEUROSURGERY because it increases CBF (potent vasoDILATOR) - s/e: psychosis, paranoia (PCP derivative), catecholamine surge (all CV values increase) -> NOT for CAD, HTN, CHF, Aneurysms - Good for asthmatics (because bronchodilates), good for rapid sequence induction (no venodilation), good for HoTN
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MAC - define - property making more potent
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- Prevents movement in 50% pts - More lipid sol = lower mac = more potent
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Thiopental - How fast is it? - Indications - s/e - What doesn't it do for anesthetic purposes?
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- Very fast, but only lasts for 8 mins because of redistribution - Indications: good for increased ICP, causes cerebral vasoconstriction and decreases CBF, can inhibit the formation of cerebral edema, decreases cerebral O2 demands - s/e: high dose can cause a flat line on EEG, peripheral venodilation (therefore increase HR and decrease BP), respiratory depression, crosses placenta - No analgesia or muscle relaxation
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When would you use total IV anesthesia?
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- Allergy to volatile agents - FHx of MH
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What types of anesthesia can't be used for craniotomy?
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- Craniotomy requires somatosensory evoked potentials and inhaled agents blunt that reflex
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What is the excretion of all of the non depolarizing NMBDs? Which has the weird side effects?
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- Roc is biliary - Vec is biliary > renal - Pancuronium is renal > biliary - Pancuronium is vagolytic and blocks pre and post junctional receptors, good for pts w/HoTN
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Ephedrine - MOA - Weird potential phenomenon
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- MOA: indirect agent, causes release of catecholamines - Tachyphylaxis can occur if stores are depleted
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Phenylephrine - MOA - S/e - Indication
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- MOA: works on alpha 1 - s/e: vasoconstriction causes increased BP and reflex bradycardia - Best to use with low BP and high HR because it will normalize them
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Esmolol vs. labetolol
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- Esmolol: Decreases HR > BP, very short acting - Labetolol: blocks alpha and beta, decreases BP > HR, venodilates
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NPO guidelines per type of food
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- No clear liquids for 2h - No milk/light meal for 6h - No fatty foods/more for 8-10h
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What conditions delay gastric emptying?
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DM, pregnancy, ileus, hernia, scleroderma, AMS/stroke
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When does risk of aspiration damage increase? What can you do to mitigate these risks?
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Stomach volume >25cc and pH<2.5 - Use sodium citrate, H2 antagonists to change pH - Glycopyrrolate decreases gastric secretions, but also LES tone - NG tube is controversial because of paradoxical aspiration - Metoclopramide stimulates gastric emptying and increases LES tone
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How do neuraxial injections work?
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Opioids get injected into the epidural or intrathecal space, then bind to receptors in the dorsal horn of the spinal horn/substantia gelatinosa (where afferent pain is processed)
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Which receptors affect somatic pain? Visceral pain? Substance P?
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- Somatic pain: mu and delta - Visceral: mu and kappa - Substance P: kappa activation inhibits release of substance P by blocking calcium from entering neuron
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S/e of neuraxial pain control
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Pruritis, n/v, urinary retention, respiratory depression
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Which abx for gyn/shoulder surgery vs. bowel surgery and why?
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- Gyn/shoulder surgery -- Ancef for gram positives - Bowel surgery -- cipro for gram negatives
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Scopolamine - MOA - Indication - Can cross BBB? - S/e and how to tx
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- MOA: anti-Ach - Indications: premedication [dry out airway (stop salivation), prevent reflex brady when vagal stimulation anticipated, sedative/amnesia] - Scopolamine and atropine can cross the BBB, glycopyrrolate cannot - S/e: confusion, anticholinergic syndrome (tx with physostigmine because it's the only Achesterase inhibitor that crosses the BBB)
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Which meds do you use for - Unconsciousness - Amnesia - Analgesia - Immobility - ANS response
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- Unconsciousness: inhalants, IV agents - Amnesia: benzos, anti-ach - Analgesia: opioids, ketamine, inhalants - Immobility: NMBDs - ANS response: Opioids and inhalants block sympathetic response, anticholinergics block post-synaptic muscarinic response
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What ANS responses occur in response to the following: - Hypovolemia - Hypothermia - Pulmonary hypoxia - Laryngeal manipulation
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- Hypovolemia -- increased HR - Hypothermia -- peripheral vasoconstriction - Pulmonary hypoxia -- pulmonary artery vasoconstriction - Laryngeal manipulation -- tachycardia and HTN
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Which drugs trigger MH?
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Succs and inhalants
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Spinal - where injected - advantages
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- intrathecal - stronger, faster, less discomfort, more of a block, easier to confirm direct placement
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Epidural - advantages - post-op pain control
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- decreased risk post-dural puncture h/a, less systemic hypotn, more control over intensity & spread - superior to PO opioids
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CI to blocks
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infection at site elevated ICP bleeding d/o CNS problems valve-problems (AS) Previous spinal sx
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Opioids - Use - MOA - SE - what happens when combo with volatile anesthetics
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- analgesia - opioid-R coupled G-protein --> hyperpolarization -->inhibit adenylylcyclase --> inhibit Ca entry and inc K efflux - inhibits presynaptic release & post-synaptic response to excitatory neurotransmitters from nociceptive nrns - supp cough reflex (good for intubation), brady/venodil/dec symp-->hypo, dec RR, n/v/dec motil, pruritis, low stress resp/dec steroids-catecholamines, Urinary Ret - Decreased MAC (balanced anesthesia)
