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UBP Pearls > Misc > Flashcards

Misc Flashcards

1
Q

BMI obesity classification

A
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2
Q

“Premedication” possibilities

A
  • Reglan or antacid (Bicitra - citric acid) for aspiration
  • Breathing tx (asthma)
  • DVT ppx
  • Abx
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3
Q

Would you give an obese pt versed?

A

“Would need to weigh risks/benefits with particular patient and see if there are any other measures they’d be okay with to decrease their anxiety (music, talking, etc) or possibility giving a bit of precedex instead - knowing that they are at higher risk of resp depression if have undiagnosed OSA. But also don’t want to cause increase in anxiety that could also lead to uncooperation/ineffective preoxygenation etc

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4
Q

How to calculate BMI?

A

To remember rough estimate…5’ 70kg person = BMI ~31 (5’ is ~ 150cm, which is 1.5m…1.5^2 = 2.25…70/2.25 = 31)

If height is in inches and weight in lbs, BMI = (lbs/in^2)*703

Remember 2.2lbs = 1kg

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5
Q

Fat embolism major/minor criteria and name

A

Gurd and Wilson:
petechiae
AMS
hypoxemia, pulm edema

unexplained thrombocytopenia, anemia
fat everywhere
tachycardia
fever

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6
Q

Tx of fat embolism?

A
  • Give 100% FIO2
  • Tx hypoTN and hypovol
  • Give blood products PRN, keep ventilating
  • Tell surgeon in case they’re able to shorten procedure
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7
Q

Explain MetHb and SpO2

A
  • cyanosis typically doesn’t occur at a sat of 85%, more like 70%, so this can be a clue
  • Traditional dual wave-length pulse oximetry is inaccurate in the setting of methemoglobinemia because these pulse oximeters measure the absorbance of light at two wavelengths - 660 and 940 nm. The ratio of this absorbance allows the distinction between oxyhemoglobin and deoxyhemoglobin, with the expressed percentage, or SpO2, indicating the measured amount of hemoglobin that is oxygenated. Methemoglobin has high absorbance at both of these wavelengths, leading to the interference that causes an inaccurate SpO2 reading. When the level of methemoglobin approaches 30-35%, the ratio of absorbance becomes 1.0. A ratio of absorbance (A660/A940) of 1.0 reads as a SpO2 of 85%.
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8
Q

Steps you’d take if your pt develops MetHb?

A

Most importantly, ID the oxidizing agent (benzocaine, prilocaine, etc) and stop it! Tissue hypoxia doesn’t occur until MetHb levels >30%. If levels were clinically significant though, would give 100% O2, consider exchange transfusion, and give methylene blue (or if G6PD def, ascorbic acid)

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9
Q

What is G6PD def? Symptoms, etc

A
  • Sxs: Fatigue, cyanosis, jaundice, anemia, hypoTN, lumbar/abd pain, hemolysis (can have all the time, intermittently, or in presence of inc oxidants and free radicals like during illness/infection, certain meds, fava beans), hematuria, renal failure
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10
Q

Explain/draw out enzyme pathways relating to MetHb, methylene blue, and G6PD deficiency

A
  • Basically, G6PD is needed to generate NADPH, which is needed for the methylene blue pathway to work, which converts ferric to ferrous heme
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11
Q

What does placing the pt in reverse T during induction do?

A
  • Improves resp mechanics
  • Dec risk of aspiration
  • Facilitates venous drainage from intracranial compartment
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12
Q

What to do if poked with HIV pt? Transmission rate?

A
  • Wash w/soap and water
  • Contact employee health for blood draw
  • rate w/perQ puncture = 0.3%
  • will likely get postexposure ppx
  • avoid transmissable activities until everything comes back
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13
Q

Myasthenia gravis sxs?

A
  • dyspnea
  • diplopia (dbl vision) –> blurred vision
  • ptosis
  • dysphagia
  • difficulty chewing
  • dysarthria (slurred speech)
  • muscle weakness
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14
Q

How to dx myasthenia gravis?

A
  • tensilon test (1st line. Edrophonium injx –> if muscle weakness improved with this AChE inhibitor, then might be MG)
  • nerve stimulation
  • AB immunoassays
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15
Q

“Bulbar sxs” - what are they, what sxs

A
  • weakness in the muscles innervated by CNs V, VII, and IX-XII
  • facial weakness, difficulty chewing, dysphagia, dysarthria
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16
Q

Risk factors (10) for CV periop complications for pts w/ant mediastinal mass?

A
  • tracheal compression >50%
  • ” “ >30% + bronchial compression
  • stridor
  • orthopnea
  • cyanosis
  • jugular distention
  • SVC syndrome
  • pericardial/pleural effusion
  • combo obstructive + restrictive pattern on PFTs
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17
Q

Explain your overall method for evaluating severity of ant mediastinal mass preop?

A

Obviously H&P, focusing on:
- tracheal compression >50%
- “ “ >30% + bronchial compression
- stridor
- orthopnea
- cyanosis
- jugular distention
- SVC syndrome
- pericardial/pleural effusion
- combo obstructive + restrictive pattern on PFTs
…as well as:

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18
Q

Congenital effects seen with Down Syndrome pts that could effect airway?

A
  • Macroglossia
  • Atlanto-axial instability
  • micrognathia
  • subglottic stenosis
  • could complicated mask ventilation, laryngoscopy, and ETT placement
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19
Q

2-3 major things to discuss with surgeon when about to perform anesthesia for a biopsy of a mass of some kind?

A
  • what kind of biopsy is needed (e.g. for this mediastinal mass, are there any extrathoracic adenopathy, cervical/supraclav nodes available to do a much less invasive bx under LA instead of intrathoracic bx under GA)
  • any chance of pt receiving chemo/radiation/steroids to decrease the size of the tumor prior to surgery if this would dec anesthetic risk, for example. However, rapid tumor lysis may affect accuracy of future histological dx so sometimes can’t
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20
Q

What can anticholinergics be used for in the OR?

A
  • aspiration ppx (this seems like it was done in the past but no longer..they dec LEW tone and not shown to dec acidity/gastric volume - ASA no longer recommend)
  • dec airway secretions
  • dec airway hyperreactivity (asthma pt)
  • obviously helps with bradycardia (esp if inducing w/inhaled sevo)
  • random**: avoid anticholinergics in MG pts, as would lead to inc muscle weakness and bulbar sxs
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21
Q

How to eval someone for atlanto-axial instability?

A
  • look at their previous anesthesia records/esp airway
  • see if any neck radiographs-look for any subluxation (ant atlantodental interval > 4-5mm in any lat view)
  • thorough H&P Re: s/s of cord compression (gait issues, paresthesias, fatigue when walking, and ask them to extend/flex neck to see if that elicits pain/motor/sensory deficits)
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22
Q

Pts with MG and Lambert Eaton…dosing of nondepols and depol agents?

A
  • MG: will be RESISTANT to sux (not as many Rs available to create large depolarizing effect, so will need to give ~1.5x normal dose) and SENSITIVE to roc (the disease has already destroyed Rs so kind of already getting a head start on a nondepol mechanism)
  • LE: lambs are SENSITIVE to both
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23
Q

Signs of cholinergic crisis?

A
  • dyspnea
  • constricted pupils
  • weakness/muscle fasciculations
  • brady
  • salivation, N/V/abd cramps
  • diarrhea, urinary freq/urgency
  • diaphoresis
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24
Q

SEs of methylpred (or just high dose steroids in general)

A
  • infx, impaired wound healing, immunosuppression, GI bleeding, resp compromise
  • fluid retention, HTN, lyte imbalances, hyperglycemia,

**random side note: giving high dose steroids after acute spinal cord injury used to be recommended, but is no longer d/t lack of clinical benefit shown and all of the above named SEs

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25
Q

Alcohol w/d timeline and s/s?

A
  • 6-8 hrs: tremors
  • 24-36hrs: hallucinations/seizures
  • w/in 72hrs: life threatening DTs (confusion, perceptual distortions, agitation, autonomic instability w/fever, tachy, HTN)
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26
Q

How would you proceed preoperatively with a chronic alcoholic?

A
  • history: type, freq, quantity, and time of last alcohol
  • PE: cirrhosis, HE, Wernicke-Korsakoff, gait issues, CM
  • CBC, BUN, Cr, lytes, glu, coags, LFTs, ECG, CXR
  • consider BDZ to prevent acute w/d
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27
Q

What effects does alcohol have on the body (esp those related to anesthesia)

A
  • inc MAC, tolerance to drugs, cerebral atrophy/cerebellar degeneration, peripheral neuropathy, acute w/d sxs
  • CM
  • cirrhosis, GI bleeding, inc risk of aspiration (inc gastric acid, dec LES tone, delayed gastric emptying), nutritional deficiency, hypoglycemia
    -thrombocytopenia, lyte abnlties
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28
Q

Risks of poor periop glu control?

Lab work you’d order for diabetic pt?

A
  • worse neuro outcomes iso TBIs
  • impaired wound healing, inc risk of infx, osmotic diuresis
  • Just think of anything that would ID end organ disease…
  • CBC, BUN, Cr, K, glu, UA
  • possibly ECG (early atherosclerosis and silent ischemia in these pts)
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29
Q

Any special monitoring for spine cases?

A
  • Remember SSEP and MEPs!!! Apparently, MEPs are not necessarily the standard of care yet technically, but have inc sensitivity than SSEPs so if spinal cord ischemia is a significant risk, you could always say that you wanted to dec the false negative rate that you’d have if only monitoring SSEPs, thus you’d want both.
  • if >4 hrs, have to remember Foley
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30
Q

Describe with autonomic neuropathy is, and clinical manifestations?

A
  • Longstanding, poorly controlled DM –> excessive glycosylation –> neuropathy of the ANS
  • GI: gastroparesis, GERD, early satiety, bloating, N/V/D, epigastric pain
  • extremities: peripheral neuropathy, no sweating
  • CV: HTN, resting tachycardia, orthostasis, no reflex tachy w/hypovolemia, resistance to ephedrine
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31
Q

Causes of AGMA?

A
  • MUDPILES: methanol, urea, DKA, paraldehyde, iron/isoniazid, lactic acidosis, ethanol/ethylene glycol, salicylates/ASA
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32
Q

When would you administer bicarb? Issues with doing it?

A
  • if pH < 7.1, bicarb < 10, or if pt developed life threatening hyperK (bc can lead to dysrhythmias, hypoTN, myocardial dep, resistance to exogenous catecholamines)

-1) bicarb + H –> CO2 + H2O (additional CO2 diffuses into cells –> worsening acidosis).
2) leftward shift of curve –> less unloading of O2 at tissues
3) causing hyperosmolar state 2/2 excessive Na (review this?)
4) causing hypoK d/t extra- to intra-cellular movement

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33
Q

Causes of postop vision loss? (3)

Steps to take?

A

-PION: post ischemic optic neuropathy
- RAO: retinal artery occlusion
- cortical blindness
- all likely 2/2 impaired O2 delivery, so you should…

  • assess and correct any metabolic disurbances, elevate HOB to facilitate venous drainage, ensure adequate BP/Hgb/oxygenation/cardiac fxn, ophtho consult

-ASA states NO role for antiplatelets, steroids, IOP lowering agents in periop ION

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34
Q

Describe PION - what it stands for, what it is, who is at high risk? How to reduce risk?

A
  • posterior ischemic optic neuropathy
  • postop vision loss (dec acuity to blindness) 2/2 dec O2 delivery to part of optic nerve –> nerve damage. Poor prognosis, presents w/in 24-48 hrs postop, painless vision loss/field defects/etc
  • risk: prolonged procedures (>6.5 hrs), substantial blood loss (50% of blood vol).

Could dec risk by:
- head neutral or higher than heart
- monitor BP and keep near baseline (esp in HTN pts)
- consider CVP monitoring and admin fluids PRN
- monitor Hct levels
- consider staging long procedures (weighing risk/benefit)

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35
Q

Good way of describing decision to/not to get further cardiac evaluation if METS <4 or unknown + intervention would change management?

A

“I would consider pharmacological stress testing (e.g. dobutamine stress echocardiography to ID any myocardium at risk)”

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36
Q

Periop complications associated with DM?

A
  • hyper/hypoglycemia
  • hemodyn instability (autonomic neuropathy)
  • silent ischemia
  • neurologic injury
  • aspiration
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37
Q

Potential deleterious effects of hypothermia?

A
  • inc O2 consumption
  • inc PVR (+ possible cardiac shunting if have PFO, VSD, PDA)
  • altered drug response
  • postop hypovent, apnea
  • coagulopathy
  • delayed emergence
  • cardiac irritability
  • impaired wound healing
  • metabolic acidosis
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38
Q

What’s a good framework for answering the question “what concerns do you have in providing anesthesia to this patient”?

A
  • first, state the urgency of the case if it’s urgent or emergent, “since this may limit the time I have to evaluate and optimize the patient”
  • think through in your head all of the data you’ve been given about the patient and every possible issue that is r/t his PMH etc…he’s at “inc risk for ___ d/t his ___ disease”
  • any particular concerns about the type of surgery itself or what they have to do for it
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39
Q

Name the signs of hyper- and hypo- volemia

A

Hypervol: peripheral edema, pulm edema, elevated JVD, HTN

Hypovol: dry mucous membranes, poor skin turger, hypoTN, orthostasis

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40
Q

What’s a good way to approach the questions where they ask if you would cancel the case due to a lab value or whatever?

A
  • “Assuming nothing terrible is happening (like symptomatic from said lab derangement, EKG changes, etc), I would not cancel the case due to the urgency of the procedure
  • However, I understand that ___ has the potential to ___
  • Therefore, I would do these things to prepare/help the situation in general
  • Proceed with the case and monitor closely for signs of really bad stuff”
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41
Q

Preop labwork you’d order for a pt with chronic renal failure?

A
  • CBC (anemia)
  • lyte panel (Na, Ca, K)
  • ECG (hypertrophy, ischemia, conduction abnlties)
  • CXR (fluid overload, pulm status)
  • if dyspneic, ABG
  • if regional, coags
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42
Q

Describe how you would induce a patient whom you are concerned about aspiration in?

A
  • insert NGT
  • aspiration ppx
  • reverse T to improve resp mechanics, dec passive regurg, facilitate rapid intubation
  • pre-ox w/100% FiO2
  • if reassuring airway, RSI w/cricoid pressure
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43
Q

Drugs that you’d want to avoid in someone with kidney disease?

A
  • drugs dep on renal elim or had active metabolites that could accumulate:
  • pancuronium, atropine, glyco, ketamine, morphine, diazepam, meperidine
    -BDZs also may exert exaggerated response due to dec protein binding ass w/CRF
44
Q

Replacement of insensible and third space losses w/isotonic crystalloids at what rate during procedure? How to replace blood loss?

A

1-2mL/kg/hr

Blood loss replacement w/colloid solution vs pRBCs (rather than 3:1 crystalloid ratio)

45
Q

What fluid has some K in it?

A

LR contains 4mEq/L of K (avoid in pts where you’re concerned about hyperK)

46
Q

Definition of third spacing?

A

When fluids in the intravasc compartment are lost into the interstitial space d/t traumatized, inflamed, or infected tissue. Will vary depending on extent and type of surgery

47
Q

Describe how to extubate a patient?

A
  • ensure complete muscle relaxant reversal, adequate oxygenation/ventilation with normocarbia, stable hemodynamics, sufficient TVs w/spontaneous ventilation
  • +/- NGT to empty stomach of high aspiration risk (but should say suction everyone)
  • extubate as soon as pt exhibits signs of being awake/alert and exhibiting intact airway reflexes
48
Q

What is the pathogenesis of sickle cell disease?

A
  • mutation in chr 11 that causes valine substitution for glutamate in beta chains of Hb –> HbS
  • HbS can link together and polymerize –> contorts RBC membrane into sickled shape –> hemolysis
  • microvasc occlusion of capillaries , ischemic injury to end organs, infarcts, hemolytic crisis
49
Q

Comorbidities associated with sickle cell disease?

A
  • chronic hypoxia, anemia, hemochromotosis may lead to:
  • neuro deficits, retinopathy, painful crises
  • CM, CHF, pulm HTN, acute chest syndrome
  • renal insufficiency/failure, asplenia by adolescence (so prone to infx)
  • aseptic necrosis of head
50
Q

When would you order an exchange transfusion for a sickle cell patient preop?

A
  • I wouldn’t, bc evidence shows maintaining Hct of 30% and above for mod-high risk surgeries (low risk surgeries don’t need anything) is just as effective and avoids the risks of multiple transfusions and those complications
51
Q

How to prevent sickling in pt with SCD?

A
  • anything that promotes dissociation of O2 from Hb predisposes to red cell sickling, so avoid: hypoxemia, hypoTN, hypothermia, acidosis, hypovolemia
  • use supplemental O2 perioperatively, avoid hypoventilation, assure adequate hydration w/IVFs, maintain Hct 30-40%, use warmers, postop pain control
52
Q

Tx of sickle cell disease?

A

1) ensuring adequate pain control
2) IV hydration
3) suppl O2
4) maintain adequate Hct levels
5) tx infx
6) consider exchange transfusions to reduce fraction of HbS to <40%

53
Q

What should you think about if the patient has a hx of masseter muscle spasm?

A

MH!
MHAUS recommends immediately starting MH tx and cancelling any elective procedure s/p significant MMR (masseter muscle rigidity). If emergent case, can continue anesthetic with nontriggering agents only

54
Q

Steps to take after pt has had severe masseter muscle spasm “jaws of steel”? After either waking patient up or securing airway

A
  • Due to likelihood of developing rhabdo, need to observe as inpatient for 12-24 hrs. Place art line
  • monitor ETCO2, CK, temp, acid/base status, lyte levels (rhabdo can –> hyperK)
  • CTM for pigmenturia, myoglobinuria, generalized rigidity, s/s of hypermetabolism
  • recommend testing for MH susceptibility
  • if procedure is elective and developed MMR s/p sux, should be cancelled and postponed until further testing for MH (caffeine halothane contracture test - CHCT) has been completed. If emergent, can continue w/nontriggering agents and all precautions taken. Likelihood of MH susceptibility as high as 50%
55
Q

S/s of thyroitoxicosis?

A
  • cardiac (tachy, arrhythmias, CM, inc SV and CO, dec SVR and PVR)
  • neuro (anxiety, agitation, tremors, insomnia, muscle weakness)
  • nonspecific (sweating, heat intolerance, weight loss)
56
Q

Lab tests to assess thyroid fxn?

A
  • TSH, free T3 and T4
  • hyperthyroid pt will have high free T3/T4 and low TSH
57
Q

What kind of condition is PTU administered for? Mech?

A

Hyperthyroid pts!
PTU inhibits organification of iodide, synth of thyroid hormone, and peripheral conversion of T4 to T3

Should be continued in patient presenting with thyrotoxicosis sxs…I believe should always continue it?

58
Q

What would you administer (premed) for someone who you’re concerned about delayed gastric emptying/aspiration?

A

1) reglan (blocks dopamine Rs –> speeds up muscle movement)
2) H2 antagonist (block histamine type 2 Rs –> dec prod and secretion of gastric acid)
3) antacid

59
Q

Where do you place a precordial doppler to detect venous air embolism?

A

Between 2-4th ribs

60
Q

Risks of a PAC?

A
  • arrhythmias
  • pulm infarction
  • pulm artery rupture (esp iso pulm HTN)
  • thrombosis
  • infx
  • errors in data interpretation
61
Q

Risks of a CVC?

A
  • art puncture
  • PTX/hemothorax
  • air embolism
  • thrombosis
  • thoracic duct injury
  • pseudoaneurysm formation
  • arterial/venous hematoma
62
Q

Strategies to minimize transfusion requirements during bloody case?

A
  • preop autologous blood donation (think about C/Is to this though, like myocardial dysfxn, anemia, etc - this is done weeks in advance)
  • acute normovolemic hemodilution
  • intraop blood salvage
  • deliberate hypoTN
  • antifibrinolytic tx (TXA, aminocap acid)
  • avoid hypothermia
  • minimize intra-abd pressure (can cause excessive shunting to vertebral venous plexus –> more bleeding)
63
Q

Ways to see if clinical picture of dec CO2 and hypoTN was 2/2 VAE?

A
  • listen for sporadic roaring sounds from precordial doppler
  • auscultate heart for millwheel murmur
  • attempt to aspirate air from CVC
  • consider TEE
64
Q

Steps to take if heard sporadic roaring sounds from precordial doppler?

A
  • VAE is likely!
  • ask surgeon to flood field w/saline
  • d/c nitrous if on and deliver 100% FIO2
  • attempt to aspirate the air using CVC
  • supportive BP tx
  • place pt in L lat decub so that air stays in RA and away from pulm outflow tract
65
Q

Can a patient have MH if had a previously uncomplicated anesthetic?

A

Yes - the variable expressivity of MH means possible for pt to experience one or more exposures to a triggering agent w/o complication, then have MH on next exposure. However, once pt has MH reaction to triggering agent –> subsequent exposures will always result in MH

66
Q

Steps to take to prepare the anesthesia machine if you were concerned about MH?

A
  • remove all sux from area
  • disengage all vaporizers
  • replace circuit and CO2 absorbent
  • flush anesth machine for 10 mins
  • (+/-) filter?
  • presence of ice solutions, appropriate monitors, and dantrolene supplies
67
Q

What to do if suspect oculocardiac reflex? Mech?

A
  • ask surgeon to stop
  • ensure ETT placement, auscultate lungs, assess other vitals
  • deepen anesthetic
  • correct hypercarbia/hypoxemia
  • admin atropine 0.02mg/kg
  • if nothing else works, have surgeon infiltrate rectus muscles with LA
  • usually medial rectus muscle manipulation –> afferent: ophthalmic part of trigeminal n and ciliary nerves –> efferent: vagal n
68
Q

Central O2 supply is compromised during a GA. Steps you take?

A
69
Q

Possible complications of autonomic hyperreflexia episode?

Pathophys of AH?

A
  • everything that has to do with high BP spike…
  • cerebral, retinal, subarachnoid hemorrhage
  • seizures, MI, dysrhythmias, pulm edema (LV failure d/t inc afterload)
  • random things: rarely can get AH if SCI below T7 (has to do w/splanchnic sympathetic control and cause of HTN). Also, usually don’t get AH w/in 1-3 weeks of injury d/t spinal shock
70
Q

Ddx for hypoTN and inc PIP in laparoscopic surgery?

A
  • pneumoperitoneum (inc in vagal tone from upward pressure on diaphragm)
  • mainstem intubation
  • tension PTX
  • capnothorax (from insufflated gas)
  • CO2 embolism w/gas lock in vena cava/RA
  • anaphylaxis w/bronchospasm and CV collapse
  • severe bronchospasm –> hypoxia –> CV depression
  • stiff chest syndrome (if high dose narcotics administered)
71
Q

Definition of anaphylaxis vs anaphylactoid?

A
  • anaphylaxis: second exposure to Ag –> IgE production –> stimulate mast cells and basophils to release histamine, leukotrienes, PGs, TNF, etc –> cap permeability, vasodil, bronchoconstriction, negative inotropy. S/s w/in 10 mins of exposure. Non dose dependent since everything just gets rapidly set off and chain rxn
  • anaphylactoid: clinically the same. But Mast cells and basophils degranulate after direct exposure to Ags instead of IgE ABs. So don’t require previous sensitization. Dose dependent since responding directly to the Ags.
72
Q

Steps to take if c/f true type 1 hypersensitivity rxn (anaphylaxis)?

A
  • inform surgeon and call for help
  • d/c all infusions and inhalational agents
  • FiO2 100%, 1-2L IVF bolus
  • IV epi (or subQ if normotensive) - dbl dose q1-2m until goal SBP achieved. Last resort: bicarb to correct acidemia, vaso gtt if refractory hypoTN
  • corticosteroids (enhances B agonist effects of other drugs and inhibits prod of leukotrienes + PGs, delayed by 4-6 hrs), histamine blockers (benadryl),
  • eval cardiac fxn w/TTE
73
Q

Mech of why epi helps in anaphylaxis? What kind of doses would you give in an adult?

A
  • a agonist –> vasoconstriction –> inc BP
  • B agonist –> relaxes bronchial smooth m + inc cAMP (restores mem permeability)
  • if CV collapse: start w/100mcg. If just hypoTN, start w/10mcg IV. If normotensive, 0.3-0.5mg subQ
  • for all doses, repeat q1-2m
74
Q

Risk factors for latex allergy?

A
  • kids w/spina bifida
  • congenital urinary tract abnlties
  • multiple surgeries/medical tx
  • working in healthcare/rubber industry (workers should use latex-free gloves to dec work-related exposure)
  • other allergy to avocados, bananas, chestnuts, kiwis, passion fruit (similar allergens, could have ABs that cross react)
75
Q

How would you prepare a pt preop w/esophageal ca for esophagectomy?

A
  • eval nutritional status (inc M&M if malnourished)
  • ID any chemo/rad complications (CM, pulm tox. Pneumonitis, pericarditis, coagulopathy)
  • ID any pulm, hepatic, cardiac dz (if tobacco, alcohol use)
  • aspiration ppx
  • consider diltiazem (inc risk of periop afib, esp if old, CAD, COPD, etc. No BB unless already on one, d/t inc risk for hypoTN –> gastric tube anastomotic leak/dehiscence)
  • 2 large PIVs, thoracic epidural
76
Q

What does the blood bank actually do when they T&S? Rates of hemolytic rxn in type-specific blood, T&S, and T&C?

A
  • Mix recipient plasma w/panel of commercial RBCs to detect presence of various known ABs (can ID rare ABs)
  • 2/1000, 6/10,000, and 5/10,000
77
Q

Complications of intraop blood salvage?

A
  • hemolysis (high vacuum settings)
  • systemic contamination: urine, amniotic fluid, bacteria, cancer cells (washing, filtering clears most)
  • nephrotoxicity (lots of free Hb)
  • coagulopathy
  • fever
78
Q

Several possible postop complications a/w/ esophagectomy?

A
  • pulm: aspiration pneumonitis, PNA, BPF, PE, ARDS
  • phrenic, vagal, laryngeal n injury
  • anastomotic leak/dehiscence
  • arrhythmias (afib, flutter, PSVT)
  • hypoTN
  • esophageal stricture/stenosis
  • dumping syndrome (rapid fluid/gastric food into small intestine. Can happen w/any gastric surgery. Abd cramps, N/V/D, flushing, tachy, etc)
79
Q

What is another name for CRPS I? What’s the cause of this vs type II?

A
  • reflex sympathetic dystrophy
  • events like crush injuries, lacerations, fractures, surgery, sprains, burns (Type II is 2/2 NERVE injury w/sxs not limited to distribution of the injured nerve)
80
Q

Ddx for extremity w/burning pain for 6 months

A
  • CRPS
  • soft tissue vs nerve injury
  • vascular insuff (Raynaud’s)
  • peripheral neuropathy
  • nerve entrapment syndrome (e.g. carpal tunnel)
81
Q

Tx for CRPS?

A
  • PT, CBT, TENS, spinal cord stimulation
  • gaba
  • antidepressants (amitriptyline)
  • opioids
  • symp n blockade (stellate ganglion block for arm, etc)
  • somatic block (spinal/bier)
  • IV ketamine gtt
82
Q

Pros/cons of thoracic epidural for an esophagectomy?

A

Pros:
- facilitate early extubation
- better postop pulm fxn
- improved gastric tube blood flow and dec risk of anastomotic leak

Cons:
- sympathectomy –> hypoTN –> compromise coronary/gastric tube blood flow (could delay dosing of epidural vs utilize vasoconstrictors/inotropes. Also should use hydrophilic like hydromorphone vs lipophilic d/t wide # of dermatomes necessary to cover)

83
Q

A few ddx for hypoTN during esophagectomy?

A
  • hemorrhage (esp during blunt dissection in mediastinum)
  • arrhythmias (esp atrial)
  • vagal stimulation during dissection
  • compression of heart/great vessels
  • sympathectomy (thoracic epidural)
84
Q

Why is the risk of developing hypoxia higher in esophagectomy patients vs lung resection?

A
85
Q

Steps to take when pt has emesis upon induction?

A
  • head down to allow drainage out of lungs
  • cricoid pressure
  • suction oropharynx
  • intubate
  • in line suction PRIOR to any PPV to avoid dissemination of aspirated material
  • 100% O2 and support ventilation PRN
  • OGT
  • tracheal aspirate sample for culture
  • baseline CXR and ABG
  • tx bronchospasm
  • 24-48 hrs monitoring
  • NO steroids or ppx abx (not proven effective and leads to drug resistance)
86
Q

A few things on the ddx to mention if pt under anesthesia has AGMA?

A

Esp in pt w/DM, alcohol consumption, etc:
- DKA, alcohol ketoacidosis
- poor tissue oxygenation/poor liver fxn –> LA
- dilutional acidosis

  • renal failure, rhabdo, starvation, toxins (methanol, ethylene glycol, salicylate, etc)
87
Q

Problems with giving bicarb?

A
  • combines with H ions –> more CO2 –> intracellular acidosis
  • L shift of curve
  • hypoK from shifting intracellularly
88
Q

How would you induce and intubate an uncooperative Down’s pt w/WPW and a submandibular abscess?

A
  • emergent airway equipment in room, including surgeon who has prepped and draped neck & applying cricoid pressure
  • preox w/100% FiO2, reverse Tburg
  • sedative dose of precedex (no ketamine d/t WPW and risk for tachyarrhythmia + inc risk of this w/anxiety and symp stimulation if try it all awake)
  • suction mouth carefully, in line stabilization of neck
  • mask induce w/sevo (I would get PIV during this time too), maintain spont resp
  • perform careful nasal/oral fiberoptic intubation depending on surgical preference
89
Q

What does DDAVP do?

A
  • induces release of VIII and vWF from endothelial cells –> inc circulating levels of these factors
  • inc in vWF (carrier molecule for factor VIII) may also dec the clearance of fVIII from circulation

This is all helpful for pt with Hemophilia A and certain vWD patients

90
Q

Pros/cons of flexible LMA vs ETT in tonsillectomy case?

A

LMA pros:
- better protection of lower airway from blood
- less bronchospasm (important if pt is asthmatic)
- less laryngospasm, postop desaturation

ETT:
- easier to place
- occupies less space in oropharynx
- more reliable PPV i.s.o. dec chest wall compliance

91
Q

How do you describe what can happen when patient is relatively normotensive but has lost a lot of blood?

A

“While BP is near normal, the catecholamine-induced vasoconstriction that occurs in response to blood loss may mask considerable hypovolemia”

92
Q

Name a few physical signs of hemorrhage (e.g. post tonsillectomy)

A

orthostatic hypoTN
dizziness, pallor, sweating
excessive swallowing
tachycardia
inc cap refill

93
Q

Induction meds you’d use for post-tonsillectomy massively hemorrhaging child?

A
  • etomidate, sux, atropine
94
Q

What is Addisonian crisis? All about this

A
  • prior exogenous steroids –> suppression of HPA axis –> adrenal atrophy and inability to produce cortisol under stress experienced during periop period
  • glucocorticoids are the key here!
  • s/s of this: fever, abd pain, dehydration, N/V, hypoglycemia, acidosis, hyperK, hypoNa, circ collapse, depressed mentation
95
Q

What pain meds can you give for tonsillectomy?

A
  • often toradol, though not if pt has coagulation issues
  • these patients are at risk of narcotic induced postop nausea and resp depression d/t their obstructive sleep hypopnea syndrome. So it is suggested to use half the normal narcotic dose for them
  • tylenol, decadron
96
Q

How to classify extent of burn injury?

A
  • Percent of involved BSA (using rule of 9s): head, arms = 1. Front torso, back torso, each leg = 2. Totals 11
  • Depth of burn: 1* = epidermis, 2* = dermis, 3* = full thickness, 4* = muscle, fascia, bone involvement
  • presence/absence of inhalational injury: singed hair, soot in mouth/nose, burns of nasal mucosa/lips/mouth, cough, stridor, hoarseness, dyspnea, tachypnea, dec SpO2
97
Q

When can you consider delayed intubation in a burn victim?

A
  • when 3* burns are minimal
  • no signs of inhalational injury
  • no hypoxemia, resp distress, hypercarbia, AMS
  • do PEAE to examine glottic/periglottic structures + lower airways for signs of edema/inhalational injury
  • ABG (low PaO2 suggests inhalational injury), CXR, PFTs (to get a baseline)
  • if reassuring tests, would repeat q3-4hrs x 12 hrs
98
Q

What is the mechanism of “burn shock”? Tx?

A
  • can lead to tissue hypoperfusion & multiple organ failure
  • negative imbimbition pressure in injured tissues (P gradient that –> lots of water/crystalloid absorption)
  • inc permeability throughout vasc system
  • So, need to resuscitate enough using Parkland formula! But, too much can cause airway edema, impaired perfusion of burned areas (inc tissue P –> ischemia), compartment syndrome, inc mortality. Want UOP 0.5 - 1 cc/kg/hr
99
Q

Parkland formula?

A

Fluid replacement w/crystalloid at volume of 4 cc/kg/% BSA in first 24hrs. 1/2 this volume in first 8 hrs after burn injury, then other half over next 16hrs. Titrate to UOP 0.5 - 1 cc/kg/hr

100
Q

Ddx for hypoTN s/p induction/intubation in burn trauma victim? Though many of these can be applied to other scenarios

A
  • Burn shock (distributive, hypovolemic, and cardiogenic mix)
  • sedation-induced CV depression and dec SVR
  • mechanical vent dec filling (high PEEP)
  • hemorrhagic shock
  • CO, CN poisoning (myocardial toxicity, CV depression/arrhythmias)
  • vagal response to laryngoscopy
  • tension PTX 2/2 central line
  • fat embolism 2/2 leg trauma
  • neurogenic shock (intubation w/C-spine injury)
  • allergic rxn
  • transfusion rxn
  • citrate intoxication (if MTP or whatnot)
101
Q

How do you calculate FiO2 from L of oxygen supplied?

A

For every 1L added, increases FiO2 by 4%
So, if you have someone on 2L, FiO2 ~29%

102
Q

What can “significant acidosis” lead to? What’s your cutoff for this irt administering NaHCO3?

A
  • dysrhythmias, hypoTN, myocardial depression, catecholamine resistance
  • if pH drops below 7.1
103
Q

Systemic effects of CRF?

A
  • metabolic derangements (hyperK/Mg/Phos/H+/uric acid, hypoNa/Ca), which if longstanding, can lead to:
  • peripheral and autonomic neuropathy, seizures, uremic encephalopathy, anorexia, delayed gastric emptying, insulin resistance, arrhythmias, conduction blocks, accelerated atherosclerosis, uremic pericarditis
  • Na and water retention –> HTN –> LVH, CHF, CAD, CVD
  • pulm edema
  • anemia (dec renal production of EPO)
  • impaired platelet fxn –> bleeding (despite normal labs)
104
Q

Can you use a patient’s temp dialysis catheter if absolutely necessary? If so, steps to take?

A
  • yes, but it increases risk of infx and clotting of a vital access site
  • So, access it aseptically!! Leave the line heparinized, aspirate prior to connecting an IV line. At time of disconnection, re-heparinize the line and seal it aseptically
105
Q
A

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