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Surgery > General Anesthesia and Airway Mgmt- Exam 1 > Flashcards

General Anesthesia and Airway Mgmt- Exam 1 Flashcards

1
Q

d-Tubocuraine

A 
Slow onset (6m)
Long duration (90m)
Causes hypotension=do not give to hypotensive pt
Causes histamine release and skin flushing
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2
Q

Atracurium

A

Ester hydrolysis metab (plasma)
Not metab thru liver or kidneys=safe for administration in pt w/ kidney and/or liver dz
Onset=5m
Duration=30m

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3
Q

Succinylcholine

A 
Rapid onset (30-60s)
Short duration (5m)
Metab by serum (pseudo) cholinesterase (if pt lacks enz, DO NOT GIVE=DEATH!)
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4
Q

What are the SEs a/w Succ?

A 
Bradycardia
Fasciculations
Incr gastric pressure (No pts w/ GERD)
Incr intraocular pressure (No pts w/ glaucoma)
Incr intracranial pressure
Incr K+ (No pts w/ K+ >7.5)
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5
Q

Pancuronium

A

Onset=7m
Duration 60-75m (avg length of podiatry case)
Processed in liver and excreted by kidneys
Given after pt is intubated
Used for long term relaxation in long cases

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6
Q

Roncuronium

A

Onset=3m
Duration=30-50m
Good replacement for Succ

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7
Q

Vercuronium

A

Onset=5-6m
Duration=30-60m
Metab in liver, excreted in kidneys (No pts w/ kidney or liver dz)

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8
Q

What are the NMJ reversal agents?

A

Anticholinesterase:
Neostigmine
Edrophonium
Phyostigmine

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9
Q

What is the Pathophys of Malignant Hyperthermia?

A
  1. Decr Ca++ uptake by sarcoplasmic reticulum
  2. Leads to high intracellular [Ca++]
  3. Aerobic and Anaerobic cell turnover
  4. Leads to excess heat, CO2, and lactic acid
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10
Q

How will a pt present w/ MH?

A

Fever, unexplained tachycardia and tachypnea, failure of masseter muscle relaxation

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11
Q

How is MH dx?

A
  1. Muscle biopsy

2. Serum CPK (creatinine phosphokinase) elevated

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12
Q

What drug is given to tx MH?

A

Dantrolene:

1-2 mg/kg

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13
Q

Nose and Mouth

A

Fxn: warm and humidify air
Inn: CN V (trigeminal), CN IX (glossopharyngeal)

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14
Q

Pharynx

A

Fxn: connect oral and nasal cavities to esophagus and larynx
Inn: CN IX and X (vagus)

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15
Q

Larynx

A

Fxn: modulation of sound; separates esophagus from trachea during swallowing
Inn: CN X
Location: btwn C3-C6

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16
Q

Trachea

A

Location: C6-T5

Supported by 16-20 cartilages (Cricoid has full ring structures; remainder have horseshoes)

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17
Q

Mallampati Class I

A

Soft palate, fauces, uvula, and tonsillar pillars are visible

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18
Q

Mallampati Class II

A

Soft palate, fauces, and uvula visible

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19
Q

Mallampati Class III

A

Soft palate and base of uvula visible

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20
Q

Mallampati Class IV

A

Soft palate NOT visible

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21
Q

Cormack and Lehane Score: Grade I

A

Most of the glottis is visible

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22
Q

Cormack and Lehane Score: Grade II

A

Only posterior portion of glottis visible

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23
Q

Cormack and Lehane Score: Grade III

A

The epiglottis visible, but NO PART of the glottis can be seen

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24
Q

Cormack and Lehane Score: Grade IV

A

No airway structures visualized

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25
Q

What is the primary problem of airway mgmt?

A

The inability to oxygenate, ventilate, and prevent aspiration (or a combo of these factors)

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26
Q

What are the boundaries of the facemask (for ventilation)?

A

Bridge of the nose
Upper border aligned w/ pupils
Sides seal lateral to nasolabial folds
Bottom seals between lip and chin

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27
Q

Endotracheal intubation technique

A
  1. Raise table so pt is at height of xyphoid cartilage of the anesthesiologist
  2. Elevate and extend head
  3. Align oral, pharyngeal, and laryngeal axes
  4. Apply pressure to cricoid cartilage
  5. Blade, tube, and check for placement
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28
Q

When is Fiberoptic Endotracheal Intubation indicated?

A
  1. Known that pt will be difficult to intubate by direct laryngoscopy
  2. Unstable cervical spine
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29
Q

What is the ratio of compressions:breaths in compression-only CPR?

A

30:2

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30
Q

What drugs are used to control A-flutter?

A

Beta blockers and Ca++ channel blockers

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31
Q

What drugs are used to control V-tach?

A

Lido, Procainamide, Bretyllium

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32
Q

What drugs are used for V-fib?

A

Epi, Lido, Bretyllium, Mag Sulf, and Procainamide

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33
Q

What drugs are used in Asystole?

A

Epi, Atropine, and Sod Bicarb

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34
Q

What are causes of asystole?

A

Hypoxia, hypokalemia, hyperkalemia, hypothermia, acidosis, and drug OD

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35
Q

What is normal body pH?

A

7.4

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36
Q

What are causes of metabolic acidosis?

A

Renal failure
Lactic acidosis
Ketoacidosis
Hypokalemia

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37
Q

What are causes of metabolic alkalosis?

A

Vomiting

Mineralcorticoid excess

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38
Q

What are causes of respiratory acidosis?

A

Hypoventilation
CNS depression
COPD
Guillen-Barre Syndrome

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39
Q

What are causes of respiratory alkalosis?

A 
Anxiety
Sepsis
Lung Dz
Hypothyroidism
Liver dz
Pregnancy
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40
Q

What is the definition of Local Anesthesia?

A

Drug induced REVERSIBLE blockade in a restricted region of a nerve fiber

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41
Q

What are the two types of LAs?

A

Amides and Esters

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42
Q

What is the common structures shared btwn LAs?

A

Lipophilic aromatic ring–amide/ester–hydrocarbon chain–2ry/3ry amine (hydrophilic)

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43
Q

What is the least toxic amide LA?

A

Lidocaine

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44
Q

What is the longest acting amide LA?

A

Bupivicaine

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45
Q

What is the duration of action of Lidocaine?

A

2 hours

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46
Q

Which amide LA has the most VC properties?

A

Prilocaine

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47
Q

What is the relationship btwn Ropivicaine and Bupivicaine?

A

They are both long acting but Ropivicaine is less cardiotoxic

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48
Q

What is a major complication of Prilocaine?

A

Fetal methemoglobinemia

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49
Q

Are LAs weak acids or base? What is their pKa?

A

Weak bases

8-9

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50
Q

Why are ester LAs not used very ofter?

A

Because they are short acting and take longer to take effect

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51
Q

What is the oldest, widely known, useless LA? Ester or amide? Why is it useless?

A

Procaine (Novocaine)
Ester
It’s pKa is 9.1=very long onset (relative to other LAs)

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52
Q

What is the MOA of LAs?

A

Block nerve conduction by reducing influx of Na+ into cytoplasm

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53
Q

Upon administration of LA, is it in its ionized or unionized form? Why? Acidic or basic?

A

Unionized
Because in this form it is able to penetrate the plasma membrane (lipid)
Acidic bc more stable and water soluble

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54
Q

What form, ionized or unionized, produces the actual block?

A

Ionized form

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55
Q

T or F. LA blocks occur from inside out?

A

T. LAs must penetrate the lipid membrane, ionize, and then bind to Na+ channels to prevent influx

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56
Q

How is pH, pKa, rate of diffusion, and effect of LA related?

A

If pH=pKa then the rate of diffusion would be rapid, and therefore the effect of the LA would be rapid. Conversely, higher pKa:pH ratio=slower diffusion, etc.

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57
Q

What effects the speed of onset of LAs?

A 
Type of nerve fiber
[LA]
Degree of lipid solubility
Tissue pH
Degree of protein binding
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58
Q

How man successive Nodes of Ranvier must be blocked for a LA to be effective?

A

3

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59
Q

In a non-myelinated nerve, how long of a segment must be blocked for a LA to be effective?

A

5mm

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60
Q

Arrange in order the type of neurological stimuli that is anesthetized first to last:
Temp, pressure, motor, touch, sharp pain

A

Sharp pain->temp->touch->pressure->motor

**Recovery usually happens in the reverse order

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61
Q

What is anesthetized first, cold or warm sensation?

A

Cold

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62
Q

Greater protein binding increases or decreases duration of LA?

A

Decreases

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63
Q

Where are amide LAs metabolized?

A

Liver

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64
Q

Where are ester LAs metabolized?

A

Serum

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65
Q

What do vasoconstrictors do to LAs?

A

Decr absorption into blood stream=prolong effects
Incr local effects/duration
Decr risk of toxic effects

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66
Q

What are some common VC agents?

A

EPINEPHRINE<–must know this one!!!
Phenylephrine
Levonorfedrin

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67
Q

What are common drug interactions w/ LAs? (in particular, esters)

A 
Sulfur-containing drugs:
Abx (Bactrim)
Diuretics (Acetazolamide)
Anticonvulsants
NSAIDs
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68
Q

How deep should the needle go upon injection of a LA?

A

Deep enough while leaving 1/4” exposed

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69
Q

What is the max dose of Lido 1% plain?

A

4.5 mg/kg, not to exceed 300mg

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70
Q

What is the max dose of Lido 1% w/ Epi?

A

7 mg/kg, not to exceed 500mg

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71
Q

What is the max dose of Mepivicaine 1% plain?

A

7.5 mg/kg, not to exceed 400mg

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72
Q

What is the MOA of propofol?

A

Potentiating the Cl- current mediated thru the GABA receptor complex

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73
Q

At what dose and for how long do you need to take propofol to get Propofol Infusion Syndrome?

A

> 4 mg/kg/hr for 24h

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74
Q

What is the general dose for propofol? For peds pts?

A
  • 1.0-2.5 mg/kg

- 2.5-3.5 mg/kg

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75
Q

What are barbituates used for?

A

Induction of anesthesia prior to propofol

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76
Q

What is the MOA of barbituates?

A

Enhancement of inhibitory NTs (i.e., GABA receptors)

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77
Q

In terms of the CV system, what is a difference btwn propofol and barbituates?

A

Propofol is a vasodilator and barbituates are vasoconstrictors

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78
Q

What are the two examples of barbituates used? Doses?

A

Thiopental 3.0-5.0 mg/kg IV

Methohexital 1.0-1.5 mg/kg IV

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79
Q

Where are barbituates metabolized?

A

Liver, via oxidation (methohexital is cleared more rapidly)

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80
Q

Where are barbituates excreted?

A

Kidney, bile via conjugation rxns

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81
Q

Where is propofol metabolized?

A

Mainly the liver, but lungs 30%

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82
Q

Where is propofol excreted?

A

Kidneys

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83
Q

What are the examples of Benzos used?

A

Diazepam, lorazepam, midazolam

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84
Q

What drug is a benzo antagonist?

A

Flumazenil

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85
Q

Of the benzos used, which is the most lipophilic?

A

Miazolam

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86
Q

What is the MOA of benzos?

A
  • Actication of GABAa receptor
  • Enhancement of GABA-mediated Cl- currents
  • Hyperpolarization of neurons and reduced excitability
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87
Q

Benzos have what effect on gamma-subunit receptors?

A

Anxiolysis and muscle relaxation

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88
Q

Where are benzos metabolized?

A

Liver

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89
Q

What are benzos used for, clinically?

A
  • Pre-op meds (peds pts)
  • IV sedation/induction of sedation
  • Suppression of seizure activity
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90
Q

What drug produces a “cateleptic state” in patients?

A

Ketamine

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91
Q

What is the MOA of ketamine?

A

Inhibition of the N-methyl-D-asparate (NMDA) receptor complex

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92
Q

Which drug has caused unpleasant emergence rxns (i.e., hallucinations, out of body experiences) which has limited its use?

A

Ketamine

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93
Q

Compared to other drugs, Ketamine does what to systemic BP?

A

Increases

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94
Q

Where is ketamine metab?

A
  • Liver

- Metabolite is active but less potent

95
Q

Where is ketamine excreted?

96
Q

Ketamine has a high lipid solubility. What does that mean?

A

It has a rapid onset

97
Q

What are some unique properties of ketamine?

A

Analgesia, stim of SNS, bronchodilation, minimal respiratory depression, and ability to use in uncooperative or mentally challenged pts

98
Q

What is the MOA of etomidate?

A

Potentiation of GABAa-mediated Cl- currents

99
Q

What must be done first before administration of etomidate?

A

Fluid/volume balance must be achieved bc BP lowering effects are exaggerated in the presence of hypovolemia

100
Q

What drug inhibits 11B-hydroxylase, the enzyme that converts cholesterol to cortisol?

101
Q

How is etomidate metab?

A

Ester hydrolysis

102
Q

Where is etomidate excreted?

A

Kidney and liver (bile)

103
Q

When is etomidate used clinically?

A

It’s an alternative to propofol and barbituates for rapid induction in pts w/ compromised myocardial contractility

104
Q

Dexmedetomidine is in what class of drugs?

A

Selective alpha-2 adrenergic agonist

105
Q

Where is dexmedetomidine metab?

106
Q

Where is dexmedetomidine excreted?

A

Kidney and bile

107
Q

What are the clinical uses of dexmedetomidine?

A
  • Short term sedation of intubated and ventilated pts
  • Sedation during awake fiberoptic tracheal intubation
  • Sedation during regional anesthesia
108
Q

What is Fentanyl?

A

A potent, synthetic narcotic opioid that produces analgesia

109
Q

What is the MOA of Fentanyl?

A

Agonizes the mu-opioid receptor=inhibit pain NT release by decreasing Ca++ levels

110
Q

What are the clinical uses of Fentanyl?

A

Adjunct to GA or RA, ER dislocation/relocations, post-op pain, peds pts

111
Q

What opioid is 5-10X more potent than Fentanyl and is used during surgical procedures in opioid-dependent pts?

A

Sufentanyl

112
Q

What classic drug regimen is used for Rapid Induction Anesthesia?

A

Thiopental + Succinylcholine

113
Q

What drug is used in veterinary medicine?

A

Dexmedetomidine

114
Q

Which drugs can be used in peds pts?

A

Propofol, Benzos, Ketamine, Fentanyl

115
Q

What drugs cause a barbituate-induced histmaine release?

A

Thiopental and methohexital

116
Q

Peri-op Meds:

-TCAs cause what?

A
  • HYPOtension

- Incr/decr response to sympathomimetic (DOP, NE)

117
Q

Peri-op Meds:

-What’s important regarding MAOIs?

A
  • No meperidine of ephedrine=incr risk of serotonin syndrome
  • Can cause severe HTN
  • Hold 2 weeks prior to sx (MUST!!!!!!)
118
Q

Peri-op Meds:

-Can you continue SSRIs prior to sx?

119
Q

What are the importance of B-blockers, peri-operatively?

A

B-blockers are our friends! We do not want the pt to have an MI. If the pt has LV problems, they may be given 3 doses pre-op

120
Q

What is the concern w/ ACEIs intra-op?

A
  • May cause HYPOtension
  • May stop 1 week prior to sx and be monitored intra-op
  • 99.9% of time cardiologist will allow them to be continued (esp if using Local w/ MAC; but if using GA w/ a long case=may stop 1w prior)
121
Q

When do you d/c ASA or Plavix prior to sx?

122
Q

What is the therapuetic INR pre-op?

123
Q

If you are:

  1. Low risk for VTE
  2. Mod risk for VTE
  3. High risk for VTE
    - When do you d/c coumadin?
A
  1. 4-5d prior to sx
  2. 4-5d and consider bridge therapy w/ LMWH (Fragmin or Lovenox) or unfractioned heparin 2-3d prior
  3. Bridge therapy; await hemostasis before restarting LMWH
124
Q

If you have an urgent or major procedure, what is done for coumadin pts?

A

They are given IV/PO VitK or FFP w/ VitK to initaite clotting prior to procedure

125
Q

If you have an urgent or major procedure, what is done for pts on ASA, Plavix, or both?

A

Transfuse w/ platelets or administer pro-hemostatic agent

126
Q

Endocrine meds pre-op:

  • Insulin?
  • Insulin pump?
  • Oral hypoglycemics?
A
  • Insulin=hold a.m. dose
  • Insulin pump=decr a.m./p.m. dose and give IV drip intra-op
  • Oral hypoglycemics=d/c; sulfonureas may incr risk of MI; metformin may cause LACTIC ACIDOSIS=hold 24h-2d prior to sx
127
Q

What do you do if pt is on OCP?

A
  • If they are low risk for DVT=continue

- If high risk, d/c 4w prior to sx

128
Q

If a pt is on steroid therapy, what do you do peri-op?

A
  • MUST SUPPLEMENT! With sx, you are causing them incr stress so you don’t want their levels to fall too low.
  • Give:
    1. Cortisol 25mf pre-op
    2. Solumedrol 100mg
129
Q

What Vitamin should the pt d/c prior to sx? Why?

A
  • Vitamin E

- Stop 1w prior due to risk of incr bleeding; also, do not want pt to go into tachy

130
Q

Why hold the a.m. dose of tramadol pre-op?

A

Bc it may cause seizures and there’s an incr risk of itra-op drug interactions

131
Q

What factors affect drug choice and dose peri-op?

A

Pts physical needs, pts psychological state, choice of anesthesia, and length of procedure

132
Q

What is a common peri-op LA?

133
Q

What is a common benzo ANTAGONIST?

A

Flumazenil

134
Q

What is SCIP?

A
  • Surgical Care Improvement Project
  • A nat’l quality partnership of organizations committed to improving the safety of surgical care thru the reduction of post-op complications
135
Q

What is Measure 1 of SCIP?

A

Pre-op prophylactic abx to be administered w/in 1h prior to incision (2h for vanco or fluoroquinolones)

136
Q

What is Measure 2 of SCIP?

A

Prophylactic abx selection for surgery pts. For podiatry=cefazolin, cefuroxime, or vanco. If B-lactam allergy=clinda or vanco

137
Q

What is Measure 3 of SCIP?

A

Prophylactic abx d/c w/in 24h AFTER surgical end time

138
Q

What is Measure 7 of SCIP?

A

Pts on B-blockers should receive their B-blockers prior to arrival or during the peri-op period

139
Q

What pts are at high risk for aspiration of gastric contents?

A

Pregnancy, obesity, DM, GERD, hiatal hernia

140
Q

What drugs are used to reduce pH?

A
  • Anticholinergics=Atropine and Glycopyrrolate

- RANITIDINE=LASTS UP TO 9h!!!!

141
Q

Why would you give a fluid volume reducer prior to sx?

A

These are usually given in emergency sx, bc it’s likely the pt has just eaten.

142
Q

What is a fluid volume reducer?

A

Metoclopramide=dopamine antagonist

143
Q

What are common uses for anticholinergic agents?

A
  • Decr airway secretions
  • Sedative and amnesic effects
  • Anti-reflex bradycardia
144
Q

What are some common anticholinergic drugs?

A

Scoplamine, atropine, glycopyrrolate

145
Q

What is a anticholinergic reversal drug?

A

Physostigmine

146
Q

What is a widely used H2 receptor antagonist?

A

Ranitidine=last up to 9h!!!! and less SEs than cimetidine

147
Q

Must use clippers or razors in OR for getting rid of hair?

A

Clippers ONLY!

148
Q

What drug is used as an antacid?

A

Sodium citrate=nearly 100% effective in elevating gastric pH if administered 30min prior to induction

149
Q

Why is droperidol given?

A

It’s given at the end of procedure to prevent NV

150
Q

Why is clonidine given?

A

Prevents HTN and bradycardia produced by intubation and surgical trauma

151
Q

What is the most potent benzo?

A
  • Lorazepam

- It can be used for same-day sx or in-house sx

152
Q

What is a disadvantage to using diazepam as a sedative/hypnotic?

A

It has a long half-life (20-35h) so you don’t want them to have issues post-op

153
Q

Why do you not want to give a benzo in a pt w/ liver dz?

A

Bc they are metabilized in the liver

154
Q

Why is lorazepam “our friend”?

A

Bc it is eliminated in 10-15h and is 5-10X more potent than diazepam

155
Q

What can be given to replace dexamethasone prior to someone coming out of anesthesia?

A

Droperidol=stronger than dexa

156
Q

Which benzo has “no pain on injection”?

157
Q

Which drugs ARE NOT THE BEST for sedation?

A

OPIOIDS!!!!!!

158
Q

What’s the big issue w/ benadryl, post-op?

A

Drowsiniess

159
Q

What’s the big issue w/ opioids, post-op?

A

Constipation

160
Q

How long does morphine take to take effect?

A

15-30min and lasts 4 4h

161
Q

Where is meperidine metabolized?

A

Liver=do not give to someone w/ liver dz

162
Q

What is the 1st Korotkoff sound?

A

Systolic pressure

163
Q

What is the 5th Korotfoff cound?

A

Disatolic pressure

164
Q

What is Malignant Hyperthermia?

A
  • Incr in core body temp
  • Genetic predisposition
  • More common w/ GA
  • Anticholinergics BLOCK sweating
  • Incr BMR
  • Initial signs=Incr HR and CO2
165
Q

When is a Swan-Ganz catheter used?

A

When the pt is very sick. It’s good for infusion, cardiac pressure monitoring and CO measurements

166
Q

On EKG, what type of “wave” indicates ischemia?

A

Inverted T-waves

167
Q

On EKG, what type of wave indicates infarct?

A

ST segment elevation

168
Q

On EKG, what does ST segment depression represent?

A

Subendocardial infarction

169
Q

What type of nerve palsy are you worried about in the supine position?

A

Ulnar nerve palsy

170
Q

What type of nerve palsy are you worried about in the prone position?

A

Brachial plexus palsy

171
Q

What nerve issues are you worried about in the lateral decubitus position?

A
  • Brachial plexus
  • Lateral femoral cutaneous
  • Common fibular
172
Q

What antihistamines do you want to avoid in the geriatric population?

A

Promethazine, Chlorpheniramine, and Scopolamine

173
Q

SNS produces what kind of response?

A

Adrenergic

174
Q

PSNS produces what kind of response?

A

Cholinergic

175
Q

SNS pre-ganglionic fibers use what NT?

176
Q

PSNS pre-ganglionic fibers use what NT?

177
Q

SNS post-ganglionic fibers use what NT?

178
Q

PSNS post-ganglionic fibers use what NT?

179
Q

What are the 4 Anesthesia Stages?

A
  1. Analgesia
  2. Excitation
  3. Surgical Anesthesia
  4. Medullary Depression
180
Q

What Anesthesia Stage do we want to obtain?

A

Stage 3=Surgical Anesthesia–>light to deep anesthesia, reduced muscle tone, incr loss of ocular reflex, no response to skin incision

181
Q

What is the definition of sinus tachy? How is it tx?

A
  • HR > 120

- B-blockers

182
Q

What is the definition of sinus brady? How is it tx?

A
  • HR < 60

- Atropine

183
Q

What type of BBB is more clinically significant?

A

LBB. It’s seen in HTN, CAD, and LVH

184
Q

What is essential in a pt w/ apnea during sx?

A

Maintenance and monitoring or airway

185
Q

What does Halothane lack that causes ventricular arrhythmias?

A

An ether molecule

186
Q

Why are anesthetics halogenated w/ fluorine better?

A
  • Greater stability

- Resistant to metab

187
Q

What is the main advantage of Halothane? Disadvantage?

A
  • Faster induction and faster emersion

- Fulminant hepatic necrosis=halothane hepatitis

188
Q

What are the advantages of Isoflurane? Disadvantages?

A
  • NOT a/w cardiac arrhythmias, less metab than halothane and enflurane (stays in system longer), more rapid induction and emersion
  • Pugnent=impractical for inhalation
189
Q

What is the main disadvantage of Sevoflurane and Desflurane?

A

EXPENSIVE!!

190
Q

What is the MOA (general consensus) of inhaled anesthetics?

A

Ion channels:

  • Depress fxn of excitatory channels=prevent Na+ from entering neuron
  • Enhance inhibitory channels=Cl- ions enter thru GABA channels and K+ ions leave thru K+ channels
191
Q

Non-depolarizing Muscle relaxants are…(compared to Depolarizing MRs)

A
  • More potent
  • Have a longer onset (5-10min)
  • Have a longer duration of action (30-90min)
192
Q

What is the length of the Thyromental distance?

A

3 finger breaths

193
Q

How far is the endotracheal tube inserted?

A

1-2cm past the vocal cords

194
Q

During chest compressions (CPR), how far do you depress the sternum?

A

1.5-2 inches

195
Q

During CPR, how many compressions/min?

196
Q

ASA I

A

Normal healthy pt

197
Q

ASA II

A

Pt w/ mild systemic dz; no fxnal limitation

198
Q

ASA III

A

Pt w/ severe systemic dz, not incapacitating

199
Q

ASA IV

A

Pt w/ severe systemic dz that is a constant threat to life

200
Q

ASA V

A

A moribund pt who is not expected to survive w/o the operation

201
Q

ASA VI

A

Pt who is already pronounced brain-dead and whose organs are being removed for transplant

202
Q

ASA E

A

E=emergency, and is a modifier to the ASA classification system

203
Q

What are the 4 groups of adverse medication reactions?

A
  • Allergic (most common)=Abx
  • Toxic=halothane hepatitis
  • Pharmacologic=PONV from opioids or hypoventilation from sedatives
  • Genetic=malignant hyperthermia
204
Q

How long does a pt need to be NPO before sx?

A

At least 8 hours

205
Q

If pt at risk fr gout, when is colchicine given?

A

pre-op, intra-op, and post-op

206
Q

What is the most important factor in evaluating a pt’s EKG?

A

YOU MUST COMPARE IT TO THEIR MOST RECENT EKG (if applicable)

207
Q

What are the 5 cardinal manifestations of anesthesia?

A
  • Amnesia
  • Analgesia
  • Hypnosis
  • Blunting of autonomic reflexes
  • Muscle relaxation
208
Q

What are some advantages to SAB (Sub-Arachnoid Block)?

A
  • No airway manipulation
  • Decr # and amount of meds used
  • Reduction of surgical stress
  • Ideal for many surgical procedures
209
Q

What are some disadvantages of SAB (Sub-Arachnoid Block)?

A
  • SNS blockade=HYPOtension
  • Anxiety
  • “Failed” block
  • PDPH=Post-dural-puntcure-headache (usually young female, 20-40yo)
210
Q

What valvular dz is contraindicated for SAB?

A

Aortic stenosis. Anything <1 for valve area

211
Q

What type of block:

  • is based on mg of drug delivered, and
  • is also dependent on baricity
A

SAB (Sub-Arachnoid Block)

212
Q

What is baricity? Give an example

A

Baricity=density of a substance compared to the density of the pt’s CSF
-e.g., If a LA is more dense than CSF=hyperbaric, and anesthetic will SINK

213
Q

What type of block:

  • is base on volume injected, and
  • does NOT take into acct baricity
A

Epidural block

214
Q

In the spine, where is LA usually injected?

A

Levels T5 and L4

215
Q

Landmarks: L1

A

Iliac crest

216
Q

Landmarks: T10

217
Q

Landmarks: T8

A

Lower costal margin

218
Q

Landmarks: T6

A

Xiphoid process

219
Q

Landmarks: T4

A

Nipple line

220
Q

Landmarks: C8*

A

Little finger

*This is important bc there’s a high risk of anesthetizing the diaphragm (C3-5)

221
Q

What is an advantage to the slower onset of epidurals compared to SABs?

A

It’s easier to manage vitals

222
Q

What is the “first sign of hypotension” in SAP/Epidurals?

A

Nausea=fixing BP will fix nausea

223
Q

Can sx be performed on a pt with active cardiac dz?

A

Yes, if they are stable

224
Q

What is MAC (Monitored Anesthesia Care)?

A

A type of anesthesia allowing the pt to be sedated and to transition in and out of GA, if that is required by changes in pt or sx conditions

225
Q

In post-op recovery, how often is BP measured?

A

Every 5 min for the first 15 min, then every 15 min until d/c

226
Q

AAOx3 refers to what?

A

The pt being correctly oriented to time, place, and person

227
Q

How is post-op hypotension treated?

A

Fluid bolus or vasopressors

228
Q

How is post-op HTN treated?

A

Hydralazine (slow onset=15min) or propranolol (does not incr intracranial pressure)

229
Q

What is the first line of defense for post-op hypoxemia?

230
Q

What nerve roots make up the Femoral n?

231
Q

What nerve roots make up the Lumbar Plexus?

232
Q

What nerve roots make up the Sacral Plexus?

233
Q

What nerve roots make up the Sciatic n?

234
Q

What is a unique complication of a femoral n block?

A

Potential for fall 2ry to quadricep weakness

Surgery (2 decks)

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