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Semester 4 TxWes > Principles of Anesthesia II Unit II > Flashcards

Principles of Anesthesia II Unit II Flashcards

1
Q

Memory decline occurs in what percentage of people over 60?

A

40%

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2
Q

Neuronal shrinkage leads a decrease in what?

A

Decrease in grey matter

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3
Q

Decrease in white matter increases what in size?

A

Ventricular size

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4
Q

Decrease in white matter causes progressive loss of what?

A

Memory, balance, mobility

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5
Q

What neurotransmitter release is significantly reduced as you age? Which is not affected?

A

Dopamine, Ach, norepi and serotonin. Glutamate is unchanged.

CRMO, CBF and EEG are generally unchanged with age

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6
Q

What neuraxial changes occur as you age?

A

Decreased epidural space

Increased permeability of dura

Decreased volume of CSF

Decreased diameter/number of myelinated fibers in dorsal and ventral nerve roots

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7
Q

What PNS changes occur as you age?

A

Inter-Schwann cell distance decreased

Conduction velocity decreased

In general, elderly are more sensitive to neuraxial and peripheral blocks

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8
Q

What cardiac changes occur as you age?

A

Myocyte number decreases

LV wall thickens

SA node cells decrease – sensitive to tachy/brady arrhythmias

Conduction velocity decrease

Thickened and calcific aortic valve

Decreased contractility, increased ventricular stiffness (higher filling pressure)

Less beta-adrenergic sensitivity (less fight/flight response, you lose the ability to increase HR and CO during stress)

many of these changes are d/t increased afterload as you age

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9
Q

What increases vascular stiffness as you age?

A

Breakdown of collagen and elastin
Less NO related vasodilation
Early wave deflection…increased afterload, diastolic dysfunction

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10
Q

What pulmonary changes occur as you age?

A

Loss of elastic recoil and loss of surfactant = increase in lung compliance and decrease in elastic recoil

Enlarged bronchioles/alveolar ducts coupled with early collapse of small airways during exhalation = increase in anatomic dead space, increased closing capacity and impaired gas exchange

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11
Q

Lost of vertebral height and calcification of vertebrae lead to what pulmonary changes?

A

Barrel chest
Diaphragmatic flattening
Chest wall stiffness….increased work of breathing

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12
Q

How do VC, CC and RV change as you age?

A

VC decreases, CC increases and RV increases

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13
Q

How much does FEV1 decrease per decade?

A

6 - 8% d/t decrease in muscle mass and increase in CC

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14
Q

What relationship has the greatest effect on the alveolar-arterial oxygen gradient?

A

The relationship between FRC and CC, as the mismatch increases, shunt also increases and arterial oxygenation declines

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15
Q

How much does GFR decrease each decade after 30?

A

About 10% each decade

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16
Q

Why does aging reduce the body’s ability to adjust fluid and e-lytes?

A

The body has a blunted response to aldosterone, vasopressin, renin

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17
Q

Metabolism of drugs requiring what types of metabolism are affected by aging? What types of drug metabolism are not affected by aging?

A

Affected by aging: Phase I metabolism = oxidation, reduction, hydrolysis. Very common in narcotics and anesthetics

Not affected by aging: Phase II metabolism = acetylation and conjugation

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18
Q

What occurs to subQ fat as you age?

A

SubQ fat thins

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19
Q

How much does temperature change in the 60 - 80 year old range?

A

About 1 degree C less than infants/children/younger adults

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20
Q

What are the listed significant predictors of 6 - 12 month mortality?

A

Impaired cognition

Recent fall

Hypoalbuminemia

Anemia

Functional dependence

Comorbidities

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21
Q

Surgery and anesthesia cause peripheral inflammatory responses. In a vulnerable brain, what negative outcomes can occur because of this inflammaion?

A

Dysfunctional anti-inflammatory response leads to an exaggerated neuroinflammation and acceleration of AD pathology causing long-term cognitive decline

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22
Q

What are the neurotoxic factors that are the pathogenesis of dementia?

A

Amyloid B, Tau, calcium and neuroinflammation

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23
Q

How does amyloid B accumulate? Proposed MOA in causing neuro-degeneration?

A

It’s a fragment of synaptic origin - its released as synapses break down. The proposed MOA is they coagulate to form amyloid plaques that disrupt cell membranes over time

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24
Q

What is the relationship of temperature and Tau?

A

Decreases in temperature lead to increases in Tau

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25
Q

What is the primary MOA of Tau causing neuro-degeneration?

A

By causing neurofibrillary tangles/destabilizing microtubules

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26
Q

What is Tau?

A

Phosphorylated and aggregated T-protein

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27
Q

What biomarker increases earliest before cognitive impairment begins to show?

A

Amyloid-B accumulation (Slide 30)

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28
Q

What inflammatory markers contribute to cognitive decline?

A

Cytokines, IL-6 and TNFa

inflammation mitigating drugs such as dexamethasone, lidocaine and toradol may augment this

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29
Q

Why is propofol a great choice for anesthesia in the elderly?

A

Volatiles have a high incidence rate of cognitive decline/injury, whereas propofol has significantly less cognitive decline/injury chances

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30
Q

What risk factors appear to contribute to high chances of cognitive decline after surgery?

A

Increasing age, duration of anesthesia, lesser education, a second operation, postoperative infection and respiratory complications

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31
Q

What are the basic anesthesia strategies for the elderly?

A
  1. Using neuraxial/regional anesthesia when possible
  2. Avoid long-acting NMBD and reverse adequately
  3. Opioid sparing strategies
  4. Neutralization of stomach acid with non-particulates (Bictira)
  5. Consider using EEG based titration
  6. Avoid hypotension (Try to avoid massive drops in SVR)
  7. Pad skin and nerves
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32
Q

CO decreases as you age, how does this affect drug distribution/redistribution?

A

slower distribution to initial site of action
slower redistribution
slower distribution to metabolic organs

combined, this takes drugs longer to “kick in”

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33
Q

How does the NMJ change as you age?

A

Increased distance between the axon and motor end plate

Decrease in: concentration of Ach receptors, amount of Ach in presynaptic vesicle and release of Ach upon neuronal impulse

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34
Q

T/F: anesthetic drugs that are not metabolized by the kidney/liver have little to no changes to their metabolism as we age

A

True

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35
Q

How does drug metabolism that are dependent on the kidneys/liver change as you age?

A

Drugs dependent on this route of metabolism have: a prolongation of their effect, decreased need during maintenance phase and delayed recovery phase for non-depolarizers

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36
Q

If an elderly patient needs thoracic surgery, and has a history of poor exercise tolerance, CAD, DM or CHF, what would the next appropriate step be prior to surgery?

A

Myocardial perfusion imaging. If low risk is confirmed, proceed with surgery, if increased risk is confirmed, proceed with coronary angiography

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37
Q

How man total lung subsegments are there?

A

42

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38
Q

How many lung subsegments are in each lobe of the lungs?

A

LUL = 10
LLL = 10
RUL = 6
RML = 4
RLL = 12

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39
Q

If you preop FEV1 is 80%, and take out the entire right lung, what is the predicted FEV1?

A

22/42 = 0.5238
80 x (1 - 0.5238 / 100) = 0.38096 or ~38% FEV1

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40
Q

At what predicted FEV1 after thoracotomy would allow for extubation in the OR?

A

40% or greater

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41
Q

At what predicted FEV1 after thoracotomy would you require a V/Q scan, DLCO and consideration of other associated diseases before extubating in the OR?

A

FEV1 of 30 - 40%

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42
Q

At what predicted FEV1 after thoracotomy would you likely not extubate in the OR and send to ICU for staged weaning from the ventilator?

A

FEV1 of less than 30%

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43
Q

If FEV1 is greater than 20% after surgery, what intervention would potentially allow you to extubate?

A

Thoracic epidural analgesia

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44
Q

How many patients develop nosocomial infections?

A

~ 1/31 patients

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45
Q

What are the 2 most common nosocomial infections?

A

SSIs and hospital acquired PNA

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46
Q

What are the most “contaminated” or dirty environments on the patients skin?

A

Inguinal, perineal and axillary areas

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47
Q

What type of bacteria is most likely to migrate from the skin into the body (assuming a route to get into the body is present)?

A

Coagulase-negative Staphylococci

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48
Q

What percentage of nosocomial infections occur in surgical patients?

A

38%

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49
Q

What type of SSI is just in the area of the incision?

A

Superficial incisional

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50
Q

What type of SSI is beneath the incision area and is in the muscle and/or tissues surrounding muscles?

A

Deep incisional

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51
Q

What type of SSI is any area other than skin and muscle and includes organs or space between organs.

A

Organ or space SSI

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52
Q

What types of bacteria are common sources of an SSI?

A

Staphylococcus
Streptococcus
Pseudomonas

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53
Q

What type of wound is not inflamed or contaminated; don’t involve internal organ

A

Clean

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54
Q

What type of wound has no evidence of infection; but does involve internal organ(s)?

A

Clean-contaminated

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55
Q

What type of wound does involve internal organ with spillage of contents from the organ?

A

Contaminated

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56
Q

What type of wound is a known infection at the time of surgery?

A

Dirty

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57
Q

What length of surgery increases SSI risk?

A

Surgery greater than 2 hours in length

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58
Q

What 2 types of surgery increase SSI risk?

A

Emergency and abdominal surgery

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59
Q

Approximately how many SSIs are preventable?

A

About half

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60
Q

List the grading categories of evidence for SSI prevention

A

1A: strongly recommended; moderate-to high quality of evidence

1B: strong recommendation; low quality evidence

1C: strong recommendation required by state/federal regulation

II: weak recommendation;

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61
Q

What SSI strategies are 1A level of evidence?

A

Perioperative control of BG, keep BG under 200, maintain normothermia, use an alcohol based antiseptic for skin preparation, and if pulmonary function is normal increase FiO2 after extubation (this step is controversial, see slide 24)

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62
Q

What is the most common indication for a total knee arthroplasty revision?

A

Infection

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63
Q

What is MIC?

A

Minimum inhibitory concentration of ABX in the serum and tissues

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64
Q

Why should you give ancef within 30 minutes of incision and not 1 hour?

A

If you give it 1 hour before, you will likely have to redose during the surgery

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65
Q

What are the general principles when choosing an anti-biotic?

A
  1. should be active against common surgical wound pathogens
  2. proven efficacy in clinical trials
  3. must achieve MIC in the serum and tissues
  4. shortest possible course effective….ideally 1 dose
  5. newer antibiotics reserved for resistant infections
  6. if everything equal: give oldest/cheapest
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66
Q

What antibiotics should be given within 2 hours of first incision, not 15 - 60 minutes?

A

Vanco and fluoroquinolones

So they are usually given in pre-op. Also of note, on the SCIP powerpoint slide 10, Cornholio says Clindamycin (a macrolide) is another antibiotic that is given with 2 hours of incision

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67
Q

What must be done with ABX prior to tourniquet use?

A

The antibiotic must be completely infused prior to tourniquet use

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68
Q

What is the general redosing interval for ABX?

A

2 half lives or excessive blood loss. May also be redosed s/p CBP

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69
Q

What are some beta lactam ABX?

A

Penicillins
Cephalosporins
Carbapenems

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70
Q

Gentamycin is what class of antiobiotic?

A

Aminoglycoside

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71
Q

Cipro is what class of antibiotic?

A

Fluroquinolone

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72
Q

How do penicillins/beta lactams work?

A

Inhibit bacterial cell wall synthesis

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73
Q

What is the DOC for streptococci, meningococci, pneumococci?

A

Penicillins-beta lactams

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74
Q

Penicillin G, Methicillin, Nafcillin and Amoxicillin are what class of ABX?

A

Penicillins-beta lactams

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75
Q

What bacteria are commonly causative agents for skin infections, catheter infections or URIs?

A

Gram + bacteria like streptococci, meningococci, pneumococci

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76
Q

What antibiotic class is the DOC for surgical prophylaxis?

A

Cephalosporins

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77
Q

Cefepime is what generation of cephalosporin?

A

Gen 4

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78
Q

Ceftriaxone (Rocephin), Ceftazidime (Fortaz) and Cefotaxime (Claforan) are what generation of cephalosporin?

A

Gen 3

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79
Q

Cefuroxime (Zinacef), Cefoxitin (Mefoxin) and Cefotetan (Cefotan) are what generation of cephalosporin?

A

Gen 2

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80
Q

Cefazolin (Ancef) is what generation of cephalosporin?

A

Gen 1

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81
Q

What generations of cephalosporins may be able to cross the BBB?

A

Gen 3 and 4

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82
Q

Anaphylaxis to what antibiotic class increases the chances of a reaction to a cephalosporin?

A

Penicillin

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83
Q

What antibiotic(s) is indicated if you have a true anaphylaxis allergy to cephalosporins?

A

Vancomycin or clindamycin

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84
Q

What class of antibiotics are effective against gram - rods such as enterobacter or P aeruginosa?

A

Carbapenems

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85
Q

What are our last line agents for intra-abdominal, resistant UTI’s and PNA’s?

A

Carbapenems

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86
Q

T/F: Most carbapenems penetrate the BBB?

A

True

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87
Q

What medication may be a contraindication to using a carbapenem?

A

Valproic acid (Depakote) as carbapenems can decrease it up to 90%

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88
Q

IM formulations of carbapenems have what allergy concern?

A

LA allergies as they contain lidocaine (so amide allergy concerns)

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89
Q

What type of bacteria does vancomycin work well against?

A

Gram + (vanco is too large to penetrate gram - walls). It also only works if the bacteria is actively dividing

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90
Q

What infections is vancomycin particularly useful for?

A

Blood stream infections and endocarditis caused by MRSA

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91
Q

What antibiotic class inhibits ribosomal proteins and causes mRNA to be misread?

A

Aminoglycosides

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92
Q

What antibiotic class has a very long half life?

A

Aminoglycosides

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93
Q

Aminoglycosides have a synergistic effect with what antibiotic classes?

A

Beta lactams and vancomycin (very useful in enterococcal endocarditis)

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94
Q

What s/e are common to aminoglycosides?

A

Ototoxicity (very common), nephrotoxicity and a curare like effect

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95
Q

What antibiotic class inhibits DNA protein synthesis?

A

Fluoroquinolones

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96
Q

Fluoroquinolones are good for what kinds of organisms?

A

Gram -. Common in GU surgery, UTIs, bacterial diarrhea and bone/joint infections

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97
Q

What antibiotic class can prolong the QT interval and cause cartilage damage/tendon rupture?

A

Fluoroquinolones

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98
Q

What antibiotic is an Antiprotozoal /Anaerobic antibacterial?

A

Metronidazole

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99
Q

What antibiotic works by forming toxic byproducts that cause unstable DNA molecules?

A

Metronidazole

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100
Q

What is metronidazole generally indicated for?

A

Intra-abdominal infections
Vaginitis
C-diff

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101
Q

What antibiotic can cause peripheral neuropathy and have a disulfiram-like effect with alcohol?

A

Metronidazole

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102
Q

If ancef is contraindicated d/t allergy concerns for cardiac/vascular/thoracic surgery, what are the secondary antibiotic options?

A

Clindamycin or vancomycin

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103
Q

What was the original goal of the SIP?

A

Decrease morbidity and mortality of SSI

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104
Q

What are the performance measures of the SIP?

A

Proportion of pts who get abx started within 1 hr of incision

Proportion given abx regimen consistent with guidelines

Proportion of pts whose abx is discontinued within 24 hrs of surgery stop

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105
Q

Explain the reasoning for this: For the SIP goals, we want to start ABX early/often, but stop them in a timely manner, generally within 24 hours.

A

Appropriate timing/dosing of ABX can reduce SSI incidence, but we also want to limit duration to reduce the chances of bacterial resistance

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106
Q

What is the primary goal of the SCIP?

A

To reduce surgical mortality/morbidity

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107
Q

In general, what timeframe do we stop antibiotics? What is the exception?

A

Within 24 hours. The exception is cardiac surgery which is within 48 hours

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108
Q

What is the timeframe to restart BBs for someone on chronic BB therapy?

A

Within 24 hours

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109
Q

T/F: Razors are an appropriate measure to get rid of hair from the surgical site

A

False. Clippers only.

This is because razors can cause small wounds in the skin that allow for bacterial contamination.

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110
Q

If there is not a reason to keep a surgical foley, when should it be dc’d?

A

On or before POD 2

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111
Q

What are the SCIP BG goals for cardiac patients?

A

Get to or less than 180 within 18 - 24 hours after anesthesia ends

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112
Q

What are the SCIP DVT measures?

A

SCDs placed during surgery for all procedures >/= 1 hr

Orders for appropriate DVT prophylaxis on the postoperative admission orders (Unless documentation criteria for not administering pharmacologic and mechanical prophylaxis)

RN administration of the appropriate DVT prophylaxis within 24 hours of surgery end

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113
Q

What is the goal PACU temperature after surgery?

A

Greater than 96.8 (or rather, goal temperature greater than 96.8 within 15 minutes of leaving the OR)

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114
Q

What is the temperature difference from axillary vs an oral/core temperature?

A

A 0.5 - 1 degree F difference, axillary is cooler relative to oral/core

A temporal temperature is similar to the axillary temperature in that it is also 0.5 - 1 degree F lower than an oral/core

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115
Q

What ingested material(s) requires a minimum 4 hour fasting period?

A

Breast milk

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116
Q

What ingested material(s) requires a minimum 6 hour fasting period?

A

Infant formula, non-human milk and a light meal

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117
Q

What ingested material(s) requires a minimum 8 hour fasting period?

A

Fried foods, fatty foods and meat

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118
Q

What are 4 basic goals to accomplish in pre-op?

A

Perform an H/P, ensure NPO status, explain the anesthesia choice and what to expect in the OR, set expectations for post-op recovery/pain control

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119
Q

What are the 2 big patient complaints from surgery?

A

Pain and N/V

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120
Q

If a patient has been on bowel prep, approximately how much fluid do you add to their fluid deficit?

A

2 - 3L

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121
Q

4-2-1 refresher: what is the fluid replacement rate for a 135 kg patient?

A

(4 x 10) + (2 x 10) + (1 x 115) = 175 ml/hr

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122
Q

How much fluid is lost d/t insensible losses?

A

4 - 8 ml/kg/hr

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123
Q

What is the ratio of fluid to replace blood loss?

A

3 ml of crystalloid per 1 ml of blood lost, or 3:1

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124
Q

What class of medications act on both the spinal cord and the brain to mitigate pain?

A

Opioids and A2 agonists

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125
Q

What is the standard concentration of IVP precedex?

A

4 mcg/ml

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126
Q

What are the 2 primary concerns with Toradol administration?

A

Bleeding and kidney injury

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127
Q

Why does NGT suction not prevent/reduce aspiration events?

A

Studies showed prophylactic NGT suction does not reduce aspiration events, furthermore, you can still aspirate because the NGT keeps the esophageal sphincter open

128
Q

PONV prophylaxis refresher: what are the risk factors for PONV?

A

Female, non-smoker, young, length of anesthesia, opioid use and history of PONV/motion sickness

129
Q

At what risk level of PONV is the use of 2 or 3 agents from different classes warranted to prevent PONV?

A

High risk for PONV

130
Q

(Because my fish brain struggles to remember acronyms) what does ERAS stand for?

A

Enhanced Recovery After Surgery

131
Q

What are the pre-op “must haves” for ERAS?

A

Pre-Operative- Formal, pre-surgical patient education and/or counseling

Risk assessment – intervention with standardized optimization

132
Q

What are the Intra-op “must haves” for ERAS?

A

Limited fasting, carbohydrate rich drink up to 2 hrs before surgery

Opioid sparing, multimodal analgesia that continues through discharge

133
Q

What are the post-op “must haves” for ERAS?

A

Ambulation w/in 8 hrs of surgery stop time

Formal discharge education that includes incision care and mobility recommendations

134
Q

Should education about a surgery vary based on the surgeon?

A

No, it should be formal patient centered and remains consistent regardless of the surgeon

you MUST document the educational process

135
Q

The STRONG for Surgery checklist mentions 4 things a patient should do to prep for surgery, what are they?

A

Eat well, quit smoking, control your BG and ensure the healthcare team knows about all medications you are taking

136
Q

What interventions may be warranted if you Hgb drops below 11.5 prior to surgery?

A

Start iron and/or EPO (erythropoietin)

137
Q

At what BMI is surgery generally avoided?

A

A BMI greater than 40

138
Q

What is required during the intra-op phase (think newer school of thinking)?

A

Limit fasting and carb rich beverage up to 2 hours prior to surgery and use opioid sparing multimodal analgesia

139
Q

List the steps of the catabolic pathway

A

Post op lean tissue loss -> increase in IL 1 and IL 6 -> increase in cortisol, glucagon and GH -> catecholamine surge -> increase in gluconeogenesis -> decreased glucose uptake -> immunosuppression and insulin resistance

140
Q

CHO loading (carb loading with carbohydrate drinks) resulted in what post-operative events?

A

Improved insulin resistance, improved patient comfort (less thirst, hunger), no conclusions on preservation of muscle mass, no aspiration events and “probably safe”

141
Q

Based on the Penn neurosurgery ERAS multi-modal protocol, what medication is given in pre-op only?

A

Gabapentin

142
Q

What are the “suggested” post-op phase goals?

A

Early nutrition (eat in chair, not bed), post-DC call within 7 days (discuss pain, concerns, incisions and clarify post-op instructions) and a follow up clinic visit within 14 days

143
Q

What type of crystalloid should we generally avoid giving in the OR?

A

NS

144
Q

What is the Clearsight monitor?

A

A non-invasive BP cuff that sits on your finger and mimics an arterial line

145
Q

What have recent studies shown occur if a patient is not ordered a bowel prep prior to a surgery that normally uses one?

A

They have an earlier return of bowel function, shorter hospital stay with no difference in the rate of anastomotic leaks or wound infections

146
Q

Carbohydrate loading up to 2 hours prior to surgery is associated with what outcomes?

A

Rate of pulmonary aspiration has not increased
Reduced thirst, hunger, anxiety
Reduced insulin resistance
More muscle strength and lean body mass
Accelerated recovery
Shorter hospital stay

147
Q

What regional anesthesia may be helpful in thoracic surgery?

A

Erector spinae or a TAP block

148
Q

What regional anesthesia may be helpful in abdominal surgery?

A

a Quadratus lumborum or TAP block

149
Q

The multi-modal PONV prophylaxis chart says medium risk dictates use of how many interventions? High risk?

A

Medium = 1 - 2 interventions
High = 2+ interventions

150
Q

What does standard 2 of the PACU dictate that anesthesia staff must do?

A

A member of the anesthesia team who is knowledgeable about the patient’s condition must accompany the patient to PACU

151
Q

What should be done with the patient upon arrival to PACU?

A

Assess the airway, vitals, mental status, pain and PONV. If hypoxemic assess and treat. Connect to the PACU monitors

152
Q

What are some common causes/risk factors for hypoxia in the PACU?

A

Room air, Obesity, Sedation, Respiratory rate, advanced age (> 60)

153
Q

How many phases of recovery are there in the PACU?

A

2

154
Q

What phase is the immediate post-op recovery phase?

A

Phase I

155
Q

How is phase I different from phase II in anesthesia recovery?

A

It is the more “intense” phase, vitals and airway patency are rigorously monitored. If intubated, neuromuscular function is also monitored.

156
Q

How frequently are VS done during phase I?

A

q5m for the first 15 minutes, then q15m throughout phase I

157
Q

What are the 3 primary scores used to determine if the patient is appropriate for d/c from phase II?

A

Standard Aldrete Score.

Modified Aldrete Score.

Postanthesia Discharge Score.

158
Q

What factors does the standard aldrete score measure?

A

Activity, respiration, circulation, consciousness and oxygen saturation

all are scored on a scale of 0 - 2, the higher the score the safer the patient is for D/C

159
Q

Determine the standard aldrete score: The patient is moving their legs, is shallowly breathing, pre-op BP was 130/80 and is currently 118/65, is arousable and is currently 94% on RA

A

7

160
Q

Determine the standard aldrete score: The patient is not moving, has a poor respiratory drive, the current BP is 102/55 and was 157/78 in pre-op, is arousable and is satting 91% on 15L NRB

A

4

The respiratory drive, though poor, is still breathing so the get a score of 1 for respiration

161
Q

What does the post-anesthesia discharges scoring system measure?

A

VS (BP/HR), activity, N/V, Pain and Bleeding

162
Q

Determine the post-anesthesia discharge score: BP and HR are 92/40 and 55, in pre-op it was 101/55 and 62, has no trouble ambulating, is nauseous but not vomiting with PO zofran, reports that the PO pain meds are not adequate and you have had to change the surgical dressing twice

A

8

163
Q

Determine the post-anesthesia discharge score: BP and HR are 127/91 and 88, pre-op they were 166/87, patient needed help to get to the bathroom, reports recurrent nausea with PO and IM medication, says pain is acceptable and has required 1 dressing change

A

6

164
Q

How does phase II differ from phase I?

A

Vitals taken every 30 - 60 minutes.
Monitor:
Airway and ventilation status.
Pain level & PONV.
Fluid balance.
Integrity of the wound.

165
Q

Per lecture, what are the 3 most common complications in the PACU (reference slide 24)?

A

N/V, upper airway support is needed and hypotension

166
Q

Other than a history of HTN, what are some common reasons for HTN in the PACU?

A

Pain and urinary retention

167
Q

What pharmacologic intervention could help resolve airway obstruction without giving a paralytic?

A

A small dose of propofol

Have a low threshold for further intervention, if you give the low dose propofol, and are even slightly uncomfortable with how the patient is breathing, continue scaling up interventions

168
Q

What are the patient related risk factors for airway complications?

A

COPD, Asthma, OSA, obesity, heart failure, Pulmonary HTN, Upper respiratory tract infection, tobacco use, & higher ASA score.

169
Q

What are the procedure related risk factors for airway complications?

A

Surgery near diaphragm, ENT procedures, severe incisional pain, IV fluids, long procedure (3 hours).

170
Q

What are the anesthetic related risk factors for airway complications?

A

General, muscle relaxers, administration of opioids.

171
Q

What are the common causes of airway obstruction? Treatment?

A

Cause = loss of pharyngeal muscle tone and paradoxical breathing (chest wall moves in on inspiration and out during expiration)

Tx: Jaw thrust, continuous positive airway pressure and an OPA/NPA

172
Q

Common causes of laryngospasms?

A

Stimulation of pharynx or vocal cords.

Secretions, blood, foreign material.

Regular extubations.

173
Q

Other than hypoxemia and loss of the airway, what is a major concern of a laryngospasm?

A

Negative pressure pulmonary edema

174
Q

What is the timeframe for negative pressure pulmonary edema to resolve?

A

Generally in 12 - 48 hours

175
Q

What is the most common cause of negative pressure pulmonary edema?

A

Laryngospasm, followed closely by breathing against a closed airway tube (think the patient trying to breath while biting on the tube)

176
Q

The stimulation of what nerve can cause exaggerated closure of the glottis?

A

The superior laryngeal nerve

177
Q

What early s/sx can indicate laryngospasm?

A

Early = faint inspiratory stridor d/t increased respiratory effort and increased diaphragmatic excursion along with flailing of the lower ribs

later sign is “fish out of water”

178
Q

What steps do you take if laryngospasm occurs?

A

Get help in the OR,
Apply the facemask on the patient with a very tight seal. 100% FiO2, close your APL valve to about 40 cm H2O. Do NOT squeze the bag - wait for them to breath.

Suction airway.

Chin lift/jaw thrust, oral or nasal airways.

Pressure on the “laryngospasm notch”.

179
Q

What is the primary risk of applying pressure to Larson’s point?

A

Jaw dislocation

Larson’s point is another name for the laryngospasm notch

180
Q

Describe how to apply pressure to Larson’s point to help treat a laryngospasm

A

Forcible jaw thrust with bilateral digital pressure resolves the spasm by clearing airway and stimulation.

Apply for 3-5 seconds, then release for 5-10 seconds, while maintaining tight seal with the facemask

181
Q

If you can’t break the laryngospasm, what are the appropriate next steps?

A

Atropine, Propofol, Succinylcholine.
Re-Intubate.

182
Q

Airway edema is generally associated with what?

A

Prolonged intubation or long surgical procedures in the prone or Trendelenburg position.

Cases with large blood loss = aggressive fluid resuscitation.

Facial and scleral edema alert the CRNA that the patient most likely has airway edema.

183
Q

If you suspect airway edema, what test should you do before extubating the patient?

A

ETT cuff leak test

184
Q

What surgeries carry the highest risk of airway hematoma?

A

Thyroid and carotid

185
Q

What physical s/sx may indicate an airway hematoma is forming?

A

Can see deviated trachea & compression of the trachea below the level of the cricoid cartilage.

186
Q

Treatment of airway hematoma?

A

Decompress the airway by releasing the clips or sutures on surgical incision, subcutaneous clot removed before attempting reintubation.

Re-intubate - have advanced airway equipment ready.

Surgical backup - tracheostomy.

Be very judicious if you release the surgical site, if you release sutures on a carotid and it opens up, you will bleed out very quickly

187
Q

Vocal cord palsy is associated with what surgeries?

A

Otolaryngologic surgery, thyroidectomy, parathyroidectomy, rigid bronchoscopy, over inflated ETT cuff

188
Q

Upon direct laryngoscopy, you notice the vocal cords appear wavy, what does this indicate?

A

There is loss of tension to the vocal cord, which indicates damage to the external branch of the superior laryngeal nerve

The cricothyroid muscle may also be paralyzed

189
Q

If bilateral recurrent laryngeal nerve damage has occurred, when are the vocal cords most likely to cause an obstruction?

A

During inspiration

190
Q

After thyroid surgery, what timeframe can hypocalcemia occur?

A

24 - 48 hours post-op

191
Q

What are the 2 classic s/sx of hypocalcemia?

A

Chvostek’s sign = facial spasm
Trousseau’s sign = carpal spasm

192
Q

Per lecture, what evaluation of return of muscle function did Cornelius spend time explaining as a solid indicator of adequate reversal, though not definitive?

A

Holding up the head for 5 seconds

193
Q

What type of extubation should you avoid if a patient has a history of OSA?

A

Deep extubation - you want them as awake as possible

194
Q

What questionnaire evaluates sleep apnea?

A

STOP-BANG

195
Q

What does STOP-BANG measure (list out each part)?

A

S = snore
T = tired/sleepy during the day
O = observed a stoppage of breathing by someone else
P = pressure, HTN
B = BMI over 35
A = age over 50
N = neck circumference greater than 16 inches
G = gender, male

196
Q

What is low, medium, and high risk of OSA on the STOP-BANG?

A

Low = 0 - 2
Med = 3 - 4
High = 5 - 8

197
Q

What is the common cause of diffusion hypoxia?

A

Nitrous oxide

it dilutes alveolar gas, including oxygen and CO2 which can decrease both PAO2 and PaCO2

198
Q

Why does diffusion hypoxia cause such profound hypoxia?

A

Because it dilutes oxygen (self explanatory why this is bad) but it also reduces PaCO2, which can depress the drive to breathe.

quite the double whammy

199
Q

In the absence of oxygen, how long does diffusion hypoxia generally persist?

A

5 - 10 minutes after DC of nitrous oxide

200
Q

What are some common causes of systemic HTN in PACU?

A

Emergence excitement, shivering, hypercapnia, pain, agitation, bowel distention, urinary retention

201
Q

Treatment of HTN in PACU?

A

Treat the underlying cause first (pain, agitation, full bladder etc), if you are confident there are no other underlying causes, then treat with: Labetalol, Hydralazine and/or Metoprolol

202
Q

What are the 3 most common drugs used to treat HTN in the PACU (include dosage range)? Which one can be given in consecutive doses in a short timeframe?

A

Labetalol 5 - 25 mg
Hydralazine 5 - 10 mg
Metoprolol 1 - 5 mg

Labetalol can have several doses in a short timeframe

203
Q

What type of hypotension is caused by decreased preload?

A

Hypovolemic

204
Q

What type of hypotension is caused by decreased afterload?

A

Distributive

205
Q

What type of hypotension is caused by intrinsic pump failure?

A

Cardiogenic

206
Q

What are some common causes of decreased pre-load relative to surgery and anesthesia?

A

Third spacing.

Inadequate intraoperative IV fluid replacement.

Loss of sympathetic nervous system tone due to neuraxial blockade.

Ongoing bleeding.

207
Q

What are some common causes of distributive shock?

A

Decreased afterload from: Sepsis, allergic reactions, critical illness and iatrogenic sympathectomy

208
Q

What are the primary types of allergic reactions (define them as well)?

A

Anaphylactic = an IgE mediated immune response that occurs when the body rapidly releases mediators from mast cells and basophils in response to an allergen

Anaphylactoid = an IgE independent reaction that occurs when mast cells and basophils release mediators due to non-IgE-mediated triggering events

In both cases, epinephrine is generally the initial treatment

209
Q

What drug class most commonly causes anaphylactic reactions and why?

A

Muscle relaxants like Rocuronium because they contain quaternary ammonium compounds

210
Q

What are the 3 most common allergic reactions in the hospital?

A

Allergic reactions to: muscle relaxants, rubber latex and antibiotics

211
Q

GETA masks many of the s/sx of an allergic reaction, what is the one reaction mentioned in lecture that can be easily identified?

A

Increase in airway pressure

212
Q

What populations are at risk for developing a latex allergy?

A

Repeated exposure people, those who have had numerous surgeries, spina bifida patients and us

213
Q

What type of reactions can cause latex mediated reactions?

A

Irritant contact dermatitis.
Type IV cell - mediated reactions.
Type I IgE - mediated hypersensitivity reactions

214
Q

What class of abx most commonly have allergic reactions?

A

Penicillin

215
Q

3 common causes of intrinsic pump failure?

A

Myocardial ischemia & infarctions.
Cardiac tamponade.
Cardiac dysrhythmias.

216
Q

What leads do you want to use to monitor for myocardial ischemia?

A

II and V5

217
Q

Common causes of cardiac dysrhythmias?

A

Hypoxemia.
Hypoventilation.
Endogenous and exogenous catecholamines.
Electrolyte abnormalities.
Anemia.
Fluid overload.

218
Q

What types of surgery have a higher incidence rate of atrial dysrhythmias?

A

Cardiac and thoracic surgery

219
Q

What is the treatment of new onset stable vs unstable A Fib?

A

Stable = rate control with CCBs or BBs

Unstable = cardioversion

do NOT cardiovert chronic A. Fib even if unstable d/t atrial clot concerns

220
Q

What 2 factors commonly contribute to PVCs?

A

A mixture of underlying pathology and hypoxia

221
Q

A spinal block can cause a brady dysrhythmia when it reaches what spinal level? Why?

A

T1-4, this is there the cardio accelerator fibers are, and blockade of them = profound bradycardia

222
Q

Risk factors for postoperative cognitive dysfunction?

A

Advanced age > 70 years old.
Preoperative cognitive impairment.
Decreased functional status.
Alcohol abuse.

223
Q

What Intra-operative factors are associated with delirium?

A

Surgical blood loss (hematocrit < 30% & increased number of intra-operative blood transfusions).

Periods of hypotension.

Administration of nitrous oxide and volatiles.

Anesthetic technique (general vs regional, propofol based also has a lower rate of delirium)

224
Q

If the surgery is minor, what may help reduce the chance of post-op delirium in an elderly patient?

A

Do the surgery outpatient in a surgery center (they return home faster which may help stabilize their mental state).

225
Q

What interventions should you do if delayed awakening occurs?

A

Evaluate the vital signs. Too high ETCO2 = sleepy patient.

Perform neurological exam.

Monitor patient’s oxygenation status.

Send lab for potential electrolyte abnormalities or high or low glucose concentrations.

226
Q

What is the most common cause of delayed awakening?

A

Residual sedation from the anesthetic

227
Q

What is the common s/e from over administration of flumenazail and narcan?

A

Seizure

228
Q

What drug can you use to treat over administration of scopolamine?

A

Physostigmine

229
Q

List the dosage of: narcan, flumenazil and physostigmine

A

Narcan: 20 - 40 mcg
Flumenazil: 0.2 mg
Physostigmine: 0.5 - 2 mg IV

230
Q

Repeated exposure to volatiles increases the chances of cognitive decline/dementia via what mechanism?

A

Increase in phosphorylated tau protein

231
Q

What type of pain affects skin, subQ tissue and mucous membraines?

A

Somatic (specifically, this is superficial somatic pain)

It may also affect deep muscles, tendons, joints and bones or deep somatic pain

232
Q

What pain is generally more organ related?

A

Visceral

233
Q

What specific type of pain is localized to the area around the organ?

A

Visceral parietal pain

234
Q

What specific type of pain is cutaneous pain that converges with visceral and somatic afferent input into the CNS?

A

Visceral referred pain

235
Q

What are the 3 phases of pain?

A

Acute, chronic nociceptive and neuropathic pain

These are non-exclusive, you could have 1 or any combination of the 3

236
Q

What are the pain “red flags?”

A

Constitutional symptoms (pain with loss of bowel/bladder problems)

Pain that wakes patient up

Immunosuppression

Severe or progressive neurologic deficit

Cold, pale mottled or cyanotic limb

New bowel/bladder dysfunction

Severe abdominal pain or signs of shock/peritonitis

237
Q

The theory that the intensity of pain is directly related to the amount/degree of tissue injury is what pain theory?

A

The specificity theory (the theory was made by Rene Descartes)

238
Q

What is the theory that states that pain is more of an emotional experience rather than sensory?

A

Intensity theory - defined by Plato

Think stoicism; you have to “grin and bear it”

239
Q

What is the more modern theory of how pain transmission works?

A

The gate control theory of pain

240
Q

Surgery releases what pain/inflammation related mediators?

A

Peptides (bradykinin), Lipids (prostaglandins), & Neurotransmitters (serotonin).

241
Q

What nerves make up our nociceptors?

A

They are afferent nerve endings of myelinated A-delta & unmyelinated C fibers

242
Q

Where would you find first order neurons?

A

In the periphery and entering into the spinal

243
Q

Where would you find second order neurons?

A

In the spinal cord contralateral to the peripheral entry point and ascends via the spinothalamic tract to the thalamus

244
Q

Where would you find third order neurons?

A

In the thalamus ascending to the cortex

245
Q

Pain related nerves ascend in what part of the spinal cord?

A

In the spinothalamic tract

246
Q

Third order neurons project from the thalamus to what?

A

The internal capsule and then to the post-central gyrus of the cerebral cortex

247
Q

List the 4 elements of pain processing and where they occur

A

Transduction - In the periphery, converting stimulus into an AP

Transmission - the AP is conducted from the periphery to the spinal cord

Modulation - the pain transmission can be altered in the spinal cord

Perception - the pain is the integrated in the somatosensory and limbic cortices in the brain

248
Q

Define allodynia and hyperalgesia

A

Allodynia = A stimulus that is NOT normally painful becomes painful

Hyperalgesia = An exaggerated response to a painful stimuli

249
Q

Increased excitability of neurons in the CNS due to glutamate activation of the N-methyl-D-aspartate (NMDA) receptors is what type of hyperalgesia?

A

Secondary

250
Q

Augmented sensitivity to painful response or allodynia misinterpretation of non-painful stimulation is what type of hyperalgesia?

A

Primary

251
Q

What is the hallmark of neuropathy?

A

Numbness from complete denervation of a body part

252
Q

How does aging affect drug distribution?

A

There is an increase in body fat percentage and a decrease in muscle mass, total body water and albumin

253
Q

What 2 factors from aging decrease the liver’s ability to eliminate drugs?

A

Decreased hepatic blood flow and a decrease in liver mass/intrinsic metabolic activity

254
Q

What decreases the kidney’s ability to excrete drugs as you age?

A

Decrease in blood flow, kidney mass, number of functioning nephrons

Decrease in glomerular filtration rate‐ considered one of the most important changes with aging

255
Q

T/F: Non-opioid analgesics act centrally

A

False - they act peripherally

256
Q

T/F: Opioid analgesics have a ceiling effect

A

False

non-opiods do have a ceiling effect, increasing a dose of say tylenol will not increase it’s pain reduction but you will get a higher/more severe incidence rate of s/e

257
Q

What opioid receptor(s) only has analgesia as a response to binding?

A

Delta

258
Q

What opioid receptor(s) have respiratory depression as a response to binding?

A

Mu and Kappa

259
Q

What opioid receptor(s) have euphoria as a response to binding?

A

Mu

260
Q

What opioid receptor(s) have miosis as a response to binding?

A

Kappa

261
Q

What opioid receptor has Analgesia, respiratory depression, euphoria, and reduced GI motility as a response to binding?

A

Mu

262
Q

What opioid receptor has Analgesia, dysphoria, psychosis, delusion/delirium, miosis, respiratory depression
as a response to binding?

A

Kappa

263
Q

What opioid receptors would you want to target if you wanted to avoid reduced GI motility?

A

Kappa and Delta

264
Q

What opioid receptors would you target if you wanted to avoid delirium?

A

Mu and Delta

265
Q

What opioid has more than 50 polymorphisms resulting in a variability of analgesia?

A

Codeine

266
Q

What opioid should be avoided in children less than 12?

A

Codeine - because at that age the enzyme to process codeine is not fully mature, meaning you get no analgesia but get all the lovely s/e

267
Q

If 30 mg of codeine is insufficient for analgesia, is it appropriate to upscale the dose?

A

Generally no as the analgesic effect of codeine does not increase appreciably with an increased dose

268
Q

What opioid is contraindicated if you have acute/severe asthma?

A

Codeine

269
Q

What opioid inhibits norepinephrine reuptake, opposes serotonin reuptake and simulates a2 receptors?

A

Tramadol

270
Q

What opioid is problematic for its potential to create hypotension if the patient undergoes anesthesia?

A

Tramadol (it reduces norepinephrine reuptake, opposes serotonin reuptake and simulates a2 receptors, all of which can cause hypotension)

271
Q

What opioid is contraindicated if you have seizure disorder?

A

Tramadol

272
Q

What opioid has a low incidence rate of dependence/tolerance/addiction?

A

Tramadol

273
Q

What opioid is ideal if you want to avoid constipation?

A

Tramadol

274
Q

What opioid should be avoided if PONV is a concern?

A

Tramadol

275
Q

What opioid is primarily metabolized via conjugation with glucuronic acid in both the liver and kidneys?

A

Morphine

275
Q

What is the ratio of oral morphine to equivalent IV/IM dose?

A

3:1

so 30 mg of PO morphine is equivalent to 10 mg of IV morphine

276
Q

What metabolite of morphine contributes to analgesia?

A

Morphine-6-glucuronide

277
Q

What metabolite of morphine contributes to adverse effects like neurotoxicity and hyperalgesia?

A

Morphine-3-glucuronide

278
Q

What 3 factors make morphine be poorly absorbed into the CNS?

A

Poor lipid solubility, highly protein bound and highly ionized at physiologic pH

279
Q

What opioid has greater analgesic potency and slower offset in women?

A

Morphine

280
Q

What opioid is contraindicated in renal impairment?

A

Morphine - it’s metabolites are metabolized by both the liver and kidneys, if the kidneys aren’t working, toxic metabolites can accumulate and cause respiratory depression

hydromorphone may also accumulate with renal insufficiency because of its toxic metabolite, but the risk is much higher with morphine

281
Q

What opioid is subject to an extensive first pass effect?

A

Oxycodone

282
Q

What opioid is primarily a prodrug?

A

Oxycodone

283
Q

What opioid has a very long and unpredictable terminal half life?

A

Methadone

284
Q

What opioid is a weak non-competitive NMDA receptor antagonist, serotonin reuptake inhibitor, monoamine transmitter reuptake inhibitor and has an affinity for mu?

A

Methadone

285
Q

What opioids particularly sensitive to CYP enzyme inducers (like carbamazepine) and enzyme inhibitors (like grapefruit juice)?

A

Methadone, hydrocodone is another that is particularly sensitive to inducers/inhibitors

286
Q

How many days does it take for methadone to reach steady state?

A

5 - 10

287
Q

What opioid is extensively metabolized by N-demethylation?

A

Fentanyl

288
Q

What opioid has a large inactive reservoir in the lungs?

A

Fentanyl

289
Q

What opioid is a hydrogenated ketone analogue of morphine?

A

Hydromorphone

290
Q

What metabolite of hydromorphone has no analgesic effects but may potentiate neurotoxic effects?

A

Hydromorphone-3-glucuronide

291
Q

What opioid is sensitive to magnesium and CCBs (increasing it’s effect on the body)?

A

Hydrocodone

292
Q

What opioid has less respiratory depression, less immune suppression, less constipation and limited accumulation if your renal function is impaired?

A

Buprenorphine

293
Q

What opioid has a partial agonism for mu, an antagonist of kappa with a high receptor affinity for both, and is a weak delta receptor agonist?

A

Buprenorphine

294
Q

What opioid is highly unlikely to cause dysphoria?

A

Buprenorphine

295
Q

Buprenorphine can cause withdrawal s/sx if the patient is physically dependent on what drug?

A

Morphine

296
Q

What are the benefits of long term opioid use?

A

Pain reduction

Fewer episodes of severe pain “spikes”

Increase in functionality

297
Q

T/F: non-opioids bind to receptors to exert their effects?

A

Per the lecture (slide 78) this is false, they work on peripheral tissues to inhibit formation of pain causing substances

298
Q

What is the dose of celecoxib?

A

100 mg daily

299
Q

What is the dose of naproxen?

A

220 mg twice daily

300
Q

What is the dose of diclofenac?

A

50 mg twice daily

301
Q

What class of anti-depressants work as an adjuvant medication in reducing pain?

A

TCAs (the triptyline drugs, like amitriptyline, nortriptyline etc)

302
Q

Carbamazepine (tegretol) is an example of what general class of drugs?

A

Anti-convulsants

303
Q

List the skeletal muscle relaxants listed in the powerpoint (slide 82)

A

Baclofen( Lioresal®)
Carisoprodol(Soma®)
Cyclobenzaprine(Flexeril®)
Methocarbamol(Robaxin®)
Tizanidine(Zanaflex®)

304
Q

What antibiotics tend to work well on gram - bacteria?

A

Fluoroquinolones and carbapenems

305
Q

What is the basic MOA of beta lactams?

A

They inhibit bacterial cell wall synthesis

306
Q

What cephalosporin is indicated for gram + infections, cellulitis, abscesses, URI or UTI?

A

Ancef (Cefazolin)

307
Q

What cephalosporin is indicated for gram - bacteria, h-influenzae PNA, UTI and otitis media?

A
308
Q

What cephalosporin is indicated for gram - bacteria, a better option for ABX resistant bacteria and meningitis?

A
309
Q

What cephalosporin treats gonorrhea?

A

Ceftriaxone (Rocephin)

310
Q

What cephalosporin is most resistant to lactamases, penetrates the BBB well and is reserved for multi-resistant organisms?

A

Cefepime (Maxipime)

311
Q

What class of ABX should be given with care in clotting disorders?

A

Cephalosporins

They can cause a potential production deficit of Vitamin K

312
Q

What opioid could be a good choice for pain management in someone with hepatic and/or renal impairment?

A

Methadone

313
Q

What opioid may be resistant to antagonism with narcan?

A

Buprenorphine

314
Q

What is the MOA of anti-depressants in reducing pain?

A

Increase transmission in spinal cord to reduce pain signals

315
Q

What opioid can strongly potentiate precedex?

A

Tramadol

Semester 4 TxWes (4 decks)

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