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Ane Principles II > E2 > Flashcards

E2 Flashcards

1
Q

Define:
Nausea
Vomiting

A

Nausea
• comes from the Greek word - nautia = “seasickness”.
• Described as ‘a feeling of sensation of unease and discomfort in the stomach with the urge to vomit.’

Vomiting
• forceful expulsion of gastric contents through the mouth or nose

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2
Q

Define:
Retching
Emetic episode

A

Retching
• Similar to vomiting
• Except that NO gastric content enters the pharynx.

Emetic episode
• one or more instances of vomiting and/or retching
• separated by no more than 1 min between episodes.

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3
Q

Describe some examples of historical treatments for nausea from 1914 to 1930

A

1914:

  • tincture of iodine in 1 tsp of H2O q30min
  • inhalation of vinegar fumes
  • rectal injection of opium

1930:

  • Essence of orange on gauze
  • Lateral position
  • Strong black coffee
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4
Q

Describe some examples of historical progression of medication treatments for nausea from 1950s to 1991

A 
1950:
-antihistamines
-neuroleptic chlorpromazine
1957:
-promethazine prophylaxis
1960:
-droperidol
1991:
-Zofran
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5
Q

Describe the incidence of PONV

A
  • Most common pt complaint
  • Overall ~20-30%
  • Intractable vomiting 0.1%
  • Calculated risk could be high as 80%
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6
Q

What are pathophysiologic mechanisms of introduction of n/v

A
  • Peripheral mechanisms
  • Central mechanisms
  • Drug
  • Toxins
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7
Q

Name receptors that mediate N/V

A 
Muscarinic--M1
Dopamine--D2
Serotonin 5-hydroxytryptamine-3--5-HT3
Histamine--H1
Neurokinin 1--NK1/substance P
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8
Q

Describe the central mechanisms that mediate n/v and potential causes preoperatively

A

Higher cortical centers
-communicate w/ vomiting center in the MEDULLA

Potential causes preoperatively
-fear, pain, anxiety

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9
Q

escribe the peripheral mechanisms that mediate n/v

A
  • Direct gastric stimulation which induces the release of substance P and serotonin from enterochromaffin cells
  • activates vagal and splanchnic nerve 5-HT3 receptors
  • Nerve afferents end in the CTZ
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10
Q

What mediators a receptors are utilized in peripheral mechanisms of n/v

A

NT mediator:
substance P and 5HT3

Receptors
5-HT3

area
CTZ

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11
Q

Describe toxic materials and drugs that mediate n/v

A

Our own gut
-Toxin ingestion activates enterochromaffin (5HT3 release?)

Things we put in our body
-Drugs, food, alcohol

What other ppl administer
-anesthetic

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12
Q

How does motion sickness r/t PONV

A

h/o motion sickness INC risk of PONV

MOA = vestibulat system stimulation. V system can be affected by anesthetic

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13
Q

What are general factors that contribute to PONV

A

Pt factors
Surgical factors
Anesthetic factor

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14
Q

What are some pt factors r/t PONV

A 
Age
Gender
H/o motion sickness
H/o PONV
NONsmoker
Genetic polymorphism
Gastric distention
GE junction dx
Delayed gastric emptying
INC gastric vol
Pre-op N/V
Autonomic imbalance
Obesity
Menstruation
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15
Q

What are surgical factors that contribute to PONV

A

Specific procedures

  • chole, gyn, lap procedures
  • strabismus sx for peds

Procedures loosely related

  • HEENT
  • URO
  • Breast
  • Major ortho
  • Abd

Surgeries specific to peds

  • Adenotonsillectomy
  • hernia repair
  • orchipexy
  • penile sx
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16
Q

Anesthesia factors that contribute to PONV

A
  • Anesthetic technique
  • Volatile
  • IV anesthetic
  • N2O
  • Duration
  • Opioid admin
  • Neostigmine
  • Sugammadex
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17
Q

How does anesthetic technique contribute to PONV

A

GA has higher PONV rate than regional

TIVA has less PONV incidence than GA

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18
Q

How does IV medication contribute to PONV. Give an example of an induction med that contributes to PONV.

A

Induction meds may have POS or NEG association w/ PONV

ETOMIDATE
-INC PONV
-DEC CBF 
-DEC ICP
recent studies show low association
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19
Q

How does nitrous contribute to PONV

A

May modestly INC PONV risk

Mostly in women

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20
Q

How does duration of anesthesia contribute to PONV

A

INC exposure to inhaled anesthetic and opioids

Usually more invasive procedures

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21
Q

How does MR reversal contribute to PONV

A

Neostigmine = LOW association

Sugammadex = questionable association

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22
Q

How do opioids contribute to PONV especially r/t pre/postop-period

A
  • Significant association
  • Studies focus on dosage and duration in association w/ PONV
  • Admin of postop opioids INC PONV incidence
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23
Q

How do volatile anesthetics contribute to PONV

A

Leading culprit for PONV

Greater than Propofol

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24
Q

What is the general expectation for the occurrence of PONV

A

Timeline

  • Immediately postop
  • Peak around 6 hrs
  • Can linger longer than pos-op period
  • Approx 35% of pts experience PONV
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25
Q

Overall risk factors for PONV

A
  • laparotomy
  • laparoscopy
  • major breast sx
  • middle ear sx
  • gyn sx
  • female
  • Age >50 yo
  • h/o PONV
  • h/o motion sickness
  • h/o vertigo
  • Dental procedures
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26
Q

What is the purpose and major predictors of risk stratification for PONV

A

Purpose
-add up all risk factors to obtain score which can guide decisions for ponv tx

Major predictors

  • female
  • h/o motion sickness and ponv
  • postop opioids
  • nonsmoker
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27
Q

What is the APFEL risk score and relation to PONV

A
  • 0 factors = 10% chance of PONV
  • 1 factor = 20% chance of PONV
  • 2 factors = 40% chance of PONV
  • 3 factors = 60% chance of PONV
  • 4 factors = 80% chance of PONV
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28
Q

How should risk score treatment be approached. Questions to ask yourself

A

Decide treatment based on the pts calculated risk stratification:
• What’s the patient’s risk of PONV?
• The consequences of N/V r/t the surgical procedure?
• What are the pt & clinician preferences?
• Implications for a change in our routine anesthesia plan.

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29
Q

How is PONV treated w/ 0-1 risk factors

A

No prophylaxis recommended

Many anesthetists still give meds

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30
Q

How is a moderate risk of ponv treated and what are the # of risk factors

A

2-3 risk factors

Prophylaxis indicated

\+Chose 1-2 interventions
>1 antiemetic PLUS
-regional 
-TIVA
-acupuncture
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31
Q

How is high risk of ponv treated and what are the # of risks factors

A

4+ risk factors

Multimodal prophylaxis indicated

Choose >/=3 interventions

> 1 antiemetic PLUS

  • regional
  • TIVA
  • acupuncture
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32
Q

What are approaches to managing PONV

A

pharmacologic
-antiemetic drugs

non-pharmacologic

  • acupuncture
  • acupressure
  • O2
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33
Q

Classes of drugs used for pharmacologic tx of ponv

A

dopamine antagonist

histamine

antagonist
anticholinergic

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34
Q

What are the 2 types of dopamine antagonists and their corresponding drugs

A

butyrophenones

  • droperidol
  • haldol

phenothiazines

  • promethazine
  • chlorpromazine
  • prochlorperazine
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35
Q 
Droperidol 
Class: 
Dose: 
Onset: 
Peak: 
Duration: 
Cost: 
MOA: 
Blackbox warning:
A 
Class: dopamine antagonist butyrophenones	
Dose: 0.625 mg - 1.25 mg IV.
Onset: 3 - 10 minutes
Peak: 30 minutes
Duration: 2-4 hours
Cost: ~$4.50 for 2.5mg/ml.
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36
Q

Droperidol MOA and what is the blackbox

A

MOA:
-it is an antipsychotic
•blocks dopamine in the CTZ.
•α-adrenergic blockade DEC pressor effect of Epinephrine

Blackbox warning
•for prolonged QT
•FDA recommends 2 hours of EKG after admin

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37
Q

How does droperidol compare to zofran

A

droperidol dose of 0.625 is equivalent to 4 mg zofran

 No difference in side effects, recovery, time of discharge.
 Droperidol is more cost effective.
 Both prolong QT

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38
Q

Where is the action phenothiazines and SE r/t admin

A

Work in the CTZ

SE

  • sedation
  • hypotension
  • EPS
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39
Q

MOA of 5-ht3 antagonists, medications, and SE

A

MOA:
-Primarily antagonize serotonin

Medications:
Zofran
dolesetron
granisetron
palonosetron

SE:
minimal
H/A, constipation

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40
Q 
Ondansetron
	IV onset: 
	Half-life: 
	Dose: 
	Rescue dose: 
	Cost:
A 
	IV onset: 10 minutes.
	Half-life: 3 hours.
	Dose: 4 mg.
	Rescue dose: 1 mg.
	Cost: $43 for 4 mgs.
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41
Q

Dolesetron
 Dose:

Granisetron 
	Dose: 
	Duration: 
	Half-life:
	Cost:

Palonosetron
 half-life:
 MOA:

A

Dolesetron
 Dose: 12.5mg - 25 mg

Granisetron 
	Dose: 1mg,
	Duration: longer acting, 
	Half-life: 9 - 12hrs
	Cost: \$\$$

Palonosetron
 2nd generation
 half-life: 40hrs,
 MOA: exhibits allosteric binding to 5-ht3 receptors.

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42
Q

Anticholinergic med used for PONV. MOA and SE

A

Scopolamine

MOA
-centrally acting antimuscarinergic w/ short half-life

SE:

  • visual disturbances
  • dilated pupils
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43
Q

Antihistamine med used for ponv, exhibits similar results to what drugs.
Side effects and dosing

A

Dimenhydrinate, diphenhydramine

sim results as:
decadron, droperidol, zofran

SE:
drowsy

dosing:
1 mg/kg

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44
Q

MOA of neurokinin-1 receptor antagonist and drug examples

A

Antiemetic that antagonizes substance P receptors

Aprepitant
Rolapitant

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45
Q

Aprepitant and Rolapitant
 Dose:
 Half-life:
 Cost:

A 
•	Aprepitant 
	Dose: 40 - 80 mg oral preoperatively 
	as early has 3 hours prior to onset of anesthesia
	Half-life: 40 hours
	Cost: >$ 200 for each dose.
Rolapitant 
	Dose: 90 mg oral preoperatively
	Half-life:180 hours
	Well known in the chemotherapy communities
	Cost: Almost $400 per dose.
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46
Q 
Glucocorticoids used for ponv. 
dose:
efficacy:
onset: give when?
considerations:
A

Dexamethasone
 Dose: adults 4mg, children 0.25mg/kg
 Max 4 mgs.
 Efficacy is similar to Zofran & droperidol.
 Onset: Slow
 Give at the beginning of the case.
 Consideration: high glucose measurements.

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47
Q

List possible alternative medications for the tx of ponv

A

cannabinoids-Nabilone
adequate hydration
midazolam
isopropyl alcohol

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48
Q

Guidelines for ponv rescue therapy

A 
#1 rule:
rescue w/ different drug class than already given

Serotonin antagonists are very good tx for ponv rescue

rescue dosage can be smaller

give small dose of narcan for ponv r/t opioids

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49
Q

What is post-discharge n/v and associated independent factors

A

Defined:
ponv ocurring w/in 48 hrs post d/c in nearly 37% of pts

Independent risk factors:

  • female gender
  • age<50
  • h/o ponv
  • opioids in pacu
  • nausea in pacu
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50
Q

What are some preventative measures for ponv (11)

A 
	Use of local and regional anesthesia.
	Use propofol.
	Avoid nitrous oxide.
	Minimize opioids.
	Nonopioid analgesics.
	Control pain.
	Adequate hydration.
	Limit motion.
	Avoid early ambulation.
	Avoid early oral intake.
	Antiemetic prophylaxis.
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51
Q

What is standard 11 from AANA standard of practice

A

Standard 11
• Evaluate pt status
• Determine when appropriate to txfr care to another qualified healthcare provider
• Communicate pt condition & essential infor for continuity of care

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52
Q

Describe standard 1 and 2 for post-anesthesia care

A

Standard 1
• All patients who have received GA, RA, or MAC
• Must receive appropriate postanesthesia management.

Standard 2
• Pt must be transported to PACU by anesthesia care team member
 That individual must be knowledgeable about the patient’s condition

• During transport pt is
 Continually evaluated & treated
 with monitoring and support
 appropriate to the pts condition

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53
Q

Describe Standard 3, 4, and 5 of post-anesthesia care

A

Standard 3
• on PACU arrival, pt shall be re-evaluated
• Verbal report provided to the responsible PACU RN by accompanying anesthesia team member

Standard 4
• The pts condition is evaluated continually in PACU.

Standard 5
• A physician is responsible for the discharge from PAC

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54
Q

General h/o PACU evolution in the US

A

1920 several PACUs opened in the United States.
• After WW II the number of PACUs increased.

1947 studies showed that 50% of deaths in the first 24 hours following surgery were preventable.

1949 PACU became Standard of Care.

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55
Q

What staff works in the PACU and their general role

A 
	Specially trained nurses
•	Highly skilled @ assessment
	Respiratory therapists.
•	Emergent breathing tx
•	Vents for short-term use
	Anesthesia personnel.
•	MDA
	Intensivist or House MD
•	Continue care for pt post-op
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56
Q

Where is the PACU located and what are requirements for travel from OR to PACU

A

Close to the OR (or ICU)

Travel requirements
Monitoring - 
•	Oxygenation  Pulse-Ox.
•	Ventilation  Make sure they are breathing.
•	Circulation  systemic BP &amp; HR.
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57
Q

What should be done on arrival to the PACU from OR

A

ASSESS
-airway patency, RR, Sat, HR, BP, mental status, pain, n/v

Assess and treat
-hypoxemia r/t RA, obesity, sedation, RR, advanced age >60 yo

Connect pt to PACU monitors

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58
Q

What is performed on pt admission to PACU

A
  • CRNA assesses pt
  • Pt connected to PACU monitors
  • Report given to PACU RN
  • PACU RN assesses pt
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59
Q

Describe the components of CRNA PACU report

A

Should be

  • specific
  • organized
  • completed when full attention of receiving RN
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60
Q

Consequences of poor report

A
  • Wrong tests
  • Delay in treatment
  • Failure to continue certain tx
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61
Q

What are 3 communication tools that can be used for handoff

A

SBAR

Simplified handoff tool

PACU admission report (comprehensive)

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62
Q

Describe the SBAR handoff and the 7 advantages

A

Situation ,Background, Assessment, Recommendations

Structured handoff
• Improves transition of care
• ↓ communication errors and Errors in general
• Improves staff satisfaction
 Standardized method of communication
 Covers pertinent surgical and pt factors
 Easy to remember

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63
Q

Concerns and guidelines for phase 1 recovery

A

Concern:

  • Most intense phase
  • ideally 1:1 ratio

Guidelines:

  • continuous monitoring (HR, Sat RR, EKG, airway patency)
  • Assessment
  • NM fxn for intubated pts
  • Frequent VS
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64
Q

What should be included in the phase 1 recovery PACU assessment

A

mental status
BP
temp
pain

Out–UO, EBL, wounds, drains
Ins–IVF, how much and what tupe

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65
Q

How often are VS assessed during phase 1 recovery. VS goal

A

1st 15 min = q5min
Duration of phase 1 = q15min

Goal: w/in 20% of baseline, be sure to notify pacu RN about pt baseline VS

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66
Q

What is phase II recovery

A

Less intense

Pt preparing to meet criteria for DC

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67
Q

Means of measuring readiness for DC

A

Aldrete score
modified aldrete score
Post-anesthesia dc scoring system

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68
Q

What are the assessment categories for the aldrete scoring tool. Describe the corresponding scores of 2 for each category

A

activity-moves all extremities voluntarily

respirations-Breaths deeply and coughs freely

circulation-BP +20 min preanesthetic level

consciousness-fully awake

O2 sat-SpO2 > 92% on RA

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69
Q

What is monitored in phase II recovery? Frequency of VS

A

Monitor:

  • Airway and ventilation
  • pain level
  • ponv
  • fluid balance
  • wound integrity

VS frequency
q30-60 min

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70
Q

What are common airway complications during recovery

A
  • Airway obstruction
  • Negative pressure pulm edema
  • laryngospasms
  • airway edema or hematoma
  • VC pralysis
  • residual neuromuscular blockade
  • OSA
  • Arterial hypoxemia
  • Diffusion hypoxemia
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71
Q

What are patient and procedural related risk factors for PACU airway complications

A 
Patient related 
•	COPD
•	Asthma
•	OSA
•	Obesity
•	heart failure
•	Pulmonary HTN
•	URI
•	tobacco use
•	higher ASA score.

Procedure related
• Surgery near diaphragm
• ENT procedures
• severe incisional pain poor ventilation

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72
Q

What are anesthetic related risk factors for airway complications in PACU

A

Largest contributor to airway complications
• Due to

General anesthetic

MR
 How much
 When
 What reversal

opioids
 When are they given??

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73
Q

Causes of upper airway obstruction in PACU and treatments

A

Causes:
•Loss of pharyngeal muscle tone
 ↑ upper airway resistance
•Paradoxical breathing

Treatment

  • Jaw thrust
  • CPAP
  • OPA/NPA (opa for deep sedation; npa for more awake pt)
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74
Q

How does loss of pharyngeal tone lead to upper airway obstruction

A

Pharyngeal muscle normally tenses on NEG pressure inspiration and opens airway

Loss of tone means airway wont open

This increases upper airway resistance

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75
Q

What is negative pressure pulmonary edema and how does it happen

A

It is a form on noncardiogenic pulm edema

  • results from generation of high negative ITP
  • Leading to capillary leakage in lungs from INC hydrostatic pressures
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76
Q

What are causes of negative pressure pulm edema

A
  • NEG ITP against an obstructed airway
  • Blocked ett
  • laryngospasm (most common)
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77
Q

What are s/sx of negative pressure pulm edema and how does it resolve

A

S/Sx:

  • pink, frothy sputum
  • Makes oxygenation difficult

Resolves in 12-48

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78
Q

What is a laryngospasm and associated causes

A

VC closure that prevents air movement resulting in hypoxemia and possibly neg pressure pulm edema

causes:
Stimulation of pharynx or VC from blood, secretions or foreign material

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79
Q

Physiology and symptoms of laryngospasm

A

physiology

  • prolong exaggeration of glottic closure reflex
  • d/t stimulation of SLN

Symptoms
-Inspiratory stridor
d/t INC respiratory effort, INC diaphragmatic excursion
-Silence = ominous sign of NO air movement

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80
Q

Treatment for laryngospasm

A
  • Get help
  • Apply FM w/ tight seal, 100% FiO2 and APL @40 cmH2O
  • suction airway
  • chin lift/jaw thrust
  • OPA/NPA
  • Pressure to laryngospasm notch
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81
Q

Describe how to perform the larson’s manuever

A

Apply bilat digital pressure behind the lobule of the pinna of each ear

  • clears airway and stimulates pt
  • apply for 3-5 seconds w/ forcible jaw thrust
  • Maintain FM w/ tight seal
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82
Q

What may be evident on assessment if unable to break laryngospasm
What should be your next actions

A

Assessment

  • Fast desat
  • INC HR followed by bradycardia

Your actions:
Give atropine and propofol
Give succs 0.1 mg/kg IV or 3-4 mg/kg IM
RE-INTUBATE

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83
Q

Contributions to airway edema in the post-op pt

A 
Prolonged intubation
Prolonged positioning (prone and tburg)
Cases w/ large blood loss that receive
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84
Q

what is an important assessment clue that a pt may have airway edema

A

Facial and scleral edema are present

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85
Q

What assessments and interventions should be performed prior to extubation on a pt w/ possible airway edema

A

Assessment

  • Perform cuff leak test
  • -remove small amount of air from cuff
  • -no air heard
  • -leave ETT and raise HOB

Intervention
suction oral pharynx

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86
Q

What surgeries may contribute to airway hematoma

Biggest concerns w/ airway hematoma

A

neck dissections
thyroid removal
carotid surgeries

  • Rapidly expanding hematoma causing supraglottic edema
  • tracheal lumen <5 mm is LIFE-THREATENING SITUATION
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87
Q

What can airway hematoma post-op lead to and treatment

A

Leads to:

  • Deviated trachea
  • compression of trachea below level of cricoid cartilage
  • VERY difficult intubation dt blood or edema

Treatment:

  • Decompress the airway (release clips or surgical incision)
  • RE-INTUBATE
  • Surgical backup for tracheostomy
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88
Q

What procedures are associated w/ VC paralysis

A
  • otolaryngologic sx
  • thyroidectomy
  • parathyroidectomy
  • Rigid bronchoscopy
  • over inflated ETT cuff
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89
Q

What is the cause of VS paralysis

A

Unilateral or bilateral nerve injury

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90
Q

What symptoms are present w/ unilateral SLN injury

A

usually asymptomatic

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91
Q

What can occur w/ the VCs as a result of damage to the external branch of the SLN

A
  • Produce weakness and huskiness of voice as VCs cannot tense up
  • cricothyroid muscle is paralyzed
  • Injury is r/t loss of tension of VCs
  • -appear wavy
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92
Q

What can occur w/ the VCs as a result of damage to bilateral recurrent laryngeal nerve

A
  • Results in aphonia and paralyzed cords
  • Each cord in intermediate position
  • VCs can close causing airway obstruction during INSPIRATION
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93
Q

What are airway problems r/t recurrent laryngeal nerve damage

A
  • Difficult intubation

- Likely tracheostomy for emergent airway

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94
Q

What are some post-op complications r/t thyroid surgery

A

Hypocalcemia

-w/in 24-48 hrs post-op

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95
Q

s/sx associated w/ hypocalcemia

when are ca++ levels considered low

A

S/sx:

  • chovsteks sign (facial spasm)
  • trouseau’s sign (carpal sign)
  • paresthesia in fingers
  • muscle cramps
  • irritability

Ca++ levels
Serum = <8.5
iCa = <3.8 mg/dL

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96
Q

What are the greatest concerns and considerations related to the effects of residual neuromuscular blockade on the airway in PACU

A
  • complete reversal of MR is necessary
  • Partial reversal can be worse than NO reversal b/c
  • –assessment for extubation readiness can be misleading w/ partial reversal
  • –Thus masking pt inability to maintain airway
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97
Q

Clinical evaluation to assess the level of residual NMB

A
  • grip strength
  • tongue protrusion
  • can lift legs off of bed
  • hold head up >/= 5 sec
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98
Q

What factors can contribute to recurarization in the PACU affecting the airway

A

Meds:
abx, lasix, propranolol, phenytoin

conditions:
low Ca++ and Mg++

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99
Q

What are the components of the STOP-BANG assessment and why is it useful?

A

Useful:
to identify pts at risk for OSA

Components:
SNORE
TIRED
OBSERVED not breathing
PRESSURE (HTN)
BMI >35
AGE >50
NECK >16
GENDER
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100
Q

How can a h/o OSA affect pts PACU recovery and why.

How might this affect the anesthetic recovery plan

A

Pts are prone to airway obstruction
–b/c partial or complete blockage of upper airway
Sensitive to opioids

Anesthetic plan:

  • Awake extubation, make sure pt is FC
  • Try regional techniques for post-op pain
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101
Q

Describe post-op care and d/c criteria for pts w/ OSA

A

Post-op care:
May need CPAP
Use home CPAP if provided

D/C criteria
SpO2 >90% while sleeping

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102
Q

What are low, intermediate, high OSA risk screening scores…

A

Low risk = 0-2
intermediate = 3-4
high risk = 5-8

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103
Q

What are causes of arterial hypoxemia in the PACU

A

Pt on RA:
–all pts should be on O2 from OR to PACU

Hypoventilation
–Too much pain meds or BZDS (poor clearance)

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104
Q

What treatments are indicated when arterial hypoxemia is present in PACU

A
  • Apply O2 via NC or FM
  • Reverse opioid or BZDs
  • –Narcan 40-80 mcg small incremental doses
  • –flumazenil 0.2 mg (repeat, max of 1 mg)
  • Stimulate pt
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105
Q

Describe the difference between hypoxia vs hypoxemia

A

hypoxia:

  • Not enough O2 DELIVERED to tissue
  • Cyanide poisoning is only time hypoxia W/O hypoxemia

Hypoxemia:
-Not enough O2 IN blood

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106
Q

What can cause diffusion hypoxia post-op?

What can this lead to?

A

Rapid diffusion of N2O into alveoli at the end of anesthetic

  • If on RA s/p N2O
  • -DEC alveolar PO2
  • -DEC PaCO2

Leads to:

  • dilution of alveolar gas
  • DEC PaO2 and PaCO2
  • DEC respiratory drive from DEC PaCO2
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107
Q

How long can diffusion hypoxia persist following N2O d/c?

What is the treatment?

A

Can persist for 5-10 min

Treatment:
Apply O2
Stimulate RR
Watch

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108
Q

What are circulatory complications that may be present in PACU

A

Systemic HTN

Systemic HoTN

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109
Q

What are parameters for post-op HTN, considerations for BP assessment and common causes

A

Parameters:
SBP>180 mmHg
DBP>110 mmHg

Assessment:
-ensure BP cuff is in appropriate place before treatment

Common causes

  • Emergence excitement
  • shivering
  • hypercapnia
  • pain
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110
Q

Suggested treatment and considerations for post-op HTN. Give dosages for medications

A
  • Use rapid acting BP meds
  • –Labetolol 5-25 mg
  • –Hydralazine 5-10 mg
  • –Metoprolol 1-5 mg

Considerations

  • Treat underlying cause
  • –Surgeon will give range for BP
  • –bring meds on transport
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111
Q

What are some causes of systemic hypotension in PACU

A

Hypovolemic–DEC preload
Distributive–DEC afterload (sepsis, allergic rxn, critical illness, iatrogenic sympathectomy)
Cardiogenic–pump failure (MI, Cardiac dysrhythmias)

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112
Q

What are causes of hypovolemic hypotension post-op

A
  1. Third spacing
  2. Inadequate intraop IV fluid replacement
  3. Loss of SNS tone d/t neuraxial blockade
  4. Ongoing bleeding
  5. ACE-i
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113
Q

How can the presence of tachycardia guide hypovolemic hypotension treatment

A

Tachycardia is NOT a reliable indicate of hypovolemia
–ESP in pts w/ BB or CCB on board
Consider pain vs hypovolemia

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114
Q

What are causes of distributive hypotension post-op

A

DEC afterload

  • Sepsis
  • Allergic rxn
  • Critical illness
  • Iatrogenic sympathectomy
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115
Q

Describe how iatrogenic sympathectomy affect BP post-op.

What does HoTN and bradycardia indicate and interventions

A

D/t surgery, disease or high spinal level (>T4)

  • Loss of vascular tone
  • Block cardioaccelerator fibers
  • Alters vascular distribution

HoTN + bradycardia

  • ominous that pt wil CODE
  • TX: vaso, neo, ephedrin
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116
Q

How is HoTN addressed in the critically ill pt pos-operatively.

A

Small doses of meds can cause exaggerated effects
–possible exaggerated SNS tone

Return on meds they were on prior to surgery?

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117
Q

Type of allergic responses leading to HoTN

Treatment

A

Anaphylactic: IgE (prior exposure)
Anaphylactoid: non-IgE

Treatment:
Epi = treat HoTN r/t allergic rxn

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118
Q

What is the most common cause of allergic rxns in perioperative period and why

What population is more prone…

A

MRs*** (most common)
-Engineered w/ quaternary ammonium ions that lead to a histamine reaction

Females more prone than men

119
Q

List common medications leading to allergic rxns from most common to least

A 
most
NMBD
Latex
Abx
Hypnotics
Colloids
Opioids
120
Q

How do NMB lead to allergic rxns w/ histamine release. Treatment

A

Histamine release

Leads to:
Erythema
Vasodilation
Edema
HoTN
GI constriction tachycardia
pruritus

Treatment:
diphenhydramine

121
Q

What are associated responses r/t potent inflammatory leukotrienes and prostaglandins release when NMB drugs cause allergic rxns
What treatment should be used

A
  • Bronchial constriction
  • INC vascular permeability

Treatment
Bronchodilators
EPI
Ephedrine

122
Q

Which NMB drugs are more prone to cause allergic rxn from greatest to least

A

Roc
Succs
Vec

123
Q

What populations are more prone to latex allergy.

A
  • Repeated exposure
  • several surgical procedures
  • spina bifida pts
  • healthcare workers
124
Q

What are the latex-mediated rxn types

A

Irritant contact dermatitis
Type IV cell mediated rxn
Type I IgE mediated hypersensitivity rxn

125
Q

What is the incidence of latex allergy and timeframe of rxn

A

Incidence:
as high as 20%

Timeframe:
30-60 min s/p exposure

126
Q

What are high and low eluding sources of latex rxns

A

high eluding:
gloves, drains, catheters
(soft rubber)

Low eluding:
____ strap, BP cuff tubing
(hard rubber)

127
Q

What are the most common allergy causing abx

A

PCN

Vanc = histamine release

128
Q

Cardiogenic causes of HoTN post-op

A

Pump failure

  • MI
  • Cardiac dysrhythmias (ST, AF, VT, VF, SB)
129
Q

What should be included in a post-op assessment for possible MI

A

EKG monitor w/ lead II and V5

  • ST segment analysis
  • 12 lead EKG
  • Troponin
130
Q

What treatments should be considered for possible MI in the PACU

A

IMPROVE MYOCARDIAL OXYGENATION

Treat brady or tachycardia
Treat HTN or HoTN
Give O2 for low O2
Avoid hypothermia
Avoid fluid overload
131
Q

What are factors that decrease O2 supply to myocardium

A

INC HR

DEC PaO2

  • LOW hgb
  • LOW SaO2

DEC coronary BF

  • LOW CPP
  • LOW DBP
  • LOW LVEDP

INC coronary vascular resistance

132
Q

What are factors that INC O2 demand on myocardium post-op

A

INC HR

INC LV systolic wall stress

  • INC SBP
  • INC LVEDV
  • DEC LV wall thickness

INC contractility

133
Q

List some causes leading to post-op cardiac dysrhythmias

A
  • hypoxemia
  • hypoventilation
  • endogenous and exogenous catecholamine
  • electrolyte abnormalities
  • anemia
  • fld overload
134
Q

Describe causes and characteristics of sinus tachycardia,

A

Causes (most common**):

  • bleeding
  • cardiogenic/septic shock
  • thyroid storm
  • PE
  • SNS**
  • hypovolemia**
  • Anemia**
  • shivering**
  • agitation**

Characteristics:
QRS: narrow
Rhythm: regular
Rate: >100 bpm

135
Q

What treatments may be indicated for sinus tach post-op

A
  • Identify and treat the cause
  • PAIN = give opioids
  • Hypovolemia = fld challenge
136
Q

What are risk factors leading to atrial dysrhythmias post-op.
When is it more likely to occur

A

Risk factors:

  • pre-existing cardiac risk factors
  • positive fld balance
  • electrolyte abnormalities
  • O2 desat

Higher after cardiac and thoracic sx
-10% pts w/ major non-cardiac sx

137
Q

Causes of post-op atrial fibrillation and considerations for treatment

A

Causes:

  • hypovolemia
  • anemia
  • trauma
  • pain
Considerations for tx:
-Rate control = immediately address >150 bpm w/ HoTN
-hemodynamically unstable
=cardioversion followed by amio
=Esmolol short-term
-hemodynamically stable
=most pts respond wo BB or CCB
138
Q

Characteristics of VT in PACU

Concerns r/t PVCs in post-op period

A

QRS >120 ms

PVC more common
-d/t INC SNS stimulation from intubation, pain, transient hypercapnia

139
Q

Causes of ventricular dysrhythmias in the PACU (6 Hs, 4 Ts)

A 
Hypoxia
Hypovolemia
hypothermia
hypokalemia
hyperkalemia
High H+

Tension PTX
Tamponade
Thrombosis
Toursades

140
Q

Possible causes of toursades in the pos-op period

A

prolong QT d/t

-amio, droperidol, procainamide

141
Q

Characteristics and causes of sinus bradycardia in the PACU

A 
Causes:
Too many to list
Long-term BB use
ACh reversal 
NMB drugs

Characteristics:
HR<60 bpm (what is baseline)

142
Q

Procedures that can cause bradycardia

A 
bowel distension 
INC ICP
INC intra-ocular pressure
Spinal anesthesia
Spinal blocks
143
Q

Why do spinal blocks lead to bradycardia.

What can this lead to and why?

A

high spinal = T1-T4 level

  • -block cardioaccelerator fibers
  • -results in profound bradycardia
Can lead to:
Cardiac arrest
--Sympathectomy
--Bradycardia
--Lack of intravascular vol
144
Q

Define delirium

A
  • Acute change in cognition or disturbance of consciousness

- cannot be attributed to pre-existing medical condition, substance intoxication or medication

145
Q

Describe the incidence of delirium in PACU

A

10% of adults >50 yo btwn POD 1-5

Higher incidence:

  • elderly
  • specific surgical procedures (TKR)
146
Q

List some factors that influence and mask postop delirium

A

influence:

  • age
  • fxntl status
  • h/o substance abuse

Mask:

  • sedation
  • anesthetic/pain meds
147
Q

What are risk factors r/t post-op delirium

A
  • Advanced age >70 yo
  • Preop cognitive impairment
  • DEC functional status
  • alcohol abuse
148
Q

What is the importance of a preop cognitive assessment

A

To determine if there is preop cognitive impairment that could lead to postop delirium

  • can alter anesthetic plan
  • may lead you to check for underlying metabolic causes
149
Q

List some intra-op factors associated w/ delirium

A
  • Surgical blood loss (HCT<30% + INC # intraop txfn)
  • HoTN
  • Admin of N2O
  • Anesthetic technique
150
Q

Describe methods for managing post-op delirium

A
  • Identify high-risk pt prior to surgery
  • severely agitated pt may require additional PACU eyes
  • Early identification can help guide meds and anesthetic
151
Q

Considerations to DEC post-op delirium effects for elderly pts undergoing minor surgery

A
  • Should be treated at an outpt center

- Allows return to normal environment ASAP to dec post-op delirium

152
Q

Considerations or assessments for pts w/ delayed awakening post-op

A
  • Evaluate VS
  • -is EtCO2 high
  • Perform neuro exam
  • -may need CT
  • Monitor SpO2
  • Assess labs for electrolyte, glucose abnormalities
153
Q

What are some causes for delayed awakening post-op

A
  • Anesthetic (#1 residual sedation)
  • Opioids
  • BZDs
  • Scopalomine
  • Hypothermia <33*C
  • Hypoglycemia
  • INC ICP
  • Residual MR
154
Q

What meds/doses would be given to address delayed awakening post-op from opioids, BZDs or scopalamine

A

Opioids:
Narcan 20-40 mcg increments

BZDs:
flumazenil 0.2 mg (max 1 mg)

Scopalomine:
Physostigmine 0.5-2mg IV

155
Q 
Describe some ways pain effects each body system
Cardiac
Pulm
Endo
Immune
Coag
GI/GU
A 
Cardiac: INC HR, HTN
Pulm: Splinting, DEC VC, atelectasis, hypoxia
Endo: INC stress response
Immune: Impaired
Coag: INC risk thrombosis
GI/GU: Ileus, urinary retention
156
Q

How is acute pain sensed. Describe mechanism…

A

At nociceptors
-Free afferent nerve endings of fibers:
+myelinated A delta
+unmyelinated C

-Tissue damage activates nociceptors via thermal, mechanical or chemical damage

157
Q

Mechanisms of tissue injury during surgery and mechanism of pain sensing

A

Surgical incision
Dissection of muscle
Burns

Stimulates release of histamine, inflammatory mediators (bradykinin, PGs, 5HT3)

158
Q

What are inflammatory mediators of pain

A

Peptides (bradykinins)
Lipids (PGs)
NT (serotonin)

159
Q

How does direct nerve injury contribute to pain perception

A

Nerve transection
Poor positioning causing:
-stretching
-compression

160
Q

What are the components of pain processing. Describe each

A

Transduction:
CONVERSION of noxious stimuli into APs

Transmission:
CONDUCTION of AP through nervous sys

Modulation:
ALTERATION of afferent pain transmission (i.e. the DIC response)

Perception:
INTEGRATION of painful input into somatosensory or limbic cortices

161
Q

Define hyperalgesia?

What is opioid-induced hyperalgesia and what meds are more prone to lead to it? Treatment?

A

Hyperalgesia:
Augmented sensitivity to painful stimuli

Opioid-induced hyperalgesia:
Reception of opioids causes more sensitivity to pain
-Remifentanyl = Tx give long acting pain med w/ dose
-Fentanyl = follow w/ infusion
-Maybe give ketamine

162
Q

Describe primary and secondary hyperalgesia

A

Primary:

  • Augmented sensitivity to painful response
  • misinterpretation of non-painful stimulation

Secondary:

  • INC excitability of neurons in the CNS
  • –d/t glutamate activation of NMDA receptors
163
Q

Describe some goals of pain control

A
  • optimal pt comfort
  • attenuation of adverse physiologic responses to pain
  • control anxiety/agitation
164
Q

Considerations for attaining pain control goals post-op

A

Preemptive and preventative analgesia:

  • -What is the most painful part of the surgery
  • -What is the primary source of pain (i.e. spasms vs incisional pain)

Multimodal approach:

  • -Use of multiple drugs from different calsses w/ various MOA/DOA
  • -Variety of drugs and techniques

Opioid free approach

165
Q

What are some drugs or techniques to be considered for the treatment of post-op pain

A

Drugs w/ variety of MOA in central and peripheral NS

Drugs:
opioids, ketamine, neuropathic, NSAIDs

Techniques:
regional or local anesthetics

166
Q 
Dosing and route for the following post-op opioids
Morphine
Codeine
Hydromorphone
Fentanyl
A

Morphine
IV 2.5-15 mg
IM 10-15 mg
PO 30-60 mg

Codeine
PO 15-60

Hydromorphone
IV 0.2-1.0 mg
IM 1-4 mg
PO 1-4 mg

Fentanyl
IV 20-50 mcg
Transmucosal 200-1600 mcg
Transderm 12.5-100 mcg

167
Q 
Dosing and route for the following post-op opioids
Oxymorphone
Hydrocodone
Oxycodone
Methadone
Propoxyphene
Tramadol
A 
Oxymorphone
PO 5-10 mg
IV 0.5-1 mg
SQ 1-1.5 mg
IM 1-1.5

Hydrocodone
PO 5-7.5

Oxycodone
PO 5 mg

Methadone
PO 2.5-10 mg

Propoxyphene
PO 32-65 mg

Tramadol
PO 50-100 mg

168
Q

What are recommendations for pacu discharge

A
  • PT should be AOx3 or return to baseline
  • VS should be stable
  • PT must meet specified criteria
  • Use score to document fitness for DC
  • Outpt DC home w/ responsible adult
  • Give written instructions
169
Q

What are not considered requirements for discharge from pacu

A
  • No minimum stay

- Requirements for urination or PO intake are NOT part of routine dc protocol

170
Q

What information should be included in written DC instructions from the PACU

A
  • Diet
  • Medications
  • Activities
  • Phone # for emergency
171
Q

What are components of evaluation criteria for DC

A

Activity:
able to move all 4 extremities on command

Breathing:
Able to breathe deeply and cough freely

Circulation:
SBP /=20% of preanesthetic level

Consciousness:
Fully awake

O2 sat:
>92% on RA

172
Q

What are HAIs

Common reasons for HAI

A

Nosocomial acquired infections

Not present or incubating at item of admission

Reasons:
Most likely from break in our technique
-Poor/No handwashing, improper preop prep etc

173
Q

What are sources for HAIs?

What are the 2 most common?

A

-Central line associated sepsis
-CAUTI
-SSI
-Hospital acquired PNA
-VAP
C-Diff

2 most common:
SSI (21.8%)
Hospital acquired PNA (21.8%)

174
Q 
Pt awaiting R inguinal repair:
-Intermittent episodes of chest tightness and dizziness w/ exertion x3 weeks
-Syncopal episode last week w/ MI
-On ASA, nonsmoker
VS: 186/106 mmHg, HR 84, RR 16/min
EKG = LBBB

Assessment: systolic murmur over R sternal edge, radiates to neck

What are your current concerns

Anesthetic plan

A

HTN:

  • INC risk of ischemia, stroke, LV dysfunction
  • DBP should be w/in 20% of normal prior to sx

Possible AS:

  • Untreated = LVH and failure
  • Echo/Cath to determine severity

Possible inferior MI on EKG:

  • Comparing this EKG to prior ED EKG
  • Elective Sx w/in 3 months very high risk

Anesthetic plan:
Delay case vs continue (likely delay)

175
Q

Cholecystectomy:
55 yo M, 80 kg w/ cholelithiasis

h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years

ABG: pH 7.36, PCO2 60, PO2 70

Is pt having acute or chronic changes on ABG.
What pulm test should be assessed and what may be seen in his case?

A

ABG changes:
CHRONIC b/c inc PCO2 and lower PO2

Pulm tests:

  • Spirometry w/ flow-vol loops
  • -Concavity on expiration d/t obstruction
  • FVC, FEV1, RV, FRC
  • -norm FVC, low FEV1 (<40%**), inc RV, inc FRC
  • Chest xray
  • –intercostal space wide
  • –Ribs are flattened, not angled
  • –diaphragm and apical flattening
  • –hyperlucency (from less lung tissue)
  • –thin, narrow heart
176
Q

Cholecystectomy:
55 yo M, 80 kg w/ cholelithiasis

h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years

ABG: pH 7.36, PCO2 60, PO2 70

What is our anesthetic plan? (monitor, airway, meds, other):
Preop
Induction
Maintenance
Emergence
A

Preop:
+MONITORS-SpO2, ekg etc
+AIRWAY- No need for O2?
+MEDS-bronchodilator (anticholinergic, beta-agonist), steroid (esp if taking at home), maybe multimodal pain premedication
+OTHER- avoid meds w/ histamine release to prevent airway reactivity

Induction:
+MONITORS- EtCO2, typical monitors
+AIRWAY- GETA, ETT, 8.0 w/ rsi induction risk r/t n/v
+MEDS- RSI?? to secure airway rapidly in the presence of N/V; succs vs roc
+OTHER-

Maintenance:
\+MONITORS-all
\+AIRWAY- ETA w/ VG-PCV setting
\+MEDS- Sevo (avoid des to dec airway reactivity)
\+OTHER-
Emergence:
\+MONITORS- same
\+AIRWAY- awake extubation
\+MEDS- reversal, lido on extubation (concern for laryngospasm), inhaler prior to pulling tube
\+OTHER-
177
Q

Cholecystectomy:
55 yo M, 80 kg w/ cholelithiasis

h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years

ABG: pH 7.36, PCO2 60, PO2 70

Anesthetic plan = GETA w/ sevo

During the case, PIP suddenly increases and there are NO BS. What is the most common cause and what should be done?

A

Common cause:
Bronchospasms B/C the pt is too light**

Treatment:

  • Turn off vent and manually vent
  • Deepen anesthetic
  • INC FiO2
  • inhaled beta-agonist
178
Q

Cholecystectomy:
55 yo M, 80 kg w/ cholelithiasis

h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years

ABG: pH 7.36, PCO2 60, PO2 70
Anesthetic plan = GETA w/ sevo
episode of bronchospasm treated successfully

How do you decide if/when pt should be discharged from PACU

A
  • SpO2 >90% on RA
  • Wait 30 min to ensure no resp depression post opioid admin (?)
  • Awake
  • Pain control
179
Q

86 yo M, s/p R hemicolectomy POD2, for cecal carcinoma

Assessment:
Preop BP meds not restarted, UO 75 ml over 8 hrs, Poor PO intake, AOx3, AFeb, 110/70, 110, Chest and heart clear, abd tender at incision but soft, + BS w/ gas

What are his expected labs: Na, K, Ca, A-B balance, BUN/Crt

What is normal, minimal UO in a 70 kg man in 8 hrs

Calculate hourly maintenance rate?
What fld would be used?

A 
Hypernatremia
Hyperkalemia
Hypocalcemia
Inc BUN/Crt ratio
INC crt
Met acidosis

Normal:
0.5-1 ml/kg/hr
35-70 ml/hr
280 ml MIN in 8 hrs UO

Hourly maintenance
110 ml/hr
60 ml for 1st 20 kg
1 ml per remaining 50 kg
60+50 = 110 ml/hr

Replacement fluid
Small bolus
LR (maybe has high Na)
encourage PO intake

180
Q

What are etiology of ARF types and typical causes

A

Prerenal:
hypovolemia, LOW CO, blood loss, HoTN

Intrarenal:
drugs, toxins, glomerulonephritis, contrast, infxn

Post-renal:
Obstruction in ureter, bladder, stones, stricture

181
Q

Identify the type of renal failure based on the description

  1. Direct damage to glomerulus or tubule
  2. GFR declines d/t poor renal perfusion, easily restored
  3. typically r/t obstructed urinary flow
A

1= intrarenal

2= prerenal

3= Postrenal

182
Q

86 yo M, s/p R hemicolectomy POD2, for cecal carcinoma

Assessment:
Preop BP meds not restarted, UO 75 ml over 8 hrs, Poor PO intake, AOx3

Started maintenance LR at 110 ml/hr
THEN
BP drops to 80/50, HR 120, UO <30ml/hr

What can be given?
How can fluid vol be assessed?

A

Does pt have CVC?

  • CVP
  • SVV
  • CO

US/Echo
-IVC collapsibility

GU cath

Give:
Colloid-albumin

183
Q

23 yo, 84 kg F for breast biopsy
Preop preparation

What preop labs MUST be done
What cath size placed preop?
What type of IVF?
What preop meds would you give?

A

preop-lab
PREGNANCY

Cath size:
what you can get, can usually get bigger cath once asleep, if needed

Fluid:
LR

Preop meds:
PONV prevention
Zofran, decadron, midazolam

184
Q

23 yo, 84 kg F for breast biopsy
In the OR
What type of anesthetic used?
Type of airway?

If not general, what can be used?
Type of airway

How do you decide which to use

A

Type of anesthetic:
GETA

Airway = ETT

Alternative anesthetic:
local w/ sedation

Airway = LMA

How to decide:
d/w pt; consider pt comfort

185
Q

A 23 yo 84 kg F undergoing breast biopsy is having GETA
What drugs w/ doses, in order are given

What inhalation could be given

A

PREOP = midaz 2 mg

  1. Fentanyl 150 mcg
  2. Lido 90 mg
  3. Propofol 170 mg
  4. Roccuronium 130 mg

Volatile
Sevo or Des (no iso)

186
Q

A 23 yo 84 kg F undergoing breast biopsy
Surgeon plans to inject a dye to track the lymph node distribution and asks for premedication to decrease likelihood of histamine reaction..

What 2 classes, specific drug for each class and dose

A

class:

  1. antihistamine
  2. H2 blocker

Drug/Dose

  1. Diphenhydramine 25-50 mg IV
  2. Famotidine 20 mg
187
Q

A 23 yo 84 kg F having breast biopsy under GETA

Surgeon is done w/ case, what are the things you must do to awaken the pt and move to the PACU…

A
  1. turn off gas
  2. Reverse NMBD
  3. Turn off vent to assess spont resp
  4. Pull LMA deep
  5. Give pain meds
  6. PONV prevention
188
Q

54 yo, 136 kg F undergoing lap-chole
-No PMH, no home meds, PCN all, postmenopausal
-IV in place, consents signed, Midaz 2 mg given and taken to OR
-Induced and intubated
Vt 650, RR 10, FiO2 40%, Vol control

Surgeon requests ancef 2 GMs
Is an abx required for this case?
Can the pt receive cefazolin?
Is 2 GMs appropriate dose?

A

Abx required?
NO

Can pt receive?
Assess rxn history
Can receive if NOT anaphylaxis

2 Gms ok?
It is since it’s not SCIP??
Weight based?
Surgeon ordered?

I don’t like that question….

189
Q

54 yo, 136 kg F undergoing lap-chole
-No PMH, no home meds, PCN all, postmenopausal

Vt 650, RR 10, FiO2 40%, Vol control

What position do you place the pt in?

Following positioning and insufflation, HIGH PIP alarms
What are likely causes?

A

Positioning:
Left-tilt
Revere TBurg

Causes of PIP:
VENT SETTINGS
-she's on VC 
Poor compliance d/t obesity and Insufflation
POSITION 
(ETT migration)
190
Q

54 yo, 136 kg F undergoing lap-chole
-GETA, Vt 650, RR 10, FiO2 40%, Vol control

You notice that PIP is 63 cmH2O, Vt 220, SpO2 84%

VC vs PC

  • Why could this be the problem
  • What should be changed

Abutment of carina and ETT

  • Could this be the problem?
  • What should be changed?
A

VC vs PC

  • Problem b/c HIGH pressures are generated to achieve the volume setting
  • Change to a pressure setting, just make sure pt is still getting volumes to prevent atelectasis

ETT against carina
-Not likely? Since pt is reverse TBurg. This would be more likely in TBURG right??

191
Q

54 yo, 136 kg F undergoing lap-chole
-GETA, Vt 650, RR 10, FiO2 40%, Changed vent setting from VC to PC

As surgery proceeds, the pts HR suddenly drops to 28/min

What is the most likely cause of the drop?
What are 3 possible interventions?

A

Cause:
Celiac reflex stimulation

Interventions

  1. Glycopyrolate
  2. Dec insufflation
  3. Stop
192
Q

16 yo F getting hysteroscopy and DandC s/p incomplete miscairrage.

No PMH, in OR induced, #3 LMA placed w/ good seal and pt positioned HOW?
What are risks w/ this position?
How can risks be prevented?

A 
Position = lithotomy 
Risk = peroneal nerve damage
Prevention = PAD stirrups
193
Q

16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage.

DandC is completed w/ ease and surgeon asks for pitocin

  • What is pitocin?
  • What is the dosing?
  • How fast should pitocin be given?
A

What is it:
Aka oxytocin, vasopression (ADH)
INC uterine contractions

What dose:
20 unit/liter
(can add to IVF w/ >500 ml left)
-Can lead to fluid retention

Rate of admin:
Wide open

194
Q

16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage.
She has received pitocin w/ the DandC

The surgeon proceeds w/ hysteroscopy and asks for I/O from the “scope”

What is she looking for?
Is there a minimal expectation?
What if the expected I/O doesn’t exist?
What are the causes of unequal I/O?

A

Looking for:
-Irrigation vs output

Minimal expectation:
-Output is equal to irrigation amount used to inflate uterus

What if it is unequal I/O?
-There is a significant risk of uterine perf which could mean lead to unequal I/O

What are causes
-Uterine perf which is a surgical emergency

195
Q

16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage. She received pitocin and had unequal irrigation I/O during hysteroscopy.

How would you convert the anesthetic to an emergency open laparotomy?

A
  1. Intubate
    - –Turn off gas to exchange LMA for ETT
  2. Change position, legs down, arms etc
  3. Give NMBD, turn gas back on
  4. Convert to open
  5. Change fluid administration (open abd inc fluid loss)
  6. Change vent settings
  7. pain meds
196
Q

What are risk factors that increase the likelihood pt will get HAI (8)

A
  • Pt immune status (on chemo, immunosuppressants)
  • Infxn control practices (hygiene)
  • Prevalence of population pathogens
  • Older age (altered immunity)
  • Longer hospital stay
  • multiple chronic illnesses
  • mechanical vent
  • Critical care stay
197
Q

Methods of HAI transmission

A
  • Direct contact w/ healthcare workers (poor/improper technique)
  • Contaminated environments (specific body parts)
  • Extraluminal migration
198
Q

Importance of and symptoms on History and physical that may suggest pre-existing infxn

A

Opportunity to document pre-existing infxn

Symptoms

  • Subjective fever
  • chills
  • night-sweats
  • AMS
  • Productive cough
  • SOB
  • Rebound tenderness
  • Dysuria
  • Suprapubic pain
  • CVA tenderness
199
Q

What are VS that may suggest the presence of infxn.

Are VS 100% indicative of infxn why/why not.

A 
VS:
HoTN
Tachypnea
Low sat
tachycardia

Infxn indication:
Subtle contribution
NOT 100% indicative
–Could be r/t other factors like hypovolemia, pain etc

200
Q

What is the importance of knowing placement of lines and tubes?

A

Was it placed in the hospital vs the field?

  • -field placement more prone to infxn
  • -consider exchanging outside lines/tubes
201
Q

What lab values may be evidence of infxn?

A

Labs that show organ dysfunction

Lactic acid = INC
PTT = INC
BUN/Crt = INC
WBC = INC (or really low)
Glucose = INC/DEC
Cultures
202
Q

When do SSIs typically occur and how much is spent yearly for recovery and hospitalization

What % makeup of nosocomial infections are SSI in surgical pts

A

Occur w/in 30 days of surgery

$$$
$3.5 - 8 billion spent yearly

% makeup
SSI = 38% of nosocomial infxn in surgical pts

203
Q

What are 3 types of SSI and examples.

A

Superficial incisional:
around the area of the incision

Deep incisional:
Just beneath the incisional area in muscle and tissue

Organ or space:
Any area other than skin and muscle. Includes organs or space btwn organs

204
Q

What are signs of SSI

A 
Redness
Delayed healing
Fever
Pain
Warmth
Swelling
Drainage of pus
205
Q

What types of bacteria are most commonly associated w/ SSI

A

Staphylococcus (native to skin)
Streptococcus
Pseudomonas

206
Q

Name, describe and give example of the 4 different types of SSI wounds.

A

Clean:
-NOT inflamed or contaminated
-NOT internal organ involvement
(deep stab wound in the thigh)

Clean-contaminated:
-NO evidence of infection
-INVOLVES internal organ
(deep abd stab wound that lacerates the diaphragm)

Contaminated:
-INVOLVES internal organs w/ spillag eof organ contents
(Abd stab wound that lacerates intestines)

Dirty:
-KNOWN infected at time of surgery
(maybe gangrenous wound?)

207
Q

What are factors that increase SSI risk (6)

A
  • Type of wound
  • Surgery lasting >2 hrs
  • Comorbidities
  • Elderly
  • Emergency
  • Abd surgery
208
Q

Based on a 2017 SR of 170 studies for SSI, what recommendations were made for treatment

A
  1. parenteral abx (well established, only when indicated)
  2. Non-parenteral abx (do not apply abx ointment to incision)
  3. Glycemic control (<200 mg/dl)
  4. Normothermia
  5. Oxygenation (INC FiO2 immediately after extubation)
  6. Antiseptic prophylaxis (
  7. Blood transfusion
  8. Systemic immunosuppressive therapy
209
Q

What are the 1B parenteral and non-parenteral abx guidelines for prevention of surgical infection

A

Parenteral abx:

  1. administer only when indicated
  2. timed so that agent is established in tissue upon incision

non-parenteral:

  1. no recommendation for abx irrigation
  2. Don’t apply abx ointment
210
Q

What is the 1A guidelines for glycemic control for prevention of surgical infeciton

A

Preop control:

-Glucose target <200 mg/dL

211
Q

What is the 1A recommendation for normothermia in prevention of surgical infectoin

A

Maintain periop normothermia to prevent bacteria flourishing (hot) and slow metabolism of anesthetic (cold)

212
Q

What are the 1A recommendations for FiO2 level intraop for surgical infection prevention

A

INC FiO2

  • pts w/ normal pulm fxn
  • GETA intraop
  • immediately AFTER extubation
213
Q

What are the level 1A, 1B and II antiseptic recommendations to prevent surgical infection

A

1A) intraop skin prep w/ alcohol-based antiseptic (must be 100% dry)

1B) Bathe w/ soap or antiseptic night before Sx

II) consider intraop iodine irrigation in deep tissue

214
Q

What are the recommendations for systemic immunosuppressive therapy to prevent surgical infection

A

Systemic corticosteroids:
-uncertain benefit or harm

Itra-articular:
-uncertain benefit or harm

215
Q

Most important considerations for surgical abx prophylaxis

A

Right surgery

Right time

216
Q

What is the goal of preoperative abx prophylaxis

A
  • Adequate bactericidal concentration in serum and tissue when incision is made
  • MIC prior to incision to prevent most common SSI
217
Q

Who is responsible for prophylactic abx and what is administration based on

A

anesthesia

based on evidence of specific abx based on surgical site

218
Q

6 general principles of abx prophylaxis

A
  1. Should be active against ocmmon surgical wound pathogens
  2. Proven efficacy in clinical trials
  3. Must achieve MIC
  4. Shortest course
  5. New abx for resistant infections (more $$$)
  6. Oldest and cheapest
219
Q

When should surgical abx be initiated?
What are the 3 considerations for administration?
What are the exceptions?

A

Initiated:
30 to 60 min before incision

considerations:

  • When is surgery? morning vs afternoon can affect abx timing
  • Completely infuse prior to tourniquet
  • may hold abx for cxr but must document

Exceptions:

  • Vanc or fluoroquinolones w/in 2 hrs
  • hold for drawing cxrs
220
Q

When does redosing of surgical abx occur

A
  • 2 half-lives (long procedures)
  • W/ excess blood loss
  • Following bypass
221
Q

Which abx is not redosing not necessary when pt is placed on cardiopulm bypass intraoperatively

A

vancomycin

222
Q

What are common surgical abx classes

A 
beta-lactams
vancomycin
aminoglycosides
fluoroquinolones
metronidazoles
223
Q

What are the types of beta-lactams and examples

A

PCN:
Pen G, methicillin, amoxicillin

Cephalosporins:
cefazolin, cefepime, ceoxitin, cetriaxone, cefepime

carbapenems:
meropenem, ertapenem

224
Q

What is the MOA for PCN beta-lactam abx?

How does resistance occur

A

Inhibit cell wall synthesis so cell can’t grow

D/t beta-lactamase enzyme
-on outer membrane and breaksdown abx

225
Q

What are DOC for PCN and which bacteria are targeted

A

DOC:
Pen G, amoxicillin, methicillin

Bacteria:
Strep, meningococci, pneumococci

226
Q

Potential adverse rxns to pcn

A
  • hypersensitivity
  • GI upset w/ large doses
  • vaginal candidiasis
227
Q

Educational information for women who receive PCN

A

Vaginal candidiasis

  • Possibility for vaginal yeast overgrowth
  • use OTC tx if experiencing symptoms
228
Q

What is the MOA of cephalosporins?

What bacteria are the active against?

A

MOA:
-broader, more stable beta-lactam

Active against
GRAM + cocci
staph and strep

229
Q

Which abx might be the best choice if pathogen is unknown

A

Cephalosporin

230
Q

In what cases are cephalosporins the DOC?

Can they be used in the presence of PCN allergy? why/why not?

A

Surgical prophylaxis
-primary abx used

CAN be used w/ PCN allergy

  • cross-sensitivity unlikely
  • DO NOT use if pcn anaphylactic rxn
231
Q

Give examples of generation 1, 2, 3, and 4 cephalosporins

A

1:
cefazolin (ancef)

2:
Cefuroxime (ceftin)
cefoxitin (mefoxin)
cefotetan (cefotan)

3:
cefotaxime (claforan)
ceftriaxone (rocephin)
ceftazidime (fortaz)

4:
cefepime (maxipime)

232
Q

What is the big difference in the cephalosporin generations

A

How well they cross the BBB

1st gen do NOT penetrate BBB
4th gen penetrate BBB

Also, 4th gen have increased resistant to hydrolysis by beta-lactamase

233
Q

What are possible adverse rxns to cephalosporins

A

Hypersensitivity
-rashes, fever, nephritis, anaphylaxis

INC likelihood of rxn IF PCN allergy is anaphylaxis

234
Q

What abx should be used if a pt has a true pcn anaphylaxis and cannot receive cephalosporin

A

vancomycin or clindamycin

235
Q

What is the MOA of carbapenems?
Do they cross BBB
Which bacteria are they active against?

A

beta lactam = inhibit cell wall synthesis

Most penetrate BBB

Active against:
P aeruginosa
enterobactor

236
Q

Consideratins for use of carbapenems

A

Expensive $$$
Not used often b/c:
-cephalosporins have good broad-spectrum activity
Best to use when bacteria is known

237
Q

What are examples of carbapenems

A

ertapenem

meropenem

238
Q

Possible adverse reaction r/t carbapenem administration

A 
n/v
diarrhea
rashes
injeciton site rxn (w/ IM)
Cross sensitivity w/ PCN <1%
239
Q

What is the MOA of vancomycin

Types of bacteria it is effective against

A

Inhibits cell wall synthesis

bacteria:
Gram +

240
Q

Why is vanc not effective against gram - organisms

A

Vanc is too large to penetrate gram - wall

241
Q

Drawbacks to use of vancomycin

A

Very slow to treat infxn
-Must be given for several days to be effective

More adverse effects

242
Q

In what cases is vanc the DOC

A

blood-stream infxn
endocarditis

DOC for:

  • hearts and valves
  • infxns caused by MRSA
243
Q

Describe adverse rxns associated w/ vancomycin administration

A
  • Phlebitis at injection site
  • Chills, fever
  • NEPHROTOXICITY
  • RED-MAN syndrome
244
Q

How are adverse effects of vanc prevented, give specifics

A

Nephrotoxicity:
-Give vanc over 2 hrs

red-man syndrome:

  • Give antihistamine before or during admin
  • SLOW administration rate
245
Q

What is the MOA of aminoglycosides

A

Inhibition of ribosomal proteins:

  • Causes mRNA to misread
  • Bacteria replication is not identical or survivable
246
Q

Which abx has significant post-abx effect?

What does this mean?

A

Aminoglycosides

Means:

  • Long lasting
  • Works for significantly longer than other abx
247
Q

Which abx should be given 2 hrs before incision

A

Vanc
Fluroquinolones
aminoglycosides

248
Q

Example and use of aminoglycoside abx

A

Example:
gentamycin

Use:

  • Against enterococcal endocarditis
  • infected valves pre-op
249
Q

Describe the adverse reactions associated w/ aminoglycoside administration and how to prevent them

A

Ototoxicity:
give slowly to prevent

Nephrotoxicity:
-give slowly

Curare-like effect

250
Q

When is nephrotoxicity more likely to occur w/ aminoglycoside administration

A
  • In elderly
  • When using for >5 days
  • In renal insufficiency
  • w/ higher doses
  • Concurrent loop diuretic use
251
Q

Describe curare-like effects of gentamycin

A
  • Potentiates NMBDs

- Can make reversal longer

252
Q

What is the moa of fluorquinolones

What organisms are they useful against

A

inhibits DNA protein synthesis

Useful against:
GRAM -

253
Q

What are general and surgical uses of fluorquinolones

A

General:
UTI, bacterial diarrhea, bone or joint infections

Surgical use:
Prostate sx, uro cases, kidney stones, KUB sx

254
Q

Examples of fluorquinolones

A

Ciprofloxacin (cipro)

Levofloxacin (levaquin)

255
Q

Describe adverse reactions associated w/ fluoroquinolone use

A
  • n/v/d
  • prolong QT
  • cartilage damage/tendon rupture
256
Q

When is cartilage damage or tendon rupture more likely to occur in relation to fluoroquinolone use

A

Usually occurs w/ the achilles tendon

  • Renal insufficiency
  • concurrent steroid use
  • advanced age
  • teenagers
257
Q

Metronidazole MOA and uses

A

MOA:
Forms toxic byproducts that causes unstable DNA molecules
Antiprotozoal
anaerobic antibacterial

USE:
Intra-abd infxn (intestinal spill)
vaginitis
c-diff

258
Q

Adverse reactions associated w/ metronidazole administration

A

Nausea
peripheral neuropathy
Disulfiram-like effect

259
Q

Describe symptoms associated w/ disulfiram-like reaction? When can this happen

A

Symptoms:
hangover-like
flushing, dizziness, HA, chest/abd pain

Happens with metronidazole taken w/ alcohol

260
Q

How does a surgical infection impact the length of hospital stay and $$

A

Increase hospital stay 7 days

Increase cost $3,000

261
Q

How doe surgical complications last 30 days affect survival and mortality rates

A

DECREASES median survival to 69%

INCREASES mortality rate

262
Q

What is the difference between SCIP and SIP

A

SIP = surgical infection prevention
-focus is on preventing surgical infection

SCIP = surgical care improvement project
-focus is on improving ALL outcomes from surgery

263
Q

What was the goal of SIP when it was initiated in 2002 by CMS

A

DEC morbidity and mortaility of SSI

264
Q

What were the 3 performance measures used to address SIP

Why were these measures chosen?

A
  1. Proportion of pts who get abx started w/in 1 hour of incision (GIVEN ON TIME)
  2. Proportion given abx regimen consistent w/ guidelines (CORRECT ABX)
  3. proportion of pts whose abx is d/c’d w/in 24 hrs of surgery stop (STOP TIME)

Chosen b/c:

  • Timing and selection of abx have positive correlation w/ SSI incidence
  • Excessive use of abx promotes bacterial resistance
265
Q

As of 2004, which SIP measure has been most consistently followed?
Which measure has the greatest fallout?

A

Most consistently = Correct agent (92.2%)

Greatest fallout = D/C 24 hrs after surgery (52.9%)

266
Q

What was the goal of SCIP and what year did it begin

A

Goal:
reduce surgical complications by 25% by 2010

Started:
2005

267
Q

Who was involved in initiated the SCIP measures and who participated on the steering committee

A

Initiated by:
CMS
CDC

Steering committee
AHRQ
ACS
AHA
ASA
APeriopRN
CDC
CMS
VA
IHI
JC
268
Q

What measures are addressed with SCIP (7)

A 
Abx
BB 
Hair
Foley
Sugars
DVT
Temp
269
Q

Describe the abx measure of SCIP

A
  • Give w/in 1 hr of incision to achieve MIC
  • Chose correct abx for procedure
  • D/C abx w/in 24 hrs of surgery completion
270
Q

Describe BB measure of SCIP.

What are the exceptions

A

For all pts on BB therapy

  • must have any dose of any BB w/in 24 hrs prior to surgery DOCUMENTED
  • RESTART BB post-op

Exception:
HoTN, Bradycardia–documented

271
Q

Describe hair measures under SCIP

A

Hair removal must be documented

  • NO razors or shaving
  • USE clippers

Pt may perform hair removal

272
Q

Describe the foley measures of SCIP

A

REMOVAL of GU cath on or before POD 2

-order must exist to extend cath use

273
Q

What are indications for GU cath placement in surgery

A
  • Surgery >2 hrs
  • hemodynamically unstable
  • fair indicators of renal perfusion
274
Q

Describe glucose control measures of SCIP

A

-Cardiac pts =200
some evidence indicates
-=180 mg/dL w/in 18-24 hrs s/p anesthesia

275
Q

Describe DVT measures of SCIP

A
  • SCDs MUST be placed PRIOR to induction**
  • Appropriate DVT prophy on admit orders (mechanical and pharma)
  • RN to give DVT prophy w/in 24 hrs of surgery end
276
Q

Describe temp measures of SCIP

A
  • Maintain normothermia or ACTIVE warming in OR (w/ any measure)
  • 1st PACU temp >/96.8F, 36C 15 min after leaving OR
277
Q

Why is pt normothermia important to the anesthetist

A

B/c anesthetic metabolism depends on normothermia

-hypothermia = slower metabolism

278
Q

What was important outcome of the 2010 reetrospective study of 398 hospitals using SCIP….

A

All or none composite preventions SS

-More than not, SCIP is beneficial in decreasing post-op M/M than NONE of them

279
Q

How does ERAS differ from SCIP

A

ERAS has a broader scope than SCIP

  • doesn’t focus on periop outcomes
  • considers PRE-admission, perioperative and discharge outcomes
280
Q

what is the purpose of ERAS

A
  • Focus on pt needs through out surgical care
  • To DEC complications
  • Help pt feel better
  • Help pt heal and tolerate sx better
281
Q

When were first ERAS EBP protocols published and for which surgical population

A

2005

For pts undergoing colon surgery

282
Q

Who helped establish ERAS and when

Why did they do this

A

2001
Ken Fearon and Olle Ljungvist

Compare their actual practice to what was considered “best” practice

283
Q

What was the evolution of ERAS dissemination internationally

A 
2003 = 1st ERAS symposium in Stockholm, SWEDEN
2012 = 2nd symposia in SWITZERLAND
2012 = 1st world congress in FRANCE
2016 = 1st US even
284
Q

What is the intended outcome of ERAS

A
  • DEC LOS
  • DEC morbiditiy
  • DEC overall cost
285
Q

What makes for successful ERAS protocol institution

A

Protocols tailored to the facility

Buy-in and adoption from all areas

286
Q

What are some pre-hospital components included in an ERAS protocol

A
  • Pt receive preop counseling
  • –ERAS guidelines
  • –pt expectations
  • –IS demo
  • –NPO guidelines
  • – Postop prescription education

Fill prescriptions

Optimization for risks

  • Identify needs
  • Deep breathing education
  • Smoking cessation
287
Q

What are some pre-op components of an ERAS protocol

A
  • Pt weight
  • NPO status adheres to ASA guideline
  • Glucose control
  • Skin clean (bathe)
  • Normothermia
  • IVF (minimal)
  • Multimodal pain mgmt
  • colorectal/procedure specific -meds
  • PONV prophy
288
Q

What are risk factors for PONV based on the Apfel tool

A

Female gender
Nonsmoker
H/o PONV or motion-sickness
Use of opioids

289
Q

What are the PONV % incidence w/ 0-4 risk factors

A 
0 = 9%
1 = 20%
2 = 39%
3 = 60%
4 = 78%
290
Q

Apfel tool recommendations for prophylaxis strategies based on risk factors
0, 1, 2, 3, 4

A

0 = none

1:
4 mg dex
+/-2nd antiemetic

2:
avoid inhalation agent
4 mg dex
+/-2nd antiemetic

3:
avoid inhalation
+4 mg dex
+2nd prophylactic (scop)

4: 
avoid inhalation
\+4mg dex
\+NK-1 antagonist
\+/-2nd prophylactic
291
Q

What are some intra-op components of ERAS

A 
ANALGESIA  
maintenance phase:
-short acting
-minimize opioids
-BB for DL
-ketamine, Mg, precedex, prop

Emergence phase:
-toradol, decadron, ofirmev, RA

Regional:
GA + epidural/spinal/intrathecal opioids/ESP/TAP…

292
Q

What are some post-op components of ERAS

A
  • IVF therapy
  • –GDFT
  • –Avoid overload
  • –PO instead of IV
  • PONV prevention
  • Early GU cath removal
  • Early PO nutrition
  • Non-opiod analgesia
293
Q

What are some post-DC components of ERAS

A
  • Reinforce realistic pain expectations and goals
  • Tool for breakthrough opioid use
  • Schedule non-opioids and NON-scheduled opioids

Ane Principles II (3 decks)

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