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Flashcards in Aspiration Deck (81)
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1
Q

gastric aspiration

A

stuff that comes out of stomach (acid, stomach contents) and travels up esophagus into lungs

2
Q

aspiration pneumonitis - result of?

A

result of what happens after the gastric aspiration

- pulmonary aspirations syndrome

3
Q

pulmonary aspiration

A

gastric aspiration

4
Q

pneumonia

A

occurs in pts that aspirate infectious material (ex: from small bowel obstruction) or immunocompromised

5
Q

pneumonitis - what is it?

A

chemical injury results from acid or particulates in stomach coming in contact with lung tissue and damaging the tissue.

6
Q

aspiration pneumonitis- when ingested highly acidic particulate?

A

may cause severe reap damage with infectious component, possible to show no signs of infection and later develop pneumonia overtime DT lung injury and prolonged resp support. 1/2 of aspirations lead to pneumonia.

7
Q

ppl more disposed to aspiration

A

OB, peds, trauma with low GCS = 33% aspirate

8
Q

Mortality rates are dependant on?

A

amount and characteristics- Ph? is it a liquid or solid

9
Q

Swallowing - sensory innervation

A

CN V, IX, X. to brainstem in medulla. Afferent
5 - trigeminal,
9 - glossopharyngeal
10- Vagus

10
Q

swallowing- motor innervation

A
CN V, VII, IX, X, XII  Efferent
 5- trigeminal
 7- fascial 
 9- Glossopharyngeal
 10- Vagel 
 12- Hypoglossal
11
Q

3 stages of swallowing

A
  • oral cavity= where you chew the food
  • pharyngeal= where soft palate moves upward and back sealing off the nasopharynx, vocal cords close. epiglottis covers laryngeal opening.
  • esophagus= paristalic waves generated by musculature in the hallow esophagus moves food into the stomach
12
Q

Upper esophageal sphincter (UES)/ Lower esophageal sphincter (LES)

A

Thickening of the muscle that helps prevent aspiration of stomach contents

  • not true sphincters
  • helps food pass down into stomach and with increased tone they help food from regurgitation back into esophagus
  • relax in general anesthesia and increase risk of aspiration
13
Q

UES

A

in the upper airway

14
Q

LES

A

right above stomach

15
Q

stomach

A
  • Rugae= muscular ridges allowing stomach to expand allowing to hold more food and fluid
  • increased amount of food = increased gastric pressure = increased risk for regurgitation
  • inferior to diaphragm
16
Q

3 functions of the stomach

A

1- storage
2- mixing
3- propulsions

17
Q

3 functions of the stomach

mixing

A

Mixing- with hydrochloric acid (pH 1-2)
- with food or fluid, very acidic and if it regurgitates and goes to lungs it can do a huge amount of damage to the lung being so acidic –> creating a burn

18
Q

3 functions of the stomach

propulsions

A

propulsion- time is dependent on what is in the stomach and drugs can increase or decrease gastric transit time.
- stomach contracts from top to bottom –> moving food from stomach and into small intestine. H2O leaves stomach quick, fried food takes longer to move. Time is a factor.

19
Q

Gastric emptying time is dependent on:

A
  • type of food
  • amount of food
  • state of being
  • presence of pathophysiological conditions
20
Q

Gastric emptying time is dependent on:

type of food

A

clear liquid or solid, high fat

21
Q

Gastric emptying time is dependent on:

amount of food

A

increased amount = longer it takes to leave stomach

22
Q

Gastric emptying time is dependent on:

state of being

A
  • depending on the PNS and SNS and which one is in charge.

Balance each other out

23
Q

Gastric emptying time is dependent on: PNS

A

increased tone of PNS helps facilitate process.

- gastric digestion is going at a regular rate and things are moving out of stomach. Increase of PNS tone

24
Q

Gastric emptying time is dependent on: SNS

A

digestion is not a priority, decreased gastric emptying
- increased SNS= decreased gastric emptying.
pH may be low
- surgical pts, trauma, anxiety, fear

25
Q

Gastric emptying time is dependent on:

- presence of pathophysiological conditions

A

hiatel hernia
DM type 1 specifically autonomic neuropathy who develop gastroparesis. –> slow gastric emptying times
bowel obstruction- things not moving, staying in stomach increases pressure –> increased risk of vomiting.

  • cant do anything about condition but you can use different maneuvers during induction to decrease risk
26
Q

LES

A

esophagus through diaphragm at esophageal juncture and thickening of membrane in esophagus

27
Q

LES other names

A

gastroesophageal juncture

cardiac sphincter

28
Q

LES with ventilation

A

when ventilating with mask or LMA= high ventilation pressures–> push air into stomach = LES unable to remain closed.
20cm H2O is the max pressure for ventilation
>20cm H2O overcomes the LES tone allowing air to enter the stomach

29
Q

Length of LES and Length of esophagus

A

LES- 2-3cm in length

esophagus- 10 inches

30
Q

Pyloric stenosis

A

in peds- mimics bowel obstruction, sphincter becomes stenotic keeping food and fluid from passing through = increased gastric pressure –> projectile vomiting

31
Q

Anatomy of the UES

A

not a true sphincter. Constrictor muscle present in pharynx.
- after swallowing allows us to keep food in esophagus –> stomach

32
Q

Cricopharyngeus

A

constrictor muscle in UES. buildup of hypertrophy muscle that sits in esophagus btw the larynx and cricoid cartilage.

33
Q

UES and LES in anesthesia

A

tone is impaired in both –> increased risk of aspiration

34
Q

Regurgitation of gastric contents

A

barrier pressure

active vs passive

35
Q

Regurgitation of gastric contents

- barrier pressure

A

difference btw LES tone and intragastric pressure.
- if intragastric pressure is high DT food, and you give anesthetic –> decreased LES tone and increased aspiration risk
Anesthesia- we want increased LES tone and decreased intragastric pressure = so we give meds to increase tone
INCREASED BARRIER PRESSURE BY INCREASING LES TONE

36
Q

Regurgitation of gastric contents

- active

A

reverse peristalsis = throwing up

37
Q

Regurgitation of gastric contents

- passive

A

happens in anesthesia with decreased tone in supine position –> regurgitation

38
Q

aspiration and ETT

A

can still aspirate but the CUFF is the best protection against aspiration

39
Q

Causes of regurgitation

A

increased intragastric pressure

decreased LES tone

40
Q

Causes of regurgitation

- increased intragastric pressure

A

food/ fluid, blood (surgeries in mouth and throat), air from ventilator

41
Q

Causes of regurgitation

- decreased LES tone

A

most anesthetics, ETOH, heroin - decreases gastric emptying time, esophageal CA, DM type 1, self medicating
- use of gastric tube through sphincter= you inhibit the use of the sphincter and contents can travel following the tube, and if insertion is traumatic you can have increased blood in the stomach.
PREGNANCY AND OBESITY

42
Q

gastric tube

A

no evidence that it decreases risk, clinicians preference. use of gastric tube to prevent aspiration- not common practice

43
Q

pt at biggest risk for aspiration??

A

HEAD TRAUMA!

44
Q

PNS- ACH

A

increased gastric emptying, increased digestion, increased LES tone, increased peristalsis

45
Q

Hiatal Hernia

A

displaced esophageal junction, LES displaced and nonfunctional or incompetent
- stomach goes through the esophageal hiatus and is superior to the diaphragm.

46
Q

dilated esophageal hiatus

A

dilation allows the upper portion of the stomach to herniate through the esophageal hiatus

47
Q

influence of surgical procedure on regurgitation and aspiration

A

if sugery is intragastric = increased risk. bowel obstructions - increased risk

48
Q

influence on airway management on regurgitation and aspiration

A

no studies showing increased risk is higher for mask ventilation or LMA, however contraindications for LMA or mask include all the risk factors for aspiration.
ETT- use cuffed.

49
Q

influence of patients position of regurgitation and aspirations

A

prone- pressure on abdomen

50
Q

ASA classifications

A

1-2= healthy
3-5= sicker and more comorbidities with decreased ability to come back from aspiration. –> death
- higher ASA classification= increased risk of aspiration and complications
- elective surg= always less risk than emergency

51
Q

obesity

A

decreased peristalsis - has not been proven but we always treat as risk factor anyways.

52
Q

factors that increase the risk of aspiration in the pregnant patient

A
  • incompetent LES dt baby –> 3rd trimester = worst. c/o esophageal reflux
  • decreased peristalsis (increased volume)
  • increased gastric acidity
  • difficult airway from edema during pregnancy
53
Q

Pregos are considered to have full stomachs at…

A

12- 14 weeks gestation

54
Q

GERD

A

contraindication with LMA. always investigate further

55
Q

Factors that increase the risk of aspiration in obese population

A
  • decreased LES effectiveness
  • increased intragastric pressures
  • difficult airway
56
Q

Vomiting

- area postrema

A

increased receptor sites, dopamine, serotonin, histamine, ACH, and opiate receptors
- Chemoreceptos trigger zone here!

57
Q

Chemoreceptor trigger zone (CTZ)

A

in medulla below 4th ventricle in area postrema

  • posterior to medulla
  • trigger alone can cause N/V
  • affected by medications (powerful emetic affect on CTZ, anesthetics), radiation, toxins, metabolic alterations
  • sends signal to vomiting center
58
Q

cortical afferents

A

sending signal to vomiting center

  • hypoxia
  • pain
  • increased ICP
  • sight, smell, taste
  • psychologic factors
59
Q

vomiting center

A

in brainstem- triggering act of vomiting

60
Q

Visceral afferent

A

send signal to vomiting center

  • diseases of the heart, GI tract, biliary tract, or GU tract
  • Symptom of MI = Nausea
  • Spinal anesthetic= manipulating GI or GU tract -nausea
61
Q

in anesthesia we give meds to counteract vomiting by

A

drugs that antagonize dopamine, serotonin, histamine, and opiod= antagonize the receptors in the CTZ

62
Q

Severity of the S&S after pulmonary aspiration are dependant on!

A

1- volume of aspirate
2- pH of aspirate
3- type of aspirate (liquid/solid) solids continue to cause damage
4- pt condition. pts with other issues ASA 3-5, more at risk for pulm inn after aspirating, trouble compensating with decreased PO2 and increased PCO2
- Can manipulate 1 &2 with drugs and OG

63
Q

cellular changes with aspiration of gastric contents

A

1- alveolar capillary membrane degenerates and interstial edema occurs
2- alveolar type 2 degeneration, destroying alveloar type 2 cells which produce surfactant–> atelectasis, hypoxia, hypercabia
3- microhemmorrhaging in alveolar cap membrane
4- inflammatory process caused by release of inflammatory mediators and usually occurs 1-2 hours after pulm injury

64
Q

differential diagnosis after gastric aspiration

A

pulmonary edema

65
Q

neutrophils

A

cause inflammatory process.

IV lidocaine can decrease neutrophil response

66
Q

clinical sequelae associated with aspiration of gastric contents

A
  • hypoexmia = earliest and most reliable indication
  • bronchospasm
  • tachypnea
  • tachycardia
  • resp distress
  • pt develops rales
  • hypertensive –> hypotension
  • ARDS–> DIC
67
Q

clinical sequelae associated with aspiration of gastric contents
- Hypoxemia

A

Earliest and most reliable indication.

- Silent aspiration- 1st indication is hypoexmia, hypoxemia that is unexplained –> think aspiration

68
Q

clinical sequelae associated with aspiration of gastric contents
- Hyper/hypotension

A
  • Hypertension= DT being hypoxic and hypercarbic
  • hypotension may develop later as a response to inflammatory mediator response and pulm edema
  • pulm edema –> decreased BP
69
Q

aspiration pneumonia and pneumonitis can lead to

A

DIC - DT release of inflammatory mediators

70
Q

Acute Lung injury (ALI) associated with gastric aspiration

- phase 1

A

immediate damage, damages the lung tissue

  • destruction of alveolar and capillary basement membranes, desquamination of cells –> increased permeability of alveoli –> interstiital edema.
  • reduced compliance of alveoli and V/Q mismatches
71
Q

ALI

- phase 2

A

inflammatory response depending on degree of damage and intense inflasmmatory rxn can occur characterized by plum edema and hemorrhage.
- release of many inflammatory mediators by alveolar macrophages

72
Q

ALI

  • phase 2
  • inflammatory mediators released
A
by alveolar macrophages
Mediators: 
- interluken 8 
- tumor necrosis
- inflammatory cytokines
- histamine
73
Q

release of mediators attracts

A

neutrophils - which play a key role in releasing O2 radicals and proteases

74
Q

if pulmonary inj is severe secondary inj can result in

A

fibrin deposits

- necrosis of alveolar cells –> V/Q mismatches and hypoxemia

75
Q

CXR

A

may not show infiltration for 4-6 hours

- will see white fluffy infiltrates

76
Q

pt condition 2 hours after aspiration show prognosis criteria for discharge

A

1- pt does not develop cough or wheeze
2- pt sats do not decrease more than 10% from preop levels on RA
3- no radiographic evidence of pulm aspiration

77
Q

non-acidic liquid aspirated

A

may have some bronchoconstriction, wheezing, atelectasis

- pH, CO2 and O2 stay normal

78
Q

Acidic liquid

A

presence of alveolar capillary destruction

  • interstitial and alveolar edema
  • may exhibit some hypoxia, hypercarbia
79
Q

solid/liquid

A

when fluid burns lung - it then dissipates and burning stops
when food enters lung it does not dissapate and becomes diluted by fluid and continues to do damage

80
Q

non-acidic food particles

A
  • alveolar destruction
  • inflammatory process occuring
  • micro hemorrhaging
81
Q

acidic food

A

total destruction of alveolar cap membrane

  • micro-hemorrhaging
  • extremely hypoxic and hypercarbic
  • require vent assistance with ETT