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APEXANESTHESIA COPY COPY > UNIT 1 Respiratory > Flashcards

UNIT 1 Respiratory Flashcards

1
Q

Which muscles tense & relax the vocal cords? Which muscles abduct & adduct the vocal cords?

A

Tense & Relax:

  • cricothyroid “cords tense”
  • thyroarytenoid “they relax” & vocalis

Abduct & Adduct:

  • thyroarytenoid & lateral cricoarytenoid: adduct
  • posterior cricoarytenoid: abduct
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2
Q

Which muscles abduct & adduct the vocal cords?

A

posterior cricoarytenoid: “please come apart”

lateral cricoarytenoid: “let’s close the airway”

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3
Q

Describe the sensory innervation of the upper airway

A

Trigeminal (CN V)
V1 (opthalmic): nares & anterior 1/3 of septum
V2 (maxillary): turbinates & septum
V3 (manidbular): anterior 2/3 of tongue

Glossopharyngeal (CN IX)
posterior 1/3 of tongue, soft palate, oropharynx, vallecula, anterior of epiglottis

SLN
internal branch: posterior side of epiglottis –> level of VC
external branch: no sensory

RLN
below VC –> trachea

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4
Q

How does RLN injury affect integrity of the airway?

A

Bilateral:
acute = respiratory distress d/t unopposed action of the CT muscles)
chronic = no respiratory distress

Unilateral
no respiratory distress

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5
Q

How does SLN injury affect the integrity of the airway?

A

Bilateral:
hoarseness but no respiratory distress

Unilateral:
no respiratory distress

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6
Q

Name 3 airway blocks, and ID the key landmarks for each one.

A
  1. glosspharyngeal block: palatoglossal arch @ the anterior tonsillar pillar.
  2. SLN block: greater cornu of hyoid.
  3. Transtracheal block: CT membrane
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7
Q

What are the 3 paired & 3 unpaired cartilages of the larynx?

A

unpaired: epiglottis, thyroid, cricoid
paired: corniculate, cuniform, arytenoid

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8
Q

What is the treatment for laryngospasm?

A 
100% FiO2
remove noxious stimuluation
deepen anesthesia
CPAP 15-20cmH2O
open airway w/ head extension, chin lift
Larson's maneuver
succinylcholine
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9
Q

Describe how the respiratory muscles function during the breathing cycle.

A

Inspiration:

  • diaphragm & external intercostals (tidal breathing)
  • accessory: sternocleidomastoid & scalene m.

Expiration:

  • usually passive
  • active via abdominal musculature (rectus abdominis, transverse abdominis, internal & external obliques) & secondarily via internal intercostals
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10
Q

What is the difference between minute ventilation & alveolar ventilation?

A

MV: air in a single breath x # breaths per minute (Ve = Vt*RR)

AV: only measures the fraction of Ve that is available for gas exchanges (i.e. it removes anatomic dead space gas) (AV = (Vt-dead space)*RR)

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11
Q

Define the 4 types of dead space.

A
  1. Anatomic (air confined to the conducting airways)
  2. Alveolar (alveoli that are ventilated but not perfused)
  3. Physiologic (Anatomic + Alveolar Vd)
  4. Apparatus (Vd added by airway equipment)
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12
Q

Provide an example for each type of dead space.

A
  1. Anatomic = trachea
  2. Alveolar = Zone 1 alveoli
  3. Physiologic = see above
  4. Apparatus = face mask
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13
Q

What does the alveolar compliance curve tell you?

A

alveolar ventilation is a function of alveolar size & it’s position on the alveolar compliance curve.

  • best ventilated alveolar are the most compliant (steep slope of curve)
  • worst ventilated alveoli are the least compliant (flat portion of the curve)
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14
Q

What does the V/Q ratio represent?

A

V/Q is the ratio of ventilation to perfusion

  • normal MV = 4L/min
  • normal CO = 5L/min
  • -> normal V/Q = 0.8

dead space V/Q –> infinity
shunt V/Q –> 0

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15
Q

Define the West zones of the lungs

A

Zone 1
PA>Pa>Pv
dead space (ventilation w/out perfusion)

Zone 2
Pa>PA>Pv
waterfall (normal physiology)

Zone 3
Pa>Pv>PA
shunt (perfusion w/out ventilation)

Zone 4
Pa>Pist>Pv>PA
pressure in the interstitial space (i.e. pulmonary edema) impairs ventilation & perfusion

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16
Q

Recite the alveolar gas equation

A

PAO2 = FiO2(Pb-PH2O)-(PaCO2/RQ)

tells us that hypoventilation can cause hypercarbia & hypoxemia.
normal = approx 106mmHg

Pb = 760mmHg sea level
PH2O = 47mmHg
RQ = CO2 elimination/O2 consumption = 200/250 = 0.8 
- RQ = 1 --> over feeding
- RQ < 0.7 --> starvation
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17
Q

What is the A-a gradient and what factors affect it?

A

difference b/n alveolar oxygen (PAO2) & arterial oxygen (PaO2)

  • helps diagnose cause of hypoxemia by quantifying the amount of venous admixture
  • it is normally 5-15mmHg
  • it is increased by high FiO2, aging, vasodilators, R–>L shunting, and diffusion limitation
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18
Q

List the 5 causes of hypoxemia. Which ones are reversed w/ supplemental oxygen?

A
  1. Reduced FiO2
  2. Hypoventilation
  3. Diffusion Limitation
  4. V/Q mismatch
  5. Shunt

1-4 are reversed w/ supplemental oxygen.

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19
Q

Define the 5 lung volumes & give reference values for each.

A
  1. inspiratory reserve volume (3000mL)
  2. tidal volume (500mL)
  3. expiratory reserve volume (1100mL)
  4. residual volume (1200mL)
  5. closing volume (variable - approaches RV in healthy young patients)
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20
Q

Define the lung capacities & give reference values for each.

A
  1. total lung capacity (5800mL)
  2. vital capacity (4500mL)
  3. inspiratory capacity (3500mL)
  4. functional residual capacity (2300mL)
  5. closing capacity (variable)
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21
Q

What factors influence FRC?

A

FRC = RV + ERV (35mL/kg)

conditions that reduce FRC tend to reduce outward lung expansion and/or reduce lung compliance –> zone III (shunt) increases. PEEP restores FRC by reducing zone III

  • position changes
  • increased intraabdominal pressure/contents
  • anesthesia/NMB
  • surgical displacement

COPD or any condition that causes air trapping increases FRC

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22
Q

Why can’t spirometry measure FRC?

A

Because it contains RV & the RV cannot be measured by spirometry

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23
Q

What tests can measure FRC?

A

nitrogen washout
helium wash in
body plethysmography

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24
Q

What is closing volume & what increases it?

A

the point at which dynamic compression of the airways begins.
the volume above residual volume where the small airways begin to close during expiration

CLOSEP:

  • COPD
  • LVF
  • Obesity
  • Supine position
  • extreme age
  • pregnancy
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25
Q

State the equation and normal value for oxygen carrying capacity

A

CaO2 = SaO2Hgb1.34 + PaO2*0.003

normal = 20mL O2/dL

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26
Q

State the equation and normal value for oxygen delivery

A

DO2 = CaO2CO10

normal = 1000mL O2/min

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27
Q

Discuss the factors that alter oxyhemoglobin dissociation curve

A

Left shift (love, increased affinity, decreased offloading to the tissues)

  • decreased temperature
  • decreased 2,3-DPG
  • decreased CO2
  • alkalosis/decreased [H+}
  • abnormal Hgb (HgbF, HgbCO, HgbMet)

Right shift (release, decreased affinity, increased offloading to the tissues)

  • increased temperature
  • increased 2,3-DPG
  • increased CO2
  • acidosis/increased [H+]
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28
Q

How is CO2 transported in the blood?

A

bicarbonate 70%
bound to Hgb 23%
dissolved in plasma 7%

CO2–> HCO3- requires carbonic anhydrase & release of HCO3- from RBC to plasma causes Cl- shift (aka Hamburger shift)
–> RBC increases in size

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29
Q

Describe the Bohr effect

A

describes O2 carriage

states that increased CO2 & decreased pH causes RBC to release O2

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30
Q

Describe the Haldane effect

A

describes CO2 carriage

states that increased O2 causes RBC to release CO2 (occurs in the lungs)

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31
Q

List the 3 primary causes of hypercapnia and provide examples of each

A
  1. increased CO2 production (sepsis, overfeeding, malignant hyperthermia, shivering, seizures, thyroid storm, burns)
  2. decreased CO2 elimination (a/w obstruction, increased Vd, increased Vd/Vt, ARDS, COPD, respiratory depression, drug OD, inadequate NMB reversal)
  3. rebreathing (incompetent one-way valve, exhausted soda lime)
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32
Q

Describe the 4 areas in the respiratory center

A

Medullary Respiratory Centers:

  1. Dorsal respiratory center: active during inspiration (respiratory pacemaker)
  2. Ventral respiratory center (active during expiration)

Pontine Respiratory Centers:

  1. Pneumotaxic center (upper pons): inhibits the DRC
  2. Apneuristic center (lower pons): stimulates DRC
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33
Q

Contrast the location & function of the central & peripheral chemoreceptors.

A

Central:

  • located in the medulla
  • responds to the [H+] in the CSF ([H+] is a function of the PaCO2 of the blood)

Peripheral:

  • located in the carotid bodies: nerves of Hering –> CN IX (glossopharyngeal)
  • located in the aortic arch (vagus CN X)
  • respond to decreased O2, increased CO2, and increased H+
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34
Q

Which reflex prevents overinflation of the lungs?

A

Hering-Breuer inflation reflex

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35
Q

What is hypoxic pulmonary vasoconstriction?

A

minimizes shunt by reducing blood flow through poorly ventilated alveoli

a low PAO2 (NOT arterial) is the trigger that activates HPV.
- effect begins immediately & takes 15mins for full effect.

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36
Q

What things impair HPV & what is the consequence of this?

A

Anything that inhibits HPV increases shunt (perfusion w/out ventilation)

  • halogenated anesthetics >1-1.5MAC
  • PDE inhibitors
  • dobutamine
  • vasodilators

IV anesthetics DO NOT inhibit HPV

37
Q

What does the diffusing capacity for CO tell us?

A

DLCO is used to assess how well the lung can exchange gas.
Normal = 17-25mL/CO/min/mmHg

Using Fick’s law of diffusion, the DLCO tells us 2 key characteristics about the alveolar-capillary interface:

  • surface area (decreased w/ emphysema)
  • thickness (increased by pulmonary fibrosis & edema)
38
Q

How is tobacco smoke harmful?

A

increases SNS tone, sputum production, carboxyhemoglobin concentration, and the risk of infection

39
Q

Describe the short & intermediate term benefits of smoking cessation.

A

Short term (doesn’t reduce risk of postop pulmonary complications)

  • SNS stimulation dissipates after 20-30mins
  • P50 returns to near normal in 12hrs

Intermediate term effects (return of normal pulmonary function requires at least 6 weeks)

  • improved airway function, mucociliary clearance, sputum production, & pulmonary immune function
  • CYP450 induction subsides after 6 weeks.
40
Q

Compare & contrast PFTs in obstructive vs. restrictive lung disease.

A

Restrictive = decrease in all lung volumes & FEV1; normal FEV1/FVC ratio, normal FEF25-75

Obstructive = decreased FEV1/FVC & FEF25-75, may have normal other values

41
Q

Discuss the following pulmonary flow-volume loops: normal, obstructive, restrictive, and fixed obstruction

A

normal = upside down ice cream cone

obstructive = normal inspiration w/ expiratory obstruction (negative exponential slope)

restrictive = shape similar to normal loop but smaller & shifted to the R

fixed obstructive = inspiration & expiration are affected.

42
Q

Give an example of a disease the produces the following pulmonary flow-volume loops: obstructive, restrictive, and fixed obstruction

A

obstructive = COPD
restrictive = pulmonary fibrosis
fixed obstruction = tracheal stenosis

43
Q

What is the treatment for acute bronchospasm?

A 
100% FiO2
deepen anesthetic (IA, propofol, lidocaine, ketamine)
inhaled B2 agonist (albuterol)
inhaled anticholinergic (ipratropium)
epi 1mcg/kg IV
hydrocortisone 2-4mg/kg (takes several hours)
aminophylline
heliox to reduce airway resistnace
44
Q

What is alpha-1 antitrypsin deficiency?

A

alveolar elastase is a naturally occurring enzyme that breaks down pulmonary connective tissue; it’s kept in check by alpha-1 antitrypsin (produced in the liver)

alpha-1 antitrypsin deficiency –> increased alveolar elastase actions –> panlobular emphysema.

Liver transplant is the definitive treatment

45
Q

Describe the goals & strategies for mechanical ventilation in the patient w/ COPD.

A

prevent barotrauma & reduce air trapping:

  • low Tv 6-8mL/kg
  • increased expiratory time
  • slow inspiratory flow rate to optimize V/Q matching
  • low PEEP is ok as long as air trapping doesn’t occur
46
Q

Define restrictive lung disease

A

characterized by:

  • impaired lung expansion
  • decreased lung volumes
  • normal pulmonary flow rates
47
Q

Give examples of intrinsic lung diseases (acute & chronic)

A

Acute: aspiration, negative pressure pulmonary edema

Chronic: pulmonary fibrosis, sarcoidosis

48
Q

Give examples of extrinsic lung diseases (acute & chronic)

A

Chest wall/mediastinum: kyphoscoliosis, flail chest, NM disorders, mediastinal mass

Increased intraabdominal pressure: pregnancy, obesity, ascites

49
Q

List the risk factors for aspiration pneumonitis.

A 
trauma
emergency surgery
pregnancy
GI obstruction
GERD
peptic ulcer disease
hiatal hernia
ascites
difficult airway management
cricoid pressure
impaired airway reflexes
head injury
seizures
residual NM blockade
50
Q

Describe the pharmacologic prophylaxis of aspiration pneumonitis.

A

antacids: sodium citrate, sodium bicarbonate, magnesium trisilicate

H2 antagonists: ranitidine, cimetidine, famotidine

GI stimulants: metoclopramide

PPI: omeprazole, lansoprazole, pantoprazole

antiemetics: droperidol, ondansetron

routine use of these agents for prophylaxis isn’t recommended

51
Q

What is Mendelson’s syndrome?

A

chemical aspiration pneumonitis
risk factors
- gastric pH <2.5
- gastric volume >25mL (0.4mL/kg)

52
Q

Describe the treatment of aspiration.

A

tilt head downward or to the side (first action)

  • upper airway suction
  • lower airway suction is only useful for removing particulate matter (not helpful for acidic burn)
  • secure airway
  • PEEP to reduce shunt
  • bronchodilators to reduce wheezing
  • lidocaine to reduce neutrophil response
  • steroids probably don’t help
  • Abx only if WBC or fever >48hrs
53
Q

Discuss the pathophysiology and treatment of flail chest.

A

Consequence of blunt chest trauma w/ multiple rib fractures. The key characteristic is paradoxical movement of the chest wall at the site of the fractures

Inspiration: injured ribs move inward & collapse affected region
Expiration: injured ribs move outward & affected region doesn’t empty

TX: epidural catheter or intercostal nerve blocks

54
Q

Discuss pulmonary HTN, and discuss goals of anesthetic management.

A

mean PAP>25mmHg
causes: COPD, L heart disease, connective tissue disorders

goals: optimize PVR
- increase PaO2
- hypocarbia
- alkalosis
- decreased intrathoracic pressure (prevent coughing, normal lung volumes, spontaneous ventilation)
- drugs: inhaled NO, NTG, phosphodiesterase inhibitors, PGs, CCB, ACEI

55
Q

Discuss the pathophysiology of CO poisoning

A

reduces O2 carrying capacity of the blood (L shift)
CO binds O2 binding site of HgB w/ 200x affinity of O2
–> oxidative phosphorylation & metabolic acidosis

56
Q

Discuss the treatment of CO poisoning

A

100% FiO2 x6hrs

hyperbaric oxygen if COHgb >25% or if the patient is symptomatic

57
Q

List the absolute & relative indications for OLV

A

Absolute:

  1. Isolation of one lung to avoid contamination
  2. Control of Distribution of ventilation
  3. Unilateral bronchopulmonary lavage

Relative:

  1. surgical exposure
  2. pulmonary edema s/p CABG
  3. severe hypoxemia r/t lung disease
58
Q

Discuss how anesthesia in the LDP affects the VQ relationship.

A

nondependent lung

  • moves from flatter region (less compliant) to an area of better compliance (slope)
  • ventilation is optimal in this lung

dependent lung

  • moves from the slope to the lower, flatter area of the curve (less compliant)
  • perfusion is best in this lung (gravity)
  • reduction of alveolar volume contributes to atelectasis

net effect: ventilation is better in nondependent lung & perfusion is better in dependent lung. This creates VQ mismatch & increases the risk of hypoxemia during OLV

59
Q

Discuss the management of hypoxemia during OLV

A 
100% FiO2
confirm DLT position w/ bronchoscope
CPAP 10cmH2O to nonventilated lung
PEEP 5-10 to ventilated lung
alveolar recruitment maneuver
clamp pulmonary artery to non-ventilated lung
resume two-lung ventilation
60
Q

What is mediastinoscopy, and why is it performed

A

performed to obtain biopsy of the paratracheal lymph nodes at the level of the carina. Helps to stage the tumor prior to lung resection

61
Q

What are the potential complications of mediastinoscopy. What is most common?

A

hemorrhage & pneumothorax are most common

others:
- impaired cerebral perfusion
- dysrhythmias
- air embolism
- chylothorax
- hoarseness and/or VC paralysis

62
Q

describe the mallampati score

A

assesses teh oropharyngeal space, helps quantify the size of the tongue relative to the volume in the mouth

I: pillars, uvula, soft palate, hard palate
II: uvula, soft palate, hard palate
III: soft palate, hard palate
IV: hard palate

63
Q

describe the interincisor gap. What is normal?

A

ability to open the mouth directly affects ability to align the oral, pharyngeal, and laryngeal axes. A small interincisor gap creates a more acute angle b/n the oral & glottic openings, increasing the difficulty of intubation

normal = 2-3FB or 4cm

64
Q

what is the thyromental distance & what values suggest an increased risk of difficult intubation?

A

helps estimate the size of the submandibular space

w/ neck extended & mouth closed, you can measure the distance from the tip of the thyroid cartilage to the tip of the mentum. DL may be more difficult if the TMD is <6cm (3FB) or greater than 9cm

65
Q

What is the mandibular protrusion test and what values suggest an increased risk of difficult intubation?

A

assesses the function of the TMJ. Pt is asked to sublux the jaw, and the position of the lower incisors is compared to the position of the upper incisors

Class I: LI past UI & bite the vermilion of the lip
Class II: LI in line w/ UI
Class III: LI cannot move past UI (increased risk of difficult intubation)

66
Q

What conditions impair atlanto-occipital joint mobility?

A 
DJD
RA
ankylosing spondylitis
trauma
surgical fixation
Klippel-Feil
Down syndrome
67
Q

Describe the Cormack & Lehanne score

A

helps measure the view we obtain during DVL

Grade I: full view
Grade II: partial cords, arytenoids
Grade III: epiglottis
Grade IV: soft tissue

68
Q

5 risk factors for difficult mask ventilation

A 
BONES
beard
obese (usually BMI>26)
no teeth
elderly (age >55)
snoring
69
Q

list 10 risk factors for difficult tracheal intubation

A 
small mouth opening
narrow palate w/ high arch
long upper incisors
interincisor distance <3cm
MP class 3 or 4
mandibular protrusion class 3
poor compliance of submandibular spce
TM distance <6cm or >9cm
neck is thick &amp; short
poor AO joint mobility
70
Q

list 6 risk factors for difficult supraglottic device placement

A 
limited mouth opening
upper airway obstruction 
altered pharyngeal anatomy
poor airway compliance
increased airway resistance
lower airway obstruction
71
Q

list 5 risk factors for difficult invasive airway placement

A 
abnormal neck anatomy
obesity
short neck
limited access to CT membrane
laryngeal trauma
72
Q

what is angioedema?

A

result of increased vascular permeability that can lead to swelling of the face, tongue and airway: airway obstruction is an extreme concern

73
Q

what are two common causes of angioedema? what is the treatment for each?

A

ACEI; tx = epi, antihistamines, steroids (just like anaphylaxis)

hereditary angioedema (C1 esterase deficiency); tx = C1 esterase concentrate or FFP (i.e. not epi, antihistamines, or steroids)

74
Q

What is Ludwig’s angina?

A

bacterial infection characterized by a rapidly progressing cellulitis in the floor of the mouth. Inflammation & edema compress the submandibular, submaxillary, and sublingual spaces.

the most significant concern is posterior displacement of the tongue resulting in complete, supraglottic airway obstruction

75
Q

What is the best way to secure the airway in the patient w/ Ludwig’s angina?

A

awake nasal intubation or awake trach

76
Q

Describe the practice guidelines for preoperative fasting & use of pharmacologic agents to reduce the risk of pulmonary aspiration.

A 
2hrs = clear liquids
4hrs = breast milk
6hrs = nonhuman milk, formula, solid food
8hrs = fried or fatty foods

ingestion of clear liquids 2hrs before surgery reduces gastric volume & increases gastric pH

77
Q

list the 4 types of oropharyngeal airways. which are best suited for fiberoptic intubation?

A

Guedel
Berman
Williams**
Ovassapian**

**best for fiberoptic intubation

78
Q

What is the best time to use an ESchmann introducer?

A

best time to use is when grade 3 view is obtained during DL (grade 2 is the next best time).

Likelihood of successful intubation is unacceptably low when a grade 4 view is obtained.

79
Q

When is a nasopharyngeal airway contraindicated?

A 
cribiform plate injury (LeFort II or III, basilar skull fx, CSF rhinorrhea, raccoon eyes, periorbital edema)
coagulopathy
previous transsphenoidal hypophysectomy
previous Caldwell-Luc procedure
nasal fracture
80
Q

contrast the maximum recommended cuff pressures for an ETT vs. LMA

A

ETT <25cmH2O

LMA <60cmH2O

81
Q

contrast the maximum recommended PIP for an LMA-unique vs. LMA-proseal vs. LMA-supreme

A

LMA-unique <20cmH2O
LMA-proseal <30cmH2O
LMA-supreme <30cmH2O

82
Q

what is the largest size ETT that can be passed through each LMA size?

A 
1 = 3.5
1.5 = 4
2 = 4.5
2.5 = 5
3 = 6
4 = 6
5 = 7
83
Q

list 6 indications for the Bullard laryngoscope

A 
small mouth opening (minimum 7mm)
impaired C-spine mobility 
short, thick neck
Treacher Collins
Pierre Robins
84
Q

Describe the proper placement of the lighted stylet

A

when the patient is supine, the trachea is anterior to the esophagus. therefore we can look at the quality of the light shining through the neck to determine if the tip is in the trachea or the esophagus

  • looking for a well-defined circumscribed glow below the thyroid prominence
  • if it’s diffuse, then it’s in the esophagus
85
Q

5 indications for the use of a bronchial blocker

A

indicated for lung separation in the following patients

  • age <8
  • requires nasotracheal intubation
  • have a trach
  • have a single lumen ETT in place
  • require intubation after surgery & you want to avoid changing the DLT out
86
Q

How can the lumen of the bronchial blocker be used during OLV?

A

insufflate O2 into the nonventilated lung
&
suction air from the nonventilated lung to improve surgical exposure

cannot:
- ventilate
- suction blood, pus, or secretions

87
Q

2 indications for retrograde intubation

A

unstable C-spine

upper airway bleeding (cannot visualize glottis)

88
Q

compare & contrast the benefits of awake vs. deep extubation

A

awake:
- airway reflexes intact
- ability to maintain a/w patency
- decreased risk of aspiration

deep

  • decreased CV & SNS stimulation
  • decreased coughing
89
Q

when is the best time to use an airway exchange catheter, and what can you do with it?

A

maintains direct access to the airway following tracheal extubation, thus is helpful during extubation of the difficult airway

what else can you do with it?
EtCO2 measurement
Jet ventilation
O2 insufflation

APEXANESTHESIA COPY COPY (12 decks)

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