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!!!! Board Review !!!! > Airway/Respiratory > Flashcards

Airway/Respiratory Flashcards

1
Q

Explain the nerve pathway of laryngospasm

A
  1. Afferent SENSORY stimulation of INTERNAL branch of Superior laryngeal nerve
  2. Efferent MOTOR innervation via EXTERNAL branch of SLN + Recurrent laryngeal nerve
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2
Q

the upper airway extends from 1 to 2 .

A
  1. Mouth and Nares
  2. Cricoid Cartilage
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3
Q

What increases as the airways bifurcates?

What decreases?

A

Increases:

  • number of airways
  • cross sectional area
  • muscular areas

Decreases:

  • airflow velocity
  • amount of cartilage
  • goblet cells (which produce mucous)
  • cilliated cells(Clears Mucous)
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4
Q

Explain minute ventilation compared to alveolar ventilation

A

Minute Venilation = TV x RR

  • Volume of air moved in a single minute

Alveolar Ventilation = ((TV - Anatomical Deadspace) x (RR)

  • Alveolar ventilation does NOT factor in the conducting airways.
  • Alveoloar ventilation measure fraction of minute ventilation availible for gas exchange

(Note: TV = volume of gas in conduction airways + volume of gas in the respiratory zone)

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5
Q

Definition of deadspace

A

gas that does not participate in gas exchange.

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6
Q

Normal deadspace in spontaneously ventilating patient

A

2 ml/kg

About 33%

(Vd/Vt) = 150mL/450 = 0.33

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7
Q

Bohr Equation

A

Uses CO<strong>2</strong> calculate physiologic deadspace

  • partial pressure of CO2 in blood compared to EtCO2
  • the greater difference between = the MORE deadspace

Vd = PaCo2 - PeCO2

Vt PaCO2

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8
Q

Explain V/Q in an upright spontaneously ventilating patient

A
  1. Normal V/Q = 0.8
    • ventilation = 4 L/min
    • Perfusion = CO = 5 L/min
  2. Higher V/Q ratios at apex
    • more ventilation and less perfusion = deadspace
  3. Lower V/Q ratios at base
    • more perfusion and less ventilation = shunt
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9
Q

What is the bodies compensatory mechanism to V/Q mismatch causing shunt?

A

Hypoxic Pulmonary Vasoconstriction → decreases pulmonary blood flow to alveoli with LESS ventilation which minimizes shunt

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10
Q

What is the bodies compensatory mechanism to V/Q mismatch causing deadspace?

A

Bronchioles constrict

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11
Q

Laplace’s law

A

Tension = (Pressure x Radius) / (Wall thickness)

As radius increases wall tension increases.

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12
Q

What type of cells produce surfactant and when?

A
  • Surfactant produce by Type II Pneumocytes
  • Starts between 22-26 weeks of age
  • Peak production is at 36-35 weeks
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13
Q

3 Sites of anatomical shunt

A
  1. Thebesian veins → drain left heart
  2. Bronchiolar veins →drain bronchial circulation
  3. Pleaural veins → drain bronchial circulation
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14
Q

How can we approximate alveolar oxygen from an arterial blood gas? Why is this important ?

A

Alveolar Oxygen Equation

Alveolar oxygen = FiO2 X (Pb - PH2O) - PaCO2

RQ

  • We can treat hypoxia by increasing FiO2, However, we cannot correct hypercarbia by increasing FiO2.
  • The only way to treat the hypercarbia is to increase alveolar ventilation (i.e minute ventilation) - Blow off CO2

__________________________________________________

Alveolar oxygen = Fraction of inspired oxygen TIMES (barometric pressure MINUS pressure of humidity of inhaled gas (assume 47mmHg) MINUS Arterial CO2 divided by the respiratory quotient (0.8)

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15
Q

What conditions have/cause an INCREASED FRC?

A
  1. Advanced age→ decreased elastic lung tissue/air trapping which increases residual volume
  2. Sitting & Prone Position→ changes in position of the diaphram and changes in pulmonary blood flow
  3. Obstructive Lung disease→ air trapping which increases residual volume
  4. PEEP→ recruits colapsed alveoli, partially overcomes effects of GA, decreased venous admixture = increased PaO2
  5. Sigh Breaths→ recruits colapsed alveoli
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16
Q

What is closing capacity?

A
  1. ERV = closing volume = point at which dynamic compression of the airway begins (just above residual volume)
    • where the pleural pressure exceeds airway pressure compressing the small airways (without cartilage) and traps cas distally in the alveoli
  2. CLOSING CAPACITY = closing volume + RV
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17
Q

Under normal circumstances FRC is _______ than CC.

A

Under normal circumstances FRC is GREATER than CC.

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18
Q

What happens when CC is greater than FRC?

How do we remedy this?

A

Airway closure occurs during normal tidal breathing

Remedy → need to increase FRC = ADD PEEP

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19
Q

What conditions increase closing volume

A

CLOSE -P

  1. C = COPD
  2. L = LV failure
  3. O = Obesity
  4. S = Smoking
  5. E = Extreme age
  6. P = Pregnancy

(Small airways begin to close at higher lung volumes increaseing intrapulmonary shunt and hypoxemia)

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20
Q

Lung volumes associated with agiing

A
  1. INCREASED
    • FRC
    • Closing Capacity
    • Residual Volume
  2. DECREASED
    • Vital Capacity
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21
Q

Spirometry cannot measure

A

Anything that includes residual volume

  1. Total lung Capacity (TLC)
  2. Functional Residual Capacity (FRC)
  3. Closing Volume and Closing Capacity

(Use Nitorgen Washout or Xenon 133)

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22
Q

Arterial Oxygen content equation

A

CaO2 = (1.39 x Hgb x SaO2) + (PaO2 x 0.003)

  • ≈ 3% dissolves in plasma
  • 97% reversibly binds with Hemoglobin
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23
Q

Gas Law that explains the amount of oxygen dissolved in plasma

A

Henry’s Law

(the partial pressure of gas in a solution is directly related to the partial pressure of the gas above the solution)

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24
Q

Oxygen is _____________ soluable than CO2

(O2 solubility coef. = ______)

(CO2 solubility coef. = ______)

A

Oxygen is 20x LESS soluable than CO2

( O2 solubility coef. = 0.003)

(CO2 solubility coef. = 0.067)

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25
Q

Where does 1.39 come from in the arterial oxygen content equation

A

Each gram of hemoglobin can carry 1.39 mL’s of oxygen

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26
Q

Oxygen Delivery Equation

A

DO2 = (CaO2) X (Cardiac Output) X (10)

CaO2​ = Areerial oxygen content (g/dL)

Cardiac Output = L/Min

10 = conversion factor

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27
Q

Oxygen Consumption Equation

A

VO2 = CO x (CaO2 - CvO2)

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28
Q

In an aberage 70 kg male what is the oxygen consumtion?

A

Oxygen Consumption (VO2) = 3.5 mL/kg/min

So in a 70kg male VO2 ≈ 250 mL/min

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29
Q

P50 of adult and fetal Hgb

A
  1. Adult Hgb P50 = 26.5 mmHg
  2. Fetal Hgb P50 = 19mmHg
    • does NOT produce 2,3 DPG which shift the curve to the right!!!!
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30
Q

What describes the primary mechanisms of gas exchange at the level of the tissues and lungs?

A

The Bohr effect and Haldane effect work together to deliver oxygen remeove CO2 . Both have significance at the level of the tissues and lungs.

_______________________________________________

Bohr Effect → describes carriage of oxygen to tissues

  • CO2 + H+ casue Hgb to offload OXYGEN to the tissues.
  • Presence of CO2 + H+ cause a conformational change in the Hgb molocule
  • Explains RIGHT shift from acidosis + increased metabolism )

Haldane Effect → describes CO2 carriage from tissues to the lungs

  • Oxygen causes erythrocytes to release CO2
  • Deoxygenated Hgb is able to carry more CO2 →when brougt to the lungs CO2 is then offloaded d/t the presence of oxygen and thus excreted form the body
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31
Q

What are the three mechanisms of CO2 transport?

A
  1. Transproted in the form of HCO3 →(70%)
  2. Bound to Hgb →(23%)
  3. Dissolved in plasma →(7%)
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32
Q

Venous Hematocrit vs Arterial Hematocrit

A
  1. Venous Hematocrit is 3% HIGHER than Arterial dt/t chloride (hamburger) shift.
    • Cl- adds osmotically active ions (Cl- follows Na+) which causes erythrocyte to swell.
    • This Swelling is reversed in the lungs
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33
Q
A
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34
Q

In acute respiratory acidosis, if the CO2 increases by 10mm Hg the pH will ________________________

A

In acute respiratory acidosis, if the CO2 increases by 10mm Hg the pH will DECREASE by 0.08

35
Q

In chronic respiratory acidosis, if the CO2 increases by 10mm Hg the pH will ________________________

A

In acute respiratory acidosis, if the CO2 increases by 10mm Hg the pH will DECREASE by 0.03 d/t renal bicarb retention

36
Q

Differentiate Central vs Peripheal Chemoreceptors role

A
  1. Central chemoreceptors respond primarily to CO2
  2. Peripheral chemoreceptors respond primarily to O2
37
Q

Explain the control of ventilation via the central chemoreceptors

A
  1. H+ and HCO3- DO NOT cross the BBB
  2. CO2 freely difuses across the BBB then is converted to HCO3- + H+ via carbonic anhydrase.
  3. H+ then stimulates the Dorsal Respiratory center (inspiratory group) to increase minute ventilation.
  4. HCO3- will slowly equiliberate between blood and CSF after a few hours and peaks after a few days
  5. This is why hyperventilation to decrease ICP only works for a short/acute period of time
38
Q

Random airway reflexes

  1. Hering-Breuer Inflation reflex
  2. Hering-Breuer Denflation reflex
  3. J receptor (Pulmonary C fiberreceptors)
  4. Paradoxical Reflex of Head
A

Random airway reflexes

  1. Hering-Breuer Inflation reflex→
    • lung inflation >1.5L above FRC stops insprilation (stops dorsal respiratory center)
  2. Hering-Breuer Denflation reflex→
    • lung volume too small stimulates patient to take a deep breath
  3. J receptor (Pulmonary C fiberreceptors)→
    • Traffic Jam (PE or CHF) causes tachypnea
  4. Paradoxical Reflex of Head→
    • causes newborn baby to take first breath
39
Q

Hypoxic Pulmonary Vasoconstriction

What is it?

A

Decreased alveolar oxygen tension (alveolar hypoxia) causes pulmonary vascular vasoconstriction

Decreased blood flow to poorly ventilatied areas to minimize shunt.

40
Q

Hypoxic Pulmonary Vasoconstriction

Onset and Peak?

A

Begins within seconds and peaks at 15 minutes

41
Q

Hypoxic Pulmonary Vasoconstriction

Drugs that influence it.

A

Increase HPV

  • Volitile anesthetics
  • Vasodilators, PDE inhibitors, dobutamine and some CCB inhibit HPV
  • Vasoconstrictive drugs futher constrict oxygenated vessels and increase shunt

(NOTE: IV induction agents Propofol, etomidate and ketamine DO NOT affect HPV)

42
Q

Physiologic basis for airway resistance?

(Mechanisms of bronchoconstriction and dilation)

A
  1. PNS mediated Bronchoconstriction
    • ​​Vagus nerve releases ACH onto M3 receptors
    • this activates Gq coupled proteins signalinng a downstream cascade (PIP1 to IP<strong>​3</strong> via phosphalipase C) INCREASING intracellular calcium causing smooth muscle contraction
  2. SNS mediated Bronchodilation
    • ​Circulating catchecholamines EPI stimulates ß2 receptors
    • this activating Gs coupled proteins signaling a downsteram cascade (ATP to cAMP via Adenylate Cyclace and Protein kinase A) thereby DECREASING intracellualr calcium causing smooth muscle dilation
  3. Non-cholinergic PNS mediated Bronchodilation
    • ​Nitric oxide pathway signals cGMP to casuse smooth muscle dilation
43
Q

Minimum airway pressure needed to reverse anesthesia induced atelectesis (open alveoli)

A

30 cm H2O minimum

40 cm H2O for 8 seconds almost completely reverses anesthesia induced atelectesis

44
Q

Regional and COPD

A
  1. ALWAYS consider for lower extemety and lower abdominal procedures
  2. If sesory blockade is needed >T6 → DO NOT USE NEUROAXIAL
    • Impairs expiratory muscle function and decreases ERV
    • Decreases ability to clear secretions
45
Q

Nitrous and COPD

A

Risk of rupturing pulmonary blebs and causing PTX

46
Q

Best VA for COPD

A

SEVO - least irritating to airway.

47
Q

Mechanical ventilation perameters for COPD

A
  1. TV→ 6-8 mL/kg
  2. RR→ low 7
  3. I:E→ 1:> 2
  4. +PEEP
  5. Slow inspiratory flow to redistribute gas from areas of high compliance to low compliance.
48
Q

Mendelson syndrome TWO risk factors

A
  1. Gastric pH <2.5
  2. Gastric volume >25 mL (0.4 mL/kg)

Anyone that would be an RSI:

(trauma, emergency surgery, pregnancy, GI obstruction,GERD, PUD, hiatal hernia, ascites, difficult airway management, cricoid pressure, impaired airway reflexes, head injury, seizures, residual NMB)

49
Q

When are patients MOST at risk for aspiration perioperatively

A
  1. During induction
  2. During intubation
  3. Within 5 minutes of extubation
50
Q

Three types of Pneumothorax

A
  1. Closed→ lung collapses but NO communication btwn pleural cavity and atmosphere
  2. Communicating→allows air to pass btwn pleural space and atmosphere
    • inhalation = affected lung partially collapses
    • exhalation = aggected side partially expands
  • Tension→ air enters pleuraul cavity but can NOT EXIT
    • x-ray = mediastinal shift, hemidiaphragmatic compression, tracheal deviation
51
Q

Hallmark characteristics of a tension PTX

A
  1. hypoxemia
  2. increased airway pressures
  3. tachycardia
  4. increased CVP
52
Q

ABSOLUTE Indications for One Lung Ventilaton

A
  1. Isolation of One lung to Avoid Infection/Contamination
  2. Controll of distribution of Ventilation
    • bronchopleural fistula
  3. Unilateral bronchopulmonary lavage
    • alveolar proteinosis
53
Q

What is the barrier between the upper and lower airway?

A

Glottis

54
Q

This is the only muscle that ABDUCTS the vocal ligaments

A

Posterior cricoarytenoid muscles

55
Q

What is the most narrow part of the adult and pediatric airways?

A

Pediatric - cricoid cartilage

Adults - glottis (6 - 9 mm)

58
Q

Normal mouth opening distance

A

3 - 4 cm (2-3 FB)

59
Q

Posterior cricoarytenoid

what do they do

who innervates it

A

Opens the glottis → Pull Cords Apart

Only ABductor!!

Recurrent laryngeal nerve

Intrinsic muscle

60
Q

Lateral cricoarytenoid

function

nerve

A

Adducts the cords → Lets Close Cords!

Recurrent laryngeal nerve

intrinsic muscle

61
Q

Transverse Arytenoids

function

nerve

A

Adductor = Closes the glottis (esp the posterior)

Recurrent laryngeal nerve

intrinsic muscle

62
Q

Crycothyroid

function

nerve

A

Cricothyroid = Cords Tense

Produces tension and elongates the cords

superior laryngeal nerve

63
Q

Thyroarytenoid & Vocalis

Function

Nerve inervation

A

ThyroaRytenoid = They Relax → (vocalis does the same)

Shortens and relaxes the cords

recurrent laryngeal nerve

64
Q

Superior Laryngeal Nerve (Internal branch)

Sensory and Motor Function

A

Sensory only!!

Posterior epiglotis → Vocal cords

  • Supraglottic mucosa
  • 2 joints (thyroepiglottic and cricothyroid joints)
65
Q

Superior Laryngeal Nerve (External branch)

Sensory and Motor Function

A

Motor Only!!!

  • Cricothyroid muscle (Cords TENSE)
66
Q

Recurrent laryngeal nerve

Sensory and Motor Function

A
  • Sensory
    • Subglottic mucosa
    • Muscle spindles
  • Motor (all intrinsinc muscles except the cricothyroid)
    • Thyroarytenoid
    • Lateral cricothyroid
    • Interarytenoid
    • Posterior arytenoid
67
Q

Precautions for nasal airways

A

Epistaxis and anticoagulants

Nasal and basilar skull fractures

Adenoid hypertrophy

68
Q

Big caution with oral airways

A

LARYNGOSPASM

bleeding

soft tissue damage

77
Q

What should we remember to do before placing a nasal airway?

A

Lube that sucker up

78
Q

When is a mask case ok?

A
  1. Pt doesn’t have difficult airway
  2. Airway obstruction is easily relieved with oral/nasal airway or chin lift
  3. Short case duration
  4. Surgeon doesn’t need access to head/neck (exception to the rule: bilateral myringotomy tubes)
  5. Head will be accessible for the entire case
  6. No airway bleeding/secretions
  7. No table position changes
79
Q

When in the induction sequence can an LMA be placed?

A

After loss of lash reflex and confirmation of mask ventilation

80
Q

Proper Snifing position

A

pillow under the head (not soulders)

35° neck flexion and 15° head extension

(angles relative to horizontal planes)

81
Q

Who should not have an LMA placed?

A

Anyone considered a full stomach

(non-fasting, parturients 34+ weeks, uncontrolled GERD, trauma, acute abdomens, diabetics d/t autonomic neuropathy, low pulmonary complience)

82
Q

LMA advantages

A
  • ↑ speed & ease of placement by inexperienced personnel
  • Improved hemodynamic stability at induction & during emergence
  • ↓ anesthetic requirements for airway tolerance
  • Lower frequency of coughing during emergence
  • Lower incidence of sore throats in adults (10% vs 30%)
    • Avoids “foreign body” in the trachea
  • Patient can be fully emerged prior to removal of LMA → good for asthmatic patients
83
Q

LMA disadvantages

A
  • Lower seal pressure
  • Higher frequency of gastric insufflation → risk for aspiration
  • Esophageal reflux more likely
  • Inability to use mechanical ventilation at higher pressures
84
Q

LMA - when do you deflate the cuff

A

Keep the cuff inflated until the patient is awake → DO NOT DEFLATE at END OF CASE

Keeps secretions from getting on vocal cords

85
Q

ETT indications

A
  1. Airway compromise
  2. Airway inaccessible
  3. Long surgical time
  4. Surgery of head, neck, chest, or abdomen
  5. Need for controlled ventilation & positive end-expiratory pressure
  6. Inability to maintain airway with mask/LMA
  7. Aspiration risk
  8. Airway disease
  9. Pregnancy
86
Q

How far to insert the ETT

A

males - 23 cm

females 21 cm

87
Q

RSI Sequence of Events

A
  1. Adjuncts → aspiration prophylaxis
    • Bicitra, reglan, protonix
  2. Monitors, suction on & placed at head of bed
  3. Supine “sniffing” position
  4. Sedation (Versed) if applicable
  5. Pre-Oxygenate 5 minutes or Minimum 4-5 VC Breaths!
  6. Sellick’s Maneuver = Cricoid pressure
  7. Induction agent followed by succinylcholine
    • Wait 60 seconds → watch the clock NOT the block!
  8. Attempt Laryngoscopy → visualize vocal cords → place ETT inflate cuff
  9. Confirm tracheal tube placement:
    • Chest rise
    • BBSE
    • Confirm presence of EtCO2
  10. Give assistant permission to release cricoid pressure
  11. Ventilate
  12. Start inhaled anesthetic or anesthetic infusion
  13. Ventilator on
  14. Secure ETT/tape eyes
88
Q

Potential Hazards in Airway Management

A
  • Dental damage
  • Soft tissue/mechanical injury
  • Laryngospasm
  • Bronchospasm
  • Vomiting/Aspiration
  • Hypoxemia/Hypercarbia
  • SNS stimulation
  • Esophageal/Endobronchial intubation
  • Endobronchial intubation evident by → high airway pressures, unilateral chest rise & breath sounds, ↓ O2 saturation
89
Q

Extubation Criteria

A
  • TV: >6 mL/kg
  • VC: >10 mL/kg
  • RR:
  • If >30 could mean pain or anxious
  • SaO2: >90%
  • ETCO2:
  • If EtCO2 is too low → can ↓ RR or ↓ VT
  • Sustained tetanic contraction
  • Closed grip fist for 5 seconds
  • Sustained head lift for 5 seconds
90
Q

Laryngospasm interventions

A
  • Jaw-Lift Maneuver
    • Forward displacement of the mandible with O2 administered by mask with positive pressure
  • Administration of O2 with continuous positive pressure
    • Strong intermittent pressure applied manually to a bag full of O2 can force gas effectively through the upper airway & adducted cords
  • Immediate removal of the offending stimulus
  • Small dose of short acting muscle relaxant succinylcholine 20-40 mg
92
Q

when is it allowed not to test-ventilate a patient before insertion of the ETT/LMA?

A

in RSI

93
Q

Nasal Tracheal Intubation: Asleep Sequence of Events

A
  • Phenylephrine to nose (AFRIN) or consider Anticholinergic/Antisialogogue (glycopyrrolate)
  • Monitors, Supine “sniffing” position, Sedate (Versed)
  • Pre-Oxygenate
  • Induction Agent
  • Confirm loss of consciousness
  • Attempt ventilation if able to ventilate →
  • Muscle Relaxant
  • Consider dilation of nare with sequential sizes of nasal airways → choose nare that is easily able to breathe through in preop
    • Consider induction agent may be wearing off
  • Insert LUBRICATED ETT through nare (that was dilated)
  • Continue to ventilate
  • Attempt direct visual laryngoscopy → visualize VC → use Magill forceps to pick up end of ETT & advance through cords
  • Inflate cuff
  • Confirm tracheal tube placement:
    • Chest rise
    • BBSE in all lung fields & over stomach
    • Confirm presence of EtCO2
  • Ventilate
  • Start inhaled anesthetic or anesthetic infusion
  • Ventilator On
  • Secure ETT/tape eyes
94
Q

Extubation guidelines

A
  • Nearly fully awake extubation is performed when the patient has
    • Purposeful movement
    • ready to maintain & protect his/her own airway
  • Muscle relaxant must be fully reversed & confirmed with PNS
  • Anesthetic medications, including anesthetic gases & infusions, turned OFF
  • Oropharynx is suctioned
  • The patient is self-maintaining an acceptable respiratory rate & depth (see respiratory extubation criteria*)
  • Assess for responsiveness / purposeful movement &/or responding to commands
    • A sustained (5 second) head lift is an excellent way to assess clinically adequate reversal
  • ETT is removed while a positive-pressure breath is given with the anesthesia bag to allow subsequent expulsion or secretions away from the glottis
95
Q
A

!!!! Board Review !!!! (3 decks)

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