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Flashcards in Airway/Respiratory Deck (84):

Explain the nerve pathway of laryngospasm

1. Afferent SENSORY stimulation of INTERNAL branch of Superior laryngeal nerve 

2. Efferent MOTOR innervation via EXTERNAL branch of SLN + Recurrent laryngeal nerve


the upper airway extends from        1       to        2      

1. Mouth and Nares

2. Cricoid Cartilage


What increases as the airways bifurcates? 

What decreases?


  • number of airways
  • cross sectional area
  • muscular areas


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



Explain minute ventilation compared to alveolar ventilation


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)


Definition of deadspace 

gas that does not participate in gas exchange. 


Normal deadspace in spontaneously ventilating patient

2 ml/kg


About 33%

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


Bohr Equation

Uses CO2  calculate physiologic deadspace

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


Vd = PaCo- PeCO2 

Vt                 PaCO2


Explain V/Q in an upright spontaneously ventilating patient

  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


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

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


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

Bronchioles constrict 


Laplace's law

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

As radius increases wall tension increases. 


What type of cells produce surfactant and when?

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


3 Sites of anatomical shunt

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


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

Alveolar Oxygen Equation

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


  • 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)



What conditions have/cause an INCREASED FRC

  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 Breathsrecruits colapsed alveoli


What is closing capacity? 

  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


Under normal circumstances FRC is _______ than CC. 

Under normal circumstances FRC is GREATER than CC. 


What happens when CC is greater than FRC? 


How do we remedy this?

Airway closure occurs during normal tidal breathing


Remedy → need to increase FRC = ADD PEEP


What conditions increase closing volume


  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)


Lung volumes associated with agiing

    • FRC
    • Closing Capacity
    • Residual Volume


    • Vital Capacity


Spirometry cannot measure

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)


Arterial Oxygen content equation

CaO= (1.39 x Hgb x SaO2) + (PaOx 0.003)


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


Gas Law that explains the amount of oxygen dissolved in plasma

Henry's Law

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


Oxygen is _____________ soluable than CO2


(O2 solubility coef. = ______)

(CO2 solubility coef. = ______)

Oxygen is 20x LESS soluable than CO2


( O2 solubility coef. = 0.003)

(CO2 solubility coef. = 0.067)


Where does 1.39 come from in the arterial oxygen content equation

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


Oxygen Delivery Equation

DO = (CaO2) X (Cardiac Output) X (10)

CaO2​ = Areerial oxygen content (g/dL) 

Cardiac Output = L/Min

10 = conversion factor


Oxygen Consumption Equation

VO= CO x (CaO- CvO2)


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

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

So in a 70kg male VO2 ≈ 250 mL/min


P50 of adult and fetal Hgb

  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!!!!


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


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


What are the three mechanisms of CO2 transport?

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


Venous Hematocrit vs Arterial Hematocrit

  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



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

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


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

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


Differentiate Central vs Peripheal Chemoreceptors role

  1. Central chemoreceptors respond primarily to CO2
  2. Peripheral chemoreceptors respond primarily to O2


Explain the control of ventilation via the central chemoreceptors

  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


Random airway reflexes

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

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


Hypoxic Pulmonary Vasoconstriction

What is it?


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


Decreased blood flow to poorly ventilatied areas to minimize shunt. 


Hypoxic Pulmonary Vasoconstriction


Onset and Peak?


Begins within seconds and peaks at 15 minutes


Hypoxic Pulmonary Vasoconstriction


Drugs that influence it.

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)


Physiologic basis for airway resistance?

(Mechanisms of bronchoconstriction and dilation)

  1. PNS mediated Bronchoconstriction 
    • ​​Vagus nerve releases ACH onto M3 receptors
    • this activates Gq coupled proteins signalinng a downstream cascade (PIPto IP​3 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


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

30 cm H2O minimum

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


Regional and COPD

  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


Nitrous and COPD

Risk of rupturing pulmonary blebs and causing PTX


Best VA for COPD

SEVO - least irritating to airway.


Mechanical ventilation perameters for COPD

  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.


Mendelson syndrome TWO risk factors

  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)


When are patients MOST at risk for aspiration perioperatively

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


Three types of Pneumothorax

  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


Hallmark characteristics of a tension PTX

  1. hypoxemia
  2. increased airway pressures
  3. tachycardia
  4. increased CVP


ABSOLUTE Indications for One Lung Ventilaton

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


What is the barrier between the upper and lower airway?



This is the only muscle that ABDUCTS the vocal ligaments

Posterior cricoarytenoid muscles

A image thumb

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

Pediatric - cricoid cartilage

Adults - glottis (6 - 9 mm)

A image thumb

Normal mouth opening distance

3 - 4 cm (2-3 FB)


Posterior cricoarytenoid


what do they do

who innervates it

Opens the glottis → Pull Cords Apart

Only ABductor!!


Recurrent laryngeal nerve

Intrinsic muscle

A image thumb

Lateral cricoarytenoid




Adducts the cords → Lets Close Cords!

Recurrent laryngeal nerve

intrinsic muscle

A image thumb

Transverse Arytenoids




Adductor = Closes the glottis (esp the posterior)

Recurrent laryngeal nerve

intrinsic muscle

A image thumb





Cricothyroid = Cords Tense


Produces tension and elongates the cords

superior laryngeal nerve

A image thumb

Thyroarytenoid & Vocalis



Nerve inervation

ThyroaRytenoid = They Relax → (vocalis does the same)


Shortens and relaxes the cords

recurrent laryngeal nerve

A image thumb

Superior Laryngeal Nerve (Internal branch)


Sensory and Motor Function

Sensory only!!


Posterior epiglotis → Vocal cords

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

A image thumb

Superior Laryngeal Nerve (External branch)


Sensory and Motor Function 

Motor Only!!!

  • Cricothyroid muscle (Cords TENSE)

A image thumb

 Recurrent laryngeal nerve


Sensory and Motor Function 

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

A image thumb

Precautions for nasal airways

Epistaxis and anticoagulants

Nasal and basilar skull fractures

Adenoid hypertrophy


Big caution with oral airways



soft tissue damage


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

Lube that sucker up


When is a mask case ok?

  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


When in the induction sequence can an LMA be placed?

After loss of lash reflex and confirmation of mask ventilation


Proper Snifing position

pillow under the head (not soulders) 

35° neck flexion and 15° head extension


(angles relative to horizontal planes)

A image thumb

Who should not have an LMA placed?

Anyone considered a full stomach

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


LMA advantages

  • ↑ 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


LMA disadvantages

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


LMA - when do you deflate the cuff

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

Keeps secretions from getting on vocal cords 


ETT indications 

  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


How far to insert the ETT

males - 23 cm

females 21 cm


RSI Sequence of Events

  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


Potential Hazards in Airway Management

  • 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


Extubation Criteria 

  • 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

    Laryngospasm interventions

    • 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


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

    in RSI 


    Nasal Tracheal Intubation: Asleep Sequence of Events

    • 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


    Extubation guidelines

    • 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