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What muscle abducts the vocal cords?
posterior cricoarytenoid
What is the only muscle that tenses (elongates) the vocal cords?
cricothyroid "cords tense"
What muscle opens the glottis?
thyroepiglottic
What two muscles close the glottis?
aryepiglottic
oblique arytenoid
What muscles adduct the vocal cords and arytenoids?
- there are two
lateral cricoarytenoid
transverse arytenoid
What muscle shortens the vocal cords? (relaxes?)
- there are two
thyroarytenoid "they relax"
vocalis
The cricothyroid muscle is innervated by?
external branch of SLN
- the only branch that tenses (elongates) the VCs
The internal branch of the SLN is purely?
- sensory or motor?
sensory
Recurrent laryngeal innervates...
below vocal cords --> the trachea
Branches off vagus in thorax
Motor: all intrinsic except cricothyroid
Glossopharyngeal innervates...
the vallecula
topside of epiglottis
soft palate
oropharynx
post 1/3 of tongue
tonsils
afferent limb of gag reflex
CN IX - sensory
Superior laryngeal innervates...
posterior epiglottis --> vocal cords
Internal branch is sensory - underside of epiglottis
External branch is motor - cricothyroid muscle
Trigeminal (V) V3 innervates...
anterior 2/3 tongue
Trigeminal nerve (V) contains what 3 branches?
V1 ophthalmic (anterior ethmoidal) - nares/ant 1/3 septum
V2 maxillary (sphenopalatine) - turbinates/septum
V3 Mandibular (lingual)
Superior laryngeal nerve block:
3ml at the inferior aspect of the greater cornu of hyoid bone bilaterally
- helps tolerate FO intubation once past the oropharynx
Glossopharyngeal block:
1-2 ml at the tonsillar pillar bilaterally
Transtracheal block:
3-5 ml through the cricothyroid membrane
What is most likely to injure the left RLN while sparing the right RLN?
Mitral stenosis (LA enlargement compresses the nerve and may present as hoarseness)
PDA ligation
Aortic arch aneurysm
Thoracic tumor
Causes of left OR right RLN injury:
parathyroid or thyroid surgery
external pressure from LMA/ETT
neck tumor
neck extension
Where does the right RLN loop?
left RLN loop?
under the right subclavian artery
- left under the aorta (more susceptible to injury)
For the patient in sitting position, order the cartilages from superior to inferior:
cricoid
epiglottis
arytenoid
corniculate
epiglottis
corniculate
arytenoid
cricoid
How many unpaired cartilages present in the larynx?
Paired?
3 unpaired
3 paired
9 cartilages total
Where is the adult larynx located?
Infant larynx?
C3-C6
Infant is C2-C4
What is the narrowest part of the airway? adult/infant
Vocal cords for adult
Cricoid for infant, if paralyzed = vocal cords
Risk factors for intraoperative laryngospasm?
GERD
Exposure to 2nd hand smoke
recent URI
Age < 1 year
HYPOcapnia
light anesthesia
saliva or blood in the upper airway
What is the definition of laryngospasm?
Sustained and involuntary contraction of the vocal cord Adductors that result in the inability to ventilate.
Tensor palatine opens?
nasopharynx
Genioglossus opens?
the oropharynx
Hyoid muscles open?
the hypopharynx
Landmarks for the Larson's maneuver?
posterior: mastoid process
superior: skull base
Anterior: ramus of mandible
Muller's maneuver?
inhaling against a closed glottis
Which type of pneumocystis produce surfactant?
type 2
Three types of pneumocytes?
type 1 - 3
type 1 - cover 80% of alveolar surface
type 3 - macrophages that fight lung infection
Most common etiology of hypoxemia in the PACU?
V/Q mismatch: specifically atelectasis
Result as FRC becomes smaller and there is less radial traction to hold the airways open:
result is atelectasis, R -> L shunt, and hypoxemia
Intrapleural pressure becomes positive during:
The ONLY time intrapleural pressure becomes positive is during forced exhalation, and pneumothorax
What is transpulmonary pressure?
alveolar pressure - intrapleural pressure
- always positive, keeps airway open
- Intrapleural always negative - keeps lungs inflated
What muscles provide the most significant contribution to forced exhalation?
rectus abdominus
Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume, what law is this?
boyles law
What muscles contract during inspiration?
diaphragm and external intercostals (tidal breathing)
accessory muscles: sternocleidomastoid and scalenes
Muscles of exhalation?
active exhalation: abdominal muscles
internal intercostals serve as secondary role in active
Alveolar compliance =
alveolar volume / alveolar pressure
The best ventilated alveoli are the?
most compliant!
- exchange more gas, volumes change more.
these alveoli reside at the steep slope of the curve
The least ventilated alveoli are the?
least compliant!
- exchange less gas, volumes change very little
reside near the top of the curve
Dead space is...
ventilation without perfusion
Shunt is...
perfusion without ventilation
Perfusion is what L/min?
Ventilation?
perfusion = 5L/min (greatest at lung base - gravity)
ventilation = 4L/min (greatest at base - higher compliance)
Compared to spontaneous ventilation, what happens to the Vd/Vt ratio when a patient is placed on a ventilator?
The ratio increases.
What does the Vd/Vt ratio mean?
fraction of the tidal volume lost to dead space
- gas not involved in alveolar gas exchange
Calculations for Vd/Vt ratio?
Vd = 2ml/kg
Vt = 6ml/kg
ex: 150/450 = 0.33%
Mechanical ventilation increases what west zone?
1
- increases alveolar pressure and this increases ventilation relative to perfusion. Increases to 0.5 or 50%
A patients PaCO2 has increases while his etCO2 has decreased, what is likely to contribute to this phenomenon?
Hypotension
COPD
amniotic fluid embolism
When asked about an increased PaCO2-etCO2 ratio, what is it referring to?
what increases dead space ventilation or West Zone 1
What is the most common cause of increased dead space under GA?
other causes?
decreased cardiac output
- other causes: COPD, pulmonary embolism
Anticholinergics, mechanical ventilation, neck extension, adding an HME between y-piece and ETT, and an incompetent unidirectional valve
Where does dead space begin?
at the y-piece
What is the consequence of adding a HME btw the ETT and y-piece?
PaCO2 increases (increased alveolar conc of CO2)
PaO2 decreases
*It increases apparatus dead space
What happens when PaCO2 increases?
increased alveolar concentration of CO2, which causes the alveolar partial pressure of oxygen to DECREASE
What variables are required to calculate the partial pressure of alveolar oxygen?
PAO2 - PP of O2 inside the alveolus
FiO2
Pb - barometric pressure
PH2O -humidity of inspired gas (assume 47)
PaCO2 - PP of CO2 in the blood
RQ - (CO2 production/O2 consumption = 0.8)
What is the alveolar gas equation?
PAO2 = FiO2 x (Pb - PH20) - (PaCO2/RQ)
PAO2 = 0.21 x (760-47) - (PaCO2/0.8)
PAO2 = 0.21 x (713) - (PaCO2/0.8)
What does the alveolar gas equation give context to?
to evaluate the PaO2 provided by an ABG
You can calculate the A-a gradient
How to identify an abnormal A-a gradient?
normal: A-a gradient < FiO2
Abnormal: A-a gradient > FiO2
What is the A-a gradient?
difference between PAO2 and PaO2
helps diagnose the cause of hypoxemia
Causes of a increased A-a gradient?
aging
vasodilators
R -> L shunt (can't fix with supplemental O2) (PFO, DA, VSD)
Diffusion limitation - alveocapilary thickening
Why is the alveolar gas equation important? Examples.
Hypoventilation --> hypercarbia and hypoxemia
supplemental O2 can reverse hypoxemia but NOT hypercarbia....which can go undetected with a pt on supplemental O2
Shunt increases by ____ % for every ____ mmHg of A-a gradient
1% for every 20 mmHg
What venous systems contribute to anatomic shunt?
Empties directly into left side of the heart:
Thebesian veins (drains left heart)
bronchiolar and pleural veins (drains bronchial circ)
Causes of R --> L shunt and increased A-a gradient?
atelectasis
pneumonia
bronchial intubation
intracardiac defect
What are the 3 causes of anatomic shunt?
1. venous blood that empties into the LA
2. R --> L shunt d/t intracardiac lesion (PFO, DA, VSD)
3. AVM that develops as a consequence of liver dx
Venous admixture increases when:
expiratory reserve volume decreases
Whenever you see shunt or venous admixture, what should you think of?!
FRC!!!
Decreased ERV = decreased FRC
Pulmonary vascular resistance is DIRECT/INVERSELY proportional to lung volume?
What does this mean clinically?
Inversely
When FRC decreases, PVR increases.
Venous admixture increases b/c less blood coming into contact with oxygenated alveoli
Clinically: faster rate of arterial desat during arena and an increased A-a gradient
Residual volume is what percentage of TLC?
20%
IRV - volume
3000ml - amount of gas that can be forcibly inhaled after a tidal inhalation
Vt - volume
500 - amt of gas that enters and exits the lungs during tidal breathing
ERV - volume
1100 - volume of gas that can be forcibly exhaled after a tidal exhalation
RV - volume
1200 - volume of gas that remains in lungs after complete exhalation, can't leave the lungs
Closing volume
variable - volume above RV where the small airways begin to close
TLC - volume
5800 IRV+Vt+ERV+RV
VC - volume
4500 IRV+Vt+ERV
IC - volume
3500 IRV+Vt
FRC - volume
2300 RV+ERV
Closing capacity
variable - RV+CV
Causes of decreased FRC!
GA
obesity
pregnancy
neonate
supine, lithotomy, T-burg
paralysis
light GA
High IVF
High FiO2
decreased pulmonary compliance
Causes of increased FRC:
old age
prone, sitting lateral, reverse Tburg
COPD
PEEP
sigh breaths
The etCO2 is 5%, what is this in mmHg?
What law?
38mmHg
Daltons law of partial pressure
Basically (5*760)/100
How much oxygen is consumed by a 70kg healthy adult at rest?
answer in ml/100g/min
0.357 ml/100g/min
VO2 as ml/min = 250ml/min
3.5 ml/kg/min
VO2 as ml/kg/min: 250/70 = 3.57 ml/kg/min or just 3.5
VO2 as ml/100g/min: change kg to 100g
3.57 ml/kg/min = 0.357 ml/100g/min
or if you used 3.5, 0.350 ml/100g/min
EMLA cream toxicity does what to P50 and oxyhemoglobin dissociation curve?
Why?
Tx?
decreases P50 and shifts the curve to the left
EMLA --> prilocaine, which is metabolized to o-toluidine and causes methemoglobinemia
Methemoglobin decreases P50
Tx: Methylene blue 1-2 mg/kg
Bohr effect
describes how changes in acid (PCO2 or H+) alter the carrying capacity of O2 in the blood. It explains why hemoglobin releases O2 at the tissue level and binds O2 in the lungs
REMEMBER: bOHr = Oxygen and Hgb
Haldane effect
describes how changes in PO2 in the blood alter the carrying capacity of CO2 in the blood, and it explains why venous blood can carry more CO2 than arterial blood
Hamburger phenomenon
describes how Cl- is exchanged for HCO3- to maintain electroneutrality when the erythrocyte acts as a buffer
What is the inspiratory pacemaker?
dorsal respiratory center = resp pacemaker
- active during respiration
Ventral respiratory center
active during exalation - in the medulla, tractus solitarius
quiet during normal breathing
Pontine respiratory centers include?
pneumotaxic center and apneustic center
- regulate DRG
Pneumotaxic center?
upper pons
inhibits the DRG (inhibits the PM)
triggers end expiration
strong stimulus = rapid shallow breathing
weak - slow and deep breathing
apneustic center?
lower pons
stimulates the DRG
antagonizes pneumotaxic center
inhibited by pulmonary stretch receptors
What phenomena is responsible for tachypnea that accompanies PE?
J-receptor stimulation
What is J-receptor stimulation?
causes tachypnea, activated by PE or during pulmonary vascular congestion, such as CHF
Hering-Breuer inflation reflex does what?
stops inspiration when the lungs become hyperinflated
Describe hypoxic pulmonary vasoconstriction.
What activates it?
Effect begins?
minimizes shunt by reducing blood flow through poorly ventilated alveoli.
- a low alveolar PO2 (not arterial) is the trigger that activates HPV
- effect beings almost immediately and reaches full effect in 15min
What are some examples that inhibit HPV, therefor increasing shunt?
How do IV anesthetics affect HPV?
Halogenated anesthetics > 1-1.5 MAC
phosphodiesterase inhibitors
dobutamine
vasodilators - nipride
IV ANESTHETICS DO NOT INHIBIT HPV!
What are three causes of hypercapnia?
Increased CO2 production
Decreased CO2 elimination
Rebreathing