Respiratory A & P Flashcards
Olfactory mucosa contains
afferent fibers from olfactory nerve (cranial nerve 1)
damage from covid = parosomia-stellate ganglion block
Sensory nerve of upper respiratory tract
Both branches of cranial V: opthamic and maxillary
Tonsils act as
first line of defense for bacterial invasion of nose and mouth
Tonsils are three types of lymph tissue:
- palatine tonsils - major
- lingual tonsil
- Pharyngeal tonsils (adenoids)
Pharynx upper airway innervation is what nerve(s)?
sensory or motor?
Trigeminal (V) (V1, V2, V3)
Glossopharyngeal (IX)
sensory and motor
Larynx level
C3-6
Circothyroid membrane
site for emergency laryngotomy and transtracheal block
Thyrohyoid membrae
suspends larynx from the hyoid bone
Vestibule
supraglottic area of 1st compartment of larynx
Laryngeal ventricles
area between false cords and true cords (in 2nd compartment)
Rima glottdis aka _____ is ____
true glottis is the space between the vocal cords
Which muscles cause abduction of the cords?
- Posterior CricoArytenoids (please come apart)
- ThyroaRtyenoid (They Relax)
Which muscles cause adduction of the cords?
- Lateral CricoArytenoid (lets close airway)
2.CricoThyroid muscle (CordsTense)
Injury to the superior laryngeal nerve causes
inability to adduct (close)
Injury to recurrent laryngeal nerve causes
inability to abduct (open)
Bilateral injury
emergency
Primary muscular barrier to regurgitation in awake mt
cricopharyngeus msucle
Superior laryngeal nere innervation
crycothyroid muscle (SCAR)
what provides sensation from laryngeal side of epiglottis to true cords
internal branch of superior laryngeal nerve
Laryngospast man be caused by
simulation of the superior laryngeal nerve external branch
Damage to inferior laryngeal nerves (Recurrent laryngeal nerve) may lead to
hoarseness or dyspnea
True vocal cord ligaments are innervated or not?
not innervated
Superior laryngeal nerve innervates (sensory)
posterior side of epiglottis - level of VC
Recurrent laryngeal nerve innervates (sensory)
below level of vocal cords - trachea
Motor innervation of larynx
SCAR
Superior laryngeal nerve: Cricothyroid
All others: Recurrent laryngeal nerve:
Glossopharyngeal airway block
needle at base of palatoglossal archS
Superior laryngeal airway block
interior border of hyoid bone
Transtracheal airway block
cricothyroid membrane
inject local as patient takes deep breath
at the bronchi, cellular structure changes to
cuboidal epithelium
Which bronchus has a less acute angle from trachea
R bronchus less acute (25 deg)
easier to mainstem, more liekly for ETT to migrate here, more likely place of foreign bodies
Left bronchus angle is
45 degrees
Bronchopulmonary segments in right vs L
R: 10 segments
L: 8 segments
The last structures perfused by bronchial circulation:
Terminal bronchioles, at the end of the CONDUCTING airways
perfused, but no air exchange
conducting zone means:
examples:
air delivery but no gas exchange
trachea
mainstem bronchi
lobar bronchi
small bronchi
Bronchioles
Terminal bronchioles
Respiratory zone:
examples:
exchanges air with blood
Respiratory bronchioles
alveolar ducts
alveolar sacs
as airway division progress, what increases?
- number of airways
- cross sectional area
- muscle layer
as airway division progresses, what decreass?
- air flow velocity
- cartilage
- Goblet cells
- ciliated cells
mucous glands are absent in the
bronchioles
First place in airway that are perfused by pulmonary circulation?
does gas exchange occur here?
terminal bronchioles
gas exchange does NOT occur here
Most air exchange takes place in
alveolar-capillary membrane
What cell type forms alveoli
Type I, Type II pneumocytes, Type III
what do type II pneumocytes do
produce surfactant (reduces alveolar collapse from surface tensino)
Mediastinum is
the region between the parietal pleura and visceral pleura
Pleura
serous membrane that lines thoracic wall and lungs
Parietal pleura
lines chest wall, diaphragm, mediastinum
visceral pleura
lines mediastinum back toward lungs
pleural space
layer of fluid between thoracic wall and lungs
What is responsible for quiet breathing
diaphragm
diaphragm is innervated by
phrenic nerve
c3,4,5
Expiration occurs by
passive recoil - no muscular contraction
What controls breathing?
respiratory sensors in brainstem
central and peripheral sensors
Where are central censors located
medulla, pons (secondary)
Most important central sensors - chemical control
chemoreceptors that respond to changes in hydrogen ion concentration
What is most important in brain to establish ventilatory volume and rate?
CO2 via arterial and cerebrospinal fuid
Apneic threshold
CO2 at which ventilation is 0
Central receptors and hypoxia
depressed by hypoxia - NOT stimulated
Principal peripheral chemoreceptors
carotid bodies
Central chemoreceptors respond to
PaCO2
peripheral receptors are most sensitive to
PaO2 (<50)
What abolishes peripheral ventilatory response to hypoxemia?
- antidopaminergic drugs
- most anesthetics
- bilateral carotid surgery
Central sleep apnea and CO2
central sleep apnea exhibits a depressed response to CO2 during sleep
may be caused by a defect in chemoreceptors in the brain
Lung receptors are carried
centrally by the vagus nerve
Chemical or mechanial irriation can produce
reflex cough or sneeze
hyperpnea
bronchoconstriction
increased blood pressure
vagus nerve prodcues
afferent pathways for all irritant receptors (except nasal mucosa receptor)
Intrapleural pressure is
the pressure within the pleural cavity
it is always negative - acts like suction to keep lungs inflated
elasticity of lungs causes
lung recoil and pull lung inward away from thoracic wall
elasticity of thoracic wall causes
thoracic wall to pull away from the lungs, further enlarging pleural cavity and creating negative pressure
intrapleural pressure is
always negative - causes expanding effect called compliance
airflow =
pressure/resistance
Area of airway with greatest resistance
medium sized bronchi
smooth muscle tone - asthma occurs here
What constricts bronchioles?
Acetylcholine (PNS), histamine
What dilates bronchioles?
Epinephrine (SNS)
Lung compliance:
elastic ffibers - ease with which lungs expand
Factors that determine lung compliance
- stretchability of the elastic fibers
- surface tension within alveoli
How does surface tension within the alveoli effect lung compliance?
Lower surface tension = increased lung compliance
surfactant LOWERS surface tension
Compliance equastino
V/P
change in volume divided by change in pressure
CL (lung compliance) =
TV/PIP-PEEP
Pulmonary surfactant role
decreases surface tension and holds alveoli open
lines of alveoli are made of lipoprotien mixture consisting mostly of
dipalomyl lechitin
Pulmonary surfactant is secreted by
Type II alveolar epithelial cells
Surface tension law
Laplace (P=T/r)
without surfactant, law of Laplace WOULD hold true.
But because of surfactant, law of Laplace does not apply to alveoli
air velocity law
Pouseille’s
L/R ^4
At resting expiration poing:
outward recoil of chest wall is balanced by inward elastic recoil of the lung
Transpulmonary pressure
fluccuates
is zero whenever airflow is stopped (at end expiration or end inspiration)
as intra alveolar pressure oscillates between slightly negative during inspiration and slightly positive during expiration
Pleural pressure is
always negative
Compliance, volume and pressure
increased compliance = greater change in volume at a certain change in pressure
compliance is volume dependent
at age 20, closing volume is
30% of TLC
at age 70, closing volume is
55% of TLC
closing volume and shunt
if closing volume is greater than FRC, have poorly perfused or unventilated alveoli during normal respiration
= intrapulmonary shunt
lung volumes that are NOT included in spirometry:
- FRC
- RV
- TLC
FEV1 =
forced expiratory volume in 1 second
FEV1 is based on ____ and is normal if ______
based on age and gender for a predicted normal range
normal if within 80% of predicted values
FVC
forced vital capacity
volume of gas that can be exhaled during a forced expiratory maneuver
FEV1/ FVC
helps distinguish between restrictive at obstructive diseases
< 0.7 = obstruction
FEV1/FVC < 0.7
Obstruction
FEF 25 - 75
rate of flow occurring in forced expiration between 25% and 75% of flow
What is the most sensitive test for assessing small airway disease?
FEF 25-75
most effort independent test
FEF 25 - 75
more reliable measurement of early obstruction
FEF 25 - 75
When should more sophisticated split lung function testing be done?
if FEV1 is less than 2L
and
if FEV1/FVC is less than 50%
Diagnosis obstructive dises
increased FRC, RV, TLC
Diagnosis restrictive lung dises
decrease FRC, RV, TLC
What is affected by position?
FRC but NOT closing capacity
Alveoli are most compliant at
Lower volumes (lower lung)
expand/ deflate better at lower lung
Shunt causes (PAO2, PaO2)
PaO2 < PAO2
Pulmonary blood flow is regulated locally by
changes in O2 and CO2 tension
Hypoxic pulmonary vasoconstriction
Blood flow is diverted from hypoxic or atelectatic alveolie - attmept to improve matching of VQ
high O2 tension and hypocapnia/carbia
(PVR)
vasodilate pulmonary vessels to pick up more O2
opposite in other vasculature
What brings unoxygenated blood to lungs from right ventricle
pulmonary arteries
Pulmonary arteris provide blood flow to structures distal to
terminal bronchioles
as well as non respiratory tissues and respiratory units
PVR vs SVR
PVR is 1/8 SVR
PVR is increased by
- NE
- serotonin
- histamine
- hypercapnia
- hypoxia
PVR is decreased by
- acetylcholine
- isoproterenol
west lung zones describe
perfusion the lungs
not fixed
functional zones of where the blood will flow n comparison to the alveoli
zone 1
PA > Pa > Pv
top
zone 2
middle
Pa > PA > Pv
Zone 3
bottom
Pa>Pv>PA
Zone 3 has
continuoublood flow
tip of pulmonary catheter should be here
best perfusion and best ventilation
BUT still more blood flow than ventilation = shunt
dependent portion of lungs have:
- more blood flow d/t gravity
- more alveolar compliance
= optimal gas exchange
if alveoli are ventilated but not perfused, then Q =
0
infinity dead space
If alveoli are perfused (Q) bt no ventilated (V) then V =
0
so V/Q = 0
shunt
shunt-like alveoli have
low PO2 and high PCO2 (Low V/Q)
What can cause shunt
- airway obstruction
- atelectasis
- pneumonia
If hypoxemia present and unresponsive to O2
suspect significant shunt/diffusion disorder
Dead space like alveoli have
high PO2 and low PCO2 (high V/Q)
causes of dead space
- Low CO
- Pulmonary emboli
blood flow not reaching alveolar membrane, but ventilation is good
Hypoxemia is defined as
a decrease in PaO2 (<60 mmHg)
Hypoxia is defined as
reduced level of tissue oxygenation by defective delivery or utilization by tissue
Normal A-a gradient
age adjusted
5-15 mmhg normal
with supplemental O2: <100 mmHg
PaCO2-PACO2 gradient normal
2-10 mmHg regardless of inspired O2
Respiratory failure diagnosis
PaO2 <60 despite supplemental 2 and in absence of R–>L shunt
PaCO2 > 50 mmHg in absence of resp compensation
A larger than normal PAO2-PaO2 gardient assesses
shunt and v/q mismatch that is not normal
Key clinical feature to a R–>L shunt:
oxygen administration does not help the arterial PO2
why would supplemental oxygen not hel arterial PO2?
shunt
blood flow does not come into contact with the alveoli that is getting more O2
Hypoxemia without an increase in A-a gradient is
hypoventilation
Hypoxemia with an increase in A-a gradient is
- diffusion defect
- V/Q mismatch
- shunting R–> L
Respiratory quotient
constant to be used in alveolar equation
ratio of CO2 produced to amount of O2 consumed
RQ = 0.8
norma PaO2:FiO2 ratio
100mmHg/0.21 = 500
lower ratio = worse disease
PaO2: FiO2 ratio ALI
< 300
PaO2: FiO2 ratio ARDS
<200
The most direct assessment of oxygenation is the
PaO2
A-a gradients assess
v/q mismatch in the face of hypoxemia
with elevated A-a PO2 gradient, to further work up, measure _____. Then:
O2 from SVC or distal port in PA catheter (PvO2)
low = anemia, low CO, hypermetabolic state
otherwise, suspect V/Q abnormality
Alveolar levels of O2 and CO2 are determined by:
- amount of alveolar ventilation
- inspired concentrations of O2 and CO2
- flow of mixed venous blood to lungs
- Consumption of O2
- Production of CO2
O2ER
Oxygen extraction
O2ER = VO2/DO2
SVO2 is
leftover O2 after consumption
normal anatomic dead space
2mL/kg (about 1/3 of air that enters is dead space)
volume in conducting airway
increases by 50% in paralyzed, mechanically ventilated patient
alveolar dead space
alveoli that are ventilated but do not participate in gas exchange with blood
Bohr equation
calculates deadspace
Vd/Vt = [PaCO2 - PECO2]/PaCO2
3 determinants of PaCO2
- PaCO2 production
- minute ventilation
- dead space fraction
what drives ventilation?
PaCO2
a-A CO2 gradient reflects
alveolar dead space
more deadspace = more gradient
normal: 2-5 or 2-10
What in blood carries CO2
bicarbonate ions 80-90%
CO2 dissociation curve
when blood contains mostly oxygenated hgb
CO2 shifts right (releases CO2, reduced ability to hold on to CO2)
*Haldane effect
CO2 dissociation curve
when blood contains deoxygenated hgb:
curve shifts left, blood loads more CO2
When does CO2 curve shift right
right = release
occurs as blood flows through pulmonary capillaries, facilitates unloading/release of CO2 from pulmonary capillaries
What is the hamburger shift
chloride shift
bicarb moves out of red blood cells in exchange for chloride ions
Bohr effect
influence of CO2 on shift of oxyhemoglobin curve
increased CO2 = oxygen will unload
amount of dissolved CO2 in blood is
0.67 x PCO2 /dL
Oxyhemoglobin curve right shift
reduced affinity, more O2 offload to tissue
increased temp
increased 2-3 DPG
Inrceased [H]–>decreased pH/acidosis
methemoglobinemia
Oxyhemoglobin curve left shift
left = love, hgb holds onto oxygen
decreased temp
decreased 2-3 DPG
decreased [H}–>increased pH/alkalosis
CO
VO2 (what is it and normal value)
oxygen consomption
250 mL/O2/min
3.5 mL/kg/min
normal carbon dioxide excretion
200 mL CO2/min